{"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: 1,000 genomes project enables mapping of genetic sequence variation consisting of rare variants with larger penetrance effects than common variants.\n\nCANDIDATE_ABSTRACT:\nTITLE: β-Adrenergic receptor antagonism prevents anxiety-like behavior and microglial reactivity induced by repeated social defeat.\nABSTRACT: Psychosocial stress is associated with altered immune function and development of psychological disorders including anxiety and depression. Here we show that repeated social defeat in mice increased c-Fos staining in brain regions associated with fear and threat appraisal and promoted anxiety-like behavior in a β-adrenergic receptor-dependent manner. Repeated social defeat also significantly increased the number of CD11b(+)/CD45(high)/Ly6C(high) macrophages that trafficked to the brain. In addition, several inflammatory markers were increased on the surface of microglia (CD14, CD86, and TLR4) and macrophages (CD14 and CD86) after social defeat. Repeated social defeat also increased the presence of deramified microglia in the medial amygdala, prefrontal cortex, and hippocampus. Moreover, mRNA analysis of microglia indicated that repeated social defeat increased levels of interleukin (IL)-1β and reduced levels of glucocorticoid responsive genes [glucocorticoid-induced leucine zipper (GILZ) and FK506 binding protein-51 (FKBP51)]. The stress-dependent changes in microglia and macrophages were prevented by propranolol, a β-adrenergic receptor antagonist. Microglia isolated from socially defeated mice and cultured ex vivo produced markedly higher levels of IL-6, tumor necrosis factor-α, and monocyte chemoattractant protein-1 after stimulation with lipopolysaccharide compared with microglia from control mice. Last, repeated social defeat increased c-Fos activation in IL-1 receptor type-1-deficient mice, but did not promote anxiety-like behavior or microglia activation in the absence of functional IL-1 receptor type-1. These findings indicate that repeated social defeat-induced anxiety-like behavior and enhanced reactivity of microglia was dependent on activation of [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 3, "doc_id": "2436602", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Mitochondria play a trivial role in calcium homeostasis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mitochondria: Dynamic Organelles in Disease, Aging, and Development\nABSTRACT: Mitochondria are the primary energy-generating system in most eukaryotic cells. Additionally, they participate in intermediary metabolism, calcium signaling, and apoptosis. Given these well-established functions, it might be expected that mitochondrial dysfunction would give rise to a simple and predictable set of defects in all tissues. However, mitochondrial dysfunction has pleiotropic effects in multicellular organisms. Clearly, much about the basic biology of mitochondria remains to be understood. Here we discuss recent work that suggests that the dynamics (fusion and fission) of these organelles is important in development and disease.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Additionally, they participate in intermediary metabolism, calcium signaling, and apoptosis.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 798, "doc_id": "8551160", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Mutations in G-Beta protein GNB1 are present in many cancers, resulting in loss of interaction with G-alpha subunits and concomitant activation of AKT pathway.\n\nCANDIDATE_PASSAGE:\nThe Self-Incompatibility Genes of Brassica: Expression and Use in Genetic Ablation of Floral Tissues INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 394 POLLINATION AND POLLEN TUBE GROWTH . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 395 Interaction s between the M ale G ameto phyte and Pistil . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 395 SelfIncom patibili ty Systems: Gameto phytic and S poro phyti c Determin ation of Pollen Phenoty pe . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 397 DEVELOPMENTAL S TUDIES OF REPRODUCTIVE STRUCTURES . . . . . . . . .. . . ... . . . . 398 Tissues of the Pistil with Special Reference to Pollination Functions 398 The Male Gametophyte . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 399 MOLECULAR ANALYSIS OF SELF-INCOMPATIBILITY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40 1 The S-M ultigene F amily o j Brassica. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . 402 Allelism at the S-Lo cus and the SLG Gene\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\" 402 The S-Locus Related (SLR) Genes 405 Molecular Complexity oj the S-Locus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 407 EXPRESSION OF THE SLG GENE IN PIS TILS AND ANTHERS . . . . . . . . . . . . . . . . . . . . . . . 409 Expression in Cruc ifers . . . . . . . . . . . . . . . . . . . . . . . . . [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "813", "doc_id": "86217760", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Incidence rates of cervical cancer have increased due to nationwide screening programs based primarily on cytology to detect uterine cervical cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mass screening programmes and trends in cervical cancer in Finland and the Netherlands.\nABSTRACT: With respect to cervical cancer management, Finland and the Netherlands are comparable in relevant characteristics, e.g., fertility rate, age-of-mother at first birth and a national screening programme for several years. The aim of this study is to compare trends in incidence of and mortality from cervical cancer in Finland and the Netherlands in relation to the introduction and intensity of the screening programmes. Therefore, incidence and mortality rates were calculated using the Cancer Registries of Finland and the Netherlands. Data on screening intensity were obtained from the Finnish Cancer Registry and the Dutch evaluation centre at ErasmusMC-Rotterdam. Women aged 30-60 have been screened every 5 years, in Finland since 1992 and in the Netherlands since 1996. Screening protocols for smear taking and referral to the gynaecologist are comparable. Incidence and mortality rates have declined more in Finland. In 2003, age-adjusted incidence and mortality in Finland were 4.0 and 0.9 and in the Netherlands 4.9 and 1.4 per 100,000 woman-years, respectively. Excess smear use in the Netherlands was estimated to be 24 per 1,000 women during a 5-year interval compared to 121 in Finland. The decline in mortality in Finland seems to be almost completely related to the screening programme whereas in the Netherlands it was initially considered to be a natural decline. Differences in risk factors might also play a role: the Netherlands has higher population density and higher percentages of immigrants and (female) smokers. The greater excess smear use in Finland might also have affected incidence.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The decline in mortality in Finland seems to be almost completely related to the screening programme whereas in the Netherlands it was initially considered to be a natural decline.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 598, "doc_id": "25742130", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Radioiodine treatment of non-toxic multinodular goitre increases thyroid volume.\n\nCANDIDATE_PASSAGE:\nRadioiodine treatment of multinodular non-toxic goitre. OBJECTIVE To investigate the long term effect of radioactive iodine on thyroid function and size in patients with non-toxic multinodular goitre. DESIGN Consecutive patients with multinodular non-toxic goitre selected for radioactive iodine treatment and followed for a minimum of 12 months (median 48 months) after an intended dose of 3.7 MBq/g thyroid tissue corrected to a 100% uptake of iodine-131 in 24 hours. PATIENTS 69 patients with a growing multinodular non-toxic goitre causing local compression symptoms or cosmetic inconveniences. The treatment was chosen because of a high operative risk, previous thyroidectomy, or refusal to be operated on. MAIN OUTCOME MEASUREMENTS Standard thyroid function variables and ultrasonically determined thyroid volume before treatment as well as 1, 2, 3, 6, and 12 months after treatment and then once a year. RESULTS 56 patients were treated with a single dose of 131I, 12 with two doses, and one with four doses. In 45 patients treated with one dose and remaining euthyroid the median thyroid volume was reduced from 73 (interquartile range 50-106) ml to 29 (23-48) ml at 24 months in the 39 patients in whom this was measured during follow up. The median reduction was 40 (22-48) ml (60% reduction, p < 0.0001), half of which occurred within three months. Patients treated with two doses as well as those developing hypothyroidism and hyperthyroidism had a significant reduction in thyroid volume. Eleven patients developed hypothyroidism (cumulative five year risk 22%, 95% confidence interval 4.8% to 38.4%). Side effects were few: three cases of hyperthyroidism and two cases of radiation thyroiditis. Only one patient was dissatisfied with the result; she was referred for operati [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1011", "doc_id": "9745001", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Self-advocacy training is effective at decreasing homelessness.\n\nCANDIDATE_PASSAGE:\nIn vitro antimicrobial activity of mangrove plant Sonneratia alba. OBJECTIVE To investigate the antimicrobial property of mangrove plant Sonneratia alba (S. alba). METHODS The antimicrobial activity was evaluated using disc diffusion and microdilution methods against six microorganisms. Soxhlet apparatus was used for extraction with a series of solvents, n-hexane, ethyl acetate and methanol in sequence of increasing polarity. RESULTS Methanol extract appeared to be the most effective extract while n-hexane extract showed no activity. The antimicrobial activities were observed against the gram positive bacteria Staphylococcus aureus (S. aureus) and Bacillus cereus (B. cereus), the gram negative Escherichia coli (E. coli) and the yeast Cryptococcus neoformans. Pseudomonas aeruginosa and Candida albicans appeared to be not sensitive to the concentrations tested since no inhibition zone was observed. E. coli (17.5 mm) appeared to be the most sensitive strain followed by S. aureus (12.5 mm) and B. cereus (12.5 mm). CONCLUSIONS From this study, it can be concluded that S. alba exhibits antimicrobial activities against certain microorganisms.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1070", "doc_id": "43165768", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Transplanted human glial progenitor cells can mature in their host animal.\n\nCANDIDATE_PASSAGE:\nCytomegalovirus US2 destroys two components of the MHC class II pathway, preventing recognition by CD4+ T cells Human cytomegalovirus (HCMV) is a ubiquitous herpesvirus that causes life-threatening disease in patients who are immunosuppressed for bone marrow or tissue transplantation or who have AIDS (ref. 1). HCMV establishes lifelong latent infections and, after periodic reactivation from latency, uses a panel of immune evasion proteins to survive and replicate in the face of robust, fully primed host immunity. Monocyte/macrophages are important host cells for HCMV, serving as a latent reservoir and as a means of dissemination throughout the body. Macrophages and other HCMV-permissive cells, such as endothelial and glial cells, can express MHC class II proteins and present antigens to CD4+ T lymphocytes. Here, we show that the HCMV protein US2 causes degradation of two essential proteins in the MHC class II antigen presentation pathway: HLA-DR-α and DM-α. This was unexpected, as US2 has been shown to cause degradation of MHC class I (refs. 5,6), which has only limited homology with class II proteins. Expression of US2 in cells reduced or abolished their ability to present antigen to CD4+ T lymphocytes. Thus, US2 may allow HCMV-infected macrophages to remain relatively 'invisible' to CD4+ T cells, a property that would be important after virus reactivation.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1322", "doc_id": "27555165", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Major vault protein (MVP) leads to more aggressive tumors by regulating the sorting of tumor suppressive miR-193a into extracellular vesicles (EVs).\n\nCANDIDATE_ABSTRACT:\nTITLE: MVP-mediated exosomal sorting of miR-193a promotes colon cancer progression\nABSTRACT: Exosomes are emerging mediators of intercellular communication; whether the release of exosomes has an effect on the exosome donor cells in addition to the recipient cells has not been investigated to any extent. Here, we examine different exosomal miRNA expression profiles in primary mouse colon tumour, liver metastasis of colon cancer and naive colon tissues. In more advanced disease, higher levels of tumour suppressor miRNAs are encapsulated in the exosomes. miR-193a interacts with major vault protein (MVP). Knockout of MVP leads to miR-193a accumulation in the exosomal donor cells instead of exosomes, inhibiting tumour progression. Furthermore, miR-193a causes cell cycle G1 arrest and cell proliferation repression through targeting of Caprin1, which upregulates Ccnd2 and c-Myc. Human colon cancer patients with more advanced disease show higher levels of circulating exosomal miR-193a. In summary, our data demonstrate that MVP-mediated selective sorting of tumour suppressor miRNA into exosomes promotes tumour progression.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Knockout of MVP leads to miR-193a accumulation in the exosomal donor cells instead of exosomes, inhibiting tumour progression.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 751, "doc_id": "19800147", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Birth-weight is positively associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Role of birthweight in the etiology of breast cancer.\nABSTRACT: Breast cancer may originate in utero. We reviewed the available evidence on the association between birthweight and the risk of breast cancer. To date, 26 research papers addressing this issue have been published. The majority of studies identified a positive link between birthweight and premenopausal, but not postmenopausal, breast cancer. The relative risk estimate for breast cancer comparing women with high birthweight to women with low birthweight combining all studies including both pre- and postmenopausal breast cancer was 1.23 (95% confidence interval 1.13-1.34). The mechanisms underlying this association likely include elevated levels of growth factors that may increase the number of susceptible stem cells in the mammary gland or initiate tumors through DNA mutations. Loss of imprinting (LOI) of growth hormone genes relevant for intrauterine growth, such as insulin-like growth factor 2 (IGF2), leads to abnormally high levels of these hormones evidenced by high birthweight. LOI of IGF2 has also been found in mammary tumor tissue. The role of environmental factors that stimulate such epigenetic regulation of gene expression remains to be elucidated.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The majority of studies identified a positive link between birthweight and premenopausal, but not postmenopausal, breast cancer.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 179, "doc_id": "27123743", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In young and middle-aged adults, current or remote uses of ADHD medications increase the risk of serious cardiovascular events.\n\nCANDIDATE_ABSTRACT:\nTITLE: ADHD medications and risk of serious cardiovascular events in young and middle-aged adults.\nABSTRACT: CONTEXT More than 1.5 million US adults use stimulants and other medications labeled for treatment of attention-deficit/hyperactivity disorder (ADHD). These agents can increase heart rate and blood pressure, raising concerns about their cardiovascular safety. OBJECTIVE To examine whether current use of medications prescribed primarily to treat ADHD is associated with increased risk of serious cardiovascular events in young and middle-aged adults. DESIGN, SETTING, AND PARTICIPANTS Retrospective, population-based cohort study using electronic health care records from 4 study sites (OptumInsight Epidemiology, Tennessee Medicaid, Kaiser Permanente California, and the HMO Research Network), starting in 1986 at 1 site and ending in 2005 at all sites, with additional covariate assessment using 2007 survey data. Participants were adults aged 25 through 64 years with dispensed prescriptions for methylphenidate, amphetamine, or atomoxetine at baseline. Each medication user (n = 150,359) was matched to 2 nonusers on study site, birth year, sex, and calendar year (443,198 total users and nonusers). MAIN OUTCOME MEASURES Serious cardiovascular events, including myocardial infarction (MI), sudden cardiac death (SCD), or stroke, with comparison between current or new users and remote users to account for potential healthy-user bias. RESULTS During 806,182 person-years of follow-up (median, 1.3 years per person), 1357 cases of MI, 296 cases of SCD, and 575 cases of stroke occurred. There were 107,322 person-years of current use (median, 0.33 years), with a crude incidence per 1000 person-years of 1.34 (95% CI, 1.14-1.57) for MI, 0.30 (95% CI, 0.20-0.42) for SCD, and 0.56 (95% CI, 0.43-0.72) for stroke. The multivariable-adjusted rate ratio (RR) of serious cardiovascular eve [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Among young and middle-aged adults, current or new use of ADHD medications, compared with nonuse or remote use, was not associated with an increased risk of serious cardiovascular events.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 590, "doc_id": "10984005", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: H4 G94P proteins suppress degradation of free histones via Rad53-dependent mechanisms.\n\nCANDIDATE_ABSTRACT:\nTITLE: Histone levels are regulated by phosphorylation and ubiquitylation dependent proteolysis\nABSTRACT: Histone levels are tightly regulated to prevent harmful effects such as genomic instability and hypersensitivity to DNA-damaging agents due to the accumulation of these highly basic proteins when DNA replication slows down or stops. Although chromosomal histones are stable, excess (non-chromatin bound) histones are rapidly degraded in a Rad53 (radiation sensitive 53) kinase-dependent manner in Saccharomyces cerevisiae. Here we demonstrate that excess histones associate with Rad53 in vivo and seem to undergo modifications such as tyrosine phosphorylation and polyubiquitylation, before their proteolysis by the proteasome. We have identified the Tyr 99 residue of histone H3 as being critical for the efficient ubiquitylation and degradation of this histone. We have also identified the ubiquitin conjugating enzymes (E2) Ubc4 and Ubc5, as well as the ubiquitin ligase (E3) Tom1 (temperature dependent organization in mitotic nucleus 1), as enzymes involved in the ubiquitylation of excess histones. Regulated histone proteolysis has major implications for the maintenance of epigenetic marks on chromatin, genomic stability and the packaging of sperm DNA.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 487, "doc_id": "14637235", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Lack of FGF21 in mice leads to atherosclerotic plaque formation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Hyaluronan impairs vascular function and drug delivery in a mouse model of pancreatic cancer\nABSTRACT: OBJECTIVE Pancreatic ductal adenocarcinoma (PDA) is characterised by stromal desmoplasia and vascular dysfunction, which critically impair drug delivery. This study examines the role of an abundant extracellular matrix component, the megadalton glycosaminoglycan hyaluronan (HA), as a novel therapeutic target in PDA. METHODS Using a genetically engineered mouse model of PDA, the authors enzymatically depleted HA by a clinically formulated PEGylated human recombinant PH20 hyaluronidase (PEGPH20) and examined tumour perfusion, vascular permeability and drug delivery. The preclinical utility of PEGPH20 in combination with gemcitabine was assessed by short-term and survival studies. RESULTS PEGPH20 rapidly and sustainably depleted HA, inducing the re-expansion of PDA blood vessels and increasing the intratumoral delivery of two chemotherapeutic agents, doxorubicin and gemcitabine. Moreover, PEGPH20 triggered fenestrations and interendothelial junctional gaps in PDA tumour endothelia and promoted a tumour-specific increase in macromolecular permeability. Finally, combination therapy with PEGPH20 and gemcitabine led to inhibition of PDA tumour growth and prolonged survival over gemcitabine monotherapy, suggesting immediate clinical utility. CONCLUSIONS The authors demonstrate that HA impedes the intratumoral vasculature in PDA and propose that its enzymatic depletion be explored as a means to improve drug delivery and response in patients with pancreatic cancer.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 681, "doc_id": "2565138", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Obesity raises life quality.\n\nCANDIDATE_PASSAGE:\nCollective trauma in northern Sri Lanka: a qualitative psychosocial-ecological study BACKGROUND Complex situations that follow war and natural disasters have a psychosocial impact on not only the individual but also on the family, community and society. Just as the mental health effects on the individual psyche can result in non pathological distress as well as a variety of psychiatric disorders; massive and widespread trauma and loss can impact on family and social processes causing changes at the family, community and societal levels. METHOD This qualitative, ecological study is a naturalistic, psychosocial ethnography in Northern Sri Lanka, while actively involved in psychosocial and community mental health programmes among the Tamil community. Participatory observation, key informant interviews and focus group discussion with community level relief and rehabilitation workers and government and non-governmental officials were used to gather data. The effects on the community of the chronic, man-made disaster, war, in Northern Sri Lanka were compared with the contexts found before the war and after the tsunami. RESULTS Fundamental changes in the functioning of the family and the community were observed. While the changes after the tsunami were not so prominent, the chronic war situation caused more fundamental social transformations. At the family level, the dynamics of single parent families, lack of trust among members, and changes in significant relationships, and child rearing practices were seen. Communities tended to be more dependent, passive, silent, without leadership, mistrustful, and suspicious. Additional adverse effects included the breakdown in traditional structures, institutions and familiar ways of life, and deterioration in social norms a [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "876", "doc_id": "15780826", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Upon viral challenge, influenza-specific memory CD4+ T cells greatly enhance the early production of inflammatory chemokines in the lung.\n\nCANDIDATE_ABSTRACT:\nTITLE: Memory CD4+ T cells induce innate responses independently of pathogen\nABSTRACT: Inflammation induced by recognition of pathogen-associated molecular patterns markedly affects subsequent adaptive responses. We asked whether the adaptive immune system can also affect the character and magnitude of innate inflammatory responses. We found that the response of memory, but not naive, CD4+ T cells enhances production of multiple innate inflammatory cytokines and chemokines (IICs) in the lung and that, during influenza infection, this leads to early control of virus. Memory CD4+ T cell–induced IICs and viral control require cognate antigen recognition and are optimal when memory cells are either T helper type 1 (TH1) or TH17 polarized but are independent of interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) production and do not require activation of conserved pathogen recognition pathways. This represents a previously undescribed mechanism by which memory CD4+ T cells induce an early innate response that enhances immune protection against pathogens.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We found that the response of memory, but not naive, CD4+ T cells enhances production of multiple innate inflammatory cytokines and chemokines (IICs) in the lung and that, during influenza infection, this leads to early control of virus.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1348, "doc_id": "19005293", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Rapid phosphotransfer rates govern fidelity in two component systems\n\nCANDIDATE_PASSAGE:\nUsing Structural Information to Change the Phosphotransfer Specificity of a Two-Component Chemotaxis Signalling Complex Two-component signal transduction pathways comprising histidine protein kinases (HPKs) and their response regulators (RRs) are widely used to control bacterial responses to environmental challenges. Some bacteria have over 150 different two-component pathways, and the specificity of the phosphotransfer reactions within these systems is tightly controlled to prevent unwanted crosstalk. One of the best understood two-component signalling pathways is the chemotaxis pathway. Here, we present the 1.40 A crystal structure of the histidine-containing phosphotransfer domain of the chemotaxis HPK, CheA(3), in complex with its cognate RR, CheY(6). A methionine finger on CheY(6) that nestles in a hydrophobic pocket in CheA(3) was shown to be important for the interaction and was found to only occur in the cognate RRs of CheA(3), CheY(6), and CheB(2). Site-directed mutagenesis of this methionine in combination with two adjacent residues abolished binding, as shown by surface plasmon resonance studies, and phosphotransfer from CheA(3)-P to CheY(6). Introduction of this methionine and an adjacent alanine residue into a range of noncognate CheYs, dramatically changed their specificity, allowing protein interaction and rapid phosphotransfer from CheA(3)-P. The structure presented here has allowed us to identify specificity determinants for the CheA-CheY interaction and subsequently to successfully reengineer phosphotransfer signalling. In summary, our results provide valuable insight into how cells mediate specificity in one of the most abundant signalling pathways in biology, two-component signal transduction.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1019", "doc_id": "11603066", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Binding of p53 to enhancer regions (p53BERs) regulates the activity of p53 transcription and cell cycle arrest through the production of p53-dependent eRNAs.\n\nCANDIDATE_ABSTRACT:\nTITLE: eRNAs are required for p53-dependent enhancer activity and gene transcription.\nABSTRACT: Binding within or nearby target genes involved in cell proliferation and survival enables the p53 tumor suppressor gene to regulate their transcription and cell-cycle progression. Using genome-wide chromatin-binding profiles, we describe binding of p53 also to regions located distantly from any known p53 target gene. Interestingly, many of these regions possess conserved p53-binding sites and all known hallmarks of enhancer regions. We demonstrate that these p53-bound enhancer regions (p53BERs) indeed contain enhancer activity and interact intrachromosomally with multiple neighboring genes to convey long-distance p53-dependent transcription regulation. Furthermore, p53BERs produce, in a p53-dependent manner, enhancer RNAs (eRNAs) that are required for efficient transcriptional enhancement of interacting target genes and induction of a p53-dependent cell-cycle arrest. Thus, our results ascribe transcription enhancement activity to p53 with the capacity to regulate multiple genes from a single genomic binding site. Moreover, eRNA production from p53BERs is required for efficient p53 transcription enhancement.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Moreover, eRNA production from p53BERs is required for efficient p53 transcription enhancement.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 177, "doc_id": "9669099", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Increased microtubule acetylation repairs LRRK2 Roc-COR domain mutation induced locomotor deficits.\n\nCANDIDATE_PASSAGE:\nTenomodulin promotes human adipocyte differentiation and beneficial visceral adipose tissue expansion. Proper regulation of energy storage in adipose tissue is crucial for maintaining insulin sensitivity and molecules contributing to this process have not been fully revealed. Here we show that type II transmembrane protein tenomodulin (TNMD) is upregulated in adipose tissue of insulin-resistant versus insulin-sensitive individuals, who were matched for body mass index (BMI). TNMD expression increases in human preadipocytes during differentiation, whereas silencing TNMD blocks adipogenesis. Upon high-fat diet feeding, transgenic mice overexpressing Tnmd develop increased epididymal white adipose tissue (eWAT) mass, and preadipocytes derived from Tnmd transgenic mice display greater proliferation, consistent with elevated adipogenesis. In Tnmd transgenic mice, lipogenic genes are upregulated in eWAT, as is Ucp1 in brown fat, while liver triglyceride accumulation is attenuated. Despite expanded eWAT, transgenic animals display improved systemic insulin sensitivity, decreased collagen deposition and inflammation in eWAT, and increased insulin stimulation of Akt phosphorylation. Our data suggest that TNMD acts as a protective factor in visceral adipose tissue to alleviate insulin resistance in obesity.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "613", "doc_id": "3621011", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The innate immune response struggles to remove small numbers of parasites.\n\nCANDIDATE_PASSAGE:\nPartitioning regulatory mechanisms of within-host malaria dynamics using the effective propagation number. Immune clearance and resource limitation (via red blood cell depletion) shape the peaks and troughs of malaria parasitemia, which in turn affect disease severity and transmission. Quantitatively partitioning the relative roles of these effects through time is challenging. Using data from rodent malaria, we estimated the effective propagation number, which reflects the relative importance of contrasting within-host control mechanisms through time and is sensitive to the inoculating parasite dose. Our analysis showed that the capacity of innate responses to restrict initial parasite growth saturates with parasite dose and that experimentally enhanced innate immunity can affect parasite density indirectly via resource depletion. Such a statistical approach offers a tool to improve targeting of drugs or vaccines for human therapy by revealing the dynamics and interactions of within-host regulatory mechanisms.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1223", "doc_id": "5289038", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Articles published in open access format are more likely to be cited than traditional journals.\n\nCANDIDATE_ABSTRACT:\nTITLE: Open Access Increases Citation Rate\nABSTRACT: PLoS Biology publishes today a research article by Gunther Eysenbach that is not about biology. It is about citations. It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles. As such, it adds objective support to the belief we have always held that open-access publication speeds up scientific dialog between researchers and, consequently, should be extended to the whole scientific literature as quickly as possible. It is therefore fitting that we publish such a paper. We have long argued that papers freely available in a journal will be more often read and cited than those behind a subscription barrier. However, solid evidence to support or refute such a claim has been surprisingly hard to find. Since most open-access journals are new, comparisons of the effects of open access with established subscription-based journals are easily confounded by age and reputation. In the current study, Eysenbach compared citations compiled by Thomson Scientific (formerly Thomson ISI) to individual articles published between June 2004 and December 2004 in the same journal—namely, Proceedings of the National Academy of Sciences (PNAS), which announced its open-access option for authors on June 8 of that year, with an associated publication charge of US$1,000. Non-OA articles in PNAS are subject to a six-month “toll-access” delay before the article becomes publicly available. The results of this natural experiment are clear: in the 4 to 16 months following publication, OA articles gained a significant citation advantage over non-OA articles during the same period. They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely between 10 and 16 months. Given that P [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 130, "doc_id": "27768226", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: PTEN is a regulator for the transcriptional activity of SRF\n\nCANDIDATE_ABSTRACT:\nTITLE: Nuclear PTEN functions as an essential regulator of SRF-dependent transcription to control smooth muscle differentiation\nABSTRACT: Vascular disease progression is associated with marked changes in vascular smooth muscle cell (SMC) phenotype and function. SMC contractile gene expression and, thus differentiation, is under direct transcriptional control by the transcription factor, serum response factor (SRF); however, the mechanisms dynamically regulating SMC phenotype are not fully defined. Here we report that the lipid and protein phosphatase, PTEN, has a novel role in the nucleus by functioning as an indispensible regulator with SRF to maintain the differentiated SM phenotype. PTEN interacts with the N-terminal domain of SRF and PTEN-SRF interaction promotes SRF binding to essential promoter elements in SM-specific genes. Factors inducing phenotypic switching promote loss of nuclear PTEN through nucleo-cytoplasmic translocation resulting in reduced myogenically active SRF, but enhanced SRF activity on target genes involved in proliferation. Overall decreased expression of PTEN was observed in intimal SMCs of human atherosclerotic lesions underlying the potential clinical importance of these findings.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here we report that the lipid and protein phosphatase, PTEN, has a novel role in the nucleus by functioning as an indispensible regulator with SRF to maintain the differentiated SM phenotype.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 917, "doc_id": "34071621", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Allogeneic mechanical circulatory support is not as effective as autologous mechanical circulatory support for treating acute myocardial infarction.\n\nCANDIDATE_ABSTRACT:\nTITLE: Comparison of allogeneic vs autologous bone marrow–derived mesenchymal stem cells delivered by transendocardial injection in patients with ischemic cardiomyopathy: the POSEIDON randomized trial.\nABSTRACT: CONTEXT Mesenchymal stem cells (MSCs) are under evaluation as a therapy for ischemic cardiomyopathy (ICM). Both autologous and allogeneic MSC therapies are possible; however, their safety and efficacy have not been compared. OBJECTIVE To test whether allogeneic MSCs are as safe and effective as autologous MSCs in patients with left ventricular (LV) dysfunction due to ICM. DESIGN, SETTING, AND PATIENTS A phase 1/2 randomized comparison (POSEIDON study) in a US tertiary-care referral hospital of allogeneic and autologous MSCs in 30 patients with LV dysfunction due to ICM between April 2, 2010, and September 14, 2011, with 13-month follow-up. INTERVENTION Twenty million, 100 million, or 200 million cells (5 patients in each cell type per dose level) were delivered by transendocardial stem cell injection into 10 LV sites. MAIN OUTCOME MEASURES Thirty-day postcatheterization incidence of predefined treatment-emergent serious adverse events (SAEs). Efficacy assessments included 6-minute walk test, exercise peak VO2, Minnesota Living with Heart Failure Questionnaire (MLHFQ), New York Heart Association class, LV volumes, ejection fraction (EF), early enhancement defect (EED; infarct size), and sphericity index. RESULTS Within 30 days, 1 patient in each group (treatment-emergent SAE rate, 6.7%) was hospitalized for heart failure, less than the prespecified stopping event rate of 25%. The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3% (n = 8) in the autologous group (P = .46). At 1 year, there were no ventricular arrhythmia SAEs observed among allogeneic recipients compared with 4 patients (26.7%) in the autologous group (P = .10). Relative to baseline, autologous but not allogeneic MSC therapy was associated with an improvement in the 6- [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS In this early-stage study of patients with ICM, transendocardial injection of allogeneic and autologous MSCs without a placebo control were both associated with low rates of treatment-emergent SAEs, including immunologic reactions.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 104, "doc_id": "40164383", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Antiretroviral therapy increases rates of tuberculosis across a broad range of CD4 strata.\n\nCANDIDATE_ABSTRACT:\nTITLE: Antiretroviral Therapy for Prevention of Tuberculosis in Adults with HIV: A Systematic Review and Meta-Analysis\nABSTRACT: BACKGROUND Human immunodeficiency virus (HIV) infection is the strongest risk factor for developing tuberculosis and has fuelled its resurgence, especially in sub-Saharan Africa. In 2010, there were an estimated 1.1 million incident cases of tuberculosis among the 34 million people living with HIV worldwide. Antiretroviral therapy has substantial potential to prevent HIV-associated tuberculosis. We conducted a systematic review of studies that analysed the impact of antiretroviral therapy on the incidence of tuberculosis in adults with HIV infection. METHODS AND FINDINGS PubMed, Embase, African Index Medicus, LILACS, and clinical trial registries were systematically searched. Randomised controlled trials, prospective cohort studies, and retrospective cohort studies were included if they compared tuberculosis incidence by antiretroviral therapy status in HIV-infected adults for a median of over 6 mo in developing countries. For the meta-analyses there were four categories based on CD4 counts at antiretroviral therapy initiation: (1) less than 200 cells/µl, (2) 200 to 350 cells/µl, (3) greater than 350 cells/µl, and (4) any CD4 count. Eleven studies met the inclusion criteria. Antiretroviral therapy is strongly associated with a reduction in the incidence of tuberculosis in all baseline CD4 count categories: (1) less than 200 cells/µl (hazard ratio [HR] 0.16, 95% confidence interval [CI] 0.07 to 0.36), (2) 200 to 350 cells/µl (HR 0.34, 95% CI 0.19 to 0.60), (3) greater than 350 cells/µl (HR 0.43, 95% CI 0.30 to 0.63), and (4) any CD4 count (HR 0.35, 95% CI 0.28 to 0.44). There was no evidence of hazard ratio modification with respect to baseline CD4 count category (p = 0.20). CONCLUSIONS Antiretroviral therapy is strongly associated with a reduction in the inc [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Antiretroviral therapy is strongly associated with a reduction in the incidence of tuberculosis across all CD4 count strata.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 123, "doc_id": "4883040", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Antimicrobial agents are more effective due to the pressure of antimicrobial usage.\n\nCANDIDATE_PASSAGE:\nThe challenges of overcoming antibiotic resistance: Plant extracts as potential sources of antimicrobial and resistance modifying agents The problem of antibiotic resistance, which has limited the use of cheap and old antibiotics, has necessitated the need for a continued search for new antimicrobial compounds. Understanding the mechanisms of resistance is important in the development of strategies to solving the problem. Active efflux of drugs, alteration of target sites and enzymatic degradations are the strategies by which pathogenic bacteria acquire or develop intrinsic resistance to antibiotics. Multi-drug resistance (MDR) pumps, capable of recognizing and expelling a variety of structurally unrelated compounds from the bacterial cell and conferring resistance to a wide range of antibiotics have since been characterized in many gram positive and gram negative pathogens like Staphylococcus aureus, Pseudomonas aeruginosa, Escherichia coli and, more recently, in mycobacteria. The ability of some chemical compounds (called MDR inhibitors or resistance modifying agents) to modify the resistance phenotype in bacteria by working synergistically with antibiotics in vitro has since been observed. The search for such compounds which can be combined with antibiotics in the treatment of drug resistant infections may be an alternative to overcoming the problem of resistance in bacteria. Crude extracts of medicinal plants stand out as veritable sources of potential resistance modifying agents and the African biosphere promises to be a potential source of such compounds owing to its rich plant species diversity.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "122", "doc_id": "4695107", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: H4 G94P proteins inhibit chromatin assembly, which decreases free histones.\n\nCANDIDATE_PASSAGE:\nE2F-dependent histone acetylation and recruitment of the Tip60 acetyltransferase complex to chromatin in late G1. E2F proteins can either activate or repress transcription. Following mitogenic stimulation, repressive E2F4-p130-histone deacetylase complexes dissociate from, while activating species (E2F1, -2, and -3) associate with, target promoters. Histones H3 and H4 simultaneously become hyperacetylated, but it remains unclear whether this is a prerequisite or a consequence of E2F binding. Here, we show that activating E2F species are required for hyperacetylation of target chromatin in human cells. Overexpression of a dominant-negative (DN) E2F1 mutant in serum-stimulated T98G cells blocked all E2F binding, H4 acetylation, and, albeit partially, H3 acetylation. Target gene activation and S-phase entry were also blocked by DN E2F1. Conversely, ectopic activation of E2F1 rapidly induced H3 and H4 acetylation, demonstrating a direct role for E2F in these events. E2F1 was previously shown to bind the histone acetyltransferases (HATs) p300/CBP and PCAF/GCN5. In our hands, ectopically expressed E2F1 also bound the unrelated HAT Tip60 and induced recruitment of five subunits of the Tip60 complex (Tip60, TRRAP, p400, Tip48, and Tip49) to target promoters in vivo. Moreover, E2F-dependent recruitment of Tip60 to chromatin occurred in late G(1) following serum stimulation. We speculate that the activities of multiple HAT complexes account for E2F-dependent acetylation, transcription, and S-phase entry.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "486", "doc_id": "502591", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Birth-weight is positively associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Role of birthweight in the etiology of breast cancer.\nABSTRACT: Breast cancer may originate in utero. We reviewed the available evidence on the association between birthweight and the risk of breast cancer. To date, 26 research papers addressing this issue have been published. The majority of studies identified a positive link between birthweight and premenopausal, but not postmenopausal, breast cancer. The relative risk estimate for breast cancer comparing women with high birthweight to women with low birthweight combining all studies including both pre- and postmenopausal breast cancer was 1.23 (95% confidence interval 1.13-1.34). The mechanisms underlying this association likely include elevated levels of growth factors that may increase the number of susceptible stem cells in the mammary gland or initiate tumors through DNA mutations. Loss of imprinting (LOI) of growth hormone genes relevant for intrauterine growth, such as insulin-like growth factor 2 (IGF2), leads to abnormally high levels of these hormones evidenced by high birthweight. LOI of IGF2 has also been found in mammary tumor tissue. The role of environmental factors that stimulate such epigenetic regulation of gene expression remains to be elucidated.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The majority of studies identified a positive link between birthweight and premenopausal, but not postmenopausal, breast cancer.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 179, "doc_id": "27123743", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does laser engravings as reason for mechanical failure of titanium-alloyed total hip stem?\n\nABSTRACT:\nTwo revisions of broken β-titanium total hip stems had to be performed in our hospital after 2 and 4 years in situ. Since both fractures were located at the level of a laser engraving, a failure analysis was conducted. Both retrieved hip stems were disinfected and collected in our retrieval database after patient's signed agreement. Each fragment was macroscopically photographed. Fracture surfaces were analyzed using scanning electron microscopy (SEM). Quantification of element content was conducted using energy dispersive X-ray (EDX) analysis. Both stems show fatigue fracture, as displayed by the lines of rest on the fracture surface. The origin of fracture was identified directly at the laser engraving of the company logo at both stems by means of SEM. The EDX analysis showed an oxygen level beneath the laser engraving about twice as high as in the substrate, causing material embrittlement.", "output": "{\"label\": \"yes\", \"rationale\": \"Laser engravings need to be reduced to a minimum of necessary information, and should be placed at locations with minimum mechanical load. Biomechanical analyses are recommended to identify less loaded areas in implant components to avoid such implant failures.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25920490, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Activated Cdk5 regulates DNA damage-induced neuronal death.\n\nCANDIDATE_PASSAGE:\nPhosphorylation of ATM by Cdk5 mediates DNA damage signaling and regulates neuronal death The phosphatidylinositol-3-kinase-like kinase ATM (ataxia-telangiectasia mutated) has a central role in coordinating DNA damage responses, including cell-cycle checkpoint control, DNA repair and apoptosis. Mutations of ATM cause a spectrum of defects ranging from neurodegeneration to cancer predisposition. However, the mechanism by which DNA damage activates ATM is poorly understood. Here we show that Cdk5 (cyclin-dependent kinase 5), activated by DNA damage, directly phosphorylates ATM at Ser 794 in post-mitotic neurons. Phosphorylation at Ser 794 precedes, and is required for, ATM autophosphorylation at Ser 1981, and activates ATM kinase activity. The Cdk5-ATM signal regulates phosphorylation and function of the ATM targets p53 and H2AX. Interruption of the Cdk5-ATM pathway attenuates DNA-damage-induced neuronal cell cycle re-entry and expression of the p53 targets PUMA and Bax, protecting neurons from death. Thus, activation of Cdk5 by DNA damage serves as a critical signal to initiate the ATM response and regulate ATM-dependent cellular processes.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "68", "doc_id": "21295300", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: In pediatric tissue, most T cells are naive T cell emigrants from the thymus.\n\nCANDIDATE_ABSTRACT:\nTITLE: Early life compartmentalization of human T cell differentiation and regulatory function in mucosal and lymphoid tissues\nABSTRACT: It is unclear how the immune response in early life becomes appropriately stimulated to provide protection while also avoiding excessive activation as a result of diverse new antigens. T cells are integral to adaptive immunity; mouse studies indicate that tissue localization of T cell subsets is important for both protective immunity and immunoregulation. In humans, however, the early development and function of T cells in tissues remain unexplored. We present here an analysis of lymphoid and mucosal tissue T cells derived from pediatric organ donors in the first two years of life, as compared to adult organ donors, revealing early compartmentalization of T cell differentiation and regulation. Whereas adult tissues contain a predominance of memory T cells, in pediatric blood and tissues the main subset consists of naive recent thymic emigrants, with effector memory T cells (T(EM)) found only in the lungs and small intestine. Additionally, regulatory T (T(reg)) cells comprise a high proportion (30-40%) of CD4(+) T cells in pediatric tissues but are present at much lower frequencies (1-10%) in adult tissues. Pediatric tissue T(reg) cells suppress endogenous T cell activation, and early T cell functionality is confined to the mucosal sites that have the lowest T(reg):T(EM) cell ratios, which suggests control in situ of immune responses in early life.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Whereas adult tissues contain a predominance of memory T cells, in pediatric blood and tissues the main subset consists of naive recent thymic emigrants, with effector memory T cells (T(EM)) found only in the lungs and small intestine.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 580, "doc_id": "23460562", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: B3-Galectin decreases cell resistance to tyrosine kinase inhibitors (TKIs) by engaging the alternate KRAS-RalB signaling complex downstream of EGFR.\n\nCANDIDATE_PASSAGE:\nDifferentiation of trophoblast stem cells into giant cells is triggered by p57/Kip2 inhibition of CDK1 activity. Genome endoreduplication during mammalian development is a rare event for which the mechanism is unknown. It first appears when fibroblast growth factor 4 (FGF4) deprivation induces differentiation of trophoblast stem (TS) cells into the nonproliferating trophoblast giant (TG) cells required for embryo implantation. Here we show that RO3306 inhibition of cyclin-dependent protein kinase 1 (CDK1), the enzyme required to enter mitosis, induced differentiation of TS cells into TG cells. In contrast, RO3306 induced abortive endoreduplication and apoptosis in embryonic stem cells, revealing that inactivation of CDK1 triggers endoreduplication only in cells programmed to differentiate into polyploid cells. Similarly, FGF4 deprivation resulted in CDK1 inhibition by overexpressing two CDK-specific inhibitors, p57/KIP2 and p21/CIP1. TS cell mutants revealed that p57 was required to trigger endoreduplication by inhibiting CDK1, while p21 suppressed expression of the checkpoint protein kinase CHK1, thereby preventing induction of apoptosis. Furthermore, Cdk2(-/-) TS cells revealed that CDK2 is required for endoreduplication when CDK1 is inhibited. Expression of p57 in TG cells was restricted to G-phase nuclei to allow CDK activation of S phase. Thus, endoreduplication in TS cells is triggered by p57 inhibition of CDK1 with concomitant suppression of the DNA damage response by p21.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "153", "doc_id": "1595617", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Egr3 regulates the homeostasis of B and T cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Transcription Factors Egr2 and Egr3 Are Essential for the Control of Inflammation and Antigen-Induced Proliferation of B and T Cells\nABSTRACT: Lymphocytes provide optimal responses against pathogens with minimal inflammatory pathology. However, the intrinsic mechanisms regulating these responses are unknown. Here, we report that deletion of both transcription factors Egr2 and Egr3 in lymphocytes resulted in a lethal autoimmune syndrome with excessive serum proinflammatory cytokines but also impaired antigen receptor-induced proliferation of B and T cells. Egr2- and Egr3-defective B and T cells had hyperactive signal transducer and activator of transcription-1 (STAT1) and STAT3 while antigen receptor-induced activation of transcription factor AP-1 was severely impaired. We discovered that Egr2 and/or Egr3 directly induced expression of suppressor of cytokine signaling-1 (SOCS1) and SOCS3, inhibitors of STAT1 and STAT3, and also blocked the function of Batf, an AP-1 inhibitor, in B and T cells. Thus, Egr2 and Egr3 regulate B and T cell function in adaptive immune responses and homeostasis by promoting antigen receptor signaling and controlling inflammation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here, we report that deletion of both transcription factors Egr2 and Egr3 in lymphocytes resulted in a lethal autoimmune syndrome with excessive serum proinflammatory cytokines but also impaired antigen receptor-induced proliferation of B and T cells.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 371, "doc_id": "1550937", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does platelet activation rather than endothelial injury identify risk of thrombosis in subjects positive for antiphospholipid antibodies?\n\nABSTRACT:\nAnti-phospholipid antibodies (APLA) are often associated with thrombosis, defining the antiphospholipid syndrome (APS) but it remains unclear why many subjects who are positive for APLA chiefly anti-cardiolipin (aCL) or anti-beta2GPI (abeta2GPI) do not develop thrombosis. A related question addressed in this study is whether the target of cellular injury in APS is predominately platelets or endothelial cells (EC). aCL and abeta2GPI were determined by ELISA in 88 patients, 60 of whom were thrombotic and 28 non-thrombotic. Platelet activation was measured by CD62P and by concentration of platelet microparticles (PMP) and EC activation was assessed by endothelial microparticles (EMP), both by flow cytometry. Lupus anticoagulant (LAC) was measured in the hospital laboratory. There was no difference in frequency of aCL or abeta2GPI, neither IgG or IgM, between the thrombotic and non-thrombotic groups. Both groups showed elevated EMP compared to controls but this did not differ between thrombotic and non-thrombotic groups. In contrast, PMP were not significantly elevated in non-thrombotic but were elevated in thrombotic compared to non-thrombotic (p=0.03) and controls. CD62P, an independent marker of platelet activation, was also elevated in thrombotic vs. non-thrombotic. There was a trend for increased LAC in the thrombotic group but not significant.", "output": "{\"label\": \"yes\", \"rationale\": \"Although all subjects had evidence of endothelial activation, only platelet activation differed between thrombotic and non-thrombotic. This supports the hypothesis that platelet activation predisposes to thrombosis in the presence of chronic EC activation. These data also raise the possibility of distinguishing risk-prone APLA-positive individuals.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 17582471, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: MafA ubiquitination increases the recruitment of coavtivator P/CAF by MafA.\n\nCANDIDATE_ABSTRACT:\nTITLE: In vitro characterization of the anti-PD-1 antibody nivolumab, BMS-936558, and in vivo toxicology in non-human primates.\nABSTRACT: The programmed death-1 (PD-1) receptor serves as an immunologic checkpoint, limiting bystander tissue damage and preventing the development of autoimmunity during inflammatory responses. PD-1 is expressed by activated T cells and downmodulates T-cell effector functions upon binding to its ligands, PD-L1 and PD-L2, on antigen-presenting cells. In patients with cancer, the expression of PD-1 on tumor-infiltrating lymphocytes and its interaction with the ligands on tumor and immune cells in the tumor microenvironment undermine antitumor immunity and support its rationale for PD-1 blockade in cancer immunotherapy. This report details the development and characterization of nivolumab, a fully human IgG4 (S228P) anti-PD-1 receptor-blocking monoclonal antibody. Nivolumab binds to PD-1 with high affinity and specificity, and effectively inhibits the interaction between PD-1 and its ligands. In vitro assays demonstrated the ability of nivolumab to potently enhance T-cell responses and cytokine production in the mixed lymphocyte reaction and superantigen or cytomegalovirus stimulation assays. No in vitro antibody-dependent cell-mediated or complement-dependent cytotoxicity was observed with the use of nivolumab and activated T cells as targets. Nivolumab treatment did not induce adverse immune-related events when given to cynomolgus macaques at high concentrations, independent of circulating anti-nivolumab antibodies where observed. These data provide a comprehensive preclinical characterization of nivolumab, for which antitumor activity and safety have been demonstrated in human clinical trials in various solid tumors.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 748, "doc_id": "1454773", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Natriuretic peptides protect against diabetes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Age-related changes in kynurenic acid production in rat brain.\nABSTRACT: Two separate in vitro assays were used to examine the biosynthesis of the broad spectrum excitatory amino acid receptor antagonist kynurenic acid (KYNA) during the life span of the adult rat. Assessment of KYNA's anabolic enzyme kynurenine aminotransferase revealed steady increases between 3 and 24 months of age in all five brain regions examined. No changes were observed in the liver. The changes were particularly pronounced in the cortex and in the striatum where enzyme activity increased three-fold during the period studied. KYNA production from its bioprecursor L-kynurenine was also investigated in tissue slices and was found to be significantly enhanced in the cortex and hippocampus of old animals. The effect of depolarizing agents or sodium replacement was virtually identical in tissues from young and old rats. These data, which are in excellent agreement with reports on an age-dependent increase of KYNA concentration in brain tissue, suggest an enhanced KYNA tone in the aged brain. Together with the reported decline in cerebral excitatory amino acid receptor densities with age, increased production of KYNA may play a role in cognitive and memory dysfunction in old animals.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 841, "doc_id": "1733337", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Citrullinated proteins externalized in neutrophil extracellular traps act indirectly to disrupt the inflammatory cycle.\n\nCANDIDATE_PASSAGE:\nThe Worldwide Variation in Avian Clutch Size across Species and Space Traits such as clutch size vary markedly across species and environmental gradients but have usually been investigated from either a comparative or a geographic perspective, respectively. We analyzed the global variation in clutch size across 5,290 bird species, excluding brood parasites and pelagic species. We integrated intrinsic (morphological, behavioural), extrinsic (environmental), and phylogenetic effects in a combined model that predicts up to 68% of the interspecific variation in clutch size. We then applied the same species-level model to predict mean clutch size across 2,521 assemblages worldwide and found that it explains the observed eco-geographic pattern very well. Clutches are consistently largest in cavity nesters and in species occupying seasonal environments, highlighting the importance of offspring and adult mortality that is jointly expressed in intrinsic and extrinsic correlates. The findings offer a conceptual bridge between macroecology and comparative biology and provide a global and integrative understanding of the eco-geographic and cross-species variation in a core life-history trait.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "263", "doc_id": "8502193", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: NAC destabilizes NO to increase the effect of contrast agents on renal functions.\n\nCANDIDATE_PASSAGE:\nAge-related changes in kynurenic acid production in rat brain. Two separate in vitro assays were used to examine the biosynthesis of the broad spectrum excitatory amino acid receptor antagonist kynurenic acid (KYNA) during the life span of the adult rat. Assessment of KYNA's anabolic enzyme kynurenine aminotransferase revealed steady increases between 3 and 24 months of age in all five brain regions examined. No changes were observed in the liver. The changes were particularly pronounced in the cortex and in the striatum where enzyme activity increased three-fold during the period studied. KYNA production from its bioprecursor L-kynurenine was also investigated in tissue slices and was found to be significantly enhanced in the cortex and hippocampus of old animals. The effect of depolarizing agents or sodium replacement was virtually identical in tissues from young and old rats. These data, which are in excellent agreement with reports on an age-dependent increase of KYNA concentration in brain tissue, suggest an enhanced KYNA tone in the aged brain. Together with the reported decline in cerebral excitatory amino acid receptor densities with age, increased production of KYNA may play a role in cognitive and memory dysfunction in old animals.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "826", "doc_id": "1733337", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Rapid up-regulation and higher basal expression of interferon-induced genes reduce survival of granule cell neurons that are infected by West Nile virus.\n\nCANDIDATE_PASSAGE:\nHuman NK cells in acute myeloid leukaemia patients: analysis of NK cell-activating receptors and their ligands Natural killer (NK) cell activation is strictly regulated to ensure that healthy cells are preserved, but tumour-transformed or virus-infected cells are recognized and eliminated. To carry out this selective killing, NK cells have an ample repertoire of receptors on their surface. Signalling by inhibitory and activating receptors by interaction with their ligands will determine whether the NK cell becomes activated and kills the target cell. Here, we show reduced expression of NKp46, NKp30, DNAM-1, CD244 and CD94/NKG2C activating receptors on NK cells from acute myeloid leukaemia patients. This reduction may be induced by chronic exposure to their ligands on leukaemic blasts. The analysis of ligands for NK cell-activating receptors showed that leukaemic blasts from the majority of patients express ligands for NK cell-activating receptors. DNAM-1 ligands are frequently expressed on blasts, whereas the expression of the NKG2D ligand MICA/B is found in half of the patients and CD48, a ligand for CD244, in only one-fourth of the patients. The decreased expression of NK cell-activating receptors and/or the heterogeneous expression of ligands for major receptors on leukaemic blasts can lead to an inadequate tumour immunosurveillance by NK cells. A better knowledge of the activating receptor repertoire on NK cells and their putative ligands on blasts together with the possibility to modulate their expression will open new possibilities for the use of NK cells in immunotherapy against leukaemia.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1021", "doc_id": "20690388", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is parity associated with urgency with or without urinary incontinence?\n\nABSTRACT:\nEvidence varies on the relation between parity and urgency or urge incontinence (UUI). We used data from the General Longitudinal Overactive Bladder Evaluation to determine whether differences in case definitions could account for variation in findings. We simulated case criteria to correspond to studies of urgency, UUI, and parity using data from 1,880 patients. Logistic models were run for each case-control scenario corresponding to previously used case definitions. Parity was significantly associated with urgency (odds ratios (OR) 1.70; CI: 1.30-2.22) and UUI (odds ratios (OR) 1.87; CI: 1.34-2.60) only when the case criteria included individuals with stress incontinence (SUI). Parity was not associated with UUI when individuals with SUI were excluded or with urgency when individuals with incontinence were excluded.", "output": "{\"label\": \"no\", \"rationale\": \"Neither urgency nor UUI symptoms appear to be associated with parity among women 40 years of age and older. Previous associations appear to be explained by inclusion of individuals with SUI.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 20458466, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: ATM and Rad3 related protein have no role in sensing DNA damage.\n\nCANDIDATE_PASSAGE:\nDeletion of the developmentally essential gene ATR in adult mice leads to age-related phenotypes and stem cell loss. Developmental abnormalities, cancer, and premature aging each have been linked to defects in the DNA damage response (DDR). Mutations in the ATR checkpoint regulator cause developmental defects in mice (pregastrulation lethality) and humans (Seckel syndrome). Here we show that eliminating ATR in adult mice leads to defects in tissue homeostasis and the rapid appearance of age-related phenotypes, such as hair graying, alopecia, kyphosis, osteoporosis, thymic involution, fibrosis, and other abnormalities. Histological and genetic analyses indicate that ATR deletion causes acute cellular loss in tissues in which continuous cell proliferation is required for maintenance. Importantly, thymic involution, alopecia, and hair graying in ATR knockout mice were associated with dramatic reductions in tissue-specific stem and progenitor cells and exhaustion of tissue renewal and homeostatic capacity. In aggregate, these studies suggest that reduced regenerative capacity in adults via deletion of a developmentally essential DDR gene is sufficient to cause the premature appearance of age-related phenotypes.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "64", "doc_id": "40349336", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Removal of H3K9me3 by ectopic expression of other H3K9 demethylases decreases reprogramming efficiency in SCNT experiments.\n\nCANDIDATE_ABSTRACT:\nTITLE: H3K9 demethylase KDM4E is an epigenetic regulator for bovine embryonic development and a defective factor for nuclear reprogramming.\nABSTRACT: Aberrant epigenetic reprogramming often results in developmental defects in somatic cell nuclear transfer (SCNT) embryos during embryonic genome activation (EGA). Bovine eight-cell SCNT embryos exhibit global hypermethylation of histone H3 lysine 9 tri- and di-methylation (H3K9me3/2), but the intrinsic reason for this remains elusive. Here, we provide evidence that two H3K9 demethylase genes, lysine-specific demethylase 4D (KDM4D) and 4E (KDM4E), are related to active H3K9me3/2 demethylation in in vitro fertilized (IVF) embryos and are deficiently expressed in cloned embryos at the time of EGA. Moreover, KDM4E plays a more crucial role in IVF and SCNT embryonic development, and overexpression of KDM4E can restore the global transcriptome, improve blastocyst formation and increase the cloning efficiency of SCNT embryos. Our results thereby indicate that KDM4E can function as a crucial epigenetic regulator of EGA and as an internal defective factor responsible for persistent H3K9me3/2 barriers to SCNT-mediated reprogramming. Furthermore, we show that interactions between RNA and KDM4E are essential for H3K9 demethylation during EGA. These observations advance the understanding of incomplete nuclear reprogramming and are of great importance for transgenic cattle procreation.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Moreover, KDM4E plays a more crucial role in IVF and SCNT embryonic development, and overexpression of KDM4E can restore the global transcriptome, improve blastocyst formation and increase the cloning efficiency of SCNT embryos.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1034, "doc_id": "4547102", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is diabetes-Related Burden and Distress Low in People with Diabetes at Outpatient Tertiary Care Level?\n\nABSTRACT:\nThe importance of diabetes-related distress (DRD) for the treatment of diabetes is emphasized in national and international guidelines recommending routinely screening for psychosocial problems. To detect DRD, the PAID (Problem Area In Diabetes) questionnaire provides a valid and reliable instrument. 783 patients with diabetes mellitus type 1 (DM1, n=191, age 54.5 y, diabetes duration 22.5 y, HbA1c 7.2% (55 mmol/mol)) and type 2 (DM2, n=592, age 66.6 y, diabetes duration 15.6 y, HbA1c 7.0% (60.1 mmol/mol)) were interviewed with the PAID and WHO-5 questionnaire in a University outpatient department for endocrinology and metabolic diseases in 2012. A PAID score≥40 (range 0-100) was considered as high DRD. The mean PAID score was 17.1±15.1 in all participants. Only 8.9% of all responders showed high DRD (score≥40). The PAID score neither differed in people with DM1 and DM2, nor between participants with DM2 with or without insulin therapy. Females achieved significantly higher scores than men (19.0±16.6 vs. 15.6±13.7, p=0.003). A strong negative correlation existed between the PAID score and the WHO-5 Well-being Index (r=- 0.482, p<0.001). A 10 points higher WHO-5 Well-being Index was associated with 15.9 points lower PAID score in people with DM1 (p<0.001), and 9.2 points lower PAID score in DM2 (p<0.001), respectively. One percent higher HbA1c was associated with an increase of diabetes-related distress by 2.5 points in people with DM1 and by 2.0 points in people with DM2.", "output": "{\"label\": \"yes\", \"rationale\": \"Less than 10% of our outpatients with diabetes showed high diabetes-related distress.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 27219688, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Hyperfibrinogenemia increases rates of femoropopliteal bypass thrombosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Influence of smoking and plasma factors on patency of femoropopliteal vein grafts.\nABSTRACT: OBJECTIVE To determine the effects of smoking, plasma lipids, lipoproteins, apolipoproteins, and fibrinogen on the patency of saphenous vein femoropopliteal bypass grafts at one year. DESIGN Prospective study of patients with saphenous vein femoropopliteal bypass grafts entered into a multicentre trial. SETTING Surgical wards, outpatient clinics, and home visits coordinated by two tertiary referral centres in London and Birmingham. PATIENTS 157 Patients (mean age 66.6 (SD 8.2) years), 113 with patent grafts and 44 with occluded grafts one year after bypass. MAIN OUTCOME MEASURE Cumulative percentage patency at one year. RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts. Serum cholesterol concentrations were significantly higher in patients with grafts that remained patent one year after bypass (p less than 0.005). Analysis of the smoking markers indicated that a quarter of patients (40) were untruthful in their claims to have stopped smoking. Based on smoking markers, patency of grafts in smokers was significantly lower at one year by life table analysis than in non-smokers (63% v 84%, p less than 0.02). Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002). Surprisingly, increased plasma low density lipoprotein cholesterol concentration was significantly associated with improved patency at one year (85%) at values above the median compared w [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 533, "doc_id": "12991445", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Chenodeoxycholic acid treatment increases brown adipose tissue activity.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Bile Acid Chenodeoxycholic Acid Increases Human Brown Adipose Tissue Activity.\nABSTRACT: The interest in brown adipose tissue (BAT) as a target to combat metabolic disease has recently been renewed with the discovery of functional BAT in humans. In rodents, BAT can be activated by bile acids, which activate type 2 iodothyronine deiodinase (D2) in BAT via the G-coupled protein receptor TGR5, resulting in increased oxygen consumption and energy expenditure. Here we examined the effects of oral supplementation of the bile acid chenodeoxycholic acid (CDCA) on human BAT activity. Treatment of 12 healthy female subjects with CDCA for 2 days resulted in increased BAT activity. Whole-body energy expenditure was also increased upon CDCA treatment. In vitro treatment of primary human brown adipocytes derived with CDCA or specific TGR5 agonists increased mitochondrial uncoupling and D2 expression, an effect that was absent in human primary white adipocytes. These findings identify bile acids as a target to activate BAT in humans.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Treatment of 12 healthy female subjects with CDCA for 2 days resulted in increased BAT activity.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 251, "doc_id": "1568684", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Ca2+ cycling is a UCP1-independent thermogenic mechanism.\n\nCANDIDATE_ABSTRACT:\nTITLE: UCP1-independent signaling involving SERCA2b-mediated calcium cycling regulates beige fat thermogenesis and systemic glucose homeostasis\nABSTRACT: Uncoupling protein 1 (UCP1) plays a central role in nonshivering thermogenesis in brown fat; however, its role in beige fat remains unclear. Here we report a robust UCP1-independent thermogenic mechanism in beige fat that involves enhanced ATP-dependent Ca2+ cycling by sarco/endoplasmic reticulum Ca2+-ATPase 2b (SERCA2b) and ryanodine receptor 2 (RyR2). Inhibition of SERCA2b impairs UCP1-independent beige fat thermogenesis in humans and mice as well as in pigs, a species that lacks a functional UCP1 protein. Conversely, enhanced Ca2+ cycling by activation of α1- and/or β3-adrenergic receptors or the SERCA2b-RyR2 pathway stimulates UCP1-independent thermogenesis in beige adipocytes. In the absence of UCP1, beige fat dynamically expends glucose through enhanced glycolysis, tricarboxylic acid metabolism and pyruvate dehydrogenase activity for ATP-dependent thermogenesis through the SERCA2b pathway; beige fat thereby functions as a 'glucose sink' and improves glucose tolerance independently of body weight loss. Our study uncovers a noncanonical thermogenic mechanism through which beige fat controls whole-body energy homeostasis via Ca2+ cycling.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Conversely, enhanced Ca2+ cycling by activation of α1- and/or β3-adrenergic receptors or the SERCA2b-RyR2 pathway stimulates UCP1-independent thermogenesis in beige adipocytes.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 222, "doc_id": "19205437", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Epigenetic modulating agents (EMAs) modulate antitumor immune response in a cancer model system.\n\nCANDIDATE_PASSAGE:\nIdentification of an autoantigen demonstrates a link between interstitial lung disease and a defect in central tolerance. Interstitial lung disease (ILD) is a common manifestation of systemic autoimmunity characterized by progressive inflammation or scarring of the lungs. Patients who develop these complications can exhibit significantly impaired gas exchange that may result in hypoxemia, pulmonary hypertension, and even death. Unfortunately, little is understood about how these diseases arise, including the role of specific defects in immune tolerance. Another key question is whether autoimmune responses targeting the lung parenchyma are critical to ILD pathogenesis, including that of isolated idiopathic forms. We show that a specific defect in central tolerance brought about by mutations in the autoimmune regulator gene (Aire) leads to an autoreactive T cell response to a lung antigen named vomeromodulin and the development of ILD. We found that a human patient and mice with defects in Aire develop similar lung pathology, demonstrating that the AIRE-deficient model of autoimmunity is a suitable translational system in which to unravel fundamental mechanisms of ILD pathogenesis.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "385", "doc_id": "15707049", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Post-transcriptional handling of mitochondrial transcripts occurs in mitochondrial RNA granules.\n\nCANDIDATE_ABSTRACT:\nTITLE: The mitochondrial RNA-binding protein GRSF1 localizes to RNA granules and is required for posttranscriptional mitochondrial gene expression.\nABSTRACT: RNA-binding proteins are at the heart of posttranscriptional gene regulation, coordinating the processing, storage, and handling of cellular RNAs. We show here that GRSF1, previously implicated in the binding and selective translation of influenza mRNAs, is targeted to mitochondria where it forms granules that colocalize with foci of newly synthesized mtRNA next to mitochondrial nucleoids. GRSF1 preferentially binds RNAs transcribed from three contiguous genes on the light strand of mtDNA, the ND6 mRNA, and the long noncoding RNAs for cytb and ND5, each of which contains multiple consensus binding sequences. RNAi-mediated knockdown of GRSF1 leads to alterations in mitochondrial RNA stability, abnormal loading of mRNAs and lncRNAs on the mitochondrial ribosome, and impaired ribosome assembly. This results in a specific protein synthesis defect and a failure to assemble normal amounts of the oxidative phosphorylation complexes. These data implicate GRSF1 as a key regulator of posttranscriptional mitochondrial gene expression.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We show here that GRSF1, previously implicated in the binding and selective translation of influenza mRNAs, is targeted to mitochondria where it forms granules that colocalize with foci of newly synthesized mtRNA next to mitochondrial nucleoids. These data implicate GRSF1 as a key regulator of posttranscriptional mitochondrial gene expression.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 962, "doc_id": "935538", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Reduction of purity of cytoplasmic membranes isolated from overexpressors is indicated by stronger spots for OmpA in 2D BN-PAGE gels.\n\nCANDIDATE_PASSAGE:\nAdhesion molecules and chemokines: relation to anthropometric, body composition, biochemical and dietary variables Introduction: Among the inflammatory mediators involved in the pathogenesis of obesity, the cell adhesion molecules Pselectin, E-selectin, VCAM-1, ICAM-1 and the chemokine MCP-1 stand out. They play a crucial role in adherence of cells to endothelial surfaces, in the integrity of the vascular wall and can be modulated by body composition and dietary pattern. Objectives: To describe and discuss the relation of these cell adhesion molecules and chemokines to anthropometric, body composition, dietary and biochemical markers. Methods: Papers were located using scientific databases by topic searches with no restriction on year of publication. Results: All molecules were associated positively with anthropometric markers, but controversial results were found for ICAM-1 and VCAM-1. Not only obesity, but visceral fat is more strongly correlated with E-selectin and MCP-1 levels. Weight loss influences the reduction in the levels of these molecules, except VCAM-1. The distribution of macronutrients, excessive consumption of saturated and trans fat and a Western dietary pattern are associated with increased levels. The opposite could be observed with supplementation of w-3 fatty acid, healthy dietary pattern, high calcium diet and high dairy intake. Regarding the biochemical parameters, they have inverse relation to HDLC and positive relation to total cholesterol, triglycerides, blood glucose, fasting insulin and insulin resistance. Conclusion: Normal anthropometric indicators, body composition, biochemical parameters and eating pattern positively modulate the subclinical inflammation that results from obesity by reducing the cell adhesion molecules and chemokines.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1032", "doc_id": "198309074", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Treatment with a protein named FN restores regenerative abilities of aged muscles.\n\nCANDIDATE_PASSAGE:\nAngiopoietin-1 requires p190 RhoGAP to protect against vascular leakage in vivo. Angiopoietin-1 (Ang-1), a ligand of the endothelium-specific receptor Tie-2, inhibits permeability in the mature vasculature, but the mechanism remains unknown. Here we show that Ang-1 signals Rho family GTPases to organize the cytoskeleton into a junction-fortifying arrangement that enhances the permeability barrier function of the endothelium. Ang-1 phosphorylates Tie-2 and its downstream effector phosphatidylinositol 3-kinase. This induces activation of one endogenous GTPase, Rac1, and inhibition of another, RhoA. Loss of either part of this dual effect abrogates the cytoskeletal and anti-permeability actions of Ang-1, suggesting that coordinated GTPase regulation is necessary for the vessel-sealing effects of Ang-1. p190 RhoGAP, a GTPase regulatory protein, provides this coordinating function as it is phosphorylated by Ang-1 treatment, requires Rac1 activation, and is necessary for RhoA inhibition. Ang-1 prevents the cytoskeletal and pro-permeability effects of endotoxin but requires p190 RhoGAP to do so. Treatment with p190 RhoGAP small interfering RNA completely abolishes the ability of Ang-1 to rescue endotoxemia-induced pulmonary vascular leak and inflammation in mice. We conclude that Ang-1 prevents vascular permeability by regulating the endothelial cytoskeleton through coordinated and opposite effects on the Rho GTPases Rac1 and RhoA. By linking Rac1 activation and RhoA inhibition, p190 RhoGAP is critical to the protective effects of Ang-1 against endotoxin. These results provide mechanistic evidence that targeting the endothelium through Tie-2 may offer specific therapeutic strategies in life-threatening endotoxemic conditions such as sepsis and acute respiratory dis [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1324", "doc_id": "23700330", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does timing of initial surfactant treatment make a difference in rates of chronic lung disease or mortality in premature infants?\n\nABSTRACT:\nTo compare two treatment strategies in preterm infants with or at risk of respiratory distress syndrome: early surfactant administration (within one hour of birth) versus late surfactant administration, in a geographically defined population. The primary outcome was chronic lung disease (CLD) and mortality before/at 36 weeks. Secondary outcomes included: duration of mechanical ventilation and continuous positive airway pressure (CPAP), post-natal steroids for CLD and major neonatal morbidities. Premature infants born at 22-32 weeks' gestation between January 2006 and December 2009. Ten neonatal intensive care units (NICUs) in New South Wales (NSW) and Australian Capital Territory (ACT), Australia. Retrospective analysis of prospectively collected data from the regional NICU database in NSW and ACT. Of the 2170 infants who received surfactant, 1182 (54.5%) and 988 (45.5%) received early and late surfactant, respectively. The early surfactant group was less mature (27.1 ± 2.1 versus 29.4 ± 2.1 weeks) and had more CLD and mortality (40.2% versus 20.0%). The multivariable analysis showed early surfactant to be associated with less duration of ventilation, longer duration of CPAP and longer hospital stay but had little or no impact on CLD/mortality.", "output": "{\"label\": \"maybe\", \"rationale\": \"Early surfactant administration is associated with shorter duration of ventilation but does not appear to be significantly protective against CLD/mortality among premature infants. This may support the growing evidence for consideration of CPAP as an alternative to routine intubation and early surfactant administration. Further investigation from large randomized clinical trials is warranted to confirm these results.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 25394614, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Induced hepatic stem cells possess the potential to differentiate into hepatocytic cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Reprogramming fibroblasts into bipotential hepatic stem cells by defined factors.\nABSTRACT: Recent studies have demonstrated direct reprogramming of fibroblasts into a range of somatic cell types, but to date stem or progenitor cells have only been reprogrammed for the blood and neuronal lineages. We previously reported generation of induced hepatocyte-like (iHep) cells by transduction of Gata4, Hnf1α, and Foxa3 in p19 Arf null mouse embryonic fibroblasts (MEFs). Here, we show that Hnf1β and Foxa3, liver organogenesis transcription factors, are sufficient to reprogram MEFs into induced hepatic stem cells (iHepSCs). iHepSCs can be stably expanded in vitro and possess the potential of bidirectional differentiation into both hepatocytic and cholangiocytic lineages. In the injured liver of fumarylacetoacetate hydrolase (Fah)-deficient mice, repopulating iHepSCs become hepatocyte-like cells. They also engraft as cholangiocytes into bile ducts of mice with DDC-induced bile ductular injury. Lineage conversion into bipotential expandable iHepSCs provides a strategy to enable efficient derivation of both hepatocytes and cholangiocytes for use in disease modeling and tissue engineering.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"iHepSCs can be stably expanded in vitro and possess the potential of bidirectional differentiation into both hepatocytic and cholangiocytic lineages.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 625, "doc_id": "20033112", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: ITAM phosphorylation allows for the transfer of the T cell receptor (TCR) signal from the echo-domain to the cytoplasmic tail of the T cell receptor (TCR).\n\nCANDIDATE_PASSAGE:\nMicrobiome-driven allergic lung inflammation is ameliorated by short-chain fatty acids The mammalian gastrointestinal tract harbors a microbial community with metabolic activity critical for host health, including metabolites that can modulate effector functions of immune cells. Mice treated with vancomycin have an altered microbiome and metabolite profile, exhibit exacerbated T helper type 2 cell (Th2) responses, and are more susceptible to allergic lung inflammation. Here we show that dietary supplementation with short-chain fatty acids (SCFAs) ameliorates this enhanced asthma susceptibility by modulating the activity of T cells and dendritic cells (DCs). Dysbiotic mice treated with SCFAs have fewer interleukin-4 (IL4)-producing CD4+ T cells and decreased levels of circulating immunoglobulin E (IgE). In addition, DCs exposed to SCFAs activate T cells less robustly, are less motile in response to CCL19 in vitro, and exhibit a dampened ability to transport inhaled allergens to lung draining nodes. Our data thus demonstrate that gut dysbiosis can exacerbate allergic lung inflammation through both T cell- and DC-dependent mechanisms that are inhibited by SCFAs.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "550", "doc_id": "20148808", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Removal of H3K9me3 by ectopic expression of other H3K9 demethylases improves reprogramming efficiency in SCNT experiments.\n\nCANDIDATE_PASSAGE:\nHistone Methylation-Dependent Mechanisms Impose Ligand Dependency for Gene Activation by Nuclear Receptors Nuclear receptors undergo ligand-dependent conformational changes that are required for corepressor-coactivator exchange, but whether there is an actual requirement for specific epigenetic landmarks to impose ligand dependency for gene activation remains unknown. Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases (HMTs) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals. This strategy, based at least in part on an HMT-dependent inhibitory histone code, imposes a requirement for specific histone demethylases, including LSD1, to permit ligand- and signal-dependent activation of regulated gene expression. These events link an inhibitory methylation component of the histone code to a broadly used strategy that circumvents pathological constitutive gene induction by physiologically regulated transcription factors.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1035", "doc_id": "13639330", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Cost effectiveness evaluations based on cRCT data lack external validity.\n\nCANDIDATE_PASSAGE:\nThe Danish prescription registries. The extensive computerisation of Danish pharmacies has permitted the establishment of two large prescription registries: The Odense University Pharmacoepidemiological Database (OPED) and the Pharmacoepidemiological Prescription Database of North Jutland (PDNJ). The Danish prescription registries content, coverage, completeness and the quality of the data are discussed in this article. Furthermore, conditions for access to the data are presented. The two prescription registries cover a background population of approximately one million or 18% of the Danish population. The populations covered by the registries are stable and representative of the Danish population in general. The registries cover all reimbursed medicine at the level of the individual user. Registration of a unique and permanent personal identifier enables the compilation of longitudinal drug histories and allows the linking of prescription data to other population-based Danish registries. The degree of completeness of the Danish prescription registries is excellent for reimbursed prescription drugs. A small number of comparison studies also indicate high validity of the register information. The Danish prescription registries represent a useful new data source for pharmacoepidemiological studies.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "292", "doc_id": "23841828", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is c5a/C5aR pathway essential for the pathogenesis of murine viral fulminant hepatitis by way of potentiating Fgl2/fibroleukin expression?\n\nABSTRACT:\nViral fulminant hepatitis (FH) remains a serious clinical problem with very high mortality. Lacking understanding of FH pathogenesis has in essence hindered efficient clinical treatment. Inferring from a correlation observed between the genetic differences in the complement component 5 (C5) and the susceptibility of mouse strains to murine hepatitis virus strain-3 (MHV-3) infections, we propose that excessive complement activation plays a critical role in the development of FH. We show that MHV-3 infection causes massive complement activation, along with a rapid increase in serum C5a levels and quick development of FH in susceptible strains. Mice deficient in the C5a receptor (C5aR) or the susceptible strains treated with C5aR antagonists (C5aRa) exhibit significant attenuation of the disease, accompanied by a remarkable reduction of hepatic fibrinogen-like protein 2 (Fgl2), a hallmark protein that causes necrosis of infected livers. In accordance, biopsy of FH patients shows a dramatic increase of Fgl2 expression, which correlates with C5aR up-regulation in the liver. In vitro C5a administration accelerates MHV-3-induced Fgl2 secretion by macrophages. Furthermore, inhibiting ERK1/2 and p38 efficiently blocks C5a-mediated Fgl2 production during viral infections.", "output": "{\"label\": \"yes\", \"rationale\": \"These data provide evidence that mouse susceptibility to MHV-3-induced FH may rely on C5a/C5aR interactions, for which ERK1/2 and p38 pathways participate in up-regulating Fgl2 expression. Inhibition of C5a/C5aR interactions is expected to be beneficial in the clinical treatment of FH patients.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 24604562, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The risk of breast cancer among parous women increases with placental weight of pregnancies, and this association is strongest for premenopausal breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pregnancy characteristics and maternal risk of breast cancer.\nABSTRACT: CONTEXT During pregnancy, serum levels of estrogen, progesterone, and other hormones are markedly higher than during other periods of life. Pregnancy hormones primarily are produced in the placenta, and signs of placental impairment may serve as indirect markers of hormone exposures during pregnancy. During pregnancy, these markers have been inconsistently associated with subsequent risk of breast cancer in the mother. OBJECTIVE To examine associations between indirect markers of hormonal exposures, such as placental weight and other pregnancy characteristics, and maternal risk of developing breast cancer. DESIGN AND SETTING Population-based cohort study using data from the Swedish Birth Register, the Swedish Cancer Register, the Swedish Cause of Death Register, and the Swedish Register of Population and Population Changes. PARTICIPANTS Women included in the Sweden Birth Register who delivered singletons between 1982 and 1989, with complete information on date of birth and gestational age. Women were followed up until the occurrence of breast cancer, death, or end of follow-up (December 31, 2001). Cox proportional hazards models were used to estimate associations between hormone exposures and risks of breast cancer. MAIN OUTCOME MEASURE Incidence of invasive breast cancer. RESULTS Of 314,019 women in the cohort, 2216 (0.7%) developed breast cancer during the follow-up through 2001, of whom 2100 (95%) were diagnosed before age 50 years. Compared with women who had placentas weighing less than 500 g in 2 consecutive pregnancies, the risk of breast cancer was increased among women whose placentas weighed between 500 and 699 g in their first pregnancy and at least 700 g in their second pregnancy (or vice versa) (adjusted hazard ratio, 1.82; 95% confidence interv [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Placental weight is positively associated with maternal risk of breast cancer.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1266, "doc_id": "37480103", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does limb-salvage surgery offer patients better quality of life and functional capacity than amputation?\n\nABSTRACT:\nPatients with aggressive lower extremity musculoskeletal tumors may be candidates for either above-knee amputation or limb-salvage surgery. However, the subjective and objective benefits of limb-salvage surgery compared with amputation are not fully clear.QUESTIONS/ We therefore compared functional status and quality of life for patients treated with above-knee amputation versus limb-salvage surgery. We reviewed 20 of 51 patients aged 15 years and older treated with above-knee amputation or limb-salvage surgery for aggressive musculoskeletal tumors around the knee between 1994 and 2004 as a retrospective cohort study. At last followup we obtained the Physiological Cost Index, the Reintegration to Normal Living Index, SF-36, and the Toronto Extremity Salvage Score questionnaires. The minimum followup was 12 months (median, 56 months; range, 12-108 months). Compared with patients having above-knee amputation, patients undergoing limb-salvage surgery had superior Physiological Cost Index scores and Reintegration to Normal Living Index. The Toronto Extremity Salvage scores and SF-36 scores were similar in the two groups.", "output": "{\"label\": \"maybe\", \"rationale\": \"These data suggest that limb-salvage surgery offers better gait efficiency and return to normal living compared with above-knee amputation, but does not improve the patient's perception of quality of life.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 22302658, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Concentrations of SNV and CNV in stem-cell regulatory elements and binding sites of transcription factors in iPSC-lines are distinct from their founding cells.\n\nCANDIDATE_PASSAGE:\nEndogenous miRNA sponge lincRNA-RoR regulates Oct4, Nanog, and Sox2 in human embryonic stem cell self-renewal. The embryonic stem cell (ESC) transcriptional and epigenetic networks are controlled by a multilayer regulatory circuitry, including core transcription factors (TFs), posttranscriptional modifier microRNAs (miRNAs), and some other regulators. However, the role of large intergenic noncoding RNAs (lincRNAs) in this regulatory circuitry and their underlying mechanism remains undefined. Here, we demonstrate that a lincRNA, linc-RoR, may function as a key competing endogenous RNA to link the network of miRNAs and core TFs, e.g., Oct4, Sox2, and Nanog. We show that linc-RoR shares miRNA-response elements with these core TFs and that linc-RoR prevents these core TFs from miRNA-mediated suppression in self-renewing human ESC. We suggest that linc-RoR forms a feedback loop with core TFs and miRNAs to regulate ESC maintenance and differentiation. These results may provide insights into the functional interactions of the components of genetic networks during development and may lead to new therapies for many diseases.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "281", "doc_id": "42662816", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Reduced phosphorylation of PP2A increases HDAC4 dephosphorylation by enhancing PP2A-HDAC4 interaction.\n\nCANDIDATE_ABSTRACT:\nTITLE: Nuclear accumulation of HDAC4 in ATM deficiency promotes neurodegeneration in ataxia-telangiectasia\nABSTRACT: Ataxia telangiectasia is a neurodegenerative disease caused by mutation of the Atm gene. Here we report that ataxia telangiectasia mutated (ATM) deficiency causes nuclear accumulation of histone deacetylase 4 (HDAC4) in neurons and promotes neurodegeneration. Nuclear HDAC4 binds to chromatin, as well as to myocyte enhancer factor 2A (MEF2A) and cAMP-responsive element binding protein (CREB), leading to histone deacetylation and altered neuronal gene expression. Blocking either HDAC4 activity or its nuclear accumulation blunts these neurodegenerative changes and rescues several behavioral abnormalities of ATM-deficient mice. Full rescue of the neurodegeneration, however, also requires the presence of HDAC4 in the cytoplasm, suggesting that the ataxia telangiectasia phenotype results both from a loss of cytoplasmic HDAC4 as well as its nuclear accumulation. To remain cytoplasmic, HDAC4 must be phosphorylated. The activity of the HDAC4 phosphatase, protein phosphatase 2A (PP2A), is downregulated by ATM-mediated phosphorylation. In ATM deficiency, enhanced PP2A activity leads to HDAC4 dephosphorylation and the nuclear accumulation of HDAC4. Our results define a crucial role of the cellular localization of HDAC4 in the events leading to ataxia telangiectasia neurodegeneration.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1026, "doc_id": "3113630", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does rugby headgear prevent concussion?\n\nABSTRACT:\nTo examine the attitudes of players and coaches to the use of protective headgear, particularly with respect to the prevention of concussion. A questionnaire designed to assess attitudes to headgear was administered to 63 players from four different Canadian teams, each representing a different level of play (high school, university, community club, national). In addition, coaches from all four levels were questioned about team policies and their personal opinions about the use of headgear to prevent concussion. Although the players tended to believe that the headgear could prevent concussion (62%), the coaches were less convinced (33%). Despite the players' belief that headgear offers protection against concussion, only a minority reported wearing headgear (27%) and few (24%) felt that its use should be made mandatory. Common reasons for not wearing headgear were \"its use is not mandatory\", \"it is uncomfortable\", and \"it costs too much\".", "output": "{\"label\": \"maybe\", \"rationale\": \"Although most players in the study believe that rugby headgear may prevent concussion, only a minority reported wearing it. Coaches tended to be less convinced than the players that rugby headgear can prevent concussion.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 11867487, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In rhesus macaques, daily subcutaneous injections of tenofovir protects against rectally transmitted simian-human immunodeficiency virus.\n\nCANDIDATE_ABSTRACT:\nTITLE: Prevention of Rectal SHIV Transmission in Macaques by Daily or Intermittent Prophylaxis with Emtricitabine and Tenofovir \nABSTRACT: BACKGROUND In the absence of an effective vaccine, HIV continues to spread globally, emphasizing the need for novel strategies to limit its transmission. Pre-exposure prophylaxis (PrEP) with antiretroviral drugs could prove to be an effective intervention strategy if highly efficacious and cost-effective PrEP modalities are identified. We evaluated daily and intermittent PrEP regimens of increasing antiviral activity in a macaque model that closely resembles human transmission. METHODS AND FINDINGS We used a repeat-exposure macaque model with 14 weekly rectal virus challenges. Three drug treatments were given once daily, each to a different group of six rhesus macaques. Group 1 was treated subcutaneously with a human-equivalent dose of emtricitabine (FTC), group 2 received orally the human-equivalent dosing of both FTC and tenofovir-disoproxil fumarate (TDF), and group 3 received subcutaneously a similar dosing of FTC and a higher dose of tenofovir. A fourth group of six rhesus macaques (group 4) received intermittently a PrEP regimen similar to group 3 only 2 h before and 24 h after each weekly virus challenge. Results were compared to 18 control macaques that did not receive any drug treatment. The risk of infection in macaques treated in groups 1 and 2 was 3.8- and 7.8-fold lower than in untreated macaques (p = 0.02 and p = 0.008, respectively). All six macaques in group 3 were protected. Breakthrough infections had blunted acute viremias; drug resistance was seen in two of six animals. All six animals in group 4 that received intermittent PrEP were protected. CONCLUSIONS This model suggests that single drugs for daily PrEP can be protective but a combination of antiretroviral drugs may be required to increase the level of protection. Short but potent int [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"All six macaques in group 3 were protected.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 584, "doc_id": "14260013", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Localization of PIN1 in the Arabidopsis embryo does not require VPS9a\n\nCANDIDATE_ABSTRACT:\nTITLE: Generation of cell polarity in plants links endocytosis, auxin distribution and cell fate decisions\nABSTRACT: Dynamically polarized membrane proteins define different cell boundaries and have an important role in intercellular communication—a vital feature of multicellular development. Efflux carriers for the signalling molecule auxin from the PIN family are landmarks of cell polarity in plants and have a crucial involvement in auxin distribution-dependent development including embryo patterning, organogenesis and tropisms. Polar PIN localization determines the direction of intercellular auxin flow, yet the mechanisms generating PIN polarity remain unclear. Here we identify an endocytosis-dependent mechanism of PIN polarity generation and analyse its developmental implications. Real-time PIN tracking showed that after synthesis, PINs are initially delivered to the plasma membrane in a non-polar manner and their polarity is established by subsequent endocytic recycling. Interference with PIN endocytosis either by auxin or by manipulation of the Arabidopsis Rab5 GTPase pathway prevents PIN polarization. Failure of PIN polarization transiently alters asymmetric auxin distribution during embryogenesis and increases the local auxin response in apical embryo regions. This results in ectopic expression of auxin pathway-associated root-forming master regulators in embryonic leaves and promotes homeotic transformation of leaves to roots. Our results indicate a two-step mechanism for the generation of PIN polar localization and the essential role of endocytosis in this process. It also highlights the link between endocytosis-dependent polarity of individual cells and auxin distribution-dependent cell fate establishment for multicellular patterning.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 700, "doc_id": "4350400", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Febrile seizures reduce the threshold for development of epilepsy.\n\nCANDIDATE_PASSAGE:\nHusbands' involvement in delivery care utilization in rural Bangladesh: A qualitative study BACKGROUND A primary cause of high maternal mortality in Bangladesh is lack of access to professional delivery care. Examining the role of the family, particularly the husband, during pregnancy and childbirth is important to understanding women's access to and utilization of professional maternal health services that can prevent maternal mortality. This qualitative study examines husbands' involvement during childbirth and professional delivery care utilization in a rural sub-district of Netrokona district, Bangladesh. METHODS Using purposive sampling, ten households utilizing a skilled attendant during the birth of the youngest child were selected and matched with ten households utilizing an untrained traditional birth attendant, or dhatri. Households were selected based on a set of inclusion criteria, such as approximate household income, ethnicity, and distance to the nearest hospital. Twenty semi-structured interviews were conducted in Bangla with husbands in these households in June 2010. Interviews were transcribed, translated into English, and analyzed using NVivo 9.0. RESULTS By purposefully selecting households that differed on the type of provider utilized during delivery, common themes--high costs, poor transportation, and long distances to health facilities--were eliminated as sufficient barriers to the utilization of professional delivery care. Divergent themes, namely husbands' social support and perceived social norms, were identified as underlying factors associated with delivery care utilization. We found that husbands whose wives utilized professional delivery care provided emotional, instrumental and informational support to their wives during deliv [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "411", "doc_id": "10854174", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: UCB T cells reduce TCR diversity after transplantation.\n\nCANDIDATE_PASSAGE:\nButyrate greatly enhances derivation of human induced pluripotent stem cells by promoting epigenetic remodeling and the expression of pluripotency-associated genes. We report here that butyrate, a naturally occurring fatty acid commonly used as a nutritional supplement and differentiation agent, greatly enhances the efficiency of induced pluripotent stem (iPS) cell derivation from human adult or fetal fibroblasts. After transient butyrate treatment, the iPS cell derivation efficiency is enhanced by 15- to 51-fold using either retroviral or piggyBac transposon vectors expressing 4 to 5 reprogramming genes. Butyrate stimulation is more remarkable (>100- to 200-fold) on reprogramming in the absence of either KLF4 or MYC transgene. Butyrate treatment did not negatively affect properties of iPS cell lines established by either 3 or 4 retroviral vectors or a single piggyBac DNA transposon vector. These characterized iPS cell lines, including those derived from an adult patient with sickle cell disease by either the piggyBac or retroviral vectors, show normal karyotypes and pluripotency. To gain insights into the underlying mechanisms of butyrate stimulation, we conducted genome-wide gene expression and promoter DNA methylation microarrays and other epigenetic analyses on established iPS cells and cells from intermediate stages of the reprogramming process. By days 6 to 12 during reprogramming, butyrate treatment enhanced histone H3 acetylation, promoter DNA demethylation, and the expression of endogenous pluripotency-associated genes, including DPPA2, whose overexpression partially substitutes for butyrate stimulation. Thus, butyrate as a cell permeable small molecule provides a simple tool to further investigate molecular mechanisms of cellular reprogramming. Mor [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1336", "doc_id": "8150638", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Reduced responsiveness to interleukin-2 in regulatory T cells is associated with greater resistance to autoimmune diseases such as Type 1 Diabetes.\n\nCANDIDATE_PASSAGE:\nType 1 diabetes-associated IL2RA variation lowers IL-2 signaling and contributes to diminished CD4+CD25+ regulatory T cell function. Numerous reports have demonstrated that CD4(+)CD25(+) regulatory T cells (Tregs) from individuals with a range of human autoimmune diseases, including type 1 diabetes, are deficient in their ability to control autologous proinflammatory responses when compared with nondiseased, control individuals. Treg dysfunction could be a primary, causal event or may result from perturbations in the immune system during disease development. Polymorphisms in genes associated with Treg function, such as IL2RA, confer a higher risk of autoimmune disease. Although this suggests a primary role for defective Tregs in autoimmunity, a link between IL2RA gene polymorphisms and Treg function has not been examined. We addressed this by examining the impact of an IL2RA haplotype associated with type 1 diabetes on Treg fitness and suppressive function. Studies were conducted using healthy human subjects to avoid any confounding effects of disease. We demonstrated that the presence of an autoimmune disease-associated IL2RA haplotype correlates with diminished IL-2 responsiveness in Ag-experienced CD4(+) T cells, as measured by phosphorylation of STAT5a, and is associated with lower levels of FOXP3 expression by Tregs and a reduction in their ability to suppress proliferation of autologous effector T cells. These data offer a rationale that contributes to the molecular and cellular mechanisms through which polymorphisms in the IL-2RA gene affect immune regulation, and consequently upon susceptibility to autoimmune and inflammatory diseases.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1029", "doc_id": "11899391", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Ly6C hi monocytes have a lower inflammatory capacity than Ly6C lo monocytes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Subpopulations of mouse blood monocytes differ in maturation stage and inflammatory response.\nABSTRACT: Blood monocytes are well-characterized precursors for macrophages and dendritic cells. Subsets of human monocytes with differential representation in various disease states are well known. In contrast, mouse monocyte subsets have been characterized minimally. In this study we identify three subpopulations of mouse monocytes that can be distinguished by differential expression of Ly-6C, CD43, CD11c, MBR, and CD62L. The subsets share the characteristics of extensive phagocytosis, similar expression of M-CSF receptor (CD115), and development into macrophages upon M-CSF stimulation. By eliminating blood monocytes with dichloromethylene-bisphosphonate-loaded liposomes and monitoring their repopulation, we showed a developmental relationship between the subsets. Monocytes were maximally depleted 18 h after liposome application and subsequently reappeared in the circulation. These cells were exclusively of the Ly-6C(high) subset, resembling bone marrow monocytes. Serial flow cytometric analyses of newly released Ly-6C(high) monocytes showed that Ly-6C expression on these cells was down-regulated while in circulation. Under inflammatory conditions elicited either by acute infection with Listeria monocytogenes or chronic infection with Leishmania major, there was a significant increase in immature Ly-6C(high) monocytes, resembling the inflammatory left shift of granulocytes. In addition, acute peritoneal inflammation recruited preferentially Ly-6C(med-high) monocytes. Taken together, these data identify distinct subpopulations of mouse blood monocytes that differ in maturation stage and capacity to become recruited to inflammatory sites.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In addition, acute peritoneal inflammation recruited preferentially Ly-6C(med-high) monocytes.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 728, "doc_id": "36444198", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Hypocretin neurones suppress panicprone state in rats.\n\nCANDIDATE_PASSAGE:\nCloning of rat uncoupling protein-3 and uncoupling protein-2 cDNAs: their gene expression in rats fed high-fat diet. In order to elucidate energy balance in the skeletal muscle, we cloned cDNA of a homologue of uncoupling protein (UCP) from rat skeletal muscle. We also cloned rat UCP-2 cDNA from rat brown adipose tissue (BAT). The UCP cloned from rat skeletal muscle showed 57% and 72% identity with rat UCP-1 and UCP-2. The mRNA was expressed abundantly in the skeletal muscle, moderately in the BAT, and slightly in the white adipose tissue (WAT) with a major band at 2.5 kb and a minor band at 2.8 kb, while the UCP-2 gene expression was widely detected in the whole body with substantial levels in the WAT and with slight levels in the skeletal muscle and BAT. The rat UCP cloned in the present study showed 86% identity with the recently cloned human UCP-3, which was also expressed abundantly in the skeletal muscle with a signal of 2.4 kb. Therefore, the rat UCP was considered to be rat UCP-3. In rats fed high-fat diet the UCP-3 gene expression was augmented 2-fold in the skeletal muscle while UCP-2 mRNA levels were increased significantly (1.6-fold) in the epididymal WAT. Augmented expression of UCPs may provide defense against high-fat induced obesity and impairment of glucose metabolism.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "537", "doc_id": "20363389", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: NOX2-independent pathways can generate peroxynitrite by reacting with nitrogen intermediates.\n\nCANDIDATE_ABSTRACT:\nTITLE: Altered recognition of antigen is a mechanism of CD8+ T cell tolerance in cancer\nABSTRACT: Antigen-specific CD8+ T-cell tolerance, induced by myeloid-derived suppressor cells (MDSCs), is one of the main mechanisms of tumor escape. Using in vivo models, we show here that MDSCs directly disrupt the binding of specific peptide–major histocompatibility complex (pMHC) dimers to CD8-expressing T cells through nitration of tyrosines in a T-cell receptor (TCR)-CD8 complex. This process makes CD8-expressing T cells unable to bind pMHC and to respond to the specific peptide, although they retain their ability to respond to nonspecific stimulation. Nitration of TCR-CD8 is induced by MDSCs through hyperproduction of reactive oxygen species and peroxynitrite during direct cell-cell contact. Molecular modeling suggests specific sites of nitration that might affect the conformational flexibility of TCR-CD8 and its interaction with pMHC. These data identify a previously unknown mechanism of T-cell tolerance in cancer that is also pertinent to many pathological conditions associated with accumulation of MDSCs.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 834, "doc_id": "5483793", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Pro-inflammatory cytokines are up repressed during tumor development.\n\nCANDIDATE_PASSAGE:\nParaneoplastic thrombocytosis: the secrets of tumor self-promotion. Paraneoplastic thrombocytosis is associated with many solid tumors and often correlates with reduced survival. Recent studies suggest that a pathogenic feed back loop may be operative between platelets and tumor cells, with reciprocal interactions between tumor growth/metastasis and thrombocytosis/platelet activation. Specific molecular pathways have been identified in which tumors can stimulate platelet production and activation; activated platelets can, in turn, promote tumor growth and metastasis. Taken together, these findings provide exciting new potential targets for therapeutic intervention.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "978", "doc_id": "14075252", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: In S. cerevisiae, the absence of RNA surveillance pathways causes sensitivity to high iron conditions.\n\nCANDIDATE_ABSTRACT:\nTITLE: Multiple RNA surveillance pathways limit aberrant expression of iron uptake mRNAs and prevent iron toxicity in S. cerevisiae.\nABSTRACT: Tight regulation of the expression of mRNAs encoding iron uptake proteins is essential to control iron homeostasis and avoid intracellular iron toxicity. We show that many mRNAs encoding iron uptake or iron mobilization proteins are expressed in iron-replete conditions in the absence of the S. cerevisiae RNase III ortholog Rnt1p or of the nuclear exosome component Rrp6p. Extended forms of these mRNAs accumulate in the absence of Rnt1p or of the 5'-->3' exonucleases Xrn1p and Rat1p, showing that multiple degradative pathways contribute to the surveillance of aberrant forms of these transcripts. RNase III-deficient cells are hypersensitive to high iron concentrations, suggesting that Rnt1p-mediated RNA surveillance is required to prevent iron toxicity. These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 565, "doc_id": "16120395", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Adult tissue-resident macrophages are seeded before birth.\n\nCANDIDATE_PASSAGE:\nFate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis. Mononuclear phagocytes, including monocytes, macrophages, and dendritic cells, contribute to tissue integrity as well as to innate and adaptive immune defense. Emerging evidence for labor division indicates that manipulation of these cells could bear therapeutic potential. However, specific ontogenies of individual populations and the overall functional organization of this cellular network are not well defined. Here we report a fate-mapping study of the murine monocyte and macrophage compartment taking advantage of constitutive and conditional CX(3)CR1 promoter-driven Cre recombinase expression. We have demonstrated that major tissue-resident macrophage populations, including liver Kupffer cells and lung alveolar, splenic, and peritoneal macrophages, are established prior to birth and maintain themselves subsequently during adulthood independent of replenishment by blood monocytes. Furthermore, we have established that short-lived Ly6C(+) monocytes constitute obligatory steady-state precursors of blood-resident Ly6C(-) cells and that the abundance of Ly6C(+) blood monocytes dynamically controls the circulation lifespan of their progeny.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "86", "doc_id": "7521113", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: In domesticated populations of Saccharomyces cerevisiae, whole chromosome aneuploidy is very uncommon.\n\nCANDIDATE_PASSAGE:\nQuantitative, genome-wide analysis of eukaryotic replication initiation and termination. Many fundamental aspects of DNA replication, such as the exact locations where DNA synthesis is initiated and terminated, how frequently origins are used, and how fork progression is influenced by transcription, are poorly understood. Via the deep sequencing of Okazaki fragments, we comprehensively document replication fork directionality throughout the S. cerevisiae genome, which permits the systematic analysis of initiation, origin efficiency, fork progression, and termination. We show that leading-strand initiation preferentially occurs within a nucleosome-free region at replication origins. Using a strain in which late origins can be induced to fire early, we show that replication termination is a largely passive phenomenon that does not rely on cis-acting sequences or replication fork pausing. The replication profile is predominantly determined by the kinetics of origin firing, allowing us to reconstruct chromosome-wide timing profiles from an asynchronous culture.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "575", "doc_id": "36606083", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Lamins are found within the inner layer of the mitochondrial membrane of all cells.\n\nCANDIDATE_PASSAGE:\nNeural crest cell lineage segregation in the mouse neural tube. Neural crest (NC) cells arise in the dorsal neural tube (NT) and migrate into the embryo to develop into many different cell types. A major unresolved question is when and how the fate of NC cells is decided. There is widespread evidence for multipotential NC cells, whose fates are decided during or after migration. There is also some evidence that the NC is already divided into subpopulations of discrete precursors within the NT. We have investigated this question in the mouse embryo. We find that a subpopulation of cells on the most dorsomedial aspect of the NT express the receptor tyrosine kinase Kit (previously known as c-kit), emigrate exclusively into the developing dermis, and then express definitive markers of the melanocyte lineage. These are thus melanocyte progenitor cells. They are generated predominantly at the midbrain-hindbrain junction and cervical trunk, with significant numbers also in lower trunk. Other cells within the dorsal NT are Kit-, migrate ventrally, and, from embryonic day 9.5, express the neurotrophin receptor p75. These cells most likely only give rise to ventral NC derivatives such as neurons and glia. The p75+ cells are located ventrolateral to the Kit+ cells in areas of the NT where these two cell types are found. These data provide direct in vivo evidence for NC lineage segregation within the mouse neural tube.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "686", "doc_id": "14333540", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Ca2+ cycling controls whole-body energy homeostasis in beige fat.\n\nCANDIDATE_PASSAGE:\nRelationship between activity levels, aerobic fitness, and body fat in 8- to 10-yr-old children. The relationships between children's activity, aerobic fitness, and fatness are unclear. Indirect estimates of activity, e.g., heart rate (HR) and recall, may mask any associations. The purpose of this study was to assess these relationships by using the Tritrac-R3D, a pedometer, and heart rate. Thirty-four children, ages 8-10 yr, participated in the study. The Tritrac and pedometer were worn for up to 6 days. HR was measured for 1 day. Activity measured by Tritrac or pedometer correlated positively to fitness in the whole group (Tritrac, r = 0.66; pedometer, r = 0.59; P < 0.01) and in boys and girls separately (P < 0.05) and correlated negatively to fatness in the whole group (r = -0.42, P < 0.05). In contrast, HR did not correlate significantly to fitness, and HR of >139 beats/min correlated positively to fatness in girls (r = 0.64, P < 0.05). This suggests that HR is misleading as a measure of activity. This study supports a positive relationship between activity and fitness and suggests a negative relationship between fatness and activity.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "220", "doc_id": "2575938", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Women with a lower birth weight are more likely to develop breast cancer later in life.\n\nCANDIDATE_PASSAGE:\nIdentification and characterization of subpopulations in undifferentiated ES cell culture. Embryonic stem (ES) cells are pluripotent cells derived from the inner cell mass (ICM) and the epiblast, and have been suggested to be a homogeneous population with characteristics intermediate between them. These cells express Oct3/4 and Rex1 genes, which have been used as markers to indicate the undifferentiated state of ES cells. Whereas Oct3/4 is expressed in totipotent and pluripotent cells in the mouse life cycle, Rex1 expression is restricted to the ICM, and is downregulated in pluripotent cell populations in the later stages, i.e. the epiblast and primitive ectoderm (PrE). To address whether ES cells comprise a homogeneous population equivalent to a certain developmental stage of pluripotent cells or a heterogeneous population composed of cells corresponding to various stages of differentiation, we established knock-in ES cell lines in which genes for fluorescent proteins were inserted into the Rex1 and Oct3/4 gene loci to visualize the expression of these genes. We found that undifferentiated ES cells included at least two different populations, Rex1(+)/Oct3/4(+) cells and Rex1(-)/Oct3/4(+) cells. The Rex1(-)/Oct3/4(+) and Rex1(+)/Oct3/4(+) populations could convert into each other in the presence of LIF. In accordance with our assumption that Rex1(+)/Oct3/4(+) cells and Rex1(-)/Oct3/4(+) cells have characteristics similar to those of ICM and early-PrE cells, Rex1(+)/Oct3/4(+) cells predominantly differentiated into primitive ectoderm and contributed to chimera formation, whereas Rex1(-)/Oct3/4(+) cells differentiated into cells of the somatic lineage more efficiently than non-fractionated ES cells in vitro and showed poor ability to contribute to chimera form [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1380", "doc_id": "24530633", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: In young and middle-aged adults, current or remote uses of ADHD medications increase the risk of serious cardiovascular events.\n\nCANDIDATE_PASSAGE:\nADHD medications and risk of serious cardiovascular events in young and middle-aged adults. CONTEXT More than 1.5 million US adults use stimulants and other medications labeled for treatment of attention-deficit/hyperactivity disorder (ADHD). These agents can increase heart rate and blood pressure, raising concerns about their cardiovascular safety. OBJECTIVE To examine whether current use of medications prescribed primarily to treat ADHD is associated with increased risk of serious cardiovascular events in young and middle-aged adults. DESIGN, SETTING, AND PARTICIPANTS Retrospective, population-based cohort study using electronic health care records from 4 study sites (OptumInsight Epidemiology, Tennessee Medicaid, Kaiser Permanente California, and the HMO Research Network), starting in 1986 at 1 site and ending in 2005 at all sites, with additional covariate assessment using 2007 survey data. Participants were adults aged 25 through 64 years with dispensed prescriptions for methylphenidate, amphetamine, or atomoxetine at baseline. Each medication user (n = 150,359) was matched to 2 nonusers on study site, birth year, sex, and calendar year (443,198 total users and nonusers). MAIN OUTCOME MEASURES Serious cardiovascular events, including myocardial infarction (MI), sudden cardiac death (SCD), or stroke, with comparison between current or new users and remote users to account for potential healthy-user bias. RESULTS During 806,182 person-years of follow-up (median, 1.3 years per person), 1357 cases of MI, 296 cases of SCD, and 575 cases of stroke occurred. There were 107,322 person-years of current use (median, 0.33 years), with a crude incidence per 1000 person-years of 1.34 (95% CI, 1.14-1.57) for MI, 0.30 (95% CI, 0.20-0.42) for SCD, and 0.56 (95% CI, 0.4 [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "590", "doc_id": "10984005", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Rapid up-regulation and higher basal expression of interferon-induced genes reduce survival of granule cell neurons that are infected by West Nile virus.\n\nCANDIDATE_ABSTRACT:\nTITLE: Differential innate immune response programs in neuronal subtypes determine susceptibility to infection in the brain by positive stranded RNA viruses\nABSTRACT: Although susceptibility of neurons in the brain to microbial infection is a major determinant of clinical outcome, little is known about the molecular factors governing this vulnerability. Here we show that two types of neurons from distinct brain regions showed differential permissivity to replication of several positive-stranded RNA viruses. Granule cell neurons of the cerebellum and cortical neurons from the cerebral cortex have unique innate immune programs that confer differential susceptibility to viral infection ex vivo and in vivo. By transducing cortical neurons with genes that were expressed more highly in granule cell neurons, we identified three interferon-stimulated genes (ISGs; Ifi27, Irg1 and Rsad2 (also known as Viperin)) that mediated the antiviral effects against different neurotropic viruses. Moreover, we found that the epigenetic state and microRNA (miRNA)-mediated regulation of ISGs correlates with enhanced antiviral response in granule cell neurons. Thus, neurons from evolutionarily distinct brain regions have unique innate immune signatures, which probably contribute to their relative permissiveness to infection.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"By transducing cortical neurons with genes that were expressed more highly in granule cell neurons, we identified three interferon-stimulated genes (ISGs; Ifi27, Irg1 and Rsad2 (also known as Viperin)) that mediated the antiviral effects against different neurotropic viruses.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1021, "doc_id": "9433958", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Increased microtubule acetylation exacerbates LRRK2 Roc-COR domain mutation induced locomotor deficits.\n\nCANDIDATE_ABSTRACT:\nTITLE: Activation of Frontal Neocortical Areas by Vocal Production in Marmosets\nABSTRACT: Primates often rely on vocal communication to mediate social interactions. Although much is known about the acoustic structure of primate vocalizations and the social context in which they are usually uttered, our knowledge about the neocortical control of audio-vocal interactions in primates is still incipient, being mostly derived from lesion studies in squirrel monkeys and macaques. To map the neocortical areas related to vocal control in a New World primate species, the common marmoset, we employed a method previously used with success in other vertebrate species: Analysis of the expression of the immediate early gene Egr-1 in freely behaving animals. The neocortical distribution of Egr-1 immunoreactive cells in three marmosets that were exposed to the playback of conspecific vocalizations and vocalized spontaneously (H/V group) was compared to data from three other marmosets that also heard the playback but did not vocalize (H/n group). The anterior cingulate cortex, the dorsomedial prefrontal cortex and the ventrolateral prefrontal cortex presented a higher number of Egr-1 immunoreactive cells in the H/V group than in H/n animals. Our results provide direct evidence that the ventrolateral prefrontal cortex, the region that comprises Broca's area in humans and has been associated with auditory processing of species-specific vocalizations and orofacial control in macaques, is engaged during vocal output in marmosets. Altogether, our results support the notion that the network of neocortical areas related to vocal communication in marmosets is quite similar to that of Old world primates. The vocal production role played by these areas and their importance for the evolution of speech in primates are discussed.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 612, "doc_id": "1391126", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: TMEM27 is a marker for beta cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tmem27: a cleaved and shed plasma membrane protein that stimulates pancreatic beta cell proliferation.\nABSTRACT: The signals and molecular mechanisms that regulate the replication of terminally differentiated beta cells are unknown. Here, we report the identification and characterization of transmembrane protein 27 (Tmem27, collectrin) in pancreatic beta cells. Expression of Tmem27 is reduced in Tcf1(-/-) mice and is increased in islets of mouse models with hypertrophy of the endocrine pancreas. Tmem27 forms dimers and its extracellular domain is glycosylated, cleaved and shed from the plasma membrane of beta cells. This cleavage process is beta cell specific and does not occur in other cell types. Overexpression of full-length Tmem27, but not the truncated or soluble protein, leads to increased thymidine incorporation, whereas silencing of Tmem27 using RNAi results in a reduction of cell replication. Furthermore, transgenic mice with increased expression of Tmem27 in pancreatic beta cells exhibit increased beta cell mass. Our results identify a pancreatic beta cell transmembrane protein that regulates cell growth of pancreatic islets.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Furthermore, transgenic mice with increased expression of Tmem27 in pancreatic beta cells exhibit increased beta cell mass.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1133, "doc_id": "24142891", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Mutations in RIM1 raise levels of IME1 RNA.\n\nCANDIDATE_PASSAGE:\nDrosophila MICAL regulates myofilament organization and synaptic structure The overall size and structure of a synaptic terminal is an important determinant of its function. In a large-scale mutagenesis screen, designed to identify Drosophila mutants with abnormally structured neuromuscular junctions (NMJs), we discovered mutations in Drosophila mical, a conserved gene encoding a multi-domain protein with a N-terminal monooxygenase domain. In mical mutants, synaptic boutons do not sprout normally over the muscle surface and tend to form clusters along synaptic branches and at nerve entry sites. Consistent with high expression of MICAL in somatic muscles, immunohistochemical stainings reveal that the subcellular localization and architecture of contractile muscle filaments are dramatically disturbed in mical mutants. Instead of being integrated into a regular sarcomeric pattern, actin and myosin filaments are disorganized and accumulate beneath the plasmamembrane. Whereas contractile elements are strongly deranged, the proposed organizer of sarcomeric structure, D-Titin, is much less affected. Transgenic expression of interfering RNA molecules demonstrates that MICAL is required in muscles for the higher order arrangement of myofilaments. Ultrastructural analysis confirms that myosin-rich thick filaments enter submembranous regions and interfere with synaptic development, indicating that the disorganized myofilaments may cause the synaptic growth phenotype. As a model, we suggest that the filamentous network around synaptic boutons restrains the spreading of synaptic branches.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "816", "doc_id": "16562534", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Students who perform poorly in the early years of medical school are at increased risk for professional misconduct later in their careers.\n\nCANDIDATE_ABSTRACT:\nTITLE: Risk factors at medical school for subsequent professional misconduct: multicentre retrospective case-control study\nABSTRACT: OBJECTIVE To determine whether there are risk factors in a doctor's time at medical school that are associated with subsequent professional misconduct. DESIGN Matched case-control study. Setting Records from medical schools and the General Medical Council (GMC). PARTICIPANTS 59 doctors who had graduated from any one of eight medical schools in the United Kingdom in 1958-97 and had a proved finding of serious professional misconduct in GMC proceedings in 1999-2004 (cases); 236 controls (four for each case) were selected by systematic sampling from matching graduation cohorts. Case-control status was revealed by the GMC after completion of data entry. MAIN OUTCOME MEASURE Odds ratios for being a \"case,\" with multivariable conditional logistic regression of potential risk factors including pre-admission characteristics and progress during the course. These data were obtained from anonymised copies of the students' progress files held by their original medical schools. RESULTS Univariate conditional logistic regression analysis found that cases were more likely to be men, to be of lower estimated social class, and to have had academic difficulties during their medical course, especially in the early years. Multivariable analysis showed that male sex (odds ratio 9.80, 95% confidence interval 2.43 to 39.44, P=0.001), lower social class (4.28, 1.52 to 12.09, P=0.006), and failure of early or preclinical examinations (5.47, 2.17 to 13.79, P<0.001) were independently associated with being a case. CONCLUSIONS This small study suggests that male sex, a lower socioeconomic background, and early academic difficulties at medical school could be risk factors for subsequent professional misconduct. The findings are preliminary and should be interpreted with caution. Most do [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Multivariable analysis showed that male sex (odds ratio 9.80, 95% confidence interval 2.43 to 39.44, P=0.001), lower social class (4.28, 1.52 to 12.09, P=0.006), and failure of early or preclinical examinations (5.47, 2.17 to 13.79, P<0.001) were independently associated with being a case.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1105, "doc_id": "6710713", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Lamins have no effect on nuclear membrane structure maintenance.\n\nCANDIDATE_PASSAGE:\nRibosome biogenesis: Achilles heel of cancer? It is long been known that cancer and non-cancer cells can be distinguished on the basis of their nucleolar morphologies. As early as the 19th century, it was reported that cancer cells have larger and more irregularly shaped nucleoli. Since then, pathologists have used nucleolar morphology to predict the clinical outcome [1]. Nucleolar morphology is altered due to the up-regulation of ribosomal gene transcription. Within nucleoli, ribosomal genes (rDNA) are transcribed by RNA polymerase I (pol I). The pre-ribosomal RNA (pre-rRNA) transcripts are subsequently modified and processed into the mature 18S, 5.8S and 28S rRNAs. 5S rRNA is transcribed by RNA polymerase III in the nucleoplasm. Together with the ribosomal proteins, the 5S rRNA is imported into the nucleolus where 40S and 60S ribosomal subunits are assembled prior to export to the cytoplasm [1, 2]. Oncogenes such as c-Myc can both directly and indirectly upregulate rDNA transcription, while tumour suppressors like p53 and Rb suppress ribosome biogenesis. Mutations in these genes not only result in deregulated cell cycle control, but also upregulated ribosome biogenesis. In addition to ribosome biogenesis, the nucleolus is a key cellular stress sensor and plays a central role in p53 activation [1, 2]. The increased translational capacity of cancer cells enables them to maintain higher proliferation rates. As stated by Ruggero, “compared with normal cells, cancer cells may be addicted to increases in ribosome biogenesis and number” [1]. This provides new therapeutic opportunities. As it turns out many chemotherapeutic drugs used in cancer treatment already inhibit ribosome biogenesis. In one recent survey it was shown that 20 out of 36 drugs in clinical use [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "688", "doc_id": "6670101", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The DdrB protein from Deinococcus radiodurans functions as a pentamer.\n\nCANDIDATE_PASSAGE:\nThe structure of DdrB from Deinococcus: a new fold for single-stranded DNA binding proteins Deinococcus spp. are renowned for their amazing ability to recover rapidly from severe genomic fragmentation as a result of exposure to extreme levels of ionizing radiation or desiccation. Despite having been originally characterized over 50 years ago, the mechanism underlying this remarkable repair process is still poorly understood. Here, we report the 2.8 A structure of DdrB, a single-stranded DNA (ssDNA) binding protein unique to Deinococcus spp. that is crucial for recovery following DNA damage. DdrB forms a pentameric ring capable of binding single-stranded but not double-stranded DNA. Unexpectedly, the crystal structure reveals that DdrB comprises a novel fold that is structurally and topologically distinct from all other single-stranded binding (SSB) proteins characterized to date. The need for a unique ssDNA binding function in response to severe damage, suggests a distinct role for DdrB which may encompass not only standard SSB protein function in protection of ssDNA, but also more specialized roles in protein recruitment or DNA architecture maintenance. Possible mechanisms of DdrB action in damage recovery are discussed.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1162", "doc_id": "15305881", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Adult tissue-resident macrophages are seeded before birth.\n\nCANDIDATE_PASSAGE:\nThe SMC5/6 complex maintains telomere length in ALT cancer cells through SUMOylation of telomere-binding proteins Most cancer cells activate telomerase to elongate telomeres and achieve unlimited replicative potential. Some cancer cells cannot activate telomerase and use telomere homologous recombination (HR) to elongate telomeres, a mechanism termed alternative lengthening of telomeres (ALT). A hallmark of ALT cells is the recruitment of telomeres to PML bodies (termed APBs). Here, we show that the SMC5/6 complex localizes to APBs in ALT cells and is required for targeting telomeres to APBs. The MMS21 SUMO ligase of the SMC5/6 complex SUMOylates multiple telomere-binding proteins, including TRF1 and TRF2. Inhibition of TRF1 or TRF2 SUMOylation prevents APB formation. Depletion of SMC5/6 subunits by RNA interference inhibits telomere HR, causing telomere shortening and senescence in ALT cells. Thus, the SMC5/6 complex facilitates telomere HR and elongation in ALT cells by promoting APB formation through SUMOylation of telomere-binding proteins.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "85", "doc_id": "7915836", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Stroke patients with prior use of direct oral anticoagulants have a higher risk of in-hospital mortality than stroke patients with prior use of warfarin.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association of Intracerebral Hemorrhage Among Patients Taking Non–Vitamin K Antagonist vs Vitamin K Antagonist Oral Anticoagulants With In-Hospital Mortality\nABSTRACT: Importance Although non–vitamin K antagonist oral anticoagulants (NOACs) are increasingly used to prevent thromboembolic disease, there are limited data on NOAC-related intracerebral hemorrhage (ICH). Objective To assess the association between preceding oral anticoagulant use (warfarin, NOACs, and no oral anticoagulants [OACs]) and in-hospital mortality among patients with ICH. Design, Setting, and Participants Retrospective cohort study of 141 311 patients with ICH admitted from October 2013 to December 2016 to 1662 Get With The Guidelines–Stroke hospitals. Exposures Anticoagulation therapy before ICH, defined as any use of OACs within 7 days prior to hospital arrival. Main Outcomes and Measures In-hospital mortality. Results Among 141 311 patients with ICH (mean [SD] age, 68.3 [15.3] years; 48.1% women), 15 036 (10.6%) were taking warfarin and 4918 (3.5%) were taking NOACs preceding ICH, and 39 585 (28.0%) and 5783 (4.1%) were taking concomitant single and dual antiplatelet agents, respectively. Patients with prior use of warfarin or NOACs were older and had higher prevalence of atrial fibrillation and prior stroke. Acute ICH stroke severity (measured by the National Institutes of Health Stroke Scale) was not significantly different across the 3 groups (median, 9 [interquartile range, 2-21] for warfarin, 8 [2-20] for NOACs, and 8 [2-19] for no OACs). The unadjusted in-hospital mortality rates were 32.6% for warfarin, 26.5% for NOACs, and 22.5% for no OACs. Compared with patients without prior use of OACs, the risk of in-hospital mortality was higher among patients with prior use of warfarin (adjusted risk difference [ARD], 9.0% [97.5% CI, 7.9% to 10.1%]; adjusted odds ratio [AOR], 1.62 [97.5% CI, 1.53 to 1.71]) and higher among patients with prior use of [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Compared with patients with prior use of warfarin, patients with prior use of NOACs had a lower risk of in-hospital mortality (ARD, −5.7% [97.5% CI, −7.3% to −4.2%]; AOR, 0.75 [97.5% CI, 0.69 to 0.81]).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1103, "doc_id": "3898784", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Expression of oncolytic virus antigens as peptides makes relapse more likely.\n\nCANDIDATE_ABSTRACT:\nTITLE: Detecting and targeting tumor relapse by its resistance to innate effectors at early recurrence\nABSTRACT: Tumor recurrence represents a major clinical challenge. Our data show that emergent recurrent tumors acquire a phenotype radically different from that of their originating primary tumors. This phenotype allows them to evade a host-derived innate immune response elicited by the progression from minimal residual disease (MRD) to actively growing recurrence. Screening for this innate response predicted accurately in which mice recurrence would occur. Premature induction of recurrence resensitized MRD to the primary therapy, suggesting a possible paradigm shift for clinical treatment of dormant disease in which the current expectant approach is replaced with active attempts to uncover MRD before evolution of the escape phenotype is complete. By combining screening with second-line treatments targeting innate insensitivity, up to 100% of mice that would have otherwise relapsed were cured. These data may open new avenues for early detection and appropriately timed, highly targeted treatment of tumor recurrence irrespective of tumor type or frontline treatment.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 403, "doc_id": "1921218", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Cost effectiveness evaluations based on cRCT data accurately reflect prices for patients in actual clinical practice.\n\nCANDIDATE_ABSTRACT:\nTITLE: A Comparison of Cost Effectiveness Using Data from Randomized Trials or Actual Clinical Practice: Selective Cox-2 Inhibitors as an Example\nABSTRACT: BACKGROUND Data on absolute risks of outcomes and patterns of drug use in cost-effectiveness analyses are often based on randomised clinical trials (RCTs). The objective of this study was to evaluate the external validity of published cost-effectiveness studies by comparing the data used in these studies (typically based on RCTs) to observational data from actual clinical practice. Selective Cox-2 inhibitors (coxibs) were used as an example. METHODS AND FINDINGS The UK General Practice Research Database (GPRD) was used to estimate the exposure characteristics and individual probabilities of upper gastrointestinal (GI) events during current exposure to nonsteroidal anti-inflammatory drugs (NSAIDs) or coxibs. A basic cost-effectiveness model was developed evaluating two alternative strategies: prescription of a conventional NSAID or coxib. Outcomes included upper GI events as recorded in GPRD and hospitalisation for upper GI events recorded in the national registry of hospitalisations (Hospital Episode Statistics) linked to GPRD. Prescription costs were based on the prescribed number of tables as recorded in GPRD and the 2006 cost data from the British National Formulary. The study population included over 1 million patients prescribed conventional NSAIDs or coxibs. Only a minority of patients used the drugs long-term and daily (34.5% of conventional NSAIDs and 44.2% of coxibs), whereas coxib RCTs required daily use for at least 6-9 months. The mean cost of preventing one upper GI event as recorded in GPRD was US$104k (ranging from US$64k with long-term daily use to US$182k with intermittent use) and US$298k for hospitalizations. The mean costs (for GPRD events) over calendar time were US$58k during 1990-1993 and US$174k during 2002-2005. Using RCT data rather [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS The published cost-effectiveness analyses of coxibs lacked external validity, did not represent patients in actual clinical practice, and should not have been used to inform prescribing policies.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 290, "doc_id": "15048300", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Auditory entrainment is strengthened when people see congruent visual and auditory information.\n\nCANDIDATE_ABSTRACT:\nTITLE: Auditory Cortex Tracks Both Auditory and Visual Stimulus Dynamics Using Low-Frequency Neuronal Phase Modulation\nABSTRACT: Integrating information across sensory domains to construct a unified representation of multi-sensory signals is a fundamental characteristic of perception in ecological contexts. One provocative hypothesis deriving from neurophysiology suggests that there exists early and direct cross-modal phase modulation. We provide evidence, based on magnetoencephalography (MEG) recordings from participants viewing audiovisual movies, that low-frequency neuronal information lies at the basis of the synergistic coordination of information across auditory and visual streams. In particular, the phase of the 2-7 Hz delta and theta band responses carries robust (in single trials) and usable information (for parsing the temporal structure) about stimulus dynamics in both sensory modalities concurrently. These experiments are the first to show in humans that a particular cortical mechanism, delta-theta phase modulation across early sensory areas, plays an important \"active\" role in continuously tracking naturalistic audio-visual streams, carrying dynamic multi-sensory information, and reflecting cross-sensory interaction in real time.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 141, "doc_id": "6955746", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Ultra high risk (UHR) for psychosis criteria: are there different levels of risk for transition to psychosis?\n\nABSTRACT:\nThe ultra high risk (UHR) for psychosis criteria have been validated in a number of studies. However, it is not known whether particular UHR criteria (Attenuated Psychotic Symptoms (APS), Brief Limited Intermittent Psychotic Symptoms (BLIPS) or Trait vulnerability criteria), or combination of criteria, is associated with a higher risk of transition to psychosis. The current study investigated this issue over a 6-month follow-up period. We hypothesised that the risk of transition would increase in the following order: Trait alone", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Women with a higher birth weight are more likely to develop breast cancer later in life.\n\nCANDIDATE_PASSAGE:\nRole of birthweight in the etiology of breast cancer. Breast cancer may originate in utero. We reviewed the available evidence on the association between birthweight and the risk of breast cancer. To date, 26 research papers addressing this issue have been published. The majority of studies identified a positive link between birthweight and premenopausal, but not postmenopausal, breast cancer. The relative risk estimate for breast cancer comparing women with high birthweight to women with low birthweight combining all studies including both pre- and postmenopausal breast cancer was 1.23 (95% confidence interval 1.13-1.34). The mechanisms underlying this association likely include elevated levels of growth factors that may increase the number of susceptible stem cells in the mammary gland or initiate tumors through DNA mutations. Loss of imprinting (LOI) of growth hormone genes relevant for intrauterine growth, such as insulin-like growth factor 2 (IGF2), leads to abnormally high levels of these hormones evidenced by high birthweight. LOI of IGF2 has also been found in mammary tumor tissue. The role of environmental factors that stimulate such epigenetic regulation of gene expression remains to be elucidated.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1379", "doc_id": "27123743", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Removal of H3K9me3 by ectopic expression of other H3K9 demethylases decreases reprogramming efficiency in SCNT experiments.\n\nCANDIDATE_ABSTRACT:\nTITLE: Landscape of genetic lesions in 944 patients with myelodysplastic syndromes\nABSTRACT: High-throughput DNA sequencing significantly contributed to diagnosis and prognostication in patients with myelodysplastic syndromes (MDS). We determined the biological and prognostic significance of genetic aberrations in MDS. In total, 944 patients with various MDS subtypes were screened for known/putative mutations/deletions in 104 genes using targeted deep sequencing and array-based genomic hybridization. In total, 845/944 patients (89.5%) harbored at least one mutation (median, 3 per patient; range, 0-12). Forty-seven genes were significantly mutated with TET2, SF3B1, ASXL1, SRSF2, DNMT3A, and RUNX1 mutated in >10% of cases. Many mutations were associated with higher risk groups and/or blast elevation. Survival was investigated in 875 patients. By univariate analysis, 25/48 genes (resulting from 47 genes tested significantly plus PRPF8) affected survival (P<0.05). The status of 14 genes combined with conventional factors revealed a novel prognostic model ('Model-1') separating patients into four risk groups ('low', 'intermediate', 'high', 'very high risk') with 3-year survival of 95.2, 69.3, 32.8, and 5.3% (P<0.001). Subsequently, a 'gene-only model' ('Model-2') was constructed based on 14 genes also yielding four significant risk groups (P<0.001). Both models were reproducible in the validation cohort (n=175 patients; P<0.001 each). Thus, large-scale genetic and molecular profiling of multiple target genes is invaluable for subclassification and prognostication in MDS patients.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1034, "doc_id": "2359152", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Do methamphetamine dependent individuals show attenuated brain response to pleasant interoceptive stimuli?\n\nABSTRACT:\nMechano-receptive C-fiber (MR-CF) stimulation via slow stroking of C-fiber rich skin areas can be used to probe the relationship between reward and interoception. Individuals with substance use disorders show impaired reward processing, and dysfunctional interoceptive processing of MR-CF may contribute to this dysfunction. This study predicted that methamphetamine dependent (MD) individuals would exhibit altered responses to MR-CF stimulation in brain regions important for interoception. Recently abstinent MD (n=25) and comparison (CTL, n=17) subjects received a pleasant interoceptive stimulus (\"Soft Touch\" consisting of a slow brush stroke) to the palm or forearm during functional magnetic resonance imaging. Subjects were provided with cues signaling stimulation to examine anticipatory and stimulus-related processing. Subjective responses were measured using visual analog scales (VAS). Groups were similar on behavioral performance and ratings of the interoceptive stimuli, yet MD exhibited lower anterior insula, dorsal striatum, and thalamus activation than CTL, across anticipation and soft touch conditions. The lower the anterior insula activation, the faster the reaction time across conditions in MD, whereas the opposite pattern was evident in CTL. Striatal activation in MD was greater than CTL during anticipation, but lower during soft touch. Greater striatal attenuation was associated with higher VAS pleasantness ratings of soft touch.", "output": "{\"label\": \"yes\", \"rationale\": \"MD expend fewer brain processing resources during soft touch, a form of positively-valenced interoceptive stimuli, in brain areas that are important for both interoception and reward. Future studies will ascertain if sustained abstinence from methamphetamine use can normalize aberrant neural interoceptive processing.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 23806873, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Human embryonic stem cells give rise to cell types from all three embryonic germ layers.\n\nCANDIDATE_PASSAGE:\nEstablishment and in vitro differentiation of a new embryonic stem cell line from human blastocyst. Embryonic stem cells have the ability to remain undifferentiated and proliferate indefinitely in vitro while maintaining the potential to differentiate into derivatives of all three embryonic germ layers. These cells have, therefore, potential for in vitro differentiation studies, gene function, and so on. The aim of this study was to produce a human embryonic stem cell line. An inner cell mass of a human blastocyst was separated and cultured on mouse embryonic fibroblasts in embryonic stem cell medium with related additives. The established line was evaluated by morphology; passaging; freezing and thawing; alkaline phosphatase; Oct-4 expression; anti-surface markers including Tra-1-60 and Tra-1-81; and karyotype and spontaneous differentiation. Differentiated cardiomyocytes and neurons were evaluated by transmission electron microscopy and immunocytochemistry. Here, we report the derivation of a new embryonic stem cell line (Royan H1) from a human blastocyst that remains undifferentiated in morphology during continuous passaging for more than 30 passages, maintains a normal XX karyotype, is viable after freezing and thawing, and expresses alkaline phosphatase, Oct-4, Tra-1-60, and Tra-1-81. These cells remain undifferentiated when grown on mouse embryonic fibroblast feeder layers in the presence or absence of recombinant human leukemia inhibitory factor. Royan H1 cells can differentiate in vitro in the absence of feeder cells and can produce embryoid bodies that can further differentiate into beating cardiomyocytes as well as neurons. These results define Royan H1 cells as a new human embryonic stem cell line.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "529", "doc_id": "36651210", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does overexpression of human PHEX under the human beta-actin promoter fully rescue the Hyp mouse phenotype?\n\nABSTRACT:\nXLH in humans and the Hyp phenotype in mice are caused by inactivating Phex mutations. Overexpression of human PHEX under the human beta-actin promoter in Hyp mice rescued the bone phenotype almost completely, but did not affect phosphate homeostasis, suggesting that different, possibly independent, pathophysiological mechanisms contribute to hyperphosphaturia and bone abnormalities in XLH. Mutations in PHEX, a phosphate-regulating gene with homologies to endopeptidases on the X chromosome, are responsible for X-linked hypophosphatemia (XLH) in humans, and its mouse homologs, Hyp, Phex(Hyp-2J), Phex(Hyp-Duk), Gy, and Ska1. PHEX is thought to inactivate a phosphaturic factor, which may be fibroblast growth factor 23 (FGF)-23. Consistent with this hypothesis, FGF-23 levels were shown to be elevated in most patients with XLH and in Hyp mice. The aim of this study was, therefore, to examine whether transgenic overexpression of PHEX under the human beta-actin promoter would rescue the Hyp phenotype. We tested this hypothesis by generating two mouse lines expressing human PHEX under the control of a human beta-actin promoter (PHEX-tg). With the exception of brain, RT-PCR analyses showed transgene expression in all tissues examined. PHEX protein, however, was only detected in bone, muscle, lung, skin, and heart. To assess the role of the mutant PHEX, we crossed female heterozygous Hyp mice with male heterozygous PHEX-tg mice to obtain wildtype (WT), PHEX-tg, Hyp, and Hyp/PHEX-tg offspring, which were examined at 3 months of age. PHEX-tg mice exhibited normal bone and mineral ion homeostasis. Hyp mice showed the known phenotype with reduced body weight, hypophosphatemia, hyperphosphaturia, and rickets. Hyp/PHEX-tg mice had almost normal body weight relative to WT co [TRUNCATED]", "output": "{\"label\": \"no\", \"rationale\": \"Our data suggest that different, possibly independent, pathophysiological mechanisms contribute to renal phosphate wasting and bone abnormalities in Hyp and XLH.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 15940367, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Deletion of ATM and Rad3 related protein is not predictive of acute tissue loss.\n\nCANDIDATE_PASSAGE:\nDeletion of the developmentally essential gene ATR in adult mice leads to age-related phenotypes and stem cell loss. Developmental abnormalities, cancer, and premature aging each have been linked to defects in the DNA damage response (DDR). Mutations in the ATR checkpoint regulator cause developmental defects in mice (pregastrulation lethality) and humans (Seckel syndrome). Here we show that eliminating ATR in adult mice leads to defects in tissue homeostasis and the rapid appearance of age-related phenotypes, such as hair graying, alopecia, kyphosis, osteoporosis, thymic involution, fibrosis, and other abnormalities. Histological and genetic analyses indicate that ATR deletion causes acute cellular loss in tissues in which continuous cell proliferation is required for maintenance. Importantly, thymic involution, alopecia, and hair graying in ATR knockout mice were associated with dramatic reductions in tissue-specific stem and progenitor cells and exhaustion of tissue renewal and homeostatic capacity. In aggregate, these studies suggest that reduced regenerative capacity in adults via deletion of a developmentally essential DDR gene is sufficient to cause the premature appearance of age-related phenotypes.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "325", "doc_id": "40349336", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The density of cytokine receptor bearing cells affects the distance over which cytokines act.\n\nCANDIDATE_ABSTRACT:\nTITLE: Lpcat3-dependent production of arachidonoyl phospholipids is a key determinant of triglyceride secretion\nABSTRACT: The role of specific phospholipids (PLs) in lipid transport has been difficult to assess due to an inability to selectively manipulate membrane composition in vivo. Here we show that the phospholipid remodeling enzyme lysophosphatidylcholine acyltransferase 3 (Lpcat3) is a critical determinant of triglyceride (TG) secretion due to its unique ability to catalyze the incorporation of arachidonate into membranes. Mice lacking Lpcat3 in the intestine fail to thrive during weaning and exhibit enterocyte lipid accumulation and reduced plasma TGs. Mice lacking Lpcat3 in the liver show reduced plasma TGs, hepatosteatosis, and secrete lipid-poor very low-density lipoprotein (VLDL) lacking arachidonoyl PLs. Mechanistic studies indicate that Lpcat3 activity impacts membrane lipid mobility in living cells, suggesting a biophysical basis for the requirement of arachidonoyl PLs in lipidating lipoprotein particles. These data identify Lpcat3 as a key factor in lipoprotein production and illustrate how manipulation of membrane composition can be used as a regulatory mechanism to control metabolic pathways.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1210, "doc_id": "1910120", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Knockout proximal tubule-specific deletion of the BMP receptor Alk3 causes epithelial damage.\n\nCANDIDATE_ABSTRACT:\nTITLE: Long-term outcome of patients with asystole induced by head-up tilt test.\nABSTRACT: AIMS To analyse the long-term outcome of the largest reported cohort of patients presenting asystole during head-up tilt test. METHODS AND RESULTS Since 1990, 1322 patients with syncope of unknown origin have undergone tilt-table testing. Of those, 330 patients (24 X 9%) presented an abnormal response (syncope or pre-syncope). Furthermore, 58 of those patients (17 X 5%) suffered a period of asystole (> or = 3000 ms) during the test. Asystole (median (interquartile range)) lasted 10 (4, 19 X 2) s (range 3-90). Two different protocols (angles) of tilting (Westminster (60 degrees) n=1124; isoproterenol (80 degrees) n=198)) influenced the time to the syncopal episode (13 (6 X 5, 20 X 5) vs 2 (1, 6 X 5) min, P=0,0005) but not the duration of the asystole. During this period, therapy for asystole featured three different stages: first patients were treated with pacemakers; later drug therapy (metoprolol and/or etilefrine) was recommended; lastly (from 1995), no specific treatment was given. In a cohort age- and gender-matched study, those patients without were compared to those with asystole in a 2:1 basis. During 40 X 7 months of follow-up (17 X 7, 66 X 8), 12 patients (20 X 6%) with asystole had syncopal recurrences. Furthermore, 34 patients (28 X 8%) without asystole presented syncopal episodes during a follow-up of 51 X 6 months (29 X 3, 73 X 1) (P=ns). The Kaplan-Meier analysis in patients with and without asystole showed a mean time free of recurrence of 92 X 6 +/- 6 months vs 82 X 6 +/- 4 X 7 months (P=ns). The previous number of syncopes had a significant relationship with recurrences (P=0 X 002), but not therapy. There were no cardiac related deaths. CONCLUSIONS (1) Asystole during head-up tilt test does not imply a malignant outcome and syncope recurrenc [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 670, "doc_id": "323335", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Vaccinating the gastrointestinal tract induces protection of rectal and vaginal mucosa.\n\nCANDIDATE_ABSTRACT:\nTITLE: Large intestine-targeted nanoparticle-releasing oral vaccine to control genitorectal viral infection\nABSTRACT: Both rectal and vaginal mucosal surfaces serve as transmission routes for pathogenic microorganisms. Vaccination through large intestinal mucosa, previously proven protective for both of these mucosal sites in animal studies, can be achieved successfully by direct intracolorectal (i.c.r.) administration, but this route is clinically impractical. Oral vaccine delivery seems preferable but runs the risk of the vaccine's destruction in the upper gastrointestinal tract. Therefore, we designed a large intestine-targeted oral delivery with pH-dependent microparticles containing vaccine nanoparticles, which induced colorectal immunity in mice comparably to colorectal vaccination and protected against rectal and vaginal viral challenge. Conversely, vaccine targeted to the small intestine induced only small intestinal immunity and provided no rectal or vaginal protection, demonstrating functional compartmentalization within the gut mucosal immune system. Therefore, using this oral vaccine delivery system to target the large intestine, but not the small intestine, may represent a feasible new strategy for immune protection of rectal and vaginal mucosa.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Therefore, using this oral vaccine delivery system to target the large intestine, but not the small intestine, may represent a feasible new strategy for immune protection of rectal and vaginal mucosa.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1356, "doc_id": "13764090", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Rhythmic expression of Cry1 translates directly into a circadian regulation of cAMP signaling in hepatic glucose metabolism.\n\nCANDIDATE_ABSTRACT:\nTITLE: Specific inhibition of cyclin-dependent kinase 4/6 by PD 0332991 and associated antitumor activity in human tumor xenografts.\nABSTRACT: PD 0332991 is a highly specific inhibitor of cyclin-dependent kinase 4 (Cdk4) (IC50, 0.011 micromol/L) and Cdk6 (IC50, 0.016 micromol/L), having no activity against a panel of 36 additional protein kinases. It is a potent antiproliferative agent against retinoblastoma (Rb)-positive tumor cells in vitro, inducing an exclusive G1 arrest, with a concomitant reduction of phospho-Ser780/Ser795 on the Rb protein. Oral administration of PD 0332991 to mice bearing the Colo-205 human colon carcinoma produces marked tumor regression. Therapeutic doses of PD 0332991 cause elimination of phospho-Rb and the proliferative marker Ki-67 in tumor tissue and down-regulation of genes under the transcriptional control of E2F. The results indicate that inhibition of Cdk4/6 alone is sufficient to cause tumor regression and a net reduction in tumor burden in some tumors.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1045, "doc_id": "864491", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: 7-day-old adult Caenorhabditis elegans exhibit approximately 75% of the learning capacity seen in 1-day old adults.\n\nCANDIDATE_PASSAGE:\nDeletion of the developmentally essential gene ATR in adult mice leads to age-related phenotypes and stem cell loss. Developmental abnormalities, cancer, and premature aging each have been linked to defects in the DNA damage response (DDR). Mutations in the ATR checkpoint regulator cause developmental defects in mice (pregastrulation lethality) and humans (Seckel syndrome). Here we show that eliminating ATR in adult mice leads to defects in tissue homeostasis and the rapid appearance of age-related phenotypes, such as hair graying, alopecia, kyphosis, osteoporosis, thymic involution, fibrosis, and other abnormalities. Histological and genetic analyses indicate that ATR deletion causes acute cellular loss in tissues in which continuous cell proliferation is required for maintenance. Importantly, thymic involution, alopecia, and hair graying in ATR knockout mice were associated with dramatic reductions in tissue-specific stem and progenitor cells and exhaustion of tissue renewal and homeostatic capacity. In aggregate, these studies suggest that reduced regenerative capacity in adults via deletion of a developmentally essential DDR gene is sufficient to cause the premature appearance of age-related phenotypes.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "20", "doc_id": "40349336", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Mice without IFN-γ or its receptor are resistant to EAM induced with α-MyHC/CFA.\n\nCANDIDATE_PASSAGE:\nParathyroid hormone induces E4bp4 messenger ribonucleic acid expression primarily through cyclic adenosine 3',5'-monophosphate signaling in osteoblasts. PTH binding to its receptor activates protein kinase A (PKA), protein kinase C (PKC), and calcium signaling to induce transcription of primary response genes in osteoblasts. Adenovirus E4 promoter-binding protein/nuclear factor regulated by IL-3 (E4BP4/NFIL3), a transcriptional repressor, is a PTH-induced primary response gene in primary mouse osteoblasts (MOBs). Here we investigate the signaling pathway(s) that lead to PTH induction of E4bp4 mRNA expression. Ten and 100 nm PTH induced maximum E4bp4 expression in MOBs. Forskolin (FSK), an adenylate cyclase inducer, 8-bromo-cAMP, a cAMP analog, and phorbol myristate acetate, a PKC activator, increased E4bp4 mRNA levels, whereas ionomycin, a calcium ionophore, had no effect. Pretreatment of cells with 30 microm H89, a PKA inhibitor, strongly inhibited PTH- and FSK-induced E4bp4 expression. In contrast, overnight pretreatment with 1 microm phorbol myristate acetate to down-regulate PKC signaling did not alter PTH and FSK effects. Moreover, PTH (3-34) that does not activate cAMP signaling did not increase E4bp4 expression. Prostaglandin E(2), which signals through cAMP, increased E4bp4 mRNA at all doses, whereas prostaglandin F(2alpha) that primarily activates PKC and calcium signaling, induced E4bp4 only at high doses and fluprostenol that only activates PKC and calcium signaling, had no effect. Finally, 80 microg/kg PTH (1-34) ip injection induced E4bp4 mRNA expression at 1 h in mice. In contrast, 80 microg/kg PTH (3-34) had no effect. Our data suggest that PTH-induced E4bp4 mRNA expression is mediated primarily through cAMP-PKA signaling in vitro and in vivo. [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "783", "doc_id": "21199527", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pure neural progenitor cell (NPC) populations can only be obtained from cell cultures that undergo passaging, filtration, or other isolation and cell sorting methods.\n\nCANDIDATE_ABSTRACT:\nTITLE: Niche-Independent Symmetrical Self-Renewal of a Mammalian Tissue Stem Cell\nABSTRACT: Pluripotent mouse embryonic stem (ES) cells multiply in simple monoculture by symmetrical divisions. In vivo, however, stem cells are generally thought to depend on specialised cellular microenvironments and to undergo predominantly asymmetric divisions. Ex vivo expansion of pure populations of tissue stem cells has proven elusive. Neural progenitor cells are propagated in combination with differentiating progeny in floating clusters called neurospheres. The proportion of stem cells in neurospheres is low, however, and they cannot be directly observed or interrogated. Here we demonstrate that the complex neurosphere environment is dispensable for stem cell maintenance, and that the combination of fibroblast growth factor 2 (FGF-2) and epidermal growth factor (EGF) is sufficient for derivation and continuous expansion by symmetrical division of pure cultures of neural stem (NS) cells. NS cells were derived first from mouse ES cells. Neural lineage induction was followed by growth factor addition in basal culture media. In the presence of only EGF and FGF-2, resulting NS cells proliferate continuously, are diploid, and clonogenic. After prolonged expansion, they remain able to differentiate efficiently into neurons and astrocytes in vitro and upon transplantation into the adult brain. Colonies generated from single NS cells all produce neurons upon growth factor withdrawal. NS cells uniformly express morphological, cell biological, and molecular features of radial glia, developmental precursors of neurons and glia. Consistent with this profile, adherent NS cell lines can readily be established from foetal mouse brain. Similar NS cells can be generated from human ES cells and human foetal brain. The extrinsic factors EGF plus FGF-2 are sufficient to sustain pur [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 989, "doc_id": "9988425", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: PPAR-RXRs can be activated by PPAR ligands.\n\nCANDIDATE_PASSAGE:\nDelays in the diagnosis of lung cancer. BACKGROUND Many patients with lung cancer report delays in diagnosing their disease. This may contribute to advanced stage at diagnosis and poor long term survival. This study explores the delays experienced by patients referred to a regional cancer centre with lung cancer. METHODS A prospective cohort of patients referred with newly diagnosed lung cancer were surveyed over a 3 month period to assess delays in diagnosis. Patients were asked when they first experienced symptoms, saw their doctor, what tests were done, when they saw a specialist and when they started treatment. Descriptive statistics were used to summarize the different time intervals. RESULTS 56 of 73 patients consented (RR 77%). However only 52 patients (30M, 22F) were interviewed as 2 died before being interviewed and two could not be contacted. The mean age was 68yrs. Stage distribution was as follows (IB/IIA 10%, stage IIIA 20%, IIIB/IV 70%). Patients waited a median of 21 days (iqr 7-51d) before seeing a doctor and a further 22d (iqr 0-38d) to complete any investigations. The median time from presentation to specialist referral was 27d (iqr 12-49d) and a further 23.5d (iqr 10-56d) to complete investigations. The median wait to start treatment once patients were seen at the cancer centre was 10d (iqr 2-28d). The overall time from development of first symptoms to starting treatment was 138d (iqr 79-175d). CONCLUSIONS Lung cancer patients experience substantial delays from development of symptoms to first initiating treatment. There is a need to promote awareness of lung cancer symptoms and develop and evaluate rapid assessment clinics for patients with suspected lung cancers.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "914", "doc_id": "44562904", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: MICAL redox enzymes regulate actin dynamics.\n\nCANDIDATE_PASSAGE:\nChromatin modifying enzymes as modulators of reprogramming Generation of induced pluripotent stem cells (iPSCs) by somatic cell reprogramming involves global epigenetic remodelling. Whereas several proteins are known to regulate chromatin marks associated with the distinct epigenetic states of cells before and after reprogramming, the role of specific chromatin-modifying enzymes in reprogramming remains to be determined. To address how chromatin-modifying proteins influence reprogramming, we used short hairpin RNAs (shRNAs) to target genes in DNA and histone methylation pathways, and identified positive and negative modulators of iPSC generation. Whereas inhibition of the core components of the polycomb repressive complex 1 and 2, including the histone 3 lysine 27 methyltransferase EZH2, reduced reprogramming efficiency, suppression of SUV39H1, YY1 and DOT1L enhanced reprogramming. Specifically, inhibition of the H3K79 histone methyltransferase DOT1L by shRNA or a small molecule accelerated reprogramming, significantly increased the yield of iPSC colonies, and substituted for KLF4 and c-Myc (also known as MYC). Inhibition of DOT1L early in the reprogramming process is associated with a marked increase in two alternative factors, NANOG and LIN28, which play essential functional roles in the enhancement of reprogramming. Genome-wide analysis of H3K79me2 distribution revealed that fibroblast-specific genes associated with the epithelial to mesenchymal transition lose H3K79me2 in the initial phases of reprogramming. DOT1L inhibition facilitates the loss of this mark from genes that are fated to be repressed in the pluripotent state. These findings implicate specific chromatin-modifying enzymes as barriers to or facilitators of reprogramming, and demonstrate how [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "738", "doc_id": "3669694", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Prescribed exercise training improves quality of life.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effects of exercise training on health status in patients with chronic heart failure: HF-ACTION randomized controlled trial.\nABSTRACT: CONTEXT Findings from previous studies of the effects of exercise training on patient-reported health status have been inconsistent. OBJECTIVE To test the effects of exercise training on health status among patients with heart failure. DESIGN, SETTING, AND PATIENTS Multicenter, randomized controlled trial among 2331 medically stable outpatients with heart failure with left ventricular ejection fraction of 35% or less. Patients were randomized from April 2003 through February 2007. INTERVENTIONS Usual care plus aerobic exercise training (n = 1172), consisting of 36 supervised sessions followed by home-based training, vs usual care alone (n = 1159). Randomization was stratified by heart failure etiology, which was a covariate in all models. MAIN OUTCOME MEASURES Kansas City Cardiomyopathy Questionnaire (KCCQ) overall summary scale and key subscales at baseline, every 3 months for 12 months, and annually thereafter for up to 4 years. The KCCQ is scored from 0 to 100 with higher scores corresponding to better health status. Treatment group effects were estimated using linear mixed models according to the intention-to-treat principle. RESULTS Median follow-up was 2.5 years. At 3 months, usual care plus exercise training led to greater improvement in the KCCQ overall summary score (mean, 5.21; 95% confidence interval, 4.42 to 6.00) compared with usual care alone (3.28; 95% confidence interval, 2.48 to 4.09). The additional 1.93-point increase (95% confidence interval, 0.84 to 3.01) in the exercise training group was statistically significant (P < .001). After 3 months, there were no further significant changes in KCCQ score for either group (P = .85 for the difference between slopes), resulting in a sustained, greater improvement overall for the exercise group (P [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Exercise training conferred modest but statistically significant improvements in self-reported health status compared with usual care without training.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 965, "doc_id": "40817021", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Forkhead 0 (fox0) transcription factors are involved in cellular differentiation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cell Stem Cell Review FoxO Transcription Factors and Stem Cell Homeostasis: Insights from the Hematopoietic System\nABSTRACT: The forkhead O (FoxO) family of transcription factors participates in diverse physiologic processes, including induction of cell-cycle arrest, stress resistance, differentiation, apoptosis, and metabolism. Several recent studies indicate that FoxO-dependent signaling is required for long-term regenerative potential of the hematopoietic stem cell (HSC) compartment through regulation of HSC response to physiologic oxidative stress, quiescence, and survival. These observations link FoxO function in mammalian systems with the evolutionarily conserved role of FoxO in promotion of stress resistance and longevity in lower phylogenetic systems. Furthermore, these findings have implications for aging in higher organisms and in malignant stem cell biology, and suggest that FoxOs may play an important role in the maintenance and integrity of stem cell compartments in a broad spectrum of tissues.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The forkhead O (FoxO) family of transcription factors participates in diverse physiologic processes, including induction of cell-cycle arrest, stress resistance, differentiation, apoptosis, and metabolism.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 428, "doc_id": "16728949", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Pediatric SCD patients with vaso-occlusive crisis show increased morphine use after breathing 80 ppm iNO for 4 hours.\n\nCANDIDATE_ABSTRACT:\nTITLE: Combined Impact of Lifestyle-Related Factors on Total and Cause-Specific Mortality among Chinese Women: Prospective Cohort Study\nABSTRACT: BACKGROUND Although cigarette smoking, excessive alcohol drinking, obesity, and several other well-studied unhealthy lifestyle-related factors each have been linked to the risk of multiple chronic diseases and premature death, little is known about the combined impact on mortality outcomes, in particular among Chinese and other non-Western populations. The objective of this study was to quantify the overall impact of lifestyle-related factors beyond that of active cigarette smoking and alcohol consumption on all-cause and cause-specific mortality in Chinese women. METHODS AND FINDINGS We used data from the Shanghai Women's Health Study, an ongoing population-based prospective cohort study in China. Participants included 71,243 women aged 40 to 70 years enrolled during 1996-2000 who never smoked or drank alcohol regularly. A healthy lifestyle score was created on the basis of five lifestyle-related factors shown to be independently associated with mortality outcomes (normal weight, lower waist-hip ratio, daily exercise, never exposed to spouse's smoking, higher daily fruit and vegetable intake). The score ranged from zero (least healthy) to five (most healthy) points. During an average follow-up of 9 years, 2,860 deaths occurred, including 775 from cardiovascular disease (CVD) and 1,351 from cancer. Adjusted hazard ratios for mortality decreased progressively with an increasing number of healthy lifestyle factors. Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality. The inverse association between the healthy lifestyle score and mortality was seen consistently regardless of ch [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 933, "doc_id": "1456068", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Exposure to fine particulate air pollution is relate to anxiety prevalence.\n\nCANDIDATE_ABSTRACT:\nTITLE: The relation between past exposure to fine particulate air pollution and prevalent anxiety: observational cohort study\nABSTRACT: OBJECTIVE To determine whether higher past exposure to particulate air pollution is associated with prevalent high symptoms of anxiety. DESIGN Observational cohort study. SETTING Nurses' Health Study. PARTICIPANTS 71,271 women enrolled in the Nurses' Health Study residing throughout the contiguous United States who had valid estimates on exposure to particulate matter for at least one exposure period of interest and data on anxiety symptoms. MAIN OUTCOME MEASURES Meaningfully high symptoms of anxiety, defined as a score of 6 points or greater on the phobic anxiety subscale of the Crown-Crisp index, administered in 2004. RESULTS The 71,271 eligible women were aged between 57 and 85 years (mean 70 years) at the time of assessment of anxiety symptoms, with a prevalence of high anxiety symptoms of 15%. Exposure to particulate matter was characterized using estimated average exposure to particulate matter <2.5 μm in diameter (PM2.5) and 2.5 to 10 μm in diameter (PM2.5-10) in the one month, three months, six months, one year, and 15 years prior to assessment of anxiety symptoms, and residential distance to the nearest major road two years prior to assessment. Significantly increased odds of high anxiety symptoms were observed with higher exposure to PM2.5 for multiple averaging periods (for example, odds ratio per 10 µg/m(3) increase in prior one month average PM2.5: 1.12, 95% confidence interval 1.06 to 1.19; in prior 12 month average PM2.5: 1.15, 1.06 to 1.26). Models including multiple exposure windows suggested short term averaging periods were more relevant than long term averaging periods. There was no association between anxiety and exposure to PM2.5-10. Residential proximity to major roads was not related to anxiety symptoms in a dose dependent manner. CON [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Exposure to fine particulate matter (PM2.5) was associated with high symptoms of anxiety, with more recent exposures potentially more relevant than more distant exposures.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 399, "doc_id": "791050", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: ITAM phosphorylation allows for the transfer of the T cell receptor (TCR) signal from the echo-domain to the cytoplasmic tail of the T cell receptor (TCR).\n\nCANDIDATE_PASSAGE:\nFull activation of the T cell receptor requires both clustering and conformational changes at CD3. T cell receptor (TCR-CD3) triggering involves both receptor clustering and conformational changes at the cytoplasmic tails of the CD3 subunits. The mechanism by which TCRalphabeta ligand binding confers conformational changes to CD3 is unknown. By using well-defined ligands, we showed that induction of the conformational change requires both multivalent engagement and the mobility restriction of the TCR-CD3 imposed by the plasma membrane. The conformational change is elicited by cooperative rearrangements of two TCR-CD3 complexes and does not require accompanying changes in the structure of the TCRalphabeta ectodomains. This conformational change at CD3 reverts upon ligand dissociation and is required for T cell activation. Thus, our permissive geometry model provides a molecular mechanism that rationalizes how the information of ligand binding to TCRalphabeta is transmitted to the CD3 subunits and to the intracellular signaling machinery.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "550", "doc_id": "33499189", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does risk of subsequent dementia diagnoses vary by types of adjuvant chemotherapy in older women with breast cancer?\n\nABSTRACT:\nLittle is known about long-term cognitive side effects of adjuvant chemotherapy for breast cancer. We thus examined incidence of dementia diagnoses in older women diagnosed with breast cancer, stratified by types of chemotherapy regimen. We identified patients with incident dementia diagnoses through Medicare claims linked to the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) tumor registry data. The study population (n = 6,932) consisted of women at least 68 years of age, who were diagnosed with early-stage breast cancer from 1994 through 2002 in one of the SEER areas and received chemotherapy as part of their cancer treatment. Excluded were women with a diagnosis of dementia within the 3 years prior to their cancer diagnosis. Our sample comprised mostly white women. The mean age was 74. Fifty-seven percent were estrogen receptor positive. Over 70% had no comorbidity. The use of taxol and anthracycline-based treatments increased from mid-1990s to early 2000. Increasing age at cancer diagnosis, Black ethnicity, living in a census tract with lower level of education, and increasing number of comorbidities were associated with new claims of dementia diagnoses after chemotherapy. There was no significant association between types of chemotherapy agents and risk of subsequent dementia diagnoses.", "output": "{\"label\": \"no\", \"rationale\": \"No association was found between types of adjuvant chemotherapy agents for breast cancer and risk of new dementia diagnoses. Our findings suggest that concerns about post-chemotherapy dementia should not be a major factor in determining type of adjuvant chemotherapy regimen to prescribe for older women with breast cancer.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 19067255, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Splenomegaly is observed in knockin mouse lacking the SHP-2 MAPK pathway.\n\nCANDIDATE_PASSAGE:\nCyclin-dependent kinase 2 is essential for meiosis but not for mitotic cell division in mice We targeted the locus encoding the cyclin-dependent kinase 2 (CDK2) by homologous recombination in mouse embryonic stem (ES) cells. Embryonic fibroblasts lacking CDK2 proliferate normally and become immortal after continuous passage in culture. Elimination of a conditional Cdk2 allele in immortal cells does not have a significant effect on proliferation. Cdk2−/− mice are viable and survive for up to two years, indicating that CDK2 is also dispensable for proliferation and survival of most cell types. But CDK2 is essential for completion of prophase I during meiotic cell division in male and female germ cells, an unforeseen role for this cell cycle kinase.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1097", "doc_id": "19522248", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does granulocyte Colony-Stimulating Factor improve Motor Function in Rats Developing Compression Myelopathy?\n\nABSTRACT:\nBasic animal research. The effects of granulocyte colony-stimulating factor (G-CSF) were assessed in a rat chronic spinal cord compression model to explore the potential of G-CSF as a pharmacological treatment for cervical spondylotic myelopathy. G-CSF is a hematopoietic cytokine used clinically to treat neutropenia. Recently, neuroprotective effects of G-CSF have been reported in spinal cord disorders. To introduce the chronic cervical cord compression, thin polyurethane sheets were implanted under C5-C6 laminae of rats and gradually expanded by absorbing water. This model reproduces delayed compressive myelopathy of the cervical spine. In sham operations, the sheets were immediately removed. G-CSF (15 μg/kg) or normal saline (NS) was administered subcutaneously 5 days a week. Experimental groups were sham operation given NS; cord compression given NS; and cord compression given G-CSF. To assess motor functions, rotarod performance, and grip strength were measured. Twenty-six weeks after surgery, cervical spinal cords were examined histopathologically. In the prevention experiment, G-CSF or NS administration was started immediately after surgery. In the treatment experiment, their administration was started 8 weeks after surgery. In another experiment, in three groups in the prevention experiment, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling staining was performed to assess apoptotic cell death at 8 weeks after surgery. In the prevention experiment, administration of G-CSF preserved the motor functions and motor neurons throughout the 26 weeks, and significantly decreased the number of apoptotic cells at 8 weeks. In the treatment experiment, G-CSF administration from 8 weeks after surgery markedly restore [TRUNCATED]", "output": "{\"label\": \"yes\", \"rationale\": \"G-CSF prevents the decline in motor functions and preserves motor neurons in the rat chronic cord compression model. G-CSF also improves motor function in the progressive phase of compression myelopathy.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 27120060, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Ubiquitin ligase UBC13 generates a K63-linked polyubiquitin moiety at PCNA K164.\n\nCANDIDATE_ABSTRACT:\nTITLE: Increased gene expression of brown fat uncoupling protein (UCP)1 and skeletal muscle UCP2 and UCP3 in MAC16-induced cancer cachexia.\nABSTRACT: Weight loss in cancer cachexia is attributable to decreased food intake and/or enhanced energy expenditure. We investigated the roles of the uncoupling proteins (UCPs) UCPI, -2, and -3 in a murine model of cachexia, the MAC16 adenocarcinoma. Weight fell to 24% below that of non-tumor-bearing controls (P < 0.01) 18 days after MAC16 inoculation, with significant reductions in fat-pad mass (-67%; P < 0.01) and muscle mass (-20%; P < 0.01). Food intake was 26-60% lower (P < 0.01) than in controls on days 17-18. Non-tumor-bearing mice, pair-fed to match MAC16-induced hypophagia, showed less weight loss (10% below controls, P < 0.01; 16% above MAC-16, P < 0.01) and smaller decreases in fat-pad mass (21% below controls, P < 0.01). Core temperature in MAC16 mice was significantly lower (-2.4 degrees C, P < 0.01) than in controls, and pair-feeding had no effect. MAC16 mice showed significantly higher UCP1 mRNA levels in brown adipose tissue (BAT) than in controls (+63%, P < 0.01), and pair-feeding had no effect. UCP2 and -3 expression in BAT did not differ significantly between groups. By contrast, UCP2 mRNA levels in skeletal muscle were comparably increased in both MAC16 and pair-fed groups (respectively, 183 and 163% above controls; both, P < 0.05), with no significant difference between these two groups. Similarly, UCP3 mRNA was significantly higher than controls in both MAC16 (+163%, P < 0.05) and pair-fed (+253%, P < 0.01) groups, with no significant difference between the two experimental groups. Overexpression of UCP1 in BAT in MAC16-bearing mice may be an adaptive response to hypothermia, which is apparently induced by tumor products; increased thermogenesis in BAT could increase total energy expenditure and, thus, contribute to tissue wasting. Increased UCP [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1337, "doc_id": "1507222", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Oxidative DNA damage activates STING signalling.\n\nCANDIDATE_ABSTRACT:\nTITLE: Atm-deficient mice exhibit increased sensitivity to dextran sulfate sodium-induced colitis characterized by elevated DNA damage and persistent immune activation.\nABSTRACT: The role of ataxia telangiectasia mutated (ATM), a DNA double-strand break recognition and response protein, in inflammation and inflammatory diseases is unclear. We have previously shown that high levels of systemic DNA damage are induced by intestinal inflammation in wild-type mice. To determine the effect of Atm deficiency in inflammation, we induced experimental colitis in Atm(-/-), Atm(+/-), and wild-type mice via dextran sulfate sodium (DSS) administration. Atm(-/-) mice had higher disease activity indices and rates of mortality compared with heterozygous and wild-type mice. Systemic DNA damage and immune response were characterized in peripheral blood throughout and after three cycles of treatment. Atm(-/-) mice showed increased sensitivity to levels of DNA strand breaks in peripheral leukocytes, as well as micronucleus formation in erythroblasts, compared with heterozygous and wild-type mice, especially during remission periods and after the end of treatment. Markers of reactive oxygen and nitrogen species-mediated damage, including 8-oxoguanine and nitrotyrosine, were present both in the distal colon and in peripheral leukocytes, with Atm(-/-) mice manifesting more 8-oxoguanine formation than wild-type mice. Atm(-/-) mice showed greater upregulation of inflammatory cytokines and significantly higher percentages of activated CD69+ and CD44+ T cells in the peripheral blood throughout treatment. ATM, therefore, may be a critical immunoregulatory factor dampening the deleterious effects of chronic DSS-induced inflammation, necessary for systemic genomic stability and homeostasis of the gut epithelial barrier.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 898, "doc_id": "5572127", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does bile and pancreatic juice replacement ameliorate early ligation-induced acute pancreatitis in rats?\n\nABSTRACT:\nIn healthy rats, combined bile and pancreatic juice diversion from gut has a synergistic rather than additive effect on stimulation of exocrine pancreatic protein secretion. We hypothesized that exclusion of combined bile and pancreatic juice from gut exacerbates bile and pancreatic-duct ligation-induced acute pancreatitis in rats to a greater extent than exclusion of either bile or pancreatic juice alone. Bile and pancreatic juice (obtained fresh from donor rats) were replaced, separately or together, via a duodenal fistula beginning immediately before 6 hours of duct ligation. Pancreatic morphologic changes were evaluated with an acute pancreatitis histology score and morphometric quantitation of acinar-cell necrosis. Plasma amylase and cholecystokinin concentrations and pancreatic subcellular distribution of cathepsin B activity were determined. Characteristics of bile and pancreatic juice obtained from donor rats were also studied. Combined bile and pancreatic juice replacement limited the increase in acute pancreatitis histology score by 77%, acinar cell necrosis by 95%, hyperamylasemia by 77%, and hypercholecystokininemia by 99%, while preventing subcellular redistribution of cathepsin B. Amelioration of pancreatic morphologic changes was significantly greater with combined bile and pancreatic juice replacement than with replacement of either bile or pancreatic juice alone.", "output": "{\"label\": \"yes\", \"rationale\": \"In this experimental corollary of early gallstone-induced acute pancreatitis, combined bile and pancreatic juice exclusion from gut contributes to disease pathogenesis to a greater extent than exclusion of either bile or pancreatic juice alone.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 7535017, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Bariatric surgery leads to negative outcomes in mental health.\n\nCANDIDATE_ABSTRACT:\nTITLE: Evidence that the Ipl1-Sli15 (Aurora Kinase-INCENP) Complex Promotes Chromosome Bi-orientation by Altering Kinetochore-Spindle Pole Connections\nABSTRACT: How sister kinetochores attach to microtubules from opposite spindle poles during mitosis (bi-orientation) remains poorly understood. In yeast, the ortholog of the Aurora B-INCENP protein kinase complex (Ipl1-Sli15) may have a role in this crucial process, because it is necessary to prevent attachment of sister kinetochores to microtubules from the same spindle pole. We investigated IPL1 function in cells that cannot replicate their chromosomes but nevertheless duplicate their spindle pole bodies (SPBs). Kinetochores detach from old SPBs and reattach to old and new SPBs with equal frequency in IPL1+ cells, but remain attached to old SPBs in ipl1 mutants. This raises the possibility that Ipl1-Sli15 facilitates bi-orientation by promoting turnover of kinetochore-SPB connections until traction of sister kinetochores toward opposite spindle poles creates tension in the surrounding chromatin.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 166, "doc_id": "493346", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Activated Cdk5 regulates DNA damage-induced neuronal death.\n\nCANDIDATE_PASSAGE:\nLncRNA-GAS5 induces PTEN expression through inhibiting miR-103 in endometrial cancer cells BACKGROUND Growth arrest-specific 5 (GAS5) was reported to be implicated and aberrantly express in multiple cancers. However, the expression and mechanism of action of GAS5 were largely poor understood in endometrial carcinoma. RESULTS According to the result of real-time reverse-transcriptase polymerase chain reaction (RT-PCR) and flow cytometry analysis, we identified that GAS5 was down-regulated in endometrial cancer cells and stimulated the apoptosis of endometrial cancer cells. To investigate the expression of GAS5, PTEN and miR-103, RT-PCR was performed. And we found that the expression of PTEN was up-regulated when endometrial cancer cells overexpressed GAS5. The prediction of bioinformatics online revealed that GAS5 could bind to miR-103, which was further found to be regulated by GAS5. Finally, we found that miR-103 mimic could decrease the mRNA and protein levels of PTEN through luciferase reporter assay and western blotting, and GAS5 plasmid may reverse this regulation effect in endometrial cancer cells. CONCLUSION In summary, we demonstrate that GAS5 acts as an tumor suppressor lncRNA in endometrial cancer. Through inhibiting the expression of miR-103, GAS5 significantly enhanced the expression of PTEN to promote cancer cell apoptosis, and, thus, could be an important mediator in the pathogenesis of endometrial cancer.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "68", "doc_id": "16346504", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Participating in six months of physical activity improves cognitive functioning.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effect of physical activity on cognitive function in older adults at risk for Alzheimer disease: a randomized trial.\nABSTRACT: CONTEXT Many observational studies have shown that physical activity reduces the risk of cognitive decline; however, evidence from randomized trials is lacking. OBJECTIVE To determine whether physical activity reduces the rate of cognitive decline among older adults at risk. DESIGN AND SETTING Randomized controlled trial of a 24-week physical activity intervention conducted between 2004 and 2007 in metropolitan Perth, Western Australia. Assessors of cognitive function were blinded to group membership. PARTICIPANTS We recruited volunteers who reported memory problems but did not meet criteria for dementia. Three hundred eleven individuals aged 50 years or older were screened for eligibility, 89 were not eligible, and 52 refused to participate. A total of 170 participants were randomized and 138 participants completed the 18-month assessment. INTERVENTION Participants were randomly allocated to an education and usual care group or to a 24-week home-based program of physical activity. MAIN OUTCOME MEASURE Change in Alzheimer Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) scores (possible range, 0-70) over 18 months. RESULTS In an intent-to-treat analysis, participants in the intervention group improved 0.26 points (95% confidence interval, -0.89 to 0.54) and those in the usual care group deteriorated 1.04 points (95% confidence interval, 0.32 to 1.82) on the ADAS-Cog at the end of the intervention. The absolute difference of the outcome measure between the intervention and control groups was -1.3 points (95% confidence interval,-2.38 to -0.22) at the end of the intervention. At 18 months, participants in the intervention group improved 0.73 points (95% confidence interval, -1.27 to 0.03) on the ADAS-Cog, and those in the usual care group improved 0.04 p [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS In this study of adults with subjective memory impairment, a 6-month program of physical activity provided a modest improvement in cognition over an 18-month follow-up period.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 921, "doc_id": "1642727", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Monoclonal antibody targeting of N-cadherin encourages metastasis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Monoclonal antibody targeting of N-cadherin inhibits prostate cancer growth, metastasis and castration resistance\nABSTRACT: The transition from androgen-dependent to castration-resistant prostate cancer (CRPC) is a lethal event of uncertain molecular etiology. Comparing gene expression in isogenic androgen-dependent and CRPC xenografts, we found a reproducible increase in N-cadherin expression, which was also elevated in primary and metastatic tumors of individuals with CRPC. Ectopic expression of N-cadherin in nonmetastatic, androgen-dependent prostate cancer models caused castration resistance, invasion and metastasis. Monoclonal antibodies against the ectodomain of N-cadherin reduced proliferation, adhesion and invasion of prostate cancer cells in vitro. In vivo, these antibodies slowed the growth of multiple established CRPC xenografts, blocked local invasion and metastasis and, at higher doses, led to complete regression. N-cadherin–specific antibodies markedly delayed the time to emergence of castration resistance, markedly affected tumor histology and angiogenesis, and reduced both AKT serine-threonine kinase activity and serum interleukin-8 (IL-8) secretion. These data indicate that N-cadherin is a major cause of both prostate cancer metastasis and castration resistance. Therapeutic targeting of this factor with monoclonal antibodies may have considerable clinical benefit.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In vivo, these antibodies slowed the growth of multiple established CRPC xenografts, blocked local invasion and metastasis and, at higher doses, led to complete regression.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 802, "doc_id": "22180793", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Less than 10% of patients exposed to radiation have activated markers of mesenchymal stem cells.\n\nCANDIDATE_PASSAGE:\nRNA is favourable for analysing EGFR mutations in malignant pleural effusion of lung cancer. Malignant pleural effusion (MPE) is a useful specimen allowing for the evaluation of EGFR status in nonsmall cell lung cancer (NSCLC). However, direct sequencing of genomic DNA from MPE samples was found not to be sensitive for EGFR mutation detection. To test whether EGFR analysis from RNA is less prone to interference from nontumour cells that have no or lower EGFR expression, we compared three methods (sequencing from cell-derived RNA versus sequencing and mass-spectrometric analysis from genomic DNA), in parallel, for EGFR mutation detection from MPE samples in 150 lung adenocarcinoma patients receiving first-line tyrosine kinase inhibitors (TKIs). Among these MPE samples, EGFR mutations were much more frequently identified by sequencing using RNA than by sequencing and mass-spectrometric analysis from genomic DNA (for all mutations, 67.3 versus 44.7 and 46.7%; for L858R or exon 19 deletions, 61.3 versus 41.3 and 46.7%, respectively). The better mutation detection yield of sequencing from RNA was coupled with the superior prediction of clinical efficacy of first-line TKIs. In patients with acquired resistance, EGFR sequencing from RNA provided satisfactory detection of T790M (54.2%). These results demonstrated that EGFR sequencing using RNA as template greatly improves sensitivity for EGFR mutation detection from samples of MPE, highlighting RNA as the favourable source for analysing EGFR mutations from heterogeneous MPE specimens in NSCLC.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "689", "doc_id": "711256", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: PD-1 triggering on monocytes enhances IL-10 production by monocytes.\n\nCANDIDATE_PASSAGE:\nMolecular mechanisms of (-)-epicatechin and chlorogenic acid on the regulation of the apoptotic and survival/proliferation pathways in a human hepatoma cell line. Dietary polyphenols have been associated with reduced risk of chronic diseases, but the precise molecular mechanisms of protection remain unclear. This work was aimed at studying the effect of (-)-epicatechin (EC) and chlorogenic acid (CGA) on the regulation of apoptotic and survival/proliferation pathways in a human hepatoma cell line (HepG2). EC or CGA treatment for 18 h had a slight effect on cell viability and decreased reactive oxygen species formation, and EC alone promoted cell proliferation, whereas CGA increased glutathione levels. Phenols neither induced the caspase cascade for apoptosis nor affected expression levels of Bcl-xL or Bax. A sustained activation of the major survival signals AKT/PI-3-kinase and ERK was shown in EC-treated cells, rather than in CGA-exposed cells. These data suggest that EC and CGA have no effect on apoptosis and enhance the intrinsic cellular tolerance against oxidative insults either by activating survival/proliferation pathways or by increasing antioxidant potential in HepG2.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "902", "doc_id": "9197092", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Satellite cell dysfunction is a key factor in sarcopenia development.\n\nCANDIDATE_ABSTRACT:\nTITLE: Inducible depletion of satellite cells in adult, sedentary mice impairs muscle regenerative capacity without affecting sarcopenia\nABSTRACT: A key determinant of geriatric frailty is sarcopenia, the age-associated loss of skeletal muscle mass and strength. Although the etiology of sarcopenia is unknown, the correlation during aging between the loss of activity of satellite cells, which are endogenous muscle stem cells, and impaired muscle regenerative capacity has led to the hypothesis that the loss of satellite cell activity is also a cause of sarcopenia. We tested this hypothesis in male sedentary mice by experimentally depleting satellite cells in young adult animals to a degree sufficient to impair regeneration throughout the rest of their lives. A detailed analysis of multiple muscles harvested at various time points during aging in different cohorts of these mice showed that the muscles were of normal size, despite low regenerative capacity, but did have increased fibrosis. These results suggest that lifelong reduction of satellite cells neither accelerated nor exacerbated sarcopenia and that satellite cells did not contribute to the maintenance of muscle size or fiber type composition during aging, but that their loss may contribute to age-related muscle fibrosis.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"These results suggest that lifelong reduction of satellite cells neither accelerated nor exacerbated sarcopenia and that satellite cells did not contribute to the maintenance of muscle size or fiber type composition during aging, but that their loss may contribute to age-related muscle fibrosis.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1065, "doc_id": "20418809", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does feasibility of a closed-system cell processor ( ACP215 ) for automated preparation of washed platelet concentrate?\n\nABSTRACT:\nThis study was aimed at evaluating the feasibility of the ACP215 closed-system cell processor for preparing washed platelet concentrates. Platelet washing was performed with either the ACP215 system or the manual technique with M-sol. Plasma protein removal and platelet recovery were estimated, and the washed platelet concentrates were stored for 5 days. Samples were collected after washing and on days 1, 3 and 5 of storage to determine the effects of the washing methods on the in vitro platelet qualities (platelet count, platelet volume, pH, glucose and lactate concentrations, hypotonic shock response, aggregation response and CD62P expression level). Platelet recovery was 86·9 ± 2·1% and 85·9 ± 1·9% (P = 0·305), and plasma protein removal was 95·8 ± 0·9% and 96·9 ± 0·7% (P = 0·016) after washing with the ACP215 system and manual technique, respectively. No statistically significant differences in the in vitro platelet qualities were observed between the washing methods.", "output": "{\"label\": \"yes\", \"rationale\": \"The ACP215 system is a feasible alternative to manual, labour-intensive, techniques for preparing washed platelet concentrates.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 21770954, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is perforation of the appendix a risk factor for tubal infertility and ectopic pregnancy?\n\nABSTRACT:\nTo critically assess the evidence that appendiceal perforation is a risk factor for subsequent tubal infertility or ectopic pregnancy. Epidemiologic studies investigating the relationship between appendectomy and infertility or ectopic pregnancy were identified by searching the MEDLINE database from 1966 to 1997. Appropriate citations were also extracted from a manual search of the bibliographies of selected papers. Twenty-three articles were retrieved. Only 4 presented original data including comparisons to a nonexposed control group and they form the basis for this study. Because the raw data or specific techniques of data analysis were not always explicitly described, indices of risk for exposure were extracted from the data as presented and were analysed without attempting to convert them to a common measure. Articles were assessed according to the criteria of the Evidence-Based Medicine Working Group for evaluating articles on harm. Review of the literature yielded estimates of the risk of adverse fertility outcomes ranging from 1.6 (95% confidence interval [CI] 1.1 to 2.5) for ectopic pregnancy after an appendectomy to 4.8 (95% CI 1.5 to 14.9) for tubal infertility from perforation of the appendix. Recall bias, and poor adjustment for confounding variables in some reports, weakened the validity of the studies.", "output": "{\"label\": \"maybe\", \"rationale\": \"The methodologic weaknesses of the studies do not permit acceptance of increased risk of tubal pregnancy or infertility as a consequence of perforation of the appendix, so a causal relationship cannot be supported by the data currently available. Only a well-designed case-control study with unbiased ascertainment of exposure and adjustment for confounding variables will provide a definitive answer.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 10223070, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Combining phosphatidylinositide 3-kinase and MEK 1/2 inhibitors is effective at treating KRAS mutant tumors.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effective Use of PI3K and MEK Inhibitors to Treat Mutant K-Ras G12D and PIK3CA H1047R Murine Lung Cancers\nABSTRACT: Somatic mutations that activate phosphoinositide 3-kinase (PI3K) have been identified in the p110-alpha catalytic subunit (encoded by PIK3CA). They are most frequently observed in two hotspots: the helical domain (E545K and E542K) and the kinase domain (H1047R). Although the p110-alpha mutants are transforming in vitro, their oncogenic potential has not been assessed in genetically engineered mouse models. Furthermore, clinical trials with PI3K inhibitors have recently been initiated, and it is unknown if their efficacy will be restricted to specific, genetically defined malignancies. In this study, we engineered a mouse model of lung adenocarcinomas initiated and maintained by expression of p110-alpha H1047R. Treatment of these tumors with NVP-BEZ235, a dual pan-PI3K and mammalian target of rapamycin (mTOR) inhibitor in clinical development, led to marked tumor regression as shown by positron emission tomography-computed tomography, magnetic resonance imaging and microscopic examination. In contrast, mouse lung cancers driven by mutant Kras did not substantially respond to single-agent NVP-BEZ235. However, when NVP-BEZ235 was combined with a mitogen-activated protein kinase kinase (MEK) inhibitor, ARRY-142886, there was marked synergy in shrinking these Kras-mutant cancers. These in vivo studies suggest that inhibitors of the PI3K-mTOR pathway may be active in cancers with PIK3CA mutations and, when combined with MEK inhibitors, may effectively treat KRAS mutated lung cancers.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"These in vivo studies suggest that inhibitors of the PI3K-mTOR pathway may be active in cancers with PIK3CA mutations and, when combined with MEK inhibitors, may effectively treat KRAS mutated lung cancers.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 275, "doc_id": "4961038", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Reduction of Rpl38 alters the composition of the Hox gene mRNAs translation in mice without lowering overall protein synthesis.\n\nCANDIDATE_PASSAGE:\nThe effect of folate fortification on folic acid-based homocysteine-lowering intervention and stroke risk: a meta-analysis. OBJECTIVE Folate and vitamin B12 are two vital regulators in the metabolic process of homocysteine, which is a risk factor of atherothrombotic events. Low folate intake or low plasma folate concentration is associated with increased stroke risk. Previous randomized controlled trials presented discordant findings in the effect of folic acid supplementation-based homocysteine lowering on stroke risk. The aim of the present review was to perform a meta-analysis of relevant randomized controlled trials to check the how different folate fortification status might affect the effects of folic acid supplementation in lowering homocysteine and reducing stroke risk. DESIGN Relevant randomized controlled trials were identified through formal literature search. Homocysteine reduction was compared in subgroups stratified by folate fortification status. Relative risks with 95 % confidence intervals were used as a measure to assess the association between folic acid supplementation and stroke risk. SETTING The meta-analysis included fourteen randomized controlled trials, SUBJECTS A total of 39 420 patients. RESULTS Homocysteine reductions were 26·99 (sd 1·91) %, 18·38 (sd 3·82) % and 21·30 (sd 1·98) %, respectively, in the subgroups without folate fortification, with folate fortification and with partial folate fortification. Significant difference was observed between the subgroups with folate fortification and without folate fortification (P=0·05). The relative risk of stroke was 0·88 (95 % CI 0·77, 1·00, P=0·05) in the subgroup without folate fortification, 0·94 (95 % CI 0·58, 1·54, P=0·82) in the subgroup with folate fortification and 0·91 (95 % C [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1031", "doc_id": "37424881", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Mice without IFN-γ or its receptor are highly susceptible to EAM induced with α-MyHC/CFA.\n\nCANDIDATE_ABSTRACT:\nTITLE: the Development of Autoimmune Myocarditis in Mice by an\nABSTRACT: BACKGROUND Interleukin (IL)-12 exerts a potent proinflammatory effect by stimulating T-helper (Th) 1 responses. This effect is believed to be mediated primarily through the activation of STAT4 and subsequent production of interferon (IFN)-gamma. Methods and Results- We examined the role of IL-12 receptor (IL-12R) signaling in the development of murine experimental autoimmune myocarditis (EAM) induced by cardiac myosin immunization. Both IL-12Rbeta1-deficient mice and STAT4-deficient mice were resistant to the induction of myocarditis. Treatment with exogenous IL-12 exacerbated disease. We questioned whether IFN-gamma is required for the disease-promoting activity of IL-12. On the contrary, we found that IFN-gamma suppresses EAM. Lack of IFN-gamma due to either depletion with an antibody or a genetic deficiency exacerbated myocarditis. Spleens from IFN-gamma-deficient mice immunized with cardiac myosin showed increased cellularity; greater numbers of CD3+, CD4+, CD8+, and IL-2-producing cells; and heightened ability to produce cytokines on stimulation in vitro. Treatment of mice with recombinant IFN-gamma suppressed the development of myocarditis. CONCLUSIONS IL-12/IL-12R/STAT4 signaling promotes the development of EAM. In contrast, IFN-gamma plays a protective role. The disease-limiting effects of IFN-gamma might be explained by its ability to control the expansion of activated T lymphocytes.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In contrast, IFN-gamma plays a protective role.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 782, "doc_id": "8246922", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is androgen deprivation therapy for prostate cancer associated with cardiovascular morbidity and mortality : a meta-analysis of population-based observational studies?\n\nABSTRACT:\nThere is no consensus regarding whether androgen deprivation therapy (ADT) is associated with cardiovascular disease (CVD) and cardiovascular mortality (CVM). The objective of this study was to determine the role of ADT for prostate cancer (PCa) in development of cardiovascular events (CVD and CVM). We performed a meta-analysis from population-based observational studies comparing ADT vs control aimed at treating PCa in patients with PCa, reporting either CVD or CVM as outcome. Publications were searched using Medline, Embase, Cochrane Library Central Register of observational studies database up to May 31th 2014, and supplementary searches in publications from potentially relevant journals. 6 studies were identified with a total of 129,802 ADT users and 165,605 controls investigating the relationship between ADT and CVD. The incidence of CVD was 10% higher in ADT groups, although no significant association was observed (HR = 1.10, 95%CIs: 1.00-1.21; P = 0.06). For different types of ADT, CVD was related with gonadotropin-releasing hormone (GnRH) (HR = 1.19, 95%CIs: 1.04-1.36; P<0.001) and GnRH plus oral antiandrogen (AA) (HR = 1.46, 95%CIs: 1.03-2.08; P = 0.04), but not with AA alone or orchiectomy. For CVM, 119,625 ADT users and 150,974 controls from 6 eligible studies were included, pooled results suggested that ADT was associated with CVM (HR = 1.17, 95%CIs: 1.04-1.32; P = 0.01). Significantly increased CVM was also detected in GnRH and GnRH plus AA groups. When patients received other treatments (e.g. prostatectomy and radiotherapy) were ruled out of consideration, more increased CVD (HR = 1.19, 95%CIs: 1.08-1.30; P<0.001) and CVM (HR = 1.30, 95%CIs: 1.13-1.50; P<0.001) were found in men treated with ADT monotherapy.", "output": "{\"label\": \"yes\", \"rationale\": \"ADT is associated with both CVD and CVM. Particularly, GnRH alone and GnRH plus AA can significantly increase the incidence of cardiovascular events in patients with PCa.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25264674, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Angiotensin converting enzyme inhibitors are associated with increased risk for functional renal insufficiency.\n\nCANDIDATE_ABSTRACT:\nTITLE: Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association.\nABSTRACT: Angiotensin converting enzyme (ACE) inhibitors are now one of the most frequently used classes of antihypertensive drugs. Beyond their utility in the management of hypertension, their use has been extended to the long-term management of patients with congestive heart failure (CHF), as well as diabetic and nondiabetic nephropathies. Although ACE inhibitor therapy usually improves renal blood flow (RBF) and sodium excretion rates in CHF and reduces the rate of progressive renal injury in chronic renal disease, its use can also be associated with a syndrome of “functional renal insufficiency” and/or hyperkalemia. This form of acute renal failure (ARF) most commonly develops shortly after initiation of ACE inhibitor therapy but can be observed after months or years of therapy, even in the absence of prior ill effects. ARF is most likely to occur when renal perfusion pressure cannot be sustained because of substantial decreases in mean arterial pressure (MAP) or when glomerular filtration rate (GFR) is highly angiotensin II (Ang II) dependent. Conditions that predict an adverse hemodynamic effect of ACE inhibitors in patients with CHF are preexisting hypotension and low cardiac filling pressures. The GFR is especially dependent on Ang II during extracellular fluid (ECF) volume depletion, high-grade bilateral renal artery stenosis, or stenosis of a dominant or single kidney, as in a renal transplant recipient. Understanding the pathophysiological mechanisms and the common risk factors for ACE inhibitor–induced functional ARF is critical, because preventive strategies for ARF exist, and if effectively used, they may permit use of these compounds in a less restricted fashion. Under normal physiological conditions, renal autoregulation adjusts renal vascular resistan [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Understanding the pathophysiological mechanisms and the common risk factors for ACE inhibitor–induced functional ARF is critical, because preventive strategies for ARF exist, and if effectively used, they may permit use of these compounds in a less restricted fashion.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 113, "doc_id": "6157837", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Replacement of OCT4 and SOX2 genes with GATA3 is not capable of reprogramming human cells.\n\nCANDIDATE_PASSAGE:\nReprogramming of human fibroblasts to pluripotency with lineage specifiers. Since the initial discovery that OCT4, SOX2, KLF4, and c-MYC overexpression sufficed for the induction of pluripotency in somatic cells, methodologies replacing the original factors have enhanced our understanding of the reprogramming process. However, unlike in mouse, OCT4 has not been replaced successfully during reprogramming of human cells. Here we report on a strategy to accomplish this replacement. Through a combination of transcriptome and bioinformatic analysis we have identified factors previously characterized as being lineage specifiers that are able to replace OCT4 and SOX2 in the reprogramming of human fibroblasts. Our results show that it is possible to replace OCT4 and SOX2 simultaneously with alternative lineage specifiers in the reprogramming of human cells. At a broader level, they also support a model in which counteracting lineage specification networks underlies the induction of pluripotency.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1038", "doc_id": "16287725", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nCANDIDATE_PASSAGE:\nSmall molecule inhibition of the KRAS–PDEδ interaction impairs oncogenic KRAS signalling The KRAS oncogene product is considered a major target in anticancer drug discovery. However, direct interference with KRAS signalling has not yet led to clinically useful drugs. Correct localization and signalling by farnesylated KRAS is regulated by the prenyl-binding protein PDEδ, which sustains the spatial organization of KRAS by facilitating its diffusion in the cytoplasm. Here we report that interfering with binding of mammalian PDEδ to KRAS by means of small molecules provides a novel opportunity to suppress oncogenic RAS signalling by altering its localization to endomembranes. Biochemical screening and subsequent structure-based hit optimization yielded inhibitors of the KRAS–PDEδ interaction that selectively bind to the prenyl-binding pocket of PDEδ with nanomolar affinity, inhibit oncogenic RAS signalling and suppress in vitro and in vivo proliferation of human pancreatic ductal adenocarcinoma cells that are dependent on oncogenic KRAS. Our findings may inspire novel drug discovery efforts aimed at the development of drugs targeting oncogenic RAS.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1004", "doc_id": "4320424", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Mice defective for deoxyribonucleic acid (DNA) polymerase I (polI) fail to reveal increased sensitivity to ionizing radiation (IR).\n\nCANDIDATE_ABSTRACT:\nTITLE: Nonoverlapping functions of DNA polymerases mu, lambda, and terminal deoxynucleotidyltransferase during immunoglobulin V(D)J recombination in vivo.\nABSTRACT: DNA polymerases mu (pol mu), lambda (pol lambda), and terminal deoxynucleotidyltransferase (TdT) are enzymes of the pol X family that share homology in sequence and functional domain organization. We showed previously that pol mu participates in light chain but surprisingly not heavy chain gene rearrangement. We show here that immunoglobulin heavy chain junctions from pol lambda-deficient animals have shorter length with normal N-additions, thus indicating that pol lambda is recruited during heavy chain rearrangement at a step that precedes the action of TdT. In contrast to previous in vitro studies, analysis of animals with combined inactivation of these enzymes revealed no overlapping or compensatory activities for V(D)J recombination between pol mu, pol lambda, and TdT. This complex usage of polymerases with distinct catalytic specificities may correspond to the specific function that the third hypervariable region assumes for each immunoglobulin chain, with pol lambda maintaining a large heavy chain junctional heterogeneity and pol mu ensuring a restricted light chain junctional variability.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 774, "doc_id": "32275758", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: 1-1% of colorectal cancer patients are diagnosed with regional or distant metastases.\n\nCANDIDATE_ABSTRACT:\nTITLE: Relation between Medicare screening reimbursement and stage at diagnosis for older patients with colon cancer.\nABSTRACT: CONTEXT Medicare's reimbursement policy was changed in 1998 to provide coverage for screening colonoscopies for patients with increased colon cancer risk, and expanded further in 2001 to cover screening colonoscopies for all individuals. OBJECTIVE To determine whether the Medicare reimbursement policy changes were associated with an increase in either colonoscopy use or early stage colon cancer diagnosis. DESIGN, SETTING, AND PARTICIPANTS Patients in the Surveillance, Epidemiology, and End Results Medicare linked database who were 67 years of age and older and had a primary diagnosis of colon cancer during 1992-2002, as well as a group of Medicare beneficiaries who resided in Surveillance, Epidemiology, and End Results areas but who were not diagnosed with cancer. MAIN OUTCOME MEASURES Trends in colonoscopy and sigmoidoscopy use among Medicare beneficiaries without cancer were assessed using multivariate Poisson regression. Among the patients with cancer, stage was classified as early (stage I) vs all other (stages II-IV). Time was categorized as period 1 (no screening coverage, 1992-1997), period 2 (limited coverage, January 1998-June 2001), and period 3 (universal coverage, July 2001-December 2002). A multivariate logistic regression (outcome = early stage) was used to assess temporal trends in stage at diagnosis; an interaction term between tumor site and time was included. RESULTS Colonoscopy use increased from an average rate of 285/100,000 per quarter in period 1 to 889 and 1919/100,000 per quarter in periods 2 (P<.001) and 3 (P vs 2<.001), respectively. During the study period, 44,924 eligible patients were diagnosed with colorectal cancer. The proportion of patients diagnosed at an early stage increased from 22.5% in period 1 to 25.5% in period 2 and [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 4, "doc_id": "22942787", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Allogeneic mechanical circulatory support is not as effective as autologous mechanical circulatory support for treating acute myocardial infarction.\n\nCANDIDATE_ABSTRACT:\nTITLE: Comparison of allogeneic vs autologous bone marrow–derived mesenchymal stem cells delivered by transendocardial injection in patients with ischemic cardiomyopathy: the POSEIDON randomized trial.\nABSTRACT: CONTEXT Mesenchymal stem cells (MSCs) are under evaluation as a therapy for ischemic cardiomyopathy (ICM). Both autologous and allogeneic MSC therapies are possible; however, their safety and efficacy have not been compared. OBJECTIVE To test whether allogeneic MSCs are as safe and effective as autologous MSCs in patients with left ventricular (LV) dysfunction due to ICM. DESIGN, SETTING, AND PATIENTS A phase 1/2 randomized comparison (POSEIDON study) in a US tertiary-care referral hospital of allogeneic and autologous MSCs in 30 patients with LV dysfunction due to ICM between April 2, 2010, and September 14, 2011, with 13-month follow-up. INTERVENTION Twenty million, 100 million, or 200 million cells (5 patients in each cell type per dose level) were delivered by transendocardial stem cell injection into 10 LV sites. MAIN OUTCOME MEASURES Thirty-day postcatheterization incidence of predefined treatment-emergent serious adverse events (SAEs). Efficacy assessments included 6-minute walk test, exercise peak VO2, Minnesota Living with Heart Failure Questionnaire (MLHFQ), New York Heart Association class, LV volumes, ejection fraction (EF), early enhancement defect (EED; infarct size), and sphericity index. RESULTS Within 30 days, 1 patient in each group (treatment-emergent SAE rate, 6.7%) was hospitalized for heart failure, less than the prespecified stopping event rate of 25%. The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3% (n = 8) in the autologous group (P = .46). At 1 year, there were no ventricular arrhythmia SAEs observed among allogeneic recipients compared with 4 patients (26.7%) in the autologous group (P = .10). Relative to baseline, autologous but not allogeneic MSC therapy was associated with an improvement in the 6- [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3% (n = 8) in the autologous group (P = .46).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 104, "doc_id": "40164383", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: 30-Day and 1-year mortality in emergency general surgery laparotomies: an area of concern and need for improvement?\n\nABSTRACT:\nEmergency surgery is associated with poorer outcomes and higher mortality with recent studies suggesting the 30-day mortality to be 14-15%. The aim of this study was to analyse the 30-day mortality, age-related 30-day mortality and 1-year mortality following emergency laparotomy. We hope this will encourage prospective data collection, improvement of care and initiate strategies to establish best practice in this area. This was a retrospective study of patients who underwent emergency laparotomy from June 2010 to May 2012. The primary end point of the study was 30-day mortality, age-related 30-day mortality and 1-year all-cause mortality. 477 laparotomies were performed in 446 patients. 57% were aged<70 and 43% aged>70 years. 30-day mortality was 12, 4% in those aged<70 years and 22% in those>70 years (p<0.001). 1-year mortality was 25, 15% in those aged under 70 years and 38% in those aged>70 years (p<0.001).", "output": "{\"label\": \"maybe\", \"rationale\": \"Emergency laparotomy carries a high rate of mortality, especially in those over the age of 70 years, and more needs to be done to improve outcomes, particularly in this group. This could involve increasing acute surgical care manpower, early recognition of patients requiring emergency surgery, development of clear management protocols for such patients or perhaps even considering centralisation of emergency surgical services to specialist centres with multidisciplinary teams involving emergency surgeons and care of the elderly physicians in hospital and related community outreach services for post-discharge care.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 26037986, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: TMEM27 is a marker for beta cells.\n\nCANDIDATE_PASSAGE:\nMetabolic phenotyping of human blood plasma: a powerful tool to discriminate between cancer types? BACKGROUND Accumulating evidence has shown that cancer cell metabolism differs from that of normal cells. However, up to now it is not clear whether different cancer types are characterized by a specific metabolite profile. Therefore, this study aims to evaluate whether the plasma metabolic phenotype allows to discriminate between lung and breast cancer. PATIENTS AND METHODS The proton nuclear magnetic resonance spectrum of plasma is divided into 110 integration regions, representing the metabolic phenotype. These integration regions reflect the relative metabolite concentrations and were used to train a classification model in discriminating between 80 female breast cancer patients and 54 female lung cancer patients, all with an adenocarcinoma. The validity of the model was examined by permutation testing and by classifying an independent validation cohort of 60 female breast cancer patients and 81 male lung cancer patients, all with an adenocarcinoma. RESULTS The model allows to classify 99% of the breast cancer patients and 93% of the lung cancer patients correctly with an area under the curve (AUC) of 0.96 and can be validated in the independent cohort with a sensitivity of 89%, a specificity of 82% and an AUC of 0.94. Decreased levels of sphingomyelin and phosphatidylcholine (phospholipids with choline head group) and phospholipids with short, unsaturated fatty acid chains next to increased levels of phospholipids with long, saturated fatty acid chains seem to indicate that cell membranes of lung tumors are more rigid and less sensitive to lipid peroxidation. The other discriminating metabolites are pointing to a more pronounced response of the body to the [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1133", "doc_id": "17163294", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Foxp3 represses the expression of transcriptional regulators implicated in memory T cell development.\n\nCANDIDATE_PASSAGE:\nAvailability of evidence of benefits on overall survival and quality of life of cancer drugs approved by European Medicines Agency: retrospective cohort study of drug approvals 2009-13 Objective To determine the availability of data on overall survival and quality of life benefits of cancer drugs approved in Europe. Design Retrospective cohort study. Setting Publicly accessible regulatory and scientific reports on cancer approvals by the European Medicines Agency (EMA) from 2009 to 2013.Main outcome measures Pivotal and postmarketing trials of cancer drugs according to their design features (randomisation, crossover, blinding), comparators, and endpoints. Availability and magnitude of benefit on overall survival or quality of life determined at time of approval and after market entry. Validated European Society for Medical Oncology Magnitude of Clinical Benefit Scale (ESMO-MCBS) used to assess the clinical value of the reported gains in published studies of cancer drugs. Results From 2009 to 2013, the EMA approved the use of 48 cancer drugs for 68 indications. Of these, eight indications (12%) were approved on the basis of a single arm study. At the time of market approval, there was significant prolongation of survival in 24 of the 68 (35%). The magnitude of the benefit on overall survival ranged from 1.0 to 5.8 months (median 2.7 months). At the time of market approval, there was an improvement in quality of life in seven of 68 indications (10%). Out of 44 indications for which there was no evidence of a survival gain at the time of market authorisation, in the subsequent postmarketing period there was evidence for extension of life in three (7%) and reported benefit on quality of life in five (11%). Of the 68 cancer indications with EMA approval, and with [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "435", "doc_id": "32421068", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Medications to treat obesity do not have side effects.\n\nCANDIDATE_ABSTRACT:\nTITLE: Workshop: endothelial cell dysfunction leading to diabetic nephropathy : focus on nitric oxide.\nABSTRACT: Clinical manifestations of diabetic nephropathy are an expression of diabetic microangiopathy. This review revisits the previously proposed Steno hypothesis and advances our hypothesis that development of endothelial cell dysfunction represents a common pathophysiological pathway of diabetic complications. Specifically, the ability of glucose to scavenge nitric oxide is proposed as the initiation phase of endothelial dysfunction. Gradual accumulation of advanced glycated end products and induction of plasminogen activator inhibitor-1, resulting in the decreased expression of endothelial nitric oxide synthase and reduced generation of nitric oxide, are proposed to be pathophysiologically critical for the maintenance phase of endothelial dysfunction. The proposed conceptual shift toward the role of endothelial dysfunction in diabetic complications may provide new strategies for their prevention.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 765, "doc_id": "2533768", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Microcin J25 encourages nucleoside triphosphate (NTP) binding.\n\nCANDIDATE_PASSAGE:\nUncoupling Mitochondrial Respiration for Diabesity. Until recently, the mechanism of adaptive thermogenesis was ascribed to the expression of uncoupling protein 1 (UCP1) in brown and beige adipocytes. UCP1 is known to catalyze a proton leak of the inner mitochondrial membrane, resulting in uncoupled oxidative metabolism with no production of adenosine triphosphate and increased energy expenditure. Thus increasing brown and beige adipose tissue with augmented UCP1 expression is a viable target for obesity-related disorders. Recent work demonstrates an UCP1-independent pathway to uncouple mitochondrial respiration. A secreted enzyme, PM20D1, enriched in UCP1+ adipocytes, exhibits catalytic and hydrolytic activity to reversibly form N-acyl amino acids. N-acyl amino acids act as endogenous uncouplers of mitochondrial respiration at physiological concentrations. Administration of PM20D1 or its products, N-acyl amino acids, to diet-induced obese mice improves glucose tolerance by increasing energy expenditure. In short-term studies, treated animals exhibit no toxicity while experiencing 10% weight loss primarily of adipose tissue. Further study of this metabolic pathway may identify novel therapies for diabesity, the disease state associated with diabetes and obesity.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "787", "doc_id": "29691654", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is docetaxel a major cytotoxic drug for the treatment of advanced breast cancer : a phase II trial of the Clinical Screening Cooperative Group of the European Organization for Research and Treatment of Cancer?\n\nABSTRACT:\nThis trial investigated the toxicity and efficacy of docetaxel as first-line chemotherapy in women with heavily pretreated advanced breast cancer. From April 1992 to August 1992, 35 patients with advanced breast cancer from 29 to 65 years of age with a performance status of 0 to 2 were entered onto the study. Docetaxel 100 mg/m2 was administered every 3 weeks as a 1-hour infusion on day 1 without routine premedication for hypersensitivity reactions. Thirty-one patients were assessable for response. Previous adjuvant chemotherapy had been given to 11 patients. Five complete responses (CRs) and 16 partial responses (PRs) were observed, for an overall response rate of 67.7% (95% confidence interval, 49% to 83%). A CR occurred at 13 of 45 assessable sites (four liver, two lung, three breast, three lymph node, and one skin). The median duration of response was 44+ weeks, the median time to disease progression 37+ weeks, and the median overall survival time 16+ months. Among 34 patients assessable for toxicity (177 cycles; median, five cycles per patient), the following side effects were reported: nadir neutropenia grade 3 (three patients); grade 4 (31 patients); no grade 3 to 4 infection, acute hypersensitivity-like reaction (10 patients); grade 2 to 3 alopecia (all patients); and grade 2 to 3 nausea and vomiting (six patients). Fluid retention occurred in 26 patients and consisted of weight gain, edema alone (15 patients), or edema associated with serous effusion (11 patients). This side effect led to treatment discontinuation in 16 of 21 responding patients after a median of five cycles and a median cumulative dose of docetaxel of 574 mg/m2.", "output": "{\"label\": \"yes\", \"rationale\": \"Our data suggest that docetaxel has major antitumor activity when used as a single cytotoxic agent as first-line chemotherapy in advanced breast cancer.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 7844592, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Women with a higher birth weight are more likely to develop breast cancer later in life.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cerebral perfusion and stroke.\nABSTRACT: Stroke is a heterogeneous syndrome caused by multiple disease mechanisms, but all result in a disruption of cerebral blood flow with subsequent tissue damage. This review covers the mechanisms responsible for regulation of the normal cerebral circulation, and how they are disrupted in disease states. A central concept in treating patients with acute ischaemic stroke is the existence of an ischaemic penumbra of potentially salvageable tissue, and the evidence for its existence in humans is reviewed.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1379, "doc_id": "2352142", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Birth-weight is negatively associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Birth Size and Breast Cancer Risk: Re-analysis of Individual Participant Data from 32 Studies\nABSTRACT: BACKGROUND Birth size, perhaps a proxy for prenatal environment, might be a correlate of subsequent breast cancer risk, but findings from epidemiological studies have been inconsistent. We re-analysed individual participant data from published and unpublished studies to obtain more precise estimates of the magnitude and shape of the birth size-breast cancer association. METHODS AND FINDINGS Studies were identified through computer-assisted and manual searches, and personal communication with investigators. Individual participant data from 32 studies, comprising 22,058 breast cancer cases, were obtained. Random effect models were used, if appropriate, to combine study-specific estimates of effect. Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003). Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data. Birth length and head circumference from birth records were also positively associated with breast cancer risk (pooled RR per one SD increment: 1.06 [95% CI 1.03-1.10] and 1.09 [95% CI 1.03-1.15], respectively). Simultaneous adjustment for these three birth size variables showed that length was the strongest independent predictor of risk. The birth size effec [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 178, "doc_id": "16322674", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does inactivation of the LKB1-AMPK signaling pathway contribute to salivary gland tumor development - a short report?\n\nABSTRACT:\nActivation of AMPK by the tumor suppressor LKB1 represents an essential gatekeeping step for cells under energetic stress to prevent their growth and proliferation by inhibiting mTOR activation, until the energy supply normalizes. The LKB1/AMPK pathway is frequently downregulated in various types of cancer, thereby uncoupling tumor cell growth and proliferation from energy supply. As yet, little information is available on the role of the LKB1/AMPK pathway in tumors derived from salivary gland tissues. We performed LKB1 protein expression and AMPK and mTOR activation analyses in several salivary gland tumor types and their respective healthy control tissues using immunohistochemistry. No significant downregulation of LKB1 expression or decreased activation of AMPK or mTOR were observed in any of the salivary gland tumors tested. In contrast, we found that the salivary gland tumors exhibited an increased rather than a decreased AMPK activation. Although the PI3K/Akt pathway was found to be activated in most of the analyzed tumor samples, the unchanged robust activity of LKB1/AMPK likely prevents (over)activation of mTOR.", "output": "{\"label\": \"no\", \"rationale\": \"In contrast to many other types of cancer, inactivation or downregulation of the LKB1/AMPK pathway does not substantially contribute to the pathogenesis of salivary gland tumors.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 27480082, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is lesser than diabetes hyperglycemia in pregnancy related to perinatal mortality : a cohort study in Brazil?\n\nABSTRACT:\nGestational diabetes related morbidity increases along the continuum of the glycemic spectrum. Perinatal mortality, as a complication of gestational diabetes, has been little investigated. In early studies, an association was found, but in more recent ones it has not been confirmed. The Brazilian Study of Gestational Diabetes, a cohort of untreated pregnant women enrolled in the early 1990's, offers a unique opportunity to investigate this question. Thus, our objective is to evaluate whether perinatal mortality increases in a continuum across the maternal glycemic spectrum. We prospectively enrolled and followed 4401 pregnant women attending general prenatal care clinics in six Brazilian state capitals, without history of diabetes outside of pregnancy, through to birth, and their offspring through the early neonatal period. Women answered a structured questionnaire and underwent a standardized 2-hour 75-g oral glucose tolerance test (OGTT). Obstetric care was maintained according to local protocols. We obtained antenatal, delivery and neonatal data from hospital records. Odds ratios (OR) were estimated using logistic regression. We ascertained 97 perinatal deaths (67 fetal and 31 early neonatal). Odds of dying increased according to glucose levels, statistically significantly so only for women delivering at gestational age ≥34 weeks (p < 0.05 for glycemia-gestational age interaction). ORs for a 1 standard deviation difference in glucose, when analyzed continuously, were for fasting 1.47 (95% CI 1.12, 1.92); 1-h 1.55 (95% CI 1.15, 2.07); and 2-h 1.53 (95% CI 1.15, 2.02). The adjusted OR for IADPSG criteria gestational diabetes was 2.21 (95% CI 1.15, 4.27); and for WHO criteria gestational diabetes, 3.10 (95% CI 1.39, 6.88).", "output": "{\"label\": \"yes\", \"rationale\": \"In settings of limited detection and treatment of gestational diabetes mellitus, women across a spectrum of lesser than diabetes hyperglycemia, experienced a continuous rise in perinatal death with increasing levels of glycemia after 34 weeks of pregnancy. Current GDM diagnostic criteria identified this increased risk of mortality.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 22078268, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Lamins are found within the inner layer of the mitochondrial membrane of all cells.\n\nCANDIDATE_PASSAGE:\nAutophagy mediates degradation of nuclear lamina Macroautophagy (hereafter referred to as autophagy) is a catabolic membrane trafficking process that degrades a variety of cellular constituents and is associated with human diseases. Although extensive studies have focused on autophagic turnover of cytoplasmic materials, little is known about the role of autophagy in degrading nuclear components. Here we report that the autophagy machinery mediates degradation of nuclear lamina components in mammals. The autophagy protein LC3/Atg8, which is involved in autophagy membrane trafficking and substrate delivery, is present in the nucleus and directly interacts with the nuclear lamina protein lamin B1, and binds to lamin-associated domains on chromatin. This LC3-lamin B1 interaction does not downregulate lamin B1 during starvation, but mediates its degradation upon oncogenic insults, such as by activated RAS. Lamin B1 degradation is achieved by nucleus-to-cytoplasm transport that delivers lamin B1 to the lysosome. Inhibiting autophagy or the LC3-lamin B1 interaction prevents activated RAS-induced lamin B1 loss and attenuates oncogene-induced senescence in primary human cells. Our study suggests that this new function of autophagy acts as a guarding mechanism protecting cells from tumorigenesis.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "686", "doc_id": "4452659", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Inhibiting HDAC6 increases survival of mice with ARID1A mutated tumors.\n\nCANDIDATE_PASSAGE:\nThe inflammasome component NLRP3 impairs antitumor vaccine by enhancing the accumulation of tumor-associated myeloid-derived suppressor cells. The inflammasome is a proteolysis complex that generates the active forms of the proinflammatory cytokines interleukin (IL)-1β and IL-18. Inflammasome activation is mediated by NLR proteins that respond to microbial and nonmicrobial stimuli. Among NLRs, NLRP3 senses the widest array of stimuli and enhances adaptive immunity. However, its role in antitumor immunity is unknown. Therefore, we evaluated the function of the NLRP3 inflammasome in the immune response using dendritic cell vaccination against the poorly immunogenic melanoma cell line B16-F10. Vaccination of Nlrp3(-/-) mice led to a relative 4-fold improvement in survival relative to control animals. Immunity depended on CD8(+) T cells and exhibited immune specificity and memory. Increased vaccine efficacy in Nlrp3(-/-) hosts did not reflect differences in dendritic cells but rather differences in myeloid-derived suppressor cells (MDSC). Although Nlrp3 was expressed in MDSCs, the absence of Nlrp3 did not alter either their functional capacity to inhibit T cells or their presence in peripheral lymphoid tissues. Instead, the absence of Nlrp3 caused a 5-fold reduction in the number of tumor-associated MDSCs found in host mice. Adoptive transfer experiments also showed that Nlrp3(-/-) MDSCs were less efficient in reaching the tumor site. Depleting MDSCs with an anti-Gr-1 antibody increased the survival of tumor-bearing wild-type mice but not Nlrp3(-/-) mice. We concluded that Nlrp3 was critical for accumulation of MDSCs in tumors and for inhibition of antitumor T-cell immunity after dendritic cell vaccination. Our findings establish an unexpected role for Nlrp3 in [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "631", "doc_id": "15435343", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: LSD1-positive promoters are associated with RNA polymerase II\n\nCANDIDATE_PASSAGE:\nHistone Methylation-Dependent Mechanisms Impose Ligand Dependency for Gene Activation by Nuclear Receptors Nuclear receptors undergo ligand-dependent conformational changes that are required for corepressor-coactivator exchange, but whether there is an actual requirement for specific epigenetic landmarks to impose ligand dependency for gene activation remains unknown. Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases (HMTs) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals. This strategy, based at least in part on an HMT-dependent inhibitory histone code, imposes a requirement for specific histone demethylases, including LSD1, to permit ligand- and signal-dependent activation of regulated gene expression. These events link an inhibitory methylation component of the histone code to a broadly used strategy that circumvents pathological constitutive gene induction by physiologically regulated transcription factors.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "679", "doc_id": "13639330", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The risk of breast cancer among parous women decreases with placental weight of pregnancies.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pregnancy characteristics and maternal risk of breast cancer.\nABSTRACT: CONTEXT During pregnancy, serum levels of estrogen, progesterone, and other hormones are markedly higher than during other periods of life. Pregnancy hormones primarily are produced in the placenta, and signs of placental impairment may serve as indirect markers of hormone exposures during pregnancy. During pregnancy, these markers have been inconsistently associated with subsequent risk of breast cancer in the mother. OBJECTIVE To examine associations between indirect markers of hormonal exposures, such as placental weight and other pregnancy characteristics, and maternal risk of developing breast cancer. DESIGN AND SETTING Population-based cohort study using data from the Swedish Birth Register, the Swedish Cancer Register, the Swedish Cause of Death Register, and the Swedish Register of Population and Population Changes. PARTICIPANTS Women included in the Sweden Birth Register who delivered singletons between 1982 and 1989, with complete information on date of birth and gestational age. Women were followed up until the occurrence of breast cancer, death, or end of follow-up (December 31, 2001). Cox proportional hazards models were used to estimate associations between hormone exposures and risks of breast cancer. MAIN OUTCOME MEASURE Incidence of invasive breast cancer. RESULTS Of 314,019 women in the cohort, 2216 (0.7%) developed breast cancer during the follow-up through 2001, of whom 2100 (95%) were diagnosed before age 50 years. Compared with women who had placentas weighing less than 500 g in 2 consecutive pregnancies, the risk of breast cancer was increased among women whose placentas weighed between 500 and 699 g in their first pregnancy and at least 700 g in their second pregnancy (or vice versa) (adjusted hazard ratio, 1.82; 95% confidence interv [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Placental weight is positively associated with maternal risk of breast cancer.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1265, "doc_id": "37480103", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: ADAR1 binds to Dicer to cleave pre-miRNA.\n\nCANDIDATE_ABSTRACT:\nTITLE: Partitioning the symptoms of hypoglycaemia using multi-sample confirmatory factor analysis\nABSTRACT: The allocation of hypoglycaemic symptoms to autonomie or neuroglycopenic groups tends to occur on an a priori basis. In view of the practical need for clear symptom markers of hypoglycaemia more scientific approaches must be pursued. Substantial evidence is presented from two large scale studies we performed which support a three factor model of hypoglycaemic symptomatology, based on the statistical associations discovered among symptoms reported by diabetic patients. Study 1 involved 295 insulin-treated outpatients and found that 11 key hypoglycaemic symptoms segregated into three clear factors: autonomie (sweating, palpitation, shaking and hunger) neuroglycopenic (confusion, drowsiness, odd behaviour, speech difficulty and incoordination), and malaise (nausea and headache). The three factors were validated on a separate group of 303 insulin-treated diabetic out-patients. Confirmatory factor analyses showed that the three factor model was the optimal model for explaining symptom covariance in each group. A multi-sample confirmatory factor analysis tested the rigorous assumptions that the relative loadings of symptoms on factors across groups were equal, and that the residual variance for each symptom was identical across groups. These assumptions were successful, indicating that the three factor model was replicated in detail across these two large samples. It is suggested that the results indicate valid groupings of symptoms that may be used in future research and in clinical practice.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 49, "doc_id": "1904291", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The one-child policy has created a hospitable environment for female infants.\n\nCANDIDATE_ABSTRACT:\nTITLE: Perinatal mortality in rural China: retrospective cohort study.\nABSTRACT: OBJECTIVES To explore the use of local civil registration data to assess the perinatal mortality in a typical rural county in a less developed province in China, 1999-2000. DESIGN Retrospective cohort study. Pregnancies in a cohort of women followed from registration of pregnancy to outcome of infant seven days after birth. SETTING Routine family planning records in 20 rural townships in eastern China. SUBJECTS 3697 pregnancies registered by the local family planning system during 1999. MAIN OUTCOME MEASURES Abortions, stillbirths, early neonatal mortality, perinatal mortality. RESULTS Only three cases were lost to follow up. The average age of the women at pregnancy was 25.9 years. Three hundred and twelve pregnancies were aborted and 240 ended in miscarriage (total 552, 15%). The perinatal mortality rate was 69 per 1000 births, the rate of stillbirth was 24 per 1000 births, and the early neonatal mortality was 46 per 1000 live births. The early neonatal mortality was 29 in boys and 69 in girls per 1000 live births. The perinatal mortality rate increased notably with parity and was higher in townships having lower income per capita. CONCLUSIONS The family planning system at the most local level is a useful data source for studying perinatal mortality in rural China. The perinatal mortality rate in the study county was higher than previously reported for both rural and urban areas in China. The results by parity and sex of the infant raise concern over the impact of the one child policy.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The early neonatal mortality was 29 in boys and 69 in girls per 1000 live births.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1246, "doc_id": "7662395", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The G34R/V mutation creates a hypomethylated phenotype at the H3K36 histone.\n\nCANDIDATE_PASSAGE:\nHigh CTLA-4 expression on Th17 cells results in increased sensitivity to CTLA-4 coinhibition and resistance to belatacept. The CD28/cytotoxic T-lymphocyte antigen 4 (CTLA-4)blocker belatacept selectively inhibits alloreactive T cell responses but is associated with a high incidence of acute rejection following renal transplantation,which led us to investigate the etiology of belatacept–resistant graft rejection. T cells can differentiate into functionally distinct subsets of memory T cellsthat collectively enable protection against diverse classes of pathogens and can cross-react with allogeneicantigen and mediate graft rejection. T helper 17(Th17) cells are a pro-inflammatory CD4+ lineage that provides immunity to pathogens and are pathogenic in autoimmune disease. We found that T helper 1 (Th1)and Th17 memory compartments contained a similar frequency of divided cells following allogeneic stimulation. Compared to Th1 cells, Th17 memory cells expressed significantly higher levels of the coinhibitory molecule CTLA-4. Stimulation in the presence of belatacept inhibited Th1 responses but augmented Th17 cells due to greater sensitivity to coinhibition by CTLA-4. Th17 cells from renal transplant recipients were resistant to ex vivo CD28/CTLA-4 blockade with belatacept, and an elevated frequency of Th17 memory cells was associated with acute rejection during belatacept therapy. These data highlight important differences in costimulatory and coinhibitory requirements of CD4+ memory subsets, and demonstrate that the heterogeneity of pathogen-derived memory has implications for immunomodulation strategies.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1164", "doc_id": "13398997", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Lack of FGF21 in mice slows the rate of atherosclerotic plaque formation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Fibroblast Growth Factor 21 Prevents Atherosclerosis by Suppression of Hepatic Sterol Regulatory Element-Binding Protein-2 and Induction of Adiponectin in Mice\nABSTRACT: BACKGROUND Fibroblast growth factor 21 (FGF21) is a metabolic hormone with pleiotropic effects on glucose and lipid metabolism and insulin sensitivity. It acts as a key downstream target of both peroxisome proliferator-activated receptor α and γ, the agonists of which have been used for lipid lowering and insulin sensitization, respectively. However, the role of FGF21 in the cardiovascular system remains elusive. METHODS AND RESULTS The roles of FGF21 in atherosclerosis were investigated by evaluating the impact of FGF21 deficiency and replenishment with recombinant FGF21 in apolipoprotein E(-/-) mice. FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia. Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia. Chronic treatment with adiponectin partially reverses atherosclerosis without obvious effects on hypercholesterolemia in FGF21-deficient apolipoprotein E(-/-) mice. By contrast, the cholesterol-lowering effects of FGF21 are abrogated by hepatic expression of sterol regulatory element-binding protein-2. CONCLUSIONS FGF21 protects against atherosclerosis via fine tuning the multiorgan crosstalk among liver, adipose tissue, and blood vessels.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS FGF21 protects against atherosclerosis via fine tuning the multiorgan crosstalk among liver, adipose tissue, and blood vessels.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 683, "doc_id": "9315213", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is Panton-Valentine leucocidin associated with the pathogenesis of Staphylococcus aureus bacteraemia in the UK?\n\nABSTRACT:\nThe morbidity and mortality associated with Panton-Valentine leucocidin (PVL)-positive Staphylococcus aureus suggest that this toxin is a key marker of disease severity. Nevertheless, the importance of PVL in the pathogenesis of primary bacteraemia caused by S. aureus is uncertain. We have determined the prevalence of PVL-encoding genes among isolates of S. aureus from bacteraemic patients. Consecutive bacteraemia isolates of S. aureus (n=244) from patients hospitalized in 25 centres in the UK and Ireland during 2005 were screened for PVL and mecA genes. PVL-positive isolates were characterized by toxin gene profiling, PFGE, spa-typing and MIC determinations for a range of antimicrobials. Four out of 244 isolates (1.6%) were PVL-positive and susceptible to oxacillin [methicillin-susceptible S. aureus (MSSA)]. Eighty-eight out of 244 (36%) were oxacillin-resistant (methicillin-resistant S. aureus), but none was PVL-positive. The four patients (two males: 30 and 33 years; two females: 62 and 80 years) had infection foci of: skin and soft tissue, unknown, indwelling line, and surgical site, and were located at one centre in Wales, one in England and two in Ireland. One of four PVL-positive isolates was resistant to penicillin and fusidic acid, the remainder were susceptible to all antibiotics tested. Genotypic analyses showed that the four isolates represented three distinct strains; the two isolates from Ireland were related.", "output": "{\"label\": \"maybe\", \"rationale\": \"We found that 1.6% of S. aureus (all MSSA) from bacteraemic patients were PVL-positive. This low incidence suggests that PVL-positive S.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 17562682, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Rhythmic expression of Cry1 translates directly into a circadian regulation of cAMP signaling in hepatic glucose metabolism.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cryptochrome Mediates Circadian Regulation of cAMP Signaling and Hepatic Gluconeogenesis\nABSTRACT: During fasting, mammals maintain normal glucose homeostasis by stimulating hepatic gluconeogenesis. Elevations in circulating glucagon and epinephrine, two hormones that activate hepatic gluconeogenesis, trigger the cAMP-mediated phosphorylation of cAMP response element-binding protein (Creb) and dephosphorylation of the Creb-regulated transcription coactivator-2 (Crtc2)--two key transcriptional regulators of this process. Although the underlying mechanism is unclear, hepatic gluconeogenesis is also regulated by the circadian clock, which coordinates glucose metabolism with changes in the external environment. Circadian control of gene expression is achieved by two transcriptional activators, Clock and Bmal1, which stimulate cryptochrome (Cry1 and Cry2) and Period (Per1, Per2 and Per3) repressors that feed back on Clock-Bmal1 activity. Here we show that Creb activity during fasting is modulated by Cry1 and Cry2, which are rhythmically expressed in the liver. Cry1 expression was elevated during the night-day transition, when it reduced fasting gluconeogenic gene expression by blocking glucagon-mediated increases in intracellular cAMP concentrations and in the protein kinase A-mediated phosphorylation of Creb. In biochemical reconstitution studies, we found that Cry1 inhibited accumulation of cAMP in response to G protein-coupled receptor (GPCR) activation but not to forskolin, a direct activator of adenyl cyclase. Cry proteins seemed to modulate GPCR activity directly through interaction with G(s)α. As hepatic overexpression of Cry1 lowered blood glucose concentrations and improved insulin sensitivity in insulin-resistant db/db mice, our results suggest that compounds that enhance cryptochrome activity may provide therapeutic benefit to individuals with type 2 diabetes.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Although the underlying mechanism is unclear, hepatic gluconeogenesis is also regulated by the circadian clock, which coordinates glucose metabolism with changes in the external environment. Circadian control of gene expression is achieved by two transcriptional activators, Clock and Bmal1, which stimulate cryptochrome (Cry1 and Cry2) and Period (Per1, Per2 and Per3) repressors that feed back on Clock-Bmal1 activity.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1045, "doc_id": "22500262", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Increased flux of microbial products provokes immune responses.\n\nCANDIDATE_ABSTRACT:\nTITLE: Compromised intestinal epithelial barrier induces adaptive immune compensation that protects from colitis.\nABSTRACT: Mice lacking junctional adhesion molecule A (JAM-A, encoded by F11r) exhibit enhanced intestinal epithelial permeability, bacterial translocation, and elevated colonic lymphocyte numbers, yet do not develop colitis. To investigate the contribution of adaptive immune compensation in response to increased intestinal epithelial permeability, we examined the susceptibility of F11r(-/-)Rag1(-/-) mice to acute colitis. Although negligible contributions of adaptive immunity in F11r(+/+)Rag1(-/-) mice were observed, F11r(-/-)Rag1(-/-) mice exhibited increased microflora-dependent colitis. Elimination of T cell subsets and cytokine analyses revealed a protective role for TGF-β-producing CD4(+) T cells in F11r(-/-) mice. Additionally, loss of JAM-A resulted in elevated mucosal and serum IgA that was dependent upon CD4(+) T cells and TGF-β. Absence of IgA in F11r(+/+)Igha(-/-) mice did not affect disease, whereas F11r(-/-)Igha(-/-) mice displayed markedly increased susceptibility to acute injury-induced colitis. These data establish a role for adaptive immune-mediated protection from acute colitis under conditions of intestinal epithelial barrier compromise.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 609, "doc_id": "40096222", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Nanoparticles can be targeted against specific cell types by incorporating aptamers into lipid nanoparticles.\n\nCANDIDATE_ABSTRACT:\nTITLE: Aptamer-functionalized lipid nanoparticles targeting osteoblasts as a novel RNA interference–based bone anabolic strategy\nABSTRACT: Currently, major concerns about the safety and efficacy of RNA interference (RNAi)-based bone anabolic strategies still exist because of the lack of direct osteoblast-specific delivery systems for osteogenic siRNAs. Here we screened the aptamer CH6 by cell-SELEX, specifically targeting both rat and human osteoblasts, and then we developed CH6 aptamer–functionalized lipid nanoparticles (LNPs) encapsulating osteogenic pleckstrin homology domain-containing family O member 1 (Plekho1) siRNA (CH6-LNPs-siRNA). Our results showed that CH6 facilitated in vitro osteoblast-selective uptake of Plekho1 siRNA, mainly via macropinocytosis, and boosted in vivo osteoblast-specific Plekho1 gene silencing, which promoted bone formation, improved bone microarchitecture, increased bone mass and enhanced mechanical properties in both osteopenic and healthy rodents. These results indicate that osteoblast-specific aptamer-functionalized LNPs could act as a new RNAi-based bone anabolic strategy, advancing the targeted delivery selectivity of osteogenic siRNAs from the tissue level to the cellular level.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Our results showed that CH6 facilitated in vitro osteoblast-selective uptake of Plekho1 siRNA, mainly via macropinocytosis, and boosted in vivo osteoblast-specific Plekho1 gene silencing, which promoted bone formation, improved bone microarchitecture, increased bone mass and enhanced mechanical properties in both osteopenic and healthy rodents.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 839, "doc_id": "1469751", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: DRD1 proteins enable Pol V transcription in vivo.\n\nCANDIDATE_PASSAGE:\nA Conserved MST-FOXO Signaling Pathway Mediates Oxidative-Stress Responses and Extends Life Span Oxidative stress influences cell survival and homeostasis, but the mechanisms underlying the biological effects of oxidative stress remain to be elucidated. Here, we demonstrate that the protein kinase MST1 mediates oxidative-stress-induced cell death in primary mammalian neurons by directly activating the FOXO transcription factors. MST1 phosphorylates FOXO proteins at a conserved site within the forkhead domain that disrupts their interaction with 14-3-3 proteins, promotes FOXO nuclear translocation, and thereby induces cell death in neurons. We also extend the MST-FOXO signaling link to nematodes. Knockdown of the C. elegans MST1 ortholog CST-1 shortens life span and accelerates tissue aging, while overexpression of cst-1 promotes life span and delays aging. The cst-1-induced life-span extension occurs in a daf-16-dependent manner. The identification of the FOXO transcription factors as major and evolutionarily conserved targets of MST1 suggests that MST kinases play important roles in diverse biological processes including cellular responses to oxidative stress and longevity.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "305", "doc_id": "14496749", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Obesity is determined solely by environmental factors.\n\nCANDIDATE_PASSAGE:\nHelicobacter hepaticus does not induce or potentiate colitis in interleukin-10-deficient mice. Helicobacter hepaticus has been reported to induce colitis, hepatitis, and hepatocellular carcinoma in several different murine models. The aim of this study was to determine if H. hepaticus will cause colitis in monoassociated mice lacking the interleukin-10 gene (IL-10(-/-) mice) and potentiate colitis in specific-pathogen-free (SPF) IL-10(-/-) mice. Germfree IL-10(-/-) mice on either a mixed (C57BL/6 x 129/Ola) or inbred (129/SvEv) genetic background were monoassociated with H. hepaticus ATCC 51448 by oral feeding and rectal enemas. In a second experiment, germfree IL-10(-/-) mice were colonized with stool from SPF mice that harbored or did not harbor endogenous H. hepaticus. After 7 to 9 weeks of colonization, weight loss and mortality were assessed, the colon was isolated for histology and IL-12 secretion, and mesenteric lymph node cells were assessed for T-cell activation markers. It was found that IL-10(-/-) mice monoassociated with H. hepaticus for up to 16 weeks showed almost no histologic colitis or increased IL-12 production. SPF IL-10-knockout mice had no significant difference in weight loss, mortality rate, histologic scores, colonic IL-12 secretion, or T-cell activation with or without H. hepaticus. We conclude that H. hepaticus does not induce or potentiate disease in our IL-10(-/-) mice and therefore is not required to induce colitis in genetically susceptible hosts.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "873", "doc_id": "23573229", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: A diminished ovarian reserve does not solely indicate infertility in an a priori non-infertile population.\n\nCANDIDATE_PASSAGE:\nDiminished performance on neuropsychological testing in late life depression is correlated with microstructural white matter abnormalities. BACKGROUND Traditional T2 weighted MR imaging results are non-specific for the extent of underlying white matter structural abnormalities present in late life depression (LLD). Diffusion tensor imaging provides a unique opportunity to investigate the extent and nature of structural injury, but has been limited by examining only a subset of regions of interest (ROI) and by confounds common to the study of an elderly population, including comorbid vascular pathology. Furthermore, comprehensive correlation of diffusion tensor imaging (DTI) measurements, including axial and radial diffusivity measurements, has not been demonstrated in the late life depression population. METHODS 51 depressed and 16 non-depressed, age- and cerebrovascular risk factor-matched elderly subjects underwent traditional anatomic T1 and T2 weight imaging, as well as DTI. The DTI data were skeletonized using tract based spatial statistics (TBSS), and both regional and global analyses were performed. RESULTS Widespread structural abnormalities within white matter were detected in the LLD group, accounting for age, gender and education and matched for cerebrovascular risk factors and global T2 white matter hyperintensities (T2WMH). Regional differences were most prominent in uncinate and cingulate white matter and were generally characterized by an increase in radial diffusivity. Age-related changes particularly in the cingulate bundle were more advanced in individuals with LLD relative to controls. Regression analysis demonstrated significant correlations of regional fractional anisotropy and radial diffusivity with five different neuropsychological fa [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "39", "doc_id": "1412089", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Induction of urokinase receptor signaling in podocytes causes foot process effacement and proteinuria.\n\nCANDIDATE_ABSTRACT:\nTITLE: Modification of kidney barrier function by the urokinase receptor\nABSTRACT: Podocyte dysfunction, represented by foot process effacement and proteinuria, is often the starting point for progressive kidney disease. Therapies aimed at the cellular level of the disease are currently not available. Here we show that induction of urokinase receptor (uPAR) signaling in podocytes leads to foot process effacement and urinary protein loss via a mechanism that includes lipid-dependent activation of αvβ3 integrin. Mice lacking uPAR (Plaur−/−) are protected from lipopolysaccharide (LPS)-mediated proteinuria but develop disease after expression of a constitutively active β3 integrin. Gene transfer studies reveal a prerequisite for uPAR expression in podocytes, but not in endothelial cells, for the development of LPS-mediated proteinuria. Mechanistically, uPAR is required to activate αvβ3 integrin in podocytes, promoting cell motility and activation of the small GTPases Cdc42 and Rac1. Blockade of αvβ3 integrin reduces podocyte motility in vitro and lowers proteinuria in mice. Our findings show a physiological role for uPAR signaling in the regulation of kidney permeability.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here we show that induction of urokinase receptor (uPAR) signaling in podocytes leads to foot process effacement and urinary protein loss via a mechanism that includes lipid-dependent activation of αvβ3 integrin.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 626, "doc_id": "16355392", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does serum Cystatin C Predict Mortality or Treatment Failure in Peritoneal Dialysis : A Prospective Study?\n\nABSTRACT:\n♦ Small solute clearance, especially that derived from residual renal function (RRF), is an independent risk factor for death in peritoneal dialysis (PD) patients. Assessment of solute clearance is time-consuming and prone to multiple errors. Cystatin C is a small protein which has been used as a glomerular filtration rate (GFR) marker. We investigated whether serum cystatin C concentrations are related to mortality in patients receiving PD. ♦ New and prevalent PD patients (n = 235) underwent assessment of Kt/Vurea, RRF, weekly creatinine clearance (CCr), normalized protein catabolic rate (nPCR) and a peritoneal equilibration test (PET) at intervals. Blood was collected simultaneously for cystatin C measurement. Patients were followed for a median of 1,429 days (range 12 to 2,964 days) until death or study closure. Cause of death was recorded where given. Cox regression was performed to determine whether cystatin C had prognostic value either independently or with adjustment for other factors (age, sex, dialysis modality, diabetic status, cardiovascular comorbidity, Kt/V, CCr, RRF, nPCR or 4 h dialysate to plasma creatinine ratio (4 h D/Pcr) during the PET). The primary outcomes were all-cause mortality and treatment failure. ♦ There were 93 deaths. Increasing age and 4 h D/Pcr ratio, decreased RRF and presence of diabetes were significantly [p < 0.05] negatively associated with survival and treatment failure. Serum cystatin C was not related to either outcome. ♦", "output": "{\"label\": \"no\", \"rationale\": \"Serum cystatin C concentration does not predict mortality or treatment failure in patients receiving PD.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25185011, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: 61% of colorectal cancer patients are diagnosed with regional or distant metastases.\n\nCANDIDATE_ABSTRACT:\nTITLE: Relation between Medicare screening reimbursement and stage at diagnosis for older patients with colon cancer.\nABSTRACT: CONTEXT Medicare's reimbursement policy was changed in 1998 to provide coverage for screening colonoscopies for patients with increased colon cancer risk, and expanded further in 2001 to cover screening colonoscopies for all individuals. OBJECTIVE To determine whether the Medicare reimbursement policy changes were associated with an increase in either colonoscopy use or early stage colon cancer diagnosis. DESIGN, SETTING, AND PARTICIPANTS Patients in the Surveillance, Epidemiology, and End Results Medicare linked database who were 67 years of age and older and had a primary diagnosis of colon cancer during 1992-2002, as well as a group of Medicare beneficiaries who resided in Surveillance, Epidemiology, and End Results areas but who were not diagnosed with cancer. MAIN OUTCOME MEASURES Trends in colonoscopy and sigmoidoscopy use among Medicare beneficiaries without cancer were assessed using multivariate Poisson regression. Among the patients with cancer, stage was classified as early (stage I) vs all other (stages II-IV). Time was categorized as period 1 (no screening coverage, 1992-1997), period 2 (limited coverage, January 1998-June 2001), and period 3 (universal coverage, July 2001-December 2002). A multivariate logistic regression (outcome = early stage) was used to assess temporal trends in stage at diagnosis; an interaction term between tumor site and time was included. RESULTS Colonoscopy use increased from an average rate of 285/100,000 per quarter in period 1 to 889 and 1919/100,000 per quarter in periods 2 (P<.001) and 3 (P vs 2<.001), respectively. During the study period, 44,924 eligible patients were diagnosed with colorectal cancer. The proportion of patients diagnosed at an early stage increased from 22.5% in period 1 to 25.5% in period 2 and [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 18, "doc_id": "22942787", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: 0-dimensional biomaterials lack inductive properties.\n\nCANDIDATE_PASSAGE:\nIdentification and characterization of a common set of complex I assembly intermediates in mitochondria from patients with complex I deficiency. Deficiencies in the activity of complex I (NADH: ubiquinone oxidoreductase) are an important cause of human mitochondrial disease. Complex I is composed of at least 46 structural subunits that are encoded in both nuclear and mitochondrial DNA. Enzyme deficiency can result from either impaired catalytic efficiency or an inability to assemble the holoenzyme complex; however, the assembly process remains poorly understood. We have used two-dimensional Blue-Native/SDS gel electrophoresis and a panel of 11 antibodies directed against structural subunits of the enzyme to investigate complex I assembly in the muscle mitochondria from four patients with complex I deficiency caused by either mitochondrial or nuclear gene defects. Immunoblot analyses of second dimension denaturing gels identified seven distinct complex I subcomplexes in the patients studied, five of which could also be detected in nondenaturing gels in the first dimension. Although the abundance of these intermediates varied among the different patients, a common constellation of subcomplexes was observed in all cases. A similar profile of subcomplexes was present in a human/mouse hybrid fibroblast cell line with a severe complex I deficiency due to an almost complete lack of assembly of the holoenzyme complex. The finding that diverse causes of complex I deficiency produce a similar pattern of complex I subcomplexes suggests that these are intermediates in the assembly of the holoenzyme complex. We propose a possible assembly pathway for the complex, which differs significantly from that proposed for Neurospora, the current model for complex I assembly.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "0", "doc_id": "6636088", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Omnivores produce less trimethylamine N-oxide from dietary I-carnitine than vegetarians.\n\nCANDIDATE_PASSAGE:\nAP-1/sigma1B-adaptin mediates endosomal synaptic vesicle recycling, learning and memory. Synaptic vesicle recycling involves AP-2/clathrin-mediated endocytosis, but it is not known whether the endosomal pathway is also required. Mice deficient in the tissue-specific AP-1-sigma1B complex have impaired synaptic vesicle recycling in hippocampal synapses. The ubiquitously expressed AP-1-sigma1A complex mediates protein sorting between the trans-Golgi network and early endosomes. Vertebrates express three sigma1 subunit isoforms: A, B and C. The expressions of sigma1A and sigma1B are highest in the brain. Synaptic vesicle reformation in cultured neurons from sigma1B-deficient mice is reduced upon stimulation, and large endosomal intermediates accumulate. The sigma1B-deficient mice have reduced motor coordination and severely impaired long-term spatial memory. These data reveal a molecular mechanism for a severe human X-chromosome-linked mental retardation.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "882", "doc_id": "11250124", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: ALDH1 expression is associated with better breast cancer outcomes.\n\nCANDIDATE_ABSTRACT:\nTITLE: ALDH1 is a marker of normal and malignant human mammary stem cells and a predictor of poor clinical outcome.\nABSTRACT: Application of stem cell biology to breast cancer research has been limited by the lack of simple methods for identification and isolation of normal and malignant stem cells. Utilizing in vitro and in vivo experimental systems, we show that normal and cancer human mammary epithelial cells with increased aldehyde dehydrogenase activity (ALDH) have stem/progenitor properties. These cells contain the subpopulation of normal breast epithelium with the broadest lineage differentiation potential and greatest growth capacity in a xenotransplant model. In breast carcinomas, high ALDH activity identifies the tumorigenic cell fraction, capable of self-renewal and of generating tumors that recapitulate the heterogeneity of the parental tumor. In a series of 577 breast carcinomas, expression of ALDH1 detected by immunostaining correlated with poor prognosis. These findings offer an important new tool for the study of normal and malignant breast stem cells and facilitate the clinical application of stem cell concepts.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In a series of 577 breast carcinomas, expression of ALDH1 detected by immunostaining correlated with poor prognosis.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 51, "doc_id": "45638119", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nCANDIDATE_ABSTRACT:\nTITLE: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\nABSTRACT: Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens. However, signals underlying mTEC development remain largely unclear. Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals. Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment. Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner. These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1181, "doc_id": "2734421", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: COPI coatmer is involved in lipid homeostasis.\n\nCANDIDATE_PASSAGE:\nLipid homeostasis, lipotoxicity and the metabolic syndrome. In the 20th century industrialized nations have become afflicted with an unprecedented pandemic of increased adiposity. In the United States, the epicenter of the epidemic, over 2/3 of the population, is overweight and 1 of every 6 Americans carries the diagnosis of metabolic syndrome. Although genes determine susceptibility to environmental factors, the epidemic is clearly due to increased consumption of calorie-dense, highly lipogenic foods, coupled with a marked decrease in physical exertion resulting from modern technologies. If this lifestyle continues, morbid consequences are virtually inevitable. They include type II diabetes and a cluster of disorders known as \"the metabolic syndrome\" usually appearing in middle age. The morbid consequences of the chronic caloric surplus are buffered before middle age by the partitioning of these calories as fat in the adipocyte compartment which is specifically designed to store triglycerides. Leptin has been proposed as the major hormonal regulator of the partitioning of surplus calories. However, multiple factors can determine the storage capacity of the fat tissue and when it is exceeded ectopic lipid deposition begins. The organs affected in metabolic syndrome include skeletal muscle, liver, heart and pancreas, which are now known to contain abnormal levels of triglycerides. While neutral fat is probably harmless, it is an index of ectopic lipid overload. Fatty acid derivatives can interfere with the function of the cell and ultimately lead to its demise through lipoapoptosis, the consequences of which are gradual organ failure.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "210", "doc_id": "20288322", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Drosophila supracellular actomyosin structures are found at boundaries in wing imaginal discs.\n\nCANDIDATE_ABSTRACT:\nTITLE: Localization and requirement for Myosin II at the dorsal-ventral compartment boundary of the Drosophila wing.\nABSTRACT: As organisms develop, their tissues can become separated into distinct cell populations through the establishment of compartment boundaries. Compartment boundaries have been discovered in a wide variety of tissues, but in many cases the molecular mechanisms that separate cells remain poorly understood. In the Drosophila wing, a stripe of Notch activation maintains the dorsal-ventral compartment boundary, through a process that depends on the actin cytoskeleton. Here, we show that the dorsal-ventral boundary exhibits a distinct accumulation of Myosin II, and that this accumulation is regulated downstream of Notch signaling. Conversely, the dorsal-ventral boundary is depleted for the Par-3 homologue Bazooka. We further show that mutations in the Myosin heavy chain subunit encoded by zipper can impair dorsal-ventral compartmentalization without affecting anterior-posterior compartmentalization. These observations identify a distinct accumulation and requirement for Myosin activity in dorsal-ventral compartmentalization, and suggest a novel mechanism in which contractile tension along an F-actin cable at the compartment boundary contributes to compartmentalization.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here, we show that the dorsal-ventral boundary exhibits a distinct accumulation of Myosin II, and that this accumulation is regulated downstream of Notch signaling.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 355, "doc_id": "38380061", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Bariatric surgery has a positive impact on mental health.\n\nCANDIDATE_PASSAGE:\nFBW7 ubiquitin ligase: a tumour suppressor at the crossroads of cell division, growth and differentiation FBW7 (F-box and WD repeat domain-containing 7) is the substrate recognition component of an evolutionary conserved SCF (complex of SKP1, CUL1 and F-box protein)-type ubiquitin ligase. SCFFBW7 degrades several proto-oncogenes that function in cellular growth and division pathways, including MYC, cyclin E, Notch and JUN. FBW7 is also a tumour suppressor, the regulatory network of which is perturbed in many human malignancies. Numerous cancer-associated mutations in FBW7 and its substrates have been identified, and loss of FBW7 function causes chromosomal instability and tumorigenesis. This Review focuses on structural and functional aspects of FBW7 and its role in the development of cancer.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "163", "doc_id": "13277623", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Obesity raises life quality.\n\nCANDIDATE_ABSTRACT:\nTITLE: Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies.\nABSTRACT: BACKGROUND The main associations of body-mass index (BMI) with overall and cause-specific mortality can best be assessed by long-term prospective follow-up of large numbers of people. The Prospective Studies Collaboration aimed to investigate these associations by sharing data from many studies. METHODS Collaborative analyses were undertaken of baseline BMI versus mortality in 57 prospective studies with 894 576 participants, mostly in western Europe and North America (61% [n=541 452] male, mean recruitment age 46 [SD 11] years, median recruitment year 1979 [IQR 1975-85], mean BMI 25 [SD 4] kg/m(2)). The analyses were adjusted for age, sex, smoking status, and study. To limit reverse causality, the first 5 years of follow-up were excluded, leaving 66 552 deaths of known cause during a mean of 8 (SD 6) further years of follow-up (mean age at death 67 [SD 10] years): 30 416 vascular; 2070 diabetic, renal or hepatic; 22 592 neoplastic; 3770 respiratory; 7704 other. FINDINGS In both sexes, mortality was lowest at about 22.5-25 kg/m(2). Above this range, positive associations were recorded for several specific causes and inverse associations for none, the absolute excess risks for higher BMI and smoking were roughly additive, and each 5 kg/m(2) higher BMI was on average associated with about 30% higher overall mortality (hazard ratio per 5 kg/m(2) [HR] 1.29 [95% CI 1.27-1.32]): 40% for vascular mortality (HR 1.41 [1.37-1.45]); 60-120% for diabetic, renal, and hepatic mortality (HRs 2.16 [1.89-2.46], 1.59 [1.27-1.99], and 1.82 [1.59-2.09], respectively); 10% for neoplastic mortality (HR 1.10 [1.06-1.15]); and 20% for respiratory and for all other mortality (HRs 1.20 [1.07-1.34] and 1.20 [1.16-1.25], respectively). Below the range 22.5-25 kg/m(2), BMI was associate [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 876, "doc_id": "195689316", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Omnivores produce less trimethylamine N-oxide from dietary I-carnitine than vegans.\n\nCANDIDATE_PASSAGE:\nIntestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis Intestinal microbiota metabolism of choline and phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO). We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice. Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism. The presence of specific bacterial taxa in human feces was associated with both plasma TMAO concentration and dietary status. Plasma L-carnitine levels in subjects undergoing cardiac evaluation (n = 2,595) predicted increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels. Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed. In mice with an intact intestinal microbiota, dietary supplementation with TMAO or either carnitine or choline reduced in vivo reverse cholesterol transport. Intestinal microbiota may thus contribute to the well-established link between high levels of red meat consumption and CVD risk.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "881", "doc_id": "14803797", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Adult tissue-resident macrophages are seeded before birth.\n\nCANDIDATE_ABSTRACT:\nTITLE: Fate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis.\nABSTRACT: Mononuclear phagocytes, including monocytes, macrophages, and dendritic cells, contribute to tissue integrity as well as to innate and adaptive immune defense. Emerging evidence for labor division indicates that manipulation of these cells could bear therapeutic potential. However, specific ontogenies of individual populations and the overall functional organization of this cellular network are not well defined. Here we report a fate-mapping study of the murine monocyte and macrophage compartment taking advantage of constitutive and conditional CX(3)CR1 promoter-driven Cre recombinase expression. We have demonstrated that major tissue-resident macrophage populations, including liver Kupffer cells and lung alveolar, splenic, and peritoneal macrophages, are established prior to birth and maintain themselves subsequently during adulthood independent of replenishment by blood monocytes. Furthermore, we have established that short-lived Ly6C(+) monocytes constitute obligatory steady-state precursors of blood-resident Ly6C(-) cells and that the abundance of Ly6C(+) blood monocytes dynamically controls the circulation lifespan of their progeny.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We have demonstrated that major tissue-resident macrophage populations, including liver Kupffer cells and lung alveolar, splenic, and peritoneal macrophages, are established prior to birth and maintain themselves subsequently during adulthood independent of replenishment by blood monocytes.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 85, "doc_id": "7521113", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Ultrasound guidance significantly reduces the number of traumatic procedures when attempting needle insertion.\n\nCANDIDATE_ABSTRACT:\nTITLE: Ultrasound imaging for lumbar punctures and epidural catheterisations: systematic review and meta-analysis.\nABSTRACT: OBJECTIVE To determine whether ultrasound imaging can reduce the risk of failed lumbar punctures or epidural catheterisations, when compared with standard palpation methods, and whether ultrasound imaging can reduce traumatic procedures, insertion attempts, and needle redirections. DESIGN Systematic review and meta-analysis of randomised controlled trials. DATA SOURCES Ovid Medline, Embase, and Cochrane Central Register of Controlled Trials up to May 2012, without restriction by language or publication status. REVIEW METHODS Randomised trials that compared ultrasound imaging with standard methods (no imaging) in the performance of a lumbar puncture or epidural catheterisation were identified. RESULTS 14 studies with a total of 1334 patients were included (674 patients assigned to the ultrasound group, 660 to the control group). Five studies evaluated lumbar punctures and nine evaluated epidural catheterisations. Six of 624 procedures conducted in the ultrasound group failed; 44 of 610 procedures in the control group failed. Ultrasound imaging reduced the risk of failed procedures (risk ratio 0.21 (95% confidence interval 0.10 to 0.43), P<0.001). Risk reduction was similar when subgroup analysis was performed for lumbar punctures (risk ratio 0.19 (0.07 to 0.56), P=0.002) or epidural catheterisations (0.23 (0.09 to 0.60), P=0.003). Ultrasound imaging also significantly reduced the risk of traumatic procedures (risk ratio 0.27 (0.11 to 0.67), P=0.005), the number of insertion attempts (mean difference -0.44 (-0.64 to -0.24), P<0.001), and the number of needle redirections (mean difference -1.00 (-1.24 to -0.75), P<0.001). CONCLUSIONS Ultrasound imaging can reduce the risk of failed or traumatic lumbar punctures and epidural catheterisations, as well as the numb [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Ultrasound imaging can reduce the risk of failed or traumatic lumbar punctures and epidural catheterisations, as well as the number of needle insertions and redirections.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1341, "doc_id": "15482274", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does the central venous pressure predict fluid responsiveness?\n\nABSTRACT:\nDespite a previous meta-analysis that concluded that central venous pressure should not be used to make clinical decisions regarding fluid management, central venous pressure continues to be recommended for this purpose.AIM: To perform an updated meta-analysis incorporating recent studies that investigated indices predictive of fluid responsiveness. A priori subgroup analysis was planned according to the location where the study was performed (ICU or operating room). MEDLINE, EMBASE, Cochrane Register of Controlled Trials, and citation review of relevant primary and review articles. Clinical trials that reported the correlation coefficient or area under the receiver operating characteristic curve (AUC) between the central venous pressure and change in cardiac performance following an intervention that altered cardiac preload. From 191 articles screened, 43 studies met our inclusion criteria and were included for data extraction. The studies included human adult subjects, and included healthy controls (n = 1) and ICU (n = 22) and operating room (n = 20) patients. Data were abstracted on study characteristics, patient population, baseline central venous pressure, the correlation coefficient, and/or the AUC between central venous pressure and change in stroke volume index/cardiac index and the percentage of fluid responders. Meta-analytic techniques were used to summarize the data. Overall 57% ± 13% of patients were fluid responders. The summary AUC was 0.56 (95% CI, 0.54-0.58) with no heterogenicity between studies. The summary AUC was 0.56 (95% CI, 0.52-0.60) for those studies done in the ICU and 0.56 (95% CI, 0.54-0.58) for those done in the operating room. The summary correlation coefficient between the baseline central venous pressure and change in stroke [TRUNCATED]", "output": "{\"label\": \"no\", \"rationale\": \"There are no data to support the widespread practice of using central venous pressure to guide fluid therapy. This approach to fluid resuscitation should be abandoned.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 23774337, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The deregulated and prolonged activation of monocytes has deleterious effects in chronic infectious conditions.\n\nCANDIDATE_PASSAGE:\nAssociation of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease. Crohn's disease and ulcerative colitis, the two main types of chronic inflammatory bowel disease, are multifactorial conditions of unknown aetiology. A susceptibility locus for Crohn's disease has been mapped to chromosome 16. Here we have used a positional-cloning strategy, based on linkage analysis followed by linkage disequilibrium mapping, to identify three independent associations for Crohn's disease: a frameshift variant and two missense variants of NOD2, encoding a member of the Apaf-1/Ced-4 superfamily of apoptosis regulators that is expressed in monocytes. These NOD2 variants alter the structure of either the leucine-rich repeat domain of the protein or the adjacent region. NOD2 activates nuclear factor NF-kB; this activating function is regulated by the carboxy-terminal leucine-rich repeat domain, which has an inhibitory role and also acts as an intracellular receptor for components of microbial pathogens. These observations suggest that the NOD2 gene product confers susceptibility to Crohn's disease by altering the recognition of these components and/or by over-activating NF-kB in monocytes, thus documenting a molecular model for the pathogenic mechanism of Crohn's disease that can now be further investigated.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1212", "doc_id": "4427060", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: 5% of perinatal mortality is due to low birth weight.\n\nCANDIDATE_ABSTRACT:\nTITLE: Estimates of global prevalence of childhood underweight in 1990 and 2015.\nABSTRACT: CONTEXT One key target of the United Nations Millennium Development goals is to reduce the prevalence of underweight among children younger than 5 years by half between 1990 and 2015. OBJECTIVE To estimate trends in childhood underweight by geographic regions of the world. DESIGN, SETTING, AND PARTICIPANTS Time series study of prevalence of underweight, defined as weight 2 SDs below the mean weight for age of the National Center for Health Statistics and World Health Organization (WHO) reference population. National prevalence rates derived from the WHO Global Database on Child Growth and Malnutrition, which includes data on approximately 31 million children younger than 5 years who participated in 419 national nutritional surveys in 139 countries from 1965 through 2002. MAIN OUTCOME MEASURES Linear mixed-effects modeling was used to estimate prevalence rates and numbers of underweight children by region in 1990 and 2015 and to calculate the changes (ie, increase or decrease) to these values between 1990 and 2015. RESULTS Worldwide, underweight prevalence was projected to decline from 26.5% in 1990 to 17.6% in 2015, a change of -34% (95% confidence interval [CI], -43% to -23%). In developed countries, the prevalence was estimated to decrease from 1.6% to 0.9%, a change of -41% (95% CI, -92% to 343%). In developing regions, the prevalence was forecasted to decline from 30.2% to 19.3%, a change of -36% (95% CI, -45% to -26%). In Africa, the prevalence of underweight was forecasted to increase from 24.0% to 26.8%, a change of 12% (95% CI, 8%-16%). In Asia, the prevalence was estimated to decrease from 35.1% to 18.5%, a change of -47% (95% CI, -58% to -34%). Worldwide, the number of underweight children was projected to decline from 163.8 million in 1990 to 113. [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 13, "doc_id": "1606628", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Ambulatory blood pressure monitoring is inaccurate at diagnosing hypertension.\n\nCANDIDATE_ABSTRACT:\nTITLE: Relative effectiveness of clinic and home blood pressure monitoring compared with ambulatory blood pressure monitoring in diagnosis of hypertension: systematic review\nABSTRACT: OBJECTIVE To determine the relative accuracy of clinic measurements and home blood pressure monitoring compared with ambulatory blood pressure monitoring as a reference standard for the diagnosis of hypertension. DESIGN Systematic review with meta-analysis with hierarchical summary receiver operating characteristic models. Methodological quality was appraised, including evidence of validation of blood pressure measurement equipment. DATA SOURCES Medline (from 1966), Embase (from 1980), Cochrane Database of Systematic Reviews, DARE, Medion, ARIF, and TRIP up to May 2010. Eligibility criteria for selecting studies Eligible studies examined diagnosis of hypertension in adults of all ages using home and/or clinic blood pressure measurement compared with those made using ambulatory monitoring that clearly defined thresholds to diagnose hypertension. RESULTS The 20 eligible studies used various thresholds for the diagnosis of hypertension, and only seven studies (clinic) and three studies (home) could be directly compared with ambulatory monitoring. Compared with ambulatory monitoring thresholds of 135/85 mm Hg, clinic measurements over 140/90 mm Hg had mean sensitivity and specificity of 74.6% (95% confidence interval 60.7% to 84.8%) and 74.6% (47.9% to 90.4%), respectively, whereas home measurements over 135/85 mm Hg had mean sensitivity and specificity of 85.7% (78.0% to 91.0%) and 62.4% (48.0% to 75.0%). CONCLUSIONS Neither clinic nor home measurement had sufficient sensitivity or specificity to be recommended as a single diagnostic test. If ambulatory monitoring is taken as the reference standard, then treatment decisions based on clinic or home blood pressure alone might result in substantial overdiagnosis. Ambulatory monitoring before the start of lifelong [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Compared with ambulatory monitoring thresholds of 135/85 mm Hg, clinic measurements over 140/90 mm Hg had mean sensitivity and specificity of 74.6% (95% confidence interval 60.7% to 84.8%) and 74.6% (47.9% to 90.4%), respectively, whereas home measurements over 135/85 mm Hg had mean sensitivity and specificity of 85.7% (78.0% to 91.0%) and 62.4% (48.0% to 75.0%).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 106, "doc_id": "25515907", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Sympathetic nerve activity is reduced throughout normal pregnancy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Sympathetic neural mechanisms in normal and hypertensive pregnancy in humans.\nABSTRACT: BACKGROUND Direct recordings from peripheral sympathetic nerves have shown an increased sympathetic drive in pregnancy-induced hypertension (PIH) and preeclampsia (PE). It is unknown whether sympathetic drive is altered in normal pregnancy, when arterial blood pressure can be normal or relatively low. The aim of this study was to measure and compare peripheral sympathetic discharge, its vasoconstrictor effect and its baroreceptor control, during pregnancy and postpartum in women with normal pregnancy (NP) and PIH and in normotensive nonpregnant (NN) women. METHODS AND RESULTS Twenty-one women with NP, 18 women with PIH, and 21 NN women had muscle sympathetic nerve activity assessed from multiunit discharges (MSNA) and from single units with defined vasoconstrictor properties (s-MSNA). The s-MSNA in NP (38+/-6.6 impulses/100 beats) was greater (P<0.05) than in NN women (19+/-1.8 impulses/100 beats) despite similar age and body weight but less than in PIH women (P<0.001) (146+/-23.5 impulses/100 beats). MSNA followed a similar trend. Cardiac baroreceptor reflex sensitivity (BRS) was impaired in NP and PIH women relative to NN. After delivery, sympathetic activity decreased to values similar to those obtained in NN, and there was an increase in BRS. In women with NP, the decrease in sympathetic output occurred despite an insignificant change in blood pressure. CONCLUSIONS Central sympathetic output was increased in women with normal pregnancy and was even greater in the hypertensive pregnant group. The findings suggest that the moderate sympathetic hyperactivity during the latter months of normal pregnancy may help to return the arterial pressure to nonpregnant levels, although when the increase in activity is excessive, hypertension may ensue.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The s-MSNA in NP (38+/-6.6 impulses/100 beats) was greater (P<0.05) than in NN women (19+/-1.8 impulses/100 beats) despite similar age and body weight but less than in PIH women (P<0.001) (146+/-23.5 impulses/100 beats).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1120, "doc_id": "5323845", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Androgenetic haploid mouse embryonic stem cells (ESCs) can be derived and genetically manipulated in vitro.\n\nCANDIDATE_PASSAGE:\nDerivation of novel human ground state naive pluripotent stem cells Mouse embryonic stem (ES) cells are isolated from the inner cell mass of blastocysts, and can be preserved in vitro in a naive inner-cell-mass-like configuration by providing exogenous stimulation with leukaemia inhibitory factor (LIF) and small molecule inhibition of ERK1/ERK2 and GSK3β signalling (termed 2i/LIF conditions). Hallmarks of naive pluripotency include driving Oct4 (also known as Pou5f1) transcription by its distal enhancer, retaining a pre-inactivation X chromosome state, and global reduction in DNA methylation and in H3K27me3 repressive chromatin mark deposition on developmental regulatory gene promoters. Upon withdrawal of 2i/LIF, naive mouse ES cells can drift towards a primed pluripotent state resembling that of the post-implantation epiblast. Although human ES cells share several molecular features with naive mouse ES cells, they also share a variety of epigenetic properties with primed murine epiblast stem cells (EpiSCs). These include predominant use of the proximal enhancer element to maintain OCT4 expression, pronounced tendency for X chromosome inactivation in most female human ES cells, increase in DNA methylation and prominent deposition of H3K27me3 and bivalent domain acquisition on lineage regulatory genes. The feasibility of establishing human ground state naive pluripotency in vitro with equivalent molecular and functional features to those characterized in mouse ES cells remains to be defined. Here we establish defined conditions that facilitate the derivation of genetically unmodified human naive pluripotent stem cells from already established primed human ES cells, from somatic cells through induced pluripotent stem (iPS) cell reprogramming or directly from b [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "111", "doc_id": "4462419", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does image preprocessing improve Fourier-based texture analysis of nuclear chromatin?\n\nABSTRACT:\nTo investigate whether preprocessing of digitized images can improve the image analysis of chromatin of cytologic preparations using Fast Fourier Transformation (FFT). In a preprocessing step the nuclear borders of the segmented nuclei were smoothed, thus avoiding the Airy ring artifact. We tested this method, comparing the inertia values of digitalized cardiomyocyte nuclei of rats of different ages. Furthermore, we created in silicio nuclear images with chromatin alterations at or nearby the nuclear edge in order to investigate the robustness of our method. After preprocessing, the FFT-derived variable inertia discriminated significantly better the chromatin structure of the nuclei at different ages in every frequency range. The investigation on simulated nuclei revealed that within the frequency ranges from 1.8 microm to 0.72 microm smoothing of the borders does not interfere with the detection of chromatin changes at the nuclear border.", "output": "{\"label\": \"yes\", \"rationale\": \"Smoothing of borders in segmented images can improve the analysis of Fourier-derived variables of the chromatin texture.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 18630843, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Addition of BMP4, activin A, CHIR99021, and SU504 to reprogramming fibroblasts generates, expands and maintains cardiovascular progenitor cells (CPCs)\n\nCANDIDATE_PASSAGE:\nNatural variation in the parameters of innate immune cells is preferentially driven by genetic factors The quantification and characterization of circulating immune cells provide key indicators of human health and disease. To identify the relative effects of environmental and genetic factors on variation in the parameters of innate and adaptive immune cells in homeostatic conditions, we combined standardized flow cytometry of blood leukocytes and genome-wide DNA genotyping of 1,000 healthy, unrelated people of Western European ancestry. We found that smoking, together with age, sex and latent infection with cytomegalovirus, were the main non-genetic factors that affected variation in parameters of human immune cells. Genome-wide association studies of 166 immunophenotypes identified 15 loci that showed enrichment for disease-associated variants. Finally, we demonstrated that the parameters of innate cells were more strongly controlled by genetic variation than were those of adaptive cells, which were driven by mainly environmental exposure. Our data establish a resource that will generate new hypotheses in immunology and highlight the role of innate immunity in susceptibility to common autoimmune diseases. Both environmental factors and genetic factors influence human immunity. Albert and colleagues leverage data from the Milieu Intérieur Consortium to comprehensively describe the effects of lifestyle, environment and genetics on human innate and adaptive immunity.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "82", "doc_id": "3672261", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Vitamin D deficiency effects birth weight.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association between maternal serum 25-hydroxyvitamin D level and pregnancy and neonatal outcomes: systematic review and meta-analysis of observational studies.\nABSTRACT: OBJECTIVE To assess the effect of 25-hydroxyvitamin D (25-OHD) levels on pregnancy outcomes and birth variables. DESIGN Systematic review and meta-analysis. DATA SOURCES Medline (1966 to August 2012), PubMed (2008 to August 2012), Embase (1980 to August 2012), CINAHL (1981 to August 2012), the Cochrane database of systematic reviews, and the Cochrane database of registered clinical trials. STUDY SELECTION Studies reporting on the association between serum 25-OHD levels during pregnancy and the outcomes of interest (pre-eclampsia, gestational diabetes, bacterial vaginosis, caesarean section, small for gestational age infants, birth weight, birth length, and head circumference). DATA EXTRACTION Two authors independently extracted data from original research articles, including key indicators of study quality. We pooled the most adjusted odds ratios and weighted mean differences. Associations were tested in subgroups representing different patient characteristics and study quality. RESULTS 3357 studies were identified and reviewed for eligibility. 31 eligible studies were included in the final analysis. Insufficient serum levels of 25-OHD were associated with gestational diabetes (pooled odds ratio 1.49, 95% confidence interval 1.18 to 1.89), pre-eclampsia (1.79, 1.25 to 2.58), and small for gestational age infants (1.85, 1.52 to 2.26). Pregnant women with low serum 25-OHD levels had an increased risk of bacterial vaginosis and low birthweight infants but not delivery by caesarean section. CONCLUSION Vitamin D insufficiency is associated with an increased risk of gestational diabetes, pre-eclampsia, and small for gestational age infants. Pregnant women with low 25-OHD levels had an increased risk of bacterial vaginosis and lower birth weight infants, but not de [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Pregnant women with low serum 25-OHD levels had an increased risk of bacterial vaginosis and low birthweight infants but not delivery by caesarean section.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1367, "doc_id": "2425364", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Human embryonic stem cells have the capacity to give rise to differentiated progeny representative of all three embryonic germ layers.\n\nCANDIDATE_PASSAGE:\nHuman and murine very small embryonic-like cells represent multipotent tissue progenitors, in vitro and in vivo. The purpose of this study was to determine the lineage progression of human and murine very small embryonic-like (HuVSEL or MuVSEL) cells in vitro and in vivo. In vitro, HuVSEL and MuVSEL cells differentiated into cells of all three embryonic germ layers. HuVSEL cells produced robust mineralized tissue of human origin compared with controls in calvarial defects. Immunohistochemistry demonstrated that the HuVSEL cells gave rise to neurons, adipocytes, chondrocytes, and osteoblasts within the calvarial defects. MuVSEL cells were also able to differentiate into similar lineages. First round serial transplants of MuVSEL cells into irradiated osseous sites demonstrated that ∼60% of the cells maintained their VSEL cell phenotype while other cells differentiated into multiple tissues at 3 months. Secondary transplants did not identify donor VSEL cells, suggesting limited self renewal but did demonstrate VSEL cell derivatives in situ for up to 1 year. At no point were teratomas identified. These studies show that VSEL cells produce multiple cellular structures in vivo and in vitro and lay the foundation for future cell-based regenerative therapies for osseous, neural, and connective tissue disorders.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "531", "doc_id": "36398420", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: High levels of CRP reduces the risk of exacerbations in chronic obstructive pulmonary disease (COPD).\n\nCANDIDATE_ABSTRACT:\nTITLE: Inflammatory biomarkers and exacerbations in chronic obstructive pulmonary disease.\nABSTRACT: IMPORTANCE Exacerbations of respiratory symptoms in chronic obstructive pulmonary disease (COPD) have profound and long-lasting adverse effects on patients. OBJECTIVE To test the hypothesis that elevated levels of inflammatory biomarkers in individuals with stable COPD are associated with an increased risk of having exacerbations. DESIGN, SETTING, AND PARTICIPANTS Prospective cohort study examining 61,650 participants with spirometry measurements from the Copenhagen City Heart Study (2001-2003) and the Copenhagen General Population Study (2003-2008). Of these, 6574 had COPD, defined as a ratio between forced expiratory volume in 1 second (FEV1) and forced vital capacity below 0.7. MAIN OUTCOMES AND MEASURES Baseline levels of C-reactive protein (CRP) and fibrinogen and leukocyte count were measured in participants at a time when they were not experiencing symptoms of exacerbations. Exacerbations were recorded and defined as short-course treatment with oral corticosteroids alone or in combination with an antibiotic or as a hospital admission due to COPD. Levels of CRP and fibrinogen and leukocyte count were defined as high or low according to cut points of 3 mg/L, 14 μmol/L, and 9 ×10(9)/L, respectively. RESULTS During follow-up, 3083 exacerbations were recorded (mean, 0.5/participant). In the first year of follow-up, multivariable-adjusted odds ratios for having frequent exacerbations were 1.2 (95% CI, 0.7-2.2; 17 events/1000 person-years) for individuals with 1 high biomarker, 1.7 (95% CI, 0.9-3.2; 32 events/1000 person-years) for individuals with 2 high biomarkers, and 3.7 (95% CI, 1.9-7.4; 81 events/1000 person-years) for individuals with 3 high biomarkers compared with individuals who had no elevated biomarkers (9 events/1000 person-years; trend: P = 2 × [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS AND RELEVANCE Simultaneously elevated levels of CRP and fibrinogen and leukocyte count in individuals with COPD were associated with increased risk of having exacerbations, even in those with milder COPD and in those without previous exacerbations.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 516, "doc_id": "29564505", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Omnivores produce less trimethylamine N-oxide from dietary I-carnitine than vegetarians.\n\nCANDIDATE_ABSTRACT:\nTITLE: Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis\nABSTRACT: Intestinal microbiota metabolism of choline and phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO). We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice. Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism. The presence of specific bacterial taxa in human feces was associated with both plasma TMAO concentration and dietary status. Plasma L-carnitine levels in subjects undergoing cardiac evaluation (n = 2,595) predicted increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels. Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed. In mice with an intact intestinal microbiota, dietary supplementation with TMAO or either carnitine or choline reduced in vivo reverse cholesterol transport. Intestinal microbiota may thus contribute to the well-established link between high levels of red meat consumption and CVD risk.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 882, "doc_id": "14803797", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Suboptimal nutrition is a leading cause of premature death\n\nCANDIDATE_ABSTRACT:\nTITLE: The state of US health, 1990-2010: burden of diseases, injuries, and risk factors.\nABSTRACT: IMPORTANCE Understanding the major health problems in the United States and how they are changing over time is critical for informing national health policy. OBJECTIVES To measure the burden of diseases, injuries, and leading risk factors in the United States from 1990 to 2010 and to compare these measurements with those of the 34 countries in the Organisation for Economic Co-operation and Development (OECD) countries. DESIGN We used the systematic analysis of descriptive epidemiology of 291 diseases and injuries, 1160 sequelae of these diseases and injuries, and 67 risk factors or clusters of risk factors from 1990 to 2010 for 187 countries developed for the Global Burden of Disease 2010 Study to describe the health status of the United States and to compare US health outcomes with those of 34 OECD countries. Years of life lost due to premature mortality (YLLs) were computed by multiplying the number of deaths at each age by a reference life expectancy at that age. Years lived with disability (YLDs) were calculated by multiplying prevalence (based on systematic reviews) by the disability weight (based on population-based surveys) for each sequela; disability in this study refers to any short- or long-term loss of health. Disability-adjusted life-years (DALYs) were estimated as the sum of YLDs and YLLs. Deaths and DALYs related to risk factors were based on systematic reviews and meta-analyses of exposure data and relative risks for risk-outcome pairs. Healthy life expectancy (HALE) was used to summarize overall population health, accounting for both length of life and levels of ill health experienced at different ages. RESULTS US life expectancy for both sexes combined increased from 75.2 years in 1990 to 78.2 years in 2010; during the same period, HALE inc [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The leading risk factors related to DALYs were dietary risks, tobacco smoking, high body mass index, high blood pressure, high fasting plasma glucose, physical inactivity, and alcohol use.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1109, "doc_id": "8582337", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Bariatric surgery has a positive impact on mental health.\n\nCANDIDATE_PASSAGE:\nMental Health Conditions Among Patients Seeking and Undergoing Bariatric Surgery: A Meta-analysis. IMPORTANCE Bariatric surgery is associated with sustained weight loss and improved physical health status for severely obese individuals. Mental health conditions may be common among patients seeking bariatric surgery; however, the prevalence of these conditions and whether they are associated with postoperative outcomes remains unknown. OBJECTIVE To determine the prevalence of mental health conditions among bariatric surgery candidates and recipients, to evaluate the association between preoperative mental health conditions and health outcomes following bariatric surgery, and to evaluate the association between surgery and the clinical course of mental health conditions. DATA SOURCES We searched PubMed, MEDLINE on OVID, and PsycINFO for studies published between January 1988 and November 2015. Study quality was assessed using an adapted tool for risk of bias; quality of evidence was rated based on GRADE (Grading of Recommendations Assessment, Development and Evaluation) criteria. FINDINGS We identified 68 publications meeting inclusion criteria: 59 reporting the prevalence of preoperative mental health conditions (65,363 patients) and 27 reporting associations between preoperative mental health conditions and postoperative outcomes (50,182 patients). Among patients seeking and undergoing bariatric surgery, the most common mental health conditions, based on random-effects estimates of prevalence, were depression (19% [95% CI, 14%-25%]) and binge eating disorder (17% [95% CI, 13%-21%]). There was conflicting evidence regarding the association between preoperative mental health conditions and postoperative weight loss. Neither depression nor binge eating disorder [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "163", "doc_id": "18872233", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Perigenital skin is not the primary site of HIV acquisition.\n\nCANDIDATE_PASSAGE:\nMyeloperoxidase: friend and foe. Neutrophilic polymorphonuclear leukocytes (neutrophils) are highly specialized for their primary function, the phagocytosis and destruction of microorganisms. When coated with opsonins (generally complement and/or antibody), microorganisms bind to specific receptors on the surface of the phagocyte and invagination of the cell membrane occurs with the incorporation of the microorganism into an intracellular phagosome. There follows a burst of oxygen consumption, and much, if not all, of the extra oxygen consumed is converted to highly reactive oxygen species. In addition, the cytoplasmic granules discharge their contents into the phagosome, and death of the ingested microorganism soon follows. Among the antimicrobial systems formed in the phagosome is one consisting of myeloperoxidase (MPO), released into the phagosome during the degranulation process, hydrogen peroxide (H2O2), formed by the respiratory burst and a halide, particularly chloride. The initial product of the MPO-H2O2-chloride system is hypochlorous acid, and subsequent formation of chlorine, chloramines, hydroxyl radicals, singlet oxygen, and ozone has been proposed. These same toxic agents can be released to the outside of the cell, where they may attack normal tissue and thus contribute to the pathogenesis of disease. This review will consider the potential sources of H2O2 for the MPO-H2O2-halide system; the toxic products of the MPO system; the evidence for MPO involvement in the microbicidal activity of neutrophils; the involvement of MPO-independent antimicrobial systems; and the role of the MPO system in tissue injury. It is concluded that the MPO system plays an important role in the microbicidal activity of phagocytes.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "934", "doc_id": "12489688", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Increased microtubule acetylation repairs interference of axonal transport caused by LRRK2 Roc-COR domain mutations.\n\nCANDIDATE_ABSTRACT:\nTITLE: Increasing microtubule acetylation rescues axonal transport and locomotor deficits caused by LRRK2 Roc-COR domain mutations\nABSTRACT: Leucine-rich repeat kinase 2 (LRRK2) mutations are the most common genetic cause of Parkinson's disease. LRRK2 is a multifunctional protein affecting many cellular processes and has been described to bind microtubules. Defective microtubule-based axonal transport is hypothesized to contribute to Parkinson's disease, but whether LRRK2 mutations affect this process to mediate pathogenesis is not known. Here we find that LRRK2 containing pathogenic Roc-COR domain mutations (R1441C, Y1699C) preferentially associates with deacetylated microtubules, and inhibits axonal transport in primary neurons and in Drosophila, causing locomotor deficits in vivo. In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport. In vivo knockdown of the deacetylases HDAC6 and Sirt2, or administration of TSA rescues both axonal transport and locomotor behavior. Thus, this study reveals a pathogenic mechanism and a potential intervention for Parkinson's disease.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 614, "doc_id": "9638032", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Taxation of sugar-sweetened beverages had no effect on the incidence rate of type II diabetes in India.\n\nCANDIDATE_ABSTRACT:\nTITLE: Averting Obesity and Type 2 Diabetes in India through Sugar-Sweetened Beverage Taxation: An Economic-Epidemiologic Modeling Study\nABSTRACT: BACKGROUND Taxing sugar-sweetened beverages (SSBs) has been proposed in high-income countries to reduce obesity and type 2 diabetes. We sought to estimate the potential health effects of such a fiscal strategy in the middle-income country of India, where there is heterogeneity in SSB consumption, patterns of substitution between SSBs and other beverages after tax increases, and vast differences in chronic disease risk within the population. METHODS AND FINDINGS Using consumption and price variations data from a nationally representative survey of 100,855 Indian households, we first calculated how changes in SSB price alter per capita consumption of SSBs and substitution with other beverages. We then incorporated SSB sales trends, body mass index (BMI), and diabetes incidence data stratified by age, sex, income, and urban/rural residence into a validated microsimulation of caloric consumption, glycemic load, overweight/obesity prevalence, and type 2 diabetes incidence among Indian subpopulations facing a 20% SSB excise tax. The 20% SSB tax was anticipated to reduce overweight and obesity prevalence by 3.0% (95% CI 1.6%-5.9%) and type 2 diabetes incidence by 1.6% (95% CI 1.2%-1.9%) among various Indian subpopulations over the period 2014-2023, if SSB consumption continued to increase linearly in accordance with secular trends. However, acceleration in SSB consumption trends consistent with industry marketing models would be expected to increase the impact efficacy of taxation, averting 4.2% of prevalent overweight/obesity (95% CI 2.5-10.0%) and 2.5% (95% CI 1.0-2.8%) of incident type 2 diabetes from 2014-2023. Given current consumption and BMI distributions, our results suggest the largest relative effect would be expected among young rural men, refuting our a [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The 20% SSB tax was anticipated to reduce overweight and obesity prevalence by 3.0% (95% CI 1.6%-5.9%) and type 2 diabetes incidence by 1.6% (95% CI 1.2%-1.9%) among various Indian subpopulations over the period 2014-2023, if SSB consumption continued to increase linearly in accordance with secular trends.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1144, "doc_id": "10071552", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: A 100g dose of chloroquine chemoprophylactic regimen results in retinal toxicity after 1 year of weekly intake.\n\nCANDIDATE_PASSAGE:\nTreatment of active tuberculosis in HIV-coinfected patients: a systematic review and meta-analysis. BACKGROUND Patients with human immunodeficiency virus (HIV) infection and tuberculosis have an increased risk of death, treatment failure, and relapse. METHODS A systematic review and meta-analysis of randomized, controlled trials and cohort studies was conducted to evaluate the impact of duration and dosing schedule of rifamycin and use of antiretroviral therapy in the treatment of active tuberculosis in HIV-positive patients. In included studies, the initial tuberculosis diagnosis, failure, and/or relapse were microbiologically confirmed, and patients received standardized rifampin- or rifabutin-containing regimens. Pooled cumulative incidence of treatment failure, death during treatment, and relapse were calculated using random-effects models. Multivariable meta-regression was performed using negative binomial regression. RESULTS After screening 5158 citations, 6 randomized trials and 21 cohort studies were included. Relapse was more common with regimens using 2 months rifamycin (adjusted risk ratio, 3.6; 95% confidence interval, 1.1-11.7) than with regimens using rifamycin for at least 8 months. Compared with daily therapy in the initial phase (n=3352 patients from 35 study arms), thrice-weekly therapy (n=211 patients from 5 study arms) was associated with higher rates of failure (adjusted risk ratio, 4.0; 95% confidence interval, 1.5-10.4) and relapse [adjusted risk ratio, 4.8; 95% confidence interval, 1.8-12.8). There were trends toward higher relapse rates if rifamycins were used for only 6 months, compared with > or =8 months, or if antiretroviral therapy was not used. CONCLUSIONS This review raises serious concerns regarding current recommendations fo [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "26", "doc_id": "31363207", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: A breast cancer patient's capacity to metabolize tamoxifen influences treatment outcome.\n\nCANDIDATE_PASSAGE:\nAssociation between the Medicare Modernization Act of 2003 and patient wait times and travel distance for chemotherapy. CONTEXT The Medicare Prescription Drug, Improvement, and Modernization Act of 2003 (MMA) altered reimbursements for outpatient chemotherapy drugs and drug administration services. Anecdotal reports suggest that these adjustments may have negatively affected access to chemotherapy for Medicare beneficiaries. OBJECTIVE To compare patient wait times and travel distances for chemotherapy before and after the enactment of the MMA. DESIGN, SETTING, AND PATIENTS Analysis of a nationally representative 5% sample of claims from the Centers for Medicare & Medicaid Services for the period 2003 through 2006. Patients were Medicare beneficiaries with incident breast cancer, colorectal cancer, leukemia, lung cancer, or lymphoma who received chemotherapy in inpatient hospital, institutional outpatient, or physician office settings. MAIN OUTCOME MEASURES Days from incident diagnosis to first chemotherapy visit and distance traveled for treatment, controlling for age, sex, race/ethnicity, cancer type, geographic region, comorbid conditions, and year of diagnosis and treatment. RESULTS There were 5082 incident cases of breast cancer, colorectal cancer, leukemia, lung cancer, or lymphoma in 2003; 5379 cases in 2004; 5116 cases in 2005; and 5288 cases in 2006. Approximately 70% of patients received treatment in physician office settings in each year. Although the distribution of treatment settings in 2004 and 2005 was not significantly different from 2003 (P = .24 and P = .72, respectively), there was a small but significant change from 2003 to 2006 (P = .02). The proportion of patients receiving chemotherapy in inpatient settings decreased from 10.2% in 2003 [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "30", "doc_id": "24575065", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Energy balance requires hypothalamic glutamate neurotransmission.\n\nCANDIDATE_PASSAGE:\nInflammatory cytokines in depression: neurobiological mechanisms and therapeutic implications. Mounting evidence indicates that inflammatory cytokines contribute to the development of depression in both medically ill and medically healthy individuals. Cytokines are important for development and normal brain function, and have the ability to influence neurocircuitry and neurotransmitter systems to produce behavioral alterations. Acutely, inflammatory cytokine administration or activation of the innate immune system produces adaptive behavioral responses that promote conservation of energy to combat infection or recovery from injury. However, chronic exposure to elevated inflammatory cytokines and persistent alterations in neurotransmitter systems can lead to neuropsychiatric disorders and depression. Mechanisms of cytokine behavioral effects involve activation of inflammatory signaling pathways in the brain that results in changes in monoamine, glutamate, and neuropeptide systems, and decreases in growth factors, such as brain-derived neurotrophic factor. Furthermore, inflammatory cytokines may serve as mediators of both environmental (e.g. childhood trauma, obesity, stress, and poor sleep) and genetic (functional gene polymorphisms) factors that contribute to depression's development. This review explores the idea that specific gene polymorphisms and neurotransmitter systems can confer protection from or vulnerability to specific symptom dimensions of cytokine-related depression. Additionally, potential therapeutic strategies that target inflammatory cytokine signaling or the consequences of cytokines on neurotransmitter systems in the brain to prevent or reverse cytokine effects on behavior are discussed.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "378", "doc_id": "25315295", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Early patent ductus ateriosus (PDA) screening decreases in-hospital mortality.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association Between Early Screening for Patent Ductus Arteriosus and In-Hospital Mortality Among Extremely Preterm Infants.\nABSTRACT: IMPORTANCE There is currently no consensus for the screening and treatment of patent ductus arteriosus (PDA) in extremely preterm infants. Less pharmacological closure and more supportive management have been observed without evidence to support these changes. OBJECTIVE To evaluate the association between early screening echocardiography for PDA and in-hospital mortality. DESIGN, SETTING, AND PARTICIPANTS Comparison of screened and not screened preterm infants enrolled in the EPIPAGE 2 national prospective population-based cohort study that included all preterm infants born at less than 29 weeks of gestation and hospitalized in 68 neonatal intensive care units in France from April through December 2011. Two main analyses were performed to adjust for potential selection bias, one using propensity score matching and one using neonatal unit preference for early screening echocardiography as an instrumental variable. EXPOSURES Early screening echocardiography before day 3 of life. MAIN OUTCOMES AND MEASURES The primary outcome was death between day 3 and discharge. The secondary outcomes were major neonatal morbidities (pulmonary hemorrhage, severe bronchopulmonary dysplasia, severe cerebral lesions, and necrotizing enterocolitis). RESULTS Among the 1513 preterm infants with data available to determine exposure, 847 were screened for PDA and 666 were not; 605 infants from each group could be paired. Exposed infants were treated for PDA more frequently during their hospitalization than nonexposed infants (55.1% vs 43.1%; odds ratio [OR], 1.62 [95% CI, 1.31 to 2.00]; absolute risk reduction [ARR] in events per 100 infants, -12.0 [95% CI, -17.3 to -6.7). Exposed infants had a lower hospital death rate (14.2% vs 18.5% ; OR, 0.73 [95% CI, 0.54 to 0.98]; ARR, 4.3 [95% [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Exposed infants had a lower hospital death rate (14.2% vs 18.5% ; OR, 0.73 [95% CI, 0.54 to 0.98]; ARR, 4.3 [95% CI, 0.3 to 8.3]) and a lower rate of pulmonary hemorrhage (5.6% vs 8.9%; OR, 0.60 [95% CI, 0.38 to 0.95]; ARR, 3.3 [95% CI, 0.4 to 6.3]).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 367, "doc_id": "27099731", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does prevalence of TTV DNA and GBV-C RNA in patients with systemic sclerosis , rheumatoid arthritis , and osteoarthritis differ from that in healthy blood donors?\n\nABSTRACT:\nTo determine the prevalence of GB virus-C (GBV-C) RNA and TT virus (TTV) DNA in patients with systemic sclerosis (SSc), rheumatoid arthritis (RA), and osteoarthritis (OA) as well as to compare the autoantibody pattern in patients with SSc with and without evidence of viral infection. The study included 168 patients (84 SSc, 41 RA, and 43 OA) diagnosed according to the American College of Rheumatology criteria and 122 volunteer blood donors. The presence of GBV-C RNA and TTV DNA in serum was assessed by nested reverse transcriptase-polymerase chain reaction (RT-PCR) and semi-nested PCR, respectively. Autoantibodies in patients with SSc were determined by enzyme linked immunosorbent assay (ELISA) and Hep-2 immunofluorescence. TTV-DNA was detected in 10/84 (12%) patients with SSc, 9/41 (22%) patients with RA, 3/43 (7%) patients with OA, and 16/122 (13%) blood donors. GBV-C RNA was present in 4/84 (5%) patients with SSc, 2/43 (5%) patients with OA, and 5/122 (4%) blood donors. No patient with RA was positive for GBV-C RNA. One patient with SSc and one patient with OA showed a double infection with GBV-C and TTV. 74/84 (88%) patients with SSc were positive for at least one autoantibody species tested: 18/84 (21%) showed anticentromeric autoantibodies, 55/84 (66%) a speckled (36/84 (43%) fine, 19/84 (23%) coarse), and 20/84 (24%) a homogeneous nuclear Hep-2 pattern, and 21/84 (25%) had antinucleolar autoantibodies. Anti-Scl-70 antibodies were found in 31/84 (37%) and anti-RNP antibodies in 5/84 (6%) patients with SSc. No differences in the autoantibody pattern in patients with SSc with or without viral infection could be detected.", "output": "{\"label\": \"no\", \"rationale\": \"The prevalence of GBV-C RNA and TTV DNA in serum samples from patients with SSc, RA, and OA was low and comparable with that in blood donors. A continuing infection with TTV and or GBV-C was not associated with a significant change in the autoantibody pattern in patients with SSc. These data provide no evidence for an association between GBV-C and/or TTV infections and SSc and/or arthritis (RA and OA).\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 11454648, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The density of cytokine receptor bearing cells affects the distance over which cytokines act.\n\nCANDIDATE_ABSTRACT:\nTITLE: Duration of androgen suppression in the treatment of prostate cancer.\nABSTRACT: BACKGROUND The combination of radiotherapy plus long-term medical suppression of androgens (> or = 2 years) improves overall survival in patients with locally advanced prostate cancer. We compared the use of radiotherapy plus short-term androgen suppression with the use of radiotherapy plus long-term androgen suppression in the treatment of locally advanced prostate cancer. METHODS We randomly assigned patients with locally advanced prostate cancer who had received external-beam radiotherapy plus 6 months of androgen suppression to two groups, one to receive no further treatment (short-term suppression) and the other to receive 2.5 years of further treatment with a luteinizing hormone-releasing hormone agonist (long-term suppression). An outcome of noninferiority of short-term androgen suppression as compared with long-term suppression required a hazard ratio of more than 1.35 for overall survival, with a one-sided alpha level of 0.05. An interim analysis showed futility, and the results are presented with an adjusted one-sided alpha level of 0.0429. RESULTS A total of 1113 men were registered, of whom 970 were randomly assigned, 483 to short-term suppression and 487 to long-term suppression. After a median follow-up of 6.4 years, 132 patients in the short-term group and 98 in the long-term group had died; the number of deaths due to prostate cancer was 47 in the short-term group and 29 in the long-term group. The 5-year overall mortality for short-term and long-term suppression was 19.0% and 15.2%, respectively; the observed hazard ratio was 1.42 (upper 95.71% confidence limit, 1.79; P=0.65 for noninferiority). Adverse events in both groups included fatigue, diminished sexual function, and hot flushes. CONCLUSIONS The combination of radiotherapy plus 6 mont [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1210, "doc_id": "308862", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: H4 G94P proteins induce chromatin assembly, which increases free histones.\n\nCANDIDATE_PASSAGE:\nAutonomic neuropathy, QT interval lengthening, and unexpected deaths in male diabetic patients QT intervals were measured over RR intervals ranging from 500 ms to 1000 ms in 13 normal male subjects, 13 male diabetic subjects without and 13 with autonomic neuropathy. There was a close linear relationship between QT and RR in all subjects. The slope of the regression line was significantly greater in the autonomic neuropathy group than the normal group. Thirty-two male diabetic subjects with varying degrees of autonomic dysfunction had repeat QT measurements 3 (range 2–6) years later. QT and QTC lengthened significantly at the second visit, unrelated to age or time between recordings, but which corresponded with changes in autonomic function. Of 71 male diabetic subjects under 60 years followed for 3 years, 13 had died, 8 unexpectedly. Of those with autonomic neuropathy, QT and QTC were significantly longer in those who subsequently died, despite similar ages and duration of diabetes. We conclude that QT/RR interval relationships are altered in diabetic autonomic neuropathy, and that changes in QT length with time parallel changese in autonomic function. There may be an association between QT interval prolongation and the risk of dying unexpectedly in diabetic autonomic neuropathy.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "484", "doc_id": "9047718", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Asymptomatic visual impairment screening in elderly populations leads to improved vision.\n\nCANDIDATE_PASSAGE:\nTransnationalism and identity Transnationalism and identity are concepts that inherently call for juxtaposition. This is so because many peoples' transnational networks of exchange and participation are grounded upon some perception of common identity; conversely, the identities of numerous individuals and groups of people are negotiated within social worlds that span more than one place. In this introductory article, the transnational perspective on migration studies is first discussed, followed by some critiques and outstanding questions. The final section summarises points raised by the contributing authors of the main articles in this themed issue of JEMS, especially with regard to various ways transnational settings and dynamics affect the construction, negotiation and reproduction of identities.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "138", "doc_id": "145716849", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: One in five surgical randomized controlled trials are discontinued early.\n\nCANDIDATE_ABSTRACT:\nTITLE: Discontinuation and non-publication of surgical randomised controlled trials: observational study\nABSTRACT: OBJECTIVE To determine the rate of early discontinuation and non-publication of randomised controlled trials involving patients undergoing surgery. DESIGN Cross sectional observational study of registered and published trials. SETTING Randomised controlled trials of interventions in patients undergoing a surgical procedure. DATA SOURCES The ClinicalTrials.gov database was searched for interventional trials registered between January 2008 and December 2009 using the keyword \"surgery\". Recruitment status was extracted from the ClinicalTrials.gov database. A systematic search for studies published in peer reviewed journals was performed; if they were not found, results posted on the ClinicalTrials.gov results database were sought. Email queries were sent to trial investigators of discontinued and unpublished completed trials if no reason for the respective status was disclosed. MAIN OUTCOME MEASURES Trial discontinuation before completion and non-publication after completion. Logistic regression was used to determine the effect of funding source on publication status, with adjustment for intervention type and trial size. RESULTS Of 818 registered trials found using the keyword \"surgery\", 395 met the inclusion criteria. Of these, 21% (81/395) were discontinued early, most commonly owing to poor recruitment (44%, 36/81). The remaining 314 (79%) trials proceeded to completion, with a publication rate of 66% (208/314) at a median time of 4.9 (interquartile range 4.0-6.0) years from study completion to publication search. A further 6% (20/314) of studies presented results on ClinicalTrials.gov without a corresponding peer reviewed publication. Industry funding did not affect the rate of discontinuation (adjusted odds ratio 0.91, 95% confidence interval 0.54 to 1.55) [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS One in five surgical randomised controlled trials are discontinued early, one in three completed trials remain unpublished, and investigators of unpublished studies are frequently not contactable.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 885, "doc_id": "6477536", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Lamins are associated with nuclear membrane structure maintenance.\n\nCANDIDATE_PASSAGE:\nSecDFyajC is not required for the maintenance of the proton motive force. SecDFyajC of Escherichia coli is required for efficient export of proteins in vivo. However, the functional role of SecDFyajC in protein translocation is unclear. We evaluated the postulated function of SecDFyajC in the maintenance of the proton motive force. As previously reported, inner membrane vesicles (IMVs) lacking SecDFyajC are defective in the generation of a stable proton motive force when energized with succinate. This phenomenon is, however, not observed when NADH is used as an electron donor. Moreover, the proton motive force generated in SecDFyajC-depleted vesicles stimulated translocation to the same extent as seen with IMVs containing SecDFyajC. Further analysis demonstrates that the reduced proton motive force with succinate in IMVs lacking SecDFyajC is due to a lower amount of the enzyme succinate dehydrogenase. The expression of this enzyme complex is repressed by growth on glucose media, the condition used to deplete SecDFyajC. These results demonstrate that SecDFyajC is not required for proton motive force-driven protein translocation.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "685", "doc_id": "10660080", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Headaches are not correlated with cognitive impairment.\n\nCANDIDATE_PASSAGE:\nTargeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs). GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets. We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels. To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA). Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis. The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays. The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts. In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival. Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation. Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "501", "doc_id": "33370", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Increased flux of microbial products suppresses immune responses.\n\nCANDIDATE_PASSAGE:\nDeveloping criteria for evaluation of geroprotectors as a key stage toward translation to the clinic In the coming decades, a massive shift in the aging segment of the population will have major social and economic consequences around the world. One way to offset this increase is to expedite the development of geroprotectors, substances that slow aging, repair age-associated damage and extend healthy lifespan, or healthspan. While over 200 geroprotectors are now reported in model organisms and some are in human use for specific disease indications, the path toward determining whether they affect aging in humans remains obscure. Translation to the clinic is hampered by multiple issues including absence of a common set of criteria to define, select, and classify these substances, given the complexity of the aging process and their enormous diversity in mechanism of action. Translational research efforts would benefit from the formation of a scientific consensus on the following: the definition of 'geroprotector', the selection criteria for geroprotectors, a comprehensive classification system, and an analytical model. Here, we review current approaches to selection and put forth our own suggested selection criteria. Standardizing selection of geroprotectors will streamline discovery and analysis of new candidates, saving time and cost involved in translation to clinic.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "610", "doc_id": "3707035", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is pyridoxine effective to prevent hand-foot syndrome associated with capecitabine therapy : results of a randomized , double-blind , placebo-controlled study?\n\nABSTRACT:\nTo determine whether concurrent pyridoxine therapy can prevent the development of hand-foot syndrome (HFS) in patients being treated with capecitabine. Chemotherapy-naive patients with GI tract cancers scheduled for capecitabine-containing chemotherapy were randomly assigned to concurrent oral pyridoxine (200 mg/d) or placebo. Patients were stratified by chemotherapy regimen and monitored until development of National Cancer Institute Common Toxicity Criteria grade 2 or worse HFS or capecitabine-containing chemotherapy ended. Patients in the placebo group who developed grade 2 or worse HFS were randomly assigned again to receive pyridoxine or placebo in the next chemotherapy cycle to determine whether pyridoxine could improve HFS. The median number of chemotherapy cycles to grade 2 or worse HFS was three in both groups. Grade 2 or worse HFS developed in 55 (30.6%) of 180 placebo-treated patients and in 57 (31.7%) of 180 pyridoxine patients. The cumulative dose of capecitabine to grade 2 or worse HFS was not different between the two groups (median not reached in either group; hazard ratio [HR] = 0.95; P = .788). Randomization of the 44 patients in the placebo group with grade 2 or worse HFS to placebo or pyridoxine for the next cycle resulted in no significant difference in the proportion showing improvement of HFS (42.9% v 47.8%; HR = 1.12; P = .94). By multivariate analysis, age > or = 56 years (HR = 1.768; 95% CI, 1.190 to 2.628; P = .005) was an independent risk factor for grade 2 or worse HFS, and combined use of docetaxel (HR = 2.046; 95% CI, 0.880 to 4.755; P = .096) was of borderline significance.", "output": "{\"label\": \"no\", \"rationale\": \"Pyridoxine is not effective in prevention of capecitabine-associated HFS.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 20625131, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: CDK6 shows improved binding to loss-of-function variants of p18 INK4C.\n\nCANDIDATE_PASSAGE:\nThe p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases. The cyclin-dependent kinase Cdk2 associates with cyclins A, D, and E and has been implicated in the control of the G1 to S phase transition in mammals. To identify potential Cdk2 regulators, we have employed an improved two-hybrid system to isolate human genes encoding Cdk-interacting proteins (Cips). CIP1 encodes a novel 21 kd protein that is found in cyclin A, cyclin D1, cyclin E, and Cdk2 immunoprecipitates. p21CIP1 is a potent, tight-binding inhibitor of Cdks and can inhibit the phosphorylation of Rb by cyclin A-Cdk2, cyclin E-Cdk2, cyclin D1-Cdk4, and cyclin D2-Cdk4 complexes. Cotransfection experiments indicate that CIP1 and SV40 T antigen function in a mutually antagonistic manner to control cell cycle progression.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "205", "doc_id": "13614794", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: JMJD6 catalyzes the hydroxylation of C-terminal lysine and supresses transcriptional activity.\n\nCANDIDATE_ABSTRACT:\nTITLE: JMJD6 Promotes Colon Carcinogenesis through Negative Regulation of p53 by Hydroxylation\nABSTRACT: Jumonji domain-containing 6 (JMJD6) is a member of the Jumonji C domain-containing family of proteins. Compared to other members of the family, the cellular activity of JMJD6 is still not clearly defined and its biological function is still largely unexplored. Here we report that JMJD6 is physically associated with the tumor suppressor p53. We demonstrated that JMJD6 acts as an α-ketoglutarate- and Fe(II)-dependent lysyl hydroxylase to catalyze p53 hydroxylation. We found that p53 indeed exists as a hydroxylated protein in vivo and that the hydroxylation occurs mainly on lysine 382 of p53. We showed that JMJD6 antagonizes p53 acetylation, promotes the association of p53 with its negative regulator MDMX, and represses transcriptional activity of p53. Depletion of JMJD6 enhances p53 transcriptional activity, arrests cells in the G1 phase, promotes cell apoptosis, and sensitizes cells to DNA damaging agent-induced cell death. Importantly, knockdown of JMJD6 represses p53-dependent colon cell proliferation and tumorigenesis in vivo, and significantly, the expression of JMJD6 is markedly up-regulated in various types of human cancer especially in colon cancer, and high nuclear JMJD6 protein is strongly correlated with aggressive clinical behaviors of colon adenocarcinomas. Our results reveal a novel posttranslational modification for p53 and support the pursuit of JMJD6 as a potential biomarker for colon cancer aggressiveness and a potential target for colon cancer intervention.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We demonstrated that JMJD6 acts as an α-ketoglutarate- and Fe(II)-dependent lysyl hydroxylase to catalyze p53 hydroxylation. We found that p53 indeed exists as a hydroxylated protein in vivo and that the hydroxylation occurs mainly on lysine 382 of p53.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 661, "doc_id": "37204802", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Less than 10% of patients exposed to radiation have activated markers of mesenchymal stem cells.\n\nCANDIDATE_PASSAGE:\nRNA is favourable for analysing EGFR mutations in malignant pleural effusion of lung cancer. Malignant pleural effusion (MPE) is a useful specimen allowing for the evaluation of EGFR status in nonsmall cell lung cancer (NSCLC). However, direct sequencing of genomic DNA from MPE samples was found not to be sensitive for EGFR mutation detection. To test whether EGFR analysis from RNA is less prone to interference from nontumour cells that have no or lower EGFR expression, we compared three methods (sequencing from cell-derived RNA versus sequencing and mass-spectrometric analysis from genomic DNA), in parallel, for EGFR mutation detection from MPE samples in 150 lung adenocarcinoma patients receiving first-line tyrosine kinase inhibitors (TKIs). Among these MPE samples, EGFR mutations were much more frequently identified by sequencing using RNA than by sequencing and mass-spectrometric analysis from genomic DNA (for all mutations, 67.3 versus 44.7 and 46.7%; for L858R or exon 19 deletions, 61.3 versus 41.3 and 46.7%, respectively). The better mutation detection yield of sequencing from RNA was coupled with the superior prediction of clinical efficacy of first-line TKIs. In patients with acquired resistance, EGFR sequencing from RNA provided satisfactory detection of T790M (54.2%). These results demonstrated that EGFR sequencing using RNA as template greatly improves sensitivity for EGFR mutation detection from samples of MPE, highlighting RNA as the favourable source for analysing EGFR mutations from heterogeneous MPE specimens in NSCLC.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "689", "doc_id": "711256", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does transcriptional activation of Fsp27 by the liver-enriched transcription factor CREBH promote lipid droplet growth and hepatic steatosis?\n\nABSTRACT:\nFat-specific protein 27 (Fsp27) is a lipid droplet-associated protein that promotes lipid droplet (LD) growth and triglyceride (TG) storage in white adipocytes. Fsp27 is also highly expressed in the steatotic liver and contributes to TG accumulation. In this study we discovered that the liver produces Fsp27β, an alternative Fsp27 isoform, which contains 10 additional amino acids at the N-terminus of the original Fsp27 (Fsp27α). White adipose tissue (WAT) and the liver specifically expressed Fsp27α and Fsp27β transcripts, respectively, which were driven by distinct promoters. The Fsp27β promoter was activated by the liver-enriched transcription factor cyclic-AMP-responsive-element-binding protein H (CREBH) but not by peroxisome proliferator-activated receptor gamma (PPARγ), which activated the Fsp27α promoter. Enforced expression of the constitutively active CREBH strongly induced Fsp27β and the human ortholog CIDEC2 in mouse hepatocytes and HepG2 cells, respectively. In contrast, loss of CREBH decreased hepatic Fsp27β in fasted mice, suggesting that CREBH plays a critical role in Fsp27β expression in the liver. Similar to Fsp27α, Fsp27β localized on the surface of lipid droplets and suppressed lipolysis. Consequently, enforced expression of Fsp27β or CREBH promoted lipid droplet enlargement and TG accumulation in the liver.", "output": "{\"label\": \"yes\", \"rationale\": \"The CREBH-Fsp27β axis is important for regulating lipid droplet dynamics and TG storage in the liver.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25125366, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: miR-142-5P is a known regulator of raised body temperature.\n\nCANDIDATE_ABSTRACT:\nTITLE: Extracellular vesicles from human cardiac progenitor cells inhibit cardiomyocyte apoptosis and improve cardiac function after myocardial infarction.\nABSTRACT: AIMS Recent evidence suggests that cardiac progenitor cells (CPCs) may improve cardiac function after injury. The underlying mechanisms are indirect, but their mediators remain unidentified. Exosomes and other secreted membrane vesicles, hereafter collectively referred to as extracellular vesicles (EVs), act as paracrine signalling mediators. Here, we report that EVs secreted by human CPCs are crucial cardioprotective agents. METHODS AND RESULTS CPCs were derived from atrial appendage explants from patients who underwent heart valve surgery. CPC-conditioned medium (CM) inhibited apoptosis in mouse HL-1 cardiomyocytic cells, while enhancing tube formation in human umbilical vein endothelial cells. These effects were abrogated by depleting CM of EVs. They were reproduced by EVs secreted by CPCs, but not by those secreted by human dermal fibroblasts. Transmission electron microscopy and nanoparticle tracking analysis showed most EVs to be 30-90 nm in diameter, the size of exosomes, although smaller and larger vesicles were also present. MicroRNAs most highly enriched in EVs secreted by CPCs compared with fibroblasts included miR-210, miR-132, and miR-146a-3p. miR-210 down-regulated its known targets, ephrin A3 and PTP1b, inhibiting apoptosis in cardiomyocytic cells. miR-132 down-regulated its target, RasGAP-p120, enhancing tube formation in endothelial cells. Infarcted hearts injected with EVs from CPCs, but not from fibroblasts, exhibited less cardiomyocyte apoptosis, enhanced angiogenesis, and improved LV ejection fraction (0.8 ± 6.8 vs. -21.3 ± 4.5%; P < 0.05) compared with those injected with control medium. CONCLUSION EVs are the active component of the paracrine secretion by human CPCs. As a cell-free approach, EVs could circumvent many of the limitations [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1391, "doc_id": "1905095", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: siRNA knockdown of A20 accelerates tumor progression in an in vivo murine xenograft model.\n\nCANDIDATE_PASSAGE:\nEpigenetic therapy activates type I interferon signaling in murine ovarian cancer to reduce immunosuppression and tumor burden. Ovarian cancer is the most lethal of all gynecological cancers, and there is an urgent unmet need to develop new therapies. Epithelial ovarian cancer (EOC) is characterized by an immune suppressive microenvironment, and response of ovarian cancers to immune therapies has thus far been disappointing. We now find, in a mouse model of EOC, that clinically relevant doses of DNA methyltransferase and histone deacetylase inhibitors (DNMTi and HDACi, respectively) reduce the immune suppressive microenvironment through type I IFN signaling and improve response to immune checkpoint therapy. These data indicate that the type I IFN response is required for effective in vivo antitumorigenic actions of the DNMTi 5-azacytidine (AZA). Through type I IFN signaling, AZA increases the numbers of CD45+ immune cells and the percentage of active CD8+ T and natural killer (NK) cells in the tumor microenvironment, while reducing tumor burden and extending survival. AZA also increases viral defense gene expression in both tumor and immune cells, and reduces the percentage of macrophages and myeloid-derived suppressor cells in the tumor microenvironment. The addition of an HDACi to AZA enhances the modulation of the immune microenvironment, specifically increasing T and NK cell activation and reducing macrophages over AZA treatment alone, while further increasing the survival of the mice. Finally, a triple combination of DNMTi/HDACi plus the immune checkpoint inhibitor α-PD-1 provides the best antitumor effect and longest overall survival, and may be an attractive candidate for future clinical trials in ovarian cancer.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1403", "doc_id": "9767444", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: RANK signals from CD4+3− inducer cells regulate development of Aire-expressing epithelial cells in the thymic medulla\nABSTRACT: Aire-expressing medullary thymic epithelial cells (mTECs) play a key role in preventing autoimmunity by expressing tissue-restricted antigens to help purge the emerging T cell receptor repertoire of self-reactive specificities. Here we demonstrate a novel role for a CD4+3− inducer cell population, previously linked to development of organized secondary lymphoid structures and maintenance of T cell memory in the functional regulation of Aire-mediated promiscuous gene expression in the thymus. CD4+3− cells are closely associated with mTECs in adult thymus, and in fetal thymus their appearance is temporally linked with the appearance of Aire+ mTECs. We show that RANKL signals from this cell promote the maturation of RANK-expressing CD80−Aire− mTEC progenitors into CD80+Aire+ mTECs, and that transplantation of RANK-deficient thymic stroma into immunodeficient hosts induces autoimmunity. Collectively, our data reveal cellular and molecular mechanisms leading to the generation of Aire+ mTECs and highlight a previously unrecognized role for CD4+3−RANKL+ inducer cells in intrathymic self-tolerance.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We show that RANKL signals from this cell promote the maturation of RANK-expressing CD80−Aire− mTEC progenitors into CD80+Aire+ mTECs, and that transplantation of RANK-deficient thymic stroma into immunodeficient hosts induces autoimmunity.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1004, "doc_id": "3952288", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Integrated care is ineffective at tackling multiple comorbidities.\n\nCANDIDATE_ABSTRACT:\nTITLE: Functional outcomes of multi-condition collaborative care and successful ageing: results of randomised trial\nABSTRACT: OBJECTIVE To evaluate the effectiveness of integrated care for chronic physical diseases and depression in reducing disability and improving quality of life. DESIGN A randomised controlled trial of multi-condition collaborative care for depression and poorly controlled diabetes and/or risk factors for coronary heart disease compared with usual care among middle aged and elderly people SETTING Fourteen primary care clinics in Seattle, Washington. PARTICIPANTS Patients with diabetes or coronary heart disease, or both, and blood pressure above 140/90 mm Hg, low density lipoprotein concentration >3.37 mmol/L, or glycated haemoglobin 8.5% or higher, and PHQ-9 depression scores of ≥ 10. INTERVENTION A 12 month intervention to improve depression, glycaemic control, blood pressure, and lipid control by integrating a \"treat to target\" programme for diabetes and risk factors for coronary heart disease with collaborative care for depression. The intervention combined self management support, monitoring of disease control, and pharmacotherapy to control depression, hyperglycaemia, hypertension, and hyperlipidaemia. MAIN OUTCOME MEASURES Social role disability (Sheehan disability scale), global quality of life rating, and World Health Organization disability assessment schedule (WHODAS-2) scales to measure disabilities in activities of daily living (mobility, self care, household maintenance). RESULTS Of 214 patients enrolled (106 intervention and 108 usual care), disability and quality of life measures were obtained for 97 intervention patients at six months (92%) and 92 at 12 months (87%), and for 96 usual care patients at six months (89%) and 92 at 12 months (85%). Improvements from baseline on the Sheehan disability scale (-0.9, 95% confidence interval -1.5 to -0.2; [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Integrated care that covers chronic physical disease and comorbid depression can reduce social role disability and enhance global quality of life.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 647, "doc_id": "15041758", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Side effects associated with antidepressants do not represent a mortality risk to postmenopausal women.\n\nCANDIDATE_PASSAGE:\nPlasma vitamin D metabolites and risk of colorectal cancer in women. OBJECTIVE Experimental evidence suggests that 1,25-dihydroxyvitamin D and its precursor, 25-hydroxyvitamin D [25(OH)D], may aid in the prevention of colorectal cancer. We therefore examined risk in relation to plasma concentrations of these vitamin D metabolites. METHODS In a nested case-control study among women in the Nurses' Health Study, we identified 193 colorectal cancer cases, ages 46 to 78 years, diagnosed up to 11 years after blood collection. Two controls were matched per case on year of birth and month of blood draw. Odds ratios (OR) for risk of colorectal cancer were calculated using conditional logistic regression adjusted for body mass index, physical activity, smoking, family history, use of hormone replacement therapy, aspirin use, and dietary intakes. RESULTS We found a significant inverse linear association between plasma 25(OH)D and risk of colorectal cancer (P = 0.02). Among women in the highest quintile, the OR (95% confidence interval) was 0.53 (0.27-1.04). This inverse association remained strong when limited to women > or =60 years at blood collection (P = 0.006) but was not apparent among the younger women (P = 0.70). Benefit from higher 25(OH)D concentrations was observed for cancers at the distal colon and rectum (P = 0.02) but was not evident for those at the proximal colon (P = 0.81). In contrast to 25(OH)D, we did not observe an association between 1,25-dihydroxyvitamin D and colorectal cancer, although risk was elevated among the women in the highest quintile if they were also in the lower half of the 25(OH)D distribution (OR, 2.52; 95% confidence interval, 1.04-6.11). CONCLUSION From these results and supporting evidence from previous studies, we conclude tha [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1081", "doc_id": "520579", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Amitriptyline is an effective treatment for chronic tension-type headaches.\n\nCANDIDATE_ABSTRACT:\nTITLE: Management of chronic tension-type headache with tricyclic antidepressant medication, stress management therapy, and their combination: a randomized controlled trial.\nABSTRACT: CONTEXT Chronic tension-type headaches are characterized by near-daily headaches and often are difficult to manage in primary practice. Behavioral and pharmacological therapies each appear modestly effective, but data are lacking on their separate and combined effects. OBJECTIVE To evaluate the clinical efficacy of behavioral and pharmacological therapies, singly and combined, for chronic tension-type headaches. DESIGN AND SETTING Randomized placebo-controlled trial conducted from August 1995 to January 1998 at 2 outpatient sites in Ohio. PARTICIPANTS Two hundred three adults (mean age, 37 years; 76% women) with diagnosis of chronic tension-type headaches (mean, 26 headache d/mo). INTERVENTIONS Participants were randomly assigned to receive tricyclic antidepressant (amitriptyline hydrochloride, up to 100 mg/d, or nortriptyline hydrochloride, up to 75 mg/d) medication (n = 53), placebo (n = 48), stress management (eg, relaxation, cognitive coping) therapy (3 sessions and 2 telephone contacts) plus placebo (n = 49), or stress management therapy plus antidepressant medication (n = 53). MAIN OUTCOME MEASURES Monthly headache index scores calculated as the mean of pain ratings (0-10 scale) recorded by participants in a daily diary 4 times per day; number of days per month with at least moderate pain (pain rating >/=5), analgesic medication use, and Headache Disability Inventory scores, compared by intervention group. RESULTS Tricyclic antidepressant medication and stress management therapy each produced larger reductions in headache activity, analgesic medication use, and headache-related disability than placebo, but antidepressant medication yielded more rapid improvements in headache activity. Combined therapy was more likely to produce clinically significant ( [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Combined therapy was more likely to produce clinically significant (>/=50%) reductions in headache index scores (64% of participants) than antidepressant medication (38% of participants; P =.006), stress management therapy (35%; P =.003), or placebo (29%; P =.001).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 108, "doc_id": "6191684", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Crossover hot spots are found within gene promoters in Saccharomyces cerevisiae.\n\nCANDIDATE_PASSAGE:\nVariant Histone H2A.Z Is Globally Localized to the Promoters of Inactive Yeast Genes and Regulates Nucleosome Positioning H2A.Z is an evolutionary conserved histone variant involved in transcriptional regulation, antisilencing, silencing, and genome stability. The mechanism(s) by which H2A.Z regulates these various biological functions remains poorly defined, in part due to the lack of knowledge regarding its physical location along chromosomes and the bearing it has in regulating chromatin structure. Here we mapped H2A.Z across the yeast genome at an approximately 300-bp resolution, using chromatin immunoprecipitation combined with tiling microarrays. We have identified 4,862 small regions—typically one or two nucleosomes wide—decorated with H2A.Z. Those “Z loci” are predominantly found within specific nucleosomes in the promoter of inactive genes all across the genome. Furthermore, we have shown that H2A.Z can regulate nucleosome positioning at the GAL1 promoter. Within HZAD domains, the regions where H2A.Z shows an antisilencing function, H2A.Z is localized in a wider pattern, suggesting that the variant histone regulates a silencing and transcriptional activation via different mechanisms. Our data suggest that the incorporation of H2A.Z into specific promoter-bound nucleosomes configures chromatin structure to poise genes for transcriptional activation. The relevance of these findings to higher eukaryotes is discussed.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "293", "doc_id": "15778034", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Transcription rates in S. cerevisiae range between 7 and 12 kb/min.\n\nCANDIDATE_PASSAGE:\nThe Self-Incompatibility Genes of Brassica: Expression and Use in Genetic Ablation of Floral Tissues INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 394 POLLINATION AND POLLEN TUBE GROWTH . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 395 Interaction s between the M ale G ameto phyte and Pistil . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 395 SelfIncom patibili ty Systems: Gameto phytic and S poro phyti c Determin ation of Pollen Phenoty pe . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 397 DEVELOPMENTAL S TUDIES OF REPRODUCTIVE STRUCTURES . . . . . . . . .. . . ... . . . . 398 Tissues of the Pistil with Special Reference to Pollination Functions 398 The Male Gametophyte . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 399 MOLECULAR ANALYSIS OF SELF-INCOMPATIBILITY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40 1 The S-M ultigene F amily o j Brassica. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . 402 Allelism at the S-Lo cus and the SLG Gene\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\" 402 The S-Locus Related (SLR) Genes 405 Molecular Complexity oj the S-Locus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 407 EXPRESSION OF THE SLG GENE IN PIS TILS AND ANTHERS . . . . . . . . . . . . . . . . . . . . . . . 409 Expression in Cruc ifers . . . . . . . . . . . . . . . . . . . . . . . . . [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1315", "doc_id": "86217760", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Breast cancer development is determined exclusively by genetic factors.\n\nCANDIDATE_PASSAGE:\nGene–environment interactions in 7610 women with breast cancer: prospective evidence from the Million Women Study BACKGROUND Information is scarce about the combined effects on breast cancer incidence of low-penetrance genetic susceptibility polymorphisms and environmental factors (reproductive, behavioural, and anthropometric risk factors for breast cancer). To test for evidence of gene-environment interactions, we compared genotypic relative risks for breast cancer across the other risk factors in a large UK prospective study. METHODS We tested gene-environment interactions in 7610 women who developed breast cancer and 10 196 controls without the disease, studying the effects of 12 polymorphisms (FGFR2-rs2981582, TNRC9-rs3803662, 2q35-rs13387042, MAP3K1-rs889312, 8q24-rs13281615, 2p-rs4666451, 5p12-rs981782, CASP8-rs1045485, LSP1-rs3817198, 5q-rs30099, TGFB1-rs1982073, and ATM-rs1800054) in relation to prospectively collected information about ten established environmental risk factors (age at menarche, parity, age at first birth, breastfeeding, menopausal status, age at menopause, use of hormone replacement therapy, body-mass index, height, and alcohol consumption). FINDINGS After allowance for multiple testing none of the 120 comparisons yielded significant evidence of a gene-environment interaction. By contrast with previous suggestions, there was little evidence that the genotypic relative risks were affected by use of hormone replacement therapy, either overall or for oestrogen-receptor-positive disease. Only one of the 12 polymorphisms was correlated with any of the ten other risk factors: carriers of the high-risk C allele of MAP3K1-rs889312 were significantly shorter than non-carriers (mean height 162.4 cm [95% CI 162.1-162.7] vs 163.1 cm [162.9-16 [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "185", "doc_id": "18340282", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The mean suicide rate in women is higher after miscarriage than live birth.\n\nCANDIDATE_ABSTRACT:\nTITLE: N348I in HIV-1 reverse transcriptase can counteract the nevirapine-mediated bias toward RNase H cleavage during plus-strand initiation.\nABSTRACT: Drug resistance-associated mutations in HIV-1 reverse transcriptase (RT) can affect the balance between polymerase and ribonuclease H (RNase H) activities of the enzyme. We have recently demonstrated that the N348I mutation in the connection domain causes selective dissociation from RNase H-competent complexes, whereas the functional integrity of the polymerase-competent complex remains largely unaffected. N348I has been associated with resistance to the non-nucleoside RT inhibitor (NNRTI), nevirapine; however, a possible mechanism that links changes in RNase H activity to changes in NNRTI susceptibility remains to be established. To address this problem, we consider recent findings suggesting that NNRTIs may affect the orientation of RT on its nucleic acid substrate and increase RNase H activity. Here we demonstrate that RNase H-mediated primer removal is indeed more efficient in the presence of NNRTIs; however, the N348I mutant enzyme is able to counteract this effect. Efavirenz, a tight binding inhibitor, restricts the influence of the mutation. These findings provide strong evidence to suggest that N348I can thwart the inhibitory effects of nevirapine during initiation of (+)-strand DNA synthesis, which provides a novel mechanism for resistance. The data are in agreement with clinical data, which demonstrate a stronger effect of N348I on susceptibility to nevirapine as compared with efavirenz.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1227, "doc_id": "2319305", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: ART has no effect on the infectiveness of HIV-positive people.\n\nCANDIDATE_ABSTRACT:\nTITLE: HIV Treatment as Prevention: Systematic Comparison of Mathematical Models of the Potential Impact of Antiretroviral Therapy on HIV Incidence in South Africa\nABSTRACT: BACKGROUND Many mathematical models have investigated the impact of expanding access to antiretroviral therapy (ART) on new HIV infections. Comparing results and conclusions across models is challenging because models have addressed slightly different questions and have reported different outcome metrics. This study compares the predictions of several mathematical models simulating the same ART intervention programmes to determine the extent to which models agree about the epidemiological impact of expanded ART. METHODS AND FINDINGS Twelve independent mathematical models evaluated a set of standardised ART intervention scenarios in South Africa and reported a common set of outputs. Intervention scenarios systematically varied the CD4 count threshold for treatment eligibility, access to treatment, and programme retention. For a scenario in which 80% of HIV-infected individuals start treatment on average 1 y after their CD4 count drops below 350 cells/µl and 85% remain on treatment after 3 y, the models projected that HIV incidence would be 35% to 54% lower 8 y after the introduction of ART, compared to a counterfactual scenario in which there is no ART. More variation existed in the estimated long-term (38 y) reductions in incidence. The impact of optimistic interventions including immediate ART initiation varied widely across models, maintaining substantial uncertainty about the theoretical prospect for elimination of HIV from the population using ART alone over the next four decades. The number of person-years of ART per infection averted over 8 y ranged between 5.8 and 18.7. Considering the actual scale-up of ART in South Africa, seven models estimated that current HIV incidence is 17% to 32% lower than it would have been in the absence of ART. Differences [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"For a scenario in which 80% of HIV-infected individuals start treatment on average 1 y after their CD4 count drops below 350 cells/µl and 85% remain on treatment after 3 y, the models projected that HIV incidence would be 35% to 54% lower 8 y after the introduction of ART, compared to a counterfactual scenario in which there is no ART.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 60, "doc_id": "13899137", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Glycan adaptation involves insertion-deletion events.\n\nCANDIDATE_PASSAGE:\nSerum amyloid A: An acute-phase protein involved in tumour pathogenesis The synthesis of acute-phase protein serum amyloid A (SAA) is largely regulated by inflammation- associated cytokines and a high concentration of circulating SAA may represent an ideal marker for acute and chronic inflammatory diseases. However, SAA is also synthesized in extrahepatic tissues, e.g. human carcinoma metastases and cancer cell lines. An increasing body of in vitro data supports the concept of involvement of SAA in carcinogenesis and neoplastic diseases. Accumulating evidence suggests that SAA might be included in a group of biomarkers to detect a pattern of physiological events that reflect the growth of malignancy and host response. This review is meant to provide a broad overview of the many ways that SAA could contribute to tumour development, and accelerate tumour progression and metastasis, and to gain a better understanding of this acute-phase reactant as a possible link between chronic inflammation and neoplasia.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "473", "doc_id": "31933981", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does vaginal intraepithelial neoplasia have the same evolution as cervical intraepithelial neoplasia?\n\nABSTRACT:\nVaginal intraepithelial neoplasia is a little known disease which could be related to risk factors different from simple HPV infections. To ascertain wheter vaginal lesions have a natural history similar to cervical lesions.MATERIALS & A retrospective study to identify patients with vaginal lesions and synchronous cervical lesions through biopsy. The rate of mild cervical lesions (koilocytosis, warts, CIN I with and without koilocytosis) was compared with the rate of severe cervical lesions (CIN II and III, cervical carcinoma) in patients with mild vaginal lesions (warts and koilocytosis, and low-grade VAIN) and in patients with severe vaginal lesions (high-grade VAIN). Using koilocytosis as a marker, the rate of \"active\" cervical lesions was compared with the rate of \"non active\" cervical lesions in patients with \"active\" versus \"non active\" vaginal lesions. Finally, the rates of mild and severe cervical lesions were compared among each group of VAIN (low-grade, high-grade, with or without koilocytosis). In patients with mild vaginal lesions, mild cervical lesions were significantly more frequent than severe cervical lesions. In patients with \"active\" vaginal lesions the rate of \"active\" cervical lesions was significantly higher than \"non active\" cervical lesions. The differences in rates of mild cervical lesions and severe cervical lesions among patients with high-grade VAIN and low-grade VAIN (with and without koilocytosis) were not significant.", "output": "{\"label\": \"maybe\", \"rationale\": \"These data suggest that CIN and VAIN may have some common features in certain cases, i.e., if an HPV infection is proved.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 18714572, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Cis-acting lncRNAs control the expression of genes that are positioned in the vicinity of their transcription sites.\n\nCANDIDATE_PASSAGE:\nFunctional Consequences of Splicing of the Antisense Transcript COOLAIR on FLC Transcription Antisense transcription is widespread in many genomes; however, how much is functional is hotly debated. We are investigating functionality of a set of long noncoding antisense transcripts, collectively called COOLAIR, produced at Arabidopsis FLOWERING LOCUS C (FLC). COOLAIR initiates just downstream of the major sense transcript poly(A) site and terminates either early or extends into the FLC promoter region. We now show that splicing of COOLAIR is functionally important. This was revealed through analysis of a hypomorphic mutation in the core spliceosome component PRP8. The prp8 mutation perturbs a cotranscriptional feedback mechanism linking COOLAIR processing to FLC gene body histone demethylation and reduced FLC transcription. The importance of COOLAIR splicing in this repression mechanism was confirmed by disrupting COOLAIR production and mutating the COOLAIR proximal splice acceptor site. Our findings suggest that altered splicing of a long noncoding transcript can quantitatively modulate gene expression through cotranscriptional coupling mechanisms.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "262", "doc_id": "14610165", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cost effectiveness evaluations based on cRCT data lack external validity.\n\nCANDIDATE_ABSTRACT:\nTITLE: A Comparison of Cost Effectiveness Using Data from Randomized Trials or Actual Clinical Practice: Selective Cox-2 Inhibitors as an Example\nABSTRACT: BACKGROUND Data on absolute risks of outcomes and patterns of drug use in cost-effectiveness analyses are often based on randomised clinical trials (RCTs). The objective of this study was to evaluate the external validity of published cost-effectiveness studies by comparing the data used in these studies (typically based on RCTs) to observational data from actual clinical practice. Selective Cox-2 inhibitors (coxibs) were used as an example. METHODS AND FINDINGS The UK General Practice Research Database (GPRD) was used to estimate the exposure characteristics and individual probabilities of upper gastrointestinal (GI) events during current exposure to nonsteroidal anti-inflammatory drugs (NSAIDs) or coxibs. A basic cost-effectiveness model was developed evaluating two alternative strategies: prescription of a conventional NSAID or coxib. Outcomes included upper GI events as recorded in GPRD and hospitalisation for upper GI events recorded in the national registry of hospitalisations (Hospital Episode Statistics) linked to GPRD. Prescription costs were based on the prescribed number of tables as recorded in GPRD and the 2006 cost data from the British National Formulary. The study population included over 1 million patients prescribed conventional NSAIDs or coxibs. Only a minority of patients used the drugs long-term and daily (34.5% of conventional NSAIDs and 44.2% of coxibs), whereas coxib RCTs required daily use for at least 6-9 months. The mean cost of preventing one upper GI event as recorded in GPRD was US$104k (ranging from US$64k with long-term daily use to US$182k with intermittent use) and US$298k for hospitalizations. The mean costs (for GPRD events) over calendar time were US$58k during 1990-1993 and US$174k during 2002-2005. Using RCT data rather [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The mean costs (for GPRD events) over calendar time were US$58k during 1990-1993 and US$174k during 2002-2005. Using RCT data rather than GPRD data for event probabilities, the mean cost was US$16k with the VIGOR RCT and US$20k with the CLASS RCT.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 292, "doc_id": "15048300", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Gpr124 increases BBB breakdown in mouse models of ischemic stroke.\n\nCANDIDATE_PASSAGE:\nEnhancement of anxiety-like responsiveness to the cannabinoid CB(1) receptor agonist HU-210 following chronic stress. The effect that chronic unpredictable stress had on the anxiety-like response elicited by the cannabinoid receptor agonist HU-210 [3-(1,1-dimethylheptyl)-(-)-11-hydroxy-delta 8-tetrahydrocannabinol] in the elevated plus maze was investigated here. Male Long-Evans rats were either unstressed or were subjected to a 21-day regimen of chronic unpredictable stress, and subsequently were subdivided into three testing groups (vehicle, 10 and 50 microg/kg of HU-210) and tested on the elevated plus maze. Results demonstrated that in unstressed animals, a low dose of HU-210 induced an anxiolytic response, whereas a high dose induced an anxiogenic response. Further, in stressed animals both the low and the high doses of HU-210 induced anxiogenic responses. These findings suggest that chronic stress enhances either cannabinoid receptor responsivity or one of the interacting systems implicated in emotional states.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "479", "doc_id": "41911192", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The DESMOND program caused substantial weight loss in most participants.\n\nCANDIDATE_PASSAGE:\nExploring Metabolic Configurations of Single Cells within Complex Tissue Microenvironments. Over the past years, plenty of evidence has emerged illustrating how metabolism supports many aspects of cellular function and how metabolic reprogramming can drive cell differentiation and fate. Here, we present a method to assess the metabolic configuration of single cells within their native tissue microenvironment via the visualization and quantification of multiple enzymatic activities measured at saturating substrate conditions combined with subsequent cell type identification. After careful validation of the approach and to demonstrate its potential, we assessed the intracellular metabolic configuration of different human immune cell populations in healthy and tumor colon tissue. Additionally, we analyzed the intercellular metabolic relationship between cancer cells and cancer-associated fibroblasts in a breast cancer tissue array. This study demonstrates that the determination of metabolic configurations in single cells could be a powerful complementary tool for every researcher interested to study metabolic networks in situ.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1156", "doc_id": "22712546", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Dscam1 acts as a hypervariable pattern-recognition receptor for the immune system.\n\nCANDIDATE_ABSTRACT:\nTITLE: AgDscam, a Hypervariable Immunoglobulin Domain-Containing Receptor of the Anopheles gambiae Innate Immune System \nABSTRACT: Activation of the insect innate immune system is dependent on a limited number of pattern recognition receptors (PRRs) capable of interacting with pathogen-associated molecular pattern. Here we report a novel role of an alternatively spliced hypervariable immunoglobulin domain-encoding gene, Dscam, in generating a broad range of PRRs implicated in immune defense in the malaria vector Anopheles gambiae. The mosquito Down syndrome cell adhesion molecule gene, AgDscam, has a complex genome organization with 101 exons that can produce over 31,000 potential alternative splice forms with different combinations of adhesive domains and interaction specificities. AgDscam responds to infection by producing pathogen challenge-specific splice form repertoires. Transient silencing of AgDscam compromises the mosquito's resistance to infections with bacteria and the malaria parasite Plasmodium. AgDscam is mediating phagocytosis of bacteria with which it can associate and defend against in a splice form–specific manner. AgDscam is a hypervariable PRR of the A. gambiae innate immune system.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here we report a novel role of an alternatively spliced hypervariable immunoglobulin domain-encoding gene, Dscam, in generating a broad range of PRRs implicated in immune defense in the malaria vector Anopheles gambiae.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 356, "doc_id": "6144337", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pioglitazone use is significantly associated with an increased risk of prostate cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: CD127 expression inversely correlates with FoxP3 and suppressive function of human CD4+ T reg cells\nABSTRACT: Regulatory T (T reg) cells are critical regulators of immune tolerance. Most T reg cells are defined based on expression of CD4, CD25, and the transcription factor, FoxP3. However, these markers have proven problematic for uniquely defining this specialized T cell subset in humans. We found that the IL-7 receptor (CD127) is down-regulated on a subset of CD4+ T cells in peripheral blood. We demonstrate that the majority of these cells are FoxP3+, including those that express low levels or no CD25. A combination of CD4, CD25, and CD127 resulted in a highly purified population of T reg cells accounting for significantly more cells that previously identified based on other cell surface markers. These cells were highly suppressive in functional suppressor assays. In fact, cells separated based solely on CD4 and CD127 expression were anergic and, although representing at least three times the number of cells (including both CD25+CD4+ and CD25−CD4+ T cell subsets), were as suppressive as the “classic” CD4+CD25hi T reg cell subset. Finally, we show that CD127 can be used to quantitate T reg cell subsets in individuals with type 1 diabetes supporting the use of CD127 as a biomarker for human T reg cells.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 954, "doc_id": "266641", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does timing of initial surfactant treatment make a difference in rates of chronic lung disease or mortality in premature infants?\n\nABSTRACT:\nTo compare two treatment strategies in preterm infants with or at risk of respiratory distress syndrome: early surfactant administration (within one hour of birth) versus late surfactant administration, in a geographically defined population. The primary outcome was chronic lung disease (CLD) and mortality before/at 36 weeks. Secondary outcomes included: duration of mechanical ventilation and continuous positive airway pressure (CPAP), post-natal steroids for CLD and major neonatal morbidities. Premature infants born at 22-32 weeks' gestation between January 2006 and December 2009. Ten neonatal intensive care units (NICUs) in New South Wales (NSW) and Australian Capital Territory (ACT), Australia. Retrospective analysis of prospectively collected data from the regional NICU database in NSW and ACT. Of the 2170 infants who received surfactant, 1182 (54.5%) and 988 (45.5%) received early and late surfactant, respectively. The early surfactant group was less mature (27.1 ± 2.1 versus 29.4 ± 2.1 weeks) and had more CLD and mortality (40.2% versus 20.0%). The multivariable analysis showed early surfactant to be associated with less duration of ventilation, longer duration of CPAP and longer hospital stay but had little or no impact on CLD/mortality.", "output": "{\"label\": \"maybe\", \"rationale\": \"Early surfactant administration is associated with shorter duration of ventilation but does not appear to be significantly protective against CLD/mortality among premature infants. This may support the growing evidence for consideration of CPAP as an alternative to routine intubation and early surfactant administration. Further investigation from large randomized clinical trials is warranted to confirm these results.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 25394614, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: CD44v6 is not associated with constitutive and reprogrammed cancer stem cells driving cancer metastasis.\n\nCANDIDATE_ABSTRACT:\nTITLE: CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis.\nABSTRACT: Cancer stem cells drive tumor formation and metastasis, but how they acquire metastatic traits is not well understood. Here, we show that all colorectal cancer stem cells (CR-CSCs) express CD44v6, which is required for their migration and generation of metastatic tumors. CD44v6 expression is low in primary tumors but demarcated clonogenic CR-CSC populations. Cytokines hepatocyte growth factor (HGF), osteopontin (OPN), and stromal-derived factor 1α (SDF-1), secreted from tumor associated cells, increase CD44v6 expression in CR-CSCs by activating the Wnt/β-catenin pathway, which promotes migration and metastasis. CD44v6(-) progenitor cells do not give rise to metastatic lesions but, when treated with cytokines, acquire CD44v6 expression and metastatic capacity. Importantly, phosphatidylinositol 3-kinase (PI3K) inhibition selectively killed CD44v6 CR-CSCs and reduced metastatic growth. In patient cohorts, low levels of CD44v6 predict increased probability of survival. Thus, the metastatic process in colorectal cancer is initiated by CSCs through the expression of CD44v6, which is both a functional biomarker and therapeutic target.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Cytokines hepatocyte growth factor (HGF), osteopontin (OPN), and stromal-derived factor 1α (SDF-1), secreted from tumor associated cells, increase CD44v6 expression in CR-CSCs by activating the Wnt/β-catenin pathway, which promotes migration and metastasis.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 203, "doc_id": "9558539", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: CD28 signals regulate trafficking of murine auto-reactive T cells into target tissues.\n\nCANDIDATE_ABSTRACT:\nTITLE: CD28 and ITK signals regulate autoreactive T cell trafficking\nABSTRACT: Activation of self-reactive T cells and their trafficking to target tissues leads to autoimmune organ destruction. Mice lacking the co-inhibitory receptor cytotoxic T lymphocyte antigen-4 (CTLA-4) develop fatal autoimmunity characterized by lymphocytic infiltration into nonlymphoid tissues. Here, we demonstrate that the CD28 co-stimulatory pathway regulates the trafficking of self-reactive Ctla4(-/-) T cells to tissues. Concurrent ablation of the CD28-activated Tec family kinase ITK does not block spontaneous T cell activation but instead causes self-reactive Ctla4(-/-) T cells to accumulate in secondary lymphoid organs. Despite excessive spontaneous T cell activation and proliferation in lymphoid organs, Itk(-/-); Ctla4(-/-) mice are otherwise healthy, mount antiviral immune responses and exhibit a long lifespan. We propose that ITK specifically licenses autoreactive T cells to enter tissues to mount destructive immune responses. Notably, ITK inhibitors mimic the null mutant phenotype and also prevent pancreatic islet infiltration by diabetogenic T cells in mouse models of type 1 diabetes, highlighting their potential utility for the treatment of human autoimmune disorders.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here, we demonstrate that the CD28 co-stimulatory pathway regulates the trafficking of self-reactive Ctla4(-/-) T cells to tissues.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 201, "doc_id": "2462673", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_ABSTRACT:\nTITLE: Human papillomavirus and Papanicolaou tests to screen for cervical cancer.\nABSTRACT: BACKGROUND Screening for cervical cancer based on testing for human papillomavirus (HPV) increases the sensitivity of detection of high-grade (grade 2 or 3) cervical intraepithelial neoplasia, but whether this gain represents overdiagnosis or protection against future high-grade cervical epithelial neoplasia or cervical cancer is unknown. METHODS In a population-based screening program in Sweden, 12,527 women 32 to 38 years of age were randomly assigned at a 1:1 ratio to have an HPV test plus a Papanicolaou (Pap) test (intervention group) or a Pap test alone (control group). Women with a positive HPV test and a normal Pap test result were offered a second HPV test at least 1 year later, and those who were found to be persistently infected with the same high-risk type of HPV were then offered colposcopy with cervical biopsy. A similar number of double-blinded Pap smears and colposcopies with biopsy were performed in randomly selected women in the control group. Comprehensive registry data were used to follow the women for a mean of 4.1 years. The relative rates of grade 2 or 3 cervical intraepithelial neoplasia or cancer detected at enrollment and at subsequent screening examinations were calculated. RESULTS At enrollment, the proportion of women in the intervention group who were found to have lesions of grade 2 or 3 cervical intraepithelial neoplasia or cancer was 51% greater (95% confidence interval [CI], 13 to 102) than the proportion of women in the control group who were found to have such lesions. At subsequent screening examinations, the proportion of women in the intervention group who were found to have grade 2 or 3 lesions or cancer was 42% less (95% CI, 4 to 64) and the proportion with grade 3 lesions or cancer was 47% less (95% CI, 2 to 71) than [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS The addition of an HPV test to the Pap test to screen women in their mid-30s for cervical cancer reduces the incidence of grade 2 or 3 cervical intraepithelial neoplasia or cancer detected by subsequent screening examinations.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 972, "doc_id": "46695481", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: eRNAs influence is linked to senescence, aging, and carcinogenesis.\n\nCANDIDATE_PASSAGE:\nLarge-Scale Profiling Reveals the Influence of Genetic Variation on Gene Expression in Human Induced Pluripotent Stem Cells. In this study, we used whole-genome sequencing and gene expression profiling of 215 human induced pluripotent stem cell (iPSC) lines from different donors to identify genetic variants associated with RNA expression for 5,746 genes. We were able to predict causal variants for these expression quantitative trait loci (eQTLs) that disrupt transcription factor binding and validated a subset of them experimentally. We also identified copy-number variant (CNV) eQTLs, including some that appear to affect gene expression by altering the copy number of intergenic regulatory regions. In addition, we were able to identify effects on gene expression of rare genic CNVs and regulatory single-nucleotide variants and found that reactivation of gene expression on the X chromosome depends on gene chromosomal position. Our work highlights the value of iPSCs for genetic association analyses and provides a unique resource for investigating the genetic regulation of gene expression in pluripotent cells.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1387", "doc_id": "4632921", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Post-transcriptional handling of mitochondrial transcripts occurs in mitochondrial RNA granules.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Human Mitochondrial DEAD-Box Protein DDX28 Resides in RNA Granules and Functions in Mitoribosome Assembly.\nABSTRACT: Human mitochondrial ribosomes are specialized in the synthesis of 13 proteins, which are fundamental components of the oxidative phosphorylation system. The pathway of mitoribosome biogenesis, the compartmentalization of the process, and factors involved remain largely unknown. Here, we have identified the DEAD-box protein DDX28 as an RNA granule component essential for the biogenesis of the mitoribosome large subunit (mt-LSU). DDX28 interacts with the 16S rRNA and the mt-LSU. RNAi-mediated DDX28 silencing in HEK293T cells does not affect mitochondrial mRNA stability or 16S rRNA processing or modification. However, it leads to reduced levels of 16S rRNA and mt-LSU proteins, impaired mt-LSU assembly, deeply attenuated mitochondrial protein synthesis, and consequent failure to assemble oxidative phosphorylation complexes. Our findings identify DDX28 as essential during the early stages of mitoribosome mt-LSU biogenesis, a process that takes place mainly near the mitochondrial nucleoids, in the compartment defined by the RNA granules.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here, we have identified the DEAD-box protein DDX28 as an RNA granule component essential for the biogenesis of the mitoribosome large subunit (mt-LSU).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 962, "doc_id": "4306711", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Do ultradeep 16S rRNA sequencing analysis of geographically similar but diverse unexplored marine samples reveal varied bacterial community composition?\n\nABSTRACT:\nBacterial community composition in the marine environment differs from one geographical location to another. Reports that delineate the bacterial diversity of different marine samples from geographically similar location are limited. The present study aims to understand whether the bacterial community compositions from different marine samples harbour similar bacterial diversity since these are geographically related to each other. In the present study, 16S rRNA deep sequencing analysis targeting V3 region was performed using Illumina bar coded sequencing. A total of 22.44 million paired end reads were obtained from the metagenomic DNA of Marine sediment, Rhizosphere sediment, Seawater and the epibacterial DNA of Seaweed and Seagrass. Diversity index analysis revealed that Marine sediment has the highest bacterial diversity and the least bacterial diversity was observed in Rhizosphere sediment. Proteobacteria, Actinobacteria and Bacteroidetes were the dominant taxa present in all the marine samples. Nearly 62-71% of rare species were identified in all the samples and most of these rare species were unique to a particular sample. Further taxonomic assignment at the phylum and genus level revealed that the bacterial community compositions differ among the samples.", "output": "{\"label\": \"yes\", \"rationale\": \"This is the first report that supports the fact that, bacterial community composition is specific for specific samples irrespective of its similar geographical location. Existence of specific bacterial community for each sample may drive overall difference in bacterial structural composition of each sample. Further studies like whole metagenomic sequencing will throw more insights to the key stone players and its interconnecting metabolic pathways.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 24167548, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: 90% of sudden infant death syndrome (SIDS) deaths happen in newborns aged less than 6 months.\n\nCANDIDATE_PASSAGE:\nEIF2AK3, encoding translation initiation factor 2-α kinase 3, is mutated in patients with Wolcott-Rallison syndrome Wolcott-Rallison syndrome (WRS) is a rare, autosomal recessive disorder characterized by permanent neonatal or early infancy insulin-dependent diabetes. Epiphyseal dysplasia, osteoporosis and growth retardation occur at a later age. Other frequent multisystemic manifestations include hepatic and renal dysfunction, mental retardation and cardiovascular abnormalities. On the basis of two consanguineous families, we mapped WRS to a region of less than 3 cM on chromosome 2p12, with maximal evidence of linkage and homozygosity at 4 microsatellite markers within an interval of approximately 1 cM. The gene encoding the eukaryotic translation initiation factor 2-α kinase 3 (EIF2AK3) resides in this interval; thus we explored it as a candidate. We identified distinct mutations of EIF2AK3 that segregated with the disorder in each of the families. The first mutation produces a truncated protein in which the entire catalytic domain is missing. The other changes an amino acid, located in the catalytic domain of the protein, that is highly conserved among kinases from the same subfamily. Our results provide evidence for the role of EIF2AK3 in WRS. The identification of this gene may provide insight into the understanding of the more common forms of diabetes and other pathologic manifestations of WRS.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "25", "doc_id": "24521894", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Anthrax spores can be disposed of easily after they are dispersed.\n\nCANDIDATE_ABSTRACT:\nTITLE: Secondary aerosolization of viable Bacillus anthracis spores in a contaminated US Senate Office.\nABSTRACT: CONTEXT Bioterrorist attacks involving letters and mail-handling systems in Washington, DC, resulted in Bacillus anthracis (anthrax) spore contamination in the Hart Senate Office Building and other facilities in the US Capitol's vicinity. OBJECTIVE To provide information about the nature and extent of indoor secondary aerosolization of B anthracis spores. DESIGN Stationary and personal air samples, surface dust, and swab samples were collected under semiquiescent (minimal activities) and then simulated active office conditions to estimate secondary aerosolization of B anthracis spores. Nominal size characteristics, airborne concentrations, and surface contamination of B anthracis particles (colony-forming units) were evaluated. RESULTS Viable B anthracis spores reaerosolized under semiquiescent conditions, with a marked increase in reaerosolization during simulated active office conditions. Increases were observed for B anthracis collected on open sheep blood agar plates (P<.001) and personal air monitors (P =.01) during active office conditions. More than 80% of the B anthracis particles collected on stationary monitors were within an alveolar respirable size range of 0.95 to 3.5 micro m. CONCLUSIONS Bacillus anthracis spores used in a recent terrorist incident reaerosolized under common office activities. These findings have important implications for appropriate respiratory protection, remediation, and reoccupancy of contaminated office environments.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"More than 80% of the B anthracis particles collected on stationary monitors were within an alveolar respirable size range of 0.95 to 3.5 micro m. CONCLUSIONS Bacillus anthracis spores used in a recent terrorist incident reaerosolized under common office activities.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 115, "doc_id": "33872649", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Charcoal shows no benefit for acute paraquat poisoning.\n\nCANDIDATE_PASSAGE:\nEffect of activated charcoal hemoperfusion on renal function in patients with paraquat poisoning. The present study retrospectively analyzed 19 patients diagnosed with paraquat (PQ) poisoning with the aim to investigate the effect of activated charcoal hemoperfusion on renal function and PQ elimination. The results indicated that 7 patients died and 12 survived. Non-oliguric renal failure occurred in all of the 7 patients who died. Among the 12 surviving patients, 10 had normal renal function and 2 developed non-oliguric renal failure. There was a linear correlation between plasma and urine paraquat concentration prior to and during activated charcoal hemoperfusion. The equation parameters together with the correlation coefficient on admission were as follows: Y=0.5820+1.7348X (R2=0.678; F=35.768; P<0.0001). The equation parameters together with the correlation coefficient were as follows during activated charcoal hemoperfusion: Y=0.6827+1.2649X (R2=0.626; F=50.308; P<0.0001). Therefore, it was concluded that in patients with normal renal function, the elimination kinetics of PQ by the kidneys were only associated with the plasma PQ concentration. Activated charcoal hemoperfusion had little effect on avoiding acute kidney injury in patients with severe PQ poisoning.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "246", "doc_id": "3430789", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Inhibiting glucose-6-phospate dehydrogenase improves lipogenesis by deactivating LKB1-AMPK signaling.\n\nCANDIDATE_ABSTRACT:\nTITLE: 6-phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumor growth by inhibiting LKB1-AMPK signaling\nABSTRACT: The oxidative pentose phosphate pathway (PPP) contributes to tumour growth, but the precise contribution of 6-phosphogluconate dehydrogenase (6PGD), the third enzyme in this pathway, to tumorigenesis remains unclear. We found that suppression of 6PGD decreased lipogenesis and RNA biosynthesis and elevated ROS levels in cancer cells, attenuating cell proliferation and tumour growth. 6PGD-mediated production of ribulose-5-phosphate (Ru-5-P) inhibits AMPK activation by disrupting the active LKB1 complex, thereby activating acetyl-CoA carboxylase 1 and lipogenesis. Ru-5-P and NADPH are thought to be precursors in RNA biosynthesis and lipogenesis, respectively; thus, our findings provide an additional link between the oxidative PPP and lipogenesis through Ru-5-P-dependent inhibition of LKB1-AMPK signalling. Moreover, we identified and developed 6PGD inhibitors, physcion and its derivative S3, that effectively inhibited 6PGD, cancer cell proliferation and tumour growth in nude mice xenografts without obvious toxicity, suggesting that 6PGD could be an anticancer target.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We found that suppression of 6PGD decreased lipogenesis and RNA biosynthesis and elevated ROS levels in cancer cells, attenuating cell proliferation and tumour growth. 6PGD-mediated production of ribulose-5-phosphate (Ru-5-P) inhibits AMPK activation by disrupting the active LKB1 complex, thereby activating acetyl-CoA carboxylase 1 and lipogenesis.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 635, "doc_id": "1686997", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Participating in six months of physical activity improves cognitive functioning.\n\nCANDIDATE_PASSAGE:\nThe relation between past exposure to fine particulate air pollution and prevalent anxiety: observational cohort study OBJECTIVE To determine whether higher past exposure to particulate air pollution is associated with prevalent high symptoms of anxiety. DESIGN Observational cohort study. SETTING Nurses' Health Study. PARTICIPANTS 71,271 women enrolled in the Nurses' Health Study residing throughout the contiguous United States who had valid estimates on exposure to particulate matter for at least one exposure period of interest and data on anxiety symptoms. MAIN OUTCOME MEASURES Meaningfully high symptoms of anxiety, defined as a score of 6 points or greater on the phobic anxiety subscale of the Crown-Crisp index, administered in 2004. RESULTS The 71,271 eligible women were aged between 57 and 85 years (mean 70 years) at the time of assessment of anxiety symptoms, with a prevalence of high anxiety symptoms of 15%. Exposure to particulate matter was characterized using estimated average exposure to particulate matter <2.5 μm in diameter (PM2.5) and 2.5 to 10 μm in diameter (PM2.5-10) in the one month, three months, six months, one year, and 15 years prior to assessment of anxiety symptoms, and residential distance to the nearest major road two years prior to assessment. Significantly increased odds of high anxiety symptoms were observed with higher exposure to PM2.5 for multiple averaging periods (for example, odds ratio per 10 µg/m(3) increase in prior one month average PM2.5: 1.12, 95% confidence interval 1.06 to 1.19; in prior 12 month average PM2.5: 1.15, 1.06 to 1.26). Models including multiple exposure windows suggested short term averaging periods were more relevant than long term averaging periods. There was no association between anxiety and exposur [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "921", "doc_id": "791050", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Charcoal is an effective treatment for acute paraquat poisoning.\n\nCANDIDATE_PASSAGE:\nFailure of continuous venovenous hemofiltration to prevent death in paraquat poisoning. Paraquat poisoning is characterized by multiorgan failure and pulmonary fibrosis with respiratory failure. Multiorgan failure with circulatory collapse is a major cause of early death within 3 days of paraquat ingestion. Recent studies suggested that continuous venovenous hemofiltration (CVVH) had a role in the treatment of multiorgan failure by promoting hemodynamic stability. We therefore evaluated the effect of prophylactic CVVH in 80 patients with paraquat poisoning (August 1996 to February 1999). The amount ingested was 2.1 +/- 1.0 mouthfuls (as 20% concentrate). All patients were treated with hemoperfusion (HP; duration, 6.4 +/- 3.0 hours) within 24 hours of ingestion and then randomly assigned to the HP-alone or HP-CVVH group. Forty-four patients underwent HP only, and 36 patients underwent CVVH (duration, 57.4 +/- 31.3 hours; ultrafiltration volume, 40.2 +/- 4.8 L/d) after HP. Although time to death after ingestion was significantly longer in the HP-CVVH than HP group (5.0 +/- 5.0 versus 2.5 +/- 2.1 days; P < 0.05), there was no difference in mortality rates between the two groups (66.7% versus 63.6%; P = 0.82). In the HP group, early circulatory collapse was a major cause of death compared with the HP-CVVH group, in which late respiratory failure was a major cause of death. In conclusion, prophylactic CVVH after HP prevented early death caused by circulatory collapse and prolonged survival time. However, it could not prevent late death caused by respiratory failure and did not provide a survival benefit in acute paraquat poisoning.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "245", "doc_id": "24097933", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The availability of safe places to study is effective at decreasing homelessness.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mental health problems of homeless children and families: longitudinal study.\nABSTRACT: OBJECTIVE To establish the mental health needs of homeless children and families before and after rehousing. DESIGN Cross sectional, longitudinal study. SETTING City of Birmingham. SUBJECTS 58 rehoused families with 103 children aged 2-16 years and 21 comparison families of low socioeconomic status in stable housing, with 54 children. MAIN OUTCOME MEASURES Children's mental health problems and level of communication; mothers' mental health problems and social support one year after rehousing. RESULTS Mental health problems remained significantly higher in rehoused mothers and their children than in the comparison group (mothers 26% v 5%, P = 0.04; children 39% v 11%, P = 0.0003). Homeless mothers continued to have significantly less social support at follow up. Mothers with a history of abuse and poor social integration were more likely to have children with persistent mental health problems. CONCLUSIONS Homeless families have a high level of complex needs that cannot be met by conventional health services and arrangements. Local strategies for rapid rehousing into permanent accommodation, effective social support and health care for parents and children, and protection from violence and intimidation should be developed and implemented.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1196, "doc_id": "25649714", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Do comorbidities alone explain the undertreatment of colorectal cancer in older adults : a French population-based study?\n\nABSTRACT:\nTo investigate the influence of comorbidities on treatment modalities of colorectal cancer according to the age of patients and French recommendations. Population-based study French Digestive Cancer Registry, Burgundy. Two thousand nine hundred twenty-one incident colorectal cancers diagnosed between 2004 and 2007. The independent influence of comorbidities (recorded according to the Charlson index) on treatment was analyzed using multivariate logistic regressions controlling for age, sex, and their interaction. The association between comorbidities and resection for cure was significant only in patients younger than 75 (P interaction=.008). For Stage III colon cancer, 40.4% of the patients aged 75 and older had adjuvant chemotherapy, versus 90.5% of those younger than 75 (P<.001). The association between comorbidities and adjuvant chemotherapy for Stage III colon cancer was significant only in patients younger than 75 (P interaction=.004). Patients aged 75 and older were less likely to receive chemotherapy, even when they had few or no comorbidities. Overall, 29.3% of patients aged 75 and older with advanced colorectal cancer had palliative chemotherapy, versus 77.1% of those younger than 75 (P<.001). Whatever the age, palliative chemotherapy was less frequent for a Charlson comorbidity index of 2 or greater (P interaction=.16). Radiotherapy was administered in 59.0% of patients aged 75 and older with rectal cancer, versus 85.3% of those younger than 75 (P<.001). Whatever the age, patients with a Charlson score of 2 or greater were less likely to receive radiotherapy for rectal cancer than were patients without comorbidities (P interaction=.86).", "output": "{\"label\": \"no\", \"rationale\": \"Further studies are warranted to identify more precisely the reasons for lower treatment rates for colorectal cancer in the older population.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 21438864, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: CHOP is a general endoplasmic reticulum stress marker.\n\nCANDIDATE_ABSTRACT:\nTITLE: Wolfram syndrome 1 and adenylyl cyclase 8 interact at the plasma membrane to regulate insulin production and secretion\nABSTRACT: Endoplasmic reticulum (ER) stress causes pancreatic β-cell dysfunction and contributes to β-cell loss and the progression of type 2 diabetes. Wolfram syndrome 1 (WFS1) has been shown to be an important regulator of the ER stress signalling pathway; however, its role in β-cell function remains unclear. Here we provide evidence that WFS1 is essential for glucose- and glucagon-like peptide 1 (GLP-1)-stimulated cyclic AMP production and regulation of insulin biosynthesis and secretion. Stimulation with glucose causes WFS1 translocation from the ER to the plasma membrane, where it forms a complex with adenylyl cyclase 8 (AC8), an essential cAMP-generating enzyme in the β-cell that integrates glucose and GLP-1 signalling. ER stress and mutant WFS1 inhibit complex formation and activation of AC8, reducing cAMP synthesis and insulin secretion. These findings reveal that an ER-stress-related protein has a distinct role outside the ER regulating both insulin biosynthesis and secretion. The reduction of WFS1 protein on the plasma membrane during ER stress is a contributing factor for β-cell dysfunction and progression of type 2 diabetes.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 209, "doc_id": "32587939", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does timing of initial surfactant treatment make a difference in rates of chronic lung disease or mortality in premature infants?\n\nABSTRACT:\nTo compare two treatment strategies in preterm infants with or at risk of respiratory distress syndrome: early surfactant administration (within one hour of birth) versus late surfactant administration, in a geographically defined population. The primary outcome was chronic lung disease (CLD) and mortality before/at 36 weeks. Secondary outcomes included: duration of mechanical ventilation and continuous positive airway pressure (CPAP), post-natal steroids for CLD and major neonatal morbidities. Premature infants born at 22-32 weeks' gestation between January 2006 and December 2009. Ten neonatal intensive care units (NICUs) in New South Wales (NSW) and Australian Capital Territory (ACT), Australia. Retrospective analysis of prospectively collected data from the regional NICU database in NSW and ACT. Of the 2170 infants who received surfactant, 1182 (54.5%) and 988 (45.5%) received early and late surfactant, respectively. The early surfactant group was less mature (27.1 ± 2.1 versus 29.4 ± 2.1 weeks) and had more CLD and mortality (40.2% versus 20.0%). The multivariable analysis showed early surfactant to be associated with less duration of ventilation, longer duration of CPAP and longer hospital stay but had little or no impact on CLD/mortality.", "output": "{\"label\": \"maybe\", \"rationale\": \"Early surfactant administration is associated with shorter duration of ventilation but does not appear to be significantly protective against CLD/mortality among premature infants. This may support the growing evidence for consideration of CPAP as an alternative to routine intubation and early surfactant administration. Further investigation from large randomized clinical trials is warranted to confirm these results.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 25394614, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Men are more susceptible to death due to pneumonia when compared to women.\n\nCANDIDATE_ABSTRACT:\nTITLE: Gender-dependent differences in outcome after the treatment of infection in hospitalized patients.\nABSTRACT: CONTEXT While it is established that management strategies and outcomes differ by gender for many diseases, its effect on infection has not been adequately studied. OBJECTIVE To investigate the role of gender among hospitalized patients treated for infection. DESIGN Observational cohort study conducted during a 26-month period from December 1996 through January 1999. SETTING University-affiliated hospital. PARTICIPANTS A total of 892 patients in the surgical units of the hospital with 1470 consecutive infectious episodes (782 in men and 688 in women). MAIN OUTCOME MEASURES Mortality during hospitalization by gender for infection episodes overall and for specific infectious sites, including lung, peritoneum, bloodstream, catheter, urine, surgical site, and skin/soft tissue. RESULTS Among all infections, there was no significant difference in mortality based on gender (men, 11.1% vs women, 14.2%; P = .07). After logistic regression analysis, factors independently associated with mortality included higher APACHE (Acute Physiology and Chronic Health Evaluation) II score, older age, malignancy, blood transfusion, and diagnosis of infection more than 7 days after admission, but not gender (female odds ratio [OR] for death, 1.32; 95% confidence interval [CI], 0.90-1.94; P = .16). Mortality was higher in women for lung (men, 18% vs women, 34%; P = .002) and soft tissue (men, 2% vs women, 10%; P < or = .05) infection; for other infectious sites, mortality did not differ by gender. Factors associated with mortality due to pneumonia by logistic regression included higher APACHE II score, malignancy, diabetes mellitus, diagnosis of infection more than 7 days after admission, older age, transplantation, and female gender (OR for death, 2.25; 95% CI, 1.17-4.32; P = .02). [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Although gender may not be predictive of mortality among all infections, women appear to be at increased risk for death from hospital-acquired pneumonia, even after controlling for other comorbidities.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 767, "doc_id": "2488880", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: There is no increased risk of hypospadias with clomiphene.\n\nCANDIDATE_PASSAGE:\nStructure of human RNase H1 complexed with an RNA/DNA hybrid: insight into HIV reverse transcription. We report here crystal structures of human RNase H1 complexed with an RNA/DNA substrate. Unlike B. halodurans RNase H1, human RNase H1 has a basic protrusion, which forms a DNA-binding channel and together with the conserved phosphate-binding pocket confers specificity for the B form and 2'-deoxy DNA. The RNA strand is recognized by four consecutive 2'-OH groups and cleaved by a two-metal ion mechanism. Although RNase H1 is overall positively charged, the substrate interface is neutral to acidic in character, which likely contributes to the catalytic specificity. Positions of the scissile phosphate and two catalytic metal ions are interdependent and highly coupled. Modeling of HIV reverse transcriptase (RT) with RNA/DNA in its RNase H active site suggests that the substrate cannot simultaneously occupy the polymerase active site and must undergo a conformational change to toggle between the two catalytic centers. The region that accommodates this conformational change offers a target to develop HIV-specific inhibitors.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1293", "doc_id": "39389082", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Activated Cdk5 regulates DNA damage-induced neuronal death.\n\nCANDIDATE_ABSTRACT:\nTITLE: The transcriptional program of sporulation in budding yeast\nABSTRACT: Diploid cells of budding yeast produce haploid cells through the developmental program of sporulation, which consists of meiosis and spore morphogenesis. DNA microarrays containing nearly every yeast gene were used to assay changes in gene expression during sporulation. At least seven distinct temporal patterns of induction were observed. The transcription factor Ndt80 appeared to be important for induction of a large group of genes at the end of meiotic prophase. Consensus sequences known or proposed to be responsible for temporal regulation could be identified solely from analysis of sequences of coordinately expressed genes. The temporal expression pattern provided clues to potential functions of hundreds of previously uncharacterized genes, some of which have vertebrate homologs that may function during gametogenesis.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 68, "doc_id": "680949", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Cost effectiveness evaluations based on cRCT data lack external validity.\n\nCANDIDATE_ABSTRACT:\nTITLE: Bone loss and vascular calcification: A bi-directional interplay?\nABSTRACT: Vascular calcification (VC) represents a recognized adverse predictor for cardiovascular morbidity and mortality. Previously considered passive and degenerative, VC is now recognized as an active process that resembles bone formation, and shares a number of histopathological features, mineral composition, and initiation mechanisms with bone development and metabolism. Oxidative stress and inflammation are key factors in both VC and osteoporosis (OP). Biochemical factors known to be primarily involved in the healthy bone metabolism also regulate VC. These biomarkers include vitamin D, osteoprotegerin, osteopontin, matrix Gla protein, cathepsin K, fibroblast growth factor-23, and fetuin-A. A better understanding of this highly controlled regulatory network, with multiple, nested feedback loops and cross talk between organs, may help to decrease the growing prevalence of calcific vasculopathy as well as OP in the aging population, and to advance in common preventive and therapeutic interventions targeted at both conditions.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 292, "doc_id": "2159648", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Commelina yellow mottle virus' (ComYMV) genome consists of 2140 baise pairs.\n\nCANDIDATE_PASSAGE:\nProperties of Commelina yellow mottle virus's complete DNA sequence, genomic discontinuities and transcript suggest that it is a pararetrovirus. The non-enveloped bacilliform viruses are the second group of plant viruses known to possess a genome consisting of circular double-stranded DNA. We have characterized the viral transcript and determined the complete sequence of the genome of Commelina mellow mottle virus (CoYMV), a member of this group. Analysis of the viral transcript indicates that the virus encodes a single terminally-redundant genome-length plus 120 nucleotide transcript. A fraction of the transcripts is polyadenylated, although the majority of the transcript is not polyadenylated. Analysis of the genome sequence indicates that the genome is 7489 bp in size and that the transcribed strand contains three open reading frames capable of encoding proteins of 23, 15 and 216 kd. The function of the 25 and 15 kd proteins is unknown. Similarities between the 216 kd polypeptide and the cauliflower mosaic virus coat protein and protease/reverse transcriptase polyprotein suggest that the 216 kd polypeptide is a polyprotein that is proteolytically processed to yield the virion coat protein, a protease, and replicase (reverse transcriptase and ribonuclease H). Each strand of the CoYMV genome is interrupted by site-specific discontinuities. The locations of the 5'-ends of these discontinuities, and the presence and location of a region on the CoYMV transcript capable of annealing with the 3'-end of cytosolic initiator methionine tRNA are consistent with replication by reverse transcription. We have demonstrated that a construct containing 1.3 CoYMV genomes is infective when introduced into Commelina diffusa, the host for CoYMV, using Agrobacterium-mediated infection.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "278", "doc_id": "14376683", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Androgenetic haploid mouse embryonic stem cells (ESCs) can be derived and genetically manipulated in vitro.\n\nCANDIDATE_ABSTRACT:\nTITLE: Generation of Genetically Modified Mice by Oocyte Injection of Androgenetic Haploid Embryonic Stem Cells\nABSTRACT: Haploid cells are amenable for genetic analysis. Recent success in the derivation of mouse haploid embryonic stem cells (haESCs) via parthenogenesis has enabled genetic screening in mammalian cells. However, successful generation of live animals from these haESCs, which is needed to extend the genetic analysis to the organism level, has not been achieved. Here, we report the derivation of haESCs from androgenetic blastocysts. These cells, designated as AG-haESCs, partially maintain paternal imprints, express classical ESC pluripotency markers, and contribute to various tissues, including the germline, upon injection into diploid blastocysts. Strikingly, live mice can be obtained upon injection of AG-haESCs into MII oocytes, and these mice bear haESC-carried genetic traits and develop into fertile adults. Furthermore, gene targeting via homologous recombination is feasible in the AG-haESCs. Our results demonstrate that AG-haESCs can be used as a genetically tractable fertilization agent for the production of live animals via injection into oocytes.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Strikingly, live mice can be obtained upon injection of AG-haESCs into MII oocytes, and these mice bear haESC-carried genetic traits and develop into fertile adults.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 111, "doc_id": "13513790", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Sildenafil worsens erectile function in men who experience sexual dysfunction as a result of the use of SSRI antidepressants.\n\nCANDIDATE_ABSTRACT:\nTITLE: Treatment of antidepressant-associated sexual dysfunction with sildenafil: a randomized controlled trial.\nABSTRACT: CONTEXT Sexual dysfunction is a common adverse effect of antidepressants that frequently results in treatment noncompliance. OBJECTIVE To assess the efficacy of sildenafil citrate in men with sexual dysfunction associated with the use of selective and nonselective serotonin reuptake inhibitor (SRI) antidepressants. DESIGN, SETTING, AND PATIENTS Prospective, parallel-group, randomized, double-blind, placebo-controlled trial conducted between November 1, 2000, and January 1, 2001, at 3 US university medical centers among 90 male outpatients (mean [SD] age, 45 [8] years) with major depression in remission and sexual dysfunction associated with SRI antidepressant treatment. INTERVENTION Patients were randomly assigned to take sildenafil (n = 45) or placebo (n = 45) at a flexible dose starting at 50 mg and adjustable to 100 mg before sexual activity for 6 weeks. MAIN OUTCOME MEASURES The primary outcome measure was score on the Clinical Global Impression-Sexual Function (CGI-SF); secondary measures were scores on the International Index of Erectile Function, Arizona Sexual Experience Scale, Massachusetts General Hospital-Sexual Functioning Questionnaire, and Hamilton Rating Scale for Depression (HAM-D). RESULTS Among the 90 randomized patients, 93% (83/89) of patients treated per protocol took at least 1 dose of study drug and 85% (76/89) completed week 6 end-point assessments with last observation carried forward analyses. At a CGI-SF score of 2 or lower, 54.5% (24/44) of sildenafil compared with 4.4% (2/45) of placebo patients were much or very much improved (P<.001). Erectile function, arousal, ejaculation, orgasm, and overall satisfaction domain measures improved significantly in sildenafil compared with placebo patients. Mean depression scores remained consi [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSION In our study, sildenafil effectively improved erectile function and other aspects of sexual function in men with sexual dysfunction associated with the use of SRI antidepressants.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1087, "doc_id": "39281140", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Charcoal shows no benefit for acute paraquat poisoning.\n\nCANDIDATE_PASSAGE:\nAssociation of aspirin and NSAID use with risk of colorectal cancer according to genetic variants. IMPORTANCE Use of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with lower risk of colorectal cancer. OBJECTIVE To identify common genetic markers that may confer differential benefit from aspirin or NSAID chemoprevention, we tested gene × environment interactions between regular use of aspirin and/or NSAIDs and single-nucleotide polymorphisms (SNPs) in relation to risk of colorectal cancer. DESIGN, SETTING, AND PARTICIPANTS Case-control study using data from 5 case-control and 5 cohort studies initiated between 1976 and 2003 across the United States, Canada, Australia, and Germany and including colorectal cancer cases (n=8634) and matched controls (n=8553) ascertained between 1976 and 2011. Participants were all of European descent. EXPOSURES Genome-wide SNP data and information on regular use of aspirin and/or NSAIDs and other risk factors. MAIN OUTCOMES AND MEASURES Colorectal cancer. RESULTS Regular use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer (prevalence, 28% vs 38%; odds ratio [OR], 0.69 [95% CI, 0.64-0.74]; P = 6.2 × 10(-28)) compared with nonregular use. In the conventional logistic regression analysis, the SNP rs2965667 at chromosome 12p12.3 near the MGST1 gene showed a genome-wide significant interaction with aspirin and/or NSAID use (P = 4.6 × 10(-9) for interaction). Aspirin and/or NSAID use was associated with a lower risk of colorectal cancer among individuals with rs2965667-TT genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.61-0.70]; P = 7.7 × 10(-33)) but with a higher risk among those with rare (4%) TA or AA genotypes (prevalence, 35% vs 29%; OR, 1.89 [95% CI, 1.27-2.81]; [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "246", "doc_id": "43334921", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: PrimPol degrades short DNA replication intermediates on the leading strand during DNA replication.\n\nCANDIDATE_ABSTRACT:\nTITLE: PrimPol, an Archaic Primase/Polymerase Operating in Human Cells\nABSTRACT: We describe a second primase in human cells, PrimPol, which has the ability to start DNA chains with deoxynucleotides unlike regular primases, which use exclusively ribonucleotides. Moreover, PrimPol is also a DNA polymerase tailored to bypass the most common oxidative lesions in DNA, such as abasic sites and 8-oxoguanine. Subcellular fractionation and immunodetection studies indicated that PrimPol is present in both nuclear and mitochondrial DNA compartments. PrimPol activity is detectable in mitochondrial lysates from human and mouse cells but is absent from mitochondria derived from PRIMPOL knockout mice. PRIMPOL gene silencing or ablation in human and mouse cells impaired mitochondrial DNA replication. On the basis of the synergy observed with replicative DNA polymerases Polγ and Polε, PrimPol is proposed to facilitate replication fork progression by acting as a translesion DNA polymerase or as a specific DNA primase reinitiating downstream of lesions that block synthesis during both mitochondrial and nuclear DNA replication.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 969, "doc_id": "17368516", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Choose reasons why patients referred to diabetes education programmes to attend : a systematic review?\n\nABSTRACT:\nTo identify the reasons why those offered a place on diabetes education programmes declined the opportunity. It is well established that diabetes education is critical to optimum diabetes care; it improves metabolic control, prevents complications, improves quality of life and empowers people to make informed choices to manage their condition. Despite the significant clinical and personal rewards offered by diabetes education, programmes are underused, with a significant proportion of patients choosing not to attend. A systematic search of the following databases was conducted for the period from 2005-2015: Medline; EMBASE; Scopus; CINAHL; and PsycINFO. Studies that met the inclusion criteria focusing on patient-reported reasons for non-attendance at structured diabetes education were selected. A total of 12 studies spanning quantitative and qualitative methodologies were included. The selected studies were published in Europe, USA, Pakistan, Canada and India, with a total sample size of 2260 people. Two broad categories of non-attender were identified: 1) those who could not attend for logistical, medical or financial reasons (e.g. timing, costs or existing comorbidities) and 2) those who would not attend because they perceived no benefit from doing so, felt they had sufficient knowledge already or had emotional and cultural reasons (e.g. no perceived problem, denial or negative feelings towards education). Diabetes education was declined for many reasons, and the range of expressed reasons was more diverse and complex than anticipated.", "output": "{\"label\": \"no\", \"rationale\": \"New and innovative methods of delivering diabetes education are required which address the needs of people with diabetes whilst maintaining quality and efficiency. This article is protected by copyright. All rights reserved.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 26996982, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: ATM and Rad3 related protein have no role in sensing DNA damage.\n\nCANDIDATE_ABSTRACT:\nTITLE: Deletion of the developmentally essential gene ATR in adult mice leads to age-related phenotypes and stem cell loss.\nABSTRACT: Developmental abnormalities, cancer, and premature aging each have been linked to defects in the DNA damage response (DDR). Mutations in the ATR checkpoint regulator cause developmental defects in mice (pregastrulation lethality) and humans (Seckel syndrome). Here we show that eliminating ATR in adult mice leads to defects in tissue homeostasis and the rapid appearance of age-related phenotypes, such as hair graying, alopecia, kyphosis, osteoporosis, thymic involution, fibrosis, and other abnormalities. Histological and genetic analyses indicate that ATR deletion causes acute cellular loss in tissues in which continuous cell proliferation is required for maintenance. Importantly, thymic involution, alopecia, and hair graying in ATR knockout mice were associated with dramatic reductions in tissue-specific stem and progenitor cells and exhaustion of tissue renewal and homeostatic capacity. In aggregate, these studies suggest that reduced regenerative capacity in adults via deletion of a developmentally essential DDR gene is sufficient to cause the premature appearance of age-related phenotypes.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 64, "doc_id": "40349336", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Mice without IFN-γ or its receptor are resistant to EAM induced with α-MyHC/CFA.\n\nCANDIDATE_PASSAGE:\nGpr124 is essential for blood–brain barrier integrity in central nervous system disease Although blood–brain barrier (BBB) compromise is central to the etiology of diverse central nervous system (CNS) disorders, endothelial receptor proteins that control BBB function are poorly defined. The endothelial G-protein-coupled receptor (GPCR) Gpr124 has been reported to be required for normal forebrain angiogenesis and BBB function in mouse embryos, but the role of this receptor in adult animals is unknown. Here Gpr124 conditional knockout (CKO) in the endothelia of adult mice did not affect homeostatic BBB integrity, but resulted in BBB disruption and microvascular hemorrhage in mouse models of both ischemic stroke and glioblastoma, accompanied by reduced cerebrovascular canonical Wnt–β-catenin signaling. Constitutive activation of Wnt–β-catenin signaling fully corrected the BBB disruption and hemorrhage defects of Gpr124-CKO mice, with rescue of the endothelial gene tight junction, pericyte coverage and extracellular-matrix deficits. We thus identify Gpr124 as an endothelial GPCR specifically required for endothelial Wnt signaling and BBB integrity under pathological conditions in adult mice. This finding implicates Gpr124 as a potential therapeutic target for human CNS disorders characterized by BBB disruption.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "783", "doc_id": "6325527", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Mice without IFN-γ or its receptor are highly susceptible to EAM induced with α-MyHC/CFA.\n\nCANDIDATE_ABSTRACT:\nTITLE: the Development of Autoimmune Myocarditis in Mice by an\nABSTRACT: BACKGROUND Interleukin (IL)-12 exerts a potent proinflammatory effect by stimulating T-helper (Th) 1 responses. This effect is believed to be mediated primarily through the activation of STAT4 and subsequent production of interferon (IFN)-gamma. Methods and Results- We examined the role of IL-12 receptor (IL-12R) signaling in the development of murine experimental autoimmune myocarditis (EAM) induced by cardiac myosin immunization. Both IL-12Rbeta1-deficient mice and STAT4-deficient mice were resistant to the induction of myocarditis. Treatment with exogenous IL-12 exacerbated disease. We questioned whether IFN-gamma is required for the disease-promoting activity of IL-12. On the contrary, we found that IFN-gamma suppresses EAM. Lack of IFN-gamma due to either depletion with an antibody or a genetic deficiency exacerbated myocarditis. Spleens from IFN-gamma-deficient mice immunized with cardiac myosin showed increased cellularity; greater numbers of CD3+, CD4+, CD8+, and IL-2-producing cells; and heightened ability to produce cytokines on stimulation in vitro. Treatment of mice with recombinant IFN-gamma suppressed the development of myocarditis. CONCLUSIONS IL-12/IL-12R/STAT4 signaling promotes the development of EAM. In contrast, IFN-gamma plays a protective role. The disease-limiting effects of IFN-gamma might be explained by its ability to control the expansion of activated T lymphocytes.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Lack of IFN-gamma due to either depletion with an antibody or a genetic deficiency exacerbated myocarditis.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 782, "doc_id": "8246922", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: BRCA 1 mutation carriers' risk of breast and ovarian cancer depends on where the mutation is located.\n\nCANDIDATE_ABSTRACT:\nTITLE: Selective elimination of high constitutive activity or chemokine binding in the human herpesvirus 8 encoded seven transmembrane oncogene ORF74.\nABSTRACT: Open reading frame 74 (ORF74) encoded by human herpesvirus 8 is a highly constitutively active seven transmembrane (7TM) receptor stimulated by angiogenic chemokines, e.g. growth-related oncogene-alpha, and inhibited by angiostatic chemokines e.g. interferon-gamma-inducible protein. Transgenic mice expressing ORF74 under control of the CD2 promoter develop highly vascularized Kaposi's sarcoma-like tumors. Through targeted mutagenesis we here create three distinct phenotypes of ORF74: a receptor with normal, high constitutive signaling through the phospholipase C pathway but deprived of binding and action of chemokines obtained through deletion of 22 amino acids from the N-terminal extension; an ORF74 with high constitutive activity but with selective elimination of stimulatory regulation by angiogenic chemokines obtained through substitution of basic residues at the extracellular ends of TM-V or TM-VI; and an ORF74 lacking constitutive activity but with preserved ability to be stimulated by agonist chemokines obtained through introduction of an Asp residue on the hydrophobic, presumed membrane-exposed face of TM-II. It is concluded that careful molecular dissection can selectively eliminate either agonist or inverse agonist modulation as well as high constitutive activity of the virally encoded oncogene ORF74 and that these mutant forms presumably can be used in transgenic animals to identify the molecular mechanism of its transforming activity.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 159, "doc_id": "1574014", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Auditory entrainment is strengthened when people see congruent visual and auditory information.\n\nCANDIDATE_ABSTRACT:\nTITLE: Congruent Visual Speech Enhances Cortical Entrainment to Continuous Auditory Speech in Noise-Free Conditions.\nABSTRACT: UNLABELLED Congruent audiovisual speech enhances our ability to comprehend a speaker, even in noise-free conditions. When incongruent auditory and visual information is presented concurrently, it can hinder a listener's perception and even cause him or her to perceive information that was not presented in either modality. Efforts to investigate the neural basis of these effects have often focused on the special case of discrete audiovisual syllables that are spatially and temporally congruent, with less work done on the case of natural, continuous speech. Recent electrophysiological studies have demonstrated that cortical response measures to continuous auditory speech can be easily obtained using multivariate analysis methods. Here, we apply such methods to the case of audiovisual speech and, importantly, present a novel framework for indexing multisensory integration in the context of continuous speech. Specifically, we examine how the temporal and contextual congruency of ongoing audiovisual speech affects the cortical encoding of the speech envelope in humans using electroencephalography. We demonstrate that the cortical representation of the speech envelope is enhanced by the presentation of congruent audiovisual speech in noise-free conditions. Furthermore, we show that this is likely attributable to the contribution of neural generators that are not particularly active during unimodal stimulation and that it is most prominent at the temporal scale corresponding to syllabic rate (2-6 Hz). Finally, our data suggest that neural entrainment to the speech envelope is inhibited when the auditory and visual streams are incongruent both temporally and contextually. SIGNIFICANCE STATEMENT Seeing a speaker's face as he or she talks can greatly help in understan [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We demonstrate that the cortical representation of the speech envelope is enhanced by the presentation of congruent audiovisual speech in noise-free conditions.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 141, "doc_id": "14437255", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Side effects associated with antidepressants do not represent a mortality risk to postmenopausal women.\n\nCANDIDATE_PASSAGE:\nAntidepressant use and risk of adverse outcomes in older people: population based cohort study OBJECTIVES To investigate the association between antidepressant treatment and risk of several potential adverse outcomes in older people with depression and to examine risks by class of antidepressant, duration of use, and dose. DESIGN Cohort study of people aged 65 and over diagnosed as having depression. SETTING 570 general practices in the United Kingdom supplying data to the QResearch primary care database. PARTICIPANTS 60,746 patients diagnosed as having a new episode of depression between the ages of 65 and 100 years from 1 January 1996 to 31 December 2007 and followed up until 31 December 2008. MAIN OUTCOME MEASURES Hazard ratios associated with antidepressant use for all cause mortality, attempted suicide/self harm, myocardial infarction, stroke/transient ischaemic attack, falls, fractures, upper gastrointestinal bleeding, epilepsy/seizures, road traffic accidents, adverse drug reactions, and hyponatraemia, adjusted for a range of potential confounding variables. Hazard ratios were calculated for antidepressant class (tricyclic and related antidepressants, selective serotonin reuptake inhibitors, other antidepressants), dose, and duration of use and for commonly prescribed individual drugs. RESULTS 54,038 (89.0%) patients received at least one prescription for an antidepressant during follow-up. A total of 1,398,359 antidepressant prescriptions were issued: 764,659 (54.7%) for selective serotonin reuptake inhibitors, 442,192 (31.6%) for tricyclic antidepressants, 2203 (0.2%) for monoamine oxidase inhibitors, and 189,305 (13.5%) for the group of other antidepressants. The associations with the adverse outcomes differed significantly between the antidepressa [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1081", "doc_id": "5691302", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Cell autonomous sex determination in somatic cells does not occur in Galliformes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Somatic sex identity is cell-autonomous in the chicken\nABSTRACT: In the mammalian model of sex determination, embryos are considered to be sexually indifferent until the transient action of a sex-determining gene initiates gonadal differentiation. Although this model is thought to apply to all vertebrates, this has yet to be established. Here we have examined three lateral gynandromorph chickens (a rare, naturally occurring phenomenon in which one side of the animal appears male and the other female) to investigate the sex-determining mechanism in birds. These studies demonstrated that gynandromorph birds are genuine male:female chimaeras, and indicated that male and female avian somatic cells may have an inherent sex identity. To test this hypothesis, we transplanted presumptive mesoderm between embryos of reciprocal sexes to generate embryos containing male:female chimaeric gonads. In contrast to the outcome for mammalian mixed-sex chimaeras, in chicken mixed-sex chimaeras the donor cells were excluded from the functional structures of the host gonad. In an example where female tissue was transplanted into a male host, donor cells contributing to the developing testis retained a female identity and expressed a marker of female function. Our study demonstrates that avian somatic cells possess an inherent sex identity and that, in birds, sexual differentiation is substantively cell autonomous.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In an example where female tissue was transplanted into a male host, donor cells contributing to the developing testis retained a female identity and expressed a marker of female function.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 233, "doc_id": "4388470", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Auditory entrainment is strengthened when people see congruent visual and auditory information.\n\nCANDIDATE_PASSAGE:\nMotion magnification We present motion magnification, a technique that acts like a microscope for visual motion. It can amplify subtle motions in a video sequence, allowing for visualization of deformations that would otherwise be invisible. To achieve motion magnification, we need to accurately measure visual motions, and group the pixels to be modified. After an initial image registration step, we measure motion by a robust analysis of feature point trajectories, and segment pixels based on similarity of position, color, and motion. A novel measure of motion similarity groups even very small motions according to correlation over time, which often relates to physical cause. An outlier mask marks observations not explained by our layered motion model, and those pixels are simply reproduced on the output from the original registered observations. The motion of any selected layer may be magnified by a user-specified amount; texture synthesis fills-in unseen \"holes\" revealed by the amplified motions. The resulting motion-magnified images can reveal or emphasize small motions in the original sequence, as we demonstrate with deformations in load-bearing structures, subtle motions or balancing corrections of people, and \"rigid\" structures bending under hand pressure.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "141", "doc_id": "3437084", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nCANDIDATE_PASSAGE:\nModel-based Geostatistics Geostatistics is concerned with estimation and prediction problems for spatially continuous phenomena, using data obtained at a limited number of spatial locations. Model-based geostatistics refers to the application of general statistical principles of modelling and inference to geostatisatical problems. This volume is the first book-length treatment of model-based geostatistics.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1181", "doc_id": "10743131", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The relationship between a breast cancer patient's capacity to metabolize tamoxifen and treatment outcome is independent of the patient's genetic make-up.\n\nCANDIDATE_ABSTRACT:\nTITLE: Validating a conceptual model for an inter-professional approach to shared decision making: a mixed methods study\nABSTRACT: RATIONALE, AIMS AND OBJECTIVES Following increased interest in having inter-professional (IP) health care teams engage patients in decision making, we developed a conceptual model for an IP approach to shared decision making (SDM) in primary care. We assessed the validity of the model with stakeholders in Canada. METHODS In 15 individual interviews and 7 group interviews with 79 stakeholders, we asked them to: (1) propose changes to the IP-SDM model; (2) identify barriers and facilitators to the model's implementation in clinical practice; and (3) assess the model using a theory appraisal questionnaire. We performed a thematic analysis of the transcripts and a descriptive analysis of the questionnaires. RESULTS Stakeholders suggested placing the patient at its centre; extending the concept of family to include significant others; clarifying outcomes; highlighting the concept of time; merging the micro, meso and macro levels in one figure; and recognizing the influence of the environment and emotions. The most common barriers identified were time constraints, insufficient resources and an imbalance of power among health professionals. The most common facilitators were education and training in inter-professionalism and SDM, motivation to achieve an IP approach to SDM, and mutual knowledge and understanding of disciplinary roles. Most stakeholders considered that the concepts and relationships between the concepts were clear and rated the model as logical, testable, having clear schematic representation, and being relevant to inter-professional collaboration, SDM and primary care. CONCLUSIONS Stakeholders validated the new IP-SDM model for primary care settings and proposed few modifications. Future research should assess if the model helps implement SDM in IP [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1260, "doc_id": "1338283", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The morphology change from large white adipocytes to small brown adipocytes is a sign of increased energy expenditure potential in white adipose tissue.\n\nCANDIDATE_PASSAGE:\nClonal hematopoiesis of indeterminate potential and its distinction from myelodysplastic syndromes. Recent genetic analyses of large populations have revealed that somatic mutations in hematopoietic cells leading to clonal expansion are commonly acquired during human aging. Clonally restricted hematopoiesis is associated with an increased risk of subsequent diagnosis of myeloid or lymphoid neoplasia and increased all-cause mortality. Although myelodysplastic syndromes (MDS) are defined by cytopenias, dysplastic morphology of blood and marrow cells, and clonal hematopoiesis, most individuals who acquire clonal hematopoiesis during aging will never develop MDS. Therefore, acquisition of somatic mutations that drive clonal expansion in the absence of cytopenias and dysplastic hematopoiesis can be considered clonal hematopoiesis of indeterminate potential (CHIP), analogous to monoclonal gammopathy of undetermined significance and monoclonal B-cell lymphocytosis, which are precursor states for hematologic neoplasms but are usually benign and do not progress. Because mutations are frequently observed in healthy older persons, detection of an MDS-associated somatic mutation in a cytopenic patient without other evidence of MDS may cause diagnostic uncertainty. Here we discuss the nature and prevalence of CHIP, distinction of this state from MDS, and current areas of uncertainty regarding diagnostic criteria for myeloid malignancies.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1236", "doc_id": "5782614", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does the potassium channel opener levcromakalim cause expansive remodelling of experimental vein grafts?\n\nABSTRACT:\nMaintenance of luminal area is essential for the optimal performance of venous bypass grafts. However, injury and response to the arterial circulation evoke vascular remodelling that favors intimal hyperplasia, with luminal encroachment and inward remodelling. Potassium channel-opening drugs reduce tissue workload and peripheral vascular resistance and through these mechanisms could favor outward or expansive remodelling of vein grafts. We tested the hypothesis that levcromakalim, a potassium channel opener, would enhance expansive remodelling in vein grafts. A randomized, double-blind, placebo-controlled trial was conducted in 33 rats with vena cava-to-aorta bypass grafts. Drugs were administered via osmotic pump for 7 days after surgery. Half the cohort had bromodeoxyuridine (BrdU) infused at day 6. Morphometric analysis was conducted of pressure perfusion-fixed grafts harvested at 1 week and 4 weeks. At 1 week, lumen area was similar in both groups (1.82 +/- 0.39 mm(2) placebo vs 1.85 +/- 0.36 mm(2) levcromakalim), although medial cell density and BrdU staining were significantly increased in the placebo group. At 4 weeks, lumen area was unchanged in the placebo group (1.88 +/- 0.51 mm(2)) but had increased to 2.32 +/- 0.46 mm(2) in the levcromakalim group (P = .039 vs 1 week), with a very significant reduction in the intimal area (levcromakalim, 0.06 +/- 0.02 mm(2) vs placebo, 0.33 +/- 0.17 mm(2); P = .001).", "output": "{\"label\": \"yes\", \"rationale\": \"Early, short-term treatment with levcromakalim favors expansive remodelling of experimental vein grafts to mimic the effect of external stenting. This expansive remodelling was associated with a reduction in medial cell proliferation at 1 week.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 16828441, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The NF-κB essential modulator gene induces intestinal inflammation by promoting receptor-interacting protein (RIP) kinase 1 kinase activity-mediated epithelial cell death.\n\nCANDIDATE_ABSTRACT:\nTITLE: NEMO Prevents RIP Kinase 1-Mediated Epithelial Cell Death and Chronic Intestinal Inflammation by NF-κB-Dependent and -Independent Functions\nABSTRACT: Intestinal epithelial cells (IECs) regulate gut immune homeostasis, and impaired epithelial responses are implicated in the pathogenesis of inflammatory bowel diseases (IBD). IEC-specific ablation of nuclear factor κB (NF-κB) essential modulator (NEMO) caused Paneth cell apoptosis and impaired antimicrobial factor expression in the ileum, as well as colonocyte apoptosis and microbiota-driven chronic inflammation in the colon. Combined RelA, c-Rel, and RelB deficiency in IECs caused Paneth cell apoptosis but not colitis, suggesting that NEMO prevents colon inflammation by NF-κB-independent functions. Inhibition of receptor-interacting protein kinase 1 (RIPK1) kinase activity or combined deficiency of Fas-associated via death domain protein (FADD) and RIPK3 prevented epithelial cell death, Paneth cell loss, and colitis development in mice with epithelial NEMO deficiency. Therefore, NEMO prevents intestinal inflammation by inhibiting RIPK1 kinase activity-mediated IEC death, suggesting that RIPK1 inhibitors could be effective in the treatment of colitis in patients with NEMO mutations and possibly in IBD.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Inhibition of receptor-interacting protein kinase 1 (RIPK1) kinase activity or combined deficiency of Fas-associated via death domain protein (FADD) and RIPK3 prevented epithelial cell death, Paneth cell loss, and colitis development in mice with epithelial NEMO deficiency.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1170, "doc_id": "18956141", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Whole brain radiotherapy increases the occurrence of new brain metastases.\n\nCANDIDATE_ABSTRACT:\nTITLE: Stereotactic radiosurgery plus whole-brain radiation therapy vs stereotactic radiosurgery alone for treatment of brain metastases: a randomized controlled trial.\nABSTRACT: CONTEXT In patients with brain metastases, it is unclear whether adding up-front whole-brain radiation therapy (WBRT) to stereotactic radiosurgery (SRS) has beneficial effects on mortality or neurologic function compared with SRS alone. OBJECTIVE To determine if WBRT combined with SRS results in improvements in survival, brain tumor control, functional preservation rate, and frequency of neurologic death. DESIGN, SETTING, AND PATIENTS Randomized controlled trial of 132 patients with 1 to 4 brain metastases, each less than 3 cm in diameter, enrolled at 11 hospitals in Japan between October 1999 and December 2003. INTERVENTIONS Patients were randomly assigned to receive WBRT plus SRS (65 patients) or SRS alone (67 patients). MAIN OUTCOME MEASURES The primary end point was overall survival; secondary end points were brain tumor recurrence, salvage brain treatment, functional preservation, toxic effects of radiation, and cause of death. RESULTS The median survival time and the 1-year actuarial survival rate were 7.5 months and 38.5% (95% confidence interval, 26.7%-50.3%) in the WBRT + SRS group and 8.0 months and 28.4% (95% confidence interval, 17.6%-39.2%) for SRS alone (P = .42). The 12-month brain tumor recurrence rate was 46.8% in the WBRT + SRS group and 76.4% for SRS alone group (P<.001). Salvage brain treatment was less frequently required in the WBRT + SRS group (n = 10) than with SRS alone (n = 29) (P<.001). Death was attributed to neurologic causes in 22.8% of patients in the WBRT + SRS group and in 19.3% of those treated with SRS alone (P = .64). There were no significant differences in systemic and neurologic functional preservation and toxic effects of radiation. CONCLUSIONS Compared with SRS alone, the use of WBRT plus SRS did not improve survival [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Compared with SRS alone, the use of WBRT plus SRS did not improve survival for patients with 1 to 4 brain metastases, but intracranial relapse occurred considerably more frequently in those who did not receive WBRT.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1376, "doc_id": "3944632", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Deletion of ATM and Rad3 related protein is not predictive of acute tissue loss.\n\nCANDIDATE_PASSAGE:\nGolgi Export of the Kir2.1 Channel Is Driven by a Trafficking Signal Located within Its Tertiary Structure Mechanisms that are responsible for sorting newly synthesized proteins for traffic to the cell surface from the Golgi are poorly understood. Here, we show that the potassium channel Kir2.1, mutations in which are associated with Andersen-Tawil syndrome, is selected as cargo into Golgi export carriers in an unusual signal-dependent manner. Unlike conventional trafficking signals, which are typically comprised of short linear peptide sequences, Golgi exit of Kir2.1 is dictated by residues that are embedded within the confluence of two separate domains. This signal patch forms a recognition site for interaction with the AP1 adaptor complex, thereby marking Kir2.1 for incorporation into clathrin-coated vesicles at the trans-Golgi. The identification of a trafficking signal in the tertiary structure of Kir2.1 reveals a quality control step that couples protein conformation to Golgi export and provides molecular insight into how mutations in Kir2.1 arrest the channels at the Golgi.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "325", "doc_id": "18078750", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Cell autonomous sex determination in somatic cells does not occur in Galliformes.\n\nCANDIDATE_PASSAGE:\nApoptosis in breast cancer: relationship with other pathological parameters. Apoptosis is a frequent phenomenon in breast cancer and it can be detected by light microscopy in conventional histopathological sections or by special staining techniques. The number of apoptotic cells as a percentage of cells present, or the number of apoptotic cells per square millimetre of neoplastic tissue, is usually described as the apoptotic index (AI). In breast cancer, the AI is not related to tumour size, axillary lymph node metastasis or distant metastasis at diagnosis. It is greater in invasive ductal carcinomas than in other histological types. High AI is also related to high histological grade, high nuclear grade, comedo-type necrosis, lack of tubule formation, and dense infiltration of the tumour by lymphocytes. Sex steroid receptor-negative tumours have greater AIs than the sex steroid receptor-positive ones. Aneuploid breast cancers with high S-phase fractions (SPFs) also have high AI values compared with diploid tumours with low SPFs. p53-Positive breast cancers have high AIs, whereas tumours that are Bcl-2 positive have low AIs. The AI shows a strong positive correlation to all direct or indirect indicators of cell proliferation, such as mitotic index and Ki67 immunolabelling. Univariate survival analyses show that a high AI is linked with unfavourable disease outcome in axillary lymph node-negative and -positive breast cancer, but multivariate analyses indicate that AI is not an independent prognostic factor. In conclusion, a high AI is related to malignant cellular features and indicators of invasiveness and cell proliferation in breast cancer.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "233", "doc_id": "20839751", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Basophils counteract disease development in patients with systemic lupus erythematosus (SLE).\n\nCANDIDATE_ABSTRACT:\nTITLE: BASOPHILS AND THE T HELPER 2 ENVIRONMENT CAN PROMOTE THE DEVELOPMENT OF LUPUS NEPHRITIS\nABSTRACT: In systemic lupus erythematosus (SLE), self-reactive antibodies can target the kidney (lupus nephritis), leading to functional failure and possible mortality. We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice). Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis. Basophils were also present in the lymph nodes and spleen of subjects with SLE. Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 171, "doc_id": "12670680", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: r-protein chaperones are found in complexes with their r-protein binding partners.\n\nCANDIDATE_PASSAGE:\nA single residue determines the cooperative binding property of a primosomal DNA replication protein, PriB, to single-stranded DNA. PriB is a primosomal protein required for re-initiation of replication in bacteria. We characterized and compared the DNA-binding properties of PriB from Salmonella enterica serovar Typhimurium LT2 (StPriB) and Escherichia coli (EcPriB). Only one residue of EcPriB, V6, was different in StPriB (replaced by A6). Previous structural information revealed that this residue is located on the putative dimer-dimer interface of PriB and is not involved in single-stranded DNA (ssDNA) binding. The cooperative binding mechanism of StPriB to DNA is, however, very different from that of EcPriB. Unlike EcPriB, which forms a single complex with ssDNAs of various lengths, StPriB forms two or more distinct complexes. Based on these results, as well as information on structure, binding modes for forming a stable complex of PriB with ssDNA of 25 nucleotides (nt), (EcPriB)25, and (StPriB)25 are proposed.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1402", "doc_id": "29098525", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is a chance to cut always a chance to cure- fasciotomy in the treatment of rattlesnake envenomation : A retrospective poison center study?\n\nABSTRACT:\nFasciotomy has been described in the treatment of rattlesnake-envenomation. We sought to compare the characteristics of patients undergoing fasciotomy with those where fasciotomy was discussed but not performed. A retrospective case-series constructed from a single-statewide-poison-system electronic database for cases of fasciotomy discussion or completion in rattlesnake-envenomation between January 2001 and May 2012. Age, gender, bite location, antivenom administered, compartment pressure measurements, Snakebite Severity Score (SSS) and length of hospitalization (LOS) were recorded. Comparisons were made between fasciotomy completed and where fasciotomy was only discussed. One-hundred-five cases of fasciotomy discussion or completion were identified. Fasciotomy was performed in 28 cases (27%). There was no statistically significant difference (p > 0.05) between groups in age, gender, bite site, SSS, and total number of vials of antivenom administered. Only 2 of 28 (7%) had compartment pressure measurements. Patients undergoing fasciotomy spent an additional 2 days in the hospital.", "output": "{\"label\": \"no\", \"rationale\": \"Fasciotomies continue to take place, without compartment pressure measurements, and without repeat dosing of antivenom. In the absence of clear objective evidence that limb-threatening compartment syndrome occurs despite adequate antivenom administration, fasciotomy does not favorably impact morbidity and may be associated with increased costs for care following rattlesnake envenomation.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25935457, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Distant CREs are important for transcriptional regulation.\n\nCANDIDATE_PASSAGE:\nEnhancer Evolution across 20 Mammalian Species The mammalian radiation has corresponded with rapid changes in noncoding regions of the genome, but we lack a comprehensive understanding of regulatory evolution in mammals. Here, we track the evolution of promoters and enhancers active in liver across 20 mammalian species from six diverse orders by profiling genomic enrichment of H3K27 acetylation and H3K4 trimethylation. We report that rapid evolution of enhancers is a universal feature of mammalian genomes. Most of the recently evolved enhancers arise from ancestral DNA exaptation, rather than lineage-specific expansions of repeat elements. In contrast, almost all liver promoters are partially or fully conserved across these species. Our data further reveal that recently evolved enhancers can be associated with genes under positive selection, demonstrating the power of this approach for annotating regulatory adaptations in genomic sequences. These results provide important insight into the functional genetics underpinning mammalian regulatory evolution.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "351", "doc_id": "14658685", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Auditory entrainment is strengthened when people see congruent visual and auditory information.\n\nCANDIDATE_ABSTRACT:\nTITLE: Congruent Visual Speech Enhances Cortical Entrainment to Continuous Auditory Speech in Noise-Free Conditions.\nABSTRACT: UNLABELLED Congruent audiovisual speech enhances our ability to comprehend a speaker, even in noise-free conditions. When incongruent auditory and visual information is presented concurrently, it can hinder a listener's perception and even cause him or her to perceive information that was not presented in either modality. Efforts to investigate the neural basis of these effects have often focused on the special case of discrete audiovisual syllables that are spatially and temporally congruent, with less work done on the case of natural, continuous speech. Recent electrophysiological studies have demonstrated that cortical response measures to continuous auditory speech can be easily obtained using multivariate analysis methods. Here, we apply such methods to the case of audiovisual speech and, importantly, present a novel framework for indexing multisensory integration in the context of continuous speech. Specifically, we examine how the temporal and contextual congruency of ongoing audiovisual speech affects the cortical encoding of the speech envelope in humans using electroencephalography. We demonstrate that the cortical representation of the speech envelope is enhanced by the presentation of congruent audiovisual speech in noise-free conditions. Furthermore, we show that this is likely attributable to the contribution of neural generators that are not particularly active during unimodal stimulation and that it is most prominent at the temporal scale corresponding to syllabic rate (2-6 Hz). Finally, our data suggest that neural entrainment to the speech envelope is inhibited when the auditory and visual streams are incongruent both temporally and contextually. SIGNIFICANCE STATEMENT Seeing a speaker's face as he or she talks can greatly help in understan [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We demonstrate that the cortical representation of the speech envelope is enhanced by the presentation of congruent audiovisual speech in noise-free conditions.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 141, "doc_id": "14437255", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Deltex has no known interactions with eIF3f.\n\nCANDIDATE_PASSAGE:\nThe S. cerevisiae Rrm3p DNA helicase moves with the replication fork and affects replication of all yeast chromosomes. The Saccharomyces cerevisiae DNA helicase Rrm3p is needed for normal fork progression through >1000 discrete sites scattered throughout the genome. Here we show that replication of all yeast chromosomes was markedly delayed in rrm3 cells. Delayed replication was seen even in a region that lacks any predicted Rrm3p-dependent sites. Based on the pattern of replication intermediates in two-dimensional gels, the rate of fork movement in rrm3 cells appeared similar to wild-type except at known Rrm3p-dependent sites. These data suggest that although Rrm3p has a global role in DNA replication, its activity is needed only or primarily at specific, difficult-to-replicate sites. By the criterion of chromatin immunoprecipitation, Rrm3p was associated with both Rrm3p-dependent and -independent sites, and moved with the replication fork through both. In addition, Rrm3p interacted with Pol2p, the catalytic subunit of DNA polymerase epsilon, in vivo. Thus, rather than being recruited to its sites of action when replication forks stall at these sites, Rrm3p is likely a component of the replication fork apparatus.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "330", "doc_id": "26083387", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Rapid phosphotransfer rates govern fidelity in two component systems\n\nCANDIDATE_ABSTRACT:\nTITLE: Effect of hyperosmolality on alkaline phosphatase and stress-response protein 27 of MCF-7 breast cancer cells\nABSTRACT: MCF-7, a continuous cell line derived from a human breast carcinoma, exhibits very low alkaline phosphatase (ALP) activity. The enzyme is heat-stable and is inhibited by L-phenylalanine and L-phenylalanylgly-cylglycine, but not by L-homoarginine, 1-bromotetramisole, or levamisole. These data indicate that MCF-7 produces term-placental ALP, the oncodevelopmental enzyme form inappropriately expressed by a variety of human tumors. In contrast to human cancer cells that produce this enzyme monophenotypically, ALP activity of MCF-7 cells is not significantly increased by glucocorticoids or sodium butyrate. By comparison, exposure to hyperosmolality causes a striking increase in enzyme activity. Cycloheximide blocks this effect. The results obtained with cell-free assays were confirmed by cytochemical and immunocytochemical assays on whole cells. Because some of the agents tested in the enzyme modulation experiments affect cell proliferation, their possible effect on two stress-response proteins (srp 27 and srp 72) was also examined; specific immunocytochemical assays were used. These tests revealed that neither protein is affected by glucocorticoids; that sodium butyrate has no effect on srp 27, but alters the intracellular distribution of srp 72; and that hyperosmolality, while not significantly affecting srp 72, causes an increase in srp 27.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1019, "doc_id": "1554348", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In breast cancer, the loss of myoepithelial cells promotes the transition of ductal carcinoma in situ to invasive carcinoma.\n\nCANDIDATE_ABSTRACT:\nTITLE: Regulation of in situ to invasive breast carcinoma transition.\nABSTRACT: The transition of ductal carcinoma in situ (DCIS) to invasive carcinoma is a poorly understood key event in breast tumor progression. Here, we analyzed the role of myoepithelial cells and fibroblasts in the progression of in situ carcinomas using a model of human DCIS and primary breast tumors. Progression to invasion was promoted by fibroblasts and inhibited by normal myoepithelial cells. Molecular profiles of isolated luminal epithelial and myoepithelial cells identified an intricate interaction network involving TGFbeta, Hedgehog, cell adhesion, and p63 required for myoepithelial cell differentiation, the elimination of which resulted in loss of myoepithelial cells and progression to invasion.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Progression to invasion was promoted by fibroblasts and inhibited by normal myoepithelial cells.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 570, "doc_id": "20333864", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Nonhuman primates are incapable of producing neutralizing antibodies in reponse to the Eilat virus (EILV) produced in mosquitos.\n\nCANDIDATE_PASSAGE:\nA chikungunya fever vaccine utilizing an insect-specific virus platform Traditionally, vaccine development involves tradeoffs between immunogenicity and safety. Live-attenuated vaccines typically offer rapid and durable immunity but have reduced safety when compared to inactivated vaccines. In contrast, the inability of inactivated vaccines to replicate enhances safety at the expense of immunogenicity, often necessitating multiple doses and boosters. To overcome these tradeoffs, we developed the insect-specific alphavirus, Eilat virus (EILV), as a vaccine platform. To address the chikungunya fever (CHIKF) pandemic, we used an EILV cDNA clone to design a chimeric virus containing the chikungunya virus (CHIKV) structural proteins. The recombinant EILV/CHIKV was structurally identical at 10 Å to wild-type CHIKV, as determined by single-particle cryo-electron microscopy, and it mimicked the early stages of CHIKV replication in vertebrate cells from attachment and entry to viral RNA delivery. Yet the recombinant virus remained completely defective for productive replication, providing a high degree of safety. A single dose of EILV/CHIKV produced in mosquito cells elicited rapid (within 4 d) and long-lasting (>290 d) neutralizing antibodies that provided complete protection in two different mouse models. In nonhuman primates, EILV/CHIKV elicited rapid and robust immunity that protected against viremia and telemetrically monitored fever. Our EILV platform represents the first structurally native application of an insect-specific virus in preclinical vaccine development and highlights the potential application of such viruses in vaccinology.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "853", "doc_id": "24922825", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Taxation of sugar-sweetened beverages had no effect on the incidence rate of type II diabetes in India.\n\nCANDIDATE_PASSAGE:\nAverting Obesity and Type 2 Diabetes in India through Sugar-Sweetened Beverage Taxation: An Economic-Epidemiologic Modeling Study BACKGROUND Taxing sugar-sweetened beverages (SSBs) has been proposed in high-income countries to reduce obesity and type 2 diabetes. We sought to estimate the potential health effects of such a fiscal strategy in the middle-income country of India, where there is heterogeneity in SSB consumption, patterns of substitution between SSBs and other beverages after tax increases, and vast differences in chronic disease risk within the population. METHODS AND FINDINGS Using consumption and price variations data from a nationally representative survey of 100,855 Indian households, we first calculated how changes in SSB price alter per capita consumption of SSBs and substitution with other beverages. We then incorporated SSB sales trends, body mass index (BMI), and diabetes incidence data stratified by age, sex, income, and urban/rural residence into a validated microsimulation of caloric consumption, glycemic load, overweight/obesity prevalence, and type 2 diabetes incidence among Indian subpopulations facing a 20% SSB excise tax. The 20% SSB tax was anticipated to reduce overweight and obesity prevalence by 3.0% (95% CI 1.6%-5.9%) and type 2 diabetes incidence by 1.6% (95% CI 1.2%-1.9%) among various Indian subpopulations over the period 2014-2023, if SSB consumption continued to increase linearly in accordance with secular trends. However, acceleration in SSB consumption trends consistent with industry marketing models would be expected to increase the impact efficacy of taxation, averting 4.2% of prevalent overweight/obesity (95% CI 2.5-10.0%) and 2.5% (95% CI 1.0-2.8%) of incident type 2 diabetes from 2014-2023. Given current consumpt [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1144", "doc_id": "10071552", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Activation of the Rac1 homolog CED-10 kills viable cells in SRGP-1 mutant Caenorhabditis elegans.\n\nCANDIDATE_PASSAGE:\nE-cadherin engagement stimulates proliferation via Rac1 E-cadherin has been linked to the suppression of tumor growth and the inhibition of cell proliferation in culture. We observed that progressively decreasing the seeding density of normal rat kidney-52E (NRK-52E) or MCF-10A epithelial cells from confluence, indeed, released cells from growth arrest. Unexpectedly, a further decrease in seeding density so that cells were isolated from neighboring cells decreased proliferation. Experiments using microengineered substrates showed that E-cadherin engagement stimulated the peak in proliferation at intermediate seeding densities, and that the proliferation arrest at high densities did not involve E-cadherin, but rather resulted from a crowding-dependent decrease in cell spreading against the underlying substrate. Rac1 activity, which was induced by E-cadherin engagement specifically at intermediate seeding densities, was required for the cadherin-stimulated proliferation, and the control of Rac1 activation by E-cadherin was mediated by p120-catenin. Together, these findings demonstrate a stimulatory role for E-cadherin in proliferative regulation, and identify a simple mechanism by which cell–cell contact may trigger or inhibit epithelial cell proliferation in different settings.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "71", "doc_id": "14149065", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does negative Screening Rule Out the Risk of Tuberculosis in Patients with Inflammatory Bowel Disease Undergoing Anti-TNF Treatment : A Descriptive Study on the GETAID Cohort?\n\nABSTRACT:\nto describe the characteristics of incident cases of tuberculosis [TB] despite negative TB screening tests, in patients with inflammatory bowel disease [IBD] undergoing anti-TNF treatment, and to identify the risk factors involved. A retrospective descriptive study was conducted at GETAID centers on all IBD patients undergoing anti-TNF treatment who developed TB even though their initial screening test results were negative. The following data were collected using a standardized anonymous questionnaire: IBD, and TB characteristics and evolution, initial screening methods and results, and time before anti-TNF treatment was restarted. A total of 44 IBD patients [including 23 men; median age 37 years] were identified at 20 French and Swiss centers at which TB screening was performed [before starting anti-TNF treatment] based on Tuberculin Skin Tests [n = 25], Interferon Gamma Release Assays [n = 12], or both [n = 7]. The median interval from the start of anti-TNF treatment to TB diagnosis was 14.5 months (interquartile range [IQR] 25-75: 4.9-43.3). Pulmonary TB involvement was observed in 25 [57%] patients, and 40 [91%] had at least one extrapulmonary location. One TB patient died as the result of cardiac tamponade. Mycobacterium tuberculosis exposure was thought to be a possible cause of TB in 14 cases [32%]: 7 patients [including 6 health care workers] were exposed to occupational risks, and 7 had travelled to endemic countries. Biotherapy was restarted on 27 patients after a median period of 11.2 months [IQR 25-75: 4.4-15.2] after TB diagnosis without any recurrence of the infection.", "output": "{\"label\": \"no\", \"rationale\": \"Tuberculosis can occur in IBD patients undergoing anti-TNF treatment, even if their initial screening results were negative. In the present population, TB was mostly extrapulmonary and disseminated. TB screening tests should be repeated on people exposed to occupational risks and/or travelers to endemic countries.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 27402916, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: There is a positive correlation between hip fractures and statin use.\n\nCANDIDATE_ABSTRACT:\nTITLE: HMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients.\nABSTRACT: CONTEXT Recent animal studies have found that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) lipid-lowering drugs (statins) substantially increase bone formation, but whether statin use in humans results in clinically meaningful bone formation or a reduction in the risk of osteoporotic fractures is not known. OBJECTIVE To determine whether the use of statins is associated with reduced hip fracture risk. DESIGN Case-control study. SETTING AND PATIENTS A total of 6110 New Jersey residents aged 65 years or older and enrolled in Medicare and either Medicaid or the Pharmacy Assistance for the Aged and Disabled program. Case patients (n=1222) underwent surgical repair of a hip fracture in 1994. Control patients (n=4888) were identified at a ratio of 4:1 and frequency-matched to case patients for age and sex. MAIN OUTCOME MEASURE Adjusted odds ratio (OR) of hip fracture by statin use in the 180 days and 3 years prior to the index date (the earliest date of admission for surgery), adjusted for demographic and clinical characteristics and health care utilization. RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus. No significant relationship was observed between use of nonstatin lipid-lowering agents and hip fracture risk. Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowe [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1288, "doc_id": "4687948", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Many transmembrane receptors transmit signals by long-range conformational changes in the association of alpha-helices across the plasma membrane.\n\nCANDIDATE_PASSAGE:\nConsumption of added sugars from liquid but not solid sources predicts impaired glucose homeostasis and insulin resistance among youth at risk of obesity. Little is known about longitudinal associations between added sugar consumption (solid and liquid sources) and glucose-insulin homeostasis among youth. Caucasian children (8-10 y) with at least one obese biological parent were recruited in the QUébec Adipose and Lifestyle InvesTigation in Youth (QUALITY) cohort (n = 630) and followed-up 2 y later (n = 564). Added sugars were assessed by 3 24-h dietary recalls at baseline. Two-year changes were examined in multivariate linear regression models, adjusting for baseline level, age, sex, Tanner stage, energy intake, fat mass (dual-energy X-ray absorptiometry), and physical activity (7 d accelerometer). Added sugar intake in either liquid or solid sources was not related to changes in adiposity measures (fat mass, body mass index, or waist circumference). However, a higher consumption (10 g/d) of added sugars from liquid sources was associated with 0.04 mmol/L higher fasting glucose, 2.3 pmol/L higher fasting insulin, 0.1 unit higher homeostasis model assessment of insulin resistance (HOMA-IR), and 0.4 unit lower Matsuda-insulin sensitivity index (Matsuda-ISI) in all participants (P < 0.01). No associations were observed with consumption of added sugars from solid sources. Overweight/obese children at baseline had greater increases in adiposity indicators, fasting insulin, and HOMA-IR and decreases in Matsuda-ISI during those 2 y than normal-weight children. Consumption of added sugars from liquid or solid sources was not associated with changes in adiposity, but liquid added sugars were a risk factor for the development of impaired glucose homeostasis and insul [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "757", "doc_id": "11201004", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: p16INK4A accumulation is linked to an abnormal wound response caused by the microinvasive step of advanced Oral Potentially Malignant Lesions (OPMLs).\n\nCANDIDATE_ABSTRACT:\nTITLE: Monitoring Tumorigenesis and Senescence In Vivo with a p16INK4a-Luciferase Model\nABSTRACT: Monitoring cancer and aging in vivo remains experimentally challenging. Here, we describe a luciferase knockin mouse (p16(LUC)), which faithfully reports expression of p16(INK4a), a tumor suppressor and aging biomarker. Lifelong assessment of luminescence in p16(+/LUC) mice revealed an exponential increase with aging, which was highly variable in a cohort of contemporaneously housed, syngeneic mice. Expression of p16(INK4a) with aging did not predict cancer development, suggesting that the accumulation of senescent cells is not a principal determinant of cancer-related death. In 14 of 14 tested tumor models, expression of p16(LUC) was focally activated by early neoplastic events, enabling visualization of tumors with sensitivity exceeding other imaging modalities. Activation of p16(INK4a) was noted in the emerging neoplasm and surrounding stromal cells. This work suggests that p16(INK4a) activation is a characteristic of all emerging cancers, making the p16(LUC) allele a sensitive, unbiased reporter of neoplastic transformation.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1395, "doc_id": "17717391", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: RUNX1 is downregulated or mutated in TLX1 T-ALL.\n\nCANDIDATE_ABSTRACT:\nTITLE: Reverse engineering of TLX oncogenic transcriptional networks identifies RUNX1 as tumor suppressor in T-ALL\nABSTRACT: The TLX1 and TLX3 transcription factor oncogenes have a key role in the pathogenesis of T cell acute lymphoblastic leukemia (T-ALL). Here we used reverse engineering of global transcriptional networks to decipher the oncogenic regulatory circuit controlled by TLX1 and TLX3. This systems biology analysis defined T cell leukemia homeobox 1 (TLX1) and TLX3 as master regulators of an oncogenic transcriptional circuit governing T-ALL. Notably, a network structure analysis of this hierarchical network identified RUNX1 as a key mediator of the T-ALL induced by TLX1 and TLX3 and predicted a tumor-suppressor role for RUNX1 in T cell transformation. Consistent with these results, we identified recurrent somatic loss-of-function mutations in RUNX1 in human T-ALL. Overall, these results place TLX1 and TLX3 at the top of an oncogenic transcriptional network controlling leukemia development, show the power of network analyses to identify key elements in the regulatory circuits governing human cancer and identify RUNX1 as a tumor-suppressor gene in T-ALL.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Notably, a network structure analysis of this hierarchical network identified RUNX1 as a key mediator of the T-ALL induced by TLX1 and TLX3 and predicted a tumor-suppressor role for RUNX1 in T cell transformation.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1009, "doc_id": "1982286", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Can PRISM predict length of PICU stay?\n\nABSTRACT:\nPRISM is claimed to score disease severity which has attributed an impact on length of PICU stay (LOS). To determine the impact of PRISM on LOS, and evaluate an Artificial Neural Network's (ANN) performance to estimate LOS from PRISM item patterns. Retrospectively we performed correlation and regression analyses on routinely scored PRISM data of all consecutive admissions to our level-III PICU from 1994 to 1999 (n>2000) with individual LOS. In addition, an ANN was trained on the chronologically first 75% of those data (inputs, PRISM items + age + sex; output, LOS). The ANN's performance was tested on the remaining most recent 25% of the data sets. The Spearman and Pearson coefficients of correlation between PRISM and LOS were 0.2 (p<0.001) and 0.08 (p = 0.0003), the latter being slightly higher when LOS was logarithmically transformed. Pearson's coefficient of correlation between ANN derived LOS estimate and actual LOS was 0.21 (p<0.001) (LOS logarithmically transformed: 0.34; p<0.001) in the independent validation sample.", "output": "{\"label\": \"no\", \"rationale\": \"The ANN with its intrinsic ability to detect non-linear correlation, and to relate specific item patterns to LOS, outperformed linear statistics but was still disappointing in estimating individual LOS. It might be speculated that therapeutic intervention modulates the natural course of the disease thus counteracting both disease severity as initially scored by PRISM, and LOS. This being true, the inverse of the correlation between PRISM (or PRISM based LOS estimate) and LOS might be a candidate indicator of quality of care.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 14612308, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Polymeal nutrition reduces cardiovascular mortality.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Polymeal: a more natural, safer, and probably tastier (than the Polypill) strategy to reduce cardiovascular disease by more than 75%.\nABSTRACT: OBJECTIVE Although the Polypill concept (proposed in 2003) is promising in terms of benefits for cardiovascular risk management, the potential costs and adverse effects are its main pitfalls. The objective of this study was to identify a tastier and safer alternative to the Polypill: the Polymeal. METHODS Data on the ingredients of the Polymeal were taken from the literature. The evidence based recipe included wine, fish, dark chocolate, fruits, vegetables, garlic, and almonds. Data from the Framingham heart study and the Framingham offspring study were used to build life tables to model the benefits of the Polymeal in the general population from age 50, assuming multiplicative correlations. RESULTS Combining the ingredients of the Polymeal would reduce cardiovascular disease events by 76%. For men, taking the Polymeal daily represented an increase in total life expectancy of 6.6 years, an increase in life expectancy free from cardiovascular disease of 9.0 years, and a decrease in life expectancy with cardiovascular disease of 2.4 years. The corresponding differences for women were 4.8, 8.1, and 3.3 years. CONCLUSION The Polymeal promises to be an effective, non-pharmacological, safe, cheap, and tasty alternative to reduce cardiovascular morbidity and increase life expectancy in the general population.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSION The Polymeal promises to be an effective, non-pharmacological, safe, cheap, and tasty alternative to reduce cardiovascular morbidity and increase life expectancy in the general population.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 960, "doc_id": "8780599", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Activator-inhibitor pairs are provided dorsally by Admpchordin.\n\nCANDIDATE_PASSAGE:\nTLR-activated B cells suppress T cell-mediated autoimmunity. TLR sense microbial infections, and control activation of immune responses. Dendritic cells, macrophages, and B lymphocytes express TLR and the TLR-signaling adaptor protein MyD88. The impact of TLR-activated B cells on T cell-mediated inflammation is unknown. In this study, we have used mice carrying B cell-restricted deficiencies in MyD88 or in distinct TLR to examine the impact of TLR-activated B cells on a T cell-mediated autoimmune disease, experimental autoimmune encephalomyelitis (EAE). We demonstrate that TLR-signaling in B cells suppresses inflammatory T cell responses (both Th1 and Th17), and stimulates recovery from EAE. Only certain TLR are required on B cells for resolution of EAE, and these are dispensable for disease initiation, indicating that a category of TLR agonists preferentially triggers a suppressive function in B cells and thereby limits autoimmune disease. The TLR agonists controlling the regulatory function of B cells are provided by components of Mycobacterium tuberculosis present in the adjuvant. Thus, MyD88 signaling in B cells antagonizes MyD88 signaling in other cells, which drives differentiation of Th17 cells and is required for induction of EAE. Altogether, our data indicate that B cells link recognition of microbial products via TLR to suppression of a T cell-mediated autoimmune disease.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "72", "doc_id": "14644164", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Obesity is determined solely by environmental factors.\n\nCANDIDATE_PASSAGE:\nRole of microsomal prostaglandin E synthase-1 in the facilitation of angiogenesis and the healing of gastric ulcers. The importance of prostaglandin E(2) in various pathophysiological events emphasizes the necessity of understanding the role of PGE synthases (PGESs) in vivo. However, there has been no report on the functional relevance of microsomal PGES-1 (mPGES-1) to the physiological healing processes of gastric ulcers, or to angiogenesis, which is indispensable to the healing processes. In this report, we tested whether mPGES-1 plays a role in the healing of gastric ulcers and in the enhancement of angiogenesis using mPGES-1 knockout mice (mPGES-1 KO mice) and their wild-type (WT) counterparts. Gastric ulcers were induced by the serosal application of 100% acetic acid, and the areas of the ulcers were measured thereafter. mPGES-1 together with cyclooxygenase-2 were induced in the granulation tissues compared with normal stomach tissues. The healing of acetic acid-induced ulcers was significantly delayed in mPGES-1 KO mice compared with WT. This was accompanied with reduced angiogenesis in ulcer granulation tissues, as estimated by CD31 mRNA levels determined by real-time PCR and the microvessel density in granulation tissues. The mRNA levels of proangiogenic growth factors, such as transforming growth factor-β, basic fibroblast growth factor, and connective tissue growth factor in ulcer granulation tissues determined were reduced in mPGES-1 KO mice compared with WT. The present results suggest that mPGES-1 enhances the ulcer-healing processes and the angiogenesis indispensable to ulcer healing, and that a selective mPGES-1 inhibitor should be used with care in patients with gastric ulcers.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "873", "doc_id": "12513042", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Women with a lower birth weight are more likely to develop breast cancer later in life.\n\nCANDIDATE_ABSTRACT:\nTITLE: Birth Size and Breast Cancer Risk: Re-analysis of Individual Participant Data from 32 Studies\nABSTRACT: BACKGROUND Birth size, perhaps a proxy for prenatal environment, might be a correlate of subsequent breast cancer risk, but findings from epidemiological studies have been inconsistent. We re-analysed individual participant data from published and unpublished studies to obtain more precise estimates of the magnitude and shape of the birth size-breast cancer association. METHODS AND FINDINGS Studies were identified through computer-assisted and manual searches, and personal communication with investigators. Individual participant data from 32 studies, comprising 22,058 breast cancer cases, were obtained. Random effect models were used, if appropriate, to combine study-specific estimates of effect. Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003). Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data. Birth length and head circumference from birth records were also positively associated with breast cancer risk (pooled RR per one SD increment: 1.06 [95% CI 1.03-1.10] and 1.09 [95% CI 1.03-1.15], respectively). Simultaneous adjustment for these three birth size variables showed that length was the strongest independent predictor of risk. The birth size effec [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1380, "doc_id": "16322674", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does β3-Adrenoceptor activation attenuate atherosclerotic plaque formation in ApoE ( -/- ) mice through lowering blood lipids and glucose?\n\nABSTRACT:\nTo examine the effects of β3-adrenoceptor (β3-AR) activation on atherosclerotic plaque development in ApoE(-/-) mice. Thirty six week-old male ApoE(-/-) mice on a high-fat diet were treated with atorvastatin (10 mg·kg(-1)·d(-1), po), BRL37344 (β3-AR agonist, 1.65 or 3.30 μg/kg, ip, twice a week) or SR52390A (β3-AR antagonist, 50 μg/kg, ip, twice a week) for 12 weeks. Wild-type C57BL/6J mice receiving a normal diet were taken as healthy controls. At the end of the treatments, serum levels of triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), non-high density lipoprotein cholesterol (nHDL-C), glucose and insulin were measured. The thoracic aortas were dissected out, the area of atherosclerotic plaques and extent of fibrosis in the plaques were examined using HE and Masson's trichome staining, respectively. Compared to wild-type mice, ApoE(-/-) mice fed on a high-fat diet exhibited prominent hyperlipidemia and insulin resistance, associated with large area of atherosclerotic plaques and great extent of fibrosis in aortas. Atorvastatin significantly decreased the serum levels of TC and nHDL-C, and reduced the plaque area and collagen content in aortas. BRL37344 significantly decreased the serum levels of TG, TC, nHDL-C, glucose and insulin, and increased HDL-C and the insulin sensitivity, and dose-dependently reduced the plaque area and collagen content in aortas. SR52390A treatment did not affect any parameters studied.", "output": "{\"label\": \"yes\", \"rationale\": \"The β3-AR agonist impedes the progression of atherosclerosis in ApoE(-/-) mice, through improvement of the lipid and glucose profiles.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 23892270, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Increased microtubule acetylation worsens interference of axonal transport caused by LRRK2 Roc-COR domain mutations.\n\nCANDIDATE_ABSTRACT:\nTITLE: Increasing microtubule acetylation rescues axonal transport and locomotor deficits caused by LRRK2 Roc-COR domain mutations\nABSTRACT: Leucine-rich repeat kinase 2 (LRRK2) mutations are the most common genetic cause of Parkinson's disease. LRRK2 is a multifunctional protein affecting many cellular processes and has been described to bind microtubules. Defective microtubule-based axonal transport is hypothesized to contribute to Parkinson's disease, but whether LRRK2 mutations affect this process to mediate pathogenesis is not known. Here we find that LRRK2 containing pathogenic Roc-COR domain mutations (R1441C, Y1699C) preferentially associates with deacetylated microtubules, and inhibits axonal transport in primary neurons and in Drosophila, causing locomotor deficits in vivo. In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport. In vivo knockdown of the deacetylases HDAC6 and Sirt2, or administration of TSA rescues both axonal transport and locomotor behavior. Thus, this study reveals a pathogenic mechanism and a potential intervention for Parkinson's disease.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 615, "doc_id": "9638032", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Walking in traffic areas in London improves lung function in elderly adults.\n\nCANDIDATE_ABSTRACT:\nTITLE: Respiratory and cardiovascular responses to walking down a traffic-polluted road compared with walking in a traffic-free area in participants aged 60 years and older with chronic lung or heart disease and age-matched healthy controls: a randomised, crossover study\nABSTRACT: BACKGROUND Long-term exposure to pollution can lead to an increase in the rate of decline of lung function, especially in older individuals and in those with chronic obstructive pulmonary disease (COPD), whereas shorter-term exposure at higher pollution levels has been implicated in causing excess deaths from ischaemic heart disease and exacerbations of COPD. We aimed to assess the effects on respiratory and cardiovascular responses of walking down a busy street with high levels of pollution compared with walking in a traffic-free area with lower pollution levels in older adults. METHODS In this randomised, crossover study, we recruited men and women aged 60 years and older with angiographically proven stable ischaemic heart disease or stage 2 Global initiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable for 6 months, and age-matched healthy volunteers. Individuals with ischaemic heart disease or COPD were recruited from existing databases or outpatient respiratory and cardiology clinics at the Royal Brompton & Harefield NHS Foundation Trust and age-matched healthy volunteers using advertising and existing databases. All participants had abstained from smoking for at least 12 months and medications were taken as recommended by participants' doctors during the study. Participants were randomly assigned by drawing numbered disks at random from a bag to do a 2 h walk either along a commercial street in London (Oxford Street) or in an urban park (Hyde Park). Baseline measurements of participants were taken before the walk in the hospital laboratory. During each walk session, black carbon, particulate matter (PM) concentrations, ultrafine particles, and nitrogen dioxide (NO2) concentrations were measured. FINDINGS Between October, 2012 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Participants with COPD reported more cough (odds ratio [OR] 1·95, 95% CI 0·96-3·95; p<0·1), sputum (3·15, 1·39-7·13; p<0·05), shortness of breath (1·86, 0·97-3·57; p<0·1), and wheeze (4·00, 1·52-10·50; p<0·05) after walking down Oxford Street compared with Hyde Park.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1373, "doc_id": "21003930", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does hIV exposure worsen outcome in stage III necrotizing enterocolitis with current treatment protocols?\n\nABSTRACT:\nThe heavy burden of maternal HIV infection in developing countries such as South Africa has resulted in a high prevalence of premature birth and necrotizing enterocolitis (NEC). Uninfected infants born to HIV-infected mothers also demonstrate immune deficiencies. It is, therefore, essential to have a better understanding of how to mitigate HIV as an independent risk factor for surgically treated NEC and to evaluate the relevant contributing factors in the presence of an aggressive strategy of pasteurized breast milk feeding and antiretroviral prophylaxis. Infants with stage IIIb NEC presenting over a 4-year period were retrospectively reviewed. HIV-exposed infants were compared with non-HIV-exposed infants. Contributing factors were evaluated and studied by systematic statistical methods to evaluate risk. Twenty percent (17/87) infants were HIV-exposed, and 80% (70/87), unexposed, whereas a further 10 (total, n = 97) had unknown HIV exposure status. Demographics and other perinatal risk factors between the 2 groups were not significantly different other than that HIV-exposed infants received pasteurized breast milk and nonexposed infants received unpasteurized breast milk. There were no statistically significant differences between the groups with respect to disease presentation or severity, surgical findings or type of surgery, postoperative complications, survival, or timing of death. Trends toward higher antenatal steroid exposure and increased postoperative sepsis in the HIV-exposed group (P = .03) were noted but were not related. All HIV-exposed infants received antiretrovirals; there were no significant differences on subanalysis between different antiretroviral regimens.", "output": "{\"label\": \"no\", \"rationale\": \"HIV-exposed infants do not have a more severe disease course nor more adverse outcomes in stage IIIb NEC than unexposed infants. Significant factors were antenatal steroids and post-NEC infective episodes.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 22498379, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: High levels of CRP reduces the risk of exacerbations in chronic obstructive pulmonary disease (COPD).\n\nCANDIDATE_ABSTRACT:\nTITLE: Inflammatory biomarkers and exacerbations in chronic obstructive pulmonary disease.\nABSTRACT: IMPORTANCE Exacerbations of respiratory symptoms in chronic obstructive pulmonary disease (COPD) have profound and long-lasting adverse effects on patients. OBJECTIVE To test the hypothesis that elevated levels of inflammatory biomarkers in individuals with stable COPD are associated with an increased risk of having exacerbations. DESIGN, SETTING, AND PARTICIPANTS Prospective cohort study examining 61,650 participants with spirometry measurements from the Copenhagen City Heart Study (2001-2003) and the Copenhagen General Population Study (2003-2008). Of these, 6574 had COPD, defined as a ratio between forced expiratory volume in 1 second (FEV1) and forced vital capacity below 0.7. MAIN OUTCOMES AND MEASURES Baseline levels of C-reactive protein (CRP) and fibrinogen and leukocyte count were measured in participants at a time when they were not experiencing symptoms of exacerbations. Exacerbations were recorded and defined as short-course treatment with oral corticosteroids alone or in combination with an antibiotic or as a hospital admission due to COPD. Levels of CRP and fibrinogen and leukocyte count were defined as high or low according to cut points of 3 mg/L, 14 μmol/L, and 9 ×10(9)/L, respectively. RESULTS During follow-up, 3083 exacerbations were recorded (mean, 0.5/participant). In the first year of follow-up, multivariable-adjusted odds ratios for having frequent exacerbations were 1.2 (95% CI, 0.7-2.2; 17 events/1000 person-years) for individuals with 1 high biomarker, 1.7 (95% CI, 0.9-3.2; 32 events/1000 person-years) for individuals with 2 high biomarkers, and 3.7 (95% CI, 1.9-7.4; 81 events/1000 person-years) for individuals with 3 high biomarkers compared with individuals who had no elevated biomarkers (9 events/1000 person-years; trend: P = 2 × [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In the first year of follow-up, multivariable-adjusted odds ratios for having frequent exacerbations were 1.2 (95% CI, 0.7-2.2; 17 events/1000 person-years) for individuals with 1 high biomarker, 1.7 (95% CI, 0.9-3.2; 32 events/1000 person-years) for individuals with 2 high biomarkers, and 3.7 (95% CI, 1.9-7.4; 81 events/1000 person-years) for individuals with 3 high biomarkers compared with individuals who had no elevated biomarkers (9 events/1000 person-years; trend: P = 2 × 10(-5)).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 516, "doc_id": "29564505", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: 30-Day and 1-year mortality in emergency general surgery laparotomies: an area of concern and need for improvement?\n\nABSTRACT:\nEmergency surgery is associated with poorer outcomes and higher mortality with recent studies suggesting the 30-day mortality to be 14-15%. The aim of this study was to analyse the 30-day mortality, age-related 30-day mortality and 1-year mortality following emergency laparotomy. We hope this will encourage prospective data collection, improvement of care and initiate strategies to establish best practice in this area. This was a retrospective study of patients who underwent emergency laparotomy from June 2010 to May 2012. The primary end point of the study was 30-day mortality, age-related 30-day mortality and 1-year all-cause mortality. 477 laparotomies were performed in 446 patients. 57% were aged<70 and 43% aged>70 years. 30-day mortality was 12, 4% in those aged<70 years and 22% in those>70 years (p<0.001). 1-year mortality was 25, 15% in those aged under 70 years and 38% in those aged>70 years (p<0.001).", "output": "{\"label\": \"maybe\", \"rationale\": \"Emergency laparotomy carries a high rate of mortality, especially in those over the age of 70 years, and more needs to be done to improve outcomes, particularly in this group. This could involve increasing acute surgical care manpower, early recognition of patients requiring emergency surgery, development of clear management protocols for such patients or perhaps even considering centralisation of emergency surgical services to specialist centres with multidisciplinary teams involving emergency surgeons and care of the elderly physicians in hospital and related community outreach services for post-discharge care.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 26037986, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Diabetic patients with acute coronary syndrome experience increased short-term and long-term risk for bleeding events.\n\nCANDIDATE_PASSAGE:\nPlatelet glycoprotein IIb/IIIa inhibitors reduce mortality in diabetic patients with non-ST-segment-elevation acute coronary syndromes. BACKGROUND Diabetes mellitus is a major risk factor for adverse outcomes after acute coronary syndromes (ACS). Because this disease may be associated with increased platelet aggregation, we investigated whether diabetic patients with ACS derive particular benefit from platelet glycoprotein (GP) IIb/IIIa receptor inhibition. METHODS AND RESULTS We performed a meta-analysis of the diabetic populations enrolled in the 6 large-scale platelet GP IIb/IIIa inhibitor ACS trials: PRISM, PRISM-PLUS, PARAGON A, PARAGON B, PURSUIT, and GUSTO IV. Among 6458 diabetic patients, platelet GP IIb/IIIa inhibition was associated with a significant mortality reduction at 30 days, from 6.2% to 4.6% (OR 0.74; 95% CI 0.59 to 0.92; P=0.007). Conversely, 23 072 nondiabetic patients had no survival benefit (3.0% versus 3.0%). The interaction between platelet GP IIb/IIIa inhibition and diabetic status was statistically significant (P=0.036). Among 1279 diabetic patients undergoing percutaneous coronary intervention (PCI) during index hospitalization, the use of these agents was associated with a mortality reduction at 30 days from 4.0% to 1.2% (OR 0.30; 95% CI 0.14 to 0.69; P=0.002). CONCLUSIONS This meta-analysis, including the entire large-scale trial experience of intravenous platelet GP IIb/IIIa inhibitors for the medical management of non-ST-segment-elevation ACS, shows that these agents may significantly reduce mortality at 30 days in diabetic patients. Although not based on a randomized assessment, the survival benefit appears to be of greater magnitude in patients undergoing PCI. Therefore, the use of platelet GP IIb/IIIa inhibitors should be s [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "343", "doc_id": "7873737", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Nanoparticles can be targeted against specific cell types by incorporating aptamers into lipid nanoparticles.\n\nCANDIDATE_ABSTRACT:\nTITLE: Immunosuppressant FTY720 inhibits thymocyte emigration.\nABSTRACT: One major role of the thymus is to provide the peripheral immune system with mature T cells, but the mechanisms involving the cellular export are not fully understood. In this study, we examined the ability of a novel immunosuppressive reagent, FTY720, to inhibit T cell export from the thymus. Daily administration of FTY720 at a dose of 1 mg / kg resulted in a marked decrease in the number of peripheral blood T lymphocytes. In the thymus, long-term daily administration of FTY720 caused a three- to fourfold increase in the proportion of mature medullary thymocytes (CD4(+)CD8(-) and CD4(-)CD8(+)) as well as a slight decrease in the double-positive cell (CD4(+)CD8(+)) ratio. Phenotypic analysis (TCRalpha beta, H-2K(d), CD44, CD69 and CD24) revealed that these increased subsets represent possible peripheral recent thymic emigrants. High level expression of L-selectin by these subsets further suggests that they were prevented from leaving the thymus. By intrathymic labeling with fluorescein isothiocyanate, only one fourth of labeled cells could be detected in the lymph nodes and in the spleen of FTY720-treated mice compared to saline-treated control mice. Taken together, these results suggest that the immunosuppressive action of FTY720, at least in part, could be due to its inhibitory effect on T cell emigration from the thymus to the periphery.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 839, "doc_id": "1336292", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: PPAR-RXRs are inhibited by PPAR ligands.\n\nCANDIDATE_PASSAGE:\nInvolvement of S-nitrosylation of actin in inhibition of neurotransmitter release by nitric oxide BACKGROUND The role of the diffusible messenger nitric oxide (NO) in the regulation of pain transmission is still a debate of matter, pro-nociceptive and/or anti-nociceptive. S-Nitrosylation, the reversible post-translational modification of selective cysteine residues in proteins, has emerged as an important mechanism by which NO acts as a signaling molecule. The occurrence of S-nitrosylation in the spinal cord and its targets that may modulate pain transmission remain unclarified. The \"biotin-switch\" method and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry were employed for identifying S-nitrosylated proteins. RESULTS Here we show that actin was a major protein S-nitrosylated in the spinal cord by the NO donor, S-nitroso-N-acetyl-DL-penicillamine (SNAP). Interestingly, actin was S-nitrosylated, more in the S2 fraction than in the P2 fraction of the spinal homogenate. Treatment of PC12 cells with SNAP caused rapid S-nitrosylation of actin and inhibited dopamine release from the cells. Just like cytochalasin B, which depolymerizes actin, SNAP decreased the amount of filamentous actin cytoskeleton just beneath the membrane. The inhibition of dopamine release was not attenuated by inhibitors of soluble guanylyl cyclase and cGMP-dependent protein kinase. CONCLUSION The present study demonstrates that actin is a major S-nitrosylated protein in the spinal cord and suggests that NO directly regulates neurotransmitter release by S-nitrosylation in addition to the well-known phosphorylation by cGMP-dependent protein kinase.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "913", "doc_id": "2139357", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is arch form influenced by sagittal molar relationship or Bolton tooth-size discrepancy?\n\nABSTRACT:\nOrthodontic patients show high prevalence of tooth-size discrepancy. This study investigates the possible association between arch form, clinically significant tooth-size discrepancy, and sagittal molar relationship. Pretreatment orthodontic casts of 230 Saudi patients were classified into one of three arch form types (tapered, ovoid, and square) using digitally scanned images of the mandibular arches. Bolton ratio was calculated, sagittal molar relationship was defined according to Angle classification, and correlations were analyzed using ANOVA, chi-square, and t-tests. No single arch form was significantly more common than the others. Furthermore, no association was observed between the presence of significant Bolton discrepancy and the sagittal molar relationship or arch form. Overall Bolton discrepancy is significantly more prevalent in males.", "output": "{\"label\": \"no\", \"rationale\": \"Arch form in a Saudi patient group is independent of gender, sagittal molar relationship, and Bolton discrepancy.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 26113007, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Genetic deletion of JAM-A increases gut permeability.\n\nCANDIDATE_PASSAGE:\nRegulated nucleo/cytoplasmic exchange of HOG1 MAPK requires the importin beta homologs NMD5 and XPO1. MAP kinase signaling modules serve to transduce extracellular signals to the nucleus of eukaryotic cells, but little is known about how signals cross the nuclear envelope. Exposure of yeast cells to increases in extracellular osmolarity activates the HOG1 MAP kinase cascade, which is composed of three tiers of protein kinases, namely the SSK2, SSK22 and STE11 MAPKKKs, the PBS2 MAPKK, and the HOG1 MAPK. Using green fluorescent protein (GFP) fusions of these kinases, we found that HOG1, PBS2 and STE11 localize to the cytoplasm of unstressed cells. Following osmotic stress, HOG1, but neither PBS2 nor STE11, translocates into the nucleus. HOG1 translocation occurs very rapidly, is transient, and correlates with the phosphorylation and activation of the MAP kinase by its MAPKK. HOG1 phosphorylation is necessary and sufficient for nuclear translocation, because a catalytically inactive kinase when phosphorylated is translocated to the nucleus as efficiently as the wild-type. Nuclear import of the MAPK under stress conditions requires the activity of the small GTP binding protein Ran-GSP1, but not the NLS-binding importin alpha/beta heterodimer. Rather, HOG1 import requires the activity of a gene, NMD5, that encodes a novel importin beta homolog. Similarly, export of dephosphorylated HOG1 from the nucleus requires the activity of the NES receptor XPO1/CRM1. Our findings define the requirements for the regulated nuclear transport of a stress-activated MAP kinase.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "461", "doc_id": "33063763", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Human embryonic stem cells have the capacity to give rise to differentiated progeny representative of all three embryonic germ layers.\n\nCANDIDATE_PASSAGE:\nHuman and murine very small embryonic-like cells represent multipotent tissue progenitors, in vitro and in vivo. The purpose of this study was to determine the lineage progression of human and murine very small embryonic-like (HuVSEL or MuVSEL) cells in vitro and in vivo. In vitro, HuVSEL and MuVSEL cells differentiated into cells of all three embryonic germ layers. HuVSEL cells produced robust mineralized tissue of human origin compared with controls in calvarial defects. Immunohistochemistry demonstrated that the HuVSEL cells gave rise to neurons, adipocytes, chondrocytes, and osteoblasts within the calvarial defects. MuVSEL cells were also able to differentiate into similar lineages. First round serial transplants of MuVSEL cells into irradiated osseous sites demonstrated that ∼60% of the cells maintained their VSEL cell phenotype while other cells differentiated into multiple tissues at 3 months. Secondary transplants did not identify donor VSEL cells, suggesting limited self renewal but did demonstrate VSEL cell derivatives in situ for up to 1 year. At no point were teratomas identified. These studies show that VSEL cells produce multiple cellular structures in vivo and in vitro and lay the foundation for future cell-based regenerative therapies for osseous, neural, and connective tissue disorders.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "531", "doc_id": "36398420", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Post-transcriptional handling of mitochondrial transcripts occurs in mitochondrial RNA granules.\n\nCANDIDATE_PASSAGE:\nA Null Mutation in Inositol Polyphosphate 4-Phosphatase Type I Causes Selective Neuronal Loss in Weeble Mutant Mice Weeble mutant mice have severe locomotor instability and significant neuronal loss in the cerebellum and in the hippocampal CA1 field. Genetic mapping was used to localize the mutation to the gene encoding inositol polyphosphate 4-phosphatase type I (Inpp4a), where a single nucleotide deletion results in a likely null allele. The substrates of INPP4A are intermediates in a pathway affecting intracellular Ca(2+) release but are also involved in cell cycle regulation through binding the Akt protooncogene; dysfunction in either may account for the neuronal loss of weeble mice. Although other mutations in phosphoinositide enzymes are associated with synaptic defects without neuronal loss, weeble shows that Inpp4a is critical for the survival of a subset of neurons during postnatal development in mice.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "962", "doc_id": "6492658", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Antibiotic induced alterations in the gut microbiome reduce resistance against Clostridium difficile\n\nCANDIDATE_ABSTRACT:\nTITLE: Antibiotic-induced shifts in the mouse gut microbiome and metabolome increase susceptibility to Clostridium difficile infection\nABSTRACT: Antibiotics can have significant and long-lasting effects on the gastrointestinal tract microbiota, reducing colonization resistance against pathogens including Clostridium difficile. Here we show that antibiotic treatment induces substantial changes in the gut microbial community and in the metabolome of mice susceptible to C. difficile infection. Levels of secondary bile acids, glucose, free fatty acids and dipeptides decrease, whereas those of primary bile acids and sugar alcohols increase, reflecting the modified metabolic activity of the altered gut microbiome. In vitro and ex vivo analyses demonstrate that C. difficile can exploit specific metabolites that become more abundant in the mouse gut after antibiotics, including the primary bile acid taurocholate for germination, and carbon sources such as mannitol, fructose, sorbitol, raffinose and stachyose for growth. Our results indicate that antibiotic-mediated alteration of the gut microbiome converts the global metabolic profile to one that favours C. difficile germination and growth.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Our results indicate that antibiotic-mediated alteration of the gut microbiome converts the global metabolic profile to one that favours C. difficile germination and growth.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 118, "doc_id": "6372244", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Excess gestational weight gain is associated with obesity-related pregnancy outcomes.\n\nCANDIDATE_PASSAGE:\nConstruction of an antisense CYP86MF gene plasmid vector and production of a male-sterile Chinese cabbage transformant by the pollen-tube method SummaryA plant expression vector pBIA9-AMF containing an antisense fragment of the CYP86MF gene and the tapetum-specific A9 promoter was constructed. Plasmid vectors were introduced by floral-dipping and pollen-tube transformation methods to Chinese cabbage pak-choi (Brassica campestris ssp. chinensis (L.) Makino var. communis Tsen et Lee, syn. B. rapa ssp. chinensis (L.) Makino var. communis Tsen et Lee) and flowering Chinese cabbage (B. campestris ssp. chinensis (L.) Makino var. parachinensis (Bailey) Tsen et Lee). Results showed that KanR seedlings could be obtained by the pollen-tube method through germination tests of T1 progeny seeds, but not by the floral-dipping method. One of the two KanR seedlings proved that the antisense fragment of the CYP86MF gene was integrated into the Chinese cabbage genome by PCR amplification and Southern blotting. Northern hybridization indicated that the CYP86MF gene, under the A9 promoter, was inhibited in the transformant, and self-infertility was found in the trans...", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "394", "doc_id": "87337034", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Nonhypertensive people who are 55 years old have a 90% chance of developing hypertension during their lifetime.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Sequence Alignment/Map format and SAMtools\nABSTRACT: SUMMARY The Sequence Alignment/Map (SAM) format is a generic alignment format for storing read alignments against reference sequences, supporting short and long reads (up to 128 Mbp) produced by different sequencing platforms. It is flexible in style, compact in size, efficient in random access and is the format in which alignments from the 1000 Genomes Project are released. SAMtools implements various utilities for post-processing alignments in the SAM format, such as indexing, variant caller and alignment viewer, and thus provides universal tools for processing read alignments. AVAILABILITY http://samtools.sourceforge.net.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 854, "doc_id": "2107238", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Lupus-prone mice infected with curliproducing bacteria have higher autoantibody titers compared to controls.\n\nCANDIDATE_PASSAGE:\nResults of screening for intracranial aneurysms in patients with coarctation of the aorta. BACKGROUND AND PURPOSE IAs are found in 2.3% of adults; the mean age at detection is 52 years. Prevalence is <0.5% in young adults. Early studies suggest that 10%-50% of patients with aortic coarctation have IAs. Screening recommendations are variable. We sought to examine the prevalence of IAs through screening with MRA. MATERIALS AND METHODS Consecutive patients older than 16 years of age with coarctation undergoing brain MRA between May 1999 and October 2007 were included. MRA was performed by using a 1.5T scanner with a 3D time-of-flight protocol; simultaneous MR imaging was performed of the heart and aorta. Cerebral MRAs were double-reported by a neuroradiologist. Statistics are described as mean ± SD and median ± range. Continuous variables were compared by using Student t tests and Mann-Whitney U tests (categoric variables, by using the Fisher exact test). RESULTS One hundred seventeen MRAs were double-reported. The median age was 29 ± 11 years (range, 16-59 years). IAs were found in 12 patients (10.3%). The mean diameter of IAs was 3.9 mm (range, 2.0-8.0 mm). Patients with aneurysms were older (median, 37 years; range, 16-50 years) than those without (median, 23 years; range, 16-59 years; Z = -2.01, P = .04). Hypertension was more common in those with IAs (IA 83% versus no IA 43%, P = .01). There was no association between ascending aortopathy, bicuspid aortic valves, and IAs. CONCLUSIONS Patients with coarctation have a higher prevalence of IAs, occurring at an earlier age than in population studies. Whether routine screening is appropriate for this group of patients is unclear. Hypertension is likely to be an important pathophysiologic factor.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "721", "doc_id": "13445579", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does eGR1 predict PTEN and survival in patients with non-small-cell lung cancer?\n\nABSTRACT:\nThe zinc finger transcription factor early growth response gene 1 (EGR1) is underexpressed in non-small-cell lung cancer (NSCLC) compared with normal lung. EGR1 expression has been linked to tumor suppression as a result of cell cycle arrest and apoptosis through regulation of tumor suppressor pathways including PTEN. For these reasons, we hypothesized that reduced levels of EGR1 would correlate with inferior outcome in patients with NSCLC. Patients who underwent surgical resection for NSCLC had RNA extracted from tumor tissue and EGR1 gene expression was quantified by real-time quantitative polymerase chain reaction. The levels of EGR1 expression were examined in relationship to patient characteristics, histology, tumor stage, PTEN expression, and overall and disease-free survival. EGR1 expression strongly correlated with PTEN expression (P < .0001). No correlation of EGR1 with histology or stage was detected. Patients with high levels of EGR1 had better overall and disease-free survival compared with patients with low levels of EGR1 (P = .040 and P = .096, respectively). In a stratified log-rank test, low EGR1 expression was predictive of poor survival independent of tumor stage.", "output": "{\"label\": \"yes\", \"rationale\": \"EGR1 gene expression predicts PTEN levels and survival after surgical resection of NSCLC. Consistent with its known tumor suppressor properties, lower levels of EGR1 are associated with poor outcome. Identification of patients with low EGR1 therefore may identify patients at high risk for disease recurrence and may also identify patients who have tumors resistant to therapy secondary to loss of pathways such as PTEN.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 15774784, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: A high microerythrocyte count raises vulnerability to severe anemia in homozygous alpha (+)- thalassemia trait subjects.\n\nCANDIDATE_PASSAGE:\nNovel roles for KLF1 in erythropoiesis revealed by mRNA-seq. KLF1 (formerly known as EKLF) regulates the development of erythroid cells from bi-potent progenitor cells via the transcriptional activation of a diverse set of genes. Mice lacking Klf1 die in utero prior to E15 from severe anemia due to the inadequate expression of genes controlling hemoglobin production, cell membrane and cytoskeletal integrity, and the cell cycle. We have recently described the full repertoire of KLF1 binding sites in vivo by performing KLF1 ChIP-seq in primary erythroid tissue (E14.5 fetal liver). Here we describe the KLF1-dependent erythroid transcriptome by comparing mRNA-seq from Klf1(+/+) and Klf1(-/-) erythroid tissue. This has revealed novel target genes not previously obtainable by traditional microarray technology, and provided novel insights into the function of KLF1 as a transcriptional activator. We define a cis-regulatory module bound by KLF1, GATA1, TAL1, and EP300 that coordinates a core set of erythroid genes. We also describe a novel set of erythroid-specific promoters that drive high-level expression of otherwise ubiquitously expressed genes in erythroid cells. Our study has identified two novel lncRNAs that are dynamically expressed during erythroid differentiation, and discovered a role for KLF1 in directing apoptotic gene expression to drive the terminal stages of erythroid maturation.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "42", "doc_id": "39506601", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: ALDH1 expression is associated with poorer prognosis in breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: ALDH1 is a marker of normal and malignant human mammary stem cells and a predictor of poor clinical outcome.\nABSTRACT: Application of stem cell biology to breast cancer research has been limited by the lack of simple methods for identification and isolation of normal and malignant stem cells. Utilizing in vitro and in vivo experimental systems, we show that normal and cancer human mammary epithelial cells with increased aldehyde dehydrogenase activity (ALDH) have stem/progenitor properties. These cells contain the subpopulation of normal breast epithelium with the broadest lineage differentiation potential and greatest growth capacity in a xenotransplant model. In breast carcinomas, high ALDH activity identifies the tumorigenic cell fraction, capable of self-renewal and of generating tumors that recapitulate the heterogeneity of the parental tumor. In a series of 577 breast carcinomas, expression of ALDH1 detected by immunostaining correlated with poor prognosis. These findings offer an important new tool for the study of normal and malignant breast stem cells and facilitate the clinical application of stem cell concepts.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In a series of 577 breast carcinomas, expression of ALDH1 detected by immunostaining correlated with poor prognosis.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 53, "doc_id": "45638119", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Primary cervical cytology screening with HPV detection has higher longitudinal sensitivity to detect severe cervical intraepithelial neoplasia than conventional cytology.\n\nCANDIDATE_ABSTRACT:\nTITLE: Evidence regarding human papillomavirus testing in secondary prevention of cervical cancer.\nABSTRACT: More than ever, clinicians need regularly updated reviews given the continuously increasing amount of new information regarding innovative cervical cancer prevention methods. A summary is given from recent meta-analyses and systematic reviews on 3 possible clinical applications of human papillomavirus (HPV) testing: triage of women with equivocal or low-grade cytologic abnormalities; prediction of the therapeutic outcome after treatment of cervical intraepithelial neoplasia (CIN) lesions, and last not but not least, primary screening for cervical cancer and pre-cancer. Consistent evidence is available indicating that HPV-triage with the Hybrid Capture(®) 2 assay (Qiagen Gaithersburg, Inc., MD, USA [previously Digene Corp.] (HC2) is more accurate (higher sensitivity, similar specificity) than repeat cytology to triage women with equivocal Pap smear results. Several other tests show at least similar accuracy but mRNA testing with the APTIMA(®) (Gen-Probe Inc., San Diego, CA, USA) test is similarly sensitive but more specific compared to HC2. In triage of low-grade squamous intraepithelial lesions (LSIL), HC2 is more sensitive but its specificity is substantially lower compared to repeat cytology. The APTIMA(®) test is more specific than HC2 without showing a loss in sensitivity. Identification of DNA of HPV types 16 and/or 18, or RNA from the five most carcinogenic HPV types allow selecting women at highest risk for CIN3+ but the sensitivity and negative predictive value of these markers are lower than full-range high-risk HPV (hrHPV) testing. After conservative treatment of cervical pre-cancer, HPV testing picks up more quickly, with higher sensitivity and not lower specificity, residual or recurrent high-grade CIN than follow-up cytology. Primary screening f [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"After conservative treatment of cervical pre-cancer, HPV testing picks up more quickly, with higher sensitivity and not lower specificity, residual or recurrent high-grade CIN than follow-up cytology.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 973, "doc_id": "28617573", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Varying expression levels of EBI2 affect the positioning and migration of B cells.\n\nCANDIDATE_PASSAGE:\n7α, 25-dihydroxycholesterol-mediated activation of EBI2 in immune regulation and diseases EBI2, aka GPR183, is a G-couple receptor originally identified in 1993 as one of main genes induced in Burkitt's lymphoma cell line BL41 by Epstein-Barr virus (EBV) infection. After it was reported in 2009 that the receptor played a key role in regulating B cell migration and responses, we initiated an effort in looking for its endogenous ligand. In 2011 we and another group reported the identification of 7α, 25-dihydroxyxcholesterol (7α, 25-OHC), an oxysterol, as the likely physiological ligand of EBI2. A few subsequently published studies further elucidated how 7α, 25-OHC bound to EBI2, and how a gradient of 7α, 25-OHC could be generated in vivo and regulated migration, activation, and functions of B cells, T cells, dendritic cells (DCs), monocytes/macrophages, and astrocytes. The identification of 7α, 25-OHC as a G protein-coupled receptor ligand revealed a previously unknown signaling system of oxysterols, a class of molecules which exert profound biological functions. Dysregulation of the synthesis or functions of these molecules is believed to contribute to inflammation and autoimmune diseases, cardiovascular diseases, neurodegenerative diseases, cancer as well as metabolic diseases such as diabetes, obesity, and dyslipidemia. Therefore EBI2 may represent a promising target for therapeutic interventions for human diseases.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1361", "doc_id": "15058155", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: A deficiency of vitamin B6 decreases blood levels of homocysteine.\n\nCANDIDATE_PASSAGE:\nFGF regulates TGF-β signaling and endothelial-to-mesenchymal transition via control of let-7 miRNA expression. Maintenance of normal endothelial function is critical to various aspects of blood vessel function, but its regulation is poorly understood. In this study, we show that disruption of baseline fibroblast growth factor (FGF) signaling to the endothelium leads to a dramatic reduction in let-7 miRNA levels that, in turn, increases expression of transforming growth factor (TGF)-β ligands and receptors and activation of TGF-β signaling, leading to endothelial-to-mesenchymal transition (Endo-MT). We also find that Endo-MT is an important driver of neointima formation in a murine transplant arteriopathy model and in rejection of human transplant lesions. The decline in endothelial FGF signaling input is due to the appearance of an FGF resistance state that is characterized by inflammation-dependent reduction in expression and activation of key components of the FGF signaling cascade. These results establish FGF signaling as a critical factor in maintenance of endothelial homeostasis and point to an unexpected role of Endo-MT in vascular pathology.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "37", "doc_id": "11771811", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: TMEM27 is a marker for beta cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tmem27: a cleaved and shed plasma membrane protein that stimulates pancreatic beta cell proliferation.\nABSTRACT: The signals and molecular mechanisms that regulate the replication of terminally differentiated beta cells are unknown. Here, we report the identification and characterization of transmembrane protein 27 (Tmem27, collectrin) in pancreatic beta cells. Expression of Tmem27 is reduced in Tcf1(-/-) mice and is increased in islets of mouse models with hypertrophy of the endocrine pancreas. Tmem27 forms dimers and its extracellular domain is glycosylated, cleaved and shed from the plasma membrane of beta cells. This cleavage process is beta cell specific and does not occur in other cell types. Overexpression of full-length Tmem27, but not the truncated or soluble protein, leads to increased thymidine incorporation, whereas silencing of Tmem27 using RNAi results in a reduction of cell replication. Furthermore, transgenic mice with increased expression of Tmem27 in pancreatic beta cells exhibit increased beta cell mass. Our results identify a pancreatic beta cell transmembrane protein that regulates cell growth of pancreatic islets.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"This cleavage process is beta cell specific and does not occur in other cell types.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1133, "doc_id": "24142891", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Birth-weight is positively associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Intrauterine factors and risk of breast cancer: a systematic review and meta-analysis of current evidence.\nABSTRACT: BACKGROUND Emerging evidence suggests an association between female prenatal experience and her subsequent risk of developing breast cancer. Potential underlying mechanisms include variation in amounts of maternal endogenous sex hormones and growth hormones, germ-cell mutations, formation of cancer stem-cells, and other genetic or epigenetic events. We reviewed and summarised quantitatively the available data on intrauterine exposures and risk of breast cancer. METHODS We systematically searched for studies that assessed association between perinatal factors and risk of breast cancer. We reviewed separately each of the perinatal factors, including birthweight, birth length, parental age at delivery, gestational age, intrauterine exposure to diethylstilbestrol, twin membership, maternal pre-eclampsia or eclampsia, and other factors. FINDINGS We identified 57 studies published between Oct 1, 1980, and June 21, 2007. Increased risk of breast cancer was noted with increased birthweight (relative risk [RR] 1.15 [95% CI 1.09-1.21]), birth length (1.28 [1.11-1.48]), higher maternal age (1.13 [1.02-1.25]), and paternal age (1.12 [1.05-1.19]). Decreased risk of breast cancer was noted for maternal pre-eclampsia and eclampsia (0.48 [0.30-0.78]) and twin membership (0.93 [0.87-1.00]). No association was noted between risk of breast cancer and gestational age at birth (0.95 [0.71-1.26]) or maternal diethylstilbestrol treatment (1.40 [0.86-2.28]). INTERPRETATION The intrauterine environment contributes to the predisposition of women to breast cancer in adulthood. The in-utero mechanisms responsible for such predisposition need to be elucidated.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Increased risk of breast cancer was noted with increased birthweight (relative risk [RR] 1.15 [95% CI 1.09-1.21]), birth length (1.28 [1.11-1.48]), higher maternal age (1.13 [1.02-1.25]), and paternal age (1.12 [1.05-1.19]).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 179, "doc_id": "23557241", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Vitamin D is an important factor in the relationship between calcium and parathyroid hormone.\n\nCANDIDATE_ABSTRACT:\nTITLE: Relationship between serum parathyroid hormone levels, vitamin D sufficiency, and calcium intake.\nABSTRACT: CONTEXT Adequate vitamin D status for optimum bone health has received increased recognition in recent years; however, the ideal intake is not known. Serum 25-hydroxyvitamin D is the generally accepted indicator of vitamin D status, but no universal reference level has been reached. OBJECTIVE To investigate the relative importance of high calcium intake and serum 25-hydroxyvitamin D for calcium homeostasis, as determined by serum intact parathyroid hormone (PTH). DESIGN, SETTING, AND PARTICIPANTS Cross-sectional study of 2310 healthy Icelandic adults who were divided equally into 3 age groups (30-45 years, 50-65 years, or 70-85 years) and recruited from February 2001 to January 2003. They were administered a semi-quantitative food frequency questionnaire, which assessed vitamin D and calcium intake. Participants were further divided into groups according to calcium intake (<800 mg/d, 800-1200 mg/d, and >1200 mg/d) and serum 25-hydroxyvitamin D level (<10 ng/mL, 10-18 ng/mL, and >18 ng/mL). MAIN OUTCOME MEASURE Serum intact PTH as determined by calcium intake and vitamin D. RESULTS A total of 944 healthy participants completed all parts of the study. After adjusting for relevant factors, serum PTH was lowest in the group with a serum 25-hydroxyvitamin D level of more than 18 ng/mL but highest in the group with a serum 25-hydroxyvitamin D level of less than 10 ng/mL. At the low serum 25-hydroxyvitamin D level (<10 ng/mL), calcium intake of less than 800 mg/d vs more than 1200 mg/d was significantly associated with higher serum PTH (P = .04); and at a calcium intake of more than 1200 mg/d, there was a significant difference between the lowest and highest vitamin D groups (P = .04). CONCLUSIONS As long as vitamin D status is ensured, calcium intake levels of mor [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"After adjusting for relevant factors, serum PTH was lowest in the group with a serum 25-hydroxyvitamin D level of more than 18 ng/mL but highest in the group with a serum 25-hydroxyvitamin D level of less than 10 ng/mL. At the low serum 25-hydroxyvitamin D level (<10 ng/mL), calcium intake of less than 800 mg/d vs more than 1200 mg/d was significantly associated with higher serum PTH (P = .04); and at a calcium intake of more than 1200 mg/d, there was a significant difference between the lowest and highest vitamin D groups (P = .04).\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1371, "doc_id": "16256507", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In S. cerevisiae, the absence of RNA surveillance pathways reduces sensitivity to high iron conditions.\n\nCANDIDATE_ABSTRACT:\nTITLE: Multiple RNA surveillance pathways limit aberrant expression of iron uptake mRNAs and prevent iron toxicity in S. cerevisiae.\nABSTRACT: Tight regulation of the expression of mRNAs encoding iron uptake proteins is essential to control iron homeostasis and avoid intracellular iron toxicity. We show that many mRNAs encoding iron uptake or iron mobilization proteins are expressed in iron-replete conditions in the absence of the S. cerevisiae RNase III ortholog Rnt1p or of the nuclear exosome component Rrp6p. Extended forms of these mRNAs accumulate in the absence of Rnt1p or of the 5'-->3' exonucleases Xrn1p and Rat1p, showing that multiple degradative pathways contribute to the surveillance of aberrant forms of these transcripts. RNase III-deficient cells are hypersensitive to high iron concentrations, suggesting that Rnt1p-mediated RNA surveillance is required to prevent iron toxicity. These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 566, "doc_id": "16120395", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Enhanced early production of inflammatory chemokines damages viral control in the lung.\n\nCANDIDATE_ABSTRACT:\nTITLE: Memory CD4+ T cells induce innate responses independently of pathogen\nABSTRACT: Inflammation induced by recognition of pathogen-associated molecular patterns markedly affects subsequent adaptive responses. We asked whether the adaptive immune system can also affect the character and magnitude of innate inflammatory responses. We found that the response of memory, but not naive, CD4+ T cells enhances production of multiple innate inflammatory cytokines and chemokines (IICs) in the lung and that, during influenza infection, this leads to early control of virus. Memory CD4+ T cell–induced IICs and viral control require cognate antigen recognition and are optimal when memory cells are either T helper type 1 (TH1) or TH17 polarized but are independent of interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) production and do not require activation of conserved pathogen recognition pathways. This represents a previously undescribed mechanism by which memory CD4+ T cells induce an early innate response that enhances immune protection against pathogens.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We found that the response of memory, but not naive, CD4+ T cells enhances production of multiple innate inflammatory cytokines and chemokines (IICs) in the lung and that, during influenza infection, this leads to early control of virus.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 379, "doc_id": "19005293", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Dexamethasone decreases risk of postoperative bleeding.\n\nCANDIDATE_ABSTRACT:\nTITLE: Dexamethasone and risk of nausea and vomiting and postoperative bleeding after tonsillectomy in children: a randomized trial.\nABSTRACT: CONTEXT Dexamethasone is widely used to prevent postoperative nausea and vomiting (PONV) in pediatric tonsillectomy. OBJECTIVE To assess whether dexamethasone dose-dependently reduces the risk of PONV at 24 hours after tonsillectomy. DESIGN, SETTING, AND PATIENTS Randomized placebo-controlled trial conducted among 215 children undergoing elective tonsillectomy at a major public teaching hospital in Switzerland from February 2005 to December 2007. INTERVENTIONS Children were randomly assigned to receive dexamethasone (0.05, 0.15, or 0.5 mg/kg) or placebo intravenously after induction of anesthesia. Acetaminophen-codeine and ibuprofen were given as postoperative analgesia. Follow-up continued until the 10th postoperative day. MAIN OUTCOME MEASURES The primary end point was prevention of PONV at 24 hours; secondary end points were decrease in the need for ibuprofen at 24 hours and evaluation of adverse effects. RESULTS At 24 hours, 24 of 54 participants who received placebo (44%; 95% confidence interval [CI], 31%-59%) had experienced PONV compared with 20 of 53 (38%; 95% CI, 25%-52%), 13 of 54 (24%; 95% CI, 13%-38%), and 6 of 52 (12%; 95% CI, 4%-23%) who received dexamethasone at 0.05, 0.15, and 0.5 mg/kg, respectively (P<.001 for linear trend). Children who received dexamethasone received significantly less ibuprofen. There were 26 postoperative bleeding episodes in 22 children. Two of 53 (4%; 95% CI, 0.5%-13%) children who received placebo had bleeding compared with 6 of 53 (11%; 95% CI, 4%-23%), 2 of 51 (4%; 95% CI, 0.5%-13%), and 12 of 50 (24%; 95% CI, 13%-38%) who received dexamethasone at 0.05, 0.15, and 0.5 mg/kg, respectively (P = .003). Dexamethasone, 0.5 mg/kg, was associated with the highest bleeding risk (adjusted relative risk, 6.80; 95% CI, 1.77-1 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSION In this study of children undergoing tonsillectomy, dexamethasone decreased the risk of PONV dose dependently but was associated with an increased risk of postoperative bleeding.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 338, "doc_id": "23349986", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Bone marrow cells don't contribute to adult macrophage compartments.\n\nCANDIDATE_ABSTRACT:\nTITLE: CXCR2 mediates NADPH oxidase–independent neutrophil extracellular trap formation in cystic fibrosis airway inflammation\nABSTRACT: Upon activation, neutrophils release DNA fibers decorated with antimicrobial proteins, forming neutrophil extracellular traps (NETs). Although NETs are bactericidal and contribute to innate host defense, excessive NET formation has been linked to the pathogenesis of autoinflammatory diseases. However, the mechanisms regulating NET formation, particularly during chronic inflammation, are poorly understood. Here we show that the G protein–coupled receptor (GPCR) CXCR2 mediates NET formation. Downstream analyses showed that CXCR2-mediated NET formation was independent of NADPH oxidase and involved Src family kinases. We show the pathophysiological relevance of this mechanism in cystic fibrosis lung disease, characterized by chronic neutrophilic inflammation. We found abundant NETs in airway fluids of individuals with cystic fibrosis and mouse cystic fibrosis lung disease, and NET amounts correlated with impaired obstructive lung function. Pulmonary blockade of CXCR2 by intra-airway delivery of small-molecule antagonists inhibited NET formation and improved lung function in vivo without affecting neutrophil recruitment, proteolytic activity or antibacterial host defense. These studies establish CXCR2 as a receptor mediating NADPH oxidase–independent NET formation and provide evidence that this GPCR pathway is operative and druggable in cystic fibrosis lung disease.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 184, "doc_id": "1800734", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Basophils counteract disease development in patients with systemic lupus erythematosus (SLE).\n\nCANDIDATE_ABSTRACT:\nTITLE: BASOPHILS AND THE T HELPER 2 ENVIRONMENT CAN PROMOTE THE DEVELOPMENT OF LUPUS NEPHRITIS\nABSTRACT: In systemic lupus erythematosus (SLE), self-reactive antibodies can target the kidney (lupus nephritis), leading to functional failure and possible mortality. We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice). Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis. Basophils were also present in the lymph nodes and spleen of subjects with SLE. Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 171, "doc_id": "12670680", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Neutrophil extracellular traps (NETs) are released by ANCA-stimulated neutrophils.\n\nCANDIDATE_ABSTRACT:\nTITLE: E2F-dependent histone acetylation and recruitment of the Tip60 acetyltransferase complex to chromatin in late G1.\nABSTRACT: E2F proteins can either activate or repress transcription. Following mitogenic stimulation, repressive E2F4-p130-histone deacetylase complexes dissociate from, while activating species (E2F1, -2, and -3) associate with, target promoters. Histones H3 and H4 simultaneously become hyperacetylated, but it remains unclear whether this is a prerequisite or a consequence of E2F binding. Here, we show that activating E2F species are required for hyperacetylation of target chromatin in human cells. Overexpression of a dominant-negative (DN) E2F1 mutant in serum-stimulated T98G cells blocked all E2F binding, H4 acetylation, and, albeit partially, H3 acetylation. Target gene activation and S-phase entry were also blocked by DN E2F1. Conversely, ectopic activation of E2F1 rapidly induced H3 and H4 acetylation, demonstrating a direct role for E2F in these events. E2F1 was previously shown to bind the histone acetyltransferases (HATs) p300/CBP and PCAF/GCN5. In our hands, ectopically expressed E2F1 also bound the unrelated HAT Tip60 and induced recruitment of five subunits of the Tip60 complex (Tip60, TRRAP, p400, Tip48, and Tip49) to target promoters in vivo. Moreover, E2F-dependent recruitment of Tip60 to chromatin occurred in late G(1) following serum stimulation. We speculate that the activities of multiple HAT complexes account for E2F-dependent acetylation, transcription, and S-phase entry.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 845, "doc_id": "502591", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Consumption of whole fruits increases the risk of type 2 diabetes.\n\nCANDIDATE_PASSAGE:\nSugar-sweetened beverages, weight gain, and incidence of type 2 diabetes in young and middle-aged women. CONTEXT Sugar-sweetened beverages like soft drinks and fruit punches contain large amounts of readily absorbable sugars and may contribute to weight gain and an increased risk of type 2 diabetes, but these relationships have been minimally addressed in adults. OBJECTIVE To examine the association between consumption of sugar-sweetened beverages and weight change and risk of type 2 diabetes in women. DESIGN, SETTING, AND PARTICIPANTS Prospective cohort analyses conducted from 1991 to 1999 among women in the Nurses' Health Study II. The diabetes analysis included 91,249 women free of diabetes and other major chronic diseases at baseline in 1991. The weight change analysis included 51,603 women for whom complete dietary information and body weight were ascertained in 1991, 1995, and 1999. We identified 741 incident cases of confirmed type 2 diabetes during 716,300 person-years of follow-up. MAIN OUTCOME MEASURES Weight gain and incidence of type 2 diabetes. RESULTS Those with stable consumption patterns had no difference in weight gain, but weight gain over a 4-year period was highest among women who increased their sugar-sweetened soft drink consumption from 1 or fewer drinks per week to 1 or more drinks per day (multivariate-adjusted means, 4.69 kg for 1991 to 1995 and 4.20 kg for 1995 to 1999) and was smallest among women who decreased their intake (1.34 and 0.15 kg for the 2 periods, respectively) after adjusting for lifestyle and dietary confounders. Increased consumption of fruit punch was also associated with greater weight gain compared with decreased consumption. After adjustment for potential confounders, women consuming 1 or more sugar-sweetened s [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "283", "doc_id": "9822397", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does rugby headgear prevent concussion?\n\nABSTRACT:\nTo examine the attitudes of players and coaches to the use of protective headgear, particularly with respect to the prevention of concussion. A questionnaire designed to assess attitudes to headgear was administered to 63 players from four different Canadian teams, each representing a different level of play (high school, university, community club, national). In addition, coaches from all four levels were questioned about team policies and their personal opinions about the use of headgear to prevent concussion. Although the players tended to believe that the headgear could prevent concussion (62%), the coaches were less convinced (33%). Despite the players' belief that headgear offers protection against concussion, only a minority reported wearing headgear (27%) and few (24%) felt that its use should be made mandatory. Common reasons for not wearing headgear were \"its use is not mandatory\", \"it is uncomfortable\", and \"it costs too much\".", "output": "{\"label\": \"maybe\", \"rationale\": \"Although most players in the study believe that rugby headgear may prevent concussion, only a minority reported wearing it. Coaches tended to be less convinced than the players that rugby headgear can prevent concussion.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 11867487, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Persister cells provide relapse resistance in cancer patients.\n\nCANDIDATE_PASSAGE:\nHeterogeneity Underlies the Emergence of EGFRT790 Wild-Type Clones Following Treatment of T790M-Positive Cancers with a Third-Generation EGFR Inhibitor. UNLABELLED Rociletinib is a third-generation EGFR inhibitor active in lung cancers with T790M, the gatekeeper mutation underlying most first-generation EGFR drug resistance. We biopsied patients at rociletinib progression to explore resistance mechanisms. Among 12 patients with T790M-positive cancers at rociletinib initiation, six had T790-wild-type rociletinib-resistant biopsies. Two T790-wild-type cancers underwent small cell lung cancer transformation; three T790M-positive cancers acquired EGFR amplification. We documented T790-wild-type and T790M-positive clones coexisting within a single pre-rociletinib biopsy. The pretreatment fraction of T790M-positive cells affected response to rociletinib. Longitudinal circulating tumor DNA (ctDNA) analysis revealed an increase in plasma EGFR-activating mutation, and T790M heralded rociletinib resistance in some patients, whereas in others the activating mutation increased but T790M remained suppressed. Together, these findings demonstrate the role of tumor heterogeneity when therapies targeting a singular resistance mechanism are used. To further improve outcomes, combination regimens that also target T790-wild-type clones are required. SIGNIFICANCE This report documents that half of T790M-positive EGFR-mutant lung cancers treated with rociletinib are T790-wild-type upon progression, suggesting that T790-wild-type clones can emerge as the dominant source of resistance. We show that tumor heterogeneity has important clinical implications and that plasma ctDNA analyses can sometimes predict emerging resistance mechanisms.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "938", "doc_id": "9498458", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is preoperative smoking associated with early graft failure after infrainguinal bypass surgery?\n\nABSTRACT:\nSmoking has been implicated as the single most important risk factor for the development of peripheral arterial disease. Whereas previous studies have found poor long-term outcomes in smokers undergoing lower extremity bypass, there is a lack of consistent reports describing the effects of persistent tobacco abuse on early outcomes after infrainguinal bypass. The American College of Surgeons National Surgical Quality Improvement Program database from 2005 to 2011 was queried for primary infrainguinal bypasses. A bivariate analysis was done to assess preoperative and intraoperative risk factors for the primary outcome of 30-day graft failure comparing active smokers with nonsmokers, defined as patients who did not smoke within the 12 months before surgery. Multivariable logistic regression was conducted to assess the independent association of active smoking with graft failure. In 6614 (40.0%) active smokers and 9920 (60.0%) nonsmokers, 16,534 infrainguinal bypasses were performed. Active smokers were more likely to be younger, male, and of nonwhite race and to have a history of chronic obstructive pulmonary disease (P < .001, all). Nonsmokers were more likely to be functionally dependent and had significantly more comorbidities (ie, hypertension, diabetes, obesity, congestive heart failure, history of previous cardiac surgery or intervention, and dialysis; P < .001, all). The presence of critical limb ischemia was similar in both groups (53.1% of active smokers vs 53.5% of nonsmokers; P = .61). More nonsmokers received a tibial-level bypass than did active smokers (47.8% vs 33.9%; P < .001). There was a trend toward increased early graft failure in active smokers compared with nonsmokers (5.3% vs 4.7%; P = .08). With adjustment for other variables, especiall [TRUNCATED]", "output": "{\"label\": \"yes\", \"rationale\": \"Although nonsmokers were significantly older, had more comorbidities, and required more distal revascularization, active smokers still had an increased risk for development of early graft failure. These results stress the need for immediate smoking cessation before lower extremity bypass. Further research is warranted to determine an optimal period of abstinence among smokers with peripheral arterial disease to reduce their risk for early graft failure.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 24502815, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Surgical management of the atherosclerotic ascending aorta: is endoaortic balloon occlusion safe?\n\nABSTRACT:\nOcclusion of the atherosclerotic ascending aorta by an endoaortic inflatable balloon has been proposed as an alternative to conventional cross-clamping to prevent injury to the vessel and distal embolization of debris. The safety and the effectiveness of endoaortic occlusion have not been documented in this setting. Endoaortic occlusion was employed in 52 of 2,172 consecutive patients. Surgeon's choice was based on preoperative identification of aortic calcifications or intraoperative epiaortic ultrasonographic scanning. Deaths and strokes were analyzed casewise and in aggregate. In 10 patients (19.2%), the endoaortic balloon had to be replaced by the ordinary cross-clamp because of incomplete occlusion (n = 5), hindered exposure (n = 2), or balloon rupture (n = 3). In-hospital death occurred in 13 patients (25%), and stroke on awakening from anesthesia in 2 (3.8%). The death rate of patients treated by endoaortic occlusion was significantly higher compared with all other patients (4.2%, p<0.0001) and with the expected estimate by European System for Cardiac Operative Risk Evaluation (10.5%, p = 0.05). By multivariable analysis, use of endoaortic occlusion was independently associated with in-hospital death (odds ratio = 5.609, 95% confidence interval: 2.684 to 11.719). Although the stroke rate was higher in the endoaortic occlusion group compared with all other patients, the difference was only possibly significant (3.8% versus 0.8%, p = 0.067).", "output": "{\"label\": \"no\", \"rationale\": \"In this series, the endoaortic occlusion was frequently ineffective, and was associated with a significantly higher risk of in-hospital death and a numerically higher risk of stroke.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 17062234, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Stroke patients with prior use of direct oral anticoagulants have a higher risk of in-hospital mortality than stroke patients with prior use of warfarin.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association of Intracerebral Hemorrhage Among Patients Taking Non–Vitamin K Antagonist vs Vitamin K Antagonist Oral Anticoagulants With In-Hospital Mortality\nABSTRACT: Importance Although non–vitamin K antagonist oral anticoagulants (NOACs) are increasingly used to prevent thromboembolic disease, there are limited data on NOAC-related intracerebral hemorrhage (ICH). Objective To assess the association between preceding oral anticoagulant use (warfarin, NOACs, and no oral anticoagulants [OACs]) and in-hospital mortality among patients with ICH. Design, Setting, and Participants Retrospective cohort study of 141 311 patients with ICH admitted from October 2013 to December 2016 to 1662 Get With The Guidelines–Stroke hospitals. Exposures Anticoagulation therapy before ICH, defined as any use of OACs within 7 days prior to hospital arrival. Main Outcomes and Measures In-hospital mortality. Results Among 141 311 patients with ICH (mean [SD] age, 68.3 [15.3] years; 48.1% women), 15 036 (10.6%) were taking warfarin and 4918 (3.5%) were taking NOACs preceding ICH, and 39 585 (28.0%) and 5783 (4.1%) were taking concomitant single and dual antiplatelet agents, respectively. Patients with prior use of warfarin or NOACs were older and had higher prevalence of atrial fibrillation and prior stroke. Acute ICH stroke severity (measured by the National Institutes of Health Stroke Scale) was not significantly different across the 3 groups (median, 9 [interquartile range, 2-21] for warfarin, 8 [2-20] for NOACs, and 8 [2-19] for no OACs). The unadjusted in-hospital mortality rates were 32.6% for warfarin, 26.5% for NOACs, and 22.5% for no OACs. Compared with patients without prior use of OACs, the risk of in-hospital mortality was higher among patients with prior use of warfarin (adjusted risk difference [ARD], 9.0% [97.5% CI, 7.9% to 10.1%]; adjusted odds ratio [AOR], 1.62 [97.5% CI, 1.53 to 1.71]) and higher among patients with prior use of [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The unadjusted in-hospital mortality rates were 32.6% for warfarin, 26.5% for NOACs, and 22.5% for no OACs.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1103, "doc_id": "3898784", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Clathrin stabilizes the spindle fiber apparatus during mitosis.\n\nCANDIDATE_PASSAGE:\nClathrin is required for the function of the mitotic spindle Clathrin has an established function in the generation of vesicles that transfer membrane and proteins around the cell. The formation of clathrin-coated vesicles occurs continuously in non-dividing cells, but is shut down during mitosis, when clathrin concentrates at the spindle apparatus. Here, we show that clathrin stabilizes fibres of the mitotic spindle to aid congression of chromosomes. Clathrin bound to the spindle directly by the amino-terminal domain of clathrin heavy chain. Depletion of clathrin heavy chain using RNA interference prolonged mitosis; kinetochore fibres were destabilized, leading to defective congression of chromosomes to the metaphase plate and persistent activation of the spindle checkpoint. Normal mitosis was rescued by clathrin triskelia but not the N-terminal domain of clathrin heavy chain, indicating that stabilization of kinetochore fibres was dependent on the unique structure of clathrin. The importance of clathrin for normal mitosis may be relevant to understanding human cancers that involve gene fusions of clathrin heavy chain.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "265", "doc_id": "2033917", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: There is a positive correlation between hip fractures and statin use.\n\nCANDIDATE_ABSTRACT:\nTITLE: HMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients.\nABSTRACT: CONTEXT Recent animal studies have found that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) lipid-lowering drugs (statins) substantially increase bone formation, but whether statin use in humans results in clinically meaningful bone formation or a reduction in the risk of osteoporotic fractures is not known. OBJECTIVE To determine whether the use of statins is associated with reduced hip fracture risk. DESIGN Case-control study. SETTING AND PATIENTS A total of 6110 New Jersey residents aged 65 years or older and enrolled in Medicare and either Medicaid or the Pharmacy Assistance for the Aged and Disabled program. Case patients (n=1222) underwent surgical repair of a hip fracture in 1994. Control patients (n=4888) were identified at a ratio of 4:1 and frequency-matched to case patients for age and sex. MAIN OUTCOME MEASURE Adjusted odds ratio (OR) of hip fracture by statin use in the 180 days and 3 years prior to the index date (the earliest date of admission for surgery), adjusted for demographic and clinical characteristics and health care utilization. RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus. No significant relationship was observed between use of nonstatin lipid-lowering agents and hip fracture risk. Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowe [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1288, "doc_id": "4687948", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Rhythmic expression of Cry1 translates directly into a circadian regulation of cAMP signaling in hepatic glucose metabolism.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cryptochrome Mediates Circadian Regulation of cAMP Signaling and Hepatic Gluconeogenesis\nABSTRACT: During fasting, mammals maintain normal glucose homeostasis by stimulating hepatic gluconeogenesis. Elevations in circulating glucagon and epinephrine, two hormones that activate hepatic gluconeogenesis, trigger the cAMP-mediated phosphorylation of cAMP response element-binding protein (Creb) and dephosphorylation of the Creb-regulated transcription coactivator-2 (Crtc2)--two key transcriptional regulators of this process. Although the underlying mechanism is unclear, hepatic gluconeogenesis is also regulated by the circadian clock, which coordinates glucose metabolism with changes in the external environment. Circadian control of gene expression is achieved by two transcriptional activators, Clock and Bmal1, which stimulate cryptochrome (Cry1 and Cry2) and Period (Per1, Per2 and Per3) repressors that feed back on Clock-Bmal1 activity. Here we show that Creb activity during fasting is modulated by Cry1 and Cry2, which are rhythmically expressed in the liver. Cry1 expression was elevated during the night-day transition, when it reduced fasting gluconeogenic gene expression by blocking glucagon-mediated increases in intracellular cAMP concentrations and in the protein kinase A-mediated phosphorylation of Creb. In biochemical reconstitution studies, we found that Cry1 inhibited accumulation of cAMP in response to G protein-coupled receptor (GPCR) activation but not to forskolin, a direct activator of adenyl cyclase. Cry proteins seemed to modulate GPCR activity directly through interaction with G(s)α. As hepatic overexpression of Cry1 lowered blood glucose concentrations and improved insulin sensitivity in insulin-resistant db/db mice, our results suggest that compounds that enhance cryptochrome activity may provide therapeutic benefit to individuals with type 2 diabetes.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Cry1 expression was elevated during the night-day transition, when it reduced fasting gluconeogenic gene expression by blocking glucagon-mediated increases in intracellular cAMP concentrations and in the protein kinase A-mediated phosphorylation of Creb.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1045, "doc_id": "22500262", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Integrated care is ineffective at tackling multiple comorbidities.\n\nCANDIDATE_ABSTRACT:\nTITLE: Functional outcomes of multi-condition collaborative care and successful ageing: results of randomised trial\nABSTRACT: OBJECTIVE To evaluate the effectiveness of integrated care for chronic physical diseases and depression in reducing disability and improving quality of life. DESIGN A randomised controlled trial of multi-condition collaborative care for depression and poorly controlled diabetes and/or risk factors for coronary heart disease compared with usual care among middle aged and elderly people SETTING Fourteen primary care clinics in Seattle, Washington. PARTICIPANTS Patients with diabetes or coronary heart disease, or both, and blood pressure above 140/90 mm Hg, low density lipoprotein concentration >3.37 mmol/L, or glycated haemoglobin 8.5% or higher, and PHQ-9 depression scores of ≥ 10. INTERVENTION A 12 month intervention to improve depression, glycaemic control, blood pressure, and lipid control by integrating a \"treat to target\" programme for diabetes and risk factors for coronary heart disease with collaborative care for depression. The intervention combined self management support, monitoring of disease control, and pharmacotherapy to control depression, hyperglycaemia, hypertension, and hyperlipidaemia. MAIN OUTCOME MEASURES Social role disability (Sheehan disability scale), global quality of life rating, and World Health Organization disability assessment schedule (WHODAS-2) scales to measure disabilities in activities of daily living (mobility, self care, household maintenance). RESULTS Of 214 patients enrolled (106 intervention and 108 usual care), disability and quality of life measures were obtained for 97 intervention patients at six months (92%) and 92 at 12 months (87%), and for 96 usual care patients at six months (89%) and 92 at 12 months (85%). Improvements from baseline on the Sheehan disability scale (-0.9, 95% confidence interval -1.5 to -0.2; [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"There was a trend toward greater improvement in disabilities in activities of daily living (-1.5, -3.3 to 0.4; P = 0.10).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 647, "doc_id": "15041758", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Reduction of Rpl38 alters the composition of the Hox gene mRNAs translation in mice without lowering overall protein synthesis.\n\nCANDIDATE_PASSAGE:\nRibosome-Mediated Specificity in Hox mRNA Translation and Vertebrate Tissue Patterning Historically, the ribosome has been viewed as a complex ribozyme with constitutive rather than regulatory capacity in mRNA translation. Here we identify mutations of the Ribosomal Protein L38 (Rpl38) gene in mice exhibiting surprising tissue-specific patterning defects, including pronounced homeotic transformations of the axial skeleton. In Rpl38 mutant embryos, global protein synthesis is unchanged; however the translation of a select subset of Homeobox mRNAs is perturbed. Our data reveal that RPL38 facilitates 80S complex formation on these mRNAs as a regulatory component of the ribosome to confer transcript-specific translational control. We further show that Rpl38 expression is markedly enriched in regions of the embryo where loss-of-function phenotypes occur. Unexpectedly, a ribosomal protein (RP) expression screen reveals dynamic regulation of individual RPs within the vertebrate embryo. Collectively, these findings suggest that RP activity may be highly regulated to impart a new layer of specificity in the control of gene expression and mammalian development.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1031", "doc_id": "12486491", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Sympathetic nerve activity is reduced throughout normal pregnancy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Regulation of sympathetic nerve activity during the cold pressor test in normotensive pregnant and nonpregnant women.\nABSTRACT: Baseline neurovascular transduction is reduced in normotensive pregnancy; however, little is known about changes to neurovascular transduction during periods of heightened sympathetic activation. We tested the hypothesis that, despite an exacerbated muscle sympathetic nerve activity (microneurography) response to cold pressor stimulation, the blunting of neurovascular transduction in normotensive pregnant women would result in similar changes in vascular resistance and mean arterial pressure (Finometer) relative to nonpregnant controls. Baseline neurovascular transduction was reduced in pregnant women relative to controls when expressed as the quotient of both total resistance and mean arterial pressure and sympathetic burst frequency (0.32±0.07 versus 0.58±0.16 mm Hg/L/min/bursts/min, P<0.001 and 2.4±0.7 versus 3.6±0.8 mm Hg/bursts/min, P=0.001). Sympathetic activation was greater across all 3 minutes of cold pressor stimulation in the pregnant women relative to the nonpregnant controls. Peak sympathoexcitation was also greater in pregnant than in nonpregnant women, whether expressed as sympathetic burst frequency (+17±13 versus +7±8 bursts/min, P=0.049), burst incidence (+17±9 versus +6±11 bursts/100 hb, P=0.03), or total activity (+950±660 versus +363±414 arbitrary units, P=0.04). However, neurovascular transduction during peak cold pressor-induced sympathoexcitation remained blunted in pregnant women (0.25±0.11 versus 0.45±0.08 mm Hg/L/min/bursts/min, P<0.001 and 1.9±1.0 versus 3.2±0.9 mm Hg/bursts/min, P=0.006). Therefore, mean arterial pressure (93±21 versus 99±6 mm Hg, P=0.4) and total peripheral resistance (12±3 versus 14±3 mm Hg/L/min) were not different between pregnant and nonpregnant women during peak sympathoexcitation. These data indicate that [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Sympathetic activation was greater across all 3 minutes of cold pressor stimulation in the pregnant women relative to the nonpregnant controls.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1120, "doc_id": "13907928", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Tirasemtiv has no effect on cardiac muscle.\n\nCANDIDATE_PASSAGE:\nBCL-6 represses genes that function in lymphocyte differentiation, inflammation, and cell cycle control. BCL-6, a transcriptional repressor frequently translocated in lymphomas, regulates germinal center B cell differentiation and inflammation. DNA microarray screening identified genes repressed by BCL-6, including many lymphocyte activation genes, suggesting that BCL-6 modulates B cell receptor signals. BCL-6 repression of two chemokine genes, MIP-1alpha and IP-10, may also attenuate inflammatory responses. Blimp-1, another BCL-6 target, is important for plasmacytic differentiation. Since BCL-6 expression is silenced in plasma cells, repression of blimp-1 by BCL-6 may control plasmacytic differentiation. Indeed, inhibition of BCL-6 function initiated changes indicative of plasmacytic differentiation, including decreased expression of c-Myc and increased expression of the cell cycle inhibitor p27kip1. These data suggest that malignant transformation by BCL-6 involves inhibition of differentiation and enhanced proliferation.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1302", "doc_id": "16550075", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Birth-weight is positively associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Birth Size and Breast Cancer Risk: Re-analysis of Individual Participant Data from 32 Studies\nABSTRACT: BACKGROUND Birth size, perhaps a proxy for prenatal environment, might be a correlate of subsequent breast cancer risk, but findings from epidemiological studies have been inconsistent. We re-analysed individual participant data from published and unpublished studies to obtain more precise estimates of the magnitude and shape of the birth size-breast cancer association. METHODS AND FINDINGS Studies were identified through computer-assisted and manual searches, and personal communication with investigators. Individual participant data from 32 studies, comprising 22,058 breast cancer cases, were obtained. Random effect models were used, if appropriate, to combine study-specific estimates of effect. Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003). Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data. Birth length and head circumference from birth records were also positively associated with breast cancer risk (pooled RR per one SD increment: 1.06 [95% CI 1.03-1.10] and 1.09 [95% CI 1.03-1.15], respectively). Simultaneous adjustment for these three birth size variables showed that length was the strongest independent predictor of risk. The birth size effec [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 179, "doc_id": "16322674", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Pyridostatin decreases telomere fragility in BRCA2-deficient cells.\n\nCANDIDATE_PASSAGE:\nThe BLM helicase contributes to telomere maintenance through processing of late-replicating intermediate structures Werner's syndrome (WS) and Bloom's syndrome (BS) are cancer predisposition disorders caused by loss of function of the RecQ helicases WRN or BLM, respectively. BS and WS are characterized by replication defects, hyperrecombination events and chromosomal aberrations, which are hallmarks of cancer. Inefficient replication of the G-rich telomeric strand contributes to chromosome aberrations in WS cells, demonstrating a link between WRN, telomeres and genomic stability. Herein, we provide evidence that BLM also contributes to chromosome-end maintenance. Telomere defects (TDs) are observed in BLM-deficient cells at an elevated frequency, which is similar to cells lacking a functional WRN helicase. Loss of both helicases exacerbates TDs and chromosome aberrations, indicating that BLM and WRN function independently in telomere maintenance. BLM localization, particularly its recruitment to telomeres, changes in response to replication dysfunction, such as in WRN-deficient cells or after aphidicolin treatment. Exposure to replication challenge causes an increase in decatenated deoxyribonucleic acid (DNA) structures and late-replicating intermediates (LRIs), which are visible as BLM-covered ultra-fine bridges (UFBs) in anaphase. A subset of UFBs originates from telomeric DNA and their frequency correlates with telomere replication defects. We propose that the BLM complex contributes to telomere maintenance through its activity in resolving LRIs.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "990", "doc_id": "2679511", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The severity of cardiac involvement in amyloidosis can be described by the degree of transmurality of late gadolinium enhancement in MRI.\n\nCANDIDATE_ABSTRACT:\nTITLE: Prognostic Value of Late Gadolinium Enhancement Cardiovascular Magnetic Resonance in Cardiac Amyloidosis\nABSTRACT: BACKGROUND The prognosis and treatment of the 2 main types of cardiac amyloidosis, immunoglobulin light chain (AL) and transthyretin (ATTR) amyloidosis, are substantially influenced by cardiac involvement. Cardiovascular magnetic resonance with late gadolinium enhancement (LGE) is a reference standard for the diagnosis of cardiac amyloidosis, but its potential for stratifying risk is unknown. METHODS AND RESULTS Two hundred fifty prospectively recruited subjects, 122 patients with ATTR amyloid, 9 asymptomatic mutation carriers, and 119 patients with AL amyloidosis, underwent LGE cardiovascular magnetic resonance. Subjects were followed up for a mean of 24±13 months. LGE was performed with phase-sensitive inversion recovery (PSIR) and without (magnitude only). These were compared with extracellular volume measured with T1 mapping. PSIR was superior to magnitude-only inversion recovery LGE because PSIR always nulled the tissue (blood or myocardium) with the longest T1 (least gadolinium). LGE was classified into 3 patterns: none, subendocardial, and transmural, which were associated with increasing amyloid burden as defined by extracellular volume (P<0.0001), with transitions from none to subendocardial LGE at an extracellular volume of 0.40 to 0.43 (AL) and 0.39 to 0.40 (ATTR) and to transmural at 0.48 to 0.55 (AL) and 0.47 to 0.59 (ATTR). Sixty-seven patients (27%) died. Transmural LGE predicted death (hazard ratio, 5.4; 95% confidence interval, 2.1-13.7; P<0.0001) and remained independent after adjustment for N-terminal pro-brain natriuretic peptide, ejection fraction, stroke volume index, E/E', and left ventricular mass index (hazard ratio, 4.1; 95% confidence interval, 1.3-13.1; P<0.05). CONCLUSIONS There is a continuum of cardiac involvement in systemic A [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Transmural LGE is determined reliably by PSIR and represents advanced cardiac amyloidosis.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1271, "doc_id": "13768432", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Removal of H3K9me3 by ectopic expression of other H3K9 demethylases improves reprogramming efficiency in SCNT experiments.\n\nCANDIDATE_PASSAGE:\nHistone Methylation-Dependent Mechanisms Impose Ligand Dependency for Gene Activation by Nuclear Receptors Nuclear receptors undergo ligand-dependent conformational changes that are required for corepressor-coactivator exchange, but whether there is an actual requirement for specific epigenetic landmarks to impose ligand dependency for gene activation remains unknown. Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases (HMTs) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals. This strategy, based at least in part on an HMT-dependent inhibitory histone code, imposes a requirement for specific histone demethylases, including LSD1, to permit ligand- and signal-dependent activation of regulated gene expression. These events link an inhibitory methylation component of the histone code to a broadly used strategy that circumvents pathological constitutive gene induction by physiologically regulated transcription factors.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1035", "doc_id": "13639330", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: A deficiency of vitamin B6 decreases blood levels of homocysteine.\n\nCANDIDATE_ABSTRACT:\nTITLE: Randomized trial of folic acid supplementation and serum homocysteine levels.\nABSTRACT: BACKGROUND Lowering serum homocysteine levels with folic acid is expected to reduce mortality from ischemic heart disease. Homocysteine reduction is known to be maximal at a folic acid dosage of 1 mg/d, but the effect of lower doses (relevant to food fortification) is unclear. METHODS We randomized 151 patients with ischemic heart disease to 1 of 5 dosages of folic acid (0.2, 0.4, 0.6, 0.8, and 1.0 mg/d) or placebo. Fasting blood samples for serum homocysteine and serum folate analysis were taken initially, after 3 months of supplementation, and 3 months after folic acid use was discontinued. RESULTS Median serum homocysteine level decreased with increasing folic acid dosage, to a maximum at 0.8 mg of folic acid per day, when the homocysteine reduction (placebo adjusted) was 2.7 micromol/L (23%), similar to the known effect of folic acid dosages of 1 mg/d and above. The higher a person's initial serum homocysteine level, the greater was the response to folic acid, but there were statistically significant reductions regardless of the initial level. Serum folate level increased approximately linearly (5.5 nmol/L for every 0.1 mg of folic acid). Within-person fluctuations over time in serum homocysteine levels, measured in the placebo group, were large compared with the effect of folic acid, indicating that monitoring of the reduction in an individual is impractical. CONCLUSIONS A dosage of folic acid of 0.8 mg/d appears necessary to achieve the maximum reduction in serum homocysteine level across the range of homocysteine levels in the population. Current US food fortification levels will achieve only a small proportion of the achievable homocysteine reduction.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 37, "doc_id": "11705328", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Higher plasma levels of I-carnitine, when associated with trimethylamine N-oxide, are negatively correlated with cardiovascular events in humans.\n\nCANDIDATE_PASSAGE:\nAging, habitual exercise, and dynamic arterial compliance. BACKGROUND A reduction in compliance of the large-sized cardiothoracic (central) arteries is an independent risk factor for the development of cardiovascular disease with advancing age. METHODS AND RESULTS We determined the role of habitual exercise on the age-related decrease in central arterial compliance by using both cross-sectional and interventional approaches. First, we studied 151 healthy men aged 18 to 77 years: 54 were sedentary, 45 were recreationally active, and 53 were endurance exercise-trained. Central arterial compliance (simultaneous B-mode ultrasound and arterial applanation tonometry on the common carotid artery) was lower (P:<0.05) in middle-aged and older men than in young men in all 3 groups. There were no significant differences between sedentary and recreationally active men at any age. However, arterial compliance in the endurance-trained middle-aged and older men was 20% to 35% higher than in the 2 less active groups (P:<0.01). As such, age-related differences in central arterial compliance were smaller in the endurance-trained men than in the sedentary and recreationally active men. Second, we studied 20 middle-aged and older (53+/-2 years) sedentary healthy men before and after a 3-month aerobic exercise intervention (primarily walking). Regular exercise increased central arterial compliance (P:<0.01) to levels similar to those of the middle-aged and older endurance-trained men. These effects were independent of changes in body mass, adiposity, arterial blood pressure, or maximal oxygen consumption. CONCLUSIONS Regular aerobic-endurance exercise attenuates age-related reductions in central arterial compliance and restores levels in previously sedentary healthy middle-aged [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "523", "doc_id": "752423", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Varying expression levels of EBI2 affect the positioning and migration of B cells.\n\nCANDIDATE_PASSAGE:\nA role for fibroblasts in mediating the effects of tobacco-induced epithelial cell growth and invasion. Cigarette smoke and smokeless tobacco extracts contain multiple carcinogenic compounds, but little is known about the mechanisms by which tumors develop and progress upon chronic exposure to carcinogens such as those present in tobacco products. Here, we examine the effects of smokeless tobacco extracts on human oral fibroblasts. We show that smokeless tobacco extracts elevated the levels of intracellular reactive oxygen, oxidative DNA damage, and DNA double-strand breaks in a dose-dependent manner. Extended exposure to extracts induced fibroblasts to undergo a senescence-like growth arrest, with striking accompanying changes in the secretory phenotype. Using cocultures of smokeless tobacco extracts-exposed fibroblasts and immortalized but nontumorigenic keratinocytes, we further show that factors secreted by extracts-modified fibroblasts increase the proliferation and invasiveness of partially transformed epithelial cells, but not their normal counterparts. In addition, smokeless tobacco extracts-exposed fibroblasts caused partially transformed keratinocytes to lose the expression of E-cadherin and ZO-1, as well as involucrin, changes that are indicative of compromised epithelial function and commonly associated with malignant progression. Together, our results suggest that fibroblasts may contribute to tumorigenesis indirectly by increasing epithelial cell aggressiveness. Thus, tobacco may not only initiate mutagenic changes in epithelial cells but also promote the growth and invasion of mutant cells by creating a procarcinogenic stromal environment.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1361", "doc_id": "1192458", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Having a main partner worsens HIV outcomes.\n\nCANDIDATE_PASSAGE:\nStable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study. OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART). DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study). SETTING Seven outpatient clinics throughout Switzerland. PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years). MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound. RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion. When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership. In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without. Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression. CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patien [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "498", "doc_id": "17077004", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: PD-1 triggering on monocytes enhances IL-10 production by monocytes.\n\nCANDIDATE_PASSAGE:\nBASOPHILS AND THE T HELPER 2 ENVIRONMENT CAN PROMOTE THE DEVELOPMENT OF LUPUS NEPHRITIS In systemic lupus erythematosus (SLE), self-reactive antibodies can target the kidney (lupus nephritis), leading to functional failure and possible mortality. We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice). Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis. Basophils were also present in the lymph nodes and spleen of subjects with SLE. Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "902", "doc_id": "12670680", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Sympathetic nerve activity is reduced throughout normal pregnancy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Sympathetic neural mechanisms in normal and hypertensive pregnancy in humans.\nABSTRACT: BACKGROUND Direct recordings from peripheral sympathetic nerves have shown an increased sympathetic drive in pregnancy-induced hypertension (PIH) and preeclampsia (PE). It is unknown whether sympathetic drive is altered in normal pregnancy, when arterial blood pressure can be normal or relatively low. The aim of this study was to measure and compare peripheral sympathetic discharge, its vasoconstrictor effect and its baroreceptor control, during pregnancy and postpartum in women with normal pregnancy (NP) and PIH and in normotensive nonpregnant (NN) women. METHODS AND RESULTS Twenty-one women with NP, 18 women with PIH, and 21 NN women had muscle sympathetic nerve activity assessed from multiunit discharges (MSNA) and from single units with defined vasoconstrictor properties (s-MSNA). The s-MSNA in NP (38+/-6.6 impulses/100 beats) was greater (P<0.05) than in NN women (19+/-1.8 impulses/100 beats) despite similar age and body weight but less than in PIH women (P<0.001) (146+/-23.5 impulses/100 beats). MSNA followed a similar trend. Cardiac baroreceptor reflex sensitivity (BRS) was impaired in NP and PIH women relative to NN. After delivery, sympathetic activity decreased to values similar to those obtained in NN, and there was an increase in BRS. In women with NP, the decrease in sympathetic output occurred despite an insignificant change in blood pressure. CONCLUSIONS Central sympathetic output was increased in women with normal pregnancy and was even greater in the hypertensive pregnant group. The findings suggest that the moderate sympathetic hyperactivity during the latter months of normal pregnancy may help to return the arterial pressure to nonpregnant levels, although when the increase in activity is excessive, hypertension may ensue.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The s-MSNA in NP (38+/-6.6 impulses/100 beats) was greater (P<0.05) than in NN women (19+/-1.8 impulses/100 beats) despite similar age and body weight but less than in PIH women (P<0.001) (146+/-23.5 impulses/100 beats).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1120, "doc_id": "5323845", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Increased microtubule acetylation worsens interference of axonal transport caused by LRRK2 Roc-COR domain mutations.\n\nCANDIDATE_PASSAGE:\nThe Ran GTPase regulates mitotic spindle assembly Ran is an abundant nuclear GTPase with a clear role in nuclear transport during interphase but with roles in mitotic regulation that are less well understood. The nucleotide-binding state of Ran is regulated by a GTPase activating protein, RanGAP1, and by a guanine nucleotide exchange factor, RCC1. Ran also interacts with a guanine nucleotide dissociation inhibitor, RanBP1. RanBP1 has a high affinity for GTP-bound Ran, and it acts as a cofactor for RanGAP1, increasing the rate of GAP-mediated GTP hydrolysis on Ran approximately tenfold. RanBP1 levels oscillate during the cell cycle [4], and increased concentrations of RanBP1 prolong mitosis in mammalian cells and in Xenopus egg extracts (our unpublished observations). We investigated how increased concentrations of RanBP1 disturb mitosis. We found that spindle assembly is dramatically disrupted when exogenous RanBP1 is added to M phase Xenopus egg extracts. We present evidence that the role of Ran in spindle assembly is independent of nuclear transport and is probably mediated through changes in microtubule dynamics.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "615", "doc_id": "14119470", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Gastric infection with Helicobacter pylori increases risk of gastric cancer in humans.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association between infection with Helicobacter pylori and risk of gastric cancer: evidence from a prospective investigation.\nABSTRACT: OBJECTIVE To investigate the association between gastric cancer and prior infection with Helicobacter pylori. DESIGN Case-control comparison of prevalence of IgG antibodies to H pylori in blood samples collected prospectively, before diagnosis of gastric cancer in the cases. Presence of H pylori antibody (greater than 10 micrograms IgG/ml) determined by enzyme linked immunosorbent assay (ELISA). SUBJECTS 29 men with a subsequent diagnosis of gastric cancer and 116 aged matched controls selected from over 22,000 middle aged men participating in two ongoing cohort studies (the British United Provident Association study and the Caerphilly collaborative heart disease study), who had provided blood samples during 1975-1982. RESULTS 20 of the 29 cases (69%) and 54 of the 116 controls (47%) were positive for H pylori specific antibody. The median specific IgG concentration was significantly higher in the cases than controls (90 micrograms/ml v 3.6 micrograms/ml, p less than 0.01). The estimated odds ratio for the risk of gastric cancer in those with a history of infection with H pylori was 2.77 (95% confidence interval 1.04 to 7.97, 2p = 0.039). CONCLUSIONS H pylori infection may be an important cause of gastric cancer; between 35% and 55% of all cases may be associated with such an infection.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS H pylori infection may be an important cause of gastric cancer; between 35% and 55% of all cases may be associated with such an infection.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 448, "doc_id": "2052720", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Basophils promote disease development in patients with systemic lupus erythematosus (SLE).\n\nCANDIDATE_ABSTRACT:\nTITLE: BASOPHILS AND THE T HELPER 2 ENVIRONMENT CAN PROMOTE THE DEVELOPMENT OF LUPUS NEPHRITIS\nABSTRACT: In systemic lupus erythematosus (SLE), self-reactive antibodies can target the kidney (lupus nephritis), leading to functional failure and possible mortality. We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice). Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis. Basophils were also present in the lymph nodes and spleen of subjects with SLE. Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 172, "doc_id": "12670680", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Sympathetic nerve activity is elevated throughout normal pregnancy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Regulation of sympathetic nerve activity during the cold pressor test in normotensive pregnant and nonpregnant women.\nABSTRACT: Baseline neurovascular transduction is reduced in normotensive pregnancy; however, little is known about changes to neurovascular transduction during periods of heightened sympathetic activation. We tested the hypothesis that, despite an exacerbated muscle sympathetic nerve activity (microneurography) response to cold pressor stimulation, the blunting of neurovascular transduction in normotensive pregnant women would result in similar changes in vascular resistance and mean arterial pressure (Finometer) relative to nonpregnant controls. Baseline neurovascular transduction was reduced in pregnant women relative to controls when expressed as the quotient of both total resistance and mean arterial pressure and sympathetic burst frequency (0.32±0.07 versus 0.58±0.16 mm Hg/L/min/bursts/min, P<0.001 and 2.4±0.7 versus 3.6±0.8 mm Hg/bursts/min, P=0.001). Sympathetic activation was greater across all 3 minutes of cold pressor stimulation in the pregnant women relative to the nonpregnant controls. Peak sympathoexcitation was also greater in pregnant than in nonpregnant women, whether expressed as sympathetic burst frequency (+17±13 versus +7±8 bursts/min, P=0.049), burst incidence (+17±9 versus +6±11 bursts/100 hb, P=0.03), or total activity (+950±660 versus +363±414 arbitrary units, P=0.04). However, neurovascular transduction during peak cold pressor-induced sympathoexcitation remained blunted in pregnant women (0.25±0.11 versus 0.45±0.08 mm Hg/L/min/bursts/min, P<0.001 and 1.9±1.0 versus 3.2±0.9 mm Hg/bursts/min, P=0.006). Therefore, mean arterial pressure (93±21 versus 99±6 mm Hg, P=0.4) and total peripheral resistance (12±3 versus 14±3 mm Hg/L/min) were not different between pregnant and nonpregnant women during peak sympathoexcitation. These data indicate that [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Peak sympathoexcitation was also greater in pregnant than in nonpregnant women, whether expressed as sympathetic burst frequency (+17±13 versus +7±8 bursts/min, P=0.049), burst incidence (+17±9 versus +6±11 bursts/100 hb, P=0.03), or total activity (+950±660 versus +363±414 arbitrary units, P=0.04).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1119, "doc_id": "13907928", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Primary cervical cytology screening with HPV detection has higher longitudinal sensitivity to detect severe cervical intraepithelial neoplasia than conventional cytology.\n\nCANDIDATE_ABSTRACT:\nTITLE: Hyperactive Neuroendocrine Secretion Causes Size, Feeding, and Metabolic Defects of C. elegans Bardet-Biedl Syndrome Mutants\nABSTRACT: Bardet-Biedl syndrome, BBS, is a rare autosomal recessive disorder with clinical presentations including polydactyly, retinopathy, hyperphagia, obesity, short stature, cognitive impairment, and developmental delays. Disruptions of BBS proteins in a variety of organisms impair cilia formation and function and the multi-organ defects of BBS have been attributed to deficiencies in various cilia-associated signaling pathways. In C. elegans, bbs genes are expressed exclusively in the sixty ciliated sensory neurons of these animals and bbs mutants exhibit sensory defects as well as body size, feeding, and metabolic abnormalities. Here we show that in contrast to many other cilia-defective mutants, C. elegans bbs mutants exhibit increased release of dense-core vesicles and organism-wide phenotypes associated with enhanced activities of insulin, neuropeptide, and biogenic amine signaling pathways. We show that the altered body size, feeding, and metabolic abnormalities of bbs mutants can be corrected to wild-type levels by abrogating the enhanced secretion of dense-core vesicles without concomitant correction of ciliary defects. These findings expand the role of BBS proteins to the regulation of dense-core-vesicle exocytosis and suggest that some features of Bardet-Biedl Syndrome may be caused by excessive neuroendocrine secretion.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 973, "doc_id": "1281769", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Up-regulation of the p53 pathway and related molecular events casues cancer resistance and results in a significantly shortened lifespan marked by senescent cells and accelerated organismal aging.\n\nCANDIDATE_PASSAGE:\np53 mutation in breast cancer. Correlation with cell kinetics and cell of origin. AIM Several studies have investigated the expression of the cytokeratins (CKs), vimentin, the epithelial growth factor receptor (EGFR), the oestrogen receptor (ER), and the progesterone receptor (PgR), in breast cancer, but no study has directly compared p53 mutations with these phenotypic and differentiation markers in the same case. The present study was designed to provide some of this information. METHODS The expression of the p53 and bcl-2 proteins was evaluated by immunohistochemistry in relation to phenotypic characteristics and cellular kinetic parameters (mitotic index and apoptotic index) in 37 cases of ductal carcinoma in situ (DCIS) and 27 cases of infiltrating ductal carcinoma (IDC) of the breast. In addition, p53 gene mutation was examined by polymerase chain reaction single strand conformation polymorphism analysis (SSCP). RESULTS Thirteen cases (eight DCIS and five IDC) showed expression of CK8, CK14, CK18, vimentin, and EGFR, consistent with a stem cell phenotype, whereas 44 cases (27 DCIS and 17 IDC) showed expression of CK8 and CK1, weak or negative expression of CK18, but were negative for vimentin and EGFR, consistent with a luminal cell phenotype. DCIS and IDC cases with a stem cell phenotype were ER/PgR negative and intermediately or poorly differentiated. In contrast, the cases with luminal cell phenotype were ER/PgR positive and well or intermediately differentiated. In addition, intermediately or poorly differentiated cases with a stem cell phenotype showed higher proliferative activity (per cent of MIB-l positive cells) than did intermediately or well differentiated cases with a luminal cell phenotype. Both DCIS and IDC cases with a stem cell phenotyp [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1344", "doc_id": "12762485", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Intra-cerebroventricular infusion of amyloid-β oligomers increases expression of fibronectin type-III domain-containing protein 5 mRNA in mice hippocampi.\n\nCANDIDATE_PASSAGE:\nTargeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs). GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets. We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels. To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA). Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis. The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays. The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts. In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival. Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation. Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "654", "doc_id": "33370", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Homozygous deletion of murine Sbds gene from osterix-expressing mesenchymal stem and progenitor cells (MPCs) prevents oxidative stress.\n\nCANDIDATE_PASSAGE:\nEpithelial and mesenchymal subpopulations within normal basal breast cell lines exhibit distinct stem cell/progenitor properties. It has been proposed that epithelial-mesenchymal transition (EMT) in mammary epithelial cells and breast cancer cells generates stem cell features, and that the presence of EMT characteristics in claudin-low breast tumors reveals their origin in basal stem cells. It remains to be determined, however, whether EMT is an inherent property of normal basal stem cells, and if the presence of a mesenchymal-like phenotype is required for the maintenance of all their stem cell properties. We used nontumorigenic basal cell lines as models of normal stem cells/progenitors and demonstrate that these cell lines contain an epithelial subpopulation (\"EpCAM+,\" epithelial cell adhesion molecule positive [EpCAM(pos)]/CD49f(high)) that spontaneously generates mesenchymal-like cells (\"Fibros,\" EpCAM(neg)/CD49f(med/low)) through EMT. Importantly, stem cell/progenitor properties such as regenerative potential, high aldehyde dehydrogenase 1 activity, and formation of three-dimensional acini-like structures predominantly reside within EpCAM+ cells, while Fibros exhibit invasive behavior and mammosphere-forming ability. A gene expression profiling meta-analysis established that EpCAM+ cells show a luminal progenitor-like expression pattern, while Fibros most closely resemble stromal fibroblasts but not stem cells. Moreover, Fibros exhibit partial myoepithelial traits and strong similarities with claudin-low breast cancer cells. Finally, we demonstrate that Slug and Zeb1 EMT-inducers control the progenitor and mesenchymal-like phenotype in EpCAM+ cells and Fibros, respectively, by inhibiting luminal differentiation. In conclusion, nontumorigenic basal cell [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "527", "doc_id": "43385013", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cognitive behavioral therapy is an ineffective treatment for insomnia\n\nCANDIDATE_ABSTRACT:\nTITLE: Cognitive behavioral therapy vs zopiclone for treatment of chronic primary insomnia in older adults: a randomized controlled trial.\nABSTRACT: CONTEXT Insomnia is a common condition in older adults and is associated with a number of adverse medical, social, and psychological consequences. Previous research has suggested beneficial outcomes of both psychological and pharmacological treatments, but blinded placebo-controlled trials comparing the effects of these treatments are lacking. OBJECTIVE To examine short- and long-term clinical efficacy of cognitive behavioral therapy (CBT) and pharmacological treatment in older adults experiencing chronic primary insomnia. DESIGN, SETTING, AND PARTICIPANTS A randomized, double-blinded, placebo-controlled trial of 46 adults (mean age, 60.8 y; 22 women) with chronic primary insomnia conducted between January 2004 and December 2005 in a single Norwegian university-based outpatient clinic for adults and elderly patients. INTERVENTION CBT (sleep hygiene, sleep restriction, stimulus control, cognitive therapy, and relaxation; n = 18), sleep medication (7.5-mg zopiclone each night; n = 16), or placebo medication (n = 12). All treatment duration was 6 weeks, and the 2 active treatments were followed up at 6 months. MAIN OUTCOME MEASURES Ambulant clinical polysomnographic data and sleep diaries were used to determine total wake time, total sleep time, sleep efficiency, and slow-wave sleep (only assessed using polysomnography) on all 3 assessment points. RESULTS CBT resulted in improved short- and long-term outcomes compared with zopiclone on 3 out of 4 outcome measures. For most outcomes, zopiclone did not differ from placebo. Participants receiving CBT improved their sleep efficiency from 81.4% at pretreatment to 90.1% at 6-month follow-up compared with a decrease from 82.3% to 81.9% in the zopiclone group. Participants in the CBT group spent much more time in slow- [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSION These results suggest that interventions based on CBT are superior to zopiclone treatment both in short- and long-term management of insomnia in older adults.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 267, "doc_id": "5912283", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does bicarbonate improve hemodynamics in critically ill patients who have lactic acidosis . A prospective , controlled clinical study?\n\nABSTRACT:\nTo determine whether correction of acidemia using bicarbonate improves hemodynamics in patients who have lactic acidosis. Prospective, randomized, blinded, crossover study. Each patient sequentially received sodium bicarbonate and equimolar sodium chloride. The order of the infusions was randomized. Intensive care unit of a tertiary care hospital. Fourteen patients who had metabolic acidosis (bicarbonate less than 17 mmol/L and base excess less than -10) and increased arterial lactate (mean, 7.8 mmol/L). All had pulmonary artery catheters and 13 were receiving catecholamines. Sodium bicarbonate (2 mmol/kg body weight over 15 minutes) increased arterial pH (7.22 to 7.36, P less than 0.001), serum bicarbonate (12 to 18 mmol/L, P less than 0.001), and partial pressure of CO2 in arterial blood (PaCO2) (35 to 40 mm Hg, P less than 0.001) and decreased plasma ionized calcium (0.95 to 0.87 mmol/L, P less than 0.001). Sodium bicarbonate and sodium chloride both transiently increased pulmonary capillary wedge pressure (15 to 17 mm Hg, and 14 to 17 mm Hg, P less than 0.001) and cardiac output (18% and 16%, P less than 0.01). The mean arterial pressure was unchanged. Hemodynamic responses to sodium bicarbonate and sodium chloride were the same. These data have more than 90% power of detecting a 0.5 L/min (7%) change in mean cardiac output after administration of sodium bicarbonate compared with that after sodium chloride. Even the 7 most acidemic patients (mean pH, 7.13; range, 6.90 to 7.20) had no significant hemodynamic changes after either infusion.", "output": "{\"label\": \"no\", \"rationale\": \"Correction of acidemia using sodium bicarbonate does not improve hemodynamics in critically ill patients who have metabolic acidosis and increased blood lactate or the cardiovascular response to infused catecholamines in these patients. Sodium bicarbonate decreases plasma ionized calcium and increases PaCO2.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 2156475, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Proteins synthesized at the growth cone are ubiquitinated at a higher rate than proteins from the cell body.\n\nCANDIDATE_ABSTRACT:\nTITLE: Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles.\nABSTRACT: Although genomewide RNA expression analysis has become a routine tool in biomedical research, extracting biological insight from such information remains a major challenge. Here, we describe a powerful analytical method called Gene Set Enrichment Analysis (GSEA) for interpreting gene expression data. The method derives its power by focusing on gene sets, that is, groups of genes that share common biological function, chromosomal location, or regulation. We demonstrate how GSEA yields insights into several cancer-related data sets, including leukemia and lung cancer. Notably, where single-gene analysis finds little similarity between two independent studies of patient survival in lung cancer, GSEA reveals many biological pathways in common. The GSEA method is embodied in a freely available software package, together with an initial database of 1,325 biologically defined gene sets.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 982, "doc_id": "2374637", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Aggravated inflammation is dependent on NLRP3 inflammasome activation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Gout-associated uric acid crystals activate the NALP3 inflammasome\nABSTRACT: Development of the acute and chronic inflammatory responses known as gout and pseudogout are associated with the deposition of monosodium urate (MSU) or calcium pyrophosphate dihydrate (CPPD) crystals, respectively, in joints and periarticular tissues. Although MSU crystals were first identified as the aetiological agent of gout in the eighteenth century and more recently as a ‘danger signal’ released from dying cells, little is known about the molecular mechanisms underlying MSU- or CPPD-induced inflammation. Here we show that MSU and CPPD engage the caspase-1-activating NALP3 (also called cryopyrin) inflammasome, resulting in the production of active interleukin (IL)-1β and IL-18. Macrophages from mice deficient in various components of the inflammasome such as caspase-1, ASC and NALP3 are defective in crystal-induced IL-1β activation. Moreover, an impaired neutrophil influx is found in an in vivo model of crystal-induced peritonitis in inflammasome-deficient mice or mice deficient in the IL-1β receptor (IL-1R). These findings provide insight into the molecular processes underlying the inflammatory conditions of gout and pseudogout, and further support a pivotal role of the inflammasome in several autoinflammatory diseases.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here we show that MSU and CPPD engage the caspase-1-activating NALP3 (also called cryopyrin) inflammasome, resulting in the production of active interleukin (IL)-1β and IL-18.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 93, "doc_id": "2692522", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Mutations in RIM1 decrease levels of IME1 RNA.\n\nCANDIDATE_PASSAGE:\nMolecular characterization of the yeast meiotic regulatory gene RIM1. In the yeast Saccharomyces cerevisiae, genetic studies suggest that the RIM1 gene encodes a positive regulator of meiosis. rim1 mutations cause reduced expression of IME1, which is required for expression of many meiotic genes, and thus lead to a partial defect in meiosis and spore formation. We report the sequence of RIM1 and functional analysis of its coding region. The RIM1 gene product (RIM1) contains three regions similar to C2H2 zinc fingers. Serine substitutions for cysteine in each of the putative zinc fingers abolish RIM1 function. The carboxyl-terminus of RIM1 is enriched in acidic amino acids and is required for full RIM1 activity. RIM1 also contains two putative cAMP-dependent protein kinase (cAPK) phosphorylation sites. At one site, substitution of alanine for serine does not affect RIM1 activity; at the other site, this substitution impairs activity. This analysis of RIM1 suggests that the protein may function as a transcriptional activator. We have used the cloned RIM1 gene to create a complete rim1 deletion. This null allele, like previously isolated rim1 mutations, causes a partial meiotic defect. In addition to RIM1, maximum IME1 expression requires the MCK1 and IME4 gene products. Defects associated with rim1, mck1, and ime4 mutations in expression of a meiotic reporter gene (ime2-lacZ) and in sporulation are additive. These findings suggest that RIM1 acts independently of MCK1 and IME4 to stimulate IME1 expression.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "815", "doc_id": "8148304", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Commelina yellow mottle virus (ComYMV) has three typical badnavirus ORFs, capable of encoding proteins 23, 15, and 216 kD.\n\nCANDIDATE_ABSTRACT:\nTITLE: Properties of Commelina yellow mottle virus's complete DNA sequence, genomic discontinuities and transcript suggest that it is a pararetrovirus.\nABSTRACT: The non-enveloped bacilliform viruses are the second group of plant viruses known to possess a genome consisting of circular double-stranded DNA. We have characterized the viral transcript and determined the complete sequence of the genome of Commelina mellow mottle virus (CoYMV), a member of this group. Analysis of the viral transcript indicates that the virus encodes a single terminally-redundant genome-length plus 120 nucleotide transcript. A fraction of the transcripts is polyadenylated, although the majority of the transcript is not polyadenylated. Analysis of the genome sequence indicates that the genome is 7489 bp in size and that the transcribed strand contains three open reading frames capable of encoding proteins of 23, 15 and 216 kd. The function of the 25 and 15 kd proteins is unknown. Similarities between the 216 kd polypeptide and the cauliflower mosaic virus coat protein and protease/reverse transcriptase polyprotein suggest that the 216 kd polypeptide is a polyprotein that is proteolytically processed to yield the virion coat protein, a protease, and replicase (reverse transcriptase and ribonuclease H). Each strand of the CoYMV genome is interrupted by site-specific discontinuities. The locations of the 5'-ends of these discontinuities, and the presence and location of a region on the CoYMV transcript capable of annealing with the 3'-end of cytosolic initiator methionine tRNA are consistent with replication by reverse transcription. We have demonstrated that a construct containing 1.3 CoYMV genomes is infective when introduced into Commelina diffusa, the host for CoYMV, using Agrobacterium-mediated infection.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Analysis of the genome sequence indicates that the genome is 7489 bp in size and that the transcribed strand contains three open reading frames capable of encoding proteins of 23, 15 and 216 kd.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 277, "doc_id": "14376683", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: eRNAs influence is linked to senescence, aging, and carcinogenesis.\n\nCANDIDATE_PASSAGE:\nApolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease. Apolipoprotein E is immunochemically localized to the senile plaques, vascular amyloid, and neurofibrillary tangles of Alzheimer disease. In vitro, apolipoprotein E in cerebrospinal fluid binds to synthetic beta A4 peptide (the primary constituent of the senile plaque) with high avidity. Amino acids 12-28 of the beta A4 peptide are required. The gene for apolipoprotein E is located on chromosome 19q13.2, within the region previously associated with linkage of late-onset familial Alzheimer disease. Analysis of apolipoprotein E alleles in Alzheimer disease and controls demonstrated that there was a highly significant association of apolipoprotein E type 4 allele (APOE-epsilon 4) and late-onset familial Alzheimer disease. The allele frequency of the APOE-epsilon 4 in 30 random affected patients, each from a different Alzheimer disease family, was 0.50 +/- 0.06; the allele frequency of APOE-epsilon 4 in 91 age-matched unrelated controls was 0.16 +/- 0.03 (Z = 2.44, P = 0.014). A functional role of the apolipoprotein E-E4 isoform in the pathogenesis of late-onset familial Alzheimer disease is suggested.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1387", "doc_id": "20937018", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Golli-deficient T-cells prefer to differentiate into an anergic phenotype in the adaptive immune response when there are increased levels of Ca2+ in the cytosol.\n\nCANDIDATE_ABSTRACT:\nTITLE: Golli protein negatively regulates store depletion-induced calcium influx in T cells.\nABSTRACT: Calcium influx is crucial for T cell activation and differentiation. The detailed regulation of this process remains unclear. We report here that golli protein, an alternatively spliced product of the myelin basic protein gene, plays a critical role in regulating calcium influx in T cells. Golli-deficient T cells were hyperproliferative and showed enhanced calcium entry upon T cell receptor stimulation. We further found that golli regulates calcium influx in T cells through the inhibition of the store depletion-induced calcium influx. Mutation of the myristoylation site on golli disrupted its association with the plasma membrane and reversed its inhibitory action on Ca2+ influx, indicating that membrane association of golli was essential for its inhibitory action. These results indicate that golli functions in a unique way to regulate T cell activation through a mechanism involving the modulation of the calcium homeostasis.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 478, "doc_id": "14767844", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Obesity is determined solely by environmental factors.\n\nCANDIDATE_PASSAGE:\nBiomarkers of endothelial dysfunction and risk of type 2 diabetes mellitus. CONTEXT Endothelial dysfunction occurs in diagnosed type 2 diabetes mellitus but may also precede development of diabetes. OBJECTIVE To determine whether elevated plasma levels of biomarkers reflecting endothelial dysfunction (E-selectin; intercellular adhesion molecule 1 [ICAM-1]; and vascular cell adhesion molecule 1 [VCAM-1]) predict development of type 2 diabetes in initially nondiabetic women. DESIGN AND SETTING Prospective, nested case-control study within the Nurses' Health Study, an ongoing US study initiated in 1976. PARTICIPANTS Of 121 700 women initially enrolled, 32 826 provided blood samples in 1989-1990; of those free of diabetes, cardiovascular disease, or cancer at baseline, 737 developed incident diabetes by 2000. Controls (n = 785) were selected according to matched age, fasting status, and race. MAIN OUTCOME MEASURE Risk of confirmed clinically diagnosed type 2 diabetes by baseline levels of E-selectin, ICAM-1, and VCAM-1. RESULTS Baseline median levels of the biomarkers were significantly higher among cases than among controls (E-selectin, 61.2 vs 45.4 ng/mL; ICAM-1, 264.9 vs 247.0 ng/mL; VCAM-1, 545.4 vs 526.0 ng/mL [all P values < or =.004]). Elevated E-selectin and ICAM-1 levels predicted incident diabetes in logistic regression models conditioned on matching criteria and adjusted for body mass index (BMI), family history of diabetes, smoking, diet score, alcohol intake, activity index, and postmenopausal hormone use. The adjusted relative risks for incident diabetes in the top quintile vs the bottom quintiles were 5.43 for E-selectin (95% confidence interval [CI], 3.47-8.50), 3.56 for ICAM-1 (95% CI, 2.28-5.58), and 1.12 for VCAM-1 (95% CI, 0.76-1.66). Adjustm [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "873", "doc_id": "6176498", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does use of hydrophilic guidewires significantly improve technical success rates of peripheral PTA?\n\nABSTRACT:\nTo determine whether the use of hydrophilic guidewires has increased the technical success rate of peripheral percutaneous transluminal angioplasty (PTA).MATERIAL/ We performed 125 procedures and analyzed the technical success rates of PTA using the conventional guidewire first and then if needed, the hydrophilic guidewire for iliac and SFA stenoses or occlusions. Angioplasty was performed on 25 stenosed, 25 occluded iliac arteries and 25 stenosed, 50 occluded femoral arteries. The result was defined as technical success when the lesion was crossed by a guidewire and balloon, then it was dilated with restoration of vessel lumen and less than 30% residual stenosis and the rise in ABI values was at least 0.15 after 24 hours. The technical success rate after PTA of stenosed iliac arteries was achieved in 96% (24/25) using conventional wires and 100% using hydrophilic guidewire; in iliac occlusions, the rates were 60% (15/25) and 96%, respectively; in femoral stenosis - 84% (21/25) and 100%; in occlusions in the first group: lesions<10 cm -64% (16/25) and 96%, in the second group: lesions>10 cm -48% (12/25) and 88%. In the iliac group, there was no significant difference in the success of iliac stenosis PTA. However, there were significant changes in the success rates of PTA performed for SFA stenosis and iliac and SFA occlusions.", "output": "{\"label\": \"maybe\", \"rationale\": \"In summary, we report an overall improvement and high technical success rate for peripherial PTA. The use of hydrophilic guidewires made significant difference to the technical success rate of PTA, especially in occlusion and more complicated lesions.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 16538201, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: HIF1A as a major vascular endothelial growth factor regulator: do its polymorphisms have an association with age-related macular degeneration?\n\nABSTRACT:\nTo investigate the association between age-related macular degeneration (AMD) and the polymorphisms of HIF1A, a major vascular epithelial growth factor regulator under hypoxic conditions. The associations of AMD and polymorphisms of genes CFH, SKIV2L and MYRIP were also studied. Prospective study. Eighty-seven AMD patients and 80 healthy subjects admitted to the Department of Ophthalmology at Pamukkale University Hospital, Denizli, Turkey, were included: 45 (52%) had wet type AMD, and 42 (48%) had dry type AMD. Polymorphisms rs1061170 (CFH), rs429608 (SKIV2L), rs2679798 (MYRIP) and both rs11549465 and rs11549467 (HIF1A) were investigated in DNA isolated from peripheral blood samples of the cases and controls by dye-termination DNA sequencing. Genotype distribution of rs1061170 (CFH), rs429608 (SKIV2L), rs2679798 (MYRIP) and both rs11549465 and rs11549467 (HIF1A) in AMD cases and healthy controls; association between genotypes and AMD subtypes. Given the significant difference between the mean age of case and control groups (72.13 ± 5.77 vs. 62.80 ± 5.22, respectively) (P = .000), subsequent analyses were adjusted for age. We found that having at least one C allele for polymorphism rs1061170 increases AMD risk independent of age (OR = 2.42, 95% confidence interval [CI], 1.22-4.81). The ancestral T allele for polymorphism rs1061170 has a protective effect for AMD (OR = 0.53, 95% CI, 0.34-0.83). No statistically significant difference for distributions of other single nucleotide polymorphisms (SNPs) emerged between patients and healthy subjects.", "output": "{\"label\": \"maybe\", \"rationale\": \"No associations appeared between HIF1A SNPs and AMD, which were studied here for the first time; however, polymorphism rs1061170 of the CFH gene is associated with AMD in our population.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 24995509, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Women with a lower birth weight are more likely to develop breast cancer later in life.\n\nCANDIDATE_ABSTRACT:\nTITLE: Birth Size and Breast Cancer Risk: Re-analysis of Individual Participant Data from 32 Studies\nABSTRACT: BACKGROUND Birth size, perhaps a proxy for prenatal environment, might be a correlate of subsequent breast cancer risk, but findings from epidemiological studies have been inconsistent. We re-analysed individual participant data from published and unpublished studies to obtain more precise estimates of the magnitude and shape of the birth size-breast cancer association. METHODS AND FINDINGS Studies were identified through computer-assisted and manual searches, and personal communication with investigators. Individual participant data from 32 studies, comprising 22,058 breast cancer cases, were obtained. Random effect models were used, if appropriate, to combine study-specific estimates of effect. Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003). Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data. Birth length and head circumference from birth records were also positively associated with breast cancer risk (pooled RR per one SD increment: 1.06 [95% CI 1.03-1.10] and 1.09 [95% CI 1.03-1.15], respectively). Simultaneous adjustment for these three birth size variables showed that length was the strongest independent predictor of risk. The birth size effec [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1380, "doc_id": "16322674", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Side effects associated with antidepressants increases risk of stroke.\n\nCANDIDATE_ABSTRACT:\nTITLE: Antidepressant use and risk of adverse outcomes in older people: population based cohort study\nABSTRACT: OBJECTIVES To investigate the association between antidepressant treatment and risk of several potential adverse outcomes in older people with depression and to examine risks by class of antidepressant, duration of use, and dose. DESIGN Cohort study of people aged 65 and over diagnosed as having depression. SETTING 570 general practices in the United Kingdom supplying data to the QResearch primary care database. PARTICIPANTS 60,746 patients diagnosed as having a new episode of depression between the ages of 65 and 100 years from 1 January 1996 to 31 December 2007 and followed up until 31 December 2008. MAIN OUTCOME MEASURES Hazard ratios associated with antidepressant use for all cause mortality, attempted suicide/self harm, myocardial infarction, stroke/transient ischaemic attack, falls, fractures, upper gastrointestinal bleeding, epilepsy/seizures, road traffic accidents, adverse drug reactions, and hyponatraemia, adjusted for a range of potential confounding variables. Hazard ratios were calculated for antidepressant class (tricyclic and related antidepressants, selective serotonin reuptake inhibitors, other antidepressants), dose, and duration of use and for commonly prescribed individual drugs. RESULTS 54,038 (89.0%) patients received at least one prescription for an antidepressant during follow-up. A total of 1,398,359 antidepressant prescriptions were issued: 764,659 (54.7%) for selective serotonin reuptake inhibitors, 442,192 (31.6%) for tricyclic antidepressants, 2203 (0.2%) for monoamine oxidase inhibitors, and 189,305 (13.5%) for the group of other antidepressants. The associations with the adverse outcomes differed significantly between the antidepressant classes for seven outcomes. Selective serotonin reuptake inhibitors were associated with the [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The group of other antidepressants was associated with the highest adjusted hazard ratios for all cause mortality (1.66, 1.56 to 1.77), attempted suicide/self harm (5.16, 3.90 to 6.83), stroke/transient ischaemic attack (1.37, 1.22 to 1.55), fracture (1.64, 1.46 to 1.84), and epilepsy/seizures (2.24, 1.60 to 3.15), compared with when antidepressants were not being used.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1084, "doc_id": "5691302", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Amitriptyline is an effective treatment for chronic tension-type headaches.\n\nCANDIDATE_ABSTRACT:\nTITLE: Efficacy and tolerability of amitriptylinoxide in the treatment of chronic tension-type headache: a multi-centre controlled study.\nABSTRACT: Amitriptyline is the medication of first choice in the treatment of chronic tension-type headache. In 197 patients with chronic tension-type headache (87M and 110F with a mean age of 38 +/- 13 (18-68)) efficacy and tolerability of 60-90 mg amitriptylinoxide (AO) were compared with 50-75 mg amitriptyline (AM) and placebo (PL) in a double-blind, parallel-group trial consisting of a four weeks' baseline phase and 12 weeks of treatment. The primary study endpoint was a reduction of at least 50% of the product of headache duration and frequency and a reduction of at least 50% in headache intensity. Statistics used were Fisher's exact test and analysis of variance. No significant difference emerged between AO, AM and PL with respect to the primary study endpoint. Treatment response occurred in 30.3% of the AO, 22.4% of the AM and 21.9% of the PL group. A reduction in headache duration and frequency of at least 50% was found in 39.4% on AO, in 25.4% on AM and in 26.6% on PL (PAO-PL = .1384, PAM-PL = 1.000, PAO-AM = .0973). A reduction in headache intensity of at least 50% was found in 31.8% on AO, in 26.9% on AM and in 26.6% on PL (PAO-PL = .5657, PAM-PL = 1.000, PAO-AM = .5715). Trend analysis with respect to a significant reduction of headache intensity (p < 0.05) and the product of headache duration and frequency revealed a superior effect of AO.(ABSTRACT TRUNCATED AT 250 WORDS)", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The primary study endpoint was a reduction of at least 50% of the product of headache duration and frequency and a reduction of at least 50% in headache intensity.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 108, "doc_id": "23865182", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Do the interpretation of Rome III criteria and method of assessment affect the irritable bowel syndrome classification of children?\n\nABSTRACT:\nPaediatric classification of irritable bowel syndrome (IBS) is complicated by the potential discrepancy between parent and child report and by the interpretation of pain-stool relations in the Rome III classification system. To compare IBS classification by diary and by child and parent respondents. Children (ages 7-10 years, n = 90) with recurrent abdominal pain and their parents completed IBS symptom questionnaires and 2-week pain and stool diaries. Diaries were coded with two algorithms, one defining stool changes individually and one defining changes normatively. Proportions of dichotomous classifications (IBS vs. not IBS) between pairs of classification methods/respondents were evaluated using Chi-squared tests (χ²) to determine whether coding methods were significantly related, the degree of inclusiveness, and whether differences in classification were randomly distributed. Individual and normative diary classifications were congruent in 62% of cases, but the individual method classified more children with IBS, 53% vs. 18%. Parent and child questionnaire reports were not correlated. The normative diary classifications and parent questionnaire were the most congruent pair of methods (76% of cases).", "output": "{\"label\": \"yes\", \"rationale\": \"Poor congruence among methods suggests that Rome III IBS criteria need better specification, and efforts to improve parent-child agreement are necessary.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 21138454, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: CHOP is a general endoplasmic reticulum stress marker.\n\nCANDIDATE_PASSAGE:\nReproductive and lifestyle determinants of anti-Müllerian hormone in a large population-based study. CONTEXT Anti-müllerian hormone (AMH) is an ovarian reserve marker that is increasingly applied in clinical practice as a prognostic and diagnostic tool. Despite increased use of AMH in clinical practice, large-scale studies addressing the influence of possible determinants on AMH levels are scarce. OBJECTIVE We aimed to address the role of reproductive and lifestyle determinants of AMH in a large population-based cohort of women. DESIGN In this cross-sectional study, age-specific AMH percentiles were calculated using general linear modeling with CG-LMS (Cole and Green, Lambda, Mu, and Sigma model, an established method to calculate growth curves for children). SETTING Women from the general community participating in the Doetinchem Cohort study were assessed. PARTICIPANTS Two thousand three hundred twenty premenopausal women were included. MAIN OUTCOME MEASURE The effect of female reproductive and lifestyle factors on shifts in age-specific AMH percentiles was studied. RESULTS In comparison to women with a regular menstrual cycle, current oral contraceptive (OC) users, women with menstrual cycle irregularity, and pregnant women had significantly lower age-specific AMH percentiles (for OC use, 11 percentiles lower; for cycle irregularity, 11 percentiles lower; and for pregnancy, 17 percentiles lower [P value for all <.0001]). Age at menarche and age at first childbirth were not associated with the age-specific AMH percentile. Higher parity was associated with 2 percentiles higher age-specific AMH (P = .02). Of the lifestyle factors investigated, current smoking was associated with 4 percentiles lower age-specific AMH percentiles (P = .02), irrespective of the [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "209", "doc_id": "42150015", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does glucocorticoid treatment alter early cardiac adaptations to growth restriction in preterm sheep fetuses?\n\nABSTRACT:\nTo study the consequences of glucocorticoid treatment in fetal growth restriction (FGR) on cardiac function. Laboratory. Sheep. Growth restriction was induced in sheep fetuses using single umbilical artery ligation (SUAL) on days 105-110 of gestation (term 147). Control fetuses were not ligated. Betamethasone (BM) (11.4 mg intramuscularly) or saline was administered to ewes on days 5 and 6 after surgery. Ewes were anaesthetised on day 7, the fetuses were removed, and their hearts were mounted on a Langendorff apparatus. Balloon catheters were inserted into the right and left ventricles. Ventricular contractile function and infarct area following ischaemia/reperfusion. The SUAL resulted in FGR (body weight 77% of control). The FGR was associated with increases in basal left ventricular pressure development and rates of contraction and relaxation. Right ventricular contraction was unaffected. Following brief ischaemia/reperfusion, the infarct area in FGR hearts was increased four-fold compared with controls. Antenatal BM resulted in a proportional increase in heart size and coronary flow, especially in FGR fetuses, and left ventricular pressure and heart rate responses to β-adrenoceptor activation were increased.", "output": "{\"label\": \"no\", \"rationale\": \"Fetal hearts rapidly adapt to FGR to maintain substrate delivery to the brain and heart. The FGR greatly enhanced the area of ischaemia, with implications for susceptibility in postnatal life. Antenatal BM treatment does not interfere with these cardiac changes but appears to increase left ventricle β-adrenoceptor responsiveness, which may render the offspring vulnerable to subsequent cardiac dysfunction.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 22703419, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Microglia are an innate immune cell type of the central nervous system.\n\nCANDIDATE_PASSAGE:\nRegulation and function of the E-cadherin/catenin complex in cells of the monocyte-macrophage lineage and DCs. E-cadherin is best characterized as adherens junction protein, which through homotypic interactions contributes to the maintenance of the epithelial barrier function. In epithelial cells, the cytoplasmic tail of E-cadherin forms a dynamic complex with catenins and regulates several intracellular signal transduction pathways, including Wnt/β-catenin, PI3K/Akt, Rho GTPase, and NF-κB signaling. Recent progress uncovered a novel and critical role for this adhesion molecule in mononuclear phagocyte functions. E-cadherin regulates the maturation and migration of Langerhans cells, and its ligation prevents the induction of a tolerogenic state in bone marrow-derived dendritic cells (DCs). In this respect, the functionality of β-catenin could be instrumental in determining the balance between immunogenicity and tolerogenicity of DCs in vitro and in vivo. Fusion of alternatively activated macrophages and osteoclasts is also E-cadherin-dependent. In addition, the E-cadherin ligands CD103 and KLRG1 are expressed on DC-, T-, and NK-cell subsets and contribute to their interaction with E-cadherin-expressing DCs and macrophages. Here we discuss the regulation, function, and implications of E-cadherin expression in these central orchestrators of the immune system.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "789", "doc_id": "3118719", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: HbA1c consistently overestimates glycemic control in black individuals with Sickle cell trait (SCT).\n\nCANDIDATE_ABSTRACT:\nTITLE: Association of Sickle Cell Trait With Hemoglobin A1c in African Americans\nABSTRACT: Importance Hemoglobin A1c (HbA1c) reflects past glucose concentrations, but this relationship may differ between those with sickle cell trait (SCT) and those without it. Objective To evaluate the association between SCT and HbA1c for given levels of fasting or 2-hour glucose levels among African Americans. Design, Setting, and Participants Retrospective cohort study using data collected from 7938 participants in 2 community-based cohorts, the Coronary Artery Risk Development in Young Adults (CARDIA) study and the Jackson Heart Study (JHS). From the CARDIA study, 2637 patients contributed a maximum of 2 visits (2005-2011); from the JHS, 5301 participants contributed a maximum of 3 visits (2000-2013). All visits were scheduled at approximately 5-year intervals. Participants without SCT data, those without any concurrent HbA1c and glucose measurements, and those with hemoglobin variants HbSS, HbCC, or HbAC were excluded. Analysis of the primary outcome was conducted using generalized estimating equations (GEE) to examine the association of SCT with HbA1c levels, controlling for fasting or 2-hour glucose measures. Exposures Presence of SCT. Main Outcomes and Measures Hemoglobin A1c stratified by the presence or absence of SCT was the primary outcome measure. Results The analytic sample included 4620 participants (mean age, 52.3 [SD, 11.8] years; 2835 women [61.3%]; 367 [7.9%] with SCT) with 9062 concurrent measures of fasting glucose and HbA1c levels. In unadjusted GEE analyses, for a given fasting glucose, HbA1c values were statistically significantly lower in those with (5.72%) vs those without (6.01%) SCT (mean HbA1c difference, −0.29%; 95% CI, −0.35% to −0.23%). Findings were similar in models adjusted for key risk factors and in analyses using 2001 concurre [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"These findings suggest that HbA1c may systematically underestimate past glycemia in black patients with SCT and may require further evaluation.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 499, "doc_id": "26064662", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Combining phosphatidylinositide 3-kinase and MEK 1/2 inhibitors is effective at treating KRAS mutant tumors.\n\nCANDIDATE_PASSAGE:\nCancer-Associated Fibroblasts Neutralize the Anti-tumor Effect of CSF1 Receptor Blockade by Inducing PMN-MDSC Infiltration of Tumors. Tumor-associated macrophages (TAM) contribute to all aspects of tumor progression. Use of CSF1R inhibitors to target TAM is therapeutically appealing, but has had very limited anti-tumor effects. Here, we have identified the mechanism that limited the effect of CSF1R targeted therapy. We demonstrated that carcinoma-associated fibroblasts (CAF) are major sources of chemokines that recruit granulocytes to tumors. CSF1 produced by tumor cells caused HDAC2-mediated downregulation of granulocyte-specific chemokine expression in CAF, which limited migration of these cells to tumors. Treatment with CSF1R inhibitors disrupted this crosstalk and triggered a profound increase in granulocyte recruitment to tumors. Combining CSF1R inhibitor with a CXCR2 antagonist blocked granulocyte infiltration of tumors and showed strong anti-tumor effects.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "275", "doc_id": "3559136", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: 5'-nucleotidase metabolizes 6MP.\n\nCANDIDATE_PASSAGE:\nNovel proteinaceous infectious particles cause scrapie. After infection and a prolonged incubation period, the scrapie agent causes a degenerative disease of the central nervous system in sheep and goats. Six lines of evidence including sensitivity to proteases demonstrate that this agent contains a protein that is required for infectivity. Although the scrapie agent is irreversibly inactivated by alkali, five procedures with more specificity for modifying nucleic acids failed to cause inactivation. The agent shows heterogeneity with respect to size, apparently a result of its hydrophobicity; the smallest form may have a molecular weight of 50,000 or less. Because the novel properties of the scrapie agent distinguish it from viruses, plasmids, and viroids, a new term \"prion\" is proposed to denote a small proteinaceous infectious particle which is resistant to inactivation by most procedures that modify nucleic acids. Knowledge of the scrapie agent structure may have significance for understanding the causes of several degenerative diseases.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "14", "doc_id": "7447120", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: 5% of perinatal mortality is due to low birth weight.\n\nCANDIDATE_PASSAGE:\nMechanical coupling between transsynaptic N-cadherin adhesions and actin flow stabilizes dendritic spines The morphology of neuronal dendritic spines is a critical indicator of synaptic function. It is regulated by several factors, including the intracellular actin/myosin cytoskeleton and transcellular N-cadherin adhesions. To examine the mechanical relationship between these molecular components, we performed quantitative live-imaging experiments in primary hippocampal neurons. We found that actin turnover and structural motility were lower in dendritic spines than in immature filopodia and increased upon expression of a nonadhesive N-cadherin mutant, resulting in an inverse relationship between spine motility and actin enrichment. Furthermore, the pharmacological stimulation of myosin II induced the rearward motion of actin structures in spines, showing that myosin II exerts tension on the actin network. Strikingly, the formation of stable, spine-like structures enriched in actin was induced at contacts between dendritic filopodia and N-cadherin-coated beads or micropatterns. Finally, computer simulations of actin dynamics mimicked various experimental conditions, pointing to the actin flow rate as an important parameter controlling actin enrichment in dendritic spines. Together these data demonstrate that a clutch-like mechanism between N-cadherin adhesions and the actin flow underlies the stabilization of dendritic filopodia into mature spines, a mechanism that may have important implications in synapse initiation, maturation, and plasticity in the developing brain.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "13", "doc_id": "5700349", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does perspective-taking increase patient satisfaction in medical encounters?\n\nABSTRACT:\nTo assess whether perspective-taking, which researchers in other fields have shown to induce empathy, improves patient satisfaction in encounters between student-clinicians and standardized patients (SPs). In three studies, randomly assigned students (N = 608) received either a perspective-taking instruction or a neutral instruction prior to a clinical skills examination in 2006-2007. SP satisfaction was the main outcome in all three studies. Study 1 involved 245 third-year medical students from two universities. Studies 2 and 3 extended Study 1 to examine generalizability across student and SP subpopulations. Study 2 (105 physician assistant students, one university) explored the effect of perspective-taking on African American SPs' satisfaction. Study 3 (258 third-year medical students, two universities) examined the intervention's effect on students with high and low baseline perspective-taking tendencies. Intervention students outscored controls in patient satisfaction in all studies: Study 1: P = .01, standardized effect size = 0.16; Study 2: P = .001, standardized effect size = 0.31; Study 3: P = .009, standardized effect size = 0.13. In Study 2, perspective-taking improved African American SPs' satisfaction. In Study 3, intervention students with high baseline perspective-taking tendencies outscored controls (P = .0004, standardized effect size = 0.25), whereas those with low perspective-taking tendencies did not (P = .72, standardized effect size = 0.00).", "output": "{\"label\": \"maybe\", \"rationale\": \"Perspective-taking increased patient satisfaction in all three studies, across medical schools, clinical disciplines, and racially diverse students and SPs. Perspective-taking as a means for improving patient satisfaction deserves further exploration in clinical training and practice.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 20736672, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: De novo assembly of sequence data has shorter contigs than unassembled sequence data.\n\nCANDIDATE_PASSAGE:\nA culture-independent sequence-based metagenomics approach to the investigation of an outbreak of Shiga-toxigenic Escherichia coli O104:H4. IMPORTANCE Identification of the bacterium responsible for an outbreak can aid in disease management. However, traditional culture-based diagnosis can be difficult, particularly if no specific diagnostic test is available for an outbreak strain. OBJECTIVE To explore the potential of metagenomics, which is the direct sequencing of DNA extracted from microbiologically complex samples, as an open-ended clinical discovery platform capable of identifying and characterizing bacterial strains from an outbreak without laboratory culture. DESIGN, SETTING, AND PATIENTS In a retrospective investigation, 45 samples were selected from fecal specimens obtained from patients with diarrhea during the 2011 outbreak of Shiga-toxigenic Escherichia coli (STEC) O104:H4 in Germany. Samples were subjected to high-throughput sequencing (August-September 2012), followed by a 3-phase analysis (November 2012-February 2013). In phase 1, a de novo assembly approach was developed to obtain a draft genome of the outbreak strain. In phase 2, the depth of coverage of the outbreak strain genome was determined in each sample. In phase 3, sequences from each sample were compared with sequences from known bacteria to identify pathogens other than the outbreak strain. MAIN OUTCOMES AND MEASURES The recovery of genome sequence data for the purposes of identification and characterization of the outbreak strain and other pathogens from fecal samples. RESULTS During phase 1, a draft genome of the STEC outbreak strain was obtained. During phase 2, the outbreak strain genome was recovered from 10 samples at greater than 10-fold coverage and from 26 samples at grea [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "313", "doc_id": "6173523", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The morphology change from large white adipocytes to small brown adipocytes is a sign of decreased energy expenditure potential in white adipose tissue.\n\nCANDIDATE_PASSAGE:\nObesity and Its Metabolic Complications: The Role of Adipokines and the Relationship between Obesity, Inflammation, Insulin Resistance, Dyslipidemia and Nonalcoholic Fatty Liver Disease Accumulating evidence indicates that obesity is closely associated with an increased risk of metabolic diseases such as insulin resistance, type 2 diabetes, dyslipidemia and nonalcoholic fatty liver disease. Obesity results from an imbalance between food intake and energy expenditure, which leads to an excessive accumulation of adipose tissue. Adipose tissue is now recognized not only as a main site of storage of excess energy derived from food intake but also as an endocrine organ. The expansion of adipose tissue produces a number of bioactive substances, known as adipocytokines or adipokines, which trigger chronic low-grade inflammation and interact with a range of processes in many different organs. Although the precise mechanisms are still unclear, dysregulated production or secretion of these adipokines caused by excess adipose tissue and adipose tissue dysfunction can contribute to the development of obesity-related metabolic diseases. In this review, we focus on the role of several adipokines associated with obesity and the potential impact on obesity-related metabolic diseases. Multiple lines evidence provides valuable insights into the roles of adipokines in the development of obesity and its metabolic complications. Further research is still required to fully understand the mechanisms underlying the metabolic actions of a few newly identified adipokines.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1235", "doc_id": "5268462", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: siRNA knockdown of A20 accelerates tumor progression in an in vivo murine xenograft model.\n\nCANDIDATE_PASSAGE:\nTargeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs). GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets. We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels. To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA). Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis. The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays. The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts. In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival. Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation. Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1403", "doc_id": "33370", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Ultrasound guidance significantly reduces the number of needle insertion attempts necessary for a given procedure.\n\nCANDIDATE_ABSTRACT:\nTITLE: Ultrasound imaging for lumbar punctures and epidural catheterisations: systematic review and meta-analysis.\nABSTRACT: OBJECTIVE To determine whether ultrasound imaging can reduce the risk of failed lumbar punctures or epidural catheterisations, when compared with standard palpation methods, and whether ultrasound imaging can reduce traumatic procedures, insertion attempts, and needle redirections. DESIGN Systematic review and meta-analysis of randomised controlled trials. DATA SOURCES Ovid Medline, Embase, and Cochrane Central Register of Controlled Trials up to May 2012, without restriction by language or publication status. REVIEW METHODS Randomised trials that compared ultrasound imaging with standard methods (no imaging) in the performance of a lumbar puncture or epidural catheterisation were identified. RESULTS 14 studies with a total of 1334 patients were included (674 patients assigned to the ultrasound group, 660 to the control group). Five studies evaluated lumbar punctures and nine evaluated epidural catheterisations. Six of 624 procedures conducted in the ultrasound group failed; 44 of 610 procedures in the control group failed. Ultrasound imaging reduced the risk of failed procedures (risk ratio 0.21 (95% confidence interval 0.10 to 0.43), P<0.001). Risk reduction was similar when subgroup analysis was performed for lumbar punctures (risk ratio 0.19 (0.07 to 0.56), P=0.002) or epidural catheterisations (0.23 (0.09 to 0.60), P=0.003). Ultrasound imaging also significantly reduced the risk of traumatic procedures (risk ratio 0.27 (0.11 to 0.67), P=0.005), the number of insertion attempts (mean difference -0.44 (-0.64 to -0.24), P<0.001), and the number of needle redirections (mean difference -1.00 (-1.24 to -0.75), P<0.001). CONCLUSIONS Ultrasound imaging can reduce the risk of failed or traumatic lumbar punctures and epidural catheterisations, as well as the numb [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Ultrasound imaging also significantly reduced the risk of traumatic procedures (risk ratio 0.27 (0.11 to 0.67), P=0.005), the number of insertion attempts (mean difference -0.44 (-0.64 to -0.24), P<0.001), and the number of needle redirections (mean difference -1.00 (-1.24 to -0.75), P<0.001).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1340, "doc_id": "15482274", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: B3-Galectin increases cell resistance to tyrosine kinase inhibitors (TKIs) by engaging the alternate KRAS-RalB signaling complex downstream of EGFR.\n\nCANDIDATE_PASSAGE:\nAn integrin β3–KRAS–RalB complex drives tumour stemness and resistance to EGFR inhibition Tumour cells, with stem-like properties, are highly aggressive and often show drug resistance. Here, we reveal that integrin αvβ3 serves as a marker of breast, lung and pancreatic carcinomas with stem-like properties that are highly resistant to receptor tyrosine kinase inhibitors such as erlotinib. This was observed in vitro and in mice bearing patient-derived tumour xenografts or in clinical specimens from lung cancer patients who had progressed on erlotinib. Mechanistically, αvβ3, in the unliganded state, recruits KRAS and RalB to the tumour cell plasma membrane, leading to the activation of TBK1 and NF-κB. In fact, αvβ3 expression and the resulting KRAS–RalB–NF-κB pathway were both necessary and sufficient for tumour initiation, anchorage independence, self-renewal and erlotinib resistance. Pharmacological targeting of this pathway with bortezomib reversed both tumour stemness and erlotinib resistance. These findings not only identify αvβ3 as a marker/driver of carcinoma stemness but also reveal a therapeutic strategy to sensitize such tumours to RTK inhibition.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "154", "doc_id": "4702639", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Articles published in open access format are more likely to be cited than traditional journals.\n\nCANDIDATE_ABSTRACT:\nTITLE: Open Access Increases Citation Rate\nABSTRACT: PLoS Biology publishes today a research article by Gunther Eysenbach that is not about biology. It is about citations. It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles. As such, it adds objective support to the belief we have always held that open-access publication speeds up scientific dialog between researchers and, consequently, should be extended to the whole scientific literature as quickly as possible. It is therefore fitting that we publish such a paper. We have long argued that papers freely available in a journal will be more often read and cited than those behind a subscription barrier. However, solid evidence to support or refute such a claim has been surprisingly hard to find. Since most open-access journals are new, comparisons of the effects of open access with established subscription-based journals are easily confounded by age and reputation. In the current study, Eysenbach compared citations compiled by Thomson Scientific (formerly Thomson ISI) to individual articles published between June 2004 and December 2004 in the same journal—namely, Proceedings of the National Academy of Sciences (PNAS), which announced its open-access option for authors on June 8 of that year, with an associated publication charge of US$1,000. Non-OA articles in PNAS are subject to a six-month “toll-access” delay before the article becomes publicly available. The results of this natural experiment are clear: in the 4 to 16 months following publication, OA articles gained a significant citation advantage over non-OA articles during the same period. They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely between 10 and 16 months. Given that P [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Moreover, although the evidence from the current analysis argues most strongly for a time advantage in citation for OA articles, a study over longer periods will reveal whether this translates into a sustained increase in the number of citations.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 130, "doc_id": "27768226", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The amount of publicly available DNA data doubles every 10 months.\n\nCANDIDATE_PASSAGE:\nlumi: a pipeline for processing Illumina microarray. UNLABELLED Illumina microarray is becoming a popular microarray platform. The BeadArray technology from Illumina makes its preprocessing and quality control different from other microarray technologies. Unfortunately, most other analyses have not taken advantage of the unique properties of the BeadArray system, and have just incorporated preprocessing methods originally designed for Affymetrix microarrays. lumi is a Bioconductor package especially designed to process the Illumina microarray data. It includes data input, quality control, variance stabilization, normalization and gene annotation portions. In specific, the lumi package includes a variance-stabilizing transformation (VST) algorithm that takes advantage of the technical replicates available on every Illumina microarray. Different normalization method options and multiple quality control plots are provided in the package. To better annotate the Illumina data, a vendor independent nucleotide universal identifier (nuID) was devised to identify the probes of Illumina microarray. The nuID annotation packages and output of lumi processed results can be easily integrated with other Bioconductor packages to construct a statistical data analysis pipeline for Illumina data. AVAILABILITY The lumi Bioconductor package, www.bioconductor.org", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1190", "doc_id": "24234341", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Bariatric surgery has a positive impact on mental health.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mental Health Conditions Among Patients Seeking and Undergoing Bariatric Surgery: A Meta-analysis.\nABSTRACT: IMPORTANCE Bariatric surgery is associated with sustained weight loss and improved physical health status for severely obese individuals. Mental health conditions may be common among patients seeking bariatric surgery; however, the prevalence of these conditions and whether they are associated with postoperative outcomes remains unknown. OBJECTIVE To determine the prevalence of mental health conditions among bariatric surgery candidates and recipients, to evaluate the association between preoperative mental health conditions and health outcomes following bariatric surgery, and to evaluate the association between surgery and the clinical course of mental health conditions. DATA SOURCES We searched PubMed, MEDLINE on OVID, and PsycINFO for studies published between January 1988 and November 2015. Study quality was assessed using an adapted tool for risk of bias; quality of evidence was rated based on GRADE (Grading of Recommendations Assessment, Development and Evaluation) criteria. FINDINGS We identified 68 publications meeting inclusion criteria: 59 reporting the prevalence of preoperative mental health conditions (65,363 patients) and 27 reporting associations between preoperative mental health conditions and postoperative outcomes (50,182 patients). Among patients seeking and undergoing bariatric surgery, the most common mental health conditions, based on random-effects estimates of prevalence, were depression (19% [95% CI, 14%-25%]) and binge eating disorder (17% [95% CI, 13%-21%]). There was conflicting evidence regarding the association between preoperative mental health conditions and postoperative weight loss. Neither depression nor binge eating disorder was consistently associated with differences in weight outcomes. Bariatric surgery was, however, c [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Bariatric surgery was, however, consistently associated with postoperative decreases in the prevalence of depression (7 studies; 8%-74% decrease) and the severity of depressive symptoms (6 studies; 40%-70% decrease).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 163, "doc_id": "18872233", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Cellular clocks are associated with mitosis timing in NIH 3T3 cells.\n\nCANDIDATE_PASSAGE:\nRobust synchronization of coupled circadian and cell cycle oscillators in single mammalian cells Circadian cycles and cell cycles are two fundamental periodic processes with a period in the range of 1 day. Consequently, coupling between such cycles can lead to synchronization. Here, we estimated the mutual interactions between the two oscillators by time-lapse imaging of single mammalian NIH3T3 fibroblasts during several days. The analysis of thousands of circadian cycles in dividing cells clearly indicated that both oscillators tick in a 1:1 mode-locked state, with cell divisions occurring tightly 5 h before the peak in circadian Rev-Erbα-YFP reporter expression. In principle, such synchrony may be caused by either unidirectional or bidirectional coupling. While gating of cell division by the circadian cycle has been most studied, our data combined with stochastic modeling unambiguously show that the reverse coupling is predominant in NIH3T3 cells. Moreover, temperature, genetic, and pharmacological perturbations showed that the two interacting cellular oscillators adopt a synchronized state that is highly robust over a wide range of parameters. These findings have implications for circadian function in proliferative tissues, including epidermis, immune cells, and cancer.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "241", "doc_id": "2212067", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does improvements in pulmonary and general critical care reduce mortality following ventilator-associated pneumonia?\n\nABSTRACT:\nVentilator-associated pneumonia (VAP) is the most common hospital-acquired infection in the intensive care unit, with substantial subsequent mortality. The mortality following VAP declined in the 1980s and 1990s. Experts suggest that little progress has been made in the outcomes from VAP since several novel interventions have failed. We nonetheless hypothesized that mortality following VAP has continued to decrease owing to advances in pulmonary critical care. We identified all adult patients with Centers for Disease Control and Prevention-defined, intensive care unit-acquired VAP between January 1, 1997, and December 31, 2008, from a prospectively collected database. A total of 793 cases of VAP occurred in the study period. Cases were divided into four periods (1997-1999, 2000-2002, 2003-2005, or 2006-2008) to compare outcomes over time. Acute Physiology and Chronic Health Evaluation II scores were stable, while mortality was significantly lower in Period 4 when compared with Periods 1 and 2 (p = 0.004 and 0.009, respectively). A logistic regression model predicting death (c statistic = 0.871) revealed age (odds ratio, 1.03; 95% confidence interval, 1.02-1.05), Acute Physiology and Chronic Health Evaluation II score (1.09, 1.05-1.14), white blood cell count (1.03, 1.00-1.06), transplant recipient (3.45, 1.40-8.53), transfusions (3.25, 1.37-7.68), and pulmonary disease (3.01, 1.67-5.45) were independent predictors of death, as was the presence of trauma (0.10, 0.06-0.18), chronic steroid therapy (0.39, 0.17-0.91), and patient length of stay (0.99, 0.98-0.99), with odds ratios less than 1.0. In addition, those patients treated in Period 1 (2.23, 1.16-4.29) or Period 2 (2.13, 1.12-4.06) had twice the risk of death following an episode of VAP when compared with [TRUNCATED]", "output": "{\"label\": \"yes\", \"rationale\": \"We have shown that mortality following an episode of VAP continues to decrease over time and attribute this to advancements in pulmonary and general critical care rather than any specific interventions.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 23354252, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Leukemia associated Rho guanine nucleotide-exchange factor represses RhoA in response to SRC activation.\n\nCANDIDATE_PASSAGE:\nRole of beta adrenergic receptor polymorphisms in heart failure: systematic review and meta-analysis. Heart Failure (HF) is a common disorder associated with substantial morbidity and mortality. beta adrenergic receptors (betaAR) are the primary pathway through which cardiac function is influenced. Chronic beta(1)AR activation is implicated in the pathogenesis of HF and betaAR blockade improves survival in left ventricular systolic dysfunction. Common functional polymorphisms in beta adrenergic receptor genes (ADRB) have been associated with HF phenotypes, and with pharmacogenetic interaction with beta adrenergic receptor blockers (beta blockers). However, these associations have not been consistently replicated. The evidence for ADRB variant involvement in pathogenesis, progression and response to beta blockers in HF is reviewed. In addition, a meta-analysis of three studies analysing the effect of ADRB1 Arg389Gly polymorphism on left ventricular remodelling with the use of beta blockers, demonstrating a 5% improvement in left ventricular ejection fraction in Arg389 homozygotes, is presented. There is now accumulating molecular evidence for a different functional response to beta blockers associated with this polymorphism. In the future, confirmed genotypic associations may enable patients to be identified who are either at greater risk of developing HF, whose HF may rapidly progress, or who are unlikely to benefit from beta blockers, and such patients may benefit from targeted aggressive therapy.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "691", "doc_id": "24586989", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: APOE4 expression in iPSC-derived neurons increases AlphaBeta production and tau phosphorylation, delaying GABA neuron degeneration.\n\nCANDIDATE_PASSAGE:\nGain of toxic Apolipoprotein E4 effects in Human iPSC-Derived Neurons Is Ameliorated by a Small-Molecule Structure Corrector Efforts to develop drugs for Alzheimer's disease (AD) have shown promise in animal studies, only to fail in human trials, suggesting a pressing need to study AD in human model systems. Using human neurons derived from induced pluripotent stem cells that expressed apolipoprotein E4 (ApoE4), a variant of the APOE gene product and the major genetic risk factor for AD, we demonstrated that ApoE4-expressing neurons had higher levels of tau phosphorylation, unrelated to their increased production of amyloid-β (Aβ) peptides, and that they displayed GABAergic neuron degeneration. ApoE4 increased Aβ production in human, but not in mouse, neurons. Converting ApoE4 to ApoE3 by gene editing rescued these phenotypes, indicating the specific effects of ApoE4. Neurons that lacked APOE behaved similarly to those expressing ApoE3, and the introduction of ApoE4 expression recapitulated the pathological phenotypes, suggesting a gain of toxic effects from ApoE4. Treatment of ApoE4-expressing neurons with a small-molecule structure corrector ameliorated the detrimental effects, thus showing that correcting the pathogenic conformation of ApoE4 is a viable therapeutic approach for ApoE4-related AD.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "57", "doc_id": "4709641", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: There is a positive correlation between hip fractures and statin use.\n\nCANDIDATE_PASSAGE:\nHMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients. CONTEXT Recent animal studies have found that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) lipid-lowering drugs (statins) substantially increase bone formation, but whether statin use in humans results in clinically meaningful bone formation or a reduction in the risk of osteoporotic fractures is not known. OBJECTIVE To determine whether the use of statins is associated with reduced hip fracture risk. DESIGN Case-control study. SETTING AND PATIENTS A total of 6110 New Jersey residents aged 65 years or older and enrolled in Medicare and either Medicaid or the Pharmacy Assistance for the Aged and Disabled program. Case patients (n=1222) underwent surgical repair of a hip fracture in 1994. Control patients (n=4888) were identified at a ratio of 4:1 and frequency-matched to case patients for age and sex. MAIN OUTCOME MEASURE Adjusted odds ratio (OR) of hip fracture by statin use in the 180 days and 3 years prior to the index date (the earliest date of admission for surgery), adjusted for demographic and clinical characteristics and health care utilization. RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus. No significant relationship was observed between use of nonstatin lipid-lowering agents and hip fracture risk. Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of s [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1288", "doc_id": "4687948", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The peak incidence of fractures occurs during pubertal growth spurt in early adolescents.\n\nCANDIDATE_PASSAGE:\nThe transcriptome profile of human embryonic stem cells as defined by SAGE. Human embryonic stem (ES) cell lines that have the ability to self-renew and differentiate into specific cell types have been established. The molecular mechanisms for self-renewal and differentiation, however, are poorly understood. We determined the transcriptome profiles for two proprietary human ES cell lines (HES3 and HES4, ES Cell International), and compared them with murine ES cells and other human tissues. Human and mouse ES cells appear to share a number of expressed gene products although there are numerous notable differences, including an inactive leukemia inhibitory factor pathway and the high preponderance of several important genes like POU5F1 and SOX2 in human ES cells. We have established a list of genes comprised of known ES-specific genes and new candidates that can serve as markers for human ES cells and may also contribute to the \"stemness\" phenotype. Of particular interest was the downregulation of DNMT3B and LIN28 mRNAs during ES cell differentiation. The overlapping similarities and differences in gene expression profiles of human and mouse ES cells provide a foundation for a detailed and concerted dissection of the molecular and cellular mechanisms governing their pluripotency, directed differentiation into specific cell types, and extended ability for self-renewal.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1248", "doc_id": "42484543", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: B3-Galectin increases cell resistance to tyrosine kinase inhibitors (TKIs) by engaging the alternate KRAS-RalB signaling complex downstream of EGFR.\n\nCANDIDATE_ABSTRACT:\nTITLE: An integrin β3–KRAS–RalB complex drives tumour stemness and resistance to EGFR inhibition\nABSTRACT: Tumour cells, with stem-like properties, are highly aggressive and often show drug resistance. Here, we reveal that integrin αvβ3 serves as a marker of breast, lung and pancreatic carcinomas with stem-like properties that are highly resistant to receptor tyrosine kinase inhibitors such as erlotinib. This was observed in vitro and in mice bearing patient-derived tumour xenografts or in clinical specimens from lung cancer patients who had progressed on erlotinib. Mechanistically, αvβ3, in the unliganded state, recruits KRAS and RalB to the tumour cell plasma membrane, leading to the activation of TBK1 and NF-κB. In fact, αvβ3 expression and the resulting KRAS–RalB–NF-κB pathway were both necessary and sufficient for tumour initiation, anchorage independence, self-renewal and erlotinib resistance. Pharmacological targeting of this pathway with bortezomib reversed both tumour stemness and erlotinib resistance. These findings not only identify αvβ3 as a marker/driver of carcinoma stemness but also reveal a therapeutic strategy to sensitize such tumours to RTK inhibition.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 154, "doc_id": "4702639", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Transcription rates in S. cerevisiae range between 0.7 and 2 kb/min.\n\nCANDIDATE_PASSAGE:\nThe kinase TAK1 integrates antigen and cytokine receptor signaling for T cell development, survival and function The kinase TAK1 is critical for innate and B cell immunity. The function of TAK1 in T cells is unclear, however. We show here that T cell–specific deletion of the gene encoding TAK1 resulted in reduced development of thymocytes, especially of regulatory T cells expressing the transcription factor Foxp3. In mature thymocytes, TAK1 was required for interleukin 7–mediated survival and T cell receptor–dependent activation of transcription factor NF-κB and the kinase Jnk. In effector T cells, TAK1 was dispensable for T cell receptor–dependent NF-κB activation and cytokine production, but was important for proliferation and activation of the kinase p38 in response to interleukins 2, 7 and 15. Thus, TAK1 is essential for the integration of T cell receptor and cytokine signals to regulate the development, survival and function of T cells.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1314", "doc_id": "22210434", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Are endogenous catecholamines necessary for ischaemic preconditioning in the isolated perfused rat heart?\n\nABSTRACT:\nThe mechanism of the protective effect of ischaemic preconditioning in the myocardium is not yet known. The aim of this study was to test the hypothesis that endogenous myocardial catecholamines may be mediators of preconditioning. To test whether endogenous catecholamines are involved in preconditioning, experiments were performed in hearts from rats which had been catecholamine depleted with either reserpine or 6-hydroxydopamine. Experiments were also done to determine if noradrenaline can mimic preconditioning. Catecholamine depletion with either reserpine or 6-hydroxydopamine had no effect on preischaemic coronary flow or cardiac function. Ischaemic preconditioning (four episodes of 5 min global ischaemia and 5 min reperfusion) resulted in a significant increase in postischaemic cardiac function and a 50% decrease in lactate dehydrogenase (LDH) release following 30 min ischaemia and 30 min reperfusion compared with non-preconditioned hearts. Reserpine pretreatment did not affect the response to ischaemia or to preconditioning, although LDH release tended to be greater than in normal hearts, especially in the non-preconditioned group. Although 6-hydroxydopamine significantly increased postischaemic cardiac function in the preconditioned group, no other index of ischaemic damage (for example, LDH release, left ventricular end diastolic pressure) was affected. Further studies showed that 10 nmol.min-1 noradrenaline did not affect the severity of ischaemia, indicating that it does not mimic preconditioning.", "output": "{\"label\": \"no\", \"rationale\": \"Endogenous catecholamines are not necessary for ischaemic preconditioning in isolated rat hearts and play little or no role in the functional responses to ischaemia.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 7895230, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Artefacts in 24-h pharyngeal and oesophageal pH monitoring: is simplification of pH data analysis feasible?\n\nABSTRACT:\nAmbulatory 24-h dual-channel pharyngeal and oesophageal pH monitoring is the standard test for measuring gastro-oesophageal and gastropharyngeal reflux. Artefacts caused by the intake of food may result in falsely positive gastropharyngeal reflux, which necessitates a manual review of 24-h pH data. The purpose of the study was to investigate the influence of meals and whether leaving out meals affected the reliability of the test. Patients referred for otolaryngological complaints, suspected to have been caused by gastro-oesophageal reflux, underwent 24-h dual-channel pH monitoring. The raw unprocessed pH data were corrected by visual inspection of the 24-h tracings (corrected data), by leaving out meals or meals plus a 2-h postprandrial period. The raw pH data were substantially influenced by artefacts of food intake and pseudoreflux. Data obtained by leaving out meals agreed best with manually corrected data. Many of the falsely positive reflux episodes could be removed, thereby inducing a 9%-18% chance of undetected reflux. When examining the fraction of time supine, manually corrected data and data leaving out meals were fully concordant and detected 79% of patients with gastropharyngeal reflux. However, leaving out meals plus a 2-h postprandrial period resulted in 21%-50% falsely negative tests.", "output": "{\"label\": \"maybe\", \"rationale\": \"Leaving out the period of intake of meals and beverages from the raw pH data might be the second best test after the time-consuming visual correction with a small chance of undetected gastropharyngeal reflux. For scientific purposes and when in doubt, it remains necessary to review the computer-generated data manually to discover every gastropharyngeal reflux event.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 14992556, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Consumption of whole fruits increases the risk of type 2 diabetes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Fruit consumption and risk of type 2 diabetes: results from three prospective longitudinal cohort studies\nABSTRACT: OBJECTIVE To determine whether individual fruits are differentially associated with risk of type 2 diabetes. DESIGN Prospective longitudinal cohort study. SETTING Health professionals in the United States. PARTICIPANTS 66,105 women from the Nurses' Health Study (1984-2008), 85,104 women from the Nurses' Health Study II (1991-2009), and 36,173 men from the Health Professionals Follow-up Study (1986-2008) who were free of major chronic diseases at baseline in these studies. MAIN OUTCOME MEASURE Incident cases of type 2 diabetes, identified through self report and confirmed by supplementary questionnaires. RESULTS During 3,464,641 person years of follow-up, 12,198 participants developed type 2 diabetes. After adjustment for personal, lifestyle, and dietary risk factors of diabetes, the pooled hazard ratio of type 2 diabetes for every three servings/week of total whole fruit consumption was 0.98 (95% confidence interval 0.97 [corrected] to 0.99). With mutual adjustment of individual fruits, the pooled hazard ratios of type 2 diabetes for every three servings/week were 0.74 (0.66 to 0.83) for blueberries, 0.88 (0.83 to 0.93) for grapes and raisins, 0.89 (0.79 to 1.01) for prunes, 0.93 (0.90 to 0.96) for apples and pears, 0.95 (0.91 to 0.98) for bananas, 0.95 (0.91 to 0.99) for grapefruit, 0.97 (0.92 to 1.02) for peaches, plums, and apricots, 0.99 (0.95 to 1.03) for oranges, 1.03 (0.96 to 1.10) for strawberries, and 1.10 (1.02 to 1.18) for cantaloupe. The pooled hazard ratio for the same increment in fruit juice consumption was 1.08 (1.05 to 1.11). The associations with risk of type 2 diabetes differed significantly among individual fruits (P<0.001 in all cohorts). CONCLUSION Our findings suggest the presence of heterogeneity in the associations between individual [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Greater consumption of specific whole fruits, particularly blueberries, grapes, and apples, is significantly associated with a lower risk of type 2 diabetes, whereas greater consumption of fruit juice is associated with a higher risk.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 283, "doc_id": "1974176", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Inside the body, falciparum parasites reproduce asexually.\n\nCANDIDATE_ABSTRACT:\nTITLE: Characterization of two classes of small molecule inhibitors of Arp2/3 complex\nABSTRACT: Polymerization of actin filaments directed by the actin-related protein (Arp)2/3 complex supports many types of cellular movements. However, questions remain regarding the relative contributions of Arp2/3 complex versus other mechanisms of actin filament nucleation to processes such as path finding by neuronal growth cones; this is because of the lack of simple methods to inhibit Arp2/3 complex reversibly in living cells. Here we describe two classes of small molecules that bind to different sites on the Arp2/3 complex and inhibit its ability to nucleate actin filaments. CK-0944636 binds between Arp2 and Arp3, where it appears to block movement of Arp2 and Arp3 into their active conformation. CK-0993548 inserts into the hydrophobic core of Arp3 and alters its conformation. Both classes of compounds inhibit formation of actin filament comet tails by Listeria and podosomes by monocytes. Two inhibitors with different mechanisms of action provide a powerful approach for studying the Arp2/3 complex in living cells.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 640, "doc_id": "2119889", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: A diminished ovarian reserve is a very strong indicator of infertility, even in an a priori non-infertile population.\n\nCANDIDATE_PASSAGE:\nDiverse tumorigenic pathways in ovarian serous carcinoma. This study was undertaken to analyze genetic alterations in 108 sporadic serous ovarian neoplasms to elucidate ovarian serous carcinogenesis. Our results demonstrate that K-ras mutations occur in approximately 50% of serous borderline tumors (SBTs), non-invasive micropapillary serous carcinomas (MPSCs), and invasive micropapillary serous carcinomas, which represent a morphological continuum of tumor progression. Moreover, progressive increase in the degree of allelic imbalance of chromosomes 1p, 5q, 8p, 18q, 22q, and Xp was observed comparing serous borderline tumors to noninvasive and invasive micropapillary serous carcinomas. In contrast, high-grade (conventional serous carcinoma) tumors contained wild-type K-ras in all 23 cases studied and a high frequency of allelic imbalance even in small (early) primary tumors similar to that found in advanced stage tumors. Based on these findings, we propose a dualistic model for ovarian serous carcinogenesis. One pathway involves a stepwise progression from SBT to noninvasive and then invasive MPSC. The other pathway is characterized by rapid progression from the ovarian surface epithelium or inclusion cysts to a conventional (high-grade) serous carcinoma.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "40", "doc_id": "42836872", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Cancer-associated fibroblasts (CAFs) are constituents of tumor microenvironments\n\nCANDIDATE_PASSAGE:\nHelicobacter pylori infection triggers aberrant expression of activation-induced cytidine deaminase in gastric epithelium Infection with Helicobacter pylori (H. pylori) is a risk factor for the development of gastric cancer. Here we show that infection of gastric epithelial cells with 'cag' pathogenicity island (cagPAI)-positive H. pylori induced aberrant expression of activation-induced cytidine deaminase (AID), a member of the cytidine-deaminase family that acts as a DNA- and RNA-editing enzyme, via the IκB kinase–dependent nuclear factor-κB activation pathway. H. pylori–mediated upregulation of AID resulted in the accumulation of nucleotide alterations in the TP53 tumor suppressor gene in gastric cells in vitro. Our findings provide evidence that aberrant AID expression caused by H. pylori infection might be a mechanism of mutation accumulation in the gastric mucosa during H. pylori–associated gastric carcinogenesis.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "224", "doc_id": "22703082", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Patients in stable partnerships have a slower progression from HIV to AIDS.\n\nCANDIDATE_ABSTRACT:\nTITLE: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\nABSTRACT: OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART). DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study). SETTING Seven outpatient clinics throughout Switzerland. PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years). MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound. RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion. When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership. In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without. Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression. CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 923, "doc_id": "17077004", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Post-transcriptional handling of mitochondrial transcripts occurs in mitochondrial RNA granules.\n\nCANDIDATE_PASSAGE:\nEpigenetic regulation of miR-184 by MBD1 governs neural stem cell proliferation and differentiation. Methyl-CpG binding protein 1 (MBD1) regulates gene expression via a DNA methylation-mediated epigenetic mechanism. We have previously demonstrated that MBD1 deficiency impairs adult neural stem/progenitor cell (aNSC) differentiation and neurogenesis, but the underlying mechanism was unclear. Here, we show that MBD1 regulates the expression of several microRNAs in aNSCs and, specifically, that miR-184 is directly repressed by MBD1. High levels of miR-184 promoted proliferation but inhibited differentiation of aNSCs, whereas inhibition of miR-184 rescued the phenotypes associated with MBD1 deficiency. We further found that miR-184 regulates the expression of Numblike (Numbl), a known regulator of brain development, by binding to the 3'-UTR of Numbl mRNA and affecting its translation. Expression of exogenous Numbl could rescue the aNSC defects that result from either miR-184 overexpression or MBD1 deficiency. Therefore, MBD1, miR-184, and Numbl form a regulatory network that helps control the balance between proliferation and differentiation of aNSCs.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "962", "doc_id": "2356950", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: CD44v6 is not associated with constitutive and reprogrammed cancer stem cells driving cancer metastasis.\n\nCANDIDATE_ABSTRACT:\nTITLE: CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis.\nABSTRACT: Cancer stem cells drive tumor formation and metastasis, but how they acquire metastatic traits is not well understood. Here, we show that all colorectal cancer stem cells (CR-CSCs) express CD44v6, which is required for their migration and generation of metastatic tumors. CD44v6 expression is low in primary tumors but demarcated clonogenic CR-CSC populations. Cytokines hepatocyte growth factor (HGF), osteopontin (OPN), and stromal-derived factor 1α (SDF-1), secreted from tumor associated cells, increase CD44v6 expression in CR-CSCs by activating the Wnt/β-catenin pathway, which promotes migration and metastasis. CD44v6(-) progenitor cells do not give rise to metastatic lesions but, when treated with cytokines, acquire CD44v6 expression and metastatic capacity. Importantly, phosphatidylinositol 3-kinase (PI3K) inhibition selectively killed CD44v6 CR-CSCs and reduced metastatic growth. In patient cohorts, low levels of CD44v6 predict increased probability of survival. Thus, the metastatic process in colorectal cancer is initiated by CSCs through the expression of CD44v6, which is both a functional biomarker and therapeutic target.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Importantly, phosphatidylinositol 3-kinase (PI3K) inhibition selectively killed CD44v6 CR-CSCs and reduced metastatic growth.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 203, "doc_id": "9558539", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does use of hydrophilic guidewires significantly improve technical success rates of peripheral PTA?\n\nABSTRACT:\nTo determine whether the use of hydrophilic guidewires has increased the technical success rate of peripheral percutaneous transluminal angioplasty (PTA).MATERIAL/ We performed 125 procedures and analyzed the technical success rates of PTA using the conventional guidewire first and then if needed, the hydrophilic guidewire for iliac and SFA stenoses or occlusions. Angioplasty was performed on 25 stenosed, 25 occluded iliac arteries and 25 stenosed, 50 occluded femoral arteries. The result was defined as technical success when the lesion was crossed by a guidewire and balloon, then it was dilated with restoration of vessel lumen and less than 30% residual stenosis and the rise in ABI values was at least 0.15 after 24 hours. The technical success rate after PTA of stenosed iliac arteries was achieved in 96% (24/25) using conventional wires and 100% using hydrophilic guidewire; in iliac occlusions, the rates were 60% (15/25) and 96%, respectively; in femoral stenosis - 84% (21/25) and 100%; in occlusions in the first group: lesions<10 cm -64% (16/25) and 96%, in the second group: lesions>10 cm -48% (12/25) and 88%. In the iliac group, there was no significant difference in the success of iliac stenosis PTA. However, there were significant changes in the success rates of PTA performed for SFA stenosis and iliac and SFA occlusions.", "output": "{\"label\": \"maybe\", \"rationale\": \"In summary, we report an overall improvement and high technical success rate for peripherial PTA. The use of hydrophilic guidewires made significant difference to the technical success rate of PTA, especially in occlusion and more complicated lesions.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 16538201, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Aggravated inflammation is dependent on NLRP3 inflammasome activation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Gout-associated uric acid crystals activate the NALP3 inflammasome\nABSTRACT: Development of the acute and chronic inflammatory responses known as gout and pseudogout are associated with the deposition of monosodium urate (MSU) or calcium pyrophosphate dihydrate (CPPD) crystals, respectively, in joints and periarticular tissues. Although MSU crystals were first identified as the aetiological agent of gout in the eighteenth century and more recently as a ‘danger signal’ released from dying cells, little is known about the molecular mechanisms underlying MSU- or CPPD-induced inflammation. Here we show that MSU and CPPD engage the caspase-1-activating NALP3 (also called cryopyrin) inflammasome, resulting in the production of active interleukin (IL)-1β and IL-18. Macrophages from mice deficient in various components of the inflammasome such as caspase-1, ASC and NALP3 are defective in crystal-induced IL-1β activation. Moreover, an impaired neutrophil influx is found in an in vivo model of crystal-induced peritonitis in inflammasome-deficient mice or mice deficient in the IL-1β receptor (IL-1R). These findings provide insight into the molecular processes underlying the inflammatory conditions of gout and pseudogout, and further support a pivotal role of the inflammasome in several autoinflammatory diseases.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here we show that MSU and CPPD engage the caspase-1-activating NALP3 (also called cryopyrin) inflammasome, resulting in the production of active interleukin (IL)-1β and IL-18.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 93, "doc_id": "2692522", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The combination of physical examinations with C-reactive protein values do not improve the accuracy of radiographic verified pneumonia predictions.\n\nCANDIDATE_PASSAGE:\nUse of serum C reactive protein and procalcitonin concentrations in addition to symptoms and signs to predict pneumonia in patients presenting to primary care with acute cough: diagnostic study OBJECTIVES To quantify the diagnostic accuracy of selected inflammatory markers in addition to symptoms and signs for predicting pneumonia and to derive a diagnostic tool. DESIGN Diagnostic study performed between 2007 and 2010. Participants had their history taken, underwent physical examination and measurement of C reactive protein (CRP) and procalcitonin in venous blood on the day they first consulted, and underwent chest radiography within seven days. SETTING Primary care centres in 12 European countries. PARTICIPANTS Adults presenting with acute cough. MAIN OUTCOME MEASURES Pneumonia as determined by radiologists, who were blind to all other information when they judged chest radiographs. RESULTS Of 3106 eligible patients, 286 were excluded because of missing or inadequate chest radiographs, leaving 2820 patients (mean age 50, 40% men) of whom 140 (5%) had pneumonia. Re-assessment of a subset of 1675 chest radiographs showed agreement in 94% (κ 0.45, 95% confidence interval 0.36 to 0.54). Six published \"symptoms and signs models\" varied in their discrimination (area under receiver operating characteristics curve (ROC) ranged from 0.55 (95% confidence interval 0.50 to 0.61) to 0.71 (0.66 to 0.76)). The optimal combination of clinical prediction items derived from our patients included absence of runny nose and presence of breathlessness, crackles and diminished breath sounds on auscultation, tachycardia, and fever, with an ROC area of 0.70 (0.65 to 0.75). Addition of CRP at the optimal cut off of >30 mg/L increased the ROC area to 0.77 (0.73 to 0.81) and improved [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1205", "doc_id": "5558754", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Immune responses result in the development of inflammatory Th17 cells and anti-inflammatory iTregs.\n\nCANDIDATE_PASSAGE:\nTroponin concentrations for stratification of patients with acute coronary syndromes in relation to therapeutic efficacy of tirofiban. PRISM Study Investigators. Platelet Receptor Inhibition in Ischemic Syndrome Management. BACKGROUND A major challenge for physicians is to identify patients with acute coronary syndromes who may benefit from treatment with glycoprotein-IIb/IIIa-receptor antagonists. We investigated whether troponin concentrations can be used to stratify patients for benefit from treatment with tirofiban. METHODS We enrolled 2222 patients of the Platelet Receptor Inhibition in Ischemic Syndrome Management study with coronary artery disease and who had had chest pain in the previous 24 h. All patients received aspirin and were randomly assigned treatment with tirofiban or heparin. We took baseline measurements of troponin I and troponin T. We recorded death, myocardial infarction, or recurrent ischaemia after 48 h infusion treatment and at 7 days and 30 days. FINDINGS 629 (28.3%) patients had troponin I concentrations higher than the diagnostic threshold of 1.0 microg/L and 644 (29.0%) troponin T concentrations higher than 0.1 microg/L. 30-day event rates (death, myocardial infarction) were 13.0% for troponin-I-positive patients compared with 4.9% for troponin-I-negative patients (p<0.0001), and 13.7% compared wth 3.5% for troponin T (p<0.001). At 30 days, in troponin-I-positive patients, tirofiban had lowered the risk of death (adjusted hazard ratio 0.25 [95% CI 0.09-0.68], p=0.004) and myocardial infarction (0.37 [0.16-0.84], p=0.01). This benefit was seen in medically managed patients (0.30 [0.10-0.84], p=0.004) and those undergoing revascularisation (0.37 [0.15-0.93] p=0.02) after 48 h infusion treatment. By contrast, no treatment effect wa [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "560", "doc_id": "29526125", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Hematopoietic Stem Cell purification reaches purity rate of up to 50%.\n\nCANDIDATE_PASSAGE:\nCombined Single-Cell Functional and Gene Expression Analysis Resolves Heterogeneity within Stem Cell Populations Heterogeneity within the self-renewal durability of adult hematopoietic stem cells (HSCs) challenges our understanding of the molecular framework underlying HSC function. Gene expression studies have been hampered by the presence of multiple HSC subtypes and contaminating non-HSCs in bulk HSC populations. To gain deeper insight into the gene expression program of murine HSCs, we combined single-cell functional assays with flow cytometric index sorting and single-cell gene expression assays. Through bioinformatic integration of these datasets, we designed an unbiased sorting strategy that separates non-HSCs away from HSCs, and single-cell transplantation experiments using the enriched population were combined with RNA-seq data to identify key molecules that associate with long-term durable self-renewal, producing a single-cell molecular dataset that is linked to functional stem cell activity. Finally, we demonstrated the broader applicability of this approach for linking key molecules with defined cellular functions in another stem cell system.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "508", "doc_id": "13980338", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Genes regulated by Esrrb transcription factor are sensitive to Mbd3 function.\n\nCANDIDATE_ABSTRACT:\nTITLE: An Oct4-Centered Protein Interaction Network in Embryonic Stem Cells\nABSTRACT: Transcription factors, such as Oct4, are critical for establishing and maintaining pluripotent cell identity. Whereas the genomic locations of several pluripotency transcription factors have been reported, the spectrum of their interaction partners is underexplored. Here, we use an improved affinity protocol to purify Oct4-interacting proteins from mouse embryonic stem cells (ESCs). Subsequent purification of Oct4 partners Sall4, Tcfcp2l1, Dax1, and Esrrb resulted in an Oct4 interactome of 166 proteins, including transcription factors and chromatin-modifying complexes with documented roles in self-renewal, but also many factors not previously associated with the ESC network. We find that Esrrb associated with the basal transcription machinery and also detect interactions between transcription factors and components of the TGF-beta, Notch, and Wnt signaling pathways. Acute depletion of Oct4 reduced binding of Tcfcp2l1, Dax1, and Esrrb to several target genes. In conclusion, our purification protocol allowed us to bring greater definition to the circuitry controlling pluripotent cell identity.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 456, "doc_id": "30507607", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Patients with common epithelial cancers are less likely to have an emergency event as their first hospital admission if they live in resource-deprived areas.\n\nCANDIDATE_ABSTRACT:\nTITLE: Social variations in access to hospital care for patients with colorectal, breast, and lung cancer between 1999 and 2006: retrospective analysis of hospital episode statistics\nABSTRACT: OBJECTIVES To determine the extent to which type of hospital admission (emergency compared with elective) and surgical procedure varied by socioeconomic circumstances, age, sex, and year of admission for colorectal, breast, and lung cancer. DESIGN Repeated cross sectional study with data from individual patients, 1 April 1999 to 31 March 2006. SETTING Hospital episode statistics (HES) dataset. PARTICIPANTS 564 821 patients aged 50 and over admitted with a diagnosis of colorectal, breast, or lung cancer. MAIN OUTCOME MEASURES Proportion of patients admitted as emergencies, and the proportion receiving the recommended surgical treatment. RESULTS Patients from deprived areas, older people, and women were more likely to be admitted as emergencies. For example, the adjusted odds ratio for patients with breast cancer in the least compared with most deprived fifth of deprivation was 0.63 (95% confidence interval 0.60 to 0.66) and the adjusted odds ratio for patients with lung cancer aged 80-89 compared with those aged 50-59 was 3.13 (2.93 to 3.34). There were some improvements in disparities between age groups but not for patients living in deprived areas over time. Patients from deprived areas were less likely to receive preferred procedures for rectal, breast, and lung cancer. These findings did not improve with time. For example, 67.4% (3529/5237) of patients in the most deprived fifth of deprivation had anterior resection for rectal cancer compared with 75.5% (4497/5959) of patients in the least deprived fifth (1.34, 1.22 to 1.47). Over half (54.0%, 11 256/20 849) of patients in the most deprived fifth of deprivation had breast conserving surgery compared with 63.7% (18 445/28 960) of patients in the least deprived fifth (1.21, 1.16 to 1.26). Men were less like [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"For example, the adjusted odds ratio for patients with breast cancer in the least compared with most deprived fifth of deprivation was 0.63 (95% confidence interval 0.60 to 0.66) and the adjusted odds ratio for patients with lung cancer aged 80-89 compared with those aged 50-59 was 3.13 (2.93 to 3.34). There were some improvements in disparities between age groups but not for patients living in deprived areas over time.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 927, "doc_id": "16390264", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is a MIF haplotype associated with the outcome of patients with severe sepsis : a case control study?\n\nABSTRACT:\nMacrophage migration inhibitory factor (MIF) plays an important regulatory role in sepsis. In the promoter region a C/G single nucleotide polymorphism (SNP) at position -173 (rs755622) and a CATT5-8 microsatellite at position -794 are related to modified promoter activity. The purpose of the study was to analyze their association with the incidence and outcome of severe sepsis. Genotype distributions and allele frequencies in 169 patients with severe sepsis, 94 healthy blood donors and 183 postoperative patients without signs of infection or inflammation were analyzed by real time PCR and Sequence analysis. All included individuals were Caucasians. Genotype distribution and allele frequencies of severe sepsis patients were comparable to both control groups. However, the genotype and allele frequencies of both polymorphisms were associated significantly with the outcome of severe sepsis. The highest risk of dying from severe sepsis was detectable in patients carrying a haplotype with the alleles -173 C and CATT7 (p = 0.0005, fisher exact test, RR = 1,806, CI: 1.337 to 2.439).", "output": "{\"label\": \"yes\", \"rationale\": \"The haplotype with the combination of the -173 C allele and the -794 CATT7 allele may not serve as a marker for susceptibility to sepsis, but may help identify septic patients at risk of dying.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 19941661, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Physical activity does not improve cognitive function in individuals with Alzheimers.\n\nCANDIDATE_ABSTRACT:\nTITLE: High Km soluble 5'-nucleotidase from human placenta. Properties and allosteric regulation by IMP and ATP.\nABSTRACT: A human placental soluble \"high Km\" 5'-nucleotidase has been separated from \"low Km\" 5'-nucleotidase and nonspecific phosphatase by AMP-Sepharose affinity chromatography. The enzyme was purified 8000-fold to a specific activity of 25.6 mumol/min/mg. The subunit molecular mass is 53 kDa, and the native molecular mass is 210 kDa, suggesting a tetrameric structure. Soluble high Km 5'-nucleotidase is most active with IMP and GMP and their deoxy derivatives. IMP is hydrolyzed 15 times faster than AMP. The enzyme has a virtually absolute requirement for magnesium ions and is regulated by them. Purine nucleoside 5'-triphosphates strongly activate the enzyme with the potency order dATP greater than ATP greater than GTP. 2,3-Diphosphoglycerate activates the enzyme as potently as ATP. Three millimolar ATP decreased the Km for IMP from 0.33 to 0.09 mM and increased the Vmax 12-fold. ATP activation was modified by the IMP concentration. At 20 microM IMP the ATP-dependent activation curve was sigmoidal, while at 2 mM IMP it was hyperbolic. The A0.5 values for ATP were 2.26 and 0.70 mM, and the relative maximal velocities were 32.9 and 126.0 nmol/min, respectively. Inorganic phosphate shifts the hyperbolic substrate velocity relationship for IMP to a sigmoidal one. With physiological concentrations of cofactors (3 mM ATP, 1-4 mM Pi, 150 mM KCl) at pH 7.4, the enzyme is 25-35 times more active toward 100 microM IMP than 100 microM AMP. These data show that: (a) soluble human placental high Km 5'-nucleotidase coexists in human placenta with the low Km enzyme; (b) under physiological conditions the enzyme favors the hydrolysis of IMP and is critically regulated by IMP, ATP, and Pi levels; and (c) kinetic properties of ATP and IMP are each modified by the other compound sugge [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 944, "doc_id": "393001", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Citrullinated proteins externalized in neutrophil extracellular traps act indirectly to disrupt the inflammatory cycle.\n\nCANDIDATE_ABSTRACT:\nTITLE: Neutrophil extracellular chromatin traps connect innate immune response to autoimmunity\nABSTRACT: Autoantibodies to DNA and histones (chromatin) are the defining antigen specificity in systemic lupus erythematosus (SLE) and related musculoskeletal disorders but the mechanisms responsible for their induction remain mysterious. That situation rapidly changed once neutrophil extracellular chromatin traps (NETs) were discovered and observed to play a conserved role in innate immune responses to a broad variety of microbial pathogens. At the center of an infectious process, neutrophils exert various antimicrobial defenses, including the release of nuclear chromatin into the extracellular space. The externalized NETs, a complex meshwork of nuclear chromatin and antimicrobial proteins, serve to immobilize and degrade microbial pathogens. Here, we critically evaluate the evidence supporting NETs versus apoptotic bodies as a source for nuclear antigens in autoimmunity. We also discuss the possibility that NET chromatin forms an essential component of immune deposits in the pathogenesis of glomerulonephritis in SLE and other autoimmune immune complex diseases.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 263, "doc_id": "14853989", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Replacement of histone H2A with H2A.Z accelerates gene activation in yeasts by destabilizing +1 nucleosomes.\n\nCANDIDATE_PASSAGE:\nGenome-Wide Dynamics of Htz1, a Histone H2A Variant that Poises Repressed/Basal Promoters for Activation through Histone Loss Histone variants help specialize chromatin regions; however, their impact on transcriptional regulation is largely unknown. Here, we determined the genome-wide localization and dynamics of Htz1, the yeast histone H2A variant. Htz1 localizes to hundreds of repressed/basal Pol II promoters and prefers TATA-less promoters. Specific Htz1 deposition requires the SWR1 complex, which largely colocalizes with Htz1. Htz1 occupancy correlates with particular histone modifications, and Htz1 deposition is partially reliant on Gcn5 (a histone acetyltransferase) and Bdf1, an SWR1 complex member that binds acetylated histones. Changes in growth conditions cause a striking redistribution of Htz1 from activated to repressed/basal promoters. Furthermore, Htz1 promotes full gene activation but does not generally impact repression. Importantly, Htz1 releases from purified chromatin in vitro under conditions where H2A and H3 remain associated. We suggest that Htz1-bearing nucleosomes are deposited at repressed/basal promoters but facilitate activation through their susceptibility to loss, thereby helping to expose promoter DNA.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1040", "doc_id": "16626264", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: De novo assembly of sequence data has shorter contigs than unassembled sequence data.\n\nCANDIDATE_PASSAGE:\nThe expanding problem of adipose depot remodeling and postnatal adipocyte progenitor recruitment. The rising incidence of obesity and associated metabolic diseases has increased the urgency in understanding all aspects of adipose tissue biology. This includes the function of adipocytes, how adipose tissue expands in obesity, and how expanded adipose tissues in adults can impact physiology. Here, we highlight the growing appreciation for the importance of de novo adipocyte differentiation to adipose tissue expansion in adult humans and animals. We detail recent efforts to identify adipose precursor populations that contribute to the physiological postnatal recruitment of white, brown, and beige adipocytes in mice, and summarize new data that reveal the complexity of adipose tissue development in vivo.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "313", "doc_id": "4854076", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Gastric infection with Helicobacter pylori decreases risk of gastric cancer in humans.\n\nCANDIDATE_PASSAGE:\nCombined Impact of Lifestyle-Related Factors on Total and Cause-Specific Mortality among Chinese Women: Prospective Cohort Study BACKGROUND Although cigarette smoking, excessive alcohol drinking, obesity, and several other well-studied unhealthy lifestyle-related factors each have been linked to the risk of multiple chronic diseases and premature death, little is known about the combined impact on mortality outcomes, in particular among Chinese and other non-Western populations. The objective of this study was to quantify the overall impact of lifestyle-related factors beyond that of active cigarette smoking and alcohol consumption on all-cause and cause-specific mortality in Chinese women. METHODS AND FINDINGS We used data from the Shanghai Women's Health Study, an ongoing population-based prospective cohort study in China. Participants included 71,243 women aged 40 to 70 years enrolled during 1996-2000 who never smoked or drank alcohol regularly. A healthy lifestyle score was created on the basis of five lifestyle-related factors shown to be independently associated with mortality outcomes (normal weight, lower waist-hip ratio, daily exercise, never exposed to spouse's smoking, higher daily fruit and vegetable intake). The score ranged from zero (least healthy) to five (most healthy) points. During an average follow-up of 9 years, 2,860 deaths occurred, including 775 from cardiovascular disease (CVD) and 1,351 from cancer. Adjusted hazard ratios for mortality decreased progressively with an increasing number of healthy lifestyle factors. Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for c [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "447", "doc_id": "1456068", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: T cell receptor /CD3 microdomains are required to induce the immunologic synapse.\n\nCANDIDATE_ABSTRACT:\nTITLE: Full activation of the T cell receptor requires both clustering and conformational changes at CD3.\nABSTRACT: T cell receptor (TCR-CD3) triggering involves both receptor clustering and conformational changes at the cytoplasmic tails of the CD3 subunits. The mechanism by which TCRalphabeta ligand binding confers conformational changes to CD3 is unknown. By using well-defined ligands, we showed that induction of the conformational change requires both multivalent engagement and the mobility restriction of the TCR-CD3 imposed by the plasma membrane. The conformational change is elicited by cooperative rearrangements of two TCR-CD3 complexes and does not require accompanying changes in the structure of the TCRalphabeta ectodomains. This conformational change at CD3 reverts upon ligand dissociation and is required for T cell activation. Thus, our permissive geometry model provides a molecular mechanism that rationalizes how the information of ligand binding to TCRalphabeta is transmitted to the CD3 subunits and to the intracellular signaling machinery.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"T cell receptor (TCR-CD3) triggering involves both receptor clustering and conformational changes at the cytoplasmic tails of the CD3 subunits.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1128, "doc_id": "33499189", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: p16INK4A accumulation is linked to an abnormal wound response caused by the microinvasive step of advanced Oral Potentially Malignant Lesions (OPMLs).\n\nCANDIDATE_PASSAGE:\nIdentification of Senescent Cells in the Bone Microenvironment. Cellular senescence is a fundamental mechanism by which cells remain metabolically active yet cease dividing and undergo distinct phenotypic alterations, including upregulation of p16Ink4a , profound secretome changes, telomere shortening, and decondensation of pericentromeric satellite DNA. Because senescent cells accumulate in multiple tissues with aging, these cells and the dysfunctional factors they secrete, termed the senescence-associated secretory phenotype (SASP), are increasingly recognized as promising therapeutic targets to prevent age-related degenerative pathologies, including osteoporosis. However, the cell type(s) within the bone microenvironment that undergoes senescence with aging in vivo has remained poorly understood, largely because previous studies have focused on senescence in cultured cells. Thus in young (age 6 months) and old (age 24 months) mice, we measured senescence and SASP markers in vivo in highly enriched cell populations, all rapidly isolated from bone/marrow without in vitro culture. In both females and males, p16Ink4a expression by real-time quantitative polymerase chain reaction (rt-qPCR) was significantly higher with aging in B cells, T cells, myeloid cells, osteoblast progenitors, osteoblasts, and osteocytes. Further, in vivo quantification of senescence-associated distension of satellites (SADS), ie, large-scale unraveling of pericentromeric satellite DNA, revealed significantly more senescent osteocytes in old compared with young bone cortices (11% versus 2%, p < 0.001). In addition, primary osteocytes from old mice had sixfold more (p < 0.001) telomere dysfunction-induced foci (TIFs) than osteocytes from young mice. Corresponding with the age-associated [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1395", "doc_id": "25419778", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The loss of the TET protein functions may have dire biological consequences, such as myeloid cancers.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tet1 and Tet2 regulate 5-hydroxymethylcytosine production and cell lineage specification in mouse embryonic stem cells.\nABSTRACT: TET family enzymes convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) in DNA. Here, we show that Tet1 and Tet2 are Oct4-regulated enzymes that together sustain 5hmC in mouse embryonic stem cells (ESCs) and are induced concomitantly with 5hmC during reprogramming of fibroblasts to induced pluripotent stem cells. ESCs depleted of Tet1 by RNAi show diminished expression of the Nodal antagonist Lefty1 and display hyperactive Nodal signaling and skewed differentiation into the endoderm-mesoderm lineage in embryoid bodies in vitro. In Fgf4- and heparin-supplemented culture conditions, Tet1-depleted ESCs activate the trophoblast stem cell lineage determinant Elf5 and can colonize the placenta in midgestation embryo chimeras. Consistent with these findings, Tet1-depleted ESCs form aggressive hemorrhagic teratomas with increased endoderm, reduced neuroectoderm, and ectopic appearance of trophoblastic giant cells. Thus, 5hmC is an epigenetic modification associated with the pluripotent state, and Tet1 functions to regulate the lineage differentiation potential of ESCs.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1226, "doc_id": "13777138", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The innate immune response struggles to remove small numbers of parasites.\n\nCANDIDATE_ABSTRACT:\nTITLE: Partitioning regulatory mechanisms of within-host malaria dynamics using the effective propagation number.\nABSTRACT: Immune clearance and resource limitation (via red blood cell depletion) shape the peaks and troughs of malaria parasitemia, which in turn affect disease severity and transmission. Quantitatively partitioning the relative roles of these effects through time is challenging. Using data from rodent malaria, we estimated the effective propagation number, which reflects the relative importance of contrasting within-host control mechanisms through time and is sensitive to the inoculating parasite dose. Our analysis showed that the capacity of innate responses to restrict initial parasite growth saturates with parasite dose and that experimentally enhanced innate immunity can affect parasite density indirectly via resource depletion. Such a statistical approach offers a tool to improve targeting of drugs or vaccines for human therapy by revealing the dynamics and interactions of within-host regulatory mechanisms.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Our analysis showed that the capacity of innate responses to restrict initial parasite growth saturates with parasite dose and that experimentally enhanced innate immunity can affect parasite density indirectly via resource depletion.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1223, "doc_id": "5289038", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Glioblastoma multiforme (GBM) is characterized by extensive invasion, rapid growth, necrosis, and angiogenesis.\n\nCANDIDATE_ABSTRACT:\nTITLE: A cohort study of the risk of cervical intraepithelial neoplasia grade 2 or 3 in relation to papillomavirus infection.\nABSTRACT: BACKGROUND Human papillomavirus (HPV) has been associated with cervical intraepithelial neoplasia, but the temporal relation between the infection and the neoplasia remains unclear, as does the relative importance of the specific type of HPV, other sexually transmitted diseases, and other risk factors. METHODS We studied prospectively a cohort of 241 women who presented for evaluation of sexually transmitted disease and had negative cervical cytologic tests. The women were followed every four months with cytologic and colposcopic examinations of the uterine cervix and tests for HPV DNA and other sexually transmitted diseases. RESULTS Cervical intraepithelial neoplasia grade 2 or 3 was confirmed by biopsy in 28 women. On the basis of survival analysis, the cumulative incidence of cervical intraepithelial neoplasia at two years was 28 percent among women with a positive test for HPV and 3 percent among those without detectable HPV DNA: The risk was highest among those with HPV type 16 or 18 infection (adjusted relative risk as compared with that in women without HPV infection, 11; 95 percent confidence interval, 4.6 to 26; attributable risk, 52 percent). All 24 cases of cervical intraepithelial neoplasia grade 2 or 3 among HPV-positive women were detected within 24 months after the first positive test for HPV. After adjustment for the presence of HPV infection, the development of cervical intraepithelial neoplasia was also associated with younger age at first intercourse, the presence of serum antibodies to Chlamydia trachomatis, the presence of serum antibodies to cytomegalovirus, and cervical infection with Neisseria gonorrhoeae. CONCLUSIONS Cervical intraepithelial neoplasia is a common and apparently early manifestation of cervical infection by HPV, partic [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 470, "doc_id": "829646", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Type 1 Diabetes is associated with subtle perturbations in T reg development.\n\nCANDIDATE_PASSAGE:\nVegetarian diet improves insulin resistance and oxidative stress markers more than conventional diet in subjects with Type 2 diabetes AIMS The aim of this study was to compare the effects of calorie-restricted vegetarian and conventional diabetic diets alone and in combination with exercise on insulin resistance, visceral fat and oxidative stress markers in subjects with Type 2 diabetes. METHODS A 24-week, randomized, open, parallel design was used. Seventy-four patients with Type 2 diabetes were randomly assigned to either the experimental group (n = 37), which received a vegetarian diet, or the control group (n = 37), which received a conventional diabetic diet. Both diets were isocaloric, calorie restricted (-500 kcal/day). All meals during the study were provided. The second 12 weeks of the diet were combined with aerobic exercise. Participants were examined at baseline, 12 weeks and 24 weeks. Primary outcomes were: insulin sensitivity measured by hyperinsulinaemic isoglycaemic clamp; volume of visceral and subcutaneous fat measured by magnetic resonance imaging; and oxidative stress measured by thiobarbituric acid reactive substances. Analyses were by intention to treat. RESULTS Forty-three per cent of participants in the experimental group and 5% of participants in the control group reduced diabetes medication (P < 0.001). Body weight decreased more in the experimental group than in the control group [-6.2 kg (95% CI -6.6 to -5.3) vs. -3.2 kg (95% CI -3.7 to -2.5); interaction group × time P = 0.001]. An increase in insulin sensitivity was significantly greater in the experimental group than in the control group [30% (95% CI 24.5-39) vs. 20% (95% CI 14-25), P = 0.04]. A reduction in both visceral and subcutaneous fat was greater in the experimental gro [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1334", "doc_id": "5687200", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Moderate consumption of candy and chocolate reduces the risk of cardiovascular disease (CVD).\n\nCANDIDATE_PASSAGE:\nGlobal Regulation of H2A.Z Localization by the INO80 Chromatin-Remodeling Enzyme Is Essential for Genome Integrity INO80 is an evolutionarily conserved, ATP-dependent chromatin-remodeling enzyme that plays roles in transcription, DNA repair, and replication. Here, we show that yeast INO80 facilitates these diverse processes at least in part by controlling genome-wide distribution of the histone variant H2A.Z. In the absence of INO80, H2A.Z nucleosomes are mislocalized, and H2A.Z levels at promoters show reduced responsiveness to transcriptional changes, suggesting that INO80 controls H2A.Z dynamics. Additionally, we demonstrate that INO80 has a histone-exchange activity in which the enzyme can replace nucleosomal H2A.Z/H2B with free H2A/H2B dimers. Genetic interactions between ino80 and htz1 support a model in which INO80 catalyzes the removal of unacetylated H2A.Z from chromatin as a mechanism to promote genome stability.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "799", "doc_id": "18038955", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Sympathetic nerve activity is reduced throughout normal pregnancy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Regulation of sympathetic nerve activity during the cold pressor test in normotensive pregnant and nonpregnant women.\nABSTRACT: Baseline neurovascular transduction is reduced in normotensive pregnancy; however, little is known about changes to neurovascular transduction during periods of heightened sympathetic activation. We tested the hypothesis that, despite an exacerbated muscle sympathetic nerve activity (microneurography) response to cold pressor stimulation, the blunting of neurovascular transduction in normotensive pregnant women would result in similar changes in vascular resistance and mean arterial pressure (Finometer) relative to nonpregnant controls. Baseline neurovascular transduction was reduced in pregnant women relative to controls when expressed as the quotient of both total resistance and mean arterial pressure and sympathetic burst frequency (0.32±0.07 versus 0.58±0.16 mm Hg/L/min/bursts/min, P<0.001 and 2.4±0.7 versus 3.6±0.8 mm Hg/bursts/min, P=0.001). Sympathetic activation was greater across all 3 minutes of cold pressor stimulation in the pregnant women relative to the nonpregnant controls. Peak sympathoexcitation was also greater in pregnant than in nonpregnant women, whether expressed as sympathetic burst frequency (+17±13 versus +7±8 bursts/min, P=0.049), burst incidence (+17±9 versus +6±11 bursts/100 hb, P=0.03), or total activity (+950±660 versus +363±414 arbitrary units, P=0.04). However, neurovascular transduction during peak cold pressor-induced sympathoexcitation remained blunted in pregnant women (0.25±0.11 versus 0.45±0.08 mm Hg/L/min/bursts/min, P<0.001 and 1.9±1.0 versus 3.2±0.9 mm Hg/bursts/min, P=0.006). Therefore, mean arterial pressure (93±21 versus 99±6 mm Hg, P=0.4) and total peripheral resistance (12±3 versus 14±3 mm Hg/L/min) were not different between pregnant and nonpregnant women during peak sympathoexcitation. These data indicate that [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Peak sympathoexcitation was also greater in pregnant than in nonpregnant women, whether expressed as sympathetic burst frequency (+17±13 versus +7±8 bursts/min, P=0.049), burst incidence (+17±9 versus +6±11 bursts/100 hb, P=0.03), or total activity (+950±660 versus +363±414 arbitrary units, P=0.04).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1120, "doc_id": "13907928", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Prescriptions as a proxy for asthma in children: a good choice?\n\nABSTRACT:\nStock et al. (Eur Respir J 25:47-53, 2005) recently estimated asthma prevalence in Germany using claims data on prescriptions and hospital diagnoses and found high prevalence peaks in infants. Our objective was to critically assess and discuss various aspects of identifying children with asthma using prescription data. We replicated the selection procedure of Stock et al. using data on 290,919 children aged 0-17 years insured in the Gmünder ErsatzKasse (GEK) in 2005. Asthma prevalence was also estimated in a sample of 17,641 children aged 0-17 years participating in the German Health Interview and Examination Survey for Children and Adolescents (KiGGS) from 2003 to 2006. In children aged 0-4 years insured in the GEK, prevalences were found to range from 11.7 to 17.7% for boys and from 7.2 to 11.1% for girls when the criteria of Stock et al. were applied. A steady decline in prevalences was observed in older age groups. Asthma prevalence estimated in the KiGGS data showed a quite different distribution. In the age group 0-4 years, prevalences were found to range from 0 to 2.6% in boys and from 0 to 1.0% in girls; in children>4 years, prevalences were found to increase with increasing age.", "output": "{\"label\": \"no\", \"rationale\": \"When additional validation studies were taken into account, asthma medications were found to be prescribed not only for asthma but also for other respiratory diseases. In addition, not all children with current asthma had prescriptions. We therefore conclude that asthma medications are therefore not a good proxy for the disease.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 20187289, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: miR-142-5P is a temperature-sensitive microRNA (miRNA).\n\nCANDIDATE_PASSAGE:\nCD64 expression distinguishes monocyte-derived and conventional dendritic cells and reveals their distinct role during intramuscular immunization. Although most vaccines are administered i.m., little is known about the dendritic cells (DCs) that are present within skeletal muscles. In this article, we show that expression of CD64, the high-affinity IgG receptor FcγRI, distinguishes conventional DCs from monocyte-derived DCs (Mo-DCs). By using such a discriminatory marker, we defined the distinct DC subsets that reside in skeletal muscles and identified their migratory counterparts in draining lymph nodes (LNs). We further used this capability to analyze the functional specialization that exists among muscle DCs. After i.m. administration of Ag adsorbed to alum, we showed that alum-injected muscles contained large numbers of conventional DCs that belong to the CD8α(+)- and CD11b(+)-type DCs. Both conventional DC types were capable of capturing Ag and of migrating to draining LNs, where they efficiently activated naive T cells. In alum-injected muscles, Mo-DCs were as numerous as conventional DCs, but only a small fraction migrated to draining LNs. Therefore, alum by itself poorly induces Mo-DCs to migrate to draining LNs. We showed that addition of small amounts of LPS to alum enhanced Mo-DC migration. Considering that migratory Mo-DCs had, on a per cell basis, a higher capacity to induce IFN-γ-producing T cells than conventional DCs, the addition of LPS to alum enhanced the overall immunogenicity of Ags presented by muscle-derived DCs. Therefore, a full understanding of the role of adjuvants during i.m. vaccination needs to take into account the heterogeneous migratory and functional behavior of muscle DCs and Mo-DCs revealed in this study.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1392", "doc_id": "21719289", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: In melanoma, anti-CTLA-4 treatment reinvigorates exhausted PD-1+Eomes+CD8 T cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: National study of physician awareness and adherence to cardiovascular disease prevention guidelines.\nABSTRACT: BACKGROUND Few data have evaluated physician adherence to cardiovascular disease (CVD) prevention guidelines according to physician specialty or patient characteristics, particularly gender. METHODS AND RESULTS An online study of 500 randomly selected physicians (300 primary care physicians, 100 obstetricians/gynecologists, and 100 cardiologists) used a standardized questionnaire to assess awareness of, adoption of, and barriers to national CVD prevention guidelines by specialty. An experimental case study design tested physician accuracy and determinants of CVD risk level assignment and application of guidelines among high-, intermediate-, or low-risk patients. Intermediate-risk women, as assessed by the Framingham risk score, were significantly more likely to be assigned to a lower-risk category by primary care physicians than men with identical risk profiles (P<0.0001), and trends were similar for obstetricians/gynecologists and cardiologists. Assignment of risk level significantly predicted recommendations for lifestyle and preventive pharmacotherapy. After adjustment for risk assignment, the impact of patient gender on preventive care was not significant except for less aspirin (P<0.01) and more weight management recommended (P<0.04) for intermediate-risk women. Physicians did not rate themselves as very effective in their ability to help patients prevent CVD. Fewer than 1 in 5 physicians knew that more women than men die each year from CVD. CONCLUSIONS Perception of risk was the primary factor associated with CVD preventive recommendations. Gender disparities in recommendations for preventive therapy were explained largely by the lower perceived risk despite similar calculated risk for women versus men. Educational interventions for physicians are need [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 576, "doc_id": "409280", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Post-transcriptional handling of mitochondrial transcripts occurs in mitochondrial RNA granules.\n\nCANDIDATE_ABSTRACT:\nTITLE: The mitochondrial RNA-binding protein GRSF1 localizes to RNA granules and is required for posttranscriptional mitochondrial gene expression.\nABSTRACT: RNA-binding proteins are at the heart of posttranscriptional gene regulation, coordinating the processing, storage, and handling of cellular RNAs. We show here that GRSF1, previously implicated in the binding and selective translation of influenza mRNAs, is targeted to mitochondria where it forms granules that colocalize with foci of newly synthesized mtRNA next to mitochondrial nucleoids. GRSF1 preferentially binds RNAs transcribed from three contiguous genes on the light strand of mtDNA, the ND6 mRNA, and the long noncoding RNAs for cytb and ND5, each of which contains multiple consensus binding sequences. RNAi-mediated knockdown of GRSF1 leads to alterations in mitochondrial RNA stability, abnormal loading of mRNAs and lncRNAs on the mitochondrial ribosome, and impaired ribosome assembly. This results in a specific protein synthesis defect and a failure to assemble normal amounts of the oxidative phosphorylation complexes. These data implicate GRSF1 as a key regulator of posttranscriptional mitochondrial gene expression.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We show here that GRSF1, previously implicated in the binding and selective translation of influenza mRNAs, is targeted to mitochondria where it forms granules that colocalize with foci of newly synthesized mtRNA next to mitochondrial nucleoids. These data implicate GRSF1 as a key regulator of posttranscriptional mitochondrial gene expression.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 962, "doc_id": "935538", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: 1,000 genomes project enables mapping of genetic sequence variation consisting of rare variants with larger penetrance effects than common variants.\n\nCANDIDATE_ABSTRACT:\nTITLE: Rare Variants Create Synthetic Genome-Wide Associations\nABSTRACT: Genome-wide association studies (GWAS) have now identified at least 2,000 common variants that appear associated with common diseases or related traits (http://www.genome.gov/gwastudies), hundreds of which have been convincingly replicated. It is generally thought that the associated markers reflect the effect of a nearby common (minor allele frequency >0.05) causal site, which is associated with the marker, leading to extensive resequencing efforts to find causal sites. We propose as an alternative explanation that variants much less common than the associated one may create \"synthetic associations\" by occurring, stochastically, more often in association with one of the alleles at the common site versus the other allele. Although synthetic associations are an obvious theoretical possibility, they have never been systematically explored as a possible explanation for GWAS findings. Here, we use simple computer simulations to show the conditions under which such synthetic associations will arise and how they may be recognized. We show that they are not only possible, but inevitable, and that under simple but reasonable genetic models, they are likely to account for or contribute to many of the recently identified signals reported in genome-wide association studies. We also illustrate the behavior of synthetic associations in real datasets by showing that rare causal mutations responsible for both hearing loss and sickle cell anemia create genome-wide significant synthetic associations, in the latter case extending over a 2.5-Mb interval encompassing scores of \"blocks\" of associated variants. In conclusion, uncommon or rare genetic variants can easily create synthetic associations that are credited to common variants, and this possibility requires careful consi [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We propose as an alternative explanation that variants much less common than the associated one may create \\\"synthetic associations\\\" by occurring, stochastically, more often in association with one of the alleles at the common site versus the other allele. We show that they are not only possible, but inevitable, and that under simple but reasonable genetic models, they are likely to account for or contribute to many of the recently identified signals reported in genome-wide association studies.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 3, "doc_id": "14717500", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does rugby headgear prevent concussion?\n\nABSTRACT:\nTo examine the attitudes of players and coaches to the use of protective headgear, particularly with respect to the prevention of concussion. A questionnaire designed to assess attitudes to headgear was administered to 63 players from four different Canadian teams, each representing a different level of play (high school, university, community club, national). In addition, coaches from all four levels were questioned about team policies and their personal opinions about the use of headgear to prevent concussion. Although the players tended to believe that the headgear could prevent concussion (62%), the coaches were less convinced (33%). Despite the players' belief that headgear offers protection against concussion, only a minority reported wearing headgear (27%) and few (24%) felt that its use should be made mandatory. Common reasons for not wearing headgear were \"its use is not mandatory\", \"it is uncomfortable\", and \"it costs too much\".", "output": "{\"label\": \"maybe\", \"rationale\": \"Although most players in the study believe that rugby headgear may prevent concussion, only a minority reported wearing it. Coaches tended to be less convinced than the players that rugby headgear can prevent concussion.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 11867487, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nCANDIDATE_ABSTRACT:\nTITLE: The cytokine RANKL produced by positively selected thymocytes fosters medullary thymic epithelial cells that express autoimmune regulator.\nABSTRACT: The thymic medulla provides a microenvironment where medullary thymic epithelial cells (mTECs) express autoimmune regulator and diverse tissue-restricted genes, contributing to launching self-tolerance. Positive selection is essential for thymic medulla formation via a previously unknown mechanism. Here we show that the cytokine RANK ligand (RANKL) was produced by positively selected thymocytes and regulated the cellularity of mTEC by interacting with RANK and osteoprotegerin. Forced expression of RANKL restored thymic medulla in mice lacking positive selection, whereas RANKL perturbation impaired medulla formation. These results indicate that RANKL produced by positively selected thymocytes is responsible for fostering thymic medulla formation, thereby establishing central tolerance.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here we show that the cytokine RANK ligand (RANKL) was produced by positively selected thymocytes and regulated the cellularity of mTEC by interacting with RANK and osteoprotegerin.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1181, "doc_id": "39128592", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does antiemetic prophylaxis improve outcomes after outpatient surgery when compared to symptomatic treatment?\n\nABSTRACT:\nAlthough prophylactic administration of antiemetics reduces the incidence of postoperative nausea, vomiting, or both (PONV), there is little evidence to suggest this improves patient outcomes. The authors hypothesized that early symptomatic treatment of PONV will result in outcomes, including time to discharge, unanticipated admission, patient satisfaction, and time to return to normal daily activities, that are similar to those achieved with routine prophylaxis. Men and women (n = 575) scheduled for outpatient surgery during general anesthesia were randomized to receive either 4 mg intravenous ondansetron or placebo before operation and either 1 mg intravenous ondansetron or placebo if postoperative symptomatic treatment of PONV was necessary. Patients were stratified into subgroups by risk factors for PONV. No differences occurred in the time to discharge, rate of unanticipated admission, or time to return to normal activity between the prophylaxis and treatment groups. The reported level of satisfaction with control of PONV was 93% in the treatment arm and 97% in the prophylaxis arm, which fall within the limits defined a priori as clinically equivalent. Female patients with a history of motion sickness or PONV who were undergoing highly emetogenic procedures had a higher reported level of satisfaction with prophylaxis than with treatment (100% vs. 90%, P = 0.043); however, the level of satisfaction with the overall outpatient surgical experience was not different.", "output": "{\"label\": \"no\", \"rationale\": \"Although PONV is unpleasant, the data indicate little difference in outcomes when routine prophylactic medications are administered versus simply treating PONV should symptoms occur.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 9952138, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: A total of 1,000 people in the UK are asymptomatic carriers of vCJD infection.\n\nCANDIDATE_ABSTRACT:\nTITLE: Prevalent abnormal prion protein in human appendixes after bovine spongiform encephalopathy epizootic: large scale survey\nABSTRACT: OBJECTIVES To carry out a further survey of archived appendix samples to understand better the differences between existing estimates of the prevalence of subclinical infection with prions after the bovine spongiform encephalopathy epizootic and to see whether a broader birth cohort was affected, and to understand better the implications for the management of blood and blood products and for the handling of surgical instruments. DESIGN Irreversibly unlinked and anonymised large scale survey of archived appendix samples. SETTING Archived appendix samples from the pathology departments of 41 UK hospitals participating in the earlier survey, and additional hospitals in regions with lower levels of participation in that survey. SAMPLE 32,441 archived appendix samples fixed in formalin and embedded in paraffin and tested for the presence of abnormal prion protein (PrP). RESULTS Of the 32,441 appendix samples 16 were positive for abnormal PrP, indicating an overall prevalence of 493 per million population (95% confidence interval 282 to 801 per million). The prevalence in those born in 1941-60 (733 per million, 269 to 1596 per million) did not differ significantly from those born between 1961 and 1985 (412 per million, 198 to 758 per million) and was similar in both sexes and across the three broad geographical areas sampled. Genetic testing of the positive specimens for the genotype at PRNP codon 129 revealed a high proportion that were valine homozygous compared with the frequency in the normal population, and in stark contrast with confirmed clinical cases of vCJD, all of which were methionine homozygous at PRNP codon 129. CONCLUSIONS This study corroborates previous studies and suggests a high prevalence of infection with abnormal PrP, indicating vCJD carrier [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"RESULTS Of the 32,441 appendix samples 16 were positive for abnormal PrP, indicating an overall prevalence of 493 per million population (95% confidence interval 282 to 801 per million).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 48, "doc_id": "13734012", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: HbA1c consistently overestimates glycemic control in black individuals with Sickle cell trait (SCT).\n\nCANDIDATE_ABSTRACT:\nTITLE: Association of Sickle Cell Trait With Hemoglobin A1c in African Americans\nABSTRACT: Importance Hemoglobin A1c (HbA1c) reflects past glucose concentrations, but this relationship may differ between those with sickle cell trait (SCT) and those without it. Objective To evaluate the association between SCT and HbA1c for given levels of fasting or 2-hour glucose levels among African Americans. Design, Setting, and Participants Retrospective cohort study using data collected from 7938 participants in 2 community-based cohorts, the Coronary Artery Risk Development in Young Adults (CARDIA) study and the Jackson Heart Study (JHS). From the CARDIA study, 2637 patients contributed a maximum of 2 visits (2005-2011); from the JHS, 5301 participants contributed a maximum of 3 visits (2000-2013). All visits were scheduled at approximately 5-year intervals. Participants without SCT data, those without any concurrent HbA1c and glucose measurements, and those with hemoglobin variants HbSS, HbCC, or HbAC were excluded. Analysis of the primary outcome was conducted using generalized estimating equations (GEE) to examine the association of SCT with HbA1c levels, controlling for fasting or 2-hour glucose measures. Exposures Presence of SCT. Main Outcomes and Measures Hemoglobin A1c stratified by the presence or absence of SCT was the primary outcome measure. Results The analytic sample included 4620 participants (mean age, 52.3 [SD, 11.8] years; 2835 women [61.3%]; 367 [7.9%] with SCT) with 9062 concurrent measures of fasting glucose and HbA1c levels. In unadjusted GEE analyses, for a given fasting glucose, HbA1c values were statistically significantly lower in those with (5.72%) vs those without (6.01%) SCT (mean HbA1c difference, −0.29%; 95% CI, −0.35% to −0.23%). Findings were similar in models adjusted for key risk factors and in analyses using 2001 concurre [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Findings were similar in models adjusted for key risk factors and in analyses using 2001 concurrent measures of 2-hour glucose and HbA1c concentration for those with SCT (mean, 5.35%) vs those without SCT (mean, 5.65%) for a mean HbA1c difference of −0.30% (95% CI, −0.39% to −0.21%).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 499, "doc_id": "26064662", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: MafA phosphorylation decreases its ubiquitination.\n\nCANDIDATE_ABSTRACT:\nTITLE: Spatiotemporal regulation of epithelial-mesenchymal transition is essential for squamous cell carcinoma metastasis.\nABSTRACT: Epithelial-mesenchymal transition (EMT) is implicated in converting stationary epithelial tumor cells into motile mesenchymal cells during metastasis. However, the involvement of EMT in metastasis is still controversial, due to the lack of a mesenchymal phenotype in human carcinoma metastases. Using a spontaneous squamous cell carcinoma mouse model, we show that activation of the EMT-inducing transcription factor Twist1 is sufficient to promote carcinoma cells to undergo EMT and disseminate into blood circulation. Importantly, in distant sites, turning off Twist1 to allow reversion of EMT is essential for disseminated tumor cells to proliferate and form metastases. Our study demonstrates in vivo the requirement of \"reversible EMT\" in tumor metastasis and may resolve the controversy on the importance of EMT in carcinoma metastasis.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 745, "doc_id": "1791714", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Gastric lavage is an effective treatment for acute paraquat poisoning.\n\nCANDIDATE_PASSAGE:\nRole of antioxidants in paraquat toxicity. Paraquat, a quarternary nitrogen herbicide, is a highly toxic compound for humans and animals and many cases of acute poisoning and death have been reported over the past few decades. The mechanisms of paraquat toxicity involve: the generation of the superoxide anion, which can lead to the formation of more toxic reactive oxygen species, such as hydrogen peroxide and hydroxyl radical; and the oxidation of the cellular NADPH, the major source of reducing equivalents for the intracellular reduction of paraquat, which results in the disruption of important NADPH-requiring biochemical processes. The major cause of death in paraquat poisoning is respiratory failure due to an oxidative insult to the alveolar epithelium with subsequent obliterating fibrosis. Management of paraquat poisoning has remained mostly supportive and has been directed towards the modification of the toxicokinetics of the poison. Currently, there are no true pharmacological antagonists for paraquat and there are no chelating agents capable of binding the poison in the blood or other tissues. Recognizing the fact that paraquat induces its toxic effects via oxidative stress-mediated mechanisms, innovations in the management of paraquat poisoning are directed towards the use of antioxidants. In this review, the status of antioxidants in ameliorating or treating the toxic effects produced by paraquat is presented.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "449", "doc_id": "19132741", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is response to the methylation inhibitor dihydro-5-azacytidine in mesothelioma associated with methylation of p16INK4a : results of cancer and leukemia group B 159904?\n\nABSTRACT:\nThe molecular mechanisms of oncogenesis in mesothelioma involve the loss of negative regulators of cell growth including p16INK4a. Absence of expression of the p16INK4a gene product is exhibited in virtually all mesothelioma tumors and cell lines examined to date. Loss of p16INK4a expression has also been frequently observed in more common neoplasms such as lung cancer as well. In a wide variety of these malignancies, including lung cancer, p16INK4a expression is known to be inactivated by hypermethylation of the first exon. This project (CALGB 159904) intended to test the hypothesis that in mesothelioma loss of p16INK4a via methylation would correlate with response to the cytidine analog and methylation inhibitor dihydro-5-azacytidine (DHAC). Using tissue samples from CALGB 8833 and 9031, two clinical studies which used DHAC based therapy in mesothelioma, this study tested the hypothesis that tumors possessing methylation of p16INK4a would have a better response and survival following DHAC treatment than their nonmethylated counterparts. Methylation of p16INK4a was identified in 4 of the 20 specimens. Although there was a trend towards improved survival the result was not statistically significant.", "output": "{\"label\": \"no\", \"rationale\": \"There was no significant correlation between the presence of p16INK4a methylation and response to DHAC therapy or overall survival.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 18379362, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Cancers that initially benefit from epidermal growth factor receptor targeted therapies later become refractory through several mechanisms.\n\nCANDIDATE_PASSAGE:\nActivation of the estrogen receptor through phosphorylation by mitogen-activated protein kinase. The phosphorylation of the human estrogen receptor (ER) serine residue at position 118 is required for full activity of the ER activation function 1 (AF-1). This Ser118 is phosphorylated by mitogen-activated protein kinase (MAPK) in vitro and in cells treated with epidermal growth factor (EGF) and insulin-like growth factor (IGF) in vivo. Overexpression of MAPK kinase (MAPKK) or of the guanine nucleotide binding protein Ras, both of which activate MAPK, enhanced estrogen-induced and antiestrogen (tamoxifen)-induced transcriptional activity of wild-type ER, but not that of a mutant ER with an alanine in place of Ser118. Thus, the activity of the amino-terminal AF-1 of the ER is modulated by the phosphorylation of Ser118 through the Ras-MAPK cascade of the growth factor signaling pathways.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "227", "doc_id": "4662264", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The PRR MDA5 is a sensor of RNA virus infection.\n\nCANDIDATE_PASSAGE:\nEstimating risk curves for first-degree relatives of patients with Alzheimer’s disease: The REVEAL study Purpose: The REVEAL study is a randomized, controlled study of the psychological and behavioral impact of APOE disclosure in a risk assessment protocol provided to first degree relatives of patients with Alzheimer’s disease. The protocol presents risk information as cumulative incidence curves. This article describes how these curves were estimated. Methods: Curves were calculated using Bayes’ rule to compute the posterior survival curves incorporating APOE information. Results: A combination of survival data from the MIRAGE study and gender- and age-specific APOE odds ratios were used to create risk curves for males and females within each of the 6 APOE genotypes. Conclusion: Utilizing comparative genotype relative risk information and survival data from family studies, estimates of gender-, age-, and genotype-specific risk can be generated for use in a risk assessment research study that features genotype disclosure.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1180", "doc_id": "6917133", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Destination container port throughput(CPT) is negatively related to dengue virus (DENV-1) diffusion in air traffic shipments.\n\nCANDIDATE_PASSAGE:\nPopulation Density, Water Supply, and the Risk of Dengue Fever in Vietnam: Cohort Study and Spatial Analysis BACKGROUND Aedes aegypti, the major vector of dengue viruses, often breeds in water storage containers used by households without tap water supply, and occurs in high numbers even in dense urban areas. We analysed the interaction between human population density and lack of tap water as a cause of dengue fever outbreaks with the aim of identifying geographic areas at highest risk. METHODS AND FINDINGS We conducted an individual-level cohort study in a population of 75,000 geo-referenced households in Vietnam over the course of two epidemics, on the basis of dengue hospital admissions (n = 3,013). We applied space-time scan statistics and mathematical models to confirm the findings. We identified a surprisingly narrow range of critical human population densities between around 3,000 to 7,000 people/km² prone to dengue outbreaks. In the study area, this population density was typical of villages and some peri-urban areas. Scan statistics showed that areas with a high population density or adequate water supply did not experience severe outbreaks. The risk of dengue was higher in rural than in urban areas, largely explained by lack of piped water supply, and in human population densities more often falling within the critical range. Mathematical modeling suggests that simple assumptions regarding area-level vector/host ratios may explain the occurrence of outbreaks. CONCLUSIONS Rural areas may contribute at least as much to the dissemination of dengue fever as cities. Improving water supply and vector control in areas with a human population density critical for dengue transmission could increase the efficiency of control efforts. Please see later in the [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "336", "doc_id": "2097256", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: MICAL redox enzymes regulate actin dynamics.\n\nCANDIDATE_ABSTRACT:\nTITLE: Electroporation of Cas9 protein/sgRNA into early pronuclear zygotes generates non-mosaic mutants in the mouse.\nABSTRACT: The CRISPR/Cas9 system is a powerful tool for elucidating the roles of genes in a wide variety of organisms including mice. To obtain genetically modified embryos or mice by this method, Cas9 mRNA and sgRNA are usually introduced into zygotes by microinjection or electroporation. However, most mutants generated with this method are genetically mosaic, composed of several types of cells carrying different mutations, which complicates phenotype analysis in founder embryos or mice. To simplify the analysis and to elucidate the roles of genes involved in developmental processes, a method for producing non-mosaic mutants is needed. Here, we established a method for generating non-mosaic mouse mutant embryos. We introduced Cas9 protein and sgRNA into in vitro fertilized (IVF) zygotes by electroporation, which enabled the genome editing to occur before the first replication of the mouse genome. As a result, all of the cells in the mutant carried the same set of mutations. This method solves the problem of mosaicism/allele complexity in founder mutant embryos or mice generated by the CRIPSR/Cas9 system.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 738, "doc_id": "949309", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Traditional reviews are biased in their interpretations.\n\nCANDIDATE_PASSAGE:\nARNO regulates VEGF-dependent tissue responses by stabilizing endothelial VEGFR-2 surface expression. AIMS The vascular endothelial growth factor (VEGF) stimulates angiogenesis by induction of vessel permeability, proliferation, and migration of endothelial cells, an important process in ischaemic diseases. ADP-ribosylation factor (ARF) nucleotide-binding site opener (ARNO) (cytohesin-2) is a guanine exchange factor important for cellular signalling through ARF GTPases. However, a role for ARNO in VEGF-dependent endothelial processes has so far not been documented. Therefore, we investigated whether ARNO has a role in VEGF-dependent activation of endothelial cells and thus vessel permeability. METHODS AND RESULTS ARNO expression was observed in endothelial cells in vitro by RT-PCR, western blotting, and immunofluorescence as well as ex vivo by immunohistochemical staining of mouse aorta. Treatment with the cytohesin inhibitor SecinH3 or with an ARNO siRNA prevented VEGF-dependent Akt activation, assessed by detection of phosphorylated Akt, and proliferation of endothelial cells in vitro, measured by methylthiazoletetrazolium (MTT) reduction. In addition, ARNO suppression reduced VEGF-induced permeability in vessels of the mouse (C57BL/6) cremaster muscle in vivo, as measured by extravasation of fluorescein isothiocyanate (FITC)-dextran. Moreover, ARNO knock-down accelerated ligand-induced reduction in vascular endothelial growth factor receptor-2 (VEGFR-2) surface expression, internalization, and degradation, as assessed by flow cytometry and western blotting, respectively. CONCLUSION Our findings indicate an important and novel role for endothelial ARNO in VEGF-dependent initiation of angiogenesis by regulation of VEGFR-2 internalization in endothelial cell [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1310", "doc_id": "9185195", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does caspofungin modulate in vitro adherence of Candida albicans to plastic coated with extracellular matrix proteins?\n\nABSTRACT:\nSome manifestations of candidiasis are associated with the formation of biofilms on inert or biological surfaces and the intrinsic resistance of Candida albicans biofilms to the most commonly used antifungal agents has been demonstrated. In this study, we report on the influence of the growth of C. albicans in medium containing a sub-inhibitory concentration (MIC/2) of caspofungin, on subsequent fungal adherence to plastic coated with extracellular matrix (ECM) proteins. Eleven strains of C. albicans were studied: six strains were susceptible to fluconazole in vitro and five strains were resistant to this antifungal agent. Caspofungin induced a decrease in the adherence of all the tested strains that were susceptible to fluconazole but induced a decrease in the adherence of only 60% of the fluconazole-resistant strains.", "output": "{\"label\": \"yes\", \"rationale\": \"This study demonstrated the anti-adherent activity of caspofungin but indicated a reduced effect in the case of in vitro fluconazole resistance. These results indicated a possible relationship between the efficiency of caspofungin to inhibit the first step of the development of C. albicans biofilm and the resistance of C.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 14749343, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Integrating classroom-based collaborative learning with Web-based collaborative learning leads to subpar class performance\n\nCANDIDATE_PASSAGE:\nProtein-Protein Interaction Inhibition (2P2I)-Oriented Chemical Library Accelerates Hit Discovery. Protein-protein interactions (PPIs) represent an enormous source of opportunity for therapeutic intervention. We and others have recently pinpointed key rules that will help in identifying the next generation of innovative drugs to tackle this challenging class of targets within the next decade. We used these rules to design an oriented chemical library corresponding to a set of diverse \"PPI-like\" modulators with cores identified as privileged structures in therapeutics. In this work, we purchased the resulting 1664 structurally diverse compounds and evaluated them on a series of representative protein-protein interfaces with distinct \"druggability\" potential using homogeneous time-resolved fluorescence (HTRF) technology. For certain PPI classes, analysis of the hit rates revealed up to 100 enrichment factors compared with nonoriented chemical libraries. This observation correlates with the predicted \"druggability\" of the targets. A specific focus on selectivity profiles, the three-dimensional (3D) molecular modes of action resolved by X-ray crystallography, and the biological activities of identified hits targeting the well-defined \"druggable\" bromodomains of the bromo and extraterminal (BET) family are presented as a proof-of-concept. Overall, our present study illustrates the potency of machine learning-based oriented chemical libraries to accelerate the identification of hits targeting PPIs. A generalization of this method to a larger set of compounds will accelerate the discovery of original and potent probes for this challenging class of targets.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "649", "doc_id": "11256632", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Chinese individuals with TT homozygosity in the MTHFR gene are more vulnerable to strokes caused by low levels of folate intake.\n\nCANDIDATE_PASSAGE:\nThe effect of folate fortification on folic acid-based homocysteine-lowering intervention and stroke risk: a meta-analysis. OBJECTIVE Folate and vitamin B12 are two vital regulators in the metabolic process of homocysteine, which is a risk factor of atherothrombotic events. Low folate intake or low plasma folate concentration is associated with increased stroke risk. Previous randomized controlled trials presented discordant findings in the effect of folic acid supplementation-based homocysteine lowering on stroke risk. The aim of the present review was to perform a meta-analysis of relevant randomized controlled trials to check the how different folate fortification status might affect the effects of folic acid supplementation in lowering homocysteine and reducing stroke risk. DESIGN Relevant randomized controlled trials were identified through formal literature search. Homocysteine reduction was compared in subgroups stratified by folate fortification status. Relative risks with 95 % confidence intervals were used as a measure to assess the association between folic acid supplementation and stroke risk. SETTING The meta-analysis included fourteen randomized controlled trials, SUBJECTS A total of 39 420 patients. RESULTS Homocysteine reductions were 26·99 (sd 1·91) %, 18·38 (sd 3·82) % and 21·30 (sd 1·98) %, respectively, in the subgroups without folate fortification, with folate fortification and with partial folate fortification. Significant difference was observed between the subgroups with folate fortification and without folate fortification (P=0·05). The relative risk of stroke was 0·88 (95 % CI 0·77, 1·00, P=0·05) in the subgroup without folate fortification, 0·94 (95 % CI 0·58, 1·54, P=0·82) in the subgroup with folate fortification and 0·91 (95 % C [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "254", "doc_id": "37424881", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Primary cervical cancer screening with HPV detection has higher longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_PASSAGE:\nEvidence regarding human papillomavirus testing in secondary prevention of cervical cancer. More than ever, clinicians need regularly updated reviews given the continuously increasing amount of new information regarding innovative cervical cancer prevention methods. A summary is given from recent meta-analyses and systematic reviews on 3 possible clinical applications of human papillomavirus (HPV) testing: triage of women with equivocal or low-grade cytologic abnormalities; prediction of the therapeutic outcome after treatment of cervical intraepithelial neoplasia (CIN) lesions, and last not but not least, primary screening for cervical cancer and pre-cancer. Consistent evidence is available indicating that HPV-triage with the Hybrid Capture(®) 2 assay (Qiagen Gaithersburg, Inc., MD, USA [previously Digene Corp.] (HC2) is more accurate (higher sensitivity, similar specificity) than repeat cytology to triage women with equivocal Pap smear results. Several other tests show at least similar accuracy but mRNA testing with the APTIMA(®) (Gen-Probe Inc., San Diego, CA, USA) test is similarly sensitive but more specific compared to HC2. In triage of low-grade squamous intraepithelial lesions (LSIL), HC2 is more sensitive but its specificity is substantially lower compared to repeat cytology. The APTIMA(®) test is more specific than HC2 without showing a loss in sensitivity. Identification of DNA of HPV types 16 and/or 18, or RNA from the five most carcinogenic HPV types allow selecting women at highest risk for CIN3+ but the sensitivity and negative predictive value of these markers are lower than full-range high-risk HPV (hrHPV) testing. After conservative treatment of cervical pre-cancer, HPV testing picks up more quickly, with higher sensitivity and not lower sp [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "971", "doc_id": "28617573", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In breast cancer, the loss of myoepithelial cells slows the transition of ductal carcinoma in situ to invasive carcinoma.\n\nCANDIDATE_ABSTRACT:\nTITLE: Estimates of global prevalence of childhood underweight in 1990 and 2015.\nABSTRACT: CONTEXT One key target of the United Nations Millennium Development goals is to reduce the prevalence of underweight among children younger than 5 years by half between 1990 and 2015. OBJECTIVE To estimate trends in childhood underweight by geographic regions of the world. DESIGN, SETTING, AND PARTICIPANTS Time series study of prevalence of underweight, defined as weight 2 SDs below the mean weight for age of the National Center for Health Statistics and World Health Organization (WHO) reference population. National prevalence rates derived from the WHO Global Database on Child Growth and Malnutrition, which includes data on approximately 31 million children younger than 5 years who participated in 419 national nutritional surveys in 139 countries from 1965 through 2002. MAIN OUTCOME MEASURES Linear mixed-effects modeling was used to estimate prevalence rates and numbers of underweight children by region in 1990 and 2015 and to calculate the changes (ie, increase or decrease) to these values between 1990 and 2015. RESULTS Worldwide, underweight prevalence was projected to decline from 26.5% in 1990 to 17.6% in 2015, a change of -34% (95% confidence interval [CI], -43% to -23%). In developed countries, the prevalence was estimated to decrease from 1.6% to 0.9%, a change of -41% (95% CI, -92% to 343%). In developing regions, the prevalence was forecasted to decline from 30.2% to 19.3%, a change of -36% (95% CI, -45% to -26%). In Africa, the prevalence of underweight was forecasted to increase from 24.0% to 26.8%, a change of 12% (95% CI, 8%-16%). In Asia, the prevalence was estimated to decrease from 35.1% to 18.5%, a change of -47% (95% CI, -58% to -34%). Worldwide, the number of underweight children was projected to decline from 163.8 million in 1990 to 113. [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 571, "doc_id": "1606628", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does metabolomics analysis reveal large effect of roughage types on rumen microbial metabolic profile in dairy cows?\n\nABSTRACT:\nThe aim of our study was to determine the effect of diets with different types of roughage on the ruminal microbial metabolite profile in dairy cows. Holstein dairy cows were fed a diet containing either corn stover (CS group) or a mixture of alfalfa hay, Leymus chinensis hay and corn silage (MF group) at 0700 and 1900 h daily. Rumen fluid was sampled from each cow through a ruminal cannula at 0630 and 1030 h, and the mixed ruminal fluid from 3 day in each cow was analysed using nuclear magnetic resonance (NMR) spectroscopy. A multivariate analysis revealed a significant difference between the ruminal metabolome of the CS and MF groups at both time points. The MF group had higher levels of acetate, valerate, hydrocinnamate and methylamine and lower levels of glucose, glycine, propionate and isovalerate than those in the CS group. Our results showed that different types of roughages can significantly influence the ruminal microbial metabolome, especially with regard to organic acids, amines and amino acids.", "output": "{\"label\": \"yes\", \"rationale\": \"The microbial metabolites in the rumen provide nutritional precursors that are critical for general health and milk production in dairy cows. However, studies of the effect of diet on ruminal microbial metabolism are scant. In our current study, we analysed the ruminal microbial metabolite profile of cows fed different types of roughage.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 24617926, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Participants who quit smoking reduce lung cancer risk by approximately 50%.\n\nCANDIDATE_PASSAGE:\nPredictive value of bone resorption and formation markers in cancer patients with bone metastases receiving the bisphosphonate zoledronic acid. PURPOSE Three large, randomized trials of patients with bone metastases recently demonstrated that zoledronic acid reduces the risk of skeletal-related events. These trials provide an opportunity for investigating the correlation between bone metabolism and clinical outcome during bisphosphonate therapy. PATIENTS AND METHODS Urinary measurements of N-telopeptide (Ntx) and serum bone alkaline phosphatase (BAP) were obtained in 1,824 bisphosphonate-treated patients-1,462 with zoledronic acid (breast, 490; prostate, 411; myeloma, 210; non-small-cell lung, 183; other, 168) and 362 with pamidronate (breast, 254; myeloma, 108). This exploratory cohort analysis grouped patients by baseline and most recent levels of Ntx as low (< 50 nmol/mmol creatinine), moderate (50 to 99 nmol/mmol creatinine), or high (> or = 100 nmol/mmol creatinine), and BAP as low (< 146 U/L) or high (> or = 146 U/L). The relative risks for negative clinical outcomes were estimated for each group using multiple-event and Cox regression models with time-varying covariates. RESULTS Patients with high and moderate Ntx levels had 2-fold increases in their risk of skeletal complications and disease progression compared with patients with low Ntx levels (P < .001 for all). High Ntx levels in each solid tumor category were associated with a 4- to 6-fold increased risk of death on study, and moderate Ntx levels a 2- to 4-fold increased risk compared with low Ntx levels (P < .001 for all). Bone alkaline phosphatase also showed some correlation with risk of negative clinical outcomes. CONCLUSION The bone resorption marker Ntx provides valuable prognostic informa [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "919", "doc_id": "8037453", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Active caspase-11 participate in regulating phagosome-lysosome fusion.\n\nCANDIDATE_ABSTRACT:\nTITLE: Caspase-11 promotes the fusion of phagosomes harboring pathogenic bacteria with lysosomes by modulating actin polymerization.\nABSTRACT: Inflammasomes are multiprotein complexes that include members of the NLR (nucleotide-binding domain leucine-rich repeat containing) family and caspase-1. Once bacterial molecules are sensed within the macrophage, the inflammasome is assembled, mediating the activation of caspase-1. Caspase-11 mediates caspase-1 activation in response to lipopolysaccharide and bacterial toxins, and yet its role during bacterial infection is unknown. Here, we demonstrated that caspase-11 was dispensable for caspase-1 activation in response to Legionella, Salmonella, Francisella, and Listeria. We also determined that active mouse caspase-11 was required for restriction of L. pneumophila infection. Similarly, human caspase-4 and caspase-5, homologs of mouse caspase-11, cooperated to restrict L. pneumophila infection in human macrophages. Caspase-11 promoted the fusion of the L. pneumophila vacuole with lysosomes by modulating actin polymerization through cofilin. However, caspase-11 was dispensable for the fusion of lysosomes with phagosomes containing nonpathogenic bacteria, uncovering a fundamental difference in the trafficking of phagosomes according to their cargo.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"However, caspase-11 was dispensable for the fusion of lysosomes with phagosomes containing nonpathogenic bacteria, uncovering a fundamental difference in the trafficking of phagosomes according to their cargo.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 78, "doc_id": "5099266", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Reduced phosphorylation of PP2A increases HDAC4 dephosphorylation by enhancing PP2A-HDAC4 interaction.\n\nCANDIDATE_PASSAGE:\nReproducibility of the diagnosis of atypical endometrial hyperplasia: a Gynecologic Oncology Group study. BACKGROUND Most gynecologists determine therapy based on current International Society of Gynecologic Pathologists (ISGP)/World Health Organization classification of endometrial hyperplasia, the reproducibility of which has been questioned. The Gynecologic Oncology Group (GOG) initiated a protocol to assess the efficacy of hormonal therapy of atypical endometrial hyperplasia (AEH). Primary goals of the first phase (Part A) were to prospectively determine reproducibility of referring institution's pathologist's diagnosis of AEH by a panel of 3 gynecologic pathologists and to determine reproducibility of diagnoses by panel members. METHODS Three hundred six women were entered on this protocol with a referring institution's pathologist diagnosis of AEH based on biopsy or curettage. Available slides were assessed independently and interpreted by each of a panel of 3 gynecologic pathologists who used International Society of Gynecologic Pathologists (ISGP)/World Health Organization criteria. The majority diagnosis was based on diagnostic concordance by at least 2 of the 3 panelists. RESULTS The referring institution's pathologist's diagnosis of AEH was supported by the majority of the panel in only 38% of cases. Overall kappa value for the panel diagnosis of AEH was 0.28. The majority diagnosis was adenocarcinoma in 29%, cycling endometrium in 7%, and nonatypical hyperplasia in 18% of cases. Unanimous agreement for any diagnosis was reached among all 3 of the panel in 40% of cases. For the panel, paired kappa values for any diagnosis ranged 0.34-0.43, with an overall kappa value of 0.40. CONCLUSION Reproducibility of referring institution's pathologists' diag [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1026", "doc_id": "20221907", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Primary cervical cytology screening with HPV detection has higher longitudinal sensitivity to detect severe cervical intraepithelial neoplasia than conventional cytology.\n\nCANDIDATE_PASSAGE:\nDrug-resistant Salmonella in the United States: an epidemiologic perspective. Salmonellosis poses a health problem of large proportions in the United States. Annually, it accounts for more than 40,000 reported cases, 500 deaths, and financial costs well in excess of $50 million. Antimicrobial resistance is increasing in Salmonella strains, a finding that has important public health implications. Although the chain of transmission of the bacteria is often complex, combined epidemiologic and laboratory studies with the use of new methods in molecular biology make it possible to trace antimicrobial-resistant salmonellae to their primary source--foods of animal origin. These studies suggest that the antimicrobial drugs to which food animals are exposed provide selective pressure that leads to the appearance and persistence of resistant strains.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "973", "doc_id": "36497180", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The arm density of TatAd complexes is due to structural rearrangements within Class1 TatAd complexes such as the 'charge zipper mechanism'.\n\nCANDIDATE_ABSTRACT:\nTITLE: Folding and Self-Assembly of the TatA Translocation Pore Based on a Charge Zipper Mechanism\nABSTRACT: We propose a concept for the folding and self-assembly of the pore-forming TatA complex from the Twin-arginine translocase and of other membrane proteins based on electrostatic \"charge zippers. \" Each subunit of TatA consists of a transmembrane segment, an amphiphilic helix (APH), and a C-terminal densely charged region (DCR). The sequence of charges in the DCR is complementary to the charge pattern on the APH, suggesting that the protein can be \"zipped up\" by a ladder of seven salt bridges. The length of the resulting hairpin matches the lipid bilayer thickness, hence a transmembrane pore could self-assemble via intra- and intermolecular salt bridges. The steric feasibility was rationalized by molecular dynamics simulations, and experimental evidence was obtained by monitoring the monomer-oligomer equilibrium of specific charge mutants. Similar \"charge zippers\" are proposed for other membrane-associated proteins, e.g., the biofilm-inducing peptide TisB, the human antimicrobial peptide dermcidin, and the pestiviral E(RNS) protein.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1194, "doc_id": "11419230", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The Snf1 complex regulates carbon and energy metabolism in baker's yeast (Saccharomyces cerevisiae).\n\nCANDIDATE_ABSTRACT:\nTITLE: Once-a-day Concerta methylphenidate versus three-times-daily methylphenidate in laboratory and natural settings.\nABSTRACT: OBJECTIVE Methylphenidate (MPH), the most commonly prescribed drug for attention-deficit/hyperactivity disorder (ADHD), has a short half-life, which necessitates multiple daily doses. The need for multiple doses produces problems with medication administration during school and after-school hours, and therefore with compliance. Previous long-acting stimulants and preparations have shown effects equivalent to twice-daily dosing of MPH. This study tests the efficacy and duration of action, in natural and laboratory settings, of an extended-release MPH preparation designed to last 12 hours and therefore be equivalent to 3-times-daily dosing. METHODS Sixty-eight children with ADHD, 6 to 12 years old, participated in a within-subject, double-blind comparison of placebo, immediate-release (IR) MPH 3 times a day (tid), and Concerta, a once-daily MPH formulation. Three dosing levels of medication were used: 5 mg IR MPH tid/18 mg Concerta once a day (qd); 10 mg IR MPH tid/36 mg Concerta qd; and 15 mg IR MPH tid/54 mg Concerta qd. All children were currently medicated with MPH at enrollment, and each child's dose level was based on that child's MPH dosing before the study. The doses of Concerta were selected to be comparable to the daily doses of MPH that each child received. To achieve the ascending rate of MPH delivery determined by initial investigations to provide the necessary continuous coverage, Concerta doses were 20% higher on a daily basis than a comparable tid regimen of IR MPH. Children received each medication condition for 7 days. The investigation was conducted in the context of a background clinical behavioral intervention in both the natural environment and the laboratory setting. Parents received behavioral parent training and teachers were taught to [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1182, "doc_id": "2475059", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does allogenicity of cryopreserved human fibroblasts : cryopreservation downregulate the allogenicity of fibroblasts making up the matrices of allografts?\n\nABSTRACT:\nAlthough cryopreserved tissue allografts are being widely used, long-term degeneration of implanted cryopreserved allografts has become a problem. Although immunologic rejection has been suggested to play a part in this degeneration, cryopreserved allografts are considered to be less immunogenic than fresh allografts. We investigated the effect of cryopreservation on the allogenicity of the fibroblasts that make up the matrices of allografts. Fibroblast cell strains obtained from surgically resected lung specimens were used. Allogenicity-related antigens expressed on the cell surface (human leukocyte antigen 1, human leukocyte antigen 2, and intercellular adhesion molecule 1), stimulation indices during 1-way mixed lymphocyte-fibroblast cell culture, and proliferation indices of freshly passaged fibroblasts and cryopreserved fibroblasts stored for 1, 4, and 24 weeks were examined. Flow cytometric analysis with monoclonal antibodies was used to test for cell surface antigens, and a colorimetric methyl-thiazol-diphenyl-tetrazolium assay was used to assess stimulation indices and fibroblast proliferation indices. The effect of exogenous interferon-gamma on the degree of expression of human leukocyte antigen 1, human leukocyte antigen 2, and intercellular adhesion molecule 1 was examined simultaneously. The proliferation indices of fibroblasts were well maintained by cryopreservation. Expression of human leukocyte antigen 1, human leukocyte antigen 2, and intercellular adhesion molecule 1 by fibroblasts was significantly upregulated by interferon-gamma, and cryopreservation did not downregulate this expression.", "output": "{\"label\": \"no\", \"rationale\": \"Our study suggests that although the fibroblast cell component may be beneficial in restoring allograft function properties initially, it may render the implanted allograft more immunogenic, ultimately resulting in greater rejection and inflammatory responses by the host and, in turn, degeneration of the graft.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 11003753, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Sub-classification of low-grade cerebellar astrocytoma: is it clinically meaningful?\n\nABSTRACT:\nThe objectives were to identify prognostic factors for the survival of children with cerebellar astrocytoma, and to evaluate the reproducibility and prognostic value of histological sub-classification and grading. Children aged 0-14 years treated in Denmark for a cerebellar astrocytoma in the period 1960-1984 were included and followed until January 2001 or until their death. The histological specimens from each patient were reviewed for revised grading and classification according to three different classification schemes: the WHO, the Kernohan and the Daumas-Duport grading systems. The overall survival rate was 81% after a follow-up time of 15-40 years. The significant positive prognostic factors for survival were \"surgically gross-total removal\" of the tumour at surgery and location of the tumour in the cerebellum proper as opposed to location in the fourth ventricle. No difference in survival time was demonstrated when we compared pilocytic astrocytoma and fibrillary astrocytoma. Moreover, we found that the Kernohan and the WHO classification systems had no predictive value and that the Daumas-Duport system is unsuitable as a prognostic tool for low-grade posterior fossa astrocytomas.", "output": "{\"label\": \"no\", \"rationale\": \"Discordant observations due to interobserver variability make histological sub-classification of low-grade cerebellar astrocytomas in children insufficient for predicting prognosis and biological behaviour. Similar survival rates in a population of paediatric low-grade cerebellar astrocytomas of grades I and II indicate that tumour grade has no prognostic significance within this group of patients. \\\"Surgically gross-total removal\\\", especially if the tumour is located in the fourth ventricle is of the highest importance for long-term survival.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 14631523, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Omnivores produce less trimethylamine N-oxide from dietary I-carnitine than vegetarians.\n\nCANDIDATE_ABSTRACT:\nTITLE: Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis\nABSTRACT: Intestinal microbiota metabolism of choline and phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO). We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice. Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism. The presence of specific bacterial taxa in human feces was associated with both plasma TMAO concentration and dietary status. Plasma L-carnitine levels in subjects undergoing cardiac evaluation (n = 2,595) predicted increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels. Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed. In mice with an intact intestinal microbiota, dietary supplementation with TMAO or either carnitine or choline reduced in vivo reverse cholesterol transport. Intestinal microbiota may thus contribute to the well-established link between high levels of red meat consumption and CVD risk.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 882, "doc_id": "14803797", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Bariatric surgery increases rates of colorectal cancer.\n\nCANDIDATE_PASSAGE:\nAspirin in the chemoprevention of colorectal neoplasia: an overview. Considerable evidence supports the effectiveness of aspirin for chemoprevention of colorectal cancer (CRC) in addition to its well-established benefits in the prevention of vascular disease. Epidemiologic studies have consistently observed an inverse association between aspirin use and risk of CRC. A recent pooled analysis of a long-term posttrial follow-up of nearly 14,000 patients from four randomized, cardiovascular disease prevention trials showed that daily aspirin treatment for about five years was associated with a 34% reduction in 20-year CRC mortality. A separate metaanalysis of nearly 3,000 patients with a history of colorectal adenoma or cancer in four randomized adenoma prevention trials showed that aspirin reduced the occurrence of advanced adenomas by 28% and any adenoma by 17%. Aspirin has also been shown to be beneficial in a clinical trial of patients with Lynch syndrome, a hereditary CRC syndrome; in those treated with aspirin for at least two years, there was a 50% or more reduction in the risk of CRC commencing five years after randomization and after aspirin had been discontinued. A few observational studies have shown an increase in survival among patients with CRC who use aspirin. Taken together, these findings strengthen the case for consideration of long-term aspirin use in CRC prevention. Despite these compelling data, there is a lack of consensus about the balance of risks and benefits associated with long-term aspirin use, particularly in low-risk populations. The optimal dose to use for cancer prevention and the precise mechanism underlying aspirin's anticancer effect require further investigation.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "164", "doc_id": "7613033", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Replacement of OCT4 and SOX2 genes with GATA3 is not capable of reprogramming human cells.\n\nCANDIDATE_PASSAGE:\nB-cell self-tolerance in humans. Two mechanisms account for generation of the human antibody repertoire; V(D)J recombination during the early stages of B-cell development in the bone marrow and somatic mutation of immunoglobulin genes in mature B cells responding to antigen in the periphery. V(D)J recombination produces diversity by random joining of gene segments and somatic mutation by introducing random point mutations. Both are required to attain the degree of antigen receptor diversification that is necessary for immune protection: defects in either mechanism are associated with increased susceptibility to infection. However, the downside of producing enormous random diversity in the antibody repertoire is the generation of autoantibodies. To prevent autoimmunity B cells expressing autoantibodies are regulated by strict mechanisms that either modify the specificity of autoantibodies or the fate of cells expressing such antibodies. Abnormalities in B-cell self-tolerance are associated with a large number of autoimmune diseases, but the precise nature of the defects is less well defined. Here we summarize recent data on the self-reactive B-cell repertoire in healthy humans and in patients with autoimmunity.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1038", "doc_id": "37182501", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Active Ly49Q induces neutrophil polarization.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Ly49Q receptor plays a crucial role in neutrophil polarization and migration by regulating raft trafficking.\nABSTRACT: Neutrophils rapidly undergo polarization and directional movement to infiltrate the sites of infection and inflammation. Here, we show that an inhibitory MHC I receptor, Ly49Q, was crucial for the swift polarization of and tissue infiltration by neutrophils. During the steady state, Ly49Q inhibited neutrophil adhesion by preventing focal-complex formation, likely by inhibiting Src and PI3 kinases. However, in the presence of inflammatory stimuli, Ly49Q mediated rapid neutrophil polarization and tissue infiltration in an ITIM-domain-dependent manner. These opposite functions appeared to be mediated by distinct use of effector phosphatase SHP-1 and SHP-2. Ly49Q-dependent polarization and migration were affected by Ly49Q regulation of membrane raft functions. We propose that Ly49Q is pivotal in switching neutrophils to their polarized morphology and rapid migration upon inflammation, through its spatiotemporal regulation of membrane rafts and raft-associated signaling molecules.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We propose that Ly49Q is pivotal in switching neutrophils to their polarized morphology and rapid migration upon inflammation, through its spatiotemporal regulation of membrane rafts and raft-associated signaling molecules.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 76, "doc_id": "5531479", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Occupancy of ribosomes by IncRNAs mirror 5 0-UTRs\n\nCANDIDATE_PASSAGE:\nAnxiety OBJECTIVES To examine the effect of routinely administered psychiatric questionnaires on the recognition, management, and outcome of psychiatric disorders in non-psychiatric settings. DATA SOURCES Embase, Medline, PsycLIT, Cinahl, Cochrane Controlled Trials Register, and hand searches of key journals. METHODS A systematic review of randomised controlled trials of the administration and routine feedback of psychiatric screening and outcome questionnaires to clinicians in non-psychiatric settings. Narrative overview of key design features and end points, together with a random effects quantitative synthesis of comparable studies. MAIN OUTCOME MEASURES Recognition of psychiatric disorders after feedback of questionnaire results; interventions for psychiatric disorders; and outcome of psychiatric disorders. RESULTS Nine randomised studies were identified that examined the use of common psychiatric instruments in primary care and general hospital settings. Studies compared the effect of the administration of these instruments followed by the feedback of the results to clinicians, with administration with no feedback. Meta-analytic pooling was possible for four of these studies (2457 participants), which measured the effect of feedback on the recognition of depressive disorders. Routine administration and feedback of scores for all patients (irrespective of score) did not increase the overall rate of recognition of mental disorders such as anxiety and depression (relative risk of detection of depression by clinician after feedback 0.95, 95% confidence interval 0.83 to 1.09). Two studies showed that routine administration followed by selective feedback for only high scorers increased the rate of recognition of depression (relative risk of detection of depre [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "880", "doc_id": "4695046", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The removal of reactive oxygen species by activated oncogenes contributes to the increased genomic instability of leukaemia cells.\n\nCANDIDATE_PASSAGE:\nRole of boundary conditions in an experimental model of epithelial wound healing. Coordinated cell movements in epithelial layers are essential for proper tissue morphogenesis and homeostasis, but our understanding of the mechanisms that coordinate the behavior of multiple cells in these processes is far from complete. Recent experiments with Madin-Darby canine kidney epithelial monolayers revealed a wave-like pattern of injury-induced MAPK activation and showed that it is essential for collective cell migration after wounding. To investigate the effects of the different aspects of wounding on cell sheet migration, we engineered a system that allowed us to dissect the classic wound healing assay. We studied Madin-Darby canine kidney sheet migration under three different conditions: 1) the classic wound healing assay, 2) empty space induction, where a confluent monolayer is grown adjacent to a slab of polydimethylsiloxane and the monolayer is not injured but allowed to migrate upon removal of the slab, and 3) injury via polydimethylsiloxane membrane peel-off, where an injured monolayer migrates onto plain tissue culture surface, as in the case of empty space induction allowing for direct comparison. By tracking the motion of individual cells within the sheet under these three conditions, we show how the dynamics of the individual cells' motion is responsible for the coordinated migration of the sheet and is coordinated with the activation of ERK1/2 MAPK. In addition, we demonstrate that the propagation of the waves of MAPK activation depends on the generation of reactive oxygen species at the wound edge.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1261", "doc_id": "6308416", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The DESMOND program caused substantial weight loss in most participants.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effective population size and patterns of molecular evolution and variation\nABSTRACT: The effective size of a population, Ne, determines the rate of change in the composition of a population caused by genetic drift, which is the random sampling of genetic variants in a finite population. Ne is crucial in determining the level of variability in a population, and the effectiveness of selection relative to drift. This article reviews the properties of Ne in a variety of different situations of biological interest, and the factors that influence it. In particular, the action of selection means that Ne varies across the genome, and advances in genomic techniques are giving new insights into how selection shapes Ne.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1156, "doc_id": "1067605", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: ScPif1p has reduced binding ability to G-rich ssDNA compared to non-G-rich ssDNA.\n\nCANDIDATE_PASSAGE:\nLoss of TDP43 inhibits progression of triple-negative breast cancer in coordination with SRSF3 Aberrant alternative splicing has been highlighted as a potential hallmark of cancer. Here, we identify TDP43 (TAR DNA-binding protein 43) as an important splicing regulator responsible for the unique splicing profile in triple-negative breast cancer (TNBC). Clinical data demonstrate that TDP43 is highly expressed in TNBC with poor prognosis. Knockdown of TDP43 inhibits tumor progression, including proliferation and metastasis, and overexpression of TDP43 promotes proliferation and malignancy of mammary epithelial cells. Deep sequencing analysis and functional experiments indicate that TDP43 alters most splicing events with splicing factor SRSF3 (serine/arginine-rich splicing factor 3), in the regulation of TNBC progression. The TDP43/SRSF3 complex controls specific splicing events, including downstream genes PAR3 and NUMB The effect of reduced metastasis and proliferation upon the knockdown of TDP43 or SRSF3 is mediated by the splicing regulation of PAR3 and NUMB exon 12, respectively. The TDP43/SRSF3 complex and downstream PAR3 isoform are potential therapeutic targets for TNBC.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1068", "doc_id": "4889228", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_PASSAGE:\nHuman papillomavirus and Papanicolaou tests to screen for cervical cancer. BACKGROUND Screening for cervical cancer based on testing for human papillomavirus (HPV) increases the sensitivity of detection of high-grade (grade 2 or 3) cervical intraepithelial neoplasia, but whether this gain represents overdiagnosis or protection against future high-grade cervical epithelial neoplasia or cervical cancer is unknown. METHODS In a population-based screening program in Sweden, 12,527 women 32 to 38 years of age were randomly assigned at a 1:1 ratio to have an HPV test plus a Papanicolaou (Pap) test (intervention group) or a Pap test alone (control group). Women with a positive HPV test and a normal Pap test result were offered a second HPV test at least 1 year later, and those who were found to be persistently infected with the same high-risk type of HPV were then offered colposcopy with cervical biopsy. A similar number of double-blinded Pap smears and colposcopies with biopsy were performed in randomly selected women in the control group. Comprehensive registry data were used to follow the women for a mean of 4.1 years. The relative rates of grade 2 or 3 cervical intraepithelial neoplasia or cancer detected at enrollment and at subsequent screening examinations were calculated. RESULTS At enrollment, the proportion of women in the intervention group who were found to have lesions of grade 2 or 3 cervical intraepithelial neoplasia or cancer was 51% greater (95% confidence interval [CI], 13 to 102) than the proportion of women in the control group who were found to have such lesions. At subsequent screening examinations, the proportion of women in the intervention group who were found to have grade 2 or 3 lesions or cancer was 42% less (95% CI, 4 to 64) and the pro [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "972", "doc_id": "46695481", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Mutant mice lacking SVCT2 have greatly increased ascorbic acid levels in both brain and adrenals.\n\nCANDIDATE_PASSAGE:\nAscorbic-acid transporter Slc23a1 is essential for vitamin C transport into the brain and for perinatal survival The only proven requirement for ascorbic acid (vitamin C) is in preventing scurvy, presumably because it is a cofactor for hydroxylases required for post-translational modifications that stabilize collagen. We have created mice deficient in the mouse ortholog (solute carrier family 23 member 1 or Slc23a1) of a rat ascorbic-acid transporter, Svct2 (ref. 4). Cultured embryonic fibroblasts from homozygous Slc23a1−/− mice had less than 5% of normal ascorbic-acid uptake. Ascorbic-acid levels were undetectable or markedly reduced in the blood and tissues of Slc23a1−/− mice. Prenatal supplementation of pregnant females did not elevate blood ascorbic acid in Slc23a1−/− fetuses, suggesting Slc23a1 is important in placental ascorbic-acid transport. Slc23a1−/− mice died within a few minutes of birth with respiratory failure and intraparenchymal brain hemorrhage. Lungs showed no postnatal expansion but had normal surfactant protein B levels. Brain hemorrhage was unlikely to be simply a form of scurvy since Slc23a1−/− mice showed no hemorrhage in any other tissues and their skin had normal skin 4-hydroxyproline levels despite low ascorbic-acid content. We conclude that Slc23a1 is required for transport of ascorbic acid into many tissues and across the placenta. Deficiency of the transporter is lethal in newborn mice, thereby revealing a previously unrecognized requirement for ascorbic acid in the perinatal period.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "811", "doc_id": "19799455", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Marmosets have a brain region homologous to Broca's area.\n\nCANDIDATE_PASSAGE:\nDecreased neurogenesis after cholinergic forebrain lesion in the adult rat. Adult neurogenesis has been shown to be regulated by a multitude of extracellular cues, including hormones, growth factors, and neurotransmitters. The cholinergic system of the basal forebrain is one of the key transmitter systems for learning and memory. Because adult neurogenesis has been implicated in cognitive performance, the present work aims at defining the role of cholinergic input for adult neurogenesis by using an immunotoxic lesion approach. The immunotoxin 192IgG-saporin was infused into the lateral ventricle of adult rats to selectively lesion cholinergic neurons of the cholinergic basal forebrain (CBF), which project to the two main regions of adult neurogenesis: the dentate gyrus and the olfactory bulb. Five weeks after lesioning, neurogenesis, defined by the number of cells colocalized for bromodeoxyuridine (BrdU) and the neuronal nuclei marker NeuN, declined significantly in the granule cell layers of the dentate gyrus and olfactory bulb. Furthermore, immunotoxic lesions to the CBF led to increased numbers of apoptotic cells specifically in the subgranular zone, the progenitor region of the dentate gyrus, and within the periglomerular layer of the olfactory bulb. We propose that the cholinergic system plays a survival-promoting role for neuronal progenitors and immature neurons within regions of adult neurogenesis, similar to effects observed previously during brain development. As a working hypothesis, neuronal loss within the CBF system leads not only to cognitive deficits but may also alter on a cellular level the functionality of the dentate gyrus, which in turn may aggravate cognitive deficits.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "758", "doc_id": "22549449", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Transplanted human glial progenitor cells can mature in their host animal.\n\nCANDIDATE_ABSTRACT:\nTITLE: Asthma in United States Olympic athletes who participated in the 1996 Summer Games.\nABSTRACT: BACKGROUND Asthma prevalence appears to be increasing in the general population. We sought to determine whether asthma prevalence has also increased in highly competitive athletes. OBJECTIVE Our aim was to determine how many United States Olympic athletes who were chosen to participate in the 1996 Summer Olympic Games had a past history of asthma or symptoms that suggested asthma or took asthma medications. METHODS We analyzed responses to questions that asked about allergic and respiratory diseases on the United States Olympic Committee (USOC) Medical History Questionnaire that was completed by all athletes who were chosen to represent the US at the 1996 Summer Olympic Games in Atlanta. RESULTS Of the 699 athletes who completed the questionnaire, 107 (15.3%) had a previous diagnosis of asthma, and 97 (13.9%) recorded use of an asthma medication at some time in the past. One hundred seventeen (16.7%) reported use of an asthma medication, a diagnosis of asthma, or both (which was our basis for the diagnosis of asthma). Seventy-three (10. 4%) of the athletes were currently taking an asthma medication at the time that they were processed in Atlanta or noted that they took asthma medications on a permanent or semipermanent basis and were considered to have active asthma. Athletes who participated in cycling and mountain biking had the highest prevalence of having been told that they had asthma or had taken an asthma medication in the past (50%). Frequency of active asthma varied from 45% of cyclists and emountain bikers to none of the divers and weight lifters. Only about 11% of the athletes who participated in the 1984 Summer Olympic Games were reported to have had exercise-induced asthma on the basis of other criteria that may have been less restrictive. On th [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1322, "doc_id": "641459", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does preferential allocation of marginal kidney allografts to elderly recipients combined with modified immunosuppression give good results?\n\nABSTRACT:\nThere is an increasing tendency to allocate kidneys from marginal donors in older recipients. This combination optimizes the uses of an expanded donor pool but demands attention for the higher nephrotoxic sensitivity of the kidney and the increased immunosuppression vulnerability of the elderly recipients. We aimed to reduce these hazards by means of a calcineurin-free induction therapy followed by a maintenance regimen targeted to minimize/withdraw steroid. Eighty-eight single (43%) or double (57%) transplant recipients (58.4+/-5.7 years) from 88 marginal donors (67+/-8.3 years) received monoclonal anti-IL-2 receptor antibodies, mycophenolate mofetil (MMF), and steroid. When serum creatinine was less than 2.6 mg/dL, tacrolimus was started and MMF was withdrawn when the tacrolimus trough level was above 15 ng/ml. Steroid was tapered to 5 mg at day 45 and then progressively reduced. Overall patient and graft survival at the first and fourth year were respectively 100 and 96%, and 98 and 79%. Acute rejection rate was 13.6% (12/88), creatinine clearance remained stable (48.2 ml/min at the sixth month, 50.9 ml/min at 48th month). At the first, second, third, and fourth years, 23, 69, 80, and 100% of recipients were off steroids. For those on steroids, mean dose was respectively 2.6 mg/day from month 12. No recipient re-assumed steroids", "output": "{\"label\": \"yes\", \"rationale\": \"In the \\\"old-for-old\\\" allocation, the calcineurin-inhibitor avoidance at induction and the steroid withdrawal/minimization during the tacrolimus-based maintenance regimen allow a low acute rejection rate, a stable renal function, and favorable recipient and graft outcomes.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 16249744, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Angiotensin converting enzyme inhibitors are associated with increased risk for functional renal insufficiency.\n\nCANDIDATE_PASSAGE:\nEffect of women's nutrition before and during early pregnancy on maternal and infant outcomes: a systematic review. Current understanding of biologic processes indicates that women's nutritional status before and during early pregnancy may play an important role in determining early developmental processes and ensuring successful pregnancy outcomes. We conducted a systematic review of the evidence for the impact of maternal nutrition before and during early pregnancy (<12 weeks gestation) on maternal, neonatal and child health outcomes and included 45 articles (nine intervention trials and 32 observational studies) that were identified through PubMed and EMBASE database searches and examining review articles. Intervention trials and observational studies show that periconceptional (<12 weeks gestation) folic acid supplementation significantly reduced the risk of neural tube defects. Observational studies suggest that preconceptional and periconceptional intake of vitamin and mineral supplements is associated with a reduced risk of delivering offspring who are low birthweight and/or small-for-gestational age (SGA) and preterm deliveries (PTD). Some studies report that indicators of maternal prepregnancy size, low stature, underweight and overweight are associated with increased risks of PTD and SGA. The available data indicate the importance of women's nutrition prior to and during the first trimester of pregnancy, but there is a need for well-designed prospective studies and controlled trials in developing country settings that examine relationships with low birthweight, SGA, PTD, stillbirth and maternal and neonatal mortality. The knowledge gaps that need to be addressed include the evaluation of periconceptional interventions such as food supplements, mult [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "113", "doc_id": "33740844", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cost effectiveness evaluations based on cRCT data accurately reflect prices for patients in actual clinical practice.\n\nCANDIDATE_ABSTRACT:\nTITLE: Epigenetic switch involved in activation of pioneer factor FOXA1-dependent enhancers.\nABSTRACT: Transcription factors (TFs) bind specifically to discrete regions of mammalian genomes called cis-regulatory elements. Among those are enhancers, which play key roles in regulation of gene expression during development and differentiation. Despite the recognized central regulatory role exerted by chromatin in control of TF functions, much remains to be learned regarding the chromatin structure of enhancers and how it is established. Here, we have analyzed on a genomic-scale enhancers that recruit FOXA1, a pioneer transcription factor that triggers transcriptional competency of these cis-regulatory sites. Importantly, we found that FOXA1 binds to genomic regions showing local DNA hypomethylation and that its cell-type-specific recruitment to chromatin is linked to differential DNA methylation levels of its binding sites. Using neural differentiation as a model, we showed that induction of FOXA1 expression and its subsequent recruitment to enhancers is associated with DNA demethylation. Concomitantly, histone H3 lysine 4 methylation is induced at these enhancers. These epigenetic changes may both stabilize FOXA1 binding and allow for subsequent recruitment of transcriptional regulatory effectors. Interestingly, when cloned into reporter constructs, FOXA1-dependent enhancers were able to recapitulate their cell type specificity. However, their activities were inhibited by DNA methylation. Hence, these enhancers are intrinsic cell-type-specific regulatory regions of which activities have to be potentiated by FOXA1 through induction of an epigenetic switch that includes notably DNA demethylation.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 290, "doc_id": "2151983", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Smc5/6 engagment drives the activation of SUMO E3 ligase Mms21 by ATP-dependent remolding.\n\nCANDIDATE_PASSAGE:\nTHE USE OF LEAD CITRATE AT HIGH pH AS AN ELECTRON-OPAQUE STAIN IN ELECTRON MICROSCOPY Aqueous solutions of lead salts (1, 2) and saturated solutions of lead hydroxide (1) have been used as stains to enhance the electron-scattering properties of components of biological materials examined in the electron microscope. Saturated solutions of lead hydroxide (1), while staining more intensely than either lead acetate or monobasic lead acetate (l , 2), form insoluble lead carbonate upon exposure to air. The avoidance of such precipitates which contaminate surfaces of sections during staining has been the stimulus for the development of elaborate procedures for exclusion of air or carbon dioxide (3, 4). Several modifications of Watson's lead hydroxide stain (1) have recently appeared (5-7). All utilize relatively high pH (approximately 12) and one contains small amounts of tartrate (6), a relatively weak complexing agent (8), in addition to lead. These modified lead stains are less liable to contaminate the surface of the section with precipitated stain products. The stain reported here differs from previous alkaline lead stains in that the chelating agent, citrate, is in sufficient excess to sequester all lead present. Lead citrate, soluble in high concentrations in basic solutions, is a chelate compound with an apparent association constant (log Ka) between ligand and lead ion of 6.5 (9). Tissue binding sites, presumably organophosphates, and other anionic species present in biological components following fixation, dehydration, and plastic embedding apparently have a greater affinity for this cation than lead citrate inasmuch as cellular and extracellular structures in the section sequester lead from the staining solution. Alkaline lead citrate solutions are less [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1089", "doc_id": "32827351", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Lamins are found within the inner layer of the nuclear membrane of all cells.\n\nCANDIDATE_PASSAGE:\nA novel family of sequence-specific endoribonucleases associated with the clustered regularly interspaced short palindromic repeats. Clustered regularly interspaced short palindromic repeats (CRISPRs) together with the associated CAS proteins protect microbial cells from invasion by foreign genetic elements using presently unknown molecular mechanisms. All CRISPR systems contain proteins of the CAS2 family, suggesting that these uncharacterized proteins play a central role in this process. Here we show that the CAS2 proteins represent a novel family of endoribonucleases. Six purified CAS2 proteins from diverse organisms cleaved single-stranded RNAs preferentially within U-rich regions. A representative CAS2 enzyme, SSO1404 from Sulfolobus solfataricus, cleaved the phosphodiester linkage on the 3'-side and generated 5'-phosphate- and 3'-hydroxyl-terminated oligonucleotides. The crystal structure of SSO1404 was solved at 1.6A resolution revealing the first ribonuclease with a ferredoxin-like fold. Mutagenesis of SSO1404 identified six residues (Tyr-9, Asp-10, Arg-17, Arg-19, Arg-31, and Phe-37) that are important for enzymatic activity and suggested that Asp-10 might be the principal catalytic residue. Thus, CAS2 proteins are sequence-specific endoribonucleases, and we propose that their role in the CRISPR-mediated anti-phage defense might involve degradation of phage or cellular mRNAs.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "687", "doc_id": "22003328", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Noninvasive positive pressure ventilation is not predictive of acute respiratory failure after solid organ transplantation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Noninvasive ventilation for treatment of acute respiratory failure in patients undergoing solid organ transplantation: a randomized trial.\nABSTRACT: CONTEXT Noninvasive ventilation (NIV) has been associated with lower rates of endotracheal intubation in populations of patients with acute respiratory failure. OBJECTIVE To compare NIV with standard treatment using supplemental oxygen administration to avoid endotracheal intubation in recipients of solid organ transplantation with acute hypoxemic respiratory failure. DESIGN AND SETTING Prospective randomized study conducted at a 14-bed, general intensive care unit of a university hospital. PATIENTS Of 238 patients who underwent solid organ transplantation from December 1995 to October 1997, 51 were treated for acute respiratory failure. Of these, 40 were eligible and 20 were randomized to each group. INTERVENTION Noninvasive ventilation vs standard treatment with supplemental oxygen administration. MAIN OUTCOME MEASURES The need for endotracheal intubation and mechanical ventilation at any time during the study, complications not present on admission, duration of ventilatory assistance, length of hospital stay, and intensive care unit mortality. RESULTS The 2 groups were similar at study entry. Within the first hour of treatment, 14 patients (70%) in the NIV group, and 5 patients (25%) in the standard treatment group improved their ratio of the PaO2 to the fraction of inspired oxygen (FIO2). Over time, a sustained improvement in PaO2 to FIO2 was noted in 12 patients (60%) in the NIV group, and in 5 patients (25%) randomized to standard treatment (P = .03). The use of NIV was associated with a significant reduction in the rate of endotracheal intubation (20% vs 70%; P = .002), rate of fatal complications (20% vs 50%; P = .05), length of stay in the intensive care unit by survivors (mean [SD] days, 5.5 [3] vs 9 [4]; P = .03), and intensive care unit mortality [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Within the first hour of treatment, 14 patients (70%) in the NIV group, and 5 patients (25%) in the standard treatment group improved their ratio of the PaO2 to the fraction of inspired oxygen (FIO2).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 855, "doc_id": "8190282", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Bactericidal activity of 3 cutaneous/mucosal antiseptic solutions in the presence of interfering substances: Improvement of the NF EN 13727 European Standard?\n\nABSTRACT:\nThere is no standard protocol for the evaluation of antiseptics used for skin and mucous membranes in the presence of interfering substances. Our objective was to suggest trial conditions adapted from the NF EN 13727 standard, for the evaluation of antiseptics used in gynecology and dermatology. Three antiseptic solutions were tested in vitro: a chlorhexidine-benzalkonium (CB) combination, a hexamidine-chlorhexidine-chlorocresol (HCC) combination, and povidone iodine (P). The adaptation of trial conditions to the standard involved choosing dilutions, solvent, and interfering substances. The activity of solutions was assessed on the recommended strains at concentrations of 97% (pure solution), 50%, and 10% (diluted solution), and 1%. A logarithmic reduction ≥ 5 was expected after 60seconds of contact, to meet requirements of bactericidal activity. HCC did not present any bactericidal activity except on P. aeruginosa at a concentration of 97%. P was not bactericidal on E. hirae at any concentration and on S. aureus at 97%. CB had the most homogeneous bactericidal activity with a reduction>5 log on the 4 bacterial strains at concentrations of 97%, 50% and 10%.", "output": "{\"label\": \"maybe\", \"rationale\": \"Adapting the NF EN 13727 standard allowed assessing the 3 tested solutions: only CB was bactericidal in dirty conditions. This study proved the possibility of validating antiseptic choice in vitro, in current practice conditions, for adjunctive treatment of skin and mucous membranes disorders, primarily of bacterial origin or with a potential of superinfection.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 25779009, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: 40mg/day dosage of folic acid and 2mg/day dosage of vitamin B12 does not affect chronic kidney disease (CKD) progression.\n\nCANDIDATE_ABSTRACT:\nTITLE: Selective elimination of high constitutive activity or chemokine binding in the human herpesvirus 8 encoded seven transmembrane oncogene ORF74.\nABSTRACT: Open reading frame 74 (ORF74) encoded by human herpesvirus 8 is a highly constitutively active seven transmembrane (7TM) receptor stimulated by angiogenic chemokines, e.g. growth-related oncogene-alpha, and inhibited by angiostatic chemokines e.g. interferon-gamma-inducible protein. Transgenic mice expressing ORF74 under control of the CD2 promoter develop highly vascularized Kaposi's sarcoma-like tumors. Through targeted mutagenesis we here create three distinct phenotypes of ORF74: a receptor with normal, high constitutive signaling through the phospholipase C pathway but deprived of binding and action of chemokines obtained through deletion of 22 amino acids from the N-terminal extension; an ORF74 with high constitutive activity but with selective elimination of stimulatory regulation by angiogenic chemokines obtained through substitution of basic residues at the extracellular ends of TM-V or TM-VI; and an ORF74 lacking constitutive activity but with preserved ability to be stimulated by agonist chemokines obtained through introduction of an Asp residue on the hydrophobic, presumed membrane-exposed face of TM-II. It is concluded that careful molecular dissection can selectively eliminate either agonist or inverse agonist modulation as well as high constitutive activity of the virally encoded oncogene ORF74 and that these mutant forms presumably can be used in transgenic animals to identify the molecular mechanism of its transforming activity.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 12, "doc_id": "1574014", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does nocturnal systemic hypotension increase the risk of glaucoma progression?\n\nABSTRACT:\nThe objective of this prospective, longitudinal study of patients with normal-tension glaucoma (NTG) was to determine whether patients with nocturnal hypotension are at greater risk for visual field (VF) loss over 12 months than those without nocturnal hypotension. Prospective, longitudinal study. Consecutive patients with NTG with at least 5 prior VF tests were screened for eligibility. The baseline evaluation assessed demographic and clinical characteristics, covering systemic comorbid conditions, including systemic hypertension. All oral and ophthalmologic medications were recorded. A complete ophthalmological examination was performed at baseline and follow-up. Patients had their blood pressure (BP) monitored every 30 minutes for 48 hours with an ambulatory recording device at baseline and 6 and 12 months. The primary outcome was based on the global rates of VF progression by linear regression of the mean VF threshold sensitivity over time (decibels/year). Eighty-five patients with NTG (166 eyes; mean age, 65 years; 67% were women) were included. Of the 85 patients, 29% had progressed in the 5 VFs collected before study enrollment. The nocturnal mean arterial pressure (MAP) was compared with the daytime MAP. Multivariate analysis showed that the total time that sleep MAP was 10 mmHg below the daytime MAP was a significant predictor of subsequent VF progression (P<0.02).", "output": "{\"label\": \"yes\", \"rationale\": \"Cumulative nocturnal hypotension predicted VF loss in this cohort. Our data suggest that the duration and magnitude of decrease in nocturnal blood pressure below the daytime MAP, especially pressures that are 10 mmHg lower than daytime MAP, predict progression of NTG. Low nocturnal blood pressure, whether occurring spontaneously or as a result of medications, may lead to worsening of VF defects.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 24869467, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Obesity decreases life quality.\n\nCANDIDATE_PASSAGE:\nBody-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies. BACKGROUND The main associations of body-mass index (BMI) with overall and cause-specific mortality can best be assessed by long-term prospective follow-up of large numbers of people. The Prospective Studies Collaboration aimed to investigate these associations by sharing data from many studies. METHODS Collaborative analyses were undertaken of baseline BMI versus mortality in 57 prospective studies with 894 576 participants, mostly in western Europe and North America (61% [n=541 452] male, mean recruitment age 46 [SD 11] years, median recruitment year 1979 [IQR 1975-85], mean BMI 25 [SD 4] kg/m(2)). The analyses were adjusted for age, sex, smoking status, and study. To limit reverse causality, the first 5 years of follow-up were excluded, leaving 66 552 deaths of known cause during a mean of 8 (SD 6) further years of follow-up (mean age at death 67 [SD 10] years): 30 416 vascular; 2070 diabetic, renal or hepatic; 22 592 neoplastic; 3770 respiratory; 7704 other. FINDINGS In both sexes, mortality was lowest at about 22.5-25 kg/m(2). Above this range, positive associations were recorded for several specific causes and inverse associations for none, the absolute excess risks for higher BMI and smoking were roughly additive, and each 5 kg/m(2) higher BMI was on average associated with about 30% higher overall mortality (hazard ratio per 5 kg/m(2) [HR] 1.29 [95% CI 1.27-1.32]): 40% for vascular mortality (HR 1.41 [1.37-1.45]); 60-120% for diabetic, renal, and hepatic mortality (HRs 2.16 [1.89-2.46], 1.59 [1.27-1.99], and 1.82 [1.59-2.09], respectively); 10% for neoplastic mortality (HR 1.10 [1.06-1.15]); and 20% for respiratory and for all other morta [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "871", "doc_id": "195689316", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: IgA plasma cells that are specific for transglutaminase 2 accumulate in the duodenal mucosa on commencement of a gluten-free diet.\n\nCANDIDATE_ABSTRACT:\nTITLE: High abundance of plasma cells secreting transglutaminase 2–specific IgA autoantibodies with limited somatic hypermutation in celiac disease intestinal lesions\nABSTRACT: Celiac disease is an immune-mediated disorder in which mucosal autoantibodies to the enzyme transglutaminase 2 (TG2) are generated in response to the exogenous antigen gluten in individuals who express human leukocyte antigen HLA-DQ2 or HLA-DQ8 (ref. 3). We assessed in a comprehensive and nonbiased manner the IgA anti-TG2 response by expression cloning of the antibody repertoire of ex vivo–isolated intestinal antibody-secreting cells (ASCs). We found that TG2-specific plasma cells are markedly expanded within the duodenal mucosa in individuals with active celiac disease. TG2-specific antibodies were of high affinity yet showed little adaptation by somatic mutations. Unlike infection-induced peripheral blood plasmablasts, the TG2-specific ASCs had not recently proliferated and were not short-lived ex vivo. Altogether, these observations demonstrate that there is a germline repertoire with high affinity for TG2 that may favor massive generation of autoreactive B cells. TG2-specific antibodies did not block enzymatic activity and served as substrates for TG2-mediated crosslinking when expressed as IgD or IgM but not as IgA1 or IgG1. This could result in preferential recruitment of plasma cells from naive IgD- and IgM-expressing B cells, thus possibly explaining why the antibody response to TG2 bears signs of a primary immune response despite the disease chronicity.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 552, "doc_id": "1471041", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Up-regulation of the p53 pathway and related molecular events casues cancer resistance and results in a significantly shortened lifespan marked by senescent cells and accelerated organismal aging.\n\nCANDIDATE_PASSAGE:\nSenescent Cells, Tumor Suppression, and Organismal Aging: Good Citizens, Bad Neighbors Cells from organisms with renewable tissues can permanently withdraw from the cell cycle in response to diverse stress, including dysfunctional telomeres, DNA damage, strong mitogenic signals, and disrupted chromatin. This response, termed cellular senescence, is controlled by the p53 and RB tumor suppressor proteins and constitutes a potent anticancer mechanism. Nonetheless, senescent cells acquire phenotypic changes that may contribute to aging and certain age-related diseases, including late-life cancer. Thus, the senescence response may be antagonistically pleiotropic, promoting early-life survival by curtailing the development of cancer but eventually limiting longevity as dysfunctional senescent cells accumulate.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1344", "doc_id": "9559146", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Cytochrome c is transferred from cytosol to the mitochondrial intermembrane space during apoptosis.\n\nCANDIDATE_PASSAGE:\nPrimPol, an Archaic Primase/Polymerase Operating in Human Cells We describe a second primase in human cells, PrimPol, which has the ability to start DNA chains with deoxynucleotides unlike regular primases, which use exclusively ribonucleotides. Moreover, PrimPol is also a DNA polymerase tailored to bypass the most common oxidative lesions in DNA, such as abasic sites and 8-oxoguanine. Subcellular fractionation and immunodetection studies indicated that PrimPol is present in both nuclear and mitochondrial DNA compartments. PrimPol activity is detectable in mitochondrial lysates from human and mouse cells but is absent from mitochondria derived from PRIMPOL knockout mice. PRIMPOL gene silencing or ablation in human and mouse cells impaired mitochondrial DNA replication. On the basis of the synergy observed with replicative DNA polymerases Polγ and Polε, PrimPol is proposed to facilitate replication fork progression by acting as a translesion DNA polymerase or as a specific DNA primase reinitiating downstream of lesions that block synthesis during both mitochondrial and nuclear DNA replication.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "299", "doc_id": "17368516", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Combination nicotine replacement therapies with varenicline or bupropion lead to significantly higher long-term abstinence rates at 52 weeks than varenicline monotherapy.\n\nCANDIDATE_ABSTRACT:\nTITLE: ER-associated mitochondrial division links the distribution of mitochondria and mitochondrial DNA in yeast\nABSTRACT: Mitochondrial division is important for mitochondrial distribution and function. Recent data have demonstrated that ER-mitochondria contacts mark mitochondrial division sites, but the molecular basis and functions of these contacts are not understood. Here we show that in yeast, the ER-mitochondria tethering complex, ERMES, and the highly conserved Miro GTPase, Gem1, are spatially and functionally linked to ER-associated mitochondrial division. Gem1 acts as a negative regulator of ER-mitochondria contacts, an activity required for the spatial resolution and distribution of newly generated mitochondrial tips following division. Previous data have demonstrated that ERMES localizes with a subset of actively replicating mitochondrial nucleoids. We show that mitochondrial division is spatially linked to nucleoids and that a majority of these nucleoids segregate prior to division, resulting in their distribution into newly generated tips in the mitochondrial network. Thus, we postulate that ER-associated division serves to link the distribution of mitochondria and mitochondrial nucleoids in cells. DOI:http://dx.doi.org/10.7554/eLife.00422.001.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 274, "doc_id": "1991105", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Inhibiting HDAC6 increases survival of mice with ARID1A mutated tumors.\n\nCANDIDATE_PASSAGE:\nMHC class I antigen presentation: learning from viral evasion strategies The cell surface display of peptides by MHC class I molecules to lymphocytes provides the host with an important surveillance mechanism to protect against invading pathogens. However, in turn, viruses have evolved elegant strategies to inhibit various stages of the MHC class I antigen presentation pathway and prevent the display of viral peptides. This Review highlights how the elucidation of mechanisms of viral immune evasion is important for advancing our understanding of virus–host interactions and can further our knowledge of the MHC class I presentation pathway as well as other cellular pathways.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "631", "doc_id": "9278263", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is hyperuricemia associated with an increased prevalence of atrial fibrillation in hospitalized patients with type 2 diabetes?\n\nABSTRACT:\nHyperuricemia/gout and atrial fibrillation (AF) are two pathological conditions that are highly prevalent in type 2 diabetes and share multiple cardiovascular risk factors. However, the relationship between elevated levels of serum uric acid and risk of AF in type 2 diabetes is currently poorly known. We studied a hospital-based sample of 842 (male/female = 463/379) patients with type 2 diabetes discharged from our Division of Endocrinology during 2007-2011. Hyperuricemia was defined as a serum uric acid level >7 mg/dl for men and >6 mg/dl for women or allopurinol use. The diagnosis of AF was confirmed in affected participants on the basis of ECGs and medical history by experienced cardiologists. Overall, 243 (28.9 %) patients had hyperuricemia and 91 (10.8 %) patients had persistent or permanent AF. Compared with those with normal serum uric acid levels, patients with hyperuricemia had a remarkably greater prevalence of AF (20.6 vs. 7.1 %; p < 0.001). Hyperuricemia was significantly associated with an increased risk of prevalent AF (odds ratio 3.41, 95 % CI 2.19-5.32; p < 0.001). Adjustments for age, sex, smoking, hemoglobin A1c, hypertension status, chronic kidney disease, chronic obstructive pulmonary disease and previous histories of hyperthyroidism, ischemic heart disease and valvular heart diseases did not weaken this association (adjusted-odds ratio 6.27, 95 % CI 1.82-21.5; p < 0.01).", "output": "{\"label\": \"yes\", \"rationale\": \"These results indicate that hyperuricemia is associated with an increased prevalence of AF in hospitalized patients with type 2 diabetes, independently of multiple risk factors and potential confounders.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 26178737, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pyridostatin stabilizes the G - quadruplex in the telomeric region.\n\nCANDIDATE_ABSTRACT:\nTITLE: Genetic Variation in the Interleukin-28B Gene Is Associated with Spontaneous Clearance and Progression of Hepatitis C Virus in Moroccan Patients\nABSTRACT: BACKGROUND Genetic variation in the IL28B gene has been strongly associated with treatment outcomes, spontaneous clearance and progression of the hepatitis C virus infection (HCV). The aim of the present study was to investigate the role of polymorphisms at this locus with progression and outcome of HCV infection in a Moroccan population. METHODS We analyzed a cohort of 438 individuals among them 232 patients with persistent HCV infection, of whom 115 patients had mild chronic hepatitis and 117 had advanced liver disease (cirrhosis and hepatocellular carcinoma), 68 individuals who had naturally cleared HCV and 138 healthy subjects. The IL28B SNPs rs12979860 and rs8099917 were genotyped using a TaqMan 5' allelic discrimination assay. RESULTS The protective rs12979860-C and rs8099917-T alleles were more common in subjects with spontaneous clearance (77.9% vs 55.2%; p = 0.00001 and 95.6% vs 83.2%; p = 0.0025, respectively). Individuals with clearance were 4.69 (95% CI, 1.99-11.07) times more likely to have the C/C genotype for rs12979860 polymorphism (p = 0.0017) and 3.55 (95% CI, 0.19-66.89) times more likely to have the T/T genotype at rs8099917. Patients with advanced liver disease carried the rs12979860-T/T genotype more frequently than patients with mild chronic hepatitis C (OR = 1.89; 95% CI, 0.99-3.61; p = 0.0532) and this risk was even more pronounced when we compared them with healthy controls (OR = 4.27; 95% CI, 2.08-8.76; p = 0.0005). The rs8099917-G allele was also associated with advanced liver disease (OR = 2.34; 95% CI, 1.40-3.93; p = 0.0100). CONCLUSIONS In the Moroccan population, polymorphisms near the IL28B gene play a role both in spontaneous clearance and progression of HCV infection.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1000, "doc_id": "263364", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pre-mRNAs associated with spliceosomal components are more stable than unassociated splicing substrates.\n\nCANDIDATE_ABSTRACT:\nTITLE: Analyzing mechanisms of alternative pre-mRNA splicing using in vitro splicing assays.\nABSTRACT: The development of in vitro assays to analyze pre-mRNA splicing resulted in the discovery of many fundamental features characterizing splicing signals and the machinery that completes this process. Because in vitro assays can be manipulated by various biochemical approaches, the versatility of investigating alternative pre-mRNA splicing in the test tube appears endless. Importantly, modifications in reaction conditions can lead to the accumulation, isolation, and characterization of reaction intermediates, a prerequisite for gaining mechanistic insights into how the spliceosome carries out intron removal, and how regulatory elements assist the general splicing machinery in defining splice sites and alternative exons. These considerable experimental advantages have made the in vitro splicing system a standard assay, even though this approach is independent from RNA transcription and other RNA processing events, and in some respects deviates from the natural process of mRNA biogenesis. Here, we describe the tools and techniques necessary to carry out in vitro splicing assays. Analyses of various experimental designs are presented to highlight the approaches taken to gain insights into the mechanisms by which splice site recognition and activation are communicated with the general splicing machinery. Methods to measure the kinetics of splicing, to observe the formation of the pre-spliceosomal complexes, and to manipulate and modify the in vitro system to resolve the regulatory influences in alternative splicing are presented.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 964, "doc_id": "29828242", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The deamination of cytidine to uridine on the minus strand of viral DNA can inactivate the viral genome by inducing G-to-A mutations.\n\nCANDIDATE_ABSTRACT:\nTITLE: A rapid method for extraction of cotton (Gossypium spp.) genomic DNA suitable for RFLP or PCR analysis\nABSTRACT: Extraction of high-quality genomic DNA fromGossypium (cotton) species is difficult due to high levels of polysaccharide, oxidizable quinones, and other interfering substances. We describe a procedure that consistently permits isolation of cotton genomic DNA of satisfactory size and quality for RFLP and PCR analysis, as well as for most routine cloning applications. Several antioxidants, phenol-binding reagents, and phenol oxidase inhibitors are used throughout the procedure, and most polysaccharides are eliminated early in the procedure by isolation of nuclei.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1209, "doc_id": "102662", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does ultrasound imaging before puncture facilitate internal jugular vein cannulation?\n\nABSTRACT:\nTo investigate whether prepuncture ultrasound evaluation of vascular anatomy facilitates internal jugular vein cannulation compared with landmark-guided puncture. Prospective randomized study. Single community hospital. Adult patients undergoing general anesthesia (n = 240). The right internal jugular vein was cannulated using either anatomic landmarks or prepuncture ultrasound (3.75/7.5 MHz) guidance. In the landmark group, respiratory jugular venodilation was used as the primary landmark for locating the vein. Results of cannulation and the incidence of complications were compared. Patients were randomly assigned to the ultrasound or landmark group. Respiratory jugular venodilation was identified in 188 patients (78.3%), in whom results of cannulation did not differ between the 2 techniques with respect to the venous access rate (cannulated at the first attempt: 83.5% in the landmark v 85.7% in the ultrasound group), the success rate (cannulated within 3 attempts: 96.9% v 95.6%), and the incidence of arterial puncture (1.0% v 3.3%). In the remaining 52 respiratory jugular venodilation-unidentified patients, the access rate (30.4% v 86.2%, p<0.001) and the success rate (78.3 v 100%, p<0.05) were significantly better in the ultrasound group, and no arterial puncture was recorded in the ultrasound group, whereas the incidence was 13.0% in the landmark group. The results were similar regardless of the ultrasound frequency used.", "output": "{\"label\": \"maybe\", \"rationale\": \"Prepuncture ultrasound evaluation did not improve the result of right internal jugular vein cannulation compared with the respiratory jugular venodilation-guided approach. When the landmark was not observed, however, the prepuncture ultrasound guidance was helpful in facilitating the cannulation.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 12407608, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Albendazole is used to treat soil-transmitted helminths.\n\nCANDIDATE_PASSAGE:\nSpatial co-distribution of neglected tropical diseases in the east African great lakes region: revisiting the justification for integrated control. OBJECTIVE To determine spatial patterns of co-endemicity of schistosomiasis mansoni and the soil-transmitted helminths (STHs) Ascaris lumbricoides, Trichuris trichiura and hookworm in the Great Lakes region of East Africa, to help plan integrated neglected tropical disease programmes in this region. METHOD Parasitological surveys were conducted in Uganda, Tanzania, Kenya and Burundi in 28 213 children in 404 schools. Bayesian geostatistical models were used to interpolate prevalence of these infections across the study area. Interpolated prevalence maps were overlaid to determine areas of co-endemicity. RESULTS In the Great Lakes region, prevalence was 18.1% for Schistosoma mansoni, 50.0% for hookworm, 6.8% for A. lumbricoides and 6.8% for T. trichiura. Hookworm infection was ubiquitous, whereas S. mansoni, A. lumbricoides and T. trichiura were highly focal. Most areas were endemic (prevalence >or=10%) or hyperendemic (prevalence >or=50%) for one or more STHs, whereas endemic areas for schistosomiasis mansoni were restricted to foci adjacent large perennial water bodies. CONCLUSION Because of the ubiquity of hookworm, treatment programmes are required for STH throughout the region but efficient schistosomiasis control should only be targeted at limited high-risk areas. Therefore, integration of schistosomiasis with STH control is only indicated in limited foci in East Africa.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "95", "doc_id": "13966946", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Two variants of chromosome 6q21 are associated with radiation therapy-induced second malignancies in pediatric Hodgkin lymphoma patients.\n\nCANDIDATE_PASSAGE:\nCardiovascular risk factors in childhood and carotid artery intima-media thickness in adulthood: the Cardiovascular Risk in Young Finns Study. CONTEXT Exposure to cardiovascular risk factors during childhood and adolescence may be associated with the development of atherosclerosis later in life. OBJECTIVE To study the relationship between cardiovascular risk factors measured in childhood and adolescence and common carotid artery intima-media thickness (IMT), a marker of preclinical atherosclerosis, measured in adulthood. DESIGN, SETTING, AND PARTICIPANTS Population-based, prospective cohort study conducted at 5 centers in Finland among 2229 white adults aged 24 to 39 years who were examined in childhood and adolescence at ages 3 to 18 years in 1980 and reexamined 21 years later, between September 2001 and January 2002. MAIN OUTCOME MEASURES Association between cardiovascular risk variables (levels of low-density lipoprotein cholesterol [LDL-C], high-density lipoprotein cholesterol [HDL-C], and triglycerides; LDL-C/HDL-C ratio; systolic and diastolic blood pressure; body mass index; smoking) measured in childhood and adulthood and common carotid artery IMT measured in adulthood. RESULTS In multivariable models adjusted for age and sex, IMT in adulthood was significantly associated with childhood LDL-C levels (P =.001), systolic blood pressure (P<.001), body mass index (P =.007), and smoking (P =.02), and with adult systolic blood pressure (P<.001), body mass index (P<.001), and smoking (P =.004). The number of risk factors measured in 12- to 18-year-old adolescents, including high levels (ie, extreme age- and sex-specific 80th percentile) of LDL-C, systolic blood pressure, body mass index, and cigarette smoking, were directly related to carotid IMT measured i [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1333", "doc_id": "4647303", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In young and middle-aged adults, current or remote uses of ADHD medications do not increase the risk of serious cardiovascular events.\n\nCANDIDATE_ABSTRACT:\nTITLE: ADHD medications and risk of serious cardiovascular events in young and middle-aged adults.\nABSTRACT: CONTEXT More than 1.5 million US adults use stimulants and other medications labeled for treatment of attention-deficit/hyperactivity disorder (ADHD). These agents can increase heart rate and blood pressure, raising concerns about their cardiovascular safety. OBJECTIVE To examine whether current use of medications prescribed primarily to treat ADHD is associated with increased risk of serious cardiovascular events in young and middle-aged adults. DESIGN, SETTING, AND PARTICIPANTS Retrospective, population-based cohort study using electronic health care records from 4 study sites (OptumInsight Epidemiology, Tennessee Medicaid, Kaiser Permanente California, and the HMO Research Network), starting in 1986 at 1 site and ending in 2005 at all sites, with additional covariate assessment using 2007 survey data. Participants were adults aged 25 through 64 years with dispensed prescriptions for methylphenidate, amphetamine, or atomoxetine at baseline. Each medication user (n = 150,359) was matched to 2 nonusers on study site, birth year, sex, and calendar year (443,198 total users and nonusers). MAIN OUTCOME MEASURES Serious cardiovascular events, including myocardial infarction (MI), sudden cardiac death (SCD), or stroke, with comparison between current or new users and remote users to account for potential healthy-user bias. RESULTS During 806,182 person-years of follow-up (median, 1.3 years per person), 1357 cases of MI, 296 cases of SCD, and 575 cases of stroke occurred. There were 107,322 person-years of current use (median, 0.33 years), with a crude incidence per 1000 person-years of 1.34 (95% CI, 1.14-1.57) for MI, 0.30 (95% CI, 0.20-0.42) for SCD, and 0.56 (95% CI, 0.43-0.72) for stroke. The multivariable-adjusted rate ratio (RR) of serious cardiovascular eve [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The multivariable-adjusted rate ratio (RR) of serious cardiovascular events for current use vs nonuse of ADHD medications was 0.83 (95% CI, 0.72-0.96). Among new users of ADHD medications, the adjusted RR was 0.77 (95% CI, 0.63-0.94).\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 589, "doc_id": "10984005", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pyridostatin destabilizes the G - quadruplex in the telomeric region.\n\nCANDIDATE_ABSTRACT:\nTITLE: Targeting BRCA1 and BRCA2 Deficiencies with G-Quadruplex-Interacting Compounds\nABSTRACT: G-quadruplex (G4)-forming genomic sequences, including telomeres, represent natural replication fork barriers. Stalled replication forks can be stabilized and restarted by homologous recombination (HR), which also repairs DNA double-strand breaks (DSBs) arising at collapsed forks. We have previously shown that HR facilitates telomere replication. Here, we demonstrate that the replication efficiency of guanine-rich (G-rich) telomeric repeats is decreased significantly in cells lacking HR. Treatment with the G4-stabilizing compound pyridostatin (PDS) increases telomere fragility in BRCA2-deficient cells, suggesting that G4 formation drives telomere instability. Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint activation, and deregulated G2/M progression and by enhancing the replication defect intrinsic to HR deficiency. PDS toxicity extends to HR-defective cells that have acquired olaparib resistance through loss of 53BP1 or REV7. Altogether, these results highlight the therapeutic potential of G4-stabilizing drugs to selectively eliminate HR-compromised cells and tumors, including those resistant to PARP inhibition.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Treatment with the G4-stabilizing compound pyridostatin (PDS) increases telomere fragility in BRCA2-deficient cells, suggesting that G4 formation drives telomere instability.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 993, "doc_id": "16472469", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The locus rs647161 is associated with colorectal carcinoma.\n\nCANDIDATE_PASSAGE:\nGenome-wide association analyses in East Asians identify new susceptibility loci for colorectal cancer To identify new genetic factors for colorectal cancer (CRC), we conducted a genome-wide association study in east Asians. By analyzing genome-wide data in 2,098 cases and 5,749 controls, we selected 64 promising SNPs for replication in an independent set of samples, including up to 5,358 cases and 5,922 controls. We identified four SNPs with association P values of 8.58 × 10(-7) to 3.77 × 10(-10) in the combined analysis of all east Asian samples. Three of the four were replicated in a study conducted in 26,060 individuals of European descent, with combined P values of 1.22 × 10(-10) for rs647161 (5q31.1), 6.64 × 10(-9) for rs2423279 (20p12.3) and 3.06 × 10(-8) for rs10774214 (12p13.32 near the CCND2 gene), derived from meta-analysis of data from both east Asian and European-ancestry populations. This study identified three new CRC susceptibility loci and provides additional insight into the genetics and biology of CRC.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1225", "doc_id": "9650982", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is advanced adenoma detection rate independent of nonadvanced adenoma detection rate?\n\nABSTRACT:\nAdenoma detection rate (ADR) is the accepted rate marker in colonoscopy quality. Advanced adenomas detected at index colonoscopy, while less frequent than nonadvanced adenomas, carry greater risk for future advanced neoplasia during surveillance colonoscopy. This study aimed to determine the effect of the colonoscopist and other factors on advanced ADR and to define the correlation of advanced and nonadvanced ADRs among colonoscopists. An observational study of a cohort of patients undergoing first-time colorectal cancer screening colonoscopy was conducted. Patient characteristics and colonoscopic findings were collected. Adenoma, advanced adenoma, and nonadvanced ADRs were calculated. Logistic regression was used to determine variable effects on advanced adenoma detection, and Spearman's rank-order correlation was used to evaluate the relationship between advanced and nonadvanced ADRs. A total of 1,944 patients had first-time screening colonoscopies by 14 colonoscopists. All colonoscopists had adequate (>20%) ADRs. The variability in the colonoscopist ranges of detection was 22.22 to 44.66% for adenomas and 2.00 to 18.18% for advanced adenomas. Logistic regression showed that increasing patient age (odds ratio (OR) 1.16 per 5-year increase, 95% confidence interval (CI) 1.05-1.28, P=0.008) and male gender (OR 2.15, 95% CI 1.51-3.06, P<0.0001) were variables associated with advanced adenoma detection. Colonoscopists were significantly different in detecting advanced adenomas by random effects model (P=0.002), adjusting for patient age, gender, race, year of colonoscopy, gastroenterology fellow participation during colonoscopy, and nonadvanced adenomas. Spearman's rank-order correlation coefficient of -0.42 (95% CI -0.77 to 0.14, P=0.13) was not significant an [TRUNCATED]", "output": "{\"label\": \"yes\", \"rationale\": \"Advanced ADR is variable among colonoscopists with acceptable ADRs. Colonoscopists' advanced ADRs are independent of their nonadvanced ADRs.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 23711625, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does total body potassium differ by sex and race across the adult age span?\n\nABSTRACT:\nTotal body potassium (TBK) is an index of fat-free mass. Data describing changes in TBK in African American, Asian, or Hispanic populations have not been reported. The aim was to investigate possible sex and racial differences in TBK in adults over an age range of 70 y. The study used longitudinal and cross-sectional data collected in a body-composition unit from 973 men and 1368 women of African American, Asian, white, and Hispanic race-ethnicity. Random coefficient models in which baseline weight and height were taken into account were applied to estimate sex-specific changes in TBK among the 4 racial-ethnic groups. The ages of 30 and 31 y were identified for women and men, respectively, as the cutoffs after which TBK began to decline. Both sexes had similar racial-ethnic patterns for expected mean TBK at the age cutoffs: African Americans had the highest value, followed by whites, Hispanics, and Asians. After the age cutoffs, the decline in TBK differed by race and sex. In women, African Americans showed the most rapid decline, whereas Asians had the lowest. In men, Hispanics had the most rapid decline in TBK, followed by African Americans, whites, and Asians.", "output": "{\"label\": \"yes\", \"rationale\": \"Significant sex and racial differences exist in the rate of change in TBK with age. Further studies are needed to explore the associations of declining TBK with health risks.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 12816773, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Microcin J25 encourages nucleoside triphosphate (NTP) binding.\n\nCANDIDATE_ABSTRACT:\nTITLE: Antibacterial peptide microcin J25 inhibits transcription by binding within and obstructing the RNA polymerase secondary channel.\nABSTRACT: The antibacterial peptide microcin J25 (MccJ25) inhibits transcription by bacterial RNA polymerase (RNAP). Biochemical results indicate that inhibition of transcription occurs at the level of NTP uptake or NTP binding by RNAP. Genetic results indicate that inhibition of transcription requires an extensive determinant, comprising more than 50 amino acid residues, within the RNAP secondary channel (also known as the \"NTP-uptake channel\" or \"pore\"). Biophysical results indicate that inhibition of transcription involves binding of MccJ25 within the RNAP secondary channel. Molecular modeling indicates that binding of MccJ25 within the RNAP secondary channel obstructs the RNAP secondary channel. We conclude that MccJ25 inhibits transcription by binding within and obstructing the RNAP secondary channel--acting essentially as a \"cork in a bottle. \" Obstruction of the RNAP secondary channel represents an attractive target for drug discovery.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Biochemical results indicate that inhibition of transcription occurs at the level of NTP uptake or NTP binding by RNAP.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 787, "doc_id": "4740447", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Varying expression levels of EBI2 affect the positioning and migration of B cells.\n\nCANDIDATE_PASSAGE:\n7α, 25-dihydroxycholesterol-mediated activation of EBI2 in immune regulation and diseases EBI2, aka GPR183, is a G-couple receptor originally identified in 1993 as one of main genes induced in Burkitt's lymphoma cell line BL41 by Epstein-Barr virus (EBV) infection. After it was reported in 2009 that the receptor played a key role in regulating B cell migration and responses, we initiated an effort in looking for its endogenous ligand. In 2011 we and another group reported the identification of 7α, 25-dihydroxyxcholesterol (7α, 25-OHC), an oxysterol, as the likely physiological ligand of EBI2. A few subsequently published studies further elucidated how 7α, 25-OHC bound to EBI2, and how a gradient of 7α, 25-OHC could be generated in vivo and regulated migration, activation, and functions of B cells, T cells, dendritic cells (DCs), monocytes/macrophages, and astrocytes. The identification of 7α, 25-OHC as a G protein-coupled receptor ligand revealed a previously unknown signaling system of oxysterols, a class of molecules which exert profound biological functions. Dysregulation of the synthesis or functions of these molecules is believed to contribute to inflammation and autoimmune diseases, cardiovascular diseases, neurodegenerative diseases, cancer as well as metabolic diseases such as diabetes, obesity, and dyslipidemia. Therefore EBI2 may represent a promising target for therapeutic interventions for human diseases.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1361", "doc_id": "15058155", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Patients with common epithelial cancers are less likely to have an emergency event as their first hospital admission if they live in resource-deprived areas.\n\nCANDIDATE_ABSTRACT:\nTITLE: Social variations in access to hospital care for patients with colorectal, breast, and lung cancer between 1999 and 2006: retrospective analysis of hospital episode statistics\nABSTRACT: OBJECTIVES To determine the extent to which type of hospital admission (emergency compared with elective) and surgical procedure varied by socioeconomic circumstances, age, sex, and year of admission for colorectal, breast, and lung cancer. DESIGN Repeated cross sectional study with data from individual patients, 1 April 1999 to 31 March 2006. SETTING Hospital episode statistics (HES) dataset. PARTICIPANTS 564 821 patients aged 50 and over admitted with a diagnosis of colorectal, breast, or lung cancer. MAIN OUTCOME MEASURES Proportion of patients admitted as emergencies, and the proportion receiving the recommended surgical treatment. RESULTS Patients from deprived areas, older people, and women were more likely to be admitted as emergencies. For example, the adjusted odds ratio for patients with breast cancer in the least compared with most deprived fifth of deprivation was 0.63 (95% confidence interval 0.60 to 0.66) and the adjusted odds ratio for patients with lung cancer aged 80-89 compared with those aged 50-59 was 3.13 (2.93 to 3.34). There were some improvements in disparities between age groups but not for patients living in deprived areas over time. Patients from deprived areas were less likely to receive preferred procedures for rectal, breast, and lung cancer. These findings did not improve with time. For example, 67.4% (3529/5237) of patients in the most deprived fifth of deprivation had anterior resection for rectal cancer compared with 75.5% (4497/5959) of patients in the least deprived fifth (1.34, 1.22 to 1.47). Over half (54.0%, 11 256/20 849) of patients in the most deprived fifth of deprivation had breast conserving surgery compared with 63.7% (18 445/28 960) of patients in the least deprived fifth (1.21, 1.16 to 1.26). Men were less like [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"For example, 67.4% (3529/5237) of patients in the most deprived fifth of deprivation had anterior resection for rectal cancer compared with 75.5% (4497/5959) of patients in the least deprived fifth (1.34, 1.22 to 1.47).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 927, "doc_id": "16390264", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Do episodic migraineurs selectively attend to headache-related visual stimuli?\n\nABSTRACT:\nTo assess pain-related attentional biases among individuals with episodic migraine. Prior studies have examined whether chronic pain patients selectively attend to pain-related stimuli in the environment, but these studies have produced largely mixed findings and focused primarily on patients with chronic musculoskeletal pain. Limited research has implicated attentional biases among chronic headache patients, but no studies have been conducted among episodic migraineurs, who comprise the overwhelming majority of the migraine population. This was a case-control, experimental study. Three hundred and eight participants (mean age = 19.2 years [standard deviation = 3.3]; 69.5% female; 36.4% minority), consisting of 84 episodic migraineurs, diagnosed in accordance with International Classification of Headache Disorders (2(nd) edition) criteria using a structured diagnostic interview, and 224 non-migraine controls completed a computerized dot probe task to assess attentional bias toward headache-related pictorial stimuli. The task consisted of 192 trials and utilized 2 emotional-neutral stimulus pairing conditions (headache-neutral and happy-neutral). No within-group differences for reaction time latencies to headache vs happy conditions were found among those with episodic migraine or among the non-migraine controls. Migraine status was unrelated to attentional bias indices for both headache (F [1,306] = 0.56, P = .45) and happy facial stimuli (F [1,306] = 0.37, P = .54), indicating a lack of between-group differences. Lack of within- and between-group differences was confirmed with repeated measures analysis of variance.", "output": "{\"label\": \"no\", \"rationale\": \"In light of the large sample size and prior pilot testing of presented images, results suggest that episodic migraineurs do not differentially attend to headache-related facial stimuli. Given modest evidence of attentional biases among chronic headache samples, these findings suggest potential differences in attentional processing between chronic and episodic headache subforms.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 23252468, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The cytokine receptor which regulates chemotaxis and formation of lymph nodes is involved in production of myeloperoxidase in the left atrium.\n\nCANDIDATE_PASSAGE:\nSestrin2 inhibits uncoupling protein 1 expression through suppressing reactive oxygen species. Uncoupling protein 1 (Ucp1), which is localized in the mitochondrial inner membrane of mammalian brown adipose tissue (BAT), generates heat by uncoupling oxidative phosphorylation. Upon cold exposure or nutritional abundance, sympathetic neurons stimulate BAT to express Ucp1 to induce energy dissipation and thermogenesis. Accordingly, increased Ucp1 expression reduces obesity in mice and is correlated with leanness in humans. Despite this significance, there is currently a limited understanding of how Ucp1 expression is physiologically regulated at the molecular level. Here, we describe the involvement of Sestrin2 and reactive oxygen species (ROS) in regulation of Ucp1 expression. Transgenic overexpression of Sestrin2 in adipose tissues inhibited both basal and cold-induced Ucp1 expression in interscapular BAT, culminating in decreased thermogenesis and increased fat accumulation. Endogenous Sestrin2 is also important for suppressing Ucp1 expression because BAT from Sestrin2(-/-) mice exhibited a highly elevated level of Ucp1 expression. The redox-inactive mutant of Sestrin2 was incapable of regulating Ucp1 expression, suggesting that Sestrin2 inhibits Ucp1 expression primarily through reducing ROS accumulation. Consistently, ROS-suppressing antioxidant chemicals, such as butylated hydroxyanisole and N-acetylcysteine, inhibited cold- or cAMP-induced Ucp1 expression as well. p38 MAPK, a signaling mediator required for cAMP-induced Ucp1 expression, was inhibited by either Sestrin2 overexpression or antioxidant treatments. Taken together, these results suggest that Sestrin2 and antioxidants inhibit Ucp1 expression through suppressing ROS-mediated p38 MAPK activation, [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1208", "doc_id": "36838958", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Statins increase blood cholesterol.\n\nCANDIDATE_PASSAGE:\nA Century of Cholesterol and Coronaries: From Plaques to Genes to Statins One-fourth of all deaths in industrialized countries result from coronary heart disease. A century of research has revealed the essential causative agent: cholesterol-carrying low-density lipoprotein (LDL). LDL is controlled by specific receptors (LDLRs) in liver that remove it from blood. Mutations that eliminate LDLRs raise LDL and cause heart attacks in childhood, whereas mutations that raise LDLRs reduce LDL and diminish heart attacks. If we are to eliminate coronary disease, lowering LDL should be the primary goal. Effective means to achieve this goal are currently available. The key questions are: who to treat, when to treat, and how long to treat.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1100", "doc_id": "7662206", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: RANK-RANKL pathway signalling is linked to development of Aire-expressing medullary thymic epithelial cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Vascular endothelial cadherin controls VEGFR-2 internalization and signaling from intracellular compartments\nABSTRACT: Receptor endocytosis is a fundamental step in controlling the magnitude, duration, and nature of cell signaling events. Confluent endothelial cells are contact inhibited in their growth and respond poorly to the proliferative signals of vascular endothelial growth factor (VEGF). In a previous study, we found that the association of vascular endothelial cadherin (VEC) with VEGF receptor (VEGFR) type 2 contributes to density-dependent growth inhibition (Lampugnani, G.M., A. Zanetti, M. Corada, T. Takahashi, G. Balconi, F. Breviario, F. Orsenigo, A. Cattelino, R. Kemler, T.O. Daniel, and E. Dejana. 2003. J. Cell Biol. 161:793–804). In the present study, we describe the mechanism through which VEC reduces VEGFR-2 signaling. We found that VEGF induces the clathrin-dependent internalization of VEGFR-2. When VEC is absent or not engaged at junctions, VEGFR-2 is internalized more rapidly and remains in endosomal compartments for a longer time. Internalization does not terminate its signaling; instead, the internalized receptor is phosphorylated, codistributes with active phospholipase C–γ, and activates p44/42 mitogen-activated protein kinase phosphorylation and cell proliferation. Inhibition of VEGFR-2 internalization reestablishes the contact inhibition of cell growth, whereas silencing the junction-associated density-enhanced phosphatase-1/CD148 phosphatase restores VEGFR-2 internalization and signaling. Thus, VEC limits cell proliferation by retaining VEGFR-2 at the membrane and preventing its internalization into signaling compartments.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1005, "doc_id": "2593298", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: ERAP1 SNPs are epistatic to HLA alleles for ankylosing spondylitis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Estimating prion concentration in fluids and tissues by quantitative PMCA\nABSTRACT: Prions, the proteinaceous infectious agent responsible for prion diseases, can be detected with high sensitivity by protein misfolding cyclic amplification (PMCA) technology. Here we describe a quantitative PMCA procedure to calculate the concentration of very low levels of prions in biological samples. Using this procedure, we determined the quantities of misfolded prion protein (PrPSc) in brain, spleen, blood and urine of scrapie-affected hamsters.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 366, "doc_id": "1583041", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Alirocumab treatment reduces apo(a) fractional clearance rate.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effects of PCSK9 Inhibition With Alirocumab on Lipoprotein Metabolism in Healthy Humans\nABSTRACT: BACKGROUND Alirocumab, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), lowers plasma low-density lipoprotein (LDL) cholesterol and apolipoprotein B100 (apoB). Although studies in mice and cells have identified increased hepatic LDL receptors as the basis for LDL lowering by PCSK9 inhibitors, there have been no human studies characterizing the effects of PCSK9 inhibitors on lipoprotein metabolism. In particular, it is not known whether inhibition of PCSK9 has any effects on very low-density lipoprotein or intermediate-density lipoprotein (IDL) metabolism. Inhibition of PCSK9 also results in reductions of plasma lipoprotein (a) levels. The regulation of plasma Lp(a) levels, including the role of LDL receptors in the clearance of Lp(a), is poorly defined, and no mechanistic studies of the Lp(a) lowering by alirocumab in humans have been published to date. METHODS Eighteen (10 F, 8 mol/L) participants completed a placebo-controlled, 2-period study. They received 2 doses of placebo, 2 weeks apart, followed by 5 doses of 150 mg of alirocumab, 2 weeks apart. At the end of each period, fractional clearance rates (FCRs) and production rates (PRs) of apoB and apo(a) were determined. In 10 participants, postprandial triglycerides and apoB48 levels were measured. RESULTS Alirocumab reduced ultracentrifugally isolated LDL-C by 55.1%, LDL-apoB by 56.3%, and plasma Lp(a) by 18.7%. The fall in LDL-apoB was caused by an 80.4% increase in LDL-apoB FCR and a 23.9% reduction in LDL-apoB PR. The latter was due to a 46.1% increase in IDL-apoB FCR coupled with a 27.2% decrease in conversion of IDL to LDL. The FCR of apo(a) tended to increase (24.6%) without any change in apo(a) PR. Alirocumab had no effects on FCRs or PRs of very low-density lipopro [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The FCR of apo(a) tended to increase (24.6%) without any change in apo(a) PR.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 98, "doc_id": "6540064", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Tetraspanin-3 is a causative factor in the development of acute myelogenous leukemia\n\nCANDIDATE_ABSTRACT:\nTITLE: Tetraspanin 3 Is Required for the Development and Propagation of Acute Myelogenous Leukemia.\nABSTRACT: Acute Myelogenous Leukemia (AML) is an aggressive cancer that strikes both adults and children and is frequently resistant to therapy. Thus, identifying signals needed for AML propagation is a critical step toward developing new approaches for treating this disease. Here, we show that Tetraspanin 3 is a target of the RNA binding protein Musashi 2, which plays a key role in AML. We generated Tspan3 knockout mice that were born without overt defects. However, Tspan3 deletion impaired leukemia stem cell self-renewal and disease propagation and markedly improved survival in mouse models of AML. Additionally, Tspan3 inhibition blocked growth of AML patient samples, suggesting that Tspan3 is also important in human disease. As part of the mechanism, we show that Tspan3 deficiency disabled responses to CXCL12/SDF-1 and led to defects in AML localization within the niche. These identify Tspan3 as an important regulator of aggressive leukemias and highlight a role for Tspan3 in oncogenesis.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"However, Tspan3 deletion impaired leukemia stem cell self-renewal and disease propagation and markedly improved survival in mouse models of AML.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1150, "doc_id": "11369420", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: A T helper 2 cell (Th2) environment impedes disease development in patients with systemic lupus erythematosus (SLE).\n\nCANDIDATE_ABSTRACT:\nTITLE: MicroRNA-21 is Induced by Rapamycin in a Model of Tuberous Sclerosis (TSC) and Lymphangioleiomyomatosis (LAM)\nABSTRACT: Lymphangioleiomyomatosis (LAM), a multisystem disease of women, is manifest by the proliferation of smooth muscle-like cells in the lung resulting in cystic lung destruction. Women with LAM can also develop renal angiomyolipomas. LAM is caused by mutations in the tuberous sclerosis complex genes (TSC1 or TSC2), resulting in hyperactive mammalian Target of Rapamycin (mTOR) signaling. The mTOR inhibitor, Rapamycin, stabilizes lung function in LAM and decreases the volume of renal angiomyolipomas, but lung function declines and angiomyolipomas regrow when treatment is discontinued, suggesting that factors induced by mTORC1 inhibition may promote the survival of TSC2-deficient cells. Whether microRNA (miRNA, miR) signaling is involved in the response of LAM to mTORC1 inhibition is unknown. We identified Rapamycin-dependent miRNA in LAM patient angiomyolipoma-derived cells using two separate screens. First, we assayed 132 miRNA of known significance to tumor biology. Using a cut-off of >1.5-fold change, 48 microRNA were Rapamycin-induced, while 4 miRs were downregulated. In a second screen encompassing 946 miRNA, 18 miRs were upregulated by Rapamycin, while eight were downregulated. Dysregulation of miRs 29b, 21, 24, 221, 106a and 199a were common to both platforms and were classified as candidate \"RapamiRs. \" Validation by qRT-PCR confirmed that these microRNA were increased. miR-21, a pro-survival miR, was the most significantly increased by mTOR-inhibition (p<0.01). The regulation of miR-21 by Rapamycin is cell type independent. mTOR inhibition promotes the processing of the miR-21 transcript (pri-miR-21) to a premature form (pre-miR-21). In conclusion, our findings demonstrate that Rapamycin upregulates multiple miRs, including pro-survival miRs, in TSC2-defi [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 28, "doc_id": "2266471", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does somatoform dissociation discriminate among diagnostic categories over and above general psychopathology?\n\nABSTRACT:\nThe primary aim of this study was to investigate the hypothesis that somatoform dissociation would differentiate among specific diagnostic categories after controlling for general psychopathology. The Somatoform Dissociation Questionnaire (SDQ-20), the Dissociative Experiences Scale, and the Symptom Checklist-90-R were completed by patients with DSM-IV diagnoses of dissociative disorders (n = 44), somatoform disorders (n = 47), eating disorders (n = 50), bipolar mood disorder (n = 23), and a group of consecutive psychiatric outpatients with other psychiatric disorders (n = 45), mainly including anxiety disorders, depression, and adjustment disorder. The SDQ-20 significantly differentiated among diagnostic groups in the hypothesised order of increasing somatoform dissociation, both before and after statistically controlling for general psychopathology. Somatoform dissociation was extreme in dissociative identity disorder, high in dissociative disorder, not otherwise specified, and increased in somatoform disorders, as well as in a subgroup of patients with eating disorders. In contrast with somatoform dissociation, psychological dissociation did not discriminate between bipolar mood disorder and somatoform disorders.", "output": "{\"label\": \"yes\", \"rationale\": \"Somatoform dissociation is a unique construct that discriminates among diagnostic categories. It is highly characteristic of dissociative disorder patients, a core feature in many patients with somatoform disorders, and an important symptom cluster in a subgroup of patients with eating disorders.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 10483845, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Energy balance requires hypothalamic glutamate neurotransmission.\n\nCANDIDATE_PASSAGE:\nLateral Hypothalamic Area Glutamatergic Neurons and Their Projections to the Lateral Habenula Regulate Feeding and Reward. UNLABELLED The overconsumption of calorically dense, highly palatable foods is thought to be a major contributor to the worldwide obesity epidemic; however, the precise neural circuits that directly regulate hedonic feeding remain elusive. Here, we show that lateral hypothalamic area (LHA) glutamatergic neurons, and their projections to the lateral habenula (LHb), negatively regulate the consumption of palatable food. Genetic ablation of LHA glutamatergic neurons increased daily caloric intake and produced weight gain in mice that had access to a high-fat diet, while not altering general locomotor activity. Anterior LHA glutamatergic neurons send a functional glutamatergic projection to the LHb, a brain region involved in processing aversive stimuli and negative reward prediction outcomes. Pathway-specific, optogenetic stimulation of glutamatergic LHA-LHb circuit resulted in detectable glutamate-mediated EPSCs as well as GABA-mediated IPSCs, although the net effect of neurotransmitter release was to increase the firing of most LHb neurons. In vivo optogenetic inhibition of LHA-LHb glutamatergic fibers produced a real-time place preference, whereas optogenetic stimulation of LHA-LHb glutamatergic fibers had the opposite effect. Furthermore, optogenetic inhibition of LHA-LHb glutamatergic fibers acutely increased the consumption of a palatable liquid caloric reward. Collectively, these results demonstrate that LHA glutamatergic neurons are well situated to bidirectionally regulate feeding and potentially other behavioral states via their functional circuit connectivity with the LHb and potentially other brain regions. SIGNIFICANCE STATEMEN [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "378", "doc_id": "23869951", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Lymphadenopathy is observed in knockin mouse lacking the SHP-2 MAPK pathway.\n\nCANDIDATE_PASSAGE:\nAcute exercise activates nuclear factor (NF)-kappaB signaling pathway in rat skeletal muscle. Two studies were performed to investigate the effects of an acute bout of physical exercise on the nuclear protein kappaB (NF-kappaB) signaling pathway in rat skeletal muscle. In Study 1, a group of rats (n=6) was run on the treadmill at 25 m/min, 5% grade, for 1 h or until exhaustion (Ex), and compared with a second group (n=6) injected with two doses of pyrrolidine dithiocarbamate (PDTC, 100 mg/kg, i.p.) 24 and 1 h prior to the acute exercise bout. Three additional groups of rats (n=6) were injected with either 8 mg/kg (i.p.) of lipopolysaccharide (LPS), 1 mmol/kg (i.p.) t-butylhydroperoxide (tBHP), or saline (C) and killed at resting condition. Ex rats showed higher levels of NF-kappaB binding and P50 protein content in muscle nuclear extracts compared with C rats. Cytosolic IkappaBalpha and IkappaB kinase (IKK) contents were decreased, whereas phospho-IkappaBalpha and phospho-IKK contents were increased, comparing Ex vs. C. The exercise-induced activation of NF-kappaB signaling cascade was partially abolished by PDTC treatment. LPS, but not tBHP, treatment mimicked and exaggerated the effects observed in Ex rats. In Study 2, the time course of exercise-induced NF-kappaB activation was examined. Highest levels of NF-kappaB binding were observed at 2 h postexercise. Decreased cytosolic IkappaBalpha and increased phosphor-IkappaBalpha content were found 0-1 h postexercise whereas P65 reached peak levels at 2-4 h. These data suggest that the NF-kappaB signaling pathway can be activated in a redox-sensitive manner during muscular contraction, presumably due to increased oxidant production. The cascade of intracellular events may be the overture to elevated gene expre [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "729", "doc_id": "23737024", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Do mast cells play a partial role in allergen-induced subepithelial fibrosis in a murine model of allergic asthma?\n\nABSTRACT:\nRole of mast cells in the development of allergen-induced airway remodelling has not been fully investigated in vivo. To clarify the possible role of mast cells in the development of allergen-induced airway remodelling, we compared their responses of genetically mast cell-deficient mice, WBB6F1-W/Wv (c-kit mutant) and Sl/Sld (c-kit ligand mutant) mice with those of congenic normal mice in a murine model of allergic asthma. Mice were sensitized to ovalbumin (OA) with alum, and exposed daily for 3 weeks to aerosolized OA. Twenty-four hours after the last inhalation, bronchial responsiveness to acetylcholine (Ach) was measured, and bronchoalveolar lavage (BAL), and biochemical and histological examinations were performed. In both sensitized mast cell-deficient mice, the degree of bronchial hyper-responsiveness to Ach, the number of inflammatory cells and the level of transforming growth factor-beta1 in BAL fluid, IgE response and goblet cell hyperplasia in the epithelium after repeated allergen provocation were not significantly different from those of congenic mice. In contrast, subepithelial fibrosis, evaluated in the fibrotic area around the airways, observed in congenic mice after repeated allergen challenge was partially attenuated in both mast cell-deficient mice. In addition, the amount of hydroxyproline in the lung of mast cell-deficient mice was significantly lower than that of congenic mice. Furthermore, the decreased fibrotic area and amount of hydroxyproline in W/Wv mice was completely recovered by reconstitution of tissue mast cells with bone marrow-derived mast cells of congenic mice.", "output": "{\"label\": \"yes\", \"rationale\": \"These findings suggest that mast cells play a partial role in the development of allergen-induced subepithelial fibrosis, although airway inflammation, epithelial remodelling and BHR caused by repeated allergen challenge are independent of mast cells, at least in this model.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 12752602, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: There is no association between HNF4A mutations and diabetes risks.\n\nCANDIDATE_PASSAGE:\nTranscripts of the MHM region on the chicken Z chromosome accumulate as non-coding RNA in the nucleus of female cells adjacent to the DMRT1 locus The male hypermethylated (MHM) region, located near the middle of the short arm of the Z chromosome of chickens, consists of approximately 210 tandem repeats of a BamHI 2.2-kb sequence unit. Cytosines of the CpG dinucleotides of this region are extensively methylated on the two Z chromosomes in the male but much less methylated on the single Z chromosome in the female. The state of methylation of the MHM region is established after fertilization by about the 1-day embryonic stage. The MHM region is transcribed only in the female from the particular strand into heterogeneous, high molecular-mass, non-coding RNA, which is accumulated at the site of transcription, adjacent to the DMRT1 locus, in the nucleus. The transcriptional silence of the MHM region in the male is most likely caused by the CpG methylation, since treatment of the male embryonic fibroblasts with 5-azacytidine results in hypo-methylation and active transcription of this region. In ZZW triploid chickens, MHM regions are hypomethylated and transcribed on the two Z chromosomes, whereas MHM regions are hypermethylated and transcriptionally inactive on the three Z chromosomes in ZZZ triploid chickens, suggesting a possible role of the W chromosome on the state of the MHM region.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1291", "doc_id": "4085204", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Monoclonal antibody targeting of N-cadherin inhibits metastasis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Monoclonal antibody targeting of N-cadherin inhibits prostate cancer growth, metastasis and castration resistance\nABSTRACT: The transition from androgen-dependent to castration-resistant prostate cancer (CRPC) is a lethal event of uncertain molecular etiology. Comparing gene expression in isogenic androgen-dependent and CRPC xenografts, we found a reproducible increase in N-cadherin expression, which was also elevated in primary and metastatic tumors of individuals with CRPC. Ectopic expression of N-cadherin in nonmetastatic, androgen-dependent prostate cancer models caused castration resistance, invasion and metastasis. Monoclonal antibodies against the ectodomain of N-cadherin reduced proliferation, adhesion and invasion of prostate cancer cells in vitro. In vivo, these antibodies slowed the growth of multiple established CRPC xenografts, blocked local invasion and metastasis and, at higher doses, led to complete regression. N-cadherin–specific antibodies markedly delayed the time to emergence of castration resistance, markedly affected tumor histology and angiogenesis, and reduced both AKT serine-threonine kinase activity and serum interleukin-8 (IL-8) secretion. These data indicate that N-cadherin is a major cause of both prostate cancer metastasis and castration resistance. Therapeutic targeting of this factor with monoclonal antibodies may have considerable clinical benefit.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In vivo, these antibodies slowed the growth of multiple established CRPC xenografts, blocked local invasion and metastasis and, at higher doses, led to complete regression.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 805, "doc_id": "22180793", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does elevated DDX21 regulate c-Jun activity and rRNA processing in human breast cancers?\n\nABSTRACT:\nThe DDX21 RNA helicase has been shown to be a nucleolar and nuclear protein involved in ribosome RNA processing and AP-1 transcription. DDX21 is highly expressed in colon cancer, lymphomas, and some breast cancers, but little is known about how DDX21 might promote tumorigenesis. Immunohistochemistry was performed on a breast cancer tissue array of 187 patients. In order to study the subcellular localization of DDX21 in both tumor tissue and tumor cell lines, indirect immunofluorescence was applied. The effect of DDX21 knockdown was measured by cellular apoptosis, rRNA processing assays, soft agar growth and mouse xenograft imaging. AP-1 transcriptional activity was analyzed with a luciferase reporter and bioluminescence imaging, as well as qRT-PCR analysis of downstream target, cyclin D1, to determine the mechanism of action for DDX21 in breast tumorigenesis. Herein, we show that DDX21 is highly expressed in breast cancer tissues and established cell lines. A significant number of mammary tumor tissues and established breast cancer cell lines exhibit nuclear but not nucleolar localization of DDX21. The protein expression level of DDX21 correlates with cell proliferation rate and is markedly induced by EGF signaling. Mechanistically, DDX21 is required for the phosphorylation of c-Jun on Ser73 and DDX21 deficiency markedly reduces the transcriptional activity of AP-1. Additionally, DDX21 promotes rRNA processing in multiple breast cancer cell lines. Tumor cells expressing high levels of endogenous DDX21 undergo apoptosis after acute DDX21 knockdown, resulting in significant reduction of tumorigenicity in vitro and in vivo.", "output": "{\"label\": \"yes\", \"rationale\": \"Our findings indicate that DDX21 expression in breast cancer cells can promote AP-1 activity and rRNA processing, and thus, promote tumorigenesis by two independent mechanisms. DDX21 could serve as a marker for a subset of breast cancer patients with higher proliferation potential and may be used as a therapeutic target for a subset of breast cancer patients.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25260534, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Students who perform poorly in the early years of medical school are less likely to commit professional misconduct later in their careers.\n\nCANDIDATE_ABSTRACT:\nTITLE: Risk factors at medical school for subsequent professional misconduct: multicentre retrospective case-control study\nABSTRACT: OBJECTIVE To determine whether there are risk factors in a doctor's time at medical school that are associated with subsequent professional misconduct. DESIGN Matched case-control study. Setting Records from medical schools and the General Medical Council (GMC). PARTICIPANTS 59 doctors who had graduated from any one of eight medical schools in the United Kingdom in 1958-97 and had a proved finding of serious professional misconduct in GMC proceedings in 1999-2004 (cases); 236 controls (four for each case) were selected by systematic sampling from matching graduation cohorts. Case-control status was revealed by the GMC after completion of data entry. MAIN OUTCOME MEASURE Odds ratios for being a \"case,\" with multivariable conditional logistic regression of potential risk factors including pre-admission characteristics and progress during the course. These data were obtained from anonymised copies of the students' progress files held by their original medical schools. RESULTS Univariate conditional logistic regression analysis found that cases were more likely to be men, to be of lower estimated social class, and to have had academic difficulties during their medical course, especially in the early years. Multivariable analysis showed that male sex (odds ratio 9.80, 95% confidence interval 2.43 to 39.44, P=0.001), lower social class (4.28, 1.52 to 12.09, P=0.006), and failure of early or preclinical examinations (5.47, 2.17 to 13.79, P<0.001) were independently associated with being a case. CONCLUSIONS This small study suggests that male sex, a lower socioeconomic background, and early academic difficulties at medical school could be risk factors for subsequent professional misconduct. The findings are preliminary and should be interpreted with caution. Most do [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"RESULTS Univariate conditional logistic regression analysis found that cases were more likely to be men, to be of lower estimated social class, and to have had academic difficulties during their medical course, especially in the early years.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1106, "doc_id": "6710713", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Sympathetic nerve activity is elevated throughout normal pregnancy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Sympathetic neural mechanisms in normal and hypertensive pregnancy in humans.\nABSTRACT: BACKGROUND Direct recordings from peripheral sympathetic nerves have shown an increased sympathetic drive in pregnancy-induced hypertension (PIH) and preeclampsia (PE). It is unknown whether sympathetic drive is altered in normal pregnancy, when arterial blood pressure can be normal or relatively low. The aim of this study was to measure and compare peripheral sympathetic discharge, its vasoconstrictor effect and its baroreceptor control, during pregnancy and postpartum in women with normal pregnancy (NP) and PIH and in normotensive nonpregnant (NN) women. METHODS AND RESULTS Twenty-one women with NP, 18 women with PIH, and 21 NN women had muscle sympathetic nerve activity assessed from multiunit discharges (MSNA) and from single units with defined vasoconstrictor properties (s-MSNA). The s-MSNA in NP (38+/-6.6 impulses/100 beats) was greater (P<0.05) than in NN women (19+/-1.8 impulses/100 beats) despite similar age and body weight but less than in PIH women (P<0.001) (146+/-23.5 impulses/100 beats). MSNA followed a similar trend. Cardiac baroreceptor reflex sensitivity (BRS) was impaired in NP and PIH women relative to NN. After delivery, sympathetic activity decreased to values similar to those obtained in NN, and there was an increase in BRS. In women with NP, the decrease in sympathetic output occurred despite an insignificant change in blood pressure. CONCLUSIONS Central sympathetic output was increased in women with normal pregnancy and was even greater in the hypertensive pregnant group. The findings suggest that the moderate sympathetic hyperactivity during the latter months of normal pregnancy may help to return the arterial pressure to nonpregnant levels, although when the increase in activity is excessive, hypertension may ensue.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The s-MSNA in NP (38+/-6.6 impulses/100 beats) was greater (P<0.05) than in NN women (19+/-1.8 impulses/100 beats) despite similar age and body weight but less than in PIH women (P<0.001) (146+/-23.5 impulses/100 beats).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1119, "doc_id": "5323845", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The arm density of TatAd complexes is due to structural rearrangements within Class1 TatAd complexes such as the 'charge zipper mechanism'.\n\nCANDIDATE_PASSAGE:\nXRCC4's interaction with XLF is required for coding (but not signal) end joining XRCC4 and XLF are structurally related proteins important for DNA Ligase IV function. XRCC4 forms a tight complex with DNA Ligase IV while XLF interacts directly with XRCC4. Both XRCC4 and XLF form homodimers that can polymerize as heterotypic filaments independently of DNA Ligase IV. Emerging structural and in vitro biochemical data suggest that XRCC4 and XLF together generate a filamentous structure that promotes bridging between DNA molecules. Here, we show that ablating XRCC4's affinity for XLF results in DNA repair deficits including a surprising deficit in VDJ coding, but not signal end joining. These data are consistent with a model whereby XRCC4/XLF complexes hold DNA ends together--stringently required for coding end joining, but dispensable for signal end joining. Finally, DNA-PK phosphorylation of XRCC4/XLF complexes disrupt DNA bridging in vitro, suggesting a regulatory role for DNA-PK's phosphorylation of XRCC4/XLF complexes.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1194", "doc_id": "17768946", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Bcp1 is a chaperone for Rpl23.\n\nCANDIDATE_PASSAGE:\nHistone/protein deacetylase inhibitors increase suppressive functions of human FOXP3+ Tregs. Histone/protein deacetylases (HDACs) decrease histone and protein acetylation, typically leading to suppression of gene transcription and modulation of various protein functions. We found significant differences in expression of HDAC before and after stimulation of human T regulatory (Treg) and T effector cells, suggesting the potential for future selective targeting of Tregs with HDAC inhibitors (HDACi). Use of various HDACi small molecules enhanced, by up to 4.5-fold (average 2-fold), the suppressive functions of both freshly isolated and expanded human Tregs, consistent with our previous murine data. HDACi use increased Treg expression of CTLA-4, a key negative regulator of immune response, and we found a direct and significant correlation between CTLA-4 expression and Treg suppression. Hence, HDACi compounds are promising pharmacologic tools to increase Treg suppressive functions, and this action may potentially be of use in patients with autoimmunity or post-transplantation.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "173", "doc_id": "22968257", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Increased vessel density along with a reduction in fibrosis improves the efficacy of chemotherapy treatments.\n\nCANDIDATE_ABSTRACT:\nTITLE: Hyaluronan impairs vascular function and drug delivery in a mouse model of pancreatic cancer\nABSTRACT: OBJECTIVE Pancreatic ductal adenocarcinoma (PDA) is characterised by stromal desmoplasia and vascular dysfunction, which critically impair drug delivery. This study examines the role of an abundant extracellular matrix component, the megadalton glycosaminoglycan hyaluronan (HA), as a novel therapeutic target in PDA. METHODS Using a genetically engineered mouse model of PDA, the authors enzymatically depleted HA by a clinically formulated PEGylated human recombinant PH20 hyaluronidase (PEGPH20) and examined tumour perfusion, vascular permeability and drug delivery. The preclinical utility of PEGPH20 in combination with gemcitabine was assessed by short-term and survival studies. RESULTS PEGPH20 rapidly and sustainably depleted HA, inducing the re-expansion of PDA blood vessels and increasing the intratumoral delivery of two chemotherapeutic agents, doxorubicin and gemcitabine. Moreover, PEGPH20 triggered fenestrations and interendothelial junctional gaps in PDA tumour endothelia and promoted a tumour-specific increase in macromolecular permeability. Finally, combination therapy with PEGPH20 and gemcitabine led to inhibition of PDA tumour growth and prolonged survival over gemcitabine monotherapy, suggesting immediate clinical utility. CONCLUSIONS The authors demonstrate that HA impedes the intratumoral vasculature in PDA and propose that its enzymatic depletion be explored as a means to improve drug delivery and response in patients with pancreatic cancer.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 620, "doc_id": "2565138", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cytochrome c is transferred from cytosol to the mitochondrial intermembrane space during apoptosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: At the gates of death.\nABSTRACT: Apoptosis that proceeds via the mitochondrial pathway involves mitochondrial outer membrane permeabilization (MOMP), responsible for the release of cytochrome c and other proteins of the mitochondrial intermembrane space. This essential step is controlled and mediated by proteins of the Bcl-2 family. The proapoptotic proteins Bax and Bak are required for MOMP, while the antiapoptotic Bcl-2 proteins, including Bcl-2, Bcl-xL, Mcl-1, and others, prevent MOMP. Different proapoptotic BH3-only proteins act to interfere with the function of the antiapoptotic Bcl-2 members and/or activate Bax and Bak. Here, we discuss an emerging view, proposed by Certo et al. in this issue of Cancer Cell, on how these interactions result in MOMP and apoptosis.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Apoptosis that proceeds via the mitochondrial pathway involves mitochondrial outer membrane permeabilization (MOMP), responsible for the release of cytochrome c and other proteins of the mitochondrial intermembrane space.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 299, "doc_id": "39381118", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: TNFAIP3 is a glioblastoma tumor suppressor.\n\nCANDIDATE_ABSTRACT:\nTITLE: Targeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth\nABSTRACT: Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs). GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets. We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels. To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA). Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis. The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays. The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts. In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival. Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation. Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may funct [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may function as a tumor enhancer in glioma through promotion of GSC survival.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1135, "doc_id": "33370", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Lmna knock-in models are appropriate for testing therapeutic approaches against Hutchinson-Gilford progeria syndrome (HGPS).\n\nCANDIDATE_PASSAGE:\nN- and E-cadherins in Xenopus are specifically required in the neural and non-neural ectoderm, respectively, for F-actin assembly and morphogenetic movements. Transmembrane cadherins are calcium-dependent intercellular adhesion molecules. Recently, they have also been shown to be sites of actin assembly during adhesive contact formation. However, the roles of actin assembly on transmembrane cadherins during development are not fully understood. We show here, using the developing ectoderm of the Xenopus embryo as a model, that F-actin assembly is a primary function of both N-cadherin in the neural ectoderm and E-cadherin in the non-neural (epidermal) ectoderm, and that each cadherin is essential for the characteristic morphogenetic movements of these two tissues. However, depletion of N-cadherin and E-cadherin did not cause dissociation in these tissues at the neurula stage, probably owing to the expression of C-cadherin in each tissue. Depletion of each of these cadherins is not rescued by the other, nor by the expression of C-cadherin, which is expressed in both tissues. One possible reason for this is that each cadherin is expressed in a different domain of the cell membrane. These data indicate the combinatorial nature of cadherin function, the fact that N- and E-cadherin play primary roles in F-actin assembly in addition to roles in cell adhesion, and that this function is specific to individual cadherins. They also show how cell adhesion and motility can be combined in morphogenetic tissue movements that generate the form and shape of the embryonic organs.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "698", "doc_id": "19485649", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Including pharmacists in rounding teams reduces the incidence of adverse drug events (ADEs).\n\nCANDIDATE_ABSTRACT:\nTITLE: Pharmacist participation on physician rounds and adverse drug events in the intensive care unit.\nABSTRACT: CONTEXT Pharmacist review of medication orders in the intensive care unit (ICU) has been shown to prevent errors, and pharmacist consultation has reduced drug costs. However, whether pharmacist participation in the ICU at the time of drug prescribing reduces adverse events has not been studied. OBJECTIVE To measure the effect of pharmacist participation on medical rounds in the ICU on the rate of preventable adverse drug events (ADEs) caused by ordering errors. DESIGN Before-after comparison between phase 1 (baseline) and phase 2 (after intervention implemented) and phase 2 comparison with a control unit that did not receive the intervention. SETTING A medical ICU (study unit) and a coronary care unit (control unit) in a large urban teaching hospital. PATIENTS Seventy-five patients randomly selected from each of 3 groups: all admissions to the study unit from February 1, 1993, through July 31, 1993 (baseline) and all admissions to the study unit (postintervention) and control unit from October 1, 1994, through July 7, 1995. In addition, 50 patients were selected at random from the control unit during the baseline period. INTERVENTION A senior pharmacist made rounds with the ICU team and remained in the ICU for consultation in the morning, and was available on call throughout the day. MAIN OUTCOME MEASURES Preventable ADEs due to ordering (prescribing) errors and the number, type, and acceptance of interventions made by the pharmacist. Preventable ADEs were identified by review of medical records of the randomly selected patients during both preintervention and postintervention phases. Pharmacists recorded all recommendations, which were then analyzed by type and acceptance. RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 pat [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 patient-days (95% confidence interval [CI], 7-14) before the intervention to 3.5 (95% CI, 1-5; P<.001) after the intervention.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 601, "doc_id": "12258338", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Radioiodine treatment of non-toxic multinodular goitre increases thyroid volume.\n\nCANDIDATE_ABSTRACT:\nTITLE: Radioiodine treatment of multinodular non-toxic goitre.\nABSTRACT: OBJECTIVE To investigate the long term effect of radioactive iodine on thyroid function and size in patients with non-toxic multinodular goitre. DESIGN Consecutive patients with multinodular non-toxic goitre selected for radioactive iodine treatment and followed for a minimum of 12 months (median 48 months) after an intended dose of 3.7 MBq/g thyroid tissue corrected to a 100% uptake of iodine-131 in 24 hours. PATIENTS 69 patients with a growing multinodular non-toxic goitre causing local compression symptoms or cosmetic inconveniences. The treatment was chosen because of a high operative risk, previous thyroidectomy, or refusal to be operated on. MAIN OUTCOME MEASUREMENTS Standard thyroid function variables and ultrasonically determined thyroid volume before treatment as well as 1, 2, 3, 6, and 12 months after treatment and then once a year. RESULTS 56 patients were treated with a single dose of 131I, 12 with two doses, and one with four doses. In 45 patients treated with one dose and remaining euthyroid the median thyroid volume was reduced from 73 (interquartile range 50-106) ml to 29 (23-48) ml at 24 months in the 39 patients in whom this was measured during follow up. The median reduction was 40 (22-48) ml (60% reduction, p < 0.0001), half of which occurred within three months. Patients treated with two doses as well as those developing hypothyroidism and hyperthyroidism had a significant reduction in thyroid volume. Eleven patients developed hypothyroidism (cumulative five year risk 22%, 95% confidence interval 4.8% to 38.4%). Side effects were few: three cases of hyperthyroidism and two cases of radiation thyroiditis. Only one patient was dissatisfied with the result; she was referred for operation six months after treatment. CONCLUSIONS A substantial [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS A substantial reduction in thyroid volume accompanied by a low incidence of hypothyroidism and few side effects makes the use of radioactive iodine an attractive alternative to surgery in selected cases of non-toxic multinodular goitre.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1011, "doc_id": "9745001", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Activator-inhibitor pairs are provided ventrally by Xrl-sizzled.\n\nCANDIDATE_PASSAGE:\nSurviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2016 Objective: To provide an update to “Surviving Sepsis Campaign Guidelines for Management of Sepsis and Septic Shock: 2012. ” Design: A consensus committee of 55 international experts representing 25 international organizations was convened. Nominal groups were assembled at key international meetings (for those committee members attending the conference). A formal conflict-of-interest (COI) policy was developed at the onset of the process and enforced throughout. A stand-alone meeting was held for all panel members in December 2015. Teleconferences and electronic-based discussion among subgroups and among the entire committee served as an integral part of the development. Methods: The panel consisted of five sections: hemodynamics, infection, adjunctive therapies, metabolic, and ventilation. Population, intervention, comparison, and outcomes (PICO) questions were reviewed and updated as needed, and evidence profiles were generated. Each subgroup generated a list of questions, searched for best available evidence, and then followed the principles of the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system to assess the quality of evidence from high to very low, and to formulate recommendations as strong or weak, or best practice statement when applicable. Results: The Surviving Sepsis Guideline panel provided 93 statements on early management and resuscitation of patients with sepsis or septic shock. Overall, 32 were strong recommendations, 39 were weak recommendations, and 18 were best-practice statements. No recommendation was provided for four questions. Conclusions: Substantial agreement exists among a large cohort of international [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "73", "doc_id": "52827184", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Activated Cdk5 phosphorylates the ATM protein in response to DNA damage.\n\nCANDIDATE_ABSTRACT:\nTITLE: Phosphorylation of ATM by Cdk5 mediates DNA damage signaling and regulates neuronal death\nABSTRACT: The phosphatidylinositol-3-kinase-like kinase ATM (ataxia-telangiectasia mutated) has a central role in coordinating DNA damage responses, including cell-cycle checkpoint control, DNA repair and apoptosis. Mutations of ATM cause a spectrum of defects ranging from neurodegeneration to cancer predisposition. However, the mechanism by which DNA damage activates ATM is poorly understood. Here we show that Cdk5 (cyclin-dependent kinase 5), activated by DNA damage, directly phosphorylates ATM at Ser 794 in post-mitotic neurons. Phosphorylation at Ser 794 precedes, and is required for, ATM autophosphorylation at Ser 1981, and activates ATM kinase activity. The Cdk5-ATM signal regulates phosphorylation and function of the ATM targets p53 and H2AX. Interruption of the Cdk5-ATM pathway attenuates DNA-damage-induced neuronal cell cycle re-entry and expression of the p53 targets PUMA and Bax, protecting neurons from death. Thus, activation of Cdk5 by DNA damage serves as a critical signal to initiate the ATM response and regulate ATM-dependent cellular processes.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Thus, activation of Cdk5 by DNA damage serves as a critical signal to initiate the ATM response and regulate ATM-dependent cellular processes.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 67, "doc_id": "21295300", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Charcoal is an effective treatment for acute paraquat poisoning.\n\nCANDIDATE_PASSAGE:\nFailure of continuous venovenous hemofiltration to prevent death in paraquat poisoning. Paraquat poisoning is characterized by multiorgan failure and pulmonary fibrosis with respiratory failure. Multiorgan failure with circulatory collapse is a major cause of early death within 3 days of paraquat ingestion. Recent studies suggested that continuous venovenous hemofiltration (CVVH) had a role in the treatment of multiorgan failure by promoting hemodynamic stability. We therefore evaluated the effect of prophylactic CVVH in 80 patients with paraquat poisoning (August 1996 to February 1999). The amount ingested was 2.1 +/- 1.0 mouthfuls (as 20% concentrate). All patients were treated with hemoperfusion (HP; duration, 6.4 +/- 3.0 hours) within 24 hours of ingestion and then randomly assigned to the HP-alone or HP-CVVH group. Forty-four patients underwent HP only, and 36 patients underwent CVVH (duration, 57.4 +/- 31.3 hours; ultrafiltration volume, 40.2 +/- 4.8 L/d) after HP. Although time to death after ingestion was significantly longer in the HP-CVVH than HP group (5.0 +/- 5.0 versus 2.5 +/- 2.1 days; P < 0.05), there was no difference in mortality rates between the two groups (66.7% versus 63.6%; P = 0.82). In the HP group, early circulatory collapse was a major cause of death compared with the HP-CVVH group, in which late respiratory failure was a major cause of death. In conclusion, prophylactic CVVH after HP prevented early death caused by circulatory collapse and prolonged survival time. However, it could not prevent late death caused by respiratory failure and did not provide a survival benefit in acute paraquat poisoning.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "245", "doc_id": "24097933", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Natriuretic peptides increase susceptibility to diabetes.\n\nCANDIDATE_PASSAGE:\nImaging techniques for assaying lymphocyte activation in action Imaging techniques have greatly improved our understanding of lymphocyte activation. Technical advances in spatial and temporal resolution and new labelling tools have enabled researchers to directly observe the activation process. Consequently, research using imaging approaches to study lymphocyte activation has expanded, providing an unprecedented level of cellular and molecular detail in the field. As a result, certain models of lymphocyte activation have been verified, others have been revised and yet others have been replaced with new concepts. In this article, we review the current imaging techniques that are used to assess lymphocyte activation in different contexts, from whole animals to single molecules, and discuss the advantages and potential limitations of these methods.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "840", "doc_id": "19450341", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Do human Wharton 's jelly-derived mesenchymal stem cells express oocyte developmental genes during co-culture with placental cells?\n\nABSTRACT:\nThe present day challenge is how to obtain germ cells from stem cells to treat patients with cancer and infertility. Much more efforts have been made to develop a procedure for attaining germ cells in vitro. Recently, human umbilical cord-derived mesenchymal stem cells (HUMSCs) have been introduced with higher efficacy for differentiation. In this work, we tried to explore the efficacy of HUMSCs and some effective products of placental cells such as transforming growth factors. This study is aimed to optimize a co-culture condition for HUMSCs with placental cells to obtain primordial germ cells (PGCs) and reach into oocyte-like cells in vitro. In this experimental study, HUMSCs and placental cells were co-cultured for 14 days without any external inducer in vitro. Then HUMSCs were assessed for expression of PGC markers; Octamer-binding transcription factor 4(OCT4), Tyrosine-protein kinase Kit (CKIT), Stage specific embryonic antigen 4 (SSEA4), DEAD (Asp-Glu-Ala-Asp) box polypeptide 4(DDX4) and oocyte specific markers; Growth differentiation factor-9(GDF9), Zona pellucida glycoprotein 3(ZP3). The pertinent markers were assessed by immunocytochemistry and Q-PCR. Co-cultured HUMSCs with placental cells (including amniotic and chorionic cells) presented Oct4 and DDX4, primordial germ cells specific markers significantly, but increment in expression of oocyte-like cell specific markers, GDF9 and ZP3 did not reach to statistically significant threshold.", "output": "{\"label\": \"yes\", \"rationale\": \"Placental cell supplements Transforming growth factor (TGF α, β) and basic fibroblast growth factor (bFGF) in a co-culture model can provide proper environment for induction of HUMSCs into PGCs and expression of oocyte-like markers.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25810872, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In S. cerevisiae, the absence of RNA surveillance pathways reduces sensitivity to high iron conditions.\n\nCANDIDATE_ABSTRACT:\nTITLE: Multiple RNA surveillance pathways limit aberrant expression of iron uptake mRNAs and prevent iron toxicity in S. cerevisiae.\nABSTRACT: Tight regulation of the expression of mRNAs encoding iron uptake proteins is essential to control iron homeostasis and avoid intracellular iron toxicity. We show that many mRNAs encoding iron uptake or iron mobilization proteins are expressed in iron-replete conditions in the absence of the S. cerevisiae RNase III ortholog Rnt1p or of the nuclear exosome component Rrp6p. Extended forms of these mRNAs accumulate in the absence of Rnt1p or of the 5'-->3' exonucleases Xrn1p and Rat1p, showing that multiple degradative pathways contribute to the surveillance of aberrant forms of these transcripts. RNase III-deficient cells are hypersensitive to high iron concentrations, suggesting that Rnt1p-mediated RNA surveillance is required to prevent iron toxicity. These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"RNase III-deficient cells are hypersensitive to high iron concentrations, suggesting that Rnt1p-mediated RNA surveillance is required to prevent iron toxicity.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 566, "doc_id": "16120395", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Osteocytes have an essential role in G-CSF induced HSPC mobilization.\n\nCANDIDATE_ABSTRACT:\nTITLE: Matrix-embedded osteocytes regulate mobilization of hematopoietic stem/progenitor cells.\nABSTRACT: The bone marrow (BM) niche comprises multiple cell types that regulate hematopoietic stem/progenitor cell (HSPC) migration out of the niche and into the circulation. Here, we demonstrate that osteocytes, the major cellular component of mature bone, are regulators of HSPC egress. Granulocyte colony-stimulating factor (G-CSF), used clinically to mobilize HSPCs, induces changes in the morphology and gene expression of the osteocytic network that precedes changes in osteoblasts. This rapid response is likely under control of the sympathetic nervous system, since osteocytes express the β2-adrenergic receptor and surgical sympathectomy prevents it. Mice with targeted ablation of osteocytes or a disrupted osteocyte network have comparable numbers of HSPCs in the BM but fail to mobilize HSPCs in response to G-CSF. Taken together, these results indicate that the BM/bone niche interface is critically controlled from inside of the bone matrix and establish an important physiological role for skeletal tissues in hematopoietic function.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Granulocyte colony-stimulating factor (G-CSF), used clinically to mobilize HSPCs, induces changes in the morphology and gene expression of the osteocytic network that precedes changes in osteoblasts.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 893, "doc_id": "13509809", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Ultrasound guidance significantly reduces the number of needle insertion attempts necessary for a given procedure.\n\nCANDIDATE_ABSTRACT:\nTITLE: Detecting and targeting tumor relapse by its resistance to innate effectors at early recurrence\nABSTRACT: Tumor recurrence represents a major clinical challenge. Our data show that emergent recurrent tumors acquire a phenotype radically different from that of their originating primary tumors. This phenotype allows them to evade a host-derived innate immune response elicited by the progression from minimal residual disease (MRD) to actively growing recurrence. Screening for this innate response predicted accurately in which mice recurrence would occur. Premature induction of recurrence resensitized MRD to the primary therapy, suggesting a possible paradigm shift for clinical treatment of dormant disease in which the current expectant approach is replaced with active attempts to uncover MRD before evolution of the escape phenotype is complete. By combining screening with second-line treatments targeting innate insensitivity, up to 100% of mice that would have otherwise relapsed were cured. These data may open new avenues for early detection and appropriately timed, highly targeted treatment of tumor recurrence irrespective of tumor type or frontline treatment.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1340, "doc_id": "1921218", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Hyperfibrinogenemia decreases rates of femoropopliteal bypass thrombosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Influence of smoking and plasma factors on patency of femoropopliteal vein grafts.\nABSTRACT: OBJECTIVE To determine the effects of smoking, plasma lipids, lipoproteins, apolipoproteins, and fibrinogen on the patency of saphenous vein femoropopliteal bypass grafts at one year. DESIGN Prospective study of patients with saphenous vein femoropopliteal bypass grafts entered into a multicentre trial. SETTING Surgical wards, outpatient clinics, and home visits coordinated by two tertiary referral centres in London and Birmingham. PATIENTS 157 Patients (mean age 66.6 (SD 8.2) years), 113 with patent grafts and 44 with occluded grafts one year after bypass. MAIN OUTCOME MEASURE Cumulative percentage patency at one year. RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts. Serum cholesterol concentrations were significantly higher in patients with grafts that remained patent one year after bypass (p less than 0.005). Analysis of the smoking markers indicated that a quarter of patients (40) were untruthful in their claims to have stopped smoking. Based on smoking markers, patency of grafts in smokers was significantly lower at one year by life table analysis than in non-smokers (63% v 84%, p less than 0.02). Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002). Surprisingly, increased plasma low density lipoprotein cholesterol concentration was significantly associated with improved patency at one year (85%) at values above the median compared w [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 532, "doc_id": "12991445", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In S. cerevisiae, the absence of RNA surveillance pathways reduces sensitivity to high iron conditions.\n\nCANDIDATE_ABSTRACT:\nTITLE: Multiple RNA surveillance pathways limit aberrant expression of iron uptake mRNAs and prevent iron toxicity in S. cerevisiae.\nABSTRACT: Tight regulation of the expression of mRNAs encoding iron uptake proteins is essential to control iron homeostasis and avoid intracellular iron toxicity. We show that many mRNAs encoding iron uptake or iron mobilization proteins are expressed in iron-replete conditions in the absence of the S. cerevisiae RNase III ortholog Rnt1p or of the nuclear exosome component Rrp6p. Extended forms of these mRNAs accumulate in the absence of Rnt1p or of the 5'-->3' exonucleases Xrn1p and Rat1p, showing that multiple degradative pathways contribute to the surveillance of aberrant forms of these transcripts. RNase III-deficient cells are hypersensitive to high iron concentrations, suggesting that Rnt1p-mediated RNA surveillance is required to prevent iron toxicity. These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 566, "doc_id": "16120395", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: miR-142-5P is a temperature-sensitive microRNA (miRNA).\n\nCANDIDATE_ABSTRACT:\nTITLE: RBM3 regulates temperature sensitive miR-142–5p and miR-143 (thermomiRs), which target immune genes and control fever\nABSTRACT: Fever is commonly used to diagnose disease and is consistently associated with increased mortality in critically ill patients. However, the molecular controls of elevated body temperature are poorly understood. We discovered that the expression of RNA-binding motif protein 3 (RBM3), known to respond to cold stress and to modulate microRNA (miRNA) expression, was reduced in 30 patients with fever, and in THP-1-derived macrophages maintained at a fever-like temperature (40 °C). Notably, RBM3 expression is reduced during fever whether or not infection is demonstrable. Reduced RBM3 expression resulted in increased expression of RBM3-targeted temperature-sensitive miRNAs, we termed thermomiRs. ThermomiRs such as miR-142-5p and miR-143 in turn target endogenous pyrogens including IL-6, IL6ST, TLR2, PGE2 and TNF to complete a negative feedback mechanism, which may be crucial to prevent pathological hyperthermia. Using normal PBMCs that were exogenously exposed to fever-like temperature (40 °C), we further demonstrate the trend by which decreased levels of RBM3 were associated with increased levels of miR-142-5p and miR-143 and vice versa over a 24 h time course. Collectively, our results indicate the existence of a negative feedback loop that regulates fever via reduced RBM3 levels and increased expression of miR-142-5p and miR-143.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Reduced RBM3 expression resulted in increased expression of RBM3-targeted temperature-sensitive miRNAs, we termed thermomiRs. ThermomiRs such as miR-142-5p and miR-143 in turn target endogenous pyrogens including IL-6, IL6ST, TLR2, PGE2 and TNF to complete a negative feedback mechanism, which may be crucial to prevent pathological hyperthermia.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1392, "doc_id": "6766459", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Rapamycin delays aging in fruit flies.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mechanisms of Life Span Extension by Rapamycin in the Fruit Fly Drosophila melanogaster\nABSTRACT: The target of rapamycin (TOR) pathway is a major nutrient-sensing pathway that, when genetically downregulated, increases life span in evolutionarily diverse organisms including mammals. The central component of this pathway, TOR kinase, is the target of the inhibitory drug rapamycin, a highly specific and well-described drug approved for human use. We show here that feeding rapamycin to adult Drosophila produces the life span extension seen in some TOR mutants. Increase in life span by rapamycin was associated with increased resistance to both starvation and paraquat. Analysis of the underlying mechanisms revealed that rapamycin increased longevity specifically through the TORC1 branch of the TOR pathway, through alterations to both autophagy and translation. Rapamycin could increase life span of weak insulin/Igf signaling (IIS) pathway mutants and of flies with life span maximized by dietary restriction, indicating additional mechanisms.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We show here that feeding rapamycin to adult Drosophila produces the life span extension seen in some TOR mutants.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1015, "doc_id": "6277638", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Reduction of purity of cytoplasmic membranes isolated from overexpressors is indicated by stronger spots for OmpA in 2D BN-PAGE gels.\n\nCANDIDATE_PASSAGE:\nAdhesion molecules and chemokines: relation to anthropometric, body composition, biochemical and dietary variables Introduction: Among the inflammatory mediators involved in the pathogenesis of obesity, the cell adhesion molecules Pselectin, E-selectin, VCAM-1, ICAM-1 and the chemokine MCP-1 stand out. They play a crucial role in adherence of cells to endothelial surfaces, in the integrity of the vascular wall and can be modulated by body composition and dietary pattern. Objectives: To describe and discuss the relation of these cell adhesion molecules and chemokines to anthropometric, body composition, dietary and biochemical markers. Methods: Papers were located using scientific databases by topic searches with no restriction on year of publication. Results: All molecules were associated positively with anthropometric markers, but controversial results were found for ICAM-1 and VCAM-1. Not only obesity, but visceral fat is more strongly correlated with E-selectin and MCP-1 levels. Weight loss influences the reduction in the levels of these molecules, except VCAM-1. The distribution of macronutrients, excessive consumption of saturated and trans fat and a Western dietary pattern are associated with increased levels. The opposite could be observed with supplementation of w-3 fatty acid, healthy dietary pattern, high calcium diet and high dairy intake. Regarding the biochemical parameters, they have inverse relation to HDLC and positive relation to total cholesterol, triglycerides, blood glucose, fasting insulin and insulin resistance. Conclusion: Normal anthropometric indicators, body composition, biochemical parameters and eating pattern positively modulate the subclinical inflammation that results from obesity by reducing the cell adhesion molecules and chemokines.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1032", "doc_id": "198309074", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: There was an estimated 30 million cases of pneumonia in young children worldwide in 2010.\n\nCANDIDATE_PASSAGE:\nGlobal and regional burden of hospital admissions for severe acute lower respiratory infections in young children in 2010: a systematic analysis BACKGROUND The annual number of hospital admissions and in-hospital deaths due to severe acute lower respiratory infections (ALRI) in young children worldwide is unknown. We aimed to estimate the incidence of admissions and deaths for such infections in children younger than 5 years in 2010. METHODS We estimated the incidence of admissions for severe and very severe ALRI in children younger than 5 years, stratified by age and region, with data from a systematic review of studies published between Jan 1, 1990, and March 31, 2012, and from 28 unpublished population-based studies. We applied these incidence estimates to population estimates for 2010, to calculate the global and regional burden in children admitted with severe ALRI in that year. We estimated in-hospital mortality due to severe and very severe ALRI by combining incidence estimates with case fatality ratios from hospital-based studies. FINDINGS We identified 89 eligible studies and estimated that in 2010, 11·9 million (95% CI 10·3-13·9 million) episodes of severe and 3·0 million (2·1-4·2 million) episodes of very severe ALRI resulted in hospital admissions in young children worldwide. Incidence was higher in boys than in girls, the sex disparity being greatest in South Asian studies. On the basis of data from 37 hospital studies reporting case fatality ratios for severe ALRI, we estimated that roughly 265,000 (95% CI 160,000-450,000) in-hospital deaths took place in young children, with 99% of these deaths in developing countries. Therefore, the data suggest that although 62% of children with severe ALRI are treated in hospitals, 81% of deaths happen outs [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1297", "doc_id": "9167230", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: EG7 tumors can be killed by systemic oxaliplatin primed CD8+ T cells from the tumor-draining lymph node cells.\n\nCANDIDATE_PASSAGE:\nActivation of the NLRP3 inflammasome in dendritic cells induces IL-1β–dependent adaptive immunity against tumors The therapeutic efficacy of anticancer chemotherapies may depend on dendritic cells (DCs), which present antigens from dying cancer cells to prime tumor-specific interferon-γ (IFN-γ)–producing T lymphocytes. Here we show that dying tumor cells release ATP, which then acts on P2X7 purinergic receptors from DCs and triggers the NOD-like receptor family, pyrin domain containing-3 protein (NLRP3)-dependent caspase-1 activation complex ('inflammasome'), allowing for the secretion of interleukin-1β (IL-1β). The priming of IFN-γ–producing CD8+ T cells by dying tumor cells fails in the absence of a functional IL-1 receptor 1 and in Nlpr3-deficient (Nlrp3−/−) or caspase-1–deficient (Casp-1−/−) mice unless exogenous IL-1β is provided. Accordingly, anticancer chemotherapy turned out to be inefficient against tumors established in purinergic receptor P2rx7−/− or Nlrp3−/− or Casp1−/− hosts. Anthracycline-treated individuals with breast cancer carrying a loss-of-function allele of P2RX7 developed metastatic disease more rapidly than individuals bearing the normal allele. These results indicate that the NLRP3 inflammasome links the innate and adaptive immune responses against dying tumor cells.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "363", "doc_id": "5386514", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Exercise increases cancer mortality rates among Chinese citizens.\n\nCANDIDATE_ABSTRACT:\nTITLE: Combined Impact of Lifestyle-Related Factors on Total and Cause-Specific Mortality among Chinese Women: Prospective Cohort Study\nABSTRACT: BACKGROUND Although cigarette smoking, excessive alcohol drinking, obesity, and several other well-studied unhealthy lifestyle-related factors each have been linked to the risk of multiple chronic diseases and premature death, little is known about the combined impact on mortality outcomes, in particular among Chinese and other non-Western populations. The objective of this study was to quantify the overall impact of lifestyle-related factors beyond that of active cigarette smoking and alcohol consumption on all-cause and cause-specific mortality in Chinese women. METHODS AND FINDINGS We used data from the Shanghai Women's Health Study, an ongoing population-based prospective cohort study in China. Participants included 71,243 women aged 40 to 70 years enrolled during 1996-2000 who never smoked or drank alcohol regularly. A healthy lifestyle score was created on the basis of five lifestyle-related factors shown to be independently associated with mortality outcomes (normal weight, lower waist-hip ratio, daily exercise, never exposed to spouse's smoking, higher daily fruit and vegetable intake). The score ranged from zero (least healthy) to five (most healthy) points. During an average follow-up of 9 years, 2,860 deaths occurred, including 775 from cardiovascular disease (CVD) and 1,351 from cancer. Adjusted hazard ratios for mortality decreased progressively with an increasing number of healthy lifestyle factors. Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality. The inverse association between the healthy lifestyle score and mortality was seen consistently regardless of ch [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The population attributable risks for not having 4-5 healthy lifestyle factors were 33% for total deaths, 59% for CVD deaths, and 19% for cancer deaths.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 396, "doc_id": "1456068", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does the motor component convey all the mortality prediction capacity of the Glasgow Coma Scale in trauma patients?\n\nABSTRACT:\nWe tested the hypothesis that the motor component of the Glasgow Coma Scale (GCS) conveys most of the predictive information of triage scores (Triage Revised Trauma Score [T-RTS] and the Mechanism, GCS, Age, arterial Pressure score [MGAP]) in trauma patients. We conducted a multicenter prospective observational study and evaluated 1690 trauma patients in 14 centers. We compared the GCS, T-RTS, MGAP, and Trauma Related Injury Severity Score (reference standard) using the full GCS or its motor component only using logistic regression model, area under the receiver operating characteristic curve, and reclassification technique. Although some changes were noted for the GCS itself and the Trauma Related Injury Severity Score, no significant change was observed using the motor component only for T-RTS and MGAP when considering (1) the odds ratio of variables included in the logistic model as well as their discrimination and calibration characteristics, (2) the area under the receiver operating characteristic curve (0.827 ± 0.014 vs 0.831 ± 0.014, P = .31 and 0.863 ± 0.011 vs 0.859 ± 0.012, P = .23, respectively), and (3) the reclassification technique. Although the mortality rate remained less than the predetermined threshold of 5% in the low-risk stratum, it slightly increased for MGAP (from 1.9% to 3.9%, P = .048).", "output": "{\"label\": \"no\", \"rationale\": \"The use of the motor component only of the GCS did not change the global performance of triage scores in trauma patients. However, because a subtle increase in mortality rate was observed in the low-risk stratum for MGAP, replacing the GCS by its motor component may not be recommended in every situation.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 22035584, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Nanoparticles can be targeted against specific cell types by incorporating aptamers into lipid nanoparticles.\n\nCANDIDATE_PASSAGE:\nA Common Mechanism of Cellular Death Induced by Bactericidal Antibiotics Antibiotic mode-of-action classification is based upon drug-target interaction and whether the resultant inhibition of cellular function is lethal to bacteria. Here we show that the three major classes of bactericidal antibiotics, regardless of drug-target interaction, stimulate the production of highly deleterious hydroxyl radicals in Gram-negative and Gram-positive bacteria, which ultimately contribute to cell death. We also show, in contrast, that bacteriostatic drugs do not produce hydroxyl radicals. We demonstrate that the mechanism of hydroxyl radical formation induced by bactericidal antibiotics is the end product of an oxidative damage cellular death pathway involving the tricarboxylic acid cycle, a transient depletion of NADH, destabilization of iron-sulfur clusters, and stimulation of the Fenton reaction. Our results suggest that all three major classes of bactericidal drugs can be potentiated by targeting bacterial systems that remediate hydroxyl radical damage, including proteins involved in triggering the DNA damage response, e.g., RecA.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "839", "doc_id": "1103795", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Diminished ovarian reserve is a reliable indicator of infertility in a non-infertile population.\n\nCANDIDATE_PASSAGE:\nPrevalence of cardiovascular disease risk factor in the Chinese population: the 2007-2008 China National Diabetes and Metabolic Disorders Study. AIMS Cardiovascular disease (CVD) is now the most prevalent and debilitating disease affecting the Chinese population. The goal of the present manuscript was to analyse cardiovascular risk factors and the prevalence of non-fatal CVDs from data gathered from the 2007-2008 China National Diabetes and Metabolic Disorders Study. METHODS AND RESULTS A nationally representative sample of 46 239 adults, 20 years of age or older, was randomly recruited using a multistage stratified design method. Lifestyle factors, diagnosis of CVD, stroke, diabetes, and family history of each subject were collected, and an oral glucose tolerance test or a standard meal test was performed. Various non-fatal CVDs were reported by the subjects. SUDAAN software was used to perform all weighted statistical analyses, with P < 0.05 considered statistically significant. The prevalence of coronary heart disease, stroke, and CVDs was 0.74, 1.07, and 1.78% in males; and 0.51, 0.60, and 1.10% in females, respectively. The presence of CVDs increased with age in both males and females. The prevalence of being overweight or obese, hypertension, dyslipidaemia, or hyperglycaemia was 36.67, 30.09, 67.43, and 26.69% in males; and 29.77, 24.79, 63.98, and 23.62% in females, respectively. In the total sample of 46 239 patients, the prevalence of one subject having 1, 2, 3, or ≥4 of the 5 defined risk factors (i.e. smoking, overweight or obese, hypertension, dyslipidaemia, or hyperglycaemia) was 31.17, 27.38, 17.76, and 10.19%, respectively. Following adjustment for gender and age, the odds ratio of CVDs for those who had 1, 2, 3, or ≥4 risk factors was 2.36, 4 [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "349", "doc_id": "2138767", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Nonsteroidal antinflammatory drugs show potential anticancer indications.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association of aspirin and NSAID use with risk of colorectal cancer according to genetic variants.\nABSTRACT: IMPORTANCE Use of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with lower risk of colorectal cancer. OBJECTIVE To identify common genetic markers that may confer differential benefit from aspirin or NSAID chemoprevention, we tested gene × environment interactions between regular use of aspirin and/or NSAIDs and single-nucleotide polymorphisms (SNPs) in relation to risk of colorectal cancer. DESIGN, SETTING, AND PARTICIPANTS Case-control study using data from 5 case-control and 5 cohort studies initiated between 1976 and 2003 across the United States, Canada, Australia, and Germany and including colorectal cancer cases (n=8634) and matched controls (n=8553) ascertained between 1976 and 2011. Participants were all of European descent. EXPOSURES Genome-wide SNP data and information on regular use of aspirin and/or NSAIDs and other risk factors. MAIN OUTCOMES AND MEASURES Colorectal cancer. RESULTS Regular use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer (prevalence, 28% vs 38%; odds ratio [OR], 0.69 [95% CI, 0.64-0.74]; P = 6.2 × 10(-28)) compared with nonregular use. In the conventional logistic regression analysis, the SNP rs2965667 at chromosome 12p12.3 near the MGST1 gene showed a genome-wide significant interaction with aspirin and/or NSAID use (P = 4.6 × 10(-9) for interaction). Aspirin and/or NSAID use was associated with a lower risk of colorectal cancer among individuals with rs2965667-TT genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.61-0.70]; P = 7.7 × 10(-33)) but with a higher risk among those with rare (4%) TA or AA genotypes (prevalence, 35% vs 29%; OR, 1.89 [95% CI, 1.27-2.81]; P = .002). In case-only interaction analysis, the SNP rs16973225 at chromosome 15q25.2 near the IL [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"RESULTS Regular use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer (prevalence, 28% vs 38%; odds ratio [OR], 0.69 [95% CI, 0.64-0.74]; P = 6.2 × 10(-28)) compared with nonregular use.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 857, "doc_id": "43334921", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The morphology change from large white adipocytes to small brown adipocytes is a sign of increased energy expenditure potential in white adipose tissue.\n\nCANDIDATE_ABSTRACT:\nTITLE: Human ‘brite / beige’ adipocytes develop from capillary networks and their implantation improves metabolic homeostasis in mice\nABSTRACT: Uncoupling protein 1 (UCP1) is highly expressed in brown adipose tissue, where it generates heat by uncoupling electron transport from ATP production. UCP1 is also found outside classical brown adipose tissue depots, in adipocytes that are termed 'brite' (brown-in-white) or 'beige'. In humans, the presence of brite or beige (brite/beige) adipocytes is correlated with a lean, metabolically healthy phenotype, but whether a causal relationship exists is not clear. Here we report that human brite/beige adipocyte progenitors proliferate in response to pro-angiogenic factors, in association with expanding capillary networks. Adipocytes formed from these progenitors transform in response to adenylate cyclase activation from being UCP1 negative to being UCP1 positive, which is a defining feature of the beige/brite phenotype, while displaying uncoupled respiration. When implanted into normal chow-fed, or into high-fat diet (HFD)-fed, glucose-intolerant NOD-scid IL2rg(null) (NSG) mice, brite/beige adipocytes activated in vitro enhance systemic glucose tolerance. These adipocytes express neuroendocrine and secreted factors, including the pro-protein convertase PCSK1, which is strongly associated with human obesity. Pro-angiogenic conditions therefore drive the proliferation of human beige/brite adipocyte progenitors, and activated beige/brite adipocytes can affect systemic glucose homeostasis, potentially through a neuroendocrine mechanism.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1236, "doc_id": "17973161", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Deletion of αvβ8 does not result in a spontaneous inflammatory phenotype.\n\nCANDIDATE_PASSAGE:\nAngiopoietin-1 requires p190 RhoGAP to protect against vascular leakage in vivo. Angiopoietin-1 (Ang-1), a ligand of the endothelium-specific receptor Tie-2, inhibits permeability in the mature vasculature, but the mechanism remains unknown. Here we show that Ang-1 signals Rho family GTPases to organize the cytoskeleton into a junction-fortifying arrangement that enhances the permeability barrier function of the endothelium. Ang-1 phosphorylates Tie-2 and its downstream effector phosphatidylinositol 3-kinase. This induces activation of one endogenous GTPase, Rac1, and inhibition of another, RhoA. Loss of either part of this dual effect abrogates the cytoskeletal and anti-permeability actions of Ang-1, suggesting that coordinated GTPase regulation is necessary for the vessel-sealing effects of Ang-1. p190 RhoGAP, a GTPase regulatory protein, provides this coordinating function as it is phosphorylated by Ang-1 treatment, requires Rac1 activation, and is necessary for RhoA inhibition. Ang-1 prevents the cytoskeletal and pro-permeability effects of endotoxin but requires p190 RhoGAP to do so. Treatment with p190 RhoGAP small interfering RNA completely abolishes the ability of Ang-1 to rescue endotoxemia-induced pulmonary vascular leak and inflammation in mice. We conclude that Ang-1 prevents vascular permeability by regulating the endothelial cytoskeleton through coordinated and opposite effects on the Rho GTPases Rac1 and RhoA. By linking Rac1 activation and RhoA inhibition, p190 RhoGAP is critical to the protective effects of Ang-1 against endotoxin. These results provide mechanistic evidence that targeting the endothelium through Tie-2 may offer specific therapeutic strategies in life-threatening endotoxemic conditions such as sepsis and acute respiratory dis [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "327", "doc_id": "23700330", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Microglia are an innate immune cell type of the peripheral nervous system.\n\nCANDIDATE_ABSTRACT:\nTITLE: Sublime Microglia: Expanding Roles for the Guardians of the CNS\nABSTRACT: Recent findings challenge the concept that microglia solely function in disease states in the central nervous system (CNS). Rather than simply reacting to CNS injury, infection, or pathology, emerging lines of evidence indicate that microglia sculpt the structure of the CNS, refine neuronal circuitry and network connectivity, and contribute to plasticity. These physiological functions of microglia in the normal CNS begin during development and persist into maturity. Here, we develop a conceptual framework for functions of microglia beyond neuroinflammation and discuss the rich repertoire of signaling and communication motifs in microglia that are critical both in pathology and for the normal physiology of the CNS.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"These physiological functions of microglia in the normal CNS begin during development and persist into maturity.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 790, "doc_id": "15493354", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Leuko-increased blood increases infectious complications in red blood cell transfusion.\n\nCANDIDATE_ABSTRACT:\nTITLE: Clinical outcomes following institution of the Canadian universal leukoreduction program for red blood cell transfusions.\nABSTRACT: CONTEXT A number of countries have implemented a policy of universal leukoreduction of their blood supply, but the potential role of leukoreduction in decreasing postoperative mortality and infection is unclear. OBJECTIVE To evaluate clinical outcomes following adoption of a national universal prestorage leukoreduction program for blood transfusions. DESIGN, SETTING, AND POPULATION Retrospective before-and-after cohort study conducted from August 1998 to August 2000 in 23 academic and community hospitals throughout Canada, enrolling 14 786 patients who received red blood cell transfusions following cardiac surgery or repair of hip fracture, or who required intensive care following a surgical intervention or multiple trauma. INTERVENTION Universal prestorage leukoreduction program introduced by 2 Canadian blood agencies. A total of 6982 patients were enrolled during the control period and 7804 patients were enrolled following prestorage leukoreduction. MAIN OUTCOME MEASURES All-cause in-hospital mortality and serious nosocomial infections (pneumonia, bacteremia, septic shock, all surgical site infections) occurring after first transfusion and at least 2 days after index procedure or intensive care unit admission. Secondary outcomes included rates of posttransfusion fever and antibiotic use. RESULTS Unadjusted in-hospital mortality rates were significantly lower following the introduction of leukoreduction compared with the control period (6.19% vs 7.03%, respectively; P =.04). Compared with the control period, the adjusted odds of death following leukoreduction were reduced (odds ratio [OR], 0.87; 95% confidence interval [CI], 0.75-0.99), but serious nosocomial infections did not decrease (adjusted OR, 0.97; 95% CI, 0.87-1.09). The frequency of posttransfusio [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The frequency of posttransfusion fevers decreased significantly following leukoreduction (adjusted OR, 0.86; 95% CI, 0.79-0.94), as did antibiotic use (adjusted OR, 0.90; 95% CI, 0.82-0.99).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 692, "doc_id": "24088502", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cell autonomous sex determination in somatic cells does not occur in Galliformes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Somatic sex identity is cell-autonomous in the chicken\nABSTRACT: In the mammalian model of sex determination, embryos are considered to be sexually indifferent until the transient action of a sex-determining gene initiates gonadal differentiation. Although this model is thought to apply to all vertebrates, this has yet to be established. Here we have examined three lateral gynandromorph chickens (a rare, naturally occurring phenomenon in which one side of the animal appears male and the other female) to investigate the sex-determining mechanism in birds. These studies demonstrated that gynandromorph birds are genuine male:female chimaeras, and indicated that male and female avian somatic cells may have an inherent sex identity. To test this hypothesis, we transplanted presumptive mesoderm between embryos of reciprocal sexes to generate embryos containing male:female chimaeric gonads. In contrast to the outcome for mammalian mixed-sex chimaeras, in chicken mixed-sex chimaeras the donor cells were excluded from the functional structures of the host gonad. In an example where female tissue was transplanted into a male host, donor cells contributing to the developing testis retained a female identity and expressed a marker of female function. Our study demonstrates that avian somatic cells possess an inherent sex identity and that, in birds, sexual differentiation is substantively cell autonomous.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"These studies demonstrated that gynandromorph birds are genuine male:female chimaeras, and indicated that male and female avian somatic cells may have an inherent sex identity.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 233, "doc_id": "4388470", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Decrease of p62 in prostate tumor stroma results in defective autophagy.\n\nCANDIDATE_PASSAGE:\nAlteration of the Antitumor Immune Response by Cancer-Associated Fibroblasts Among cells present in the tumor microenvironment, activated fibroblasts termed cancer-associated fibroblasts (CAFs), play a critical role in the complex process of tumor-stroma interaction. CAFs, one of the prominent stromal cell populations in most types of human carcinomas, have been involved in tumor growth, angiogenesis, cancer stemness, extracellular matrix remodeling, tissue invasion, metastasis, and even chemoresistance. During the past decade, these activated tumor-associated fibroblasts have also been involved in the modulation of the anti-tumor immune response on various levels. In this review, we describe our current understanding of how CAFs accomplish this task as well as their potential therapeutic implications.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "315", "doc_id": "32742683", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Insulin effects appetite via ventral tegmental neurons.\n\nCANDIDATE_PASSAGE:\nFibroblast growth factor 21 as an emerging metabolic regulator: clinical perspectives. Fibroblast growth factor 21 (FGF21), a metabolic hormone predominantly produced by the liver, is also expressed in adipocytes and the pancreas. It regulates glucose and lipid metabolism through pleiotropic actions in these tissues and the brain. In mice, fasting leads to increased PPAR-α mediated expression of FGF21 in the liver where it stimulates gluconeogenesis, fatty acid oxidation, and ketogenesis, as an adaptive response to fasting and starvation. In the fed state, FGF21 acts as an autocrine factor in adipocytes, regulating the activity of PPAR-γ through a feed-forward loop mechanism. Administration of recombinant FGF21 has been shown to confer multiple metabolic benefits on insulin sensitivity, blood glucose, lipid profile and body weight in obese mice and diabetic monkeys, without mitogenic or other side effects. Such findings highlight the potential role of FGF21 as a therapeutic agent for obesity-related medical conditions. However, in human studies, high circulating FGF21 levels are found in obesity and its related cardiometabolic disorders including the metabolic syndrome, type 2 diabetes, non-alcoholic fatty liver disease and coronary artery disease. These findings may indicate the presence of FGF21 resistance or compensatory responses to the underlying metabolic stress, and imply the need for supraphysiological doses of FGF21 to achieve therapeutic efficacy. On the other hand, serum FGF21 has been implicated as a potential biomarker for the early detection of these cardiometabolic disorders. This review summarizes recent developments in the understanding of FGF21, from physiological and clinical perspectives.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "643", "doc_id": "23397658", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: R2D2 stops miRNA production by increasing the selectivity of Dcr2 for long dsRNA.\n\nCANDIDATE_ABSTRACT:\nTITLE: Phosphate and R2D2 restrict the substrate specificity of Dicer-2, an ATP-driven ribonuclease.\nABSTRACT: Drosophila Dicer-2 generates small interfering RNAs (siRNAs) from long double-stranded RNA (dsRNA), whereas Dicer-1 produces microRNAs (miRNAs) from pre-miRNA. What makes the two Dicers specific for their biological substrates? We find that purified Dicer-2 can efficiently cleave pre-miRNA, but that inorganic phosphate and the Dicer-2 partner protein R2D2 inhibit pre-miRNA cleavage. Dicer-2 contains C-terminal RNase III domains that mediate RNA cleavage and an N-terminal helicase motif, whose function is unclear. We show that Dicer-2 is a dsRNA-stimulated ATPase that hydrolyzes ATP to ADP; ATP hydrolysis is required for Dicer-2 to process long dsRNA, but not pre-miRNA. Wild-type Dicer-2, but not a mutant defective in ATP hydrolysis, can generate siRNAs faster than it can dissociate from a long dsRNA substrate. We propose that the Dicer-2 helicase domain uses ATP to generate many siRNAs from a single molecule of dsRNA before dissociating from its substrate.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1001, "doc_id": "5702790", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: RANK-RANKL pathway signalling is linked to development of Aire-expressing medullary thymic epithelial cells.\n\nCANDIDATE_PASSAGE:\nAire deficiency promotes TRP-1-specific immune rejection of melanoma. The thymic transcription factor autoimmune regulator (Aire) prevents autoimmunity in part by promoting expression of tissue-specific self-antigens, which include many cancer antigens. For example, AIRE-deficient patients are predisposed to vitiligo, an autoimmune disease of melanocytes that is often triggered by efficacious immunotherapies against melanoma. Therefore, we hypothesized that Aire deficiency in mice may elevate immune responses to cancer and provide insights into how such responses might be triggered. In this study, we show that Aire deficiency decreases thymic expression of TRP-1 (TYRP1), which is a self-antigen in melanocytes and a cancer antigen in melanomas. Aire deficiency resulted in defective negative selection of TRP-1-specific T cells without affecting thymic numbers of regulatory T cells. Aire-deficient mice displayed elevated T-cell immune responses that were associated with suppression of melanoma outgrowth. Furthermore, transplantation of Aire-deficient thymic stroma was sufficient to confer more effective immune rejection of melanoma in an otherwise Aire wild-type host. Together, our work showed how Aire deficiency can enhance immune responses against melanoma and how manipulating TRP-1-specific T-cell negative selection may offer a logical strategy to enhance immune rejection of melanoma.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1005", "doc_id": "25738896", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Patients in stable partnerships progress from HIV to death at the same rate as patients not in partnerships.\n\nCANDIDATE_ABSTRACT:\nTITLE: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\nABSTRACT: OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART). DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study). SETTING Seven outpatient clinics throughout Switzerland. PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years). MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound. RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion. When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership. In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without. Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression. CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 925, "doc_id": "17077004", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Silencing of Bcl2 is important for the maintenance and progression of tumors.\n\nCANDIDATE_ABSTRACT:\nTITLE: Antiapoptotic BCL-2 is required for maintenance of a model leukemia.\nABSTRACT: Resistance to apoptosis, often achieved by the overexpression of antiapoptotic proteins, is common and perhaps required in the genesis of cancer. However, it remains uncertain whether apoptotic defects are essential for tumor maintenance. To test this, we generated mice expressing a conditional BCL-2 gene and constitutive c-myc that develop lymphoblastic leukemia. Eliminating BCL-2 yielded rapid loss of leukemic cells and significantly prolonged survival, formally validating BCL-2 as a rational target for cancer therapy. Loss of this single molecule resulted in cell death, despite or perhaps attributable to the presence of other oncogenic events. This suggests a generalizable model in which aberrations inherent to cancer generate tonic death signals that would otherwise kill the cell if not opposed by a requisite apoptotic defect(s).", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Eliminating BCL-2 yielded rapid loss of leukemic cells and significantly prolonged survival, formally validating BCL-2 as a rational target for cancer therapy.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1088, "doc_id": "37549932", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Only a minority of cells survive development after differentiation into stress-resistant spores.\n\nCANDIDATE_PASSAGE:\nCulture of Preimplantation Mouse Embryos Affects Fetal Development and the Expression of Imprinted Genes1 Abstract Culture of preimplantation mammalian embryos and cells can influence their subsequent growth and differentiation. Previously, we reported that culture of mouse embryonic stem cells is associated with deregulation of genomic imprinting and affects the potential for these cells to develop into normal fetuses. The purpose of our current study was to determine whether culture of preimplantation mouse embryos in a chemically defined medium (M16) with or without fetal calf serum (FCS) can affect their subsequent development and imprinted gene expression. Only one third of the blastocysts that had been cultured from two-cell embryos in M16 medium complemented with FCS developed into viable Day 14 fetuses after transfer into recipients. These M16 + FCS fetuses were reduced in weight as compared with controls and M16 fetuses and had decreased expression of the imprinted H19 and insulin-like growth factor 2 genes associated with a gain of DNA methylation at an imprinting control region upstream of H19. They also displayed increased expression of the imprinted gene Grb10. The growth factor receptor binding gene Grb7, in contrast, was strongly reduced in its expression in most of the M16 + FCS fetuses. No alterations were detected for the imprinted gene Mest. Preimplantation culture in the presence of serum can influence the regulation of multiple growth-related imprinted genes, thus leading to aberrant fetal growth and development.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "887", "doc_id": "13441537", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Diminished ovarian reserve is a reliable indicator of infertility in a non-infertile population.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\nABSTRACT: Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential. Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age. Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area. Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH. Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle). Conception was defined as a positive pregnancy test result. Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis. After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively). Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cy [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 349, "doc_id": "13497630", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Pediatric SCD patients with vaso-occlusive crisis show increased morphine use after breathing 80 ppm iNO for 4 hours.\n\nCANDIDATE_ABSTRACT:\nTITLE: Preliminary assessment of inhaled nitric oxide for acute vaso-occlusive crisis in pediatric patients with sickle cell disease.\nABSTRACT: CONTEXT Vaso-occlusion is central to the painful crises and acute and chronic organ damage in sickle cell disease. Abnormal nitric oxide-dependent regulation of vascular tone, adhesion, platelet activation, and inflammation contributes to the pathophysiology of vaso-occlusion. Nitric oxide may have promise as a mechanism-of-disease-based therapy for treatment of vaso-occlusion. OBJECTIVE To explore the efficacy and safety of inhaled nitric oxide (INO) for treatment of vaso-occlusive crisis in pediatric patients. DESIGN Prospective, double-blind, placebo-controlled, randomized clinical trial with enrollment between September 1999 and October 2001. SETTING Urban, tertiary care children's hospital in the United States. PARTICIPANTS Twenty patients aged 10 to 21 years with sickle cell disease and severe acute vaso-occlusive crisis. INTERVENTION Patients were randomly assigned to receive INO (80 ppm with 21% final concentration of inspired oxygen; n = 10), or placebo (21% inspired oxygen; n = 10) for 4 hours. MAIN OUTCOME MEASURES Change in pain at 4 hours of inhalation compared with preinhalation pain, measured on a 10-cm visual analog scale (VAS); secondary outcome measures were pain over 6 hours, parenteral narcotic use over 24 hours, duration of hospitalization, blood pressure, oxygen saturation, and methemoglobin concentration. RESULTS Preinhalation VAS pain scores were similar in the INO and placebo groups (P =.80). The decrease in VAS pain scores at 4 hours was 2.0 cm in the INO group and 1.2 cm in the placebo group (P =.37). Repeated-measures analysis of variance for hourly pain scores showed a 1-cm/h greater reduction in the INO group than the placebo group (P =.02). Morphine use over 6 hours was significantly less in the INO group (mean cumulative use, [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Morphine use over 6 hours was significantly less in the INO group (mean cumulative use, 0.29 vs 0.44 mg/kg; P =.03) but was not different over 4 hours (0.26 vs 0.32 mg/kg; P =.21) or 24 hours (0.63 vs 0.91 mg/kg; P =.15).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 933, "doc_id": "14711483", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The risk of male prisoners harming themselves is ten times that of female prisoners.\n\nCANDIDATE_PASSAGE:\nRisk factors at medical school for subsequent professional misconduct: multicentre retrospective case-control study OBJECTIVE To determine whether there are risk factors in a doctor's time at medical school that are associated with subsequent professional misconduct. DESIGN Matched case-control study. Setting Records from medical schools and the General Medical Council (GMC). PARTICIPANTS 59 doctors who had graduated from any one of eight medical schools in the United Kingdom in 1958-97 and had a proved finding of serious professional misconduct in GMC proceedings in 1999-2004 (cases); 236 controls (four for each case) were selected by systematic sampling from matching graduation cohorts. Case-control status was revealed by the GMC after completion of data entry. MAIN OUTCOME MEASURE Odds ratios for being a \"case,\" with multivariable conditional logistic regression of potential risk factors including pre-admission characteristics and progress during the course. These data were obtained from anonymised copies of the students' progress files held by their original medical schools. RESULTS Univariate conditional logistic regression analysis found that cases were more likely to be men, to be of lower estimated social class, and to have had academic difficulties during their medical course, especially in the early years. Multivariable analysis showed that male sex (odds ratio 9.80, 95% confidence interval 2.43 to 39.44, P=0.001), lower social class (4.28, 1.52 to 12.09, P=0.006), and failure of early or preclinical examinations (5.47, 2.17 to 13.79, P<0.001) were independently associated with being a case. CONCLUSIONS This small study suggests that male sex, a lower socioeconomic background, and early academic difficulties at medical school could be risk factors [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1270", "doc_id": "6710713", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Mice lacking Sirt1 in Sf1-expressing neurons are immune to diet-induced obesity and insulin resistance.\n\nCANDIDATE_ABSTRACT:\nTITLE: SIRT1 deacetylase in SF1 neurons protects against metabolic imbalance.\nABSTRACT: Chronic feeding on high-calorie diets causes obesity and type 2 diabetes mellitus (T2DM), illnesses that affect hundreds of millions. Thus, understanding the pathways protecting against diet-induced metabolic imbalance is of paramount medical importance. Here, we show that mice lacking SIRT1 in steroidogenic factor 1 (SF1) neurons are hypersensitive to dietary obesity owing to maladaptive energy expenditure. Also, mutant mice have increased susceptibility to developing dietary T2DM due to insulin resistance in skeletal muscle. Mechanistically, these aberrations arise, in part, from impaired metabolic actions of the neuropeptide orexin-A and the hormone leptin. Conversely, mice overexpressing SIRT1 in SF1 neurons are more resistant to diet-induced obesity and insulin resistance due to increased energy expenditure and enhanced skeletal muscle insulin sensitivity. Our results unveil important protective roles of SIRT1 in SF1 neurons against dietary metabolic imbalance.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Here, we show that mice lacking SIRT1 in steroidogenic factor 1 (SF1) neurons are hypersensitive to dietary obesity owing to maladaptive energy expenditure. Also, mutant mice have increased susceptibility to developing dietary T2DM due to insulin resistance in skeletal muscle.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 778, "doc_id": "13001323", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: A breast cancer patient's capacity to metabolize tamoxifen influences treatment outcome.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association between CYP2D6 polymorphisms and outcomes among women with early stage breast cancer treated with tamoxifen.\nABSTRACT: CONTEXT The growth inhibitory effect of tamoxifen, which is used for the treatment of hormone receptor-positive breast cancer, is mediated by its metabolites, 4-hydroxytamoxifen and endoxifen. The formation of active metabolites is catalyzed by the polymorphic cytochrome P450 2D6 (CYP2D6) enzyme. OBJECTIVE To determine whether CYP2D6 variation is associated with clinical outcomes in women receiving adjuvant tamoxifen. DESIGN, SETTING, AND PATIENTS Retrospective analysis of German and US cohorts of patients treated with adjuvant tamoxifen for early stage breast cancer. The 1325 patients had diagnoses between 1986 and 2005 of stage I through III breast cancer and were mainly postmenopausal (95.4%). Last follow-up was in December 2008; inclusion criteria were hormone receptor positivity, no metastatic disease at diagnosis, adjuvant tamoxifen therapy, and no chemotherapy. DNA from tumor tissue or blood was genotyped for CYP2D6 variants associated with reduced (*10, *41) or absent (*3, *4, *5) enzyme activity. Women were classified as having an extensive (n=609), heterozygous extensive/intermediate (n=637), or poor (n=79) CYP2D6 metabolism. MAIN OUTCOME MEASURES Time to recurrence, event-free survival, disease-free survival, and overall survival. RESULTS Median follow-up was 6.3 years. At 9 years of follow-up, the recurrence rates were 14.9% for extensive metabolizers, 20.9% for heterozygous extensive/intermediate metabolizers, and 29.0% for poor metabolizers, and all-cause mortality rates were 16.7%, 18.0%, and 22.8%, respectively. Compared with extensive metabolizers, there was a significantly increased risk of recurrence for heterozygous extensive/intermediate metabolizers (time to recurrence adjusted hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.04 [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Compared with extensive metabolizers, those with decreased CYP2D6 activity (heterozygous extensive/intermediate and poor metabolism) had worse event-free survival (HR, 1.33; 95% CI, 1.06-1.68) and disease-free survival (HR, 1.29; 95% CI, 1.03-1.61), but there was no significant difference in overall survival (HR, 1.15; 95% CI, 0.88-1.51).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 30, "doc_id": "24341590", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Klf4 is important for proper myeloid cell differentiation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Kruppel-like factor 4 is essential for inflammatory monocyte differentiation in vivo.\nABSTRACT: Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types. We demonstrate in this study that hematopoietic cells from KLF4(-/-) fetal livers (FL) contained normal numbers of functional hematopoietic progenitor cells, were radioprotective, and performed as well as KLF4(+/+) cells in competitive repopulation assays. However, hematopoietic \"KLF4(-/-) chimeras\" generated by transplantation of KLF4(-/-) fetal livers cells into lethally irradiated wild-type mice completely lacked circulating inflammatory (CD115(+)Gr1(+)) monocytes, and had reduced numbers of resident (CD115(+)Gr1(-)) monocytes. Although the numbers and function of peritoneal macrophages were normal in KLF4(-/-) chimeras, bone marrow monocytic cells from KLF4(-/-) chimeras expressed lower levels of key trafficking molecules and were more apoptotic. Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes. In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells. The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 668, "doc_id": "25148216", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Tumor development occurs in conjunction with suppression of pro-inflammatory cytokines.\n\nCANDIDATE_PASSAGE:\nOrai1/CRACM1 overexpression suppresses cell proliferation via attenuation of the store-operated calcium influx-mediated signalling pathway in A549 lung cancer cells. BACKGROUND Orai1/CRACM1 is a principal component of the store-operated calcium channels. Store-operated calcium influx is highly correlated with inflammatory reactions, immunological regulation, and cell proliferation. Epidermal growth factor (EGF), which plays an important role in the regulation of cell proliferation, can activate store-operated calcium channels. However, the consequences of Orai1/CRACM1 overexpression in EGF-mediated lung cancer cells growth are not known. METHODS To investigate the role of Orai1/CRACM1 in EGF-mediated lung cancer cell proliferation, Orai1/CRACM1 plasmids were transfected into cells by lipofection. A cell proliferation assay, immunofluorescence staining, flow cytometry, and real-time polymerase chain reaction were employed to monitor cell proliferation. The calcium influx signals were investigated using a fluorescent-based calcium assay. RESULTS Transfection of Orai1/CRACM1 plasmids resulted in the inhibition of EGF-mediated cell proliferation. ERK1/2 and Akt phosphorylation were inhibited by Orai1/CRACM1 overexpression. Expression of the cell cycle modulator p21 was induced in the Orai1/CRACM1-overexpressing cells, whereas the expression of cyclin D3 was reduced. Flow cytometry revealed that overexpression of Orai1/CRACM1 resulted in G0/G1 cell cycle arrest. Importantly, Orai1/CRACM1 overexpression significantly attenuated EGF-mediated store-operated calcium influx. In addition, application of 2-APB, a store-operated calcium channel inhibitor, resulted in the inhibition of EGF-mediated cancer cell proliferation. CONCLUSIONS We conclude that Orai1/CRACM1 overe [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1330", "doc_id": "24349430", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does ultrasound imaging before puncture facilitate internal jugular vein cannulation?\n\nABSTRACT:\nTo investigate whether prepuncture ultrasound evaluation of vascular anatomy facilitates internal jugular vein cannulation compared with landmark-guided puncture. Prospective randomized study. Single community hospital. Adult patients undergoing general anesthesia (n = 240). The right internal jugular vein was cannulated using either anatomic landmarks or prepuncture ultrasound (3.75/7.5 MHz) guidance. In the landmark group, respiratory jugular venodilation was used as the primary landmark for locating the vein. Results of cannulation and the incidence of complications were compared. Patients were randomly assigned to the ultrasound or landmark group. Respiratory jugular venodilation was identified in 188 patients (78.3%), in whom results of cannulation did not differ between the 2 techniques with respect to the venous access rate (cannulated at the first attempt: 83.5% in the landmark v 85.7% in the ultrasound group), the success rate (cannulated within 3 attempts: 96.9% v 95.6%), and the incidence of arterial puncture (1.0% v 3.3%). In the remaining 52 respiratory jugular venodilation-unidentified patients, the access rate (30.4% v 86.2%, p<0.001) and the success rate (78.3 v 100%, p<0.05) were significantly better in the ultrasound group, and no arterial puncture was recorded in the ultrasound group, whereas the incidence was 13.0% in the landmark group. The results were similar regardless of the ultrasound frequency used.", "output": "{\"label\": \"maybe\", \"rationale\": \"Prepuncture ultrasound evaluation did not improve the result of right internal jugular vein cannulation compared with the respiratory jugular venodilation-guided approach. When the landmark was not observed, however, the prepuncture ultrasound guidance was helpful in facilitating the cannulation.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 12407608, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Taxation of sugar-sweetened beverages reduced the incidence rate of type II diabetes in India.\n\nCANDIDATE_ABSTRACT:\nTITLE: A nuclear Argonaute promotes multi-generational epigenetic inheritance and germline immortality\nABSTRACT: Epigenetic information is frequently erased near the start of each new generation. In some cases, however, epigenetic information can be transmitted from parent to progeny (multigenerational epigenetic inheritance). A particularly notable example of this type of epigenetic inheritance is double-stranded RNA-mediated gene silencing in Caenorhabditis elegans. This RNA-mediated interference (RNAi) can be inherited for more than five generations. To understand this process, here we conduct a genetic screen for nematodes defective in transmitting RNAi silencing signals to future generations. This screen identified the heritable RNAi defective 1 (hrde-1) gene. hrde-1 encodes an Argonaute protein that associates with small interfering RNAs in the germ cells of progeny of animals exposed to double-stranded RNA. In the nuclei of these germ cells, HRDE-1 engages the nuclear RNAi defective pathway to direct the trimethylation of histone H3 at Lys 9 (H3K9me3) at RNAi-targeted genomic loci and promote RNAi inheritance. Under normal growth conditions, HRDE-1 associates with endogenously expressed short interfering RNAs, which direct nuclear gene silencing in germ cells. In hrde-1- or nuclear RNAi-deficient animals, germline silencing is lost over generational time. Concurrently, these animals exhibit steadily worsening defects in gamete formation and function that ultimately lead to sterility. These results establish that the Argonaute protein HRDE-1 directs gene-silencing events in germ-cell nuclei that drive multigenerational RNAi inheritance and promote immortality of the germ-cell lineage. We propose that C. elegans use the RNAi inheritance machinery to transmit epigenetic information, accrued by past generations, into future generations to regulate important biologic [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1145, "doc_id": "2541699", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Mice without IFN-γ or its receptor are highly susceptible to EAM induced with α-MyHC/CFA.\n\nCANDIDATE_PASSAGE:\nHepatitis C virus infection in a large cohort of homosexually active men: independent associations with HIV-1 infection and injecting drug use but not sexual behaviour. OBJECTIVE To determine the prevalence and risk factors for hepatitis C virus (HCV) infection in a cohort of homosexually active men, with particular reference to assessing sexual transmission. DESIGN Prevalence based on cross-sectional testing for HCV (c100 protein) antibody in a cohort using sera stored between 1984 and 1989, and assessment of risk factors using a case-control analysis based on questionnaire data from HCV positive and negative subjects. SUBJECTS/SETTING 1038 homosexually active men who were participating in a prospective study established to identify risk factors for AIDS. They had been recruited through private and public primary care and sexually transmissible disease (STD) services in central Sydney. MAIN OUTCOME MEASURES Prevalence of HCV antibody and its association with human immunodeficiency virus type 1 (HIV-1) infection and other STDs, number of sexual partners, sexual practices and recreational drug use. RESULTS Overall, 7.6% of subjects tested were seropositive for HCV antibody. In univariate analysis, HCV infection was significantly associated with injecting drug use (IDU) (OR = 8.18, p < 0.0001) and HIV infection (OR = 3.14, p < 0.0001) and with self reported history of syphilis (OR = 1.88, p = 0.016), anogenital herpes (OR = 1.93, p = 0.017), gonorrhoea (OR = 2.43, p = 0.009) and hepatitis B (OR = 1.92, p = 0.010). In case control analysis, similar sexual behaviours (partner numbers and practices) were reported by HCV positive and HCV negative subjects except that HCV negative subjects more frequently reported engaging than HCV positive subject in unprotected r [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "782", "doc_id": "5835149", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: ERAP1 SNPs are epistatic to HLA alleles for ankylosing spondylitis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Major histocompatibility complex associations of ankylosing spondylitis are complex and involve further epistasis with ERAP1\nABSTRACT: Ankylosing spondylitis (AS) is a common, highly heritable, inflammatory arthritis for which HLA-B*27 is the major genetic risk factor, although its role in the aetiology of AS remains elusive. To better understand the genetic basis of the MHC susceptibility loci, we genotyped 7,264 MHC SNPs in 22,647 AS cases and controls of European descent. We impute SNPs, classical HLA alleles and amino-acid residues within HLA proteins, and tested these for association to AS status. Here we show that in addition to effects due to HLA-B*27 alleles, several other HLA-B alleles also affect susceptibility. After controlling for the associated haplotypes in HLA-B, we observe independent associations with variants in the HLA-A, HLA-DPB1 and HLA-DRB1 loci. We also demonstrate that the ERAP1 SNP rs30187 association is not restricted only to carriers of HLA-B*27 but also found in HLA-B*40:01 carriers independently of HLA-B*27 genotype.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We also demonstrate that the ERAP1 SNP rs30187 association is not restricted only to carriers of HLA-B*27 but also found in HLA-B*40:01 carriers independently of HLA-B*27 genotype.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 366, "doc_id": "13956305", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Polymeal nutrition reduces cardiovascular mortality.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Polymeal: a more natural, safer, and probably tastier (than the Polypill) strategy to reduce cardiovascular disease by more than 75%.\nABSTRACT: OBJECTIVE Although the Polypill concept (proposed in 2003) is promising in terms of benefits for cardiovascular risk management, the potential costs and adverse effects are its main pitfalls. The objective of this study was to identify a tastier and safer alternative to the Polypill: the Polymeal. METHODS Data on the ingredients of the Polymeal were taken from the literature. The evidence based recipe included wine, fish, dark chocolate, fruits, vegetables, garlic, and almonds. Data from the Framingham heart study and the Framingham offspring study were used to build life tables to model the benefits of the Polymeal in the general population from age 50, assuming multiplicative correlations. RESULTS Combining the ingredients of the Polymeal would reduce cardiovascular disease events by 76%. For men, taking the Polymeal daily represented an increase in total life expectancy of 6.6 years, an increase in life expectancy free from cardiovascular disease of 9.0 years, and a decrease in life expectancy with cardiovascular disease of 2.4 years. The corresponding differences for women were 4.8, 8.1, and 3.3 years. CONCLUSION The Polymeal promises to be an effective, non-pharmacological, safe, cheap, and tasty alternative to reduce cardiovascular morbidity and increase life expectancy in the general population.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSION The Polymeal promises to be an effective, non-pharmacological, safe, cheap, and tasty alternative to reduce cardiovascular morbidity and increase life expectancy in the general population.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 960, "doc_id": "8780599", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Surgical treatment is not superior to non-surgical in treating adults with displaced fractures of the proximal humerus.\n\nCANDIDATE_ABSTRACT:\nTITLE: Surgical vs nonsurgical treatment of adults with displaced fractures of the proximal humerus: the PROFHER randomized clinical trial.\nABSTRACT: IMPORTANCE The need for surgery for the majority of patients with displaced proximal humeral fractures is unclear, but its use is increasing. OBJECTIVE To evaluate the clinical effectiveness of surgical vs nonsurgical treatment for adults with displaced fractures of the proximal humerus involving the surgical neck. DESIGN, SETTING, AND PARTICIPANTS A pragmatic, multicenter, parallel-group, randomized clinical trial, the Proximal Fracture of the Humerus Evaluation by Randomization (PROFHER) trial, recruited 250 patients aged 16 years or older (mean age, 66 years [range, 24-92 years]; 192 [77%] were female; and 249 [99.6%] were white) who presented at the orthopedic departments of 32 acute UK National Health Service hospitals between September 2008 and April 2011 within 3 weeks after sustaining a displaced fracture of the proximal humerus involving the surgical neck. Patients were followed up for 2 years (up to April 2013) and 215 had complete follow-up data. The data for 231 patients (114 in surgical group and 117 in nonsurgical group) were included in the primary analysis. INTERVENTIONS Fracture fixation or humeral head replacement were performed by surgeons experienced in these techniques. Nonsurgical treatment was sling immobilization. Standardized outpatient and community-based rehabilitation was provided to both groups. MAIN OUTCOMES AND MEASURES Primary outcome was the Oxford Shoulder Score (range, 0-48; higher scores indicate better outcomes) assessed during a 2-year period, with assessment and data collection at 6, 12, and 24 months. Sample size was based on a minimal clinically important difference of 5 points for the Oxford Shoulder Score. Secondary outcomes were the Short-Form 12 (SF-12), complications, subsequent therapy, and mortality. RESULTS Th [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"P = .18); the mean SF-12 mental component score (surgical group: 1.28 points lower [95% CI, -3.80 to 1.23 points]; P = .32); complications related to surgery or shoulder fracture (30 patients in surgical group vs 23 patients in nonsurgical group; P = .28), requiring secondary surgery to the shoulder (11 patients in both groups), and increased or new shoulder-related therapy (7 patients vs 4 patients, respectively; P = .58); and mortality (9 patients vs 5 patients; P = .27).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1115, "doc_id": "44048701", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Sympathetic nerve activity is reduced throughout normal pregnancy.\n\nCANDIDATE_ABSTRACT:\nTITLE: The twin-arginine translocation (Tat) protein export pathway\nABSTRACT: The twin-arginine translocation (Tat) protein export system is present in the cytoplasmic membranes of most bacteria and archaea and has the highly unusual property of transporting fully folded proteins. The system must therefore provide a transmembrane pathway that is large enough to allow the passage of structured macromolecular substrates of different sizes but that maintains the impermeability of the membrane to ions. In the Gram-negative bacterium Escherichia coli, this complex task can be achieved by using only three small membrane proteins: TatA, TatB and TatC. In this Review, we summarize recent advances in our understanding of how this remarkable machine operates.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1120, "doc_id": "1320137", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Excess gestational weight gain is associated with obesity-related pregnancy outcomes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effects of interventions in pregnancy on maternal weight and obstetric outcomes: meta-analysis of randomised evidence\nABSTRACT: OBJECTIVE To evaluate the effects of dietary and lifestyle interventions in pregnancy on maternal and fetal weight and to quantify the effects of these interventions on obstetric outcomes. DESIGN Systematic review and meta-analysis. DATA SOURCES Major databases from inception to January 2012 without language restrictions. STUDY SELECTION Randomised controlled trials that evaluated any dietary or lifestyle interventions with potential to influence maternal weight during pregnancy and outcomes of pregnancy. DATA SYNTHESIS Results summarised as relative risks for dichotomous data and mean differences for continuous data. RESULTS We identified 44 relevant randomised controlled trials (7278 women) evaluating three categories of interventions: diet, physical activity, and a mixed approach. Overall, there was 1.42 kg reduction (95% confidence interval 0.95 to 1.89 kg) in gestational weight gain with any intervention compared with control. With all interventions combined, there were no significant differences in birth weight (mean difference -50 g, -100 to 0 g) and the incidence of large for gestational age (relative risk 0.85, 0.66 to 1.09) or small for gestational age (1.00, 0.78 to 1.28) babies between the groups, though by itself physical activity was associated with reduced birth weight (mean difference -60 g, -120 to -10 g). Interventions were associated with a reduced the risk of pre-eclampsia (0.74, 0.60 to 0.92) and shoulder dystocia (0.39, 0.22 to 0.70), with no significant effect on other critically important outcomes. Dietary intervention resulted in the largest reduction in maternal gestational weight gain (3.84 kg, 2.45 to 5.22 kg), with improved pregnancy outcomes compared with other interventions. The overall evidence rating was low to very low for i [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Interventions were associated with a reduced the risk of pre-eclampsia (0.74, 0.60 to 0.92) and shoulder dystocia (0.39, 0.22 to 0.70), with no significant effect on other critically important outcomes.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 394, "doc_id": "11360768", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Nigerian physicians constitue the largest component of sub-Saharan Africa-trained physicians in the United States.\n\nCANDIDATE_ABSTRACT:\nTITLE: Physician Emigration from Sub-Saharan Africa to the United States: Analysis of the 2011 AMA Physician Masterfile\nABSTRACT: BACKGROUND The large-scale emigration of physicians from sub-Saharan Africa (SSA) to high-income nations is a serious development concern. Our objective was to determine current emigration trends of SSA physicians found in the physician workforce of the United States. METHODS AND FINDINGS We analyzed physician data from the World Health Organization (WHO) Global Health Workforce Statistics along with graduation and residency data from the 2011 American Medical Association Physician Masterfile (AMA-PM) on physicians trained or born in SSA countries who currently practice in the US. We estimated emigration proportions, year of US entry, years of practice before emigration, and length of time in the US. According to the 2011 AMA-PM, 10,819 physicians were born or trained in 28 SSA countries. Sixty-eight percent (n = 7,370) were SSA-trained, 20% (n = 2,126) were US-trained, and 12% (n = 1,323) were trained outside both SSA and the US. We estimated active physicians (age ≤ 70 years) to represent 96% (n = 10,377) of the total. Migration trends among SSA-trained physicians increased from 2002 to 2011 for all but one principal source country; the exception was South Africa whose physician migration to the US decreased by 8% (-156). The increase in last-decade migration was >50% in Nigeria (+1,113) and Ghana (+243), >100% in Ethiopia (+274), and >200% (+244) in Sudan. Liberia was the most affected by migration to the US with 77% (n = 175) of its estimated physicians in the 2011 AMA-PM. On average, SSA-trained physicians have been in the US for 18 years. They practiced for 6.5 years before US entry, and nearly half emigrated during the implementation years (1984-1999) of the structural adjustment programs. CONCLUSION Physician emigration from SSA to the US is increasi [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 848, "doc_id": "14500725", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Pseudogene PTENP1 encodes a transcript that regulates PTEN expression.\n\nCANDIDATE_PASSAGE:\nGenetic alterations and their relationship in the phosphatidylinositol 3-kinase/Akt pathway in thyroid cancer. PURPOSE To investigate the overall occurrence and relationship of genetic alterations in the phosphatidylinositol 3-kinase (PI3K)/Akt pathway in thyroid tumors and explore the scope of this pathway as a therapeutic target for thyroid cancer. EXPERIMENTAL DESIGN We examined collectively the major genetic alterations and their relationship in this pathway, including PIK3CA copy number gain and mutation, Ras mutation, and PTEN mutation, in a large series of primary thyroid tumors. RESULTS Occurrence of any of these genetic alterations was found in 25 of 81 (31%) benign thyroid adenoma (BTA), 47 of 86 (55%) follicular thyroid cancer (FTC), 21 of 86 (24%) papillary thyroid cancer (PTC), and 29 of 50 (58%) anaplastic thyroid cancer (ATC), with FTC and ATC most frequently harboring these genetic alterations. PIK3CA copy gain was associated with increased PIK3CA protein expression. A mutual exclusivity among these genetic alterations was seen in BTA, FTC, and PTC, suggesting an independent role of each of them through the PI3K/Akt pathway in the tumorigenesis of the differentiated thyroid tumors. However, coexistence of these genetic alterations was increasingly seen with progression from differentiated tumor to undifferentiated ATC. Their coexistence with BRAF mutation was also frequent in PTC and ATC. CONCLUSIONS The data provide strong genetic implication that aberrant activation of PI3K/Akt pathway plays an extensive role in thyroid tumorigenesis, particularly in FTC and ATC, and promotes progression of BTA to FTC and to ATC as the genetic alterations of this pathway accumulate. Progression of PTC to ATC may be facilitated by coexistence of PI3K/Akt pat [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "984", "doc_id": "21551568", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Antiretroviral therapy reduces rates of tuberculosis across a broad range of CD4 strata.\n\nCANDIDATE_PASSAGE:\nPlasmid-encoded proinsulin preserves C-peptide while specifically reducing proinsulin-specific CD8⁺ T cells in type 1 diabetes. In type 1 diabetes (T1D), there is an intense inflammatory response that destroys the β cells in the pancreatic islets of Langerhans, the site where insulin is produced and released. A therapy for T1D that targets the specific autoimmune response in this disease while leaving the remainder of the immune system intact, has long been sought. Proinsulin is a major target of the adaptive immune response in T1D. We hypothesized that an engineered DNA plasmid encoding proinsulin (BHT-3021) would preserve β cell function in T1D patients through reduction of insulin-specific CD8⁺ T cells. We studied 80 subjects over 18 years of age who were diagnosed with T1D within the past 5 years. Subjects were randomized 2:1 to receive intramuscular injections of BHT-3021 or BHT-placebo, weekly for 12 weeks, and then monitored for safety and immune responses in a blinded fashion. Four dose levels of BHT-3021 were evaluated: 0.3, 1.0, 3.0, and 6.0 mg. C-peptide was used both as an exploratory efficacy measure and as a safety measure. Islet-specific CD8⁺ T cell frequencies were assessed with multimers of monomeric human leukocyte antigen class I molecules loaded with peptides from pancreatic and unrelated antigens. No serious adverse events related to BHT-3021 were observed. C-peptide levels improved relative to placebo at all doses, at 1 mg at the 15-week time point (+19.5% BHT-3021 versus -8.8% BHT-placebo, P < 0.026). Proinsulin-reactive CD8⁺ T cells, but not T cells against unrelated islet or foreign molecules, declined in the BHT-3021 arm (P < 0.006). No significant changes were noted in interferon-γ, interleukin-4 (IL-4), or IL-10 production in CD4 [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "124", "doc_id": "23342845", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does iGF-I bioactivity better reflect growth hormone deficiency than total IGF-I?\n\nABSTRACT:\nGH is considered the main regulator of circulating IGF-I. Total (extractable) IGF-I is therefore routinely used for diagnosis of GH deficiency (GHD) and for monitoring treatment. Methods currently used for measurement of circulating total IGF-I may be hampered by interferences of IGF-binding proteins. Recently a kinase receptor activation assay was developed to determine IGF-I bioactivity in human serum. The principle of this assay is based on quantification of IGF-I receptor activation after stimulation with serum in vitro. The objective of the study was to investigate the diagnostic potential of IGF-I bioactivity in adults with GHD. This was a single-center observational study. Ninety-four GH-untreated patients diagnosed with GHD by GH-provocative tests were included. IGF-I bioactivity (determined by the IGF-I kinase receptor activation assay) and total IGF-I (determined by immunoassay) were measured in fasting blood samples. IGF-I bioactivity was more frequently below the normal range (<-2 sd) in untreated GH-deficient patients than total IGF-I levels (81.9 vs. 61.7%, respectively), especially in patients older than 40 years of age. IGF-I bioactivity decreased with the duration of GHD, whereas total IGF-I did not. With a decreasing number of additional pituitary deficits, total IGF-I levels more frequently remained within the normal range, whereas the percentage below the normal range was high for IGF-I bioactivity, independent of additional deficits.", "output": "{\"label\": \"yes\", \"rationale\": \"Determination of IGF-I bioactivity may offer advantages in the evaluation of adult GHD compared with total IGF-I as bioactivity better reflects GHD as defined by GH stimulation tests, especially in subjects older than 40 years of age.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 21565786, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Bone marrow cells contribute to adult macrophage compartments.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tissue-resident macrophages self-maintain locally throughout adult life with minimal contribution from circulating monocytes.\nABSTRACT: Despite accumulating evidence suggesting local self-maintenance of tissue macrophages in the steady state, the dogma remains that tissue macrophages derive from monocytes. Using parabiosis and fate-mapping approaches, we confirmed that monocytes do not show significant contribution to tissue macrophages in the steady state. Similarly, we found that after depletion of lung macrophages, the majority of repopulation occurred by stochastic cellular proliferation in situ in a macrophage colony-stimulating factor (M-Csf)- and granulocyte macrophage (GM)-CSF-dependent manner but independently of interleukin-4. We also found that after bone marrow transplantation, host macrophages retained the capacity to expand when the development of donor macrophages was compromised. Expansion of host macrophages was functional and prevented the development of alveolar proteinosis in mice transplanted with GM-Csf-receptor-deficient progenitors. Collectively, these results indicate that tissue-resident macrophages and circulating monocytes should be classified as mononuclear phagocyte lineages that are independently maintained in the steady state.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We also found that after bone marrow transplantation, host macrophages retained the capacity to expand when the development of donor macrophages was compromised.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 183, "doc_id": "12827098", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Microglia are an innate immune cell type of the central nervous system.\n\nCANDIDATE_ABSTRACT:\nTITLE: Gestational protein restriction affects trophoblast differentiation.\nABSTRACT: Whether and how gestational protein restriction (PR) affects placental development and function remain unknown. To test the hypothesis that PR can affect trophoblast differentiation in mid-and late pregnancy, rats were fed a 20% or an isocaloric 6% protein diet from Day 1 to 14 or 18 of pregnancy and effects of PR on trophoblast differentiation were determined by changes in expressions of marker gene(s) for trophoblast lineages. At Day 18 of pregnancy, PR increased expressions of Esrrb, Id1 andId2 (trophoblast stem cell markers), decreased expressions of Ascl2 (spongiotrophblast cell marker) and Prl2c1 (trophoblast giant cell marker), but did not alter expressions of Gjb3 and Pcdh12(glycogen cell markers) in the junctional zone (JZ). In the labyrinth zone (LZ), PR did not change expressions of Prl2b1 (trophoblast giant cell marker), Gcm1 and Syna (syncytiotrophoblast cell markers), but decrease expression of Ctsq (sinusoidal trophoblast giant cell marker). These results indicate that PR impairs the differentiation of trophoblast stem cell into spongiotrophoblast and trophoblast giant cells in JZ, and formation of sinusoidal trophoblast giant cells in LZ.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 789, "doc_id": "1449692", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Cancer cells can stimulate the accumulation of intra-tumoural myeloid-derived suppressor cells by promoting granulocyte colony stimulating factor production.\n\nCANDIDATE_PASSAGE:\nCENP-B Controls Centromere Formation Depending on the Chromatin Context The centromere is a chromatin region that serves as the spindle attachment point and directs accurate inheritance of eukaryotic chromosomes during cell divisions. However, the mechanism by which the centromere assembles and stabilizes at a specific genomic region is not clear. The de novo formation of a human/mammalian artificial chromosome (HAC/MAC) with a functional centromere assembly requires the presence of alpha-satellite DNA containing binding motifs for the centromeric CENP-B protein. We demonstrate here that de novo centromere assembly on HAC/MAC is dependent on CENP-B. In contrast, centromere formation is suppressed in cells expressing CENP-B when alpha-satellite DNA was integrated into a chromosomal site. Remarkably, on those integration sites CENP-B enhances histone H3-K9 trimethylation and DNA methylation, thereby stimulating heterochromatin formation. Thus, we propose that CENP-B plays a dual role in centromere formation, ensuring de novo formation on DNA lacking a functional centromere but preventing the formation of excess centromeres on chromosomes.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "223", "doc_id": "15960670", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: De novo assembly of sequence data has fewer specific contigs than unassembled sequence data.\n\nCANDIDATE_PASSAGE:\nIdentification of T6SS-dependent effector and immunity proteins by Tn-seq in Vibrio cholerae. Type VI protein secretion system (T6SS) is important for bacterial competition through contact-dependent killing of competitors. T6SS delivers effectors to neighboring cells and corresponding antagonistic proteins confer immunity against effectors that are delivered by sister cells. Although T6SS has been found in more than 100 gram-negative bacteria including many important human pathogens, few T6SS-dependent effector and immunity proteins have been experimentally determined. Here we report a high-throughput approach using transposon mutagenesis and deep sequencing (Tn-seq) to identify T6SS immunity proteins in Vibrio cholerae. Saturating transposon mutagenesis was performed in wild type and a T6SS null mutant. Genes encoding immunity proteins were predicted to be essential in the wild type but dispensable in the T6SS mutant. By comparing the relative abundance of each transposon mutant in the mutant library using deep sequencing, we identified three immunity proteins that render protection against killing by T6SS predatory cells. We also identified their three cognate T6SS-secreted effectors and show these are important for not only antibacterial and antieukaryotic activities but also assembly of T6SS apparatus. The lipase and muramidase T6SS effectors identified in this study underscore the diversity of T6SS-secreted substrates and the distinctly different mechanisms that target these for secretion by the dynamic T6SS organelle.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "310", "doc_id": "22632303", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: \"Would a man smell a rose then throw it away?\n\nABSTRACT:\nBreast cancer is the most common malignancy afflicting women, and the most common cancer overall in Jordan. A woman's decision to go for screening is influenced by her social support network. This study aims to explore Jordanian men's individual and contextual perspectives on women's breast cancer and their own role in the breast health of the females within their families. An explorative qualitative design was used to purposively recruit 24 married men aged 27 to 65 years (median 43 years) from four governorates in Jordan. Data in the form of interviews transcriptions was subjected to qualitative content analysis. Three themes were identified: a) Supporting one's wife; b) Marital needs and obligations; c) Constrained by a culture of destiny and shame. The first theme was built on men's feelings of responsibility for the family's health and well-being, their experiences of encouraging their wives to seek health care and their providing counselling and instrumental support. The second theme emerged from men's views about other men's rejection of a wife inflicted by breast cancer, their own perceptions of diminished femininity due to mastectomy and their own concerns about protecting the family from the hereditary risk of breast cancer. The third theme was seen in men's perception of breast cancer as an inevitable act of God that is far away from one's own family, in associating breast cancer with improper behaviour and in their readiness to face the culture of Eib (shame).", "output": "{\"label\": \"maybe\", \"rationale\": \"Jordanian men perceive themselves as having a vital role in supporting, guiding and encouraging their wives to follow breast cancer early detection recommendations. Breast health awareness campaigns could involve husbands to capitalize on family support.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 24160268, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Migraine with aura is associated with ischemic stroke.\n\nCANDIDATE_PASSAGE:\nThe effect of folate fortification on folic acid-based homocysteine-lowering intervention and stroke risk: a meta-analysis. OBJECTIVE Folate and vitamin B12 are two vital regulators in the metabolic process of homocysteine, which is a risk factor of atherothrombotic events. Low folate intake or low plasma folate concentration is associated with increased stroke risk. Previous randomized controlled trials presented discordant findings in the effect of folic acid supplementation-based homocysteine lowering on stroke risk. The aim of the present review was to perform a meta-analysis of relevant randomized controlled trials to check the how different folate fortification status might affect the effects of folic acid supplementation in lowering homocysteine and reducing stroke risk. DESIGN Relevant randomized controlled trials were identified through formal literature search. Homocysteine reduction was compared in subgroups stratified by folate fortification status. Relative risks with 95 % confidence intervals were used as a measure to assess the association between folic acid supplementation and stroke risk. SETTING The meta-analysis included fourteen randomized controlled trials, SUBJECTS A total of 39 420 patients. RESULTS Homocysteine reductions were 26·99 (sd 1·91) %, 18·38 (sd 3·82) % and 21·30 (sd 1·98) %, respectively, in the subgroups without folate fortification, with folate fortification and with partial folate fortification. Significant difference was observed between the subgroups with folate fortification and without folate fortification (P=0·05). The relative risk of stroke was 0·88 (95 % CI 0·77, 1·00, P=0·05) in the subgroup without folate fortification, 0·94 (95 % CI 0·58, 1·54, P=0·82) in the subgroup with folate fortification and 0·91 (95 % C [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "791", "doc_id": "37424881", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is diffuse axonal injury ( DAI ) associated with elevated intracranial pressure ( ICP )?\n\nABSTRACT:\nTraditionally, intracranial pressure (ICP) monitoring has been utilized in all patients with severe head injury (Glasgow coma score of 3-8). Ventriculostomy placement, however, does carry a 4 to 10 percent complication rate consisting mostly of hematoma and infection. The authors propose that a subgroup of patients presenting with severe head trauma and diffuse axonal injury without associated mass lesion, do not need ICP monitoring. Additionally, the monitoring data from ICP, MAP, and CPP for a comparison severe head injury group, and subgroups of DAI would be presented. Thirty-six patients sustaining blunt head trauma and fitting our strict clinical and radiographic diagnosis of DAI were enrolled in our study. Inclusion criteria were severe head injury patients who did not regain consciousness after the initial impact, and whose CT scan demonstrated characteristic punctate hemorrhages of < 10 mm diameter at the greywhite junction, basal ganglia, corpus callosum, upper brainstem, or a combination of the above. Patients with significant mass lesions and documented anoxia were excluded. Their intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were compared to a control group of 36 consecutive patients with severe non-penetrating non-operative head injury, using the Analysis for Variance method. Eighteen (50.0%), six (16.7%), and twelve (33.3%) patients had types I, II, and III DAI, respectively. The admission Glasgow Coma Score (GCS) was higher for types I and II than for type III DAI. ICP was monitored from 23 to 165 hours, with a mean ICP for 36 patients of 11.70 mmHg (SEM = 0.75) and a range from 4.3 to 17.3 mmHg. Of all ICP recordings, of which 89.7%, (2421/2698) were < or = 20 mmHg. Average mean arterial pressure (MAP) was 96.08 mmHg (SEM [TRUNCATED]", "output": "{\"label\": \"no\", \"rationale\": \"The authors conclude that ICP elevation in DAI patients without associated mass lesions is not as prevalent as other severe head injured patients, therefore ICP monitoring may not be as critical. The presence of an ICP monitoring device may contribute to increased morbidity. Of key importance, however, is an accurate clinical history and interpretation of the CT scan.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 9522906, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does shaving the incision site increase the infection rate after spinal surgery?\n\nABSTRACT:\nA prospective randomized clinical study. To determine whether shaving the incision site before spinal surgery causes postsurgical infection. Spine surgeons usually shave the skin of the incision site immediately before surgery is performed. However, evidence from some surgical series suggests that presurgical shaving may increase the postsurgical infection rate. To our knowledge, no previously published studies have addressed this issue. A total of 789 patients scheduled to undergo spinal surgery were randomly allocated into 2 groups: those in whom the site of operation was shaved immediately before surgery (shaved group; 371 patients) and the patients in whom presurgical shaving was not performed (unshaved group; 418 patients). The mean duration of anesthesia and the infection rates in both groups were recorded and compared. The duration of anesthesia did not differ in the 2 groups (P>0.05). A postoperative infection developed in 4 patients in the shaved group and in 1 patient in the nonshaved group (P<0.01).", "output": "{\"label\": \"maybe\", \"rationale\": \"The shaving of the incision site immediately before spinal surgery may increase the rate of postoperative infection.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 17621202, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Dscam1 acts as a hypervariable pattern-recognition receptor for the immune system.\n\nCANDIDATE_ABSTRACT:\nTITLE: AgDscam, a Hypervariable Immunoglobulin Domain-Containing Receptor of the Anopheles gambiae Innate Immune System \nABSTRACT: Activation of the insect innate immune system is dependent on a limited number of pattern recognition receptors (PRRs) capable of interacting with pathogen-associated molecular pattern. Here we report a novel role of an alternatively spliced hypervariable immunoglobulin domain-encoding gene, Dscam, in generating a broad range of PRRs implicated in immune defense in the malaria vector Anopheles gambiae. The mosquito Down syndrome cell adhesion molecule gene, AgDscam, has a complex genome organization with 101 exons that can produce over 31,000 potential alternative splice forms with different combinations of adhesive domains and interaction specificities. AgDscam responds to infection by producing pathogen challenge-specific splice form repertoires. Transient silencing of AgDscam compromises the mosquito's resistance to infections with bacteria and the malaria parasite Plasmodium. AgDscam is mediating phagocytosis of bacteria with which it can associate and defend against in a splice form–specific manner. AgDscam is a hypervariable PRR of the A. gambiae innate immune system.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"AgDscam is a hypervariable PRR of the A. gambiae innate immune system.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 356, "doc_id": "6144337", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Guanine nucleotide dissociation inhibitor (Rho-GDI) interacts with the p75 NTR death domain\n\nCANDIDATE_ABSTRACT:\nTITLE: Gamma-Secretase Represents a Therapeutic Target for the Treatment of Invasive Glioma Mediated by the p75 Neurotrophin Receptor\nABSTRACT: The multifunctional signaling protein p75 neurotrophin receptor (p75(NTR)) is a central regulator and major contributor to the highly invasive nature of malignant gliomas. Here, we show that neurotrophin-dependent regulated intramembrane proteolysis (RIP) of p75(NTR) is required for p75(NTR)-mediated glioma invasion, and identify a previously unnamed process for targeted glioma therapy. Expression of cleavage-resistant chimeras of p75(NTR) or treatment of animals bearing p75(NTR)-positive intracranial tumors with clinically applicable gamma-secretase inhibitors resulted in dramatically decreased glioma invasion and prolonged survival. Importantly, proteolytic processing of p75(NTR) was observed in p75(NTR)-positive patient tumor specimens and brain tumor initiating cells. This work highlights the importance of p75(NTR) as a therapeutic target, suggesting that gamma-secretase inhibitors may have direct clinical application for the treatment of malignant glioma.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 481, "doc_id": "14706752", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is ankle/arm pressure predictive for cardiovascular mortality in older patients living in nursing homes?\n\nABSTRACT:\nlongitudinal descriptive study. 2 large nursing homes in Turin, Italy. 418 dependent elderly (83 males, 335 females, mean age 83.7+/-8.5 y, range 55-102) living in the nursing homes. the prevalence of peripheral arterial disease (PAD) was evaluated using a Doppler Ultrasound measurement of AAI (Ankle/Arm blood pressure Index). Death causes according to ICD-9-CM were ascertained on patient's clinical records. Diagnosis of PAD was made in 122 subjects (29.2%) with AAI<0.90. After a 3 year follow-up 203 patients (48.6%) died. The presence of PAD was not related to total mortality or to mortality for ischemic heart disease (IHD), cerebrovascular disease or other causes. IHD mortality was significantly and independently related to low haemoglobin values, previous cerebrovascular disease, polypharmacy and poor mobility conditions.", "output": "{\"label\": \"no\", \"rationale\": \"The prevalence of PAD is high in nursing home residents. AAI is not predictive for IHD mortality in this population. In very frail elderly traditional risk factors and PAD are less important predictors of death compared to poor functional status, nutritional factors and previous cardiovascular disease.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 12855939, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Osteocytes have an essential role in G-CSF induced HSPC mobilization.\n\nCANDIDATE_PASSAGE:\nTransglutaminase 2 Undergoes a Large Conformational Change upon Activation Human transglutaminase 2 (TG2), a member of a large family of enzymes that catalyze protein crosslinking, plays an important role in the extracellular matrix biology of many tissues and is implicated in the gluten-induced pathogenesis of celiac sprue. Although vertebrate transglutaminases have been studied extensively, thus far all structurally characterized members of this family have been crystallized in conformations with inaccessible active sites. We have trapped human TG2 in complex with an inhibitor that mimics inflammatory gluten peptide substrates and have solved, at 2-A resolution, its x-ray crystal structure. The inhibitor stabilizes TG2 in an extended conformation that is dramatically different from earlier transglutaminase structures. The active site is exposed, revealing that catalysis takes place in a tunnel, bridged by two tryptophan residues that separate acyl-donor from acyl-acceptor and stabilize the tetrahedral reaction intermediates. Site-directed mutagenesis was used to investigate the acyl-acceptor side of the tunnel, yielding mutants with a marked increase in preference for hydrolysis over transamidation. By providing the ability to visualize this activated conformer, our results create a foundation for understanding the catalytic as well as the non-catalytic roles of TG2 in biology, and for dissecting the process by which the autoantibody response to TG2 is induced in celiac sprue patients.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "893", "doc_id": "13578199", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Nasal fractures: is closed reduction satisfying?\n\nABSTRACT:\nThis study aims to evaluate the efficacy of closed reduction and the effects of timing and fracture types on patient satisfaction. Only patients with isolated nasal fractures were included in the study. Patients with additional maxillofacial fractures and patients whose application time to our clinic was more than 10 days after the trauma were excluded. Patients were classified into 5 types according to their fracture. All patients underwent closed reduction and external fixation under local anesthesia. Patients were asked about their satisfaction in a survey at 28th day and sixth month after the surgery. Patients were divided into groups according to fracture type and intervention time, and the results of the survey were evaluated. Of the 43 patients included in the study, 38 were male, 5 were female, and the average age was 24.9. The average intervention time of the patients was 5.44 days. Twenty-eight (65%) of 43 patients were satisfied with the result, whereas 15 (35%) patients were not happy with their operation. In a comparison of patient satisfaction rates according to fracture type, the mild fracture group had a higher satisfaction rate compared to the severe fracture group.", "output": "{\"label\": \"yes\", \"rationale\": \"Closed reduction is an easy and sufficient treatment for nasal fractures, especially for mild nasal fractures. Early intervention raises the patient satisfaction rate.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 23348330, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Gene expression does not vary appreciably across genetically identical cells.\n\nCANDIDATE_PASSAGE:\nGenome-wide identification of genes directly regulated by the pleiotropic transcription factor Spx in Bacillus subtilis The transcriptional regulator Spx plays a key role in maintaining the redox homeostasis of Bacillus subtilis cells exposed to disulfide stress. Defects in Spx were previously shown to lead to differential expression of numerous genes but direct and indirect regulatory effects could not be distinguished. Here we identified 283 discrete chromosomal sites potentially bound by the Spx-RNA polymerase (Spx-RNAP) complex using chromatin immunoprecipitation of Spx. Three quarters of these sites were located near Sigma(A)-dependent promoters, and upon diamide treatment, the fraction of the Spx-RNAP complex increased in parallel with the number and occupancy of DNA sites. Correlation of Spx-RNAP-binding sites with gene differential expression in wild-type and Δspx strains exposed or not to diamide revealed that 144 transcription units comprising 275 genes were potentially under direct Spx regulation. Spx-controlled promoters exhibited an extended -35 box in which nucleotide composition at the -43/-44 positions strongly correlated with observed activation. In vitro transcription confirmed activation by oxidized Spx of seven newly identified promoters, of which one was also activated by reduced Spx. Our study globally characterized the Spx regulatory network, revealing its role in the basal expression of some genes and its complex interplay with other stress responses.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "452", "doc_id": "17416520", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Articles published in open access format are less likely to be cited than traditional journals.\n\nCANDIDATE_ABSTRACT:\nTITLE: Open Access Increases Citation Rate\nABSTRACT: PLoS Biology publishes today a research article by Gunther Eysenbach that is not about biology. It is about citations. It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles. As such, it adds objective support to the belief we have always held that open-access publication speeds up scientific dialog between researchers and, consequently, should be extended to the whole scientific literature as quickly as possible. It is therefore fitting that we publish such a paper. We have long argued that papers freely available in a journal will be more often read and cited than those behind a subscription barrier. However, solid evidence to support or refute such a claim has been surprisingly hard to find. Since most open-access journals are new, comparisons of the effects of open access with established subscription-based journals are easily confounded by age and reputation. In the current study, Eysenbach compared citations compiled by Thomson Scientific (formerly Thomson ISI) to individual articles published between June 2004 and December 2004 in the same journal—namely, Proceedings of the National Academy of Sciences (PNAS), which announced its open-access option for authors on June 8 of that year, with an associated publication charge of US$1,000. Non-OA articles in PNAS are subject to a six-month “toll-access” delay before the article becomes publicly available. The results of this natural experiment are clear: in the 4 to 16 months following publication, OA articles gained a significant citation advantage over non-OA articles during the same period. They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely between 10 and 16 months. Given that P [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely between 10 and 16 months.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 129, "doc_id": "27768226", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Mice defective for deoxyribonucleic acid (DNA) polymerase I (polI) fail to reveal increased sensitivity to ionizing radiation (IR).\n\nCANDIDATE_ABSTRACT:\nTITLE: Nonoverlapping functions of DNA polymerases mu, lambda, and terminal deoxynucleotidyltransferase during immunoglobulin V(D)J recombination in vivo.\nABSTRACT: DNA polymerases mu (pol mu), lambda (pol lambda), and terminal deoxynucleotidyltransferase (TdT) are enzymes of the pol X family that share homology in sequence and functional domain organization. We showed previously that pol mu participates in light chain but surprisingly not heavy chain gene rearrangement. We show here that immunoglobulin heavy chain junctions from pol lambda-deficient animals have shorter length with normal N-additions, thus indicating that pol lambda is recruited during heavy chain rearrangement at a step that precedes the action of TdT. In contrast to previous in vitro studies, analysis of animals with combined inactivation of these enzymes revealed no overlapping or compensatory activities for V(D)J recombination between pol mu, pol lambda, and TdT. This complex usage of polymerases with distinct catalytic specificities may correspond to the specific function that the third hypervariable region assumes for each immunoglobulin chain, with pol lambda maintaining a large heavy chain junctional heterogeneity and pol mu ensuring a restricted light chain junctional variability.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 774, "doc_id": "32275758", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The PPR MDA5 has two N-terminal CARD domains.\n\nCANDIDATE_ABSTRACT:\nTITLE: Immune signaling by RIG-I-like receptors.\nABSTRACT: The RIG-I-like receptors (RLRs) RIG-I, MDA5, and LGP2 play a major role in pathogen sensing of RNA virus infection to initiate and modulate antiviral immunity. The RLRs detect viral RNA ligands or processed self RNA in the cytoplasm to trigger innate immunity and inflammation and to impart gene expression that serves to control infection. Importantly, RLRs cooperate in signaling crosstalk networks with Toll-like receptors and other factors to impart innate immunity and to modulate the adaptive immune response. RLR regulation occurs at a variety of levels ranging from autoregulation to ligand and cofactor interactions and posttranslational modifications. Abberant RLR signaling or dysregulation of RLR expression is now implicated in the development of autoimmune diseases. Understanding the processes of RLR signaling and response will provide insights to guide RLR-targeted therapeutics for antiviral and immune-modifying applications.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1175, "doc_id": "31272411", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: cSMAC formation enhances weak ligand signalling.\n\nCANDIDATE_PASSAGE:\nPituitary adenylate cyclase-activating polypeptide (PACAP(1-38)) enhances N-methyl-D-aspartate receptor function and brain-derived neurotrophic factor expression via RACK1. We recently identified a novel mechanism for modulation of the phosphorylation state and function of the N-methyl-d-aspartate (NMDA) receptor via the scaffolding protein RACK1. We found that RACK1 binds both the NR2B subunit of the NMDA receptor and the nonreceptor protein-tyrosine kinase, Fyn. RACK1 inhibits Fyn phosphorylation of NR2B and decreases NMDA receptor-mediated currents in CA1 hippocampal slices (Yaka, R., Thornton, C., Vagts, A. J., Phamluong, K., Bonci, A., and Ron, D. (2002) Proc. Natl. Acad. Sci. U. S. A. 99, 5710-5715). Here, we identified the signaling cascade by which RACK1 is released from the NMDA receptor complex and identified the consequences of the dissociation. We found that activation of the cAMP/protein kinase A pathway in hippocampal slices induced the release of RACK1 from NR2B and Fyn. This resulted in the induction of NR2B phosphorylation and the enhancement of NMDA receptor-mediated activity via Fyn. We identified the neuropeptide, pituitary adenylate cyclase activating polypeptide (PACAP(1-38)), as a ligand that induced phosphorylation of NR2B and enhanced NMDA receptor potentials. Finally, we found that activation of the cAMP/protein kinase A pathway induced the movement of RACK1 to the nuclear compartment in dissociated hippocampal neurons. Nuclear RACK1 in turn was found to regulate the expression of brain-derived neurotrophic factor induced by PACAP(1-38). Taken together our results suggest that activation of adenylate cyclase by PACAP(1-38) results in the release of RACK1 from the NMDA receptor and Fyn. This in turn leads to NMDA receptor phosphoryla [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1385", "doc_id": "23076291", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The relationship between a breast cancer patient's capacity to metabolize tamoxifen and treatment outcome is independent of the patient's genetic make-up.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association between CYP2D6 polymorphisms and outcomes among women with early stage breast cancer treated with tamoxifen.\nABSTRACT: CONTEXT The growth inhibitory effect of tamoxifen, which is used for the treatment of hormone receptor-positive breast cancer, is mediated by its metabolites, 4-hydroxytamoxifen and endoxifen. The formation of active metabolites is catalyzed by the polymorphic cytochrome P450 2D6 (CYP2D6) enzyme. OBJECTIVE To determine whether CYP2D6 variation is associated with clinical outcomes in women receiving adjuvant tamoxifen. DESIGN, SETTING, AND PATIENTS Retrospective analysis of German and US cohorts of patients treated with adjuvant tamoxifen for early stage breast cancer. The 1325 patients had diagnoses between 1986 and 2005 of stage I through III breast cancer and were mainly postmenopausal (95.4%). Last follow-up was in December 2008; inclusion criteria were hormone receptor positivity, no metastatic disease at diagnosis, adjuvant tamoxifen therapy, and no chemotherapy. DNA from tumor tissue or blood was genotyped for CYP2D6 variants associated with reduced (*10, *41) or absent (*3, *4, *5) enzyme activity. Women were classified as having an extensive (n=609), heterozygous extensive/intermediate (n=637), or poor (n=79) CYP2D6 metabolism. MAIN OUTCOME MEASURES Time to recurrence, event-free survival, disease-free survival, and overall survival. RESULTS Median follow-up was 6.3 years. At 9 years of follow-up, the recurrence rates were 14.9% for extensive metabolizers, 20.9% for heterozygous extensive/intermediate metabolizers, and 29.0% for poor metabolizers, and all-cause mortality rates were 16.7%, 18.0%, and 22.8%, respectively. Compared with extensive metabolizers, there was a significantly increased risk of recurrence for heterozygous extensive/intermediate metabolizers (time to recurrence adjusted hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.04 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSION Among women with breast cancer treated with tamoxifen, there was an association between CYP2D6 variation and clinical outcomes, such that the presence of 2 functional CYP2D6 alleles was associated with better clinical outcomes and the presence of nonfunctional or reduced-function alleles with worse outcomes.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1260, "doc_id": "24341590", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: DRD1 proteins enable Pol V transcription in vivo.\n\nCANDIDATE_PASSAGE:\nEarly lymphocyte expansion is severely impaired in interleukin 7 receptor-deficient mice Interleukin 7 (IL-7) stimulates the proliferation of B cell progenitors, thymocytes, and mature T cells through an interaction with a high affinity receptor (IL-7R) belonging to the hematopoietin receptor superfamily. We have further addressed the role of IL-7 and its receptor during B and T cell development by generating mice genetically deficient in IL-7R. Mutant mice display a profound reduction in thymic and peripheral lymphoid cellularity. Analyses of lymphoid progenitor populations in IL-7R-deficient mice define precisely those developmental stages affected by the mutation and reveal a critical role for IL-7R during early lymphoid development. Significantly, these studies indicate that the phase of thymocyte expansion occurring before the onset of T cell receptor gene rearrangement is critically dependent upon, and mediated by the high affinity receptor for IL-7.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "305", "doc_id": "9160947", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Birth-weight is positively associated with breast cancer.\n\nCANDIDATE_PASSAGE:\nIntegrated molecular genetic profiling of pediatric high-grade gliomas reveals key differences with the adult disease. PURPOSE To define copy number alterations and gene expression signatures underlying pediatric high-grade glioma (HGG). PATIENTS AND METHODS We conducted a high-resolution analysis of genomic imbalances in 78 de novo pediatric HGGs, including seven diffuse intrinsic pontine gliomas, and 10 HGGs arising in children who received cranial irradiation for a previous cancer using single nucleotide polymorphism microarray analysis. Gene expression was analyzed with gene expression microarrays for 53 tumors. Results were compared with publicly available data from adult tumors. RESULTS Significant differences in copy number alterations distinguish childhood and adult glioblastoma. PDGFRA was the predominant target of focal amplification in childhood HGG, including diffuse intrinsic pontine gliomas, and gene expression analyses supported an important role for deregulated PDGFRalpha signaling in pediatric HGG. No IDH1 hotspot mutations were found in pediatric tumors, highlighting molecular differences with adult secondary glioblastoma. Pediatric and adult glioblastomas were clearly distinguished by frequent gain of chromosome 1q (30% v 9%, respectively) and lower frequency of chromosome 7 gain (13% v 74%, respectively) and 10q loss (35% v 80%, respectively). PDGFRA amplification and 1q gain occurred at significantly higher frequency in irradiation-induced tumors, suggesting that these are initiating events in childhood gliomagenesis. A subset of pediatric HGGs showed minimal copy number changes. CONCLUSION Integrated molecular profiling showed substantial differences in the molecular features underlying pediatric and adult HGG, indicating that findings [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "179", "doc_id": "2360905", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: AMP-activated protein kinase (AMPK) activation increases inflammation-related fibrosis in the lungs.\n\nCANDIDATE_ABSTRACT:\nTITLE: Metformin reverses established lung fibrosis in a bleomycin model\nABSTRACT: Fibrosis is a pathological result of a dysfunctional repair response to tissue injury and occurs in a number of organs, including the lungs1. Cellular metabolism regulates tissue repair and remodelling responses to injury2-4. AMPK is a critical sensor of cellular bioenergetics and controls the switch from anabolic to catabolic metabolism5. However, the role of AMPK in fibrosis is not well understood. Here, we demonstrate that in humans with idiopathic pulmonary fibrosis (IPF) and in an experimental mouse model of lung fibrosis, AMPK activity is lower in fibrotic regions associated with metabolically active and apoptosis-resistant myofibroblasts. Pharmacological activation of AMPK in myofibroblasts from lungs of humans with IPF display lower fibrotic activity, along with enhanced mitochondrial biogenesis and normalization of sensitivity to apoptosis. In a bleomycin model of lung fibrosis in mice, metformin therapeutically accelerates the resolution of well-established fibrosis in an AMPK-dependent manner. These studies implicate deficient AMPK activation in non-resolving, pathologic fibrotic processes, and support a role for metformin (or other AMPK activators) to reverse established fibrosis by facilitating deactivation and apoptosis of myofibroblasts.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"These studies implicate deficient AMPK activation in non-resolving, pathologic fibrotic processes, and support a role for metformin (or other AMPK activators) to reverse established fibrosis by facilitating deactivation and apoptosis of myofibroblasts.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 54, "doc_id": "49556906", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The ureABIEFGH gene cluster encodes urease maturation proteins : UreD/UreH, UreE, UreF, and UreG.\n\nCANDIDATE_ABSTRACT:\nTITLE: Structure of the proton-gated urea channel from the gastric pathogen Helicobacter pylori\nABSTRACT: Half the world's population is chronically infected with Helicobacter pylori, causing gastritis, gastric ulcers and an increased incidence of gastric adenocarcinoma. Its proton-gated inner-membrane urea channel, HpUreI, is essential for survival in the acidic environment of the stomach. The channel is closed at neutral pH and opens at acidic pH to allow the rapid access of urea to cytoplasmic urease. Urease produces NH(3) and CO(2), neutralizing entering protons and thus buffering the periplasm to a pH of roughly 6.1 even in gastric juice at a pH below 2.0. Here we report the structure of HpUreI, revealing six protomers assembled in a hexameric ring surrounding a central bilayer plug of ordered lipids. Each protomer encloses a channel formed by a twisted bundle of six transmembrane helices. The bundle defines a previously unobserved fold comprising a two-helix hairpin motif repeated three times around the central axis of the channel, without the inverted repeat of mammalian-type urea transporters. Both the channel and the protomer interface contain residues conserved in the AmiS/UreI superfamily, suggesting the preservation of channel architecture and oligomeric state in this superfamily. Predominantly aromatic or aliphatic side chains line the entire channel and define two consecutive constriction sites in the middle of the channel. Mutation of Trp 153 in the cytoplasmic constriction site to Ala or Phe decreases the selectivity for urea in comparison with thiourea, suggesting that solute interaction with Trp 153 contributes specificity. The previously unobserved hexameric channel structure described here provides a new model for the permeation of urea and other small amide solutes in prokaryotes and archaea.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1280, "doc_id": "4387784", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Having a main partner improves HIV outcomes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\nABSTRACT: OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART). DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study). SETTING Seven outpatient clinics throughout Switzerland. PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years). MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound. RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion. When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership. In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without. Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression. CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 495, "doc_id": "17077004", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Reduced levels of lipolysis leads to higher P38 phosphorylation in adipose tissue.\n\nCANDIDATE_PASSAGE:\nLoss of fibronectin from the aged stem cell niche affects the regenerative capacity of skeletal muscle in mice Age-related changes in the niche have long been postulated to impair the function of somatic stem cells. Here we demonstrate that the aged stem cell niche in skeletal muscle contains substantially reduced levels of fibronectin (FN), leading to detrimental consequences for the function and maintenance of muscle stem cells (MuSCs). Deletion of the gene encoding FN from young regenerating muscles replicates the aging phenotype and leads to a loss of MuSC numbers. By using an extracellular matrix (ECM) library screen and pathway profiling, we characterize FN as a preferred adhesion substrate for MuSCs and demonstrate that integrin-mediated signaling through focal adhesion kinase and the p38 mitogen-activated protein kinase pathway is strongly de-regulated in MuSCs from aged mice because of insufficient attachment to the niche. Reconstitution of FN levels in the aged niche remobilizes stem cells and restores youth-like muscle regeneration. Taken together, we identify the loss of stem cell adhesion to FN in the niche ECM as a previously unknown aging mechanism.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1025", "doc_id": "19912367", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Physical activity level is associated with the difference in maximal oxygen consumption between black and white youth.\n\nCANDIDATE_PASSAGE:\nHistone chaperones: 30 years from isolation to elucidation of the mechanisms of nucleosome assembly and disassembly Some three decades have passed since the discovery of nucleosomes in 1974 and the first isolation of a histone chaperone in 1978. While various types of histone chaperones have been isolated and functionally analyzed, the elementary processes of nucleosome assembly and disassembly have been less well characterized. Recently, the tertiary structure of a hetero-trimeric complex composed of the histone chaperone CIA/ASF1 and the histone H3-H4 dimer was determined, and this complex was proposed to be an intermediate in nucleosome assembly and disassembly reactions. In addition, CIA alone was biochemically shown to dissociate the histone (H3-H4)2 tetramer into two histone H3-H4 dimers. This activity suggested that CIA regulates the semi-conservative replication of nucleosomes. Here, we provide an overview of prominent histone chaperones with the goal of elucidating the mechanisms that preserve and modify epigenetic information. We also discuss the reactions involved in nucleosome assembly and disassembly.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "946", "doc_id": "20781656", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Do resistance profiles of coagulase-negative staphylococci contaminating blood cultures predict pathogen resistance and patient mortality?\n\nABSTRACT:\nBlood culture isolates are the cornerstone of adequate antibiotic treatment. However, many blood cultures are contaminated with bacteria residing on the skin, the most common contaminants being coagulase-negative staphylococci (CoNS). Such contaminated cultures are mostly disregarded. In this retrospective study, we show that contaminated cultures contain diagnostic information. We tested the association between resistance profiles of CoNS contaminants and those of the actual infecting bacteria isolated subsequently from the same patient, as well as their association with short-term mortality. We identified all patients in Rabin Medical Center, Israel, with positive blood cultures during 2009-12. Data included patient demographics, hospitalization records, comorbidities, blood culture results and date of death. Our cohort consists of 2518 patients with 5290 blood cultures, where 1124 patients had 1664 blood cultures with CoNS contaminants. High overall CoNS resistance predicted high overall resistance of the subsequent bacterial isolates (P<0.004 and P<0.0006, for Gram-positive and -negative bacteria, respectively). Moreover, the resistance of CoNS contaminants to a specific antibiotic predicted the resistance of the subsequent bacterial isolates to that antibiotic (OR=5.55, 95% CI=3.54-8.66, P<10(-15) and OR=2.47, 95% CI=1.61-3.78, P<3 ×10(-5), for Gram-positive and -negative bacteria, respectively). Finally, highly resistant CoNS isolates were associated with higher short-term mortality (hazard ratio=1.71, 95% CI=1.4-2.11, P<10(-6)).", "output": "{\"label\": \"yes\", \"rationale\": \"Resistance patterns of CoNS contaminants predict specific and overall resistance of subsequent blood culture isolates and short-term mortality. These results may help predict patient mortality and correct empirical antibiotic therapy if blood cultures yield contaminant bacteria and imply that skin commensals may serve as an additional, non-invasive, diagnostic tool.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 24855122, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does timing of initial surfactant treatment make a difference in rates of chronic lung disease or mortality in premature infants?\n\nABSTRACT:\nTo compare two treatment strategies in preterm infants with or at risk of respiratory distress syndrome: early surfactant administration (within one hour of birth) versus late surfactant administration, in a geographically defined population. The primary outcome was chronic lung disease (CLD) and mortality before/at 36 weeks. Secondary outcomes included: duration of mechanical ventilation and continuous positive airway pressure (CPAP), post-natal steroids for CLD and major neonatal morbidities. Premature infants born at 22-32 weeks' gestation between January 2006 and December 2009. Ten neonatal intensive care units (NICUs) in New South Wales (NSW) and Australian Capital Territory (ACT), Australia. Retrospective analysis of prospectively collected data from the regional NICU database in NSW and ACT. Of the 2170 infants who received surfactant, 1182 (54.5%) and 988 (45.5%) received early and late surfactant, respectively. The early surfactant group was less mature (27.1 ± 2.1 versus 29.4 ± 2.1 weeks) and had more CLD and mortality (40.2% versus 20.0%). The multivariable analysis showed early surfactant to be associated with less duration of ventilation, longer duration of CPAP and longer hospital stay but had little or no impact on CLD/mortality.", "output": "{\"label\": \"maybe\", \"rationale\": \"Early surfactant administration is associated with shorter duration of ventilation but does not appear to be significantly protective against CLD/mortality among premature infants. This may support the growing evidence for consideration of CPAP as an alternative to routine intubation and early surfactant administration. Further investigation from large randomized clinical trials is warranted to confirm these results.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 25394614, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Malaria has a high vectorial capacity.\n\nCANDIDATE_ABSTRACT:\nTITLE: Ranking of elimination feasibility between malaria-endemic countries\nABSTRACT: Experience gained from the Global Malaria Eradication Program (1955-72) identified a set of shared technical and operational factors that enabled some countries to successfully eliminate malaria. Spatial data for these factors were assembled for all malaria-endemic countries and combined to provide an objective, relative ranking of countries by technical, operational, and combined elimination feasibility. The analysis was done separately for Plasmodium falciparum and Plasmodium vivax, and the limitations of the approach were discussed. The relative rankings suggested that malaria elimination would be most feasible in countries in the Americas and Asia, and least feasible in countries in central and west Africa. The results differed when feasibility was measured by technical or operational factors, highlighting the different types of challenge faced by each country. The results are not intended to be prescriptive, predictive, or to provide absolute assessments of feasibility, but they do show that spatial information is available to facilitate evidence-based assessments of the relative feasibility of malaria elimination by country that can be rapidly updated.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 753, "doc_id": "1173667", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does acute renal failure worsen in-hospital outcomes in patients with intracerebral hemorrhage?\n\nABSTRACT:\nOccurrence of acute renal failure (ARF) is more common in patients with intracerebral hemorrhage (ICH) compared with those with other stroke subtypes. We sought to determine the frequency and effect of ARF on in-hospital outcomes of patients with ICH. We analyzed data from all patients admitted to the United States' hospitals between 2005 and 2011 with the primary discharge diagnosis of ICH and secondary diagnosis of ARF. The associations of ARF with mortality and discharge outcomes in ICH patients were analyzed after adjusting for potential confounders using logistic regression analyses. Of the 614,454 patients admitted with ICH, 41,694 (6.8%) had ARF. In-hospital dialysis was required in 700 (1.7%) patients. ICH patients with ARF had higher rates of moderate-to-severe disability (49.5% versus 44.2%; P < .0001) and in-hospital mortality (28.7% versus 22.4%; P < .0001) compared with those without ARF. After adjusting for age, gender, and potential confounders defined as statistically significant variables on univariate analysis, ICH patients with ARF had higher odds of moderate-to-severe disability (odds ratio [OR] 1.2; 95% confidence interval [CI], 1.1-1.3; P < .0001) and death (OR, 1.5; 95% CI, 1.4-1.6; P < .0001). The rates of moderate-to-severe disability and death were 37.5% and 50.2% among those who required dialysis, respectively.", "output": "{\"label\": \"yes\", \"rationale\": \"In patients with ICH, ARF is associated with significantly higher rates of in-hospital mortality and moderate-to-severe disability at the time of discharge.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25680664, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Human embryonic stem cells have the capacity to give rise to differentiated progeny representative of all three embryonic germ layers.\n\nCANDIDATE_ABSTRACT:\nTITLE: Evidence of a pluripotent human embryonic stem cell line derived from a cloned blastocyst.\nABSTRACT: Somatic cell nuclear transfer (SCNT) technology has recently been used to generate animals with a common genetic composition. In this study, we report the derivation of a pluripotent embryonic stem (ES) cell line (SCNT-hES-1) from a cloned human blastocyst. The SCNT-hES-1 cells displayed typical ES cell morphology and cell surface markers and were capable of differentiating into embryoid bodies in vitro and of forming teratomas in vivo containing cell derivatives from all three embryonic germ layers in severe combined immunodeficient mice. After continuous proliferation for more than 70 passages, SCNT-hES-1 cells maintained normal karyotypes and were genetically identical to the somatic nuclear donor cells. Although we cannot completely exclude the possibility that the cells had a parthenogenetic origin, imprinting analyses support a SCNT origin of the derived human ES cells.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The SCNT-hES-1 cells displayed typical ES cell morphology and cell surface markers and were capable of differentiating into embryoid bodies in vitro and of forming teratomas in vivo containing cell derivatives from all three embryonic germ layers in severe combined immunodeficient mice.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 531, "doc_id": "10546779", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: ScPif1p has higher binding ability to G-rich ssDNA than to non-G-rich ssDNA.\n\nCANDIDATE_PASSAGE:\nMyocardial muscarinic receptor upregulation and normal response to isoproterenol in denervated hearts by familial amyloid polyneuropathy. BACKGROUND Patients with familial amyloid polyneuropathy, a rare hereditary form of amyloidosis, have progressive autonomic neuropathy. The disease usually does not induce heart failure but is associated with sudden death, conduction disturbances, and an increased risk of complications during anesthesia. Although cardiac sympathetic denervation has been clearly demonstrated, the postsynaptic status of the cardiac autonomic nervous system remains unelucidated. METHODS AND RESULTS Twenty-one patients were studied (age, 39+/-11 years; normal coronary arteries; left ventricular ejection fraction 68+/-9%). To evaluate the density and affinity constants of myocardial muscarinic receptors, PET with (11)C-MQNB (methylquinuclidinyl benzilate), a specific hydrophilic antagonist, was used. Cardiac beta-receptor functional efficiency was studied by the heart rate (HR) response to intravenous infusion of isoproterenol (5 minutes after 2 mg of atropine, 5, 10, and 15 ng/kg per minute during 5 minutes per step). The mean muscarinic receptor density was higher in patients than in control subjects (B'(max), 35.5+/-8.9 versus 26.1+/-6.7 pmol/mL, P=0.003), without change in receptor affinity. The increase in HR after injection of atropine as well as of MQNB was lower in patients compared with control subjects despite a similar basal HR (DeltaHR after atropine, 11+/-21% versus 62+/-17%; P<0.001), consistent with parasympathetic denervation. Incremental infusion of isoproterenol induced a similar increase in HR in patients and control subjects. CONCLUSIONS Cardiac autonomic denervation in familial amyloid polyneuropathy results in an upregulat [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1067", "doc_id": "1686881", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The morphology change from large white adipocytes to small brown adipocytes is a sign of increased energy expenditure potential in white adipose tissue.\n\nCANDIDATE_PASSAGE:\nClonal hematopoiesis of indeterminate potential and its distinction from myelodysplastic syndromes. Recent genetic analyses of large populations have revealed that somatic mutations in hematopoietic cells leading to clonal expansion are commonly acquired during human aging. Clonally restricted hematopoiesis is associated with an increased risk of subsequent diagnosis of myeloid or lymphoid neoplasia and increased all-cause mortality. Although myelodysplastic syndromes (MDS) are defined by cytopenias, dysplastic morphology of blood and marrow cells, and clonal hematopoiesis, most individuals who acquire clonal hematopoiesis during aging will never develop MDS. Therefore, acquisition of somatic mutations that drive clonal expansion in the absence of cytopenias and dysplastic hematopoiesis can be considered clonal hematopoiesis of indeterminate potential (CHIP), analogous to monoclonal gammopathy of undetermined significance and monoclonal B-cell lymphocytosis, which are precursor states for hematologic neoplasms but are usually benign and do not progress. Because mutations are frequently observed in healthy older persons, detection of an MDS-associated somatic mutation in a cytopenic patient without other evidence of MDS may cause diagnostic uncertainty. Here we discuss the nature and prevalence of CHIP, distinction of this state from MDS, and current areas of uncertainty regarding diagnostic criteria for myeloid malignancies.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1236", "doc_id": "5782614", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Noninvasive positive pressure ventilation is not predictive of acute respiratory failure after solid organ transplantation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Noninvasive ventilation for treatment of acute respiratory failure in patients undergoing solid organ transplantation: a randomized trial.\nABSTRACT: CONTEXT Noninvasive ventilation (NIV) has been associated with lower rates of endotracheal intubation in populations of patients with acute respiratory failure. OBJECTIVE To compare NIV with standard treatment using supplemental oxygen administration to avoid endotracheal intubation in recipients of solid organ transplantation with acute hypoxemic respiratory failure. DESIGN AND SETTING Prospective randomized study conducted at a 14-bed, general intensive care unit of a university hospital. PATIENTS Of 238 patients who underwent solid organ transplantation from December 1995 to October 1997, 51 were treated for acute respiratory failure. Of these, 40 were eligible and 20 were randomized to each group. INTERVENTION Noninvasive ventilation vs standard treatment with supplemental oxygen administration. MAIN OUTCOME MEASURES The need for endotracheal intubation and mechanical ventilation at any time during the study, complications not present on admission, duration of ventilatory assistance, length of hospital stay, and intensive care unit mortality. RESULTS The 2 groups were similar at study entry. Within the first hour of treatment, 14 patients (70%) in the NIV group, and 5 patients (25%) in the standard treatment group improved their ratio of the PaO2 to the fraction of inspired oxygen (FIO2). Over time, a sustained improvement in PaO2 to FIO2 was noted in 12 patients (60%) in the NIV group, and in 5 patients (25%) randomized to standard treatment (P = .03). The use of NIV was associated with a significant reduction in the rate of endotracheal intubation (20% vs 70%; P = .002), rate of fatal complications (20% vs 50%; P = .05), length of stay in the intensive care unit by survivors (mean [SD] days, 5.5 [3] vs 9 [4]; P = .03), and intensive care unit mortality [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The use of NIV was associated with a significant reduction in the rate of endotracheal intubation (20% vs 70%; P = .002), rate of fatal complications (20% vs 50%; P = .05), length of stay in the intensive care unit by survivors (mean [SD] days, 5.5 [3] vs 9 [4]; P = .03), and intensive care unit mortality (20% vs 50%; P = .05).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 855, "doc_id": "8190282", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: PrimPol degrades short DNA replication intermediates on the leading strand during DNA replication.\n\nCANDIDATE_PASSAGE:\nThe Bloom's syndrome helicase promotes the annealing of complementary single-stranded DNA The product of the gene mutated in Bloom's syndrome, BLM, is a 3′–5′ DNA helicase belonging to the highly conserved RecQ family. In addition to a conventional DNA strand separation activity, BLM catalyzes both the disruption of non-B-form DNA, such as G-quadruplexes, and the branch migration of Holliday junctions. Here, we have characterized a new activity for BLM: the promotion of single-stranded DNA (ssDNA) annealing. This activity does not require Mg2+, is inhibited by ssDNA binding proteins and ATP, and is dependent on DNA length. Through analysis of various truncation mutants of BLM, we show that the C-terminal domain is essential for strand annealing and identify a 60 amino acid stretch of this domain as being important for both ssDNA binding and strand annealing. We present a model in which the ssDNA annealing activity of BLM facilitates its role in the processing of DNA intermediates that arise during repair of damaged replication forks.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "969", "doc_id": "16217855", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Many proteins in human cells can be post-translationally modified at lysine residues via acetylation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Protein Lysine Acetylated/Deacetylated Enzymes and the Metabolism-Related Diseases\nABSTRACT: Lysine acetylation is a reversible posttranslational modifcation, an epigenetic phenomenon, referred to as transfer of an acetyl group from acetyl CoA to lysine e- amino group of targeted protein, which is modulated by acetyltransferases (histone/ lysine (K) acetyltransferases, HATs/KATs) and deacetylases (histone/lysine (K) deacetylases, HDACs/KDACs). Lysine acetylation regulates various metabolic processes, such as fatty acid oxidation, Krebs cycle, oxidative phosphorylation, angiogenesis and so on. Thus disorders of lysine acetylation may be correlated with obesity, diabetes and cardiovascular disease, which are termed as the metabolic complication. With accumulating studies on proteomic acetylation, lysine acetylation also involves in cell immune status and degenerative diseases, for example, Alzheimer’s disease and Huntington’s disease. This review primarily summarizes the current studies of lysine acetylation in metabolism modulation and in metabolism-related diseases, such as cardiovascular disease and fat metabolism disorder.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Lysine acetylation is a reversible posttranslational modifcation, an epigenetic phenomenon, referred to as transfer of an acetyl group from acetyl CoA to lysine e- amino group of targeted protein, which is modulated by acetyltransferases (histone/ lysine (K) acetyltransferases, HATs/KATs) and deacetylases (histone/lysine (K) deacetylases, HDACs/KDACs).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 756, "doc_id": "2831620", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Traditional reviews are biased in their interpretations.\n\nCANDIDATE_PASSAGE:\nFindings to date from the ASCUS-LSIL Triage Study (ALTS). Controversy exists in the United States regarding the proper evaluation and management of low-grade squamous intraepithelial lesion (LSIL) and equivocal (atypical squamous cells of undetermined significance [ASCUS, now ASC-US]) cervical cytologic interpretations. To address this issue, the National Cancer Institute initiated the ASCUS-LSIL Triage Study (ALTS). ALTS is a multicenter, randomized clinical trial designed to evaluate 3 alternative methods of management, namely, immediate colposcopy, cytologic follow-up, and triage by human papillomavirus (HPV) DNA testing. This article summarizes the major findings of ALTS that have been published to date. Patients with ASCUS (n = 3488) or LSIL (n = 1572) were randomly assigned to research arms between November 1996 and December 1998, and were monitored for 2 years. The disease outcome was histologic cervical intraepithelial neoplasia (CIN) 3/cancer. The prevalence of oncogenic HPV was too high to permit effective triage of LSIL using HPV DNA testing by Hybrid Capture 2. However, for the women referred with a cytologic interpretation of ASCUS, HPV triage proved useful, with sensitivity equivalent to immediate colposcopy and a halving of colposcopic referrals. Among older women with ASCUS, HPV testing remained sensitive for detecting CIN 3 and cancer, but the referral percentage was dramatically lower compared to younger women. ALTS yielded insight into the performance of cytology and histopathology; experienced pathologists differed significantly in their interpretations of cervical abnormalities, especially histologic CIN 1 and cytologic ASCUS. Nonetheless, it was possible to distinguish a relatively uncommon type of ASCUS, equivocal for high-grade squamo [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1310", "doc_id": "20422174", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Anthrax spores can be disposed of easily after they are dispersed.\n\nCANDIDATE_PASSAGE:\nSecondary aerosolization of viable Bacillus anthracis spores in a contaminated US Senate Office. CONTEXT Bioterrorist attacks involving letters and mail-handling systems in Washington, DC, resulted in Bacillus anthracis (anthrax) spore contamination in the Hart Senate Office Building and other facilities in the US Capitol's vicinity. OBJECTIVE To provide information about the nature and extent of indoor secondary aerosolization of B anthracis spores. DESIGN Stationary and personal air samples, surface dust, and swab samples were collected under semiquiescent (minimal activities) and then simulated active office conditions to estimate secondary aerosolization of B anthracis spores. Nominal size characteristics, airborne concentrations, and surface contamination of B anthracis particles (colony-forming units) were evaluated. RESULTS Viable B anthracis spores reaerosolized under semiquiescent conditions, with a marked increase in reaerosolization during simulated active office conditions. Increases were observed for B anthracis collected on open sheep blood agar plates (P<.001) and personal air monitors (P =.01) during active office conditions. More than 80% of the B anthracis particles collected on stationary monitors were within an alveolar respirable size range of 0.95 to 3.5 micro m. CONCLUSIONS Bacillus anthracis spores used in a recent terrorist incident reaerosolized under common office activities. These findings have important implications for appropriate respiratory protection, remediation, and reoccupancy of contaminated office environments.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "115", "doc_id": "33872649", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does rugby headgear prevent concussion?\n\nABSTRACT:\nTo examine the attitudes of players and coaches to the use of protective headgear, particularly with respect to the prevention of concussion. A questionnaire designed to assess attitudes to headgear was administered to 63 players from four different Canadian teams, each representing a different level of play (high school, university, community club, national). In addition, coaches from all four levels were questioned about team policies and their personal opinions about the use of headgear to prevent concussion. Although the players tended to believe that the headgear could prevent concussion (62%), the coaches were less convinced (33%). Despite the players' belief that headgear offers protection against concussion, only a minority reported wearing headgear (27%) and few (24%) felt that its use should be made mandatory. Common reasons for not wearing headgear were \"its use is not mandatory\", \"it is uncomfortable\", and \"it costs too much\".", "output": "{\"label\": \"maybe\", \"rationale\": \"Although most players in the study believe that rugby headgear may prevent concussion, only a minority reported wearing it. Coaches tended to be less convinced than the players that rugby headgear can prevent concussion.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 11867487, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Alteration of origin firing causes changes in termination zones of Okazaki fragments.\n\nCANDIDATE_PASSAGE:\nMechanical regulation of cell function with geometrically modulated elastomeric substrates We report the establishment of a library of micromolded elastomeric micropost arrays to modulate substrate rigidity independently of effects on adhesive and other material surface properties. We demonstrated that micropost rigidity impacts cell morphology, focal adhesions, cytoskeletal contractility and stem cell differentiation. Furthermore, early changes in cytoskeletal contractility predicted later stem cell fate decisions in single cells.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "105", "doc_id": "17388232", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Birth-weight is negatively associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Role of birthweight in the etiology of breast cancer.\nABSTRACT: Breast cancer may originate in utero. We reviewed the available evidence on the association between birthweight and the risk of breast cancer. To date, 26 research papers addressing this issue have been published. The majority of studies identified a positive link between birthweight and premenopausal, but not postmenopausal, breast cancer. The relative risk estimate for breast cancer comparing women with high birthweight to women with low birthweight combining all studies including both pre- and postmenopausal breast cancer was 1.23 (95% confidence interval 1.13-1.34). The mechanisms underlying this association likely include elevated levels of growth factors that may increase the number of susceptible stem cells in the mammary gland or initiate tumors through DNA mutations. Loss of imprinting (LOI) of growth hormone genes relevant for intrauterine growth, such as insulin-like growth factor 2 (IGF2), leads to abnormally high levels of these hormones evidenced by high birthweight. LOI of IGF2 has also been found in mammary tumor tissue. The role of environmental factors that stimulate such epigenetic regulation of gene expression remains to be elucidated.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The relative risk estimate for breast cancer comparing women with high birthweight to women with low birthweight combining all studies including both pre- and postmenopausal breast cancer was 1.23 (95% confidence interval 1.13-1.34).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 178, "doc_id": "27123743", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Ribosomopathies have a low degree of cell and tissue specific pathology.\n\nCANDIDATE_PASSAGE:\nFinding the right niche: B-cell migration in the early phases of T-dependent antibody responses. Humoral immune responses depend on B cells encountering antigen, interacting with helper T cells, proliferating and differentiating into low-affinity plasma cells or, after organizing into a germinal center (GC), high-affinity plasma cells and memory B cells. Remarkably, each of these events occurs in association with distinct stromal cells in separate subcompartments of the lymphoid tissue. B cells must migrate from niche to niche in a rapid and highly regulated manner to successfully mount a response. The chemokine, CXCL13, plays a central role in guiding B cells to follicles whereas T-zone chemokines guide activated B cells to the T zone. Sphingosine-1-phosphate (S1P) promotes cell egress from the tissue, as well as marginal-zone B-cell positioning in the spleen. Recent studies have identified a role for the orphan receptor, EBV-induced molecule 2 (EBI2; GPR183), in guiding activated B cells to inter and outer follicular niche(s) and down-regulation of this receptor is essential for organizing cells into GCs. In this review, we discuss current understanding of the roles played by chemokines, S1P and EBI2 in the migration events that underlie humoral immune responses.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1049", "doc_id": "38587347", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Citrullinated proteins externalized in neutrophil extracellular traps act indirectly to disrupt the inflammatory cycle.\n\nCANDIDATE_PASSAGE:\nNetting neutrophils are major inducers of type I IFN production in pediatric systemic lupus erythematosus. Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by a breakdown of tolerance to nuclear antigens and the development of immune complexes. Genomic approaches have shown that human SLE leukocytes homogeneously express type I interferon (IFN)-induced and neutrophil-related transcripts. Increased production and/or bioavailability of IFN-α and associated alterations in dendritic cell (DC) homeostasis have been linked to lupus pathogenesis. Although neutrophils have long been shown to be associated with lupus, their potential role in disease pathogenesis remains elusive. Here, we show that mature SLE neutrophils are primed in vivo by type I IFN and die upon exposure to SLE-derived anti-ribonucleoprotein antibodies, releasing neutrophil extracellular traps (NETs). SLE NETs contain DNA as well as large amounts of LL37 and HMGB1, neutrophil proteins that facilitate the uptake and recognition of mammalian DNA by plasmacytoid DCs (pDCs). Indeed, SLE NETs activate pDCs to produce high levels of IFN-α in a DNA- and TLR9 (Toll-like receptor 9)-dependent manner. Our results reveal an unsuspected role for neutrophils in SLE pathogenesis and identify a novel link between nucleic acid-recognizing antibodies and type I IFN production in this disease.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "263", "doc_id": "28015516", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Comparative transcriptome analysis identified new platelet proteins with structural features suggesting a role in platelet function.\n\nCANDIDATE_PASSAGE:\nThe ‘definitive’ (and ‘primitive’) guide to zebrafish hematopoiesis Progressive advances using zebrafish as a model organism have provided hematologists with an additional genetic system to study blood cell formation and hematological malignancies. Despite extensive evolutionary divergence between bony fish (teleosts) and mammals, the molecular pathways governing hematopoiesis have been highly conserved. As a result, most (if not all) of the critical hematopoietic transcription factor genes identified in mammals have orthologues in zebrafish. As in other vertebrates, all of the teleost blood lineages are believed to originate from a pool of pluripotent, self-renewing hematopoietic stem cells. Here, we provide a detailed review of the timing, anatomical location, and transcriptional regulation of zebrafish ‘primitive’ and ‘definitive’ hematopoiesis as well as discuss a model of T-cell leukemia and recent advances in blood cell transplantation. Given that many of the regulatory genes that control embryonic hematopoiesis have been implicated in oncogenic pathways in adults, an understanding of blood cell ontogeny is likely to provide insights into the pathophysiology of human leukemias.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "280", "doc_id": "30152134", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Bactericidal activity of 3 cutaneous/mucosal antiseptic solutions in the presence of interfering substances: Improvement of the NF EN 13727 European Standard?\n\nABSTRACT:\nThere is no standard protocol for the evaluation of antiseptics used for skin and mucous membranes in the presence of interfering substances. Our objective was to suggest trial conditions adapted from the NF EN 13727 standard, for the evaluation of antiseptics used in gynecology and dermatology. Three antiseptic solutions were tested in vitro: a chlorhexidine-benzalkonium (CB) combination, a hexamidine-chlorhexidine-chlorocresol (HCC) combination, and povidone iodine (P). The adaptation of trial conditions to the standard involved choosing dilutions, solvent, and interfering substances. The activity of solutions was assessed on the recommended strains at concentrations of 97% (pure solution), 50%, and 10% (diluted solution), and 1%. A logarithmic reduction ≥ 5 was expected after 60seconds of contact, to meet requirements of bactericidal activity. HCC did not present any bactericidal activity except on P. aeruginosa at a concentration of 97%. P was not bactericidal on E. hirae at any concentration and on S. aureus at 97%. CB had the most homogeneous bactericidal activity with a reduction>5 log on the 4 bacterial strains at concentrations of 97%, 50% and 10%.", "output": "{\"label\": \"maybe\", \"rationale\": \"Adapting the NF EN 13727 standard allowed assessing the 3 tested solutions: only CB was bactericidal in dirty conditions. This study proved the possibility of validating antiseptic choice in vitro, in current practice conditions, for adjunctive treatment of skin and mucous membranes disorders, primarily of bacterial origin or with a potential of superinfection.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 25779009, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Hypocretin neurones induce panicprone state in rats.\n\nCANDIDATE_PASSAGE:\nIn vitro characterization of the anti-PD-1 antibody nivolumab, BMS-936558, and in vivo toxicology in non-human primates. The programmed death-1 (PD-1) receptor serves as an immunologic checkpoint, limiting bystander tissue damage and preventing the development of autoimmunity during inflammatory responses. PD-1 is expressed by activated T cells and downmodulates T-cell effector functions upon binding to its ligands, PD-L1 and PD-L2, on antigen-presenting cells. In patients with cancer, the expression of PD-1 on tumor-infiltrating lymphocytes and its interaction with the ligands on tumor and immune cells in the tumor microenvironment undermine antitumor immunity and support its rationale for PD-1 blockade in cancer immunotherapy. This report details the development and characterization of nivolumab, a fully human IgG4 (S228P) anti-PD-1 receptor-blocking monoclonal antibody. Nivolumab binds to PD-1 with high affinity and specificity, and effectively inhibits the interaction between PD-1 and its ligands. In vitro assays demonstrated the ability of nivolumab to potently enhance T-cell responses and cytokine production in the mixed lymphocyte reaction and superantigen or cytomegalovirus stimulation assays. No in vitro antibody-dependent cell-mediated or complement-dependent cytotoxicity was observed with the use of nivolumab and activated T cells as targets. Nivolumab treatment did not induce adverse immune-related events when given to cynomolgus macaques at high concentrations, independent of circulating anti-nivolumab antibodies where observed. These data provide a comprehensive preclinical characterization of nivolumab, for which antitumor activity and safety have been demonstrated in human clinical trials in various solid tumors.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "536", "doc_id": "1454773", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Exercise increases cancer mortality rates among Chinese citizens.\n\nCANDIDATE_ABSTRACT:\nTITLE: Combined Impact of Lifestyle-Related Factors on Total and Cause-Specific Mortality among Chinese Women: Prospective Cohort Study\nABSTRACT: BACKGROUND Although cigarette smoking, excessive alcohol drinking, obesity, and several other well-studied unhealthy lifestyle-related factors each have been linked to the risk of multiple chronic diseases and premature death, little is known about the combined impact on mortality outcomes, in particular among Chinese and other non-Western populations. The objective of this study was to quantify the overall impact of lifestyle-related factors beyond that of active cigarette smoking and alcohol consumption on all-cause and cause-specific mortality in Chinese women. METHODS AND FINDINGS We used data from the Shanghai Women's Health Study, an ongoing population-based prospective cohort study in China. Participants included 71,243 women aged 40 to 70 years enrolled during 1996-2000 who never smoked or drank alcohol regularly. A healthy lifestyle score was created on the basis of five lifestyle-related factors shown to be independently associated with mortality outcomes (normal weight, lower waist-hip ratio, daily exercise, never exposed to spouse's smoking, higher daily fruit and vegetable intake). The score ranged from zero (least healthy) to five (most healthy) points. During an average follow-up of 9 years, 2,860 deaths occurred, including 775 from cardiovascular disease (CVD) and 1,351 from cancer. Adjusted hazard ratios for mortality decreased progressively with an increasing number of healthy lifestyle factors. Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality. The inverse association between the healthy lifestyle score and mortality was seen consistently regardless of ch [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS In this first study, to our knowledge, to quantify the combined impact of lifestyle-related factors on mortality outcomes in Chinese women, a healthier lifestyle pattern-including being of normal weight, lower central adiposity, participation in physical activity, nonexposure to spousal smoking, and higher fruit and vegetable intake-was associated with reductions in total and cause-specific mortality among lifetime nonsmoking and nondrinking women, supporting the importance of overall lifestyle modification in disease prevention.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 396, "doc_id": "1456068", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is perforation of the appendix a risk factor for tubal infertility and ectopic pregnancy?\n\nABSTRACT:\nTo critically assess the evidence that appendiceal perforation is a risk factor for subsequent tubal infertility or ectopic pregnancy. Epidemiologic studies investigating the relationship between appendectomy and infertility or ectopic pregnancy were identified by searching the MEDLINE database from 1966 to 1997. Appropriate citations were also extracted from a manual search of the bibliographies of selected papers. Twenty-three articles were retrieved. Only 4 presented original data including comparisons to a nonexposed control group and they form the basis for this study. Because the raw data or specific techniques of data analysis were not always explicitly described, indices of risk for exposure were extracted from the data as presented and were analysed without attempting to convert them to a common measure. Articles were assessed according to the criteria of the Evidence-Based Medicine Working Group for evaluating articles on harm. Review of the literature yielded estimates of the risk of adverse fertility outcomes ranging from 1.6 (95% confidence interval [CI] 1.1 to 2.5) for ectopic pregnancy after an appendectomy to 4.8 (95% CI 1.5 to 14.9) for tubal infertility from perforation of the appendix. Recall bias, and poor adjustment for confounding variables in some reports, weakened the validity of the studies.", "output": "{\"label\": \"maybe\", \"rationale\": \"The methodologic weaknesses of the studies do not permit acceptance of increased risk of tubal pregnancy or infertility as a consequence of perforation of the appendix, so a causal relationship cannot be supported by the data currently available. Only a well-designed case-control study with unbiased ascertainment of exposure and adjustment for confounding variables will provide a definitive answer.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 10223070, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In domesticated populations of Saccharomyces cerevisiae, whole chromosome aneuploidy is very uncommon.\n\nCANDIDATE_ABSTRACT:\nTITLE: Domestication and Divergence of Saccharomyces cerevisiae Beer Yeasts\nABSTRACT: Whereas domestication of livestock, pets, and crops is well documented, it is still unclear to what extent microbes associated with the production of food have also undergone human selection and where the plethora of industrial strains originates from. Here, we present the genomes and phenomes of 157 industrial Saccharomyces cerevisiae yeasts. Our analyses reveal that today's industrial yeasts can be divided into five sublineages that are genetically and phenotypically separated from wild strains and originate from only a few ancestors through complex patterns of domestication and local divergence. Large-scale phenotyping and genome analysis further show strong industry-specific selection for stress tolerance, sugar utilization, and flavor production, while the sexual cycle and other phenotypes related to survival in nature show decay, particularly in beer yeasts. Together, these results shed light on the origins, evolutionary history, and phenotypic diversity of industrial yeasts and provide a resource for further selection of superior strains. PAPERCLIP.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 575, "doc_id": "10300888", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The risk of breast cancer among parous women increases with placental weight of pregnancies, and this association is strongest for premenopausal breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pregnancy characteristics and maternal risk of breast cancer.\nABSTRACT: CONTEXT During pregnancy, serum levels of estrogen, progesterone, and other hormones are markedly higher than during other periods of life. Pregnancy hormones primarily are produced in the placenta, and signs of placental impairment may serve as indirect markers of hormone exposures during pregnancy. During pregnancy, these markers have been inconsistently associated with subsequent risk of breast cancer in the mother. OBJECTIVE To examine associations between indirect markers of hormonal exposures, such as placental weight and other pregnancy characteristics, and maternal risk of developing breast cancer. DESIGN AND SETTING Population-based cohort study using data from the Swedish Birth Register, the Swedish Cancer Register, the Swedish Cause of Death Register, and the Swedish Register of Population and Population Changes. PARTICIPANTS Women included in the Sweden Birth Register who delivered singletons between 1982 and 1989, with complete information on date of birth and gestational age. Women were followed up until the occurrence of breast cancer, death, or end of follow-up (December 31, 2001). Cox proportional hazards models were used to estimate associations between hormone exposures and risks of breast cancer. MAIN OUTCOME MEASURE Incidence of invasive breast cancer. RESULTS Of 314,019 women in the cohort, 2216 (0.7%) developed breast cancer during the follow-up through 2001, of whom 2100 (95%) were diagnosed before age 50 years. Compared with women who had placentas weighing less than 500 g in 2 consecutive pregnancies, the risk of breast cancer was increased among women whose placentas weighed between 500 and 699 g in their first pregnancy and at least 700 g in their second pregnancy (or vice versa) (adjusted hazard ratio, 1.82; 95% confidence interv [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Placental weight is positively associated with maternal risk of breast cancer.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1266, "doc_id": "37480103", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Active Ly49Q prevents neutrophil polarization.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Ly49Q receptor plays a crucial role in neutrophil polarization and migration by regulating raft trafficking.\nABSTRACT: Neutrophils rapidly undergo polarization and directional movement to infiltrate the sites of infection and inflammation. Here, we show that an inhibitory MHC I receptor, Ly49Q, was crucial for the swift polarization of and tissue infiltration by neutrophils. During the steady state, Ly49Q inhibited neutrophil adhesion by preventing focal-complex formation, likely by inhibiting Src and PI3 kinases. However, in the presence of inflammatory stimuli, Ly49Q mediated rapid neutrophil polarization and tissue infiltration in an ITIM-domain-dependent manner. These opposite functions appeared to be mediated by distinct use of effector phosphatase SHP-1 and SHP-2. Ly49Q-dependent polarization and migration were affected by Ly49Q regulation of membrane raft functions. We propose that Ly49Q is pivotal in switching neutrophils to their polarized morphology and rapid migration upon inflammation, through its spatiotemporal regulation of membrane rafts and raft-associated signaling molecules.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We propose that Ly49Q is pivotal in switching neutrophils to their polarized morphology and rapid migration upon inflammation, through its spatiotemporal regulation of membrane rafts and raft-associated signaling molecules.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 77, "doc_id": "5531479", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Klf2 is important for proper myeloid cell function.\n\nCANDIDATE_ABSTRACT:\nTITLE: The myeloid transcription factor KLF2 regulates the host response to polymicrobial infection and endotoxic shock.\nABSTRACT: Precise control of myeloid cell activation is required for optimal host defense. However, this activation process must be under exquisite control to prevent uncontrolled inflammation. Herein, we identify the Kruppel-like transcription factor 2 (KLF2) as a potent regulator of myeloid cell activation in vivo. Exposure of myeloid cells to hypoxia and/or bacterial products reduced KLF2 expression while inducing hypoxia inducible factor-1α (HIF-1α), findings that were recapitulated in human septic patients. Myeloid KLF2 was found to be a potent inhibitor of nuclear factor-kappaB (NF-κB)-dependent HIF-1α transcription and, consequently, a critical determinant of outcome in models of polymicrobial infection and endotoxemia. Collectively, these observations identify KLF2 as a tonic repressor of myeloid cell activation in vivo and an essential regulator of the innate immune system.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Collectively, these observations identify KLF2 as a tonic repressor of myeloid cell activation in vivo and an essential regulator of the innate immune system.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 667, "doc_id": "6493422", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: One in two surgical randomized controlled trials are discontinued early.\n\nCANDIDATE_PASSAGE:\nWhat is the best way to help caregivers in cancer and palliative care? A systematic literature review of interventions and their effectiveness. Informal carers in cancer and palliative care are known to have high needs and psychological morbidity, yet a literature review identified few targeted interventions. This systematic review of interventions for carers of patients using home cancer and palliative care services searched Medline, CancerLit, Psycinfo and Cinahl databases. The terms used were carer(s), caregiver(s), palliative and cancer. Papers that reported interventions for adults actively providing informal care for noninstitutionalized cancer and palliative care patients were reviewed. Twenty-two interventions were identified, comprising home nursing care (four), respite services (three), social networks and activity enhancement (two), problem solving and education (three) and group work (10). Of these, nine were delivered solely to carers (i.e., were targeted services). Only six of the carers' interventions had been evaluated, two of these had used a randomized control trial (RCT; grades IB), three employed a single group methodology (two prospective grades IIIC and one retrospective grade IIIC) and one was evaluated using facilitator feedback. There was a lack of outcome evaluation designs, small sample sizes and a reliance on intervention descriptions and formative evaluations. Methodological challenges may mean alternatives to 'pure' RCTs should be considered. The current evidence contributes more to understanding feasibility and acceptability than to effectiveness. Practitioners and evaluators must prioritize the further development of intervention studies.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "886", "doc_id": "22446093", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: At least 85% of patients exposed to radiation have activated markers of myofibroblasts.\n\nCANDIDATE_PASSAGE:\nDecoupling activation and exhaustion of B cells in spontaneous controllers of HIV infection. OBJECTIVE To define the impact of chronic viremia and associated immune activation on B-cell exhaustion in HIV infection. DESIGN Progressive HIV infection is marked by B-cell anergy and exhaustion coupled with dramatic hypergammaglobulinemia. Although both upregulation of CD95 and loss of CD21 have been used as markers of infection-associated B-cell dysfunction, little is known regarding the specific profiles of dysfunctional B cells and whether persistent viral replication and its associated immune activation play a central role in driving B-cell dysfunction. METHODS Multiparameter flow cytometry was used to define the profile of dysfunctional B cells. The changes in the expression of CD21 and CD95 were tracked on B-cell subpopulations in patients with differential control of viral replication. RESULTS : Although the emergence of exhausted, CD21 tissue-like memory B cells followed similar patterns in both progressors and controllers, the frequency of CD21 activated memory B cells was lower in spontaneous controllers. CONCLUSION Our results suggest that the loss of CD21 and the upregulation of CD95 occur as separate events during the development of B-cell dysfunction. The loss of CD21 is a marker of B-cell exhaustion induced in the absence of appreciable viral replication, whereas the upregulation of CD95 is tightly linked to persistent viral replication and its associated immune activation. Thus, these dysfunctional profiles potentially represent two functionally distinct states within the B-cell compartment.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "139", "doc_id": "20261352", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Adult tissue-resident macrophages possess a self-renewing capacity.\n\nCANDIDATE_PASSAGE:\nThe suture provides a niche for mesenchymal stem cells of craniofacial bones Bone tissue undergoes constant turnover supported by stem cells. Recent studies showed that perivascular mesenchymal stem cells (MSCs) contribute to the turnover of long bones. Craniofacial bones are flat bones derived from a different embryonic origin than the long bones. The identity and regulating niche for craniofacial-bone MSCs remain unknown. Here, we identify Gli1+ cells within the suture mesenchyme as the main MSC population for craniofacial bones. They are not associated with vasculature, give rise to all craniofacial bones in the adult and are activated during injury repair. Gli1+ cells are typical MSCs in vitro. Ablation of Gli1+ cells leads to craniosynostosis and arrest of skull growth, indicating that these cells are an indispensable stem cell population. Twist1(+/-) mice with craniosynostosis show reduced Gli1+ MSCs in sutures, suggesting that craniosynostosis may result from diminished suture stem cells. Our study indicates that craniofacial sutures provide a unique niche for MSCs for craniofacial bone homeostasis and repair.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "88", "doc_id": "104130", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Are homocysteine and carotid intima-media thickness in ischemic stroke patients correlated?\n\nABSTRACT:\nHyperhomocysteinemia has been linked to cardiovascular morbidity and mortality by numerous authors. Whether this association is causal or not remains uncertain. The aim of the study was to investigate the association of hyperhomocysteinemia with the degree of carotid atherosclerosis in stroke patients. We studied 97 Greek patients in our stroke unit who were hospitalized as a result of ischemic stroke between March 2006 and May 2007. The patients were divided into two groups: the first (52 patients) included stroke patients with serum levels of homocysteine below 15 mumol/L, but in the second group (45 patients) serum homocysteine exceeded this value. We measured carotid intima-media thickness (cIMT) in all patients and correlated it with serum homocysteine. The mean homocysteine concentration was 11.5 mumol/L in the first group and 21.5 mumol/L in the second group. Carotid IMT was 1.012 mm in the first group, and 1.015 mm in the second group, an insignificant difference. On the contrary, serum folate concentration was 21.3 nmol/L in the first group compared with 16.7 nmol/L in the second group (p < 0.001). VitB12 was 401 pmol/L in the first group and 340 pmol/L in the second group, a statistically significant difference (p < 0.001).", "output": "{\"label\": \"no\", \"rationale\": \"Serum levels of homocysteine were not correlated with cIMT in ischemic stroke patients. Both folate and vitB12 were decreased in hyperhomocysteinemic ischemic stroke patients.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 18728747, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: aPKCz causes tumour enhancement by affecting glutamine metabolism.\n\nCANDIDATE_ABSTRACT:\nTITLE: Control of Nutrient Stress-Induced Metabolic Reprogramming by PKCζ in Tumorigenesis\nABSTRACT: Tumor cells have high-energetic and anabolic needs and are known to adapt their metabolism to be able to survive and keep proliferating under conditions of nutrient stress. We show that PKCζ deficiency promotes the plasticity necessary for cancer cells to reprogram their metabolism to utilize glutamine through the serine biosynthetic pathway in the absence of glucose. PKCζ represses the expression of two key enzymes of the pathway, PHGDH and PSAT1, and phosphorylates PHGDH at key residues to inhibit its enzymatic activity. Interestingly, the loss of PKCζ in mice results in enhanced intestinal tumorigenesis and increased levels of these two metabolic enzymes, whereas patients with low levels of PKCζ have a poor prognosis. Furthermore, PKCζ and caspase-3 activities are correlated with PHGDH levels in human intestinal tumors. Taken together, this demonstrates that PKCζ is a critical metabolic tumor suppressor in mouse and human cancer.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Taken together, this demonstrates that PKCζ is a critical metabolic tumor suppressor in mouse and human cancer.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1382, "doc_id": "17755060", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Artefacts in 24-h pharyngeal and oesophageal pH monitoring: is simplification of pH data analysis feasible?\n\nABSTRACT:\nAmbulatory 24-h dual-channel pharyngeal and oesophageal pH monitoring is the standard test for measuring gastro-oesophageal and gastropharyngeal reflux. Artefacts caused by the intake of food may result in falsely positive gastropharyngeal reflux, which necessitates a manual review of 24-h pH data. The purpose of the study was to investigate the influence of meals and whether leaving out meals affected the reliability of the test. Patients referred for otolaryngological complaints, suspected to have been caused by gastro-oesophageal reflux, underwent 24-h dual-channel pH monitoring. The raw unprocessed pH data were corrected by visual inspection of the 24-h tracings (corrected data), by leaving out meals or meals plus a 2-h postprandrial period. The raw pH data were substantially influenced by artefacts of food intake and pseudoreflux. Data obtained by leaving out meals agreed best with manually corrected data. Many of the falsely positive reflux episodes could be removed, thereby inducing a 9%-18% chance of undetected reflux. When examining the fraction of time supine, manually corrected data and data leaving out meals were fully concordant and detected 79% of patients with gastropharyngeal reflux. However, leaving out meals plus a 2-h postprandrial period resulted in 21%-50% falsely negative tests.", "output": "{\"label\": \"maybe\", \"rationale\": \"Leaving out the period of intake of meals and beverages from the raw pH data might be the second best test after the time-consuming visual correction with a small chance of undetected gastropharyngeal reflux. For scientific purposes and when in doubt, it remains necessary to review the computer-generated data manually to discover every gastropharyngeal reflux event.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 14992556, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does perspective-taking increase patient satisfaction in medical encounters?\n\nABSTRACT:\nTo assess whether perspective-taking, which researchers in other fields have shown to induce empathy, improves patient satisfaction in encounters between student-clinicians and standardized patients (SPs). In three studies, randomly assigned students (N = 608) received either a perspective-taking instruction or a neutral instruction prior to a clinical skills examination in 2006-2007. SP satisfaction was the main outcome in all three studies. Study 1 involved 245 third-year medical students from two universities. Studies 2 and 3 extended Study 1 to examine generalizability across student and SP subpopulations. Study 2 (105 physician assistant students, one university) explored the effect of perspective-taking on African American SPs' satisfaction. Study 3 (258 third-year medical students, two universities) examined the intervention's effect on students with high and low baseline perspective-taking tendencies. Intervention students outscored controls in patient satisfaction in all studies: Study 1: P = .01, standardized effect size = 0.16; Study 2: P = .001, standardized effect size = 0.31; Study 3: P = .009, standardized effect size = 0.13. In Study 2, perspective-taking improved African American SPs' satisfaction. In Study 3, intervention students with high baseline perspective-taking tendencies outscored controls (P = .0004, standardized effect size = 0.25), whereas those with low perspective-taking tendencies did not (P = .72, standardized effect size = 0.00).", "output": "{\"label\": \"maybe\", \"rationale\": \"Perspective-taking increased patient satisfaction in all three studies, across medical schools, clinical disciplines, and racially diverse students and SPs. Perspective-taking as a means for improving patient satisfaction deserves further exploration in clinical training and practice.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 20736672, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Citrullinated proteins externalized in neutrophil extracellular traps act indirectly to perpetuate the inflammatory cycle via induction of autoantibodies.\n\nCANDIDATE_ABSTRACT:\nTITLE: NETs are a source of citrullinated autoantigens and stimulate inflammatory responses in rheumatoid arthritis.\nABSTRACT: The early events leading to the development of rheumatoid arthritis (RA) remain unclear, but formation of autoantibodies to citrullinated protein antigens (ACPAs) is considered a key pathogenic event. Neutrophils isolated from patients with various autoimmune diseases display enhanced neutrophil extracellular trap (NET) formation, a phenomenon that exposes autoantigens in the context of immunostimulatory molecules. We investigated whether aberrant NETosis occurs in RA, determined its triggers, and examined its deleterious inflammatory consequences. Enhanced NETosis was observed in circulating and RA synovial fluid neutrophils compared to neutrophils from healthy controls and from patients with osteoarthritis (OA). Further, netting neutrophils infiltrated RA synovial tissue, rheumatoid nodules, and skin. NETosis correlated with ACPA presence and levels and with systemic inflammatory markers. RA sera and immunoglobulin fractions from RA patients with high levels of ACPA and/or rheumatoid factor significantly enhanced NETosis, and the NETs induced by these autoantibodies displayed distinct protein content. Indeed, during NETosis, neutrophils externalized the citrullinated autoantigens implicated in RA pathogenesis, and anti-citrullinated vimentin antibodies potently induced NET formation. Moreover, the inflammatory cytokines interleukin-17A (IL-17A) and tumor necrosis factor-α (TNF-α) induced NETosis in RA neutrophils. In turn, NETs significantly augmented inflammatory responses in RA and OA synovial fibroblasts, including induction of IL-6, IL-8, chemokines, and adhesion molecules. These observations implicate accelerated NETosis in RA pathogenesis, through externalization of citrullinated autoantigens and immunostimulatory molecules that may promote aberrant [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Indeed, during NETosis, neutrophils externalized the citrullinated autoantigens implicated in RA pathogenesis, and anti-citrullinated vimentin antibodies potently induced NET formation. Moreover, the inflammatory cytokines interleukin-17A (IL-17A) and tumor necrosis factor-α (TNF-α) induced NETosis in RA neutrophils.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 264, "doc_id": "11328820", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Albendazole is used to treat soil-transmitted helminths.\n\nCANDIDATE_PASSAGE:\nAntihypertensive classes, cognitive decline and incidence of dementia: a network meta-analysis. OBJECTIVES Prevention of cognitive decline and dementia with blood pressure lowering treatments has shown inconsistent results. We compared the effects of different classes of antihypertensive drugs on the incidence of dementia, and on cognitive function. METHODS We conducted a systematic review and included 19 randomized trials (18 515 individuals) and 11 studies (831 674 individuals) analysing the effects of antihypertensive treatment on cognition and on the incidence of dementia, respectively, in hypertensive patients without prior cerebrovascular disorders. Network meta-analysis was used for the comparison of antihypertensive classes. RESULTS Antihypertensive treatment, regardless of the drug class, had benefits on overall cognition [effect size 0.05, 95% confidence interval (CI) 0.02-0.07] and all cognitive functions except language. Antihypertensive treatment reduced the risk of all-cause dementia by 9%, with reference to the control group (hazard ratio 0.91, 95% CI 0.89-0.94), when randomized trials and observationnal studies were combined (n = 15). Result was not significant with randomized trials alone (n = 4). Angiotensin II receptor blockers (ARBs) had larger benefits than placebo on overall cognition (adjusted effect size 0.60 ± 0.18, P = 0.02). ARBs were more effective than β-blockers (0.67 ± 0.18, P = 0.01), diuretics (0.54 ± 0.19, P = 0.04) and angiotensin-converting enzyme inhibitors (0.47 ± 0.17, P = 0.04) in rank. The mean change in blood pressure did not differ significantly between the different antihypertensive drug classes. CONCLUSION Our results support the notion that antihypertensive treatment has beneficial effects on cognitive decline an [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "95", "doc_id": "32463364", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cyclin A2 destruction is necessary to switch from unstable to stable kt-mt attachments in mitosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cyclin A Regulates Kinetochore-Microtubules to Promote Faithful Chromosome Segregation\nABSTRACT: The most conspicuous event in the cell cycle is the alignment of chromosomes in metaphase. Chromosome alignment fosters faithful segregation through the formation of bi-oriented attachments of kinetochores to spindle microtubules. Notably, numerous kinetochore-microtubule (k-MT) attachment errors are present in early mitosis (prometaphase), and the persistence of those errors is the leading cause of chromosome mis-segregation in aneuploid human tumour cells that continually mis-segregate whole chromosomes and display chromosomal instability. How robust error correction is achieved in prometaphase to ensure error-free mitosis remains unknown. Here we show that k-MT attachments in prometaphase cells are considerably less stable than in metaphase cells. The switch to more stable k-MT attachments in metaphase requires the proteasome-dependent destruction of cyclin A in prometaphase. Persistent cyclin A expression prevents k-MT stabilization even in cells with aligned chromosomes. By contrast, k-MTs are prematurely stabilized in cyclin-A-deficient cells. Consequently, cells lacking cyclin A display higher rates of chromosome mis-segregation. Thus, the stability of k-MT attachments increases decisively in a coordinated fashion among all chromosomes as cells transit from prometaphase to metaphase. Cyclin A creates a cellular environment that promotes microtubule detachment from kinetochores in prometaphase to ensure efficient error correction and faithful chromosome segregation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"By contrast, k-MTs are prematurely stabilized in cyclin-A-deficient cells.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 296, "doc_id": "4398832", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Gluten tolerance in adult patients with celiac disease 20 years after diagnosis?\n\nABSTRACT:\nCeliac disease (CD) is believed to be a permanent intolerance to gluten. A number of patients, however, discontinue the gluten-free diet (GFD) without developing symptoms or signs. The aim of our study was to investigate whether CD patients are capable of developing tolerance to gluten. All 77 adult patients from our hospital known to have biopsy-proven CD for more than 10 years were invited to participate. We investigated symptoms, gluten consumption, antibodies for CD and other autoimmunity, human leukocyte antigen (HLA)-typing, bone mineral density, and performed small bowel biopsies. Tolerance was defined as no immunological or histological signs of CD while consuming gluten. Sixty-six patients accepted participation, but after review of the diagnostic biopsies 53 were found to have true CD. Twenty-three percent of patients had a gluten-containing diet, 15% admitted gluten transgression and 62% followed the GFD. Patients on a GFD had significantly more osteoporosis. Normal small bowel mucosa was found in four of eight on gluten-containing diet and in four of four with gluten transgression. Two patients were considered to have developed tolerance to gluten. One of them was HLA-DQ2/DQ8 negative.", "output": "{\"label\": \"maybe\", \"rationale\": \"Development of tolerance to gluten seems possible in some patients with CD. Further follow-up will show whether this tolerance is permanent or only a long-term return to latency. This feature may be associated with genetic characteristics, especially with HLA genotypes that differ from DQ2 or DQ8.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 18403944, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Occupancy of ribosomes by IncRNAs do not make functional peptides.\n\nCANDIDATE_ABSTRACT:\nTITLE: Determinants of neonatal mortality in Indonesia\nABSTRACT: BACKGROUND Neonatal mortality accounts for almost 40 per cent of under-five child mortality, globally. An understanding of the factors related to neonatal mortality is important to guide the development of focused and evidence-based health interventions to prevent neonatal deaths. This study aimed to identify the determinants of neonatal mortality in Indonesia, for a nationally representative sample of births from 1997 to 2002. METHODS The data source for the analysis was the 2002-2003 Indonesia Demographic and Health Survey from which survival information of 15,952 singleton live-born infants born between 1997 and 2002 was examined. Multilevel logistic regression using a hierarchical approach was performed to analyze the factors associated with neonatal deaths, using community, socio-economic status and proximate determinants. RESULTS At the community level, the odds of neonatal death was significantly higher for infants from East Java (OR = 5.01, p = 0.00), and for North, Central and Southeast Sulawesi and Gorontalo combined (OR = 3.17, p = 0.03) compared to the lowest neonatal mortality regions of Bali, South Sulawesi and Jambi provinces. A progressive reduction in the odds was found as the percentage of deliveries assisted by trained delivery attendants in the cluster increased. The odds of neonatal death were higher for infants born to both mother and father who were employed (OR = 1.84, p = 0.00) and for infants born to father who were unemployed (OR = 2.99, p = 0.02). The odds were also higher for higher rank infants with a short birth interval (OR = 2.82, p = 0.00), male infants (OR = 1.49, p = 0.01), smaller than average-sized infants (OR = 2.80, p = 0.00), and infant's whose mother had a history of delivery complications (OR = 1.81, p = 0.00). Infa [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 879, "doc_id": "1263446", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Exposure to fine particulate air pollution is unrelated to anxiety prevalence.\n\nCANDIDATE_ABSTRACT:\nTITLE: The relation between past exposure to fine particulate air pollution and prevalent anxiety: observational cohort study\nABSTRACT: OBJECTIVE To determine whether higher past exposure to particulate air pollution is associated with prevalent high symptoms of anxiety. DESIGN Observational cohort study. SETTING Nurses' Health Study. PARTICIPANTS 71,271 women enrolled in the Nurses' Health Study residing throughout the contiguous United States who had valid estimates on exposure to particulate matter for at least one exposure period of interest and data on anxiety symptoms. MAIN OUTCOME MEASURES Meaningfully high symptoms of anxiety, defined as a score of 6 points or greater on the phobic anxiety subscale of the Crown-Crisp index, administered in 2004. RESULTS The 71,271 eligible women were aged between 57 and 85 years (mean 70 years) at the time of assessment of anxiety symptoms, with a prevalence of high anxiety symptoms of 15%. Exposure to particulate matter was characterized using estimated average exposure to particulate matter <2.5 μm in diameter (PM2.5) and 2.5 to 10 μm in diameter (PM2.5-10) in the one month, three months, six months, one year, and 15 years prior to assessment of anxiety symptoms, and residential distance to the nearest major road two years prior to assessment. Significantly increased odds of high anxiety symptoms were observed with higher exposure to PM2.5 for multiple averaging periods (for example, odds ratio per 10 µg/m(3) increase in prior one month average PM2.5: 1.12, 95% confidence interval 1.06 to 1.19; in prior 12 month average PM2.5: 1.15, 1.06 to 1.26). Models including multiple exposure windows suggested short term averaging periods were more relevant than long term averaging periods. There was no association between anxiety and exposure to PM2.5-10. Residential proximity to major roads was not related to anxiety symptoms in a dose dependent manner. CON [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Significantly increased odds of high anxiety symptoms were observed with higher exposure to PM2.5 for multiple averaging periods (for example, odds ratio per 10 µg/m(3) increase in prior one month average PM2.5: 1.12, 95% confidence interval 1.06 to 1.19; in prior 12 month average PM2.5: 1.15, 1.06 to 1.26).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 400, "doc_id": "791050", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does hepatocellular carcinoma recurrence in patients with curative resection or ablation : impact of HCV eradication depend on the use of interferon?\n\nABSTRACT:\nIn HCV-infected cirrhotic patients with successfully treated early hepatocellular carcinoma (HCC), the time to HCC recurrence and the effects of sustained viral eradication (SVR) by interferon (IFN)-based or IFN-free regimens on HCC recurrence remain unclear. To perform an indirect comparison of time to recurrence (TTR) in patients with successfully treated early HCC and active HCV infection with those of patients with SVR by IFN-based and by IFN-free regimens. We evaluated 443 patients with HCV-related cirrhosis and Barcelona Clinic Liver Cancer Stage A/0 HCC who had a complete radiological response after curative resection or ablation. Active HCV infection was present in 328, selected from the Italian Liver Cancer group cohort; 58 patients had SVR achieved by IFN-free regimens after HCC cure, and 57 patients had SVR achieved by IFN-based regimens after HCC cure. Individual data of patients in the last two groups were extracted from available publications. TTR by Kaplan-Meier curve was significantly lower in patients with active HCV infection compared with those with SVR both by IFN-free (P = 0.02) and by IFN-based (P < 0.001) treatments. TTR was similar in patients with SVR by IFN-free or by IFN-based (P = 0.49) strategies.", "output": "{\"label\": \"no\", \"rationale\": \"In HCV-infected, successfully treated patients with early HCC, SVR obtained by IFN-based or IFN-free regimens significantly reduce tumour recurrence without differences related to the anti-viral strategy used.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 27790734, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Antimicrobial agents are less effective due to the pressure of antimicrobial usage.\n\nCANDIDATE_ABSTRACT:\nTITLE: Lifeact: a versatile marker to visualize F-actin\nABSTRACT: Live imaging of the actin cytoskeleton is crucial for the study of many fundamental biological processes, but current approaches to visualize actin have several limitations. Here we describe Lifeact, a 17-amino-acid peptide, which stained filamentous actin (F-actin) structures in eukaryotic cells and tissues. Lifeact did not interfere with actin dynamics in vitro and in vivo and in its chemically modified peptide form allowed visualization of actin dynamics in nontransfectable cells.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 121, "doc_id": "1539159", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Sympathetic nerve activity is reduced throughout normal pregnancy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Sympathetic neural mechanisms in normal and hypertensive pregnancy in humans.\nABSTRACT: BACKGROUND Direct recordings from peripheral sympathetic nerves have shown an increased sympathetic drive in pregnancy-induced hypertension (PIH) and preeclampsia (PE). It is unknown whether sympathetic drive is altered in normal pregnancy, when arterial blood pressure can be normal or relatively low. The aim of this study was to measure and compare peripheral sympathetic discharge, its vasoconstrictor effect and its baroreceptor control, during pregnancy and postpartum in women with normal pregnancy (NP) and PIH and in normotensive nonpregnant (NN) women. METHODS AND RESULTS Twenty-one women with NP, 18 women with PIH, and 21 NN women had muscle sympathetic nerve activity assessed from multiunit discharges (MSNA) and from single units with defined vasoconstrictor properties (s-MSNA). The s-MSNA in NP (38+/-6.6 impulses/100 beats) was greater (P<0.05) than in NN women (19+/-1.8 impulses/100 beats) despite similar age and body weight but less than in PIH women (P<0.001) (146+/-23.5 impulses/100 beats). MSNA followed a similar trend. Cardiac baroreceptor reflex sensitivity (BRS) was impaired in NP and PIH women relative to NN. After delivery, sympathetic activity decreased to values similar to those obtained in NN, and there was an increase in BRS. In women with NP, the decrease in sympathetic output occurred despite an insignificant change in blood pressure. CONCLUSIONS Central sympathetic output was increased in women with normal pregnancy and was even greater in the hypertensive pregnant group. The findings suggest that the moderate sympathetic hyperactivity during the latter months of normal pregnancy may help to return the arterial pressure to nonpregnant levels, although when the increase in activity is excessive, hypertension may ensue.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The findings suggest that the moderate sympathetic hyperactivity during the latter months of normal pregnancy may help to return the arterial pressure to nonpregnant levels, although when the increase in activity is excessive, hypertension may ensue.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1120, "doc_id": "5323845", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Obesity is determined solely by environmental factors.\n\nCANDIDATE_ABSTRACT:\nTITLE: Genetics of obesity in adult adoptees and their biological siblings.\nABSTRACT: An adoption study of genetic effects on obesity in adulthood was carried out in which adoptees separated from their natural parents very early in life were compared with their biological full and half siblings reared by their natural parents. The adoptees represented four groups who by sampling from a larger population were categorised as either thin, medium weight, overweight, or obese. Weight and height were obtained for 115 full siblings of 57 adoptees and for 850 half siblings of 341 adoptees. In full siblings body mass index (kg/m2) significantly increased with weight of the adoptees. Body mass index of the half siblings showed a steady but weaker increase across the four weight groups of adoptees. There were no significant interactions with sex of the adoptees, sex of the siblings, or (for the half siblings) sex of the common parent. In contrast with the findings in half siblings and (previously) the natural parents there was a striking, significant increase in body mass index between full siblings of overweight and obese adoptees. The degree of fatness in adults living in the same environment appears to be influenced by genetic factors independent of sex, which may include polygenic as well as major gene effects on obesity.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In full siblings body mass index (kg/m2) significantly increased with weight of the adoptees. Body mass index of the half siblings showed a steady but weaker increase across the four weight groups of adoptees.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 873, "doc_id": "1180972", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The proportion of people with visual difficulty is two times higher in low-income countries than in high-income countries.\n\nCANDIDATE_PASSAGE:\nGlobal, regional, and national disability-adjusted life-years (DALYs) for 315 diseases and injuries and healthy life expectancy (HALE), 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015 BACKGROUND Healthy life expectancy (HALE) and disability-adjusted life-years (DALYs) provide summary measures of health across geographies and time that can inform assessments of epidemiological patterns and health system performance, help to prioritise investments in research and development, and monitor progress toward the Sustainable Development Goals (SDGs). We aimed to provide updated HALE and DALYs for geographies worldwide and evaluate how disease burden changes with development. METHODS We used results from the Global Burden of Diseases, Injuries, and Risk Factors Study 2015 (GBD 2015) for all-cause mortality, cause-specific mortality, and non-fatal disease burden to derive HALE and DALYs by sex for 195 countries and territories from 1990 to 2015. We calculated DALYs by summing years of life lost (YLLs) and years of life lived with disability (YLDs) for each geography, age group, sex, and year. We estimated HALE using the Sullivan method, which draws from age-specific death rates and YLDs per capita. We then assessed how observed levels of DALYs and HALE differed from expected trends calculated with the Socio-demographic Index (SDI), a composite indicator constructed from measures of income per capita, average years of schooling, and total fertility rate. FINDINGS Total global DALYs remained largely unchanged from 1990 to 2015, with decreases in communicable, neonatal, maternal, and nutritional (Group 1) disease DALYs offset by increased DALYs due to non-communicable diseases (NCDs). Much of this epidemiological transition was caused by chan [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1257", "doc_id": "581832", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Hyperfibrinogenemia decreases rates of femoropopliteal bypass thrombosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Influence of smoking and plasma factors on patency of femoropopliteal vein grafts.\nABSTRACT: OBJECTIVE To determine the effects of smoking, plasma lipids, lipoproteins, apolipoproteins, and fibrinogen on the patency of saphenous vein femoropopliteal bypass grafts at one year. DESIGN Prospective study of patients with saphenous vein femoropopliteal bypass grafts entered into a multicentre trial. SETTING Surgical wards, outpatient clinics, and home visits coordinated by two tertiary referral centres in London and Birmingham. PATIENTS 157 Patients (mean age 66.6 (SD 8.2) years), 113 with patent grafts and 44 with occluded grafts one year after bypass. MAIN OUTCOME MEASURE Cumulative percentage patency at one year. RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts. Serum cholesterol concentrations were significantly higher in patients with grafts that remained patent one year after bypass (p less than 0.005). Analysis of the smoking markers indicated that a quarter of patients (40) were untruthful in their claims to have stopped smoking. Based on smoking markers, patency of grafts in smokers was significantly lower at one year by life table analysis than in non-smokers (63% v 84%, p less than 0.02). Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002). Surprisingly, increased plasma low density lipoprotein cholesterol concentration was significantly associated with improved patency at one year (85%) at values above the median compared w [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 532, "doc_id": "12991445", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Do trendelenburg position , simulated Valsalva maneuver , and liver compression alter the size of the right internal jugular vein in patients with a bidirectional Glenn shunt?\n\nABSTRACT:\nUltrasound is increasingly used to facilitate right internal jugular vein (RIJV) cannulation in children. In children without cardiac disease, position changes and enhancement maneuvers increase RIJV cross-sectional area (CSA) and further facilitate cannulation. We investigated the effect of these maneuvers on RIJV CSA in children with a bidirectional Glenn (BDG) shunt presenting for a Fontan procedure. The CSA (cm(2)) of the RIJV in 21 children with a BDG shunt presenting for a Fontan procedure was assessed by ultrasonic planimetry (SonoSite). Two positions, supine (S) and 15 degrees Trendelenburg (T); and two enhancements maneuvers, manual liver compression (L) and a simulated Valsalva maneuver (V) were utilized in combination. Eight separate measurements (S, S + L, S + V, S + L + V, T, T + L, T + V, T + L + V) were made in each patient. Data were analyzed using one-way analysis of variance with repeated measures and with Tukey post hoc pairwise comparison analysis. No significant change in the RIJV CSA or % change in CSA from baseline (S) was observed.", "output": "{\"label\": \"no\", \"rationale\": \"Position changes and enhancement maneuvers are unlikely to facilitate RIJV cannulation in BDG shunt patients presenting for Fontan procedure because these interventions do not increase RIJV CSA.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 17646491, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is cumulative fluid intake minus output associated with ventilator weaning duration or extubation outcomes in children?\n\nABSTRACT:\nThe effect of fluid balance on respiratory outcomes for critically ill children has not been evaluated. The only indicator of fluid balance routinely recorded across our intensive care units was estimated fluid intake and output. We sought to determine whether cumulative intake minus output (I-O) at the start of weaning predicted weaning duration and whether cumulative I-O at extubation predicted extubation failure. Prospective observational study. Ten pediatric intensive care units. Cumulative I-O was recorded daily for 301 mechanically ventilated children (<18 yrs of age) from November 1999 through April 2001. Cumulative I-O was recorded during a study of weaning strategies and extubation failure in which mechanical ventilation of the majority of patients during weaning and extubation was managed according to a protocol that did not include fluid balance indicators. Outcomes were the time to successful removal of ventilatory support and the rate of initial extubation failure. Relationships between cumulative I-O and outcomes were assessed by means of proportional hazards and logistic regression. The mean cumulative I-O per kilogram of ideal body weight at the start of weaning was 101 mL (sd, 180). Cumulative I-O at the time weaning was initiated did not predict duration of mechanical ventilator weaning. The mean cumulative I-O per kilogram of ideal body weight at extubation was 136 mL (sd, 237). Cumulative I-O at extubation did not predict extubation outcome. There was an association between cumulative I-O at extubation and the duration of weaning in cases not managed by a protocol.", "output": "{\"label\": \"no\", \"rationale\": \"Although routinely recorded, cumulative fluid I-O does not appear to have clinical utility in cases managed according to a mechanical ventilator protocol in which tidal volume and oxygenation on minimal levels of ventilator support are systematically tested.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 16276328, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does timing of initial surfactant treatment make a difference in rates of chronic lung disease or mortality in premature infants?\n\nABSTRACT:\nTo compare two treatment strategies in preterm infants with or at risk of respiratory distress syndrome: early surfactant administration (within one hour of birth) versus late surfactant administration, in a geographically defined population. The primary outcome was chronic lung disease (CLD) and mortality before/at 36 weeks. Secondary outcomes included: duration of mechanical ventilation and continuous positive airway pressure (CPAP), post-natal steroids for CLD and major neonatal morbidities. Premature infants born at 22-32 weeks' gestation between January 2006 and December 2009. Ten neonatal intensive care units (NICUs) in New South Wales (NSW) and Australian Capital Territory (ACT), Australia. Retrospective analysis of prospectively collected data from the regional NICU database in NSW and ACT. Of the 2170 infants who received surfactant, 1182 (54.5%) and 988 (45.5%) received early and late surfactant, respectively. The early surfactant group was less mature (27.1 ± 2.1 versus 29.4 ± 2.1 weeks) and had more CLD and mortality (40.2% versus 20.0%). The multivariable analysis showed early surfactant to be associated with less duration of ventilation, longer duration of CPAP and longer hospital stay but had little or no impact on CLD/mortality.", "output": "{\"label\": \"maybe\", \"rationale\": \"Early surfactant administration is associated with shorter duration of ventilation but does not appear to be significantly protective against CLD/mortality among premature infants. This may support the growing evidence for consideration of CPAP as an alternative to routine intubation and early surfactant administration. Further investigation from large randomized clinical trials is warranted to confirm these results.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 25394614, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Birth-weight is negatively associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Intrauterine factors and risk of breast cancer: a systematic review and meta-analysis of current evidence.\nABSTRACT: BACKGROUND Emerging evidence suggests an association between female prenatal experience and her subsequent risk of developing breast cancer. Potential underlying mechanisms include variation in amounts of maternal endogenous sex hormones and growth hormones, germ-cell mutations, formation of cancer stem-cells, and other genetic or epigenetic events. We reviewed and summarised quantitatively the available data on intrauterine exposures and risk of breast cancer. METHODS We systematically searched for studies that assessed association between perinatal factors and risk of breast cancer. We reviewed separately each of the perinatal factors, including birthweight, birth length, parental age at delivery, gestational age, intrauterine exposure to diethylstilbestrol, twin membership, maternal pre-eclampsia or eclampsia, and other factors. FINDINGS We identified 57 studies published between Oct 1, 1980, and June 21, 2007. Increased risk of breast cancer was noted with increased birthweight (relative risk [RR] 1.15 [95% CI 1.09-1.21]), birth length (1.28 [1.11-1.48]), higher maternal age (1.13 [1.02-1.25]), and paternal age (1.12 [1.05-1.19]). Decreased risk of breast cancer was noted for maternal pre-eclampsia and eclampsia (0.48 [0.30-0.78]) and twin membership (0.93 [0.87-1.00]). No association was noted between risk of breast cancer and gestational age at birth (0.95 [0.71-1.26]) or maternal diethylstilbestrol treatment (1.40 [0.86-2.28]). INTERPRETATION The intrauterine environment contributes to the predisposition of women to breast cancer in adulthood. The in-utero mechanisms responsible for such predisposition need to be elucidated.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Increased risk of breast cancer was noted with increased birthweight (relative risk [RR] 1.15 [95% CI 1.09-1.21]), birth length (1.28 [1.11-1.48]), higher maternal age (1.13 [1.02-1.25]), and paternal age (1.12 [1.05-1.19]).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 178, "doc_id": "23557241", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Lack of clpC does not affect sporulation efficiency in Bacillus subtilis cells.\n\nCANDIDATE_PASSAGE:\nHigh-Throughput Genetic Screens Identify a Large and Diverse Collection of New Sporulation Genes in Bacillus subtilis The differentiation of the bacterium Bacillus subtilis into a dormant spore is among the most well-characterized developmental pathways in biology. Classical genetic screens performed over the past half century identified scores of factors involved in every step of this morphological process. More recently, transcriptional profiling uncovered additional sporulation-induced genes required for successful spore development. Here, we used transposon-sequencing (Tn-seq) to assess whether there were any sporulation genes left to be discovered. Our screen identified 133 out of the 148 genes with known sporulation defects. Surprisingly, we discovered 24 additional genes that had not been previously implicated in spore formation. To investigate their functions, we used fluorescence microscopy to survey early, middle, and late stages of differentiation of null mutants from the B. subtilis ordered knockout collection. This analysis identified mutants that are delayed in the initiation of sporulation, defective in membrane remodeling, and impaired in spore maturation. Several mutants had novel sporulation phenotypes. We performed in-depth characterization of two new factors that participate in cell-cell signaling pathways during sporulation. One (SpoIIT) functions in the activation of σE in the mother cell; the other (SpoIIIL) is required for σG activity in the forespore. Our analysis also revealed that as many as 36 sporulation-induced genes with no previously reported mutant phenotypes are required for timely spore maturation. Finally, we discovered a large set of transposon insertions that trigger premature initiation of sporulation. Our results highl [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "684", "doc_id": "4942718", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: CX3CR1 on the Th2 cells suppresses airway inflammation.\n\nCANDIDATE_ABSTRACT:\nTITLE: CX3CR1 is required for airway inflammation by promoting T helper cell survival and maintenance in inflamed lung\nABSTRACT: Allergic asthma is a T helper type 2 (T(H)2)-dominated disease of the lung. In people with asthma, a fraction of CD4(+) T cells express the CX3CL1 receptor, CX3CR1, and CX3CL1 expression is increased in airway smooth muscle, lung endothelium and epithelium upon allergen challenge. Here we found that untreated CX3CR1-deficient mice or wild-type (WT) mice treated with CX3CR1-blocking reagents show reduced lung disease upon allergen sensitization and challenge. Transfer of WT CD4(+) T cells into CX3CR1-deficient mice restored the cardinal features of asthma, and CX3CR1-blocking reagents prevented airway inflammation in CX3CR1-deficient recipients injected with WT T(H)2 cells. We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma. CX3CR1-induced survival was also observed for T(H)1 cells upon airway inflammation but not under homeostatic conditions or upon peripheral inflammation. Therefore, CX3CR1 and CX3CL1 may represent attractive therapeutic targets in asthma.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Here we found that untreated CX3CR1-deficient mice or wild-type (WT) mice treated with CX3CR1-blocking reagents show reduced lung disease upon allergen sensitization and challenge.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 219, "doc_id": "21366394", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Basophils counteract disease development in patients with systemic lupus erythematosus (SLE).\n\nCANDIDATE_ABSTRACT:\nTITLE: BASOPHILS AND THE T HELPER 2 ENVIRONMENT CAN PROMOTE THE DEVELOPMENT OF LUPUS NEPHRITIS\nABSTRACT: In systemic lupus erythematosus (SLE), self-reactive antibodies can target the kidney (lupus nephritis), leading to functional failure and possible mortality. We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice). Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis. Basophils were also present in the lymph nodes and spleen of subjects with SLE. Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 171, "doc_id": "12670680", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Do emergency medical services professionals think they should participate in disease prevention?\n\nABSTRACT:\nThe primary objective of the study was to determine emergency medical services (EMS) professionals' opinions regarding participation in disease and injury prevention programs. A secondary objective was to determine the proportion of EMS professionals who had participated in disease prevention programs. As part of the National Registry of Emergency Medical Technicians' biennial reregistration process, EMS professionals reregistering in 2006 were asked to complete an optional survey regarding their opinions on and participation in disease and injury prevention. Demographic characteristics were also collected. Data were analyzed using descriptive statistics and 99% confidence intervals (CIs). The chi-square test was used to compare differences by responder demographics (alpha = 0.01). A 10% difference between groups was determined to be clinically significant. The survey was completed by 27,233 EMS professionals. Of these responders, 82.7% (99% CI: 82.1-83.3) felt that EMS professionals should participate in disease prevention, with those working 20 to 29 hours per week being the least likely to think they should participate (67.4%, p<0.001). About a third, 33.8% (99% CI: 33.1-34.6), of the respondents reported having provided prevention services, with those having a graduate degree (43.5%, p<0.001), those working in EMS for more than 21 years (44%, p<0.001), those working for the military (57%, p<0.001), those working 60 to 69 hours per week (41%, p<0.001), and those responding to zero emergency calls in a typical week (43%, p<0.001) being the most likely to report having provided prevention services. About half, 51.1% (99% CI: 50.4-51.9), of the respondents agreed that prevention services should be provided during emergency calls, and 7.7% (99% CI: 7.3-8.1) o [TRUNCATED]", "output": "{\"label\": \"maybe\", \"rationale\": \"The majority of EMS professionals thought that they should participate in disease and injury prevention programs. The respondents were mixed as to whether prevention services should be provided while on emergency calls, but those with experience providing these services were more likely to agree with providing them during emergency calls.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 19145527, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does limb-salvage surgery offer patients better quality of life and functional capacity than amputation?\n\nABSTRACT:\nPatients with aggressive lower extremity musculoskeletal tumors may be candidates for either above-knee amputation or limb-salvage surgery. However, the subjective and objective benefits of limb-salvage surgery compared with amputation are not fully clear.QUESTIONS/ We therefore compared functional status and quality of life for patients treated with above-knee amputation versus limb-salvage surgery. We reviewed 20 of 51 patients aged 15 years and older treated with above-knee amputation or limb-salvage surgery for aggressive musculoskeletal tumors around the knee between 1994 and 2004 as a retrospective cohort study. At last followup we obtained the Physiological Cost Index, the Reintegration to Normal Living Index, SF-36, and the Toronto Extremity Salvage Score questionnaires. The minimum followup was 12 months (median, 56 months; range, 12-108 months). Compared with patients having above-knee amputation, patients undergoing limb-salvage surgery had superior Physiological Cost Index scores and Reintegration to Normal Living Index. The Toronto Extremity Salvage scores and SF-36 scores were similar in the two groups.", "output": "{\"label\": \"maybe\", \"rationale\": \"These data suggest that limb-salvage surgery offers better gait efficiency and return to normal living compared with above-knee amputation, but does not improve the patient's perception of quality of life.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 22302658, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Patients in stable partnerships have a slower progression from HIV to AIDS.\n\nCANDIDATE_ABSTRACT:\nTITLE: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\nABSTRACT: OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART). DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study). SETTING Seven outpatient clinics throughout Switzerland. PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years). MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound. RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion. When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership. In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without. Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression. CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 923, "doc_id": "17077004", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Moderate consumption of candy and chocolate reduces the risk of cardiovascular disease (CVD).\n\nCANDIDATE_ABSTRACT:\nTITLE: Life is sweet: candy consumption and longevity.\nABSTRACT: Our attitude towards candy—“if it tastes that good, it can't be healthy”—betrays society's puritanical stance towards pleasure. Candy has been blamed for various ills, including hyperactivity in children; however, clinical trials have not supported this.1 Candy—sugar confectionery and chocolate—is not a recent invention: the ancient Arabs, Chinese, and Egyptians candied fruits and nuts in honey, and the Aztecs made a chocolate drink from the bean of the cacao tree. Today, Americans gratify themselves with, on average, 5.4 kg of sugar candy and 6.5 kg of chocolate per person annually.2 Since candy has existed for centuries, we surmised that it cannot be totally unhealthy. We decided to investigate whether candy consumption was associated with longevity. Subjects were from the Harvard alumni health study, an ongoing study of men entering Harvard University as undergraduates between 1916 and 1950. We included 7841 men, free of cardiovascular disease and cancer, who responded to a health survey …", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 799, "doc_id": "5293024", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is fever a symptom of chronic rhinosinusitis?\n\nABSTRACT:\nIn the chronic rhinosinusitis (CRS) definition of the RhinoSinusitis Task Force (RSTF) of the American Academy of Otolaryngology-Head and Neck Surgery, fever is one of the minor symptoms. In the EP3OS definition, fever is not mentioned as a contributing factor. The main aim of this study was to evaluate the role of fever in CRS. Patients with CRS, scheduled for surgery were compared with a control group consisting of patients without CRS, suffering from esthetic complaints or obstruction of the nose. Temperature prior to surgery was measured and analyzed. In both groups, hundred patients were included. In the CRS group the mean temperature was 36.94 degrees C, with a maximum of 37.8 degrees C. The control group revealed a mean temperature of 36.87 degrees C. Analysis demonstrated no significant difference between the mean temperatures of the CRS patients and the controls (p = 0.306). Additional analysis, correcting for possible confounders, did not reveal significant differences between both groups either.", "output": "{\"label\": \"no\", \"rationale\": \"There have been several attempts to define CRS in the past, but an all including definition or classification system for this disorder does not currently exist. Fever is a factor under discussion. We found no significant difference between the preoperative body temperature in CRS patients and controls.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 19936365, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Ly6C hi monocytes have a lower inflammatory capacity compared to their Ly6C lo counterparts.\n\nCANDIDATE_PASSAGE:\nThe prevalence of congenital malformations is still higher in pregnant women with pregestational diabetes despite near-normal HbA1c: a literature review. AIMS/HYPOTHESIS We assessed the association between congenital malformations and maternal hyperglycemia in pregnant women with pregestational (type 1 or type 2) diabetes and investigated if the rate of congenital malformations was similar in women with near-normal glycemic control compared to the background population. We also assessed the association between congenital malformations and maternal hyperglycemia in pregnant women with pregestational diabetes with special focus on women with near-normal HbA1c in early pregnancy. MATERIALS AND METHODS This is a literature review based on an electronic literature search of the databases PubMed, Cochrane, Embase and Web of Science conducted in July 2017 using the search terms diabetes, pregnancy, HbA1c or glycemic control and congenital anomaly or congenital anomaly. We included original papers in English published after 1997 with data on congenital malformations and HbA1c in at least 250 women with pregestational diabetes. RESULTS Nine papers with in total 6225 women with type 1 diabetes and 2334 women with type 2 diabetes were included. The prevalence of congenital malformations was 6.4% in women with type 1 diabetes and 4.3% in women with type 2 diabetes and for the combined group of women with pregestational diabetes, the relative risk compared to the background population was 3.2. In women with HbA1c < 53 mmol/mol (7.0%) in early pregnancy or HbA1c 53-64 mmol/mol (7.0-8.0%) the prevalence of congenital malformations was 4.3 and 3.7%, respectively, with a relative risk of 2.2 and 1.9, respectively. CONCLUSIONS In pregnant women with pregestational diabetes th [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "727", "doc_id": "30983338", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: CD44v6 is not associated with constitutive and reprogrammed cancer stem cells driving cancer metastasis.\n\nCANDIDATE_ABSTRACT:\nTITLE: CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis.\nABSTRACT: Cancer stem cells drive tumor formation and metastasis, but how they acquire metastatic traits is not well understood. Here, we show that all colorectal cancer stem cells (CR-CSCs) express CD44v6, which is required for their migration and generation of metastatic tumors. CD44v6 expression is low in primary tumors but demarcated clonogenic CR-CSC populations. Cytokines hepatocyte growth factor (HGF), osteopontin (OPN), and stromal-derived factor 1α (SDF-1), secreted from tumor associated cells, increase CD44v6 expression in CR-CSCs by activating the Wnt/β-catenin pathway, which promotes migration and metastasis. CD44v6(-) progenitor cells do not give rise to metastatic lesions but, when treated with cytokines, acquire CD44v6 expression and metastatic capacity. Importantly, phosphatidylinositol 3-kinase (PI3K) inhibition selectively killed CD44v6 CR-CSCs and reduced metastatic growth. In patient cohorts, low levels of CD44v6 predict increased probability of survival. Thus, the metastatic process in colorectal cancer is initiated by CSCs through the expression of CD44v6, which is both a functional biomarker and therapeutic target.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Importantly, phosphatidylinositol 3-kinase (PI3K) inhibition selectively killed CD44v6 CR-CSCs and reduced metastatic growth.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 203, "doc_id": "9558539", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Gpr124 suppresses BBB breakdown in mouse models of ischemic stroke.\n\nCANDIDATE_ABSTRACT:\nTITLE: High-intensity functional exercise program and protein-enriched energy supplement for older persons dependent in activities of daily living: a randomised controlled trial.\nABSTRACT: The aims of this randomised controlled trial were to determine if a high-intensity functional exercise program improves balance, gait ability, and lower-limb strength in older persons dependent in activities of daily living and if an intake of protein-enriched energy supplement immediately after the exercises increases the effects of the training. One hundred and ninety-one older persons dependent in activities of daily living, living in residential care facilities, and with a Mini-Mental State Examination (MMSE) score of ? 10 participated. They were randomised to a high-intensity functional exercise program or a control activity, which included 29 sessions over 3 months, as well as to protein-enriched energy supplement or placebo. Berg Balance Scale, self-paced and maximum gait speed, and one-repetition maximum in lower-limb strength were followed-up at three and six months and analysed by 2 x 2 factorial ANCOVA, using the intention-to-treat principle. At three months, the exercise group had improved significantly in self-paced gait speed compared with the control group (mean difference 0.04 m/s, p = 0.02). At six months, there were significant improvements favouring the exercise group for Berg Balance Scale (1.9 points, p = 0.05), self-paced gait speed (0.05 m/s, p = 0.009), and lower-limb strength (10.8 kg, p = 0.03). No interaction effects were seen between the exercise and nutrition interventions. In conclusion, a high-intensity functional exercise program has positive long-term effects in balance, gait ability, and lower-limb strength for older persons dependent in activities of daily living. An intake of protein-enriched energy supplement immediately after the exercises does not appear to increase the effects of the training.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 480, "doc_id": "2028532", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Patients with microcytosis and higher erythrocyte count are more vulnerable to severe malarial anaemia when infected with Plasmodium falciparum.\n\nCANDIDATE_ABSTRACT:\nTITLE: Increased Microerythrocyte Count in Homozygous α+-Thalassaemia Contributes to Protection against Severe Malarial Anaemia\nABSTRACT: BACKGROUND The heritable haemoglobinopathy alpha(+)-thalassaemia is caused by the reduced synthesis of alpha-globin chains that form part of normal adult haemoglobin (Hb). Individuals homozygous for alpha(+)-thalassaemia have microcytosis and an increased erythrocyte count. Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count. We tested the hypothesis that the erythrocyte indices associated with alpha(+)-thalassaemia homozygosity provide a haematological benefit during acute malaria. METHODS AND FINDINGS Data from children living on the north coast of Papua New Guinea who had participated in a case-control study of the protection afforded by alpha(+)-thalassaemia against severe malaria were reanalysed to assess the genotype-specific reduction in erythrocyte count and Hb levels associated with acute malarial disease. We observed a reduction in median erythrocyte count of approximately 1.5 x 10(12)/l in all children with acute falciparum malaria relative to values in community children (p < 0.001). We developed a simple mathematical model of the linear relationship between Hb concentration and erythrocyte count. This model predicted that children homozygous for alpha(+)-thalassaemia lose less Hb than children of normal genotype for a reduction in erythrocyte count of >1.1 x 10(12)/l as a result of the reduced mean cell Hb in homozygous alpha(+)-thalassaemia. In addition, children homozygous for alpha(+)-thalassaemia require a 10% greater reduction in erythrocyte count than children of normal genotype (p = 0.02) for Hb concentration to fall to 50 g/l, the cutoff for SMA. We estimated that the haematological profile in [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We estimated that the haematological profile in children homozygous for alpha(+)-thalassaemia reduces the risk of SMA during acute malaria compared to children of normal genotype (relative risk 0.52; 95% confidence interval [CI] 0.24-1.12, p = 0.09).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 928, "doc_id": "18174210", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Eliminating the last sporadic cases of malaria requires considerable funding.\n\nCANDIDATE_ABSTRACT:\nTITLE: Costs and financial feasibility of malaria elimination\nABSTRACT: The marginal costs and benefits of converting malaria programmes from a control to an elimination goal are central to strategic decisions, but empirical evidence is scarce. We present a conceptual framework to assess the economics of elimination and analyse a central component of that framework-potential short-term to medium-term financial savings. After a review that showed a dearth of existing evidence, the net present value of elimination in five sites was calculated and compared with effective control. The probability that elimination would be cost-saving over 50 years ranged from 0% to 42%, with only one site achieving cost-savings in the base case. These findings show that financial savings should not be a primary rationale for elimination, but that elimination might still be a worthy investment if total benefits are sufficient to outweigh marginal costs. Robust research into these elimination benefits is urgently needed.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 376, "doc_id": "22401061", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Taking 400mg of α-tocopheryl acetate helps to prevent prostate cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Vitamins E and C in the prevention of prostate and total cancer in men: the Physicians' Health Study II randomized controlled trial.\nABSTRACT: CONTEXT Many individuals take vitamins in the hopes of preventing chronic diseases such as cancer, and vitamins E and C are among the most common individual supplements. A large-scale randomized trial suggested that vitamin E may reduce risk of prostate cancer; however, few trials have been powered to address this relationship. No previous trial in men at usual risk has examined vitamin C alone in the prevention of cancer. OBJECTIVE To evaluate whether long-term vitamin E or C supplementation decreases risk of prostate and total cancer events among men. DESIGN, SETTING, AND PARTICIPANTS The Physicians' Health Study II is a randomized, double-blind, placebo-controlled factorial trial of vitamins E and C that began in 1997 and continued until its scheduled completion on August 31, 2007. A total of 14,641 male physicians in the United States initially aged 50 years or older, including 1307 men with a history of prior cancer at randomization, were enrolled. INTERVENTION Individual supplements of 400 IU of vitamin E every other day and 500 mg of vitamin C daily. MAIN OUTCOME MEASURES Prostate and total cancer. RESULTS During a mean follow-up of 8.0 years, there were 1008 confirmed incident cases of prostate cancer and 1943 total cancers. Compared with placebo, vitamin E had no effect on the incidence of prostate cancer (active and placebo vitamin E groups, 9.1 and 9.5 events per 1000 person-years; hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.85-1.09; P = .58) or total cancer (active and placebo vitamin E groups, 17.8 and 17.3 cases per 1000 person-years; HR, 1.04; 95% CI, 0.95-1.13; P = .41). There was also no significant effect of vitamin C on total cancer (active and placebo vitamin C groups, 17.6 and 17.5 events per 1000 person-years; HR, 1.01; 95% [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS In this large, long-term trial of male physicians, neither vitamin E nor C supplementation reduced the risk of prostate or total cancer.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1140, "doc_id": "12009265", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Dexamethasone decreases risk of postoperative bleeding.\n\nCANDIDATE_ABSTRACT:\nTITLE: Dexamethasone and risk of nausea and vomiting and postoperative bleeding after tonsillectomy in children: a randomized trial.\nABSTRACT: CONTEXT Dexamethasone is widely used to prevent postoperative nausea and vomiting (PONV) in pediatric tonsillectomy. OBJECTIVE To assess whether dexamethasone dose-dependently reduces the risk of PONV at 24 hours after tonsillectomy. DESIGN, SETTING, AND PATIENTS Randomized placebo-controlled trial conducted among 215 children undergoing elective tonsillectomy at a major public teaching hospital in Switzerland from February 2005 to December 2007. INTERVENTIONS Children were randomly assigned to receive dexamethasone (0.05, 0.15, or 0.5 mg/kg) or placebo intravenously after induction of anesthesia. Acetaminophen-codeine and ibuprofen were given as postoperative analgesia. Follow-up continued until the 10th postoperative day. MAIN OUTCOME MEASURES The primary end point was prevention of PONV at 24 hours; secondary end points were decrease in the need for ibuprofen at 24 hours and evaluation of adverse effects. RESULTS At 24 hours, 24 of 54 participants who received placebo (44%; 95% confidence interval [CI], 31%-59%) had experienced PONV compared with 20 of 53 (38%; 95% CI, 25%-52%), 13 of 54 (24%; 95% CI, 13%-38%), and 6 of 52 (12%; 95% CI, 4%-23%) who received dexamethasone at 0.05, 0.15, and 0.5 mg/kg, respectively (P<.001 for linear trend). Children who received dexamethasone received significantly less ibuprofen. There were 26 postoperative bleeding episodes in 22 children. Two of 53 (4%; 95% CI, 0.5%-13%) children who received placebo had bleeding compared with 6 of 53 (11%; 95% CI, 4%-23%), 2 of 51 (4%; 95% CI, 0.5%-13%), and 12 of 50 (24%; 95% CI, 13%-38%) who received dexamethasone at 0.05, 0.15, and 0.5 mg/kg, respectively (P = .003). Dexamethasone, 0.5 mg/kg, was associated with the highest bleeding risk (adjusted relative risk, 6.80; 95% CI, 1.77-1 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Dexamethasone, 0.5 mg/kg, was associated with the highest bleeding risk (adjusted relative risk, 6.80; 95% CI, 1.77-16.5).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 338, "doc_id": "23349986", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: CX3CR1 on the Th2 cells promotes T cell survival\n\nCANDIDATE_ABSTRACT:\nTITLE: CX3CR1 is required for airway inflammation by promoting T helper cell survival and maintenance in inflamed lung\nABSTRACT: Allergic asthma is a T helper type 2 (T(H)2)-dominated disease of the lung. In people with asthma, a fraction of CD4(+) T cells express the CX3CL1 receptor, CX3CR1, and CX3CL1 expression is increased in airway smooth muscle, lung endothelium and epithelium upon allergen challenge. Here we found that untreated CX3CR1-deficient mice or wild-type (WT) mice treated with CX3CR1-blocking reagents show reduced lung disease upon allergen sensitization and challenge. Transfer of WT CD4(+) T cells into CX3CR1-deficient mice restored the cardinal features of asthma, and CX3CR1-blocking reagents prevented airway inflammation in CX3CR1-deficient recipients injected with WT T(H)2 cells. We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma. CX3CR1-induced survival was also observed for T(H)1 cells upon airway inflammation but not under homeostatic conditions or upon peripheral inflammation. Therefore, CX3CR1 and CX3CL1 may represent attractive therapeutic targets in asthma.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 217, "doc_id": "21366394", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Immune responses in immune cells are geographically segregated.\n\nCANDIDATE_PASSAGE:\nInflammatory signaling in human Tuberculosis granulomas is spatially organized Granulomas are the pathological hallmark of tuberculosis (TB). However, their function and mechanisms of formation remain poorly understood. To understand the role of granulomas in TB, we analyzed the proteomes of granulomas from subjects with tuberculosis in an unbiased manner. Using laser-capture microdissection, mass spectrometry and confocal microscopy, we generated detailed molecular maps of human granulomas. We found that the centers of granulomas have a pro-inflammatory environment that is characterized by the presence of antimicrobial peptides, reactive oxygen species and pro-inflammatory eicosanoids. Conversely, the tissue surrounding the caseum has a comparatively anti-inflammatory signature. These findings are consistent across a set of six human subjects and in rabbits. Although the balance between systemic pro- and anti-inflammatory signals is crucial to TB disease outcome, here we find that these signals are physically segregated within each granuloma. From the protein and lipid snapshots of human and rabbit lesions analyzed here, we hypothesize that the pathologic response to TB is shaped by the precise anatomical localization of these inflammatory pathways during the development of the granuloma.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "559", "doc_id": "3475317", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Early patent ductus ateriosus (PDA) screening increases in-hospital mortality.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association Between Early Screening for Patent Ductus Arteriosus and In-Hospital Mortality Among Extremely Preterm Infants.\nABSTRACT: IMPORTANCE There is currently no consensus for the screening and treatment of patent ductus arteriosus (PDA) in extremely preterm infants. Less pharmacological closure and more supportive management have been observed without evidence to support these changes. OBJECTIVE To evaluate the association between early screening echocardiography for PDA and in-hospital mortality. DESIGN, SETTING, AND PARTICIPANTS Comparison of screened and not screened preterm infants enrolled in the EPIPAGE 2 national prospective population-based cohort study that included all preterm infants born at less than 29 weeks of gestation and hospitalized in 68 neonatal intensive care units in France from April through December 2011. Two main analyses were performed to adjust for potential selection bias, one using propensity score matching and one using neonatal unit preference for early screening echocardiography as an instrumental variable. EXPOSURES Early screening echocardiography before day 3 of life. MAIN OUTCOMES AND MEASURES The primary outcome was death between day 3 and discharge. The secondary outcomes were major neonatal morbidities (pulmonary hemorrhage, severe bronchopulmonary dysplasia, severe cerebral lesions, and necrotizing enterocolitis). RESULTS Among the 1513 preterm infants with data available to determine exposure, 847 were screened for PDA and 666 were not; 605 infants from each group could be paired. Exposed infants were treated for PDA more frequently during their hospitalization than nonexposed infants (55.1% vs 43.1%; odds ratio [OR], 1.62 [95% CI, 1.31 to 2.00]; absolute risk reduction [ARR] in events per 100 infants, -12.0 [95% CI, -17.3 to -6.7). Exposed infants had a lower hospital death rate (14.2% vs 18.5% ; OR, 0.73 [95% CI, 0.54 to 0.98]; ARR, 4.3 [95% [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Exposed infants had a lower hospital death rate (14.2% vs 18.5% ; OR, 0.73 [95% CI, 0.54 to 0.98]; ARR, 4.3 [95% CI, 0.3 to 8.3]) and a lower rate of pulmonary hemorrhage (5.6% vs 8.9%; OR, 0.60 [95% CI, 0.38 to 0.95]; ARR, 3.3 [95% CI, 0.4 to 6.3]).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 368, "doc_id": "27099731", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: There is no increased risk of hypospadias with clomiphene.\n\nCANDIDATE_ABSTRACT:\nTITLE: Use of clomifene during early pregnancy and risk of hypospadias: population based case-control study.\nABSTRACT: Clomifene is widely used for inducing ovulation.1 It is structurally related to diethylstilbestrol, which has been linked to vaginal and cervical clear cell adenocarcinoma in women exposed in utero. The adverse effect is less severe in sons, although links to testicular cancer and urogenital anomalies, such as epididymal cysts, have been reported.2 3 A recent study also found an increased risk of hypospadias in the sons of women exposed to diethylstilbestrol in utero.4 Clomifene has a half life of about five days, but its metabolites have been found in blood samples on day 22 of the menstrual cycle and in faeces up to six weeks after administration.5 The occurrence of hypospadias may be increasing. Little is known about the risk of hypospadias in boys born to women who have used clomifene to induce ovulation. ### Methods and results Our case-control study was done in the Danish counties of North Jutland, Aarhus, Viborg, and …", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The adverse effect is less severe in sons, although links to testicular cancer and urogenital anomalies, such as epididymal cysts, have been reported.2 3 A recent study also found an increased risk of hypospadias in the sons of women exposed to diethylstilbestrol in utero.4 Clomifene has a half life of about five days, but its metabolites have been found in blood samples on day 22 of the menstrual cycle and in faeces up to six weeks after administration.5 The occurrence of hypospadias may be increasing.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1293, "doc_id": "43329366", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Stiff substrates encourage mesodermal differentiation by degrading beta-catenin in an integrin-dependent manner.\n\nCANDIDATE_ABSTRACT:\nTITLE: MicroRNAs can generate thresholds in target gene expression\nABSTRACT: MicroRNAs (miRNAs) are short, highly conserved noncoding RNA molecules that repress gene expression in a sequence-dependent manner. We performed single-cell measurements using quantitative fluorescence microscopy and flow cytometry to monitor a target gene's protein expression in the presence and absence of regulation by miRNA. We find that although the average level of repression is modest, in agreement with previous population-based measurements, the repression among individual cells varies dramatically. In particular, we show that regulation by miRNAs establishes a threshold level of target mRNA below which protein production is highly repressed. Near this threshold, protein expression responds sensitively to target mRNA input, consistent with a mathematical model of molecular titration. These results show that miRNAs can act both as a switch and as a fine-tuner of gene expression.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1101, "doc_id": "2000038", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does use of hydrophilic guidewires significantly improve technical success rates of peripheral PTA?\n\nABSTRACT:\nTo determine whether the use of hydrophilic guidewires has increased the technical success rate of peripheral percutaneous transluminal angioplasty (PTA).MATERIAL/ We performed 125 procedures and analyzed the technical success rates of PTA using the conventional guidewire first and then if needed, the hydrophilic guidewire for iliac and SFA stenoses or occlusions. Angioplasty was performed on 25 stenosed, 25 occluded iliac arteries and 25 stenosed, 50 occluded femoral arteries. The result was defined as technical success when the lesion was crossed by a guidewire and balloon, then it was dilated with restoration of vessel lumen and less than 30% residual stenosis and the rise in ABI values was at least 0.15 after 24 hours. The technical success rate after PTA of stenosed iliac arteries was achieved in 96% (24/25) using conventional wires and 100% using hydrophilic guidewire; in iliac occlusions, the rates were 60% (15/25) and 96%, respectively; in femoral stenosis - 84% (21/25) and 100%; in occlusions in the first group: lesions<10 cm -64% (16/25) and 96%, in the second group: lesions>10 cm -48% (12/25) and 88%. In the iliac group, there was no significant difference in the success of iliac stenosis PTA. However, there were significant changes in the success rates of PTA performed for SFA stenosis and iliac and SFA occlusions.", "output": "{\"label\": \"maybe\", \"rationale\": \"In summary, we report an overall improvement and high technical success rate for peripherial PTA. The use of hydrophilic guidewires made significant difference to the technical success rate of PTA, especially in occlusion and more complicated lesions.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 16538201, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does radiofrequency catheter ablation of the atria reduce inducibility and duration of atrial fibrillation in dogs?\n\nABSTRACT:\nThe purpose of this study was to prevent induction of sustained atrial fibrillation (AF) by radiofrequency catheter ablation (RFCA) of the atria in an open-chest canine model. In dogs randomized to acute studies, RFCA of the atria was performed after reproducible induction of sustained AF (lasting > 30 minutes) with burst stimulation or premature atrial pacing and perpetuation by low level cervical vagal stimulation or IV infusion of methacholine. Additionally, in four dogs, the long-term effectiveness of RFCA was assessed 7 to 21 days after ablation. Continuous discrete transmural lesions were produced with radiofrequency energy pulses (20 to 40 W for 60 seconds) delivered to five atrial epicardial sites and endovascularly to the coronary sinus wall. RFCA electrically isolated regions of the atria that became dissociated from the nonisolated parts. Atrial RFCA markedly attenuated vagally induced shortening of effective refractory period (ERP) at both isolated and nonisolated test sites located in the left and right atria (P < .001, n = 5). RFCA rendered noninducible sustained AF maintained by cervical vagal stimulation. The dose-response curve relating the dose of methacholine required to maintain AF was shifted down and to the right. AF was only inducible with high doses of methacholine. Atrial RFCA reduced the maximal sinus rate and prolonged the corrected sinus-node recovery time (P < .001, n = 6). However, RFCA did not affect atrial contractile function, AV-nodal ERP, or AV-nodal or His-Purkinje conduction times. In dogs in the chronic group, normal sinus rhythm and normal AV conduction were preserved and AF was only inducible with a high dose of methacholine. No atrial perforations resulted.", "output": "{\"label\": \"yes\", \"rationale\": \"RFCA in open-chest dogs produces partial vagal denervation and reduces the inducibility of AF.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 7697854, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Depletion of nitric oxide is responsible for vasospasm.\n\nCANDIDATE_ABSTRACT:\nTITLE: Nitrite infusions to prevent delayed cerebral vasospasm in a primate model of subarachnoid hemorrhage.\nABSTRACT: CONTEXT Delayed cerebral vasospasm causes permanent neurological deficits or death in at least 15% of patients following otherwise successful treatment for ruptured intracranial aneurysm. Decreased bioavailability of nitric oxide has been associated with the development of cerebral vasospasm. OBJECTIVE To determine whether infusions of nitrite will prevent delayed cerebral vasospasm. DESIGN, SETTING, AND SUBJECTS A total of 14 anesthetized cynomolgus monkeys had an autologous blood clot placed around the right middle cerebral artery. Cerebral arteriography was performed before clot placement and on days 7 and 14 to assess vasospasm. The study was conducted from August 2003 to February 2004. INTERVENTIONS A 90-mg sodium nitrite intravenous solution infused over 24 hours plus a 45-mg sodium nitrite bolus daily (n = 3); a 180-mg sodium nitrite intravenous solution infused over 24 hours (n = 3); or a control saline solution infusion (n = 8). Each was infused continuously for 14 days. MAIN OUTCOME MEASURES Nitrite, S-nitrosothiol, and methemoglobin levels in blood and cerebrospinal fluid and degree of arteriographic vasospasm. RESULTS In control monkeys, mean (SD) cerebrospinal fluid nitrite levels decreased from 3.1 (1.5) micromol/L to 0.4 (0.1) micromol/L at day 7 and to 0.4 (0.4) micromol/L at day 14 (P = .03). All 8 control monkeys developed significant vasospasm of the right middle cerebral artery, which was complicated by stroke and death in 1 animal. Sodium nitrite infusions increased the nitrite and methemoglobin levels (<2.1% of total hemoglobin) in the blood and cerebrospinal fluid without evoking systemic hypotension. Nitrite infusion prevented development of vasospasm (no animals developed significant vasospasm; mean [SD] reduction in right middle cer [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Nitrite infusion prevented development of vasospasm (no animals developed significant vasospasm; mean [SD] reduction in right middle cerebral artery area on day 7 after subarachnoid hemorrhage of 8% [9%] in nitrite-treated monkeys vs 47% [5%] in saline-treated controls; P<.001).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 334, "doc_id": "25079962", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does perspective-taking increase patient satisfaction in medical encounters?\n\nABSTRACT:\nTo assess whether perspective-taking, which researchers in other fields have shown to induce empathy, improves patient satisfaction in encounters between student-clinicians and standardized patients (SPs). In three studies, randomly assigned students (N = 608) received either a perspective-taking instruction or a neutral instruction prior to a clinical skills examination in 2006-2007. SP satisfaction was the main outcome in all three studies. Study 1 involved 245 third-year medical students from two universities. Studies 2 and 3 extended Study 1 to examine generalizability across student and SP subpopulations. Study 2 (105 physician assistant students, one university) explored the effect of perspective-taking on African American SPs' satisfaction. Study 3 (258 third-year medical students, two universities) examined the intervention's effect on students with high and low baseline perspective-taking tendencies. Intervention students outscored controls in patient satisfaction in all studies: Study 1: P = .01, standardized effect size = 0.16; Study 2: P = .001, standardized effect size = 0.31; Study 3: P = .009, standardized effect size = 0.13. In Study 2, perspective-taking improved African American SPs' satisfaction. In Study 3, intervention students with high baseline perspective-taking tendencies outscored controls (P = .0004, standardized effect size = 0.25), whereas those with low perspective-taking tendencies did not (P = .72, standardized effect size = 0.00).", "output": "{\"label\": \"maybe\", \"rationale\": \"Perspective-taking increased patient satisfaction in all three studies, across medical schools, clinical disciplines, and racially diverse students and SPs. Perspective-taking as a means for improving patient satisfaction deserves further exploration in clinical training and practice.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 20736672, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Sympathetic nerve activity is reduced throughout normal pregnancy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Regulation of sympathetic nerve activity during the cold pressor test in normotensive pregnant and nonpregnant women.\nABSTRACT: Baseline neurovascular transduction is reduced in normotensive pregnancy; however, little is known about changes to neurovascular transduction during periods of heightened sympathetic activation. We tested the hypothesis that, despite an exacerbated muscle sympathetic nerve activity (microneurography) response to cold pressor stimulation, the blunting of neurovascular transduction in normotensive pregnant women would result in similar changes in vascular resistance and mean arterial pressure (Finometer) relative to nonpregnant controls. Baseline neurovascular transduction was reduced in pregnant women relative to controls when expressed as the quotient of both total resistance and mean arterial pressure and sympathetic burst frequency (0.32±0.07 versus 0.58±0.16 mm Hg/L/min/bursts/min, P<0.001 and 2.4±0.7 versus 3.6±0.8 mm Hg/bursts/min, P=0.001). Sympathetic activation was greater across all 3 minutes of cold pressor stimulation in the pregnant women relative to the nonpregnant controls. Peak sympathoexcitation was also greater in pregnant than in nonpregnant women, whether expressed as sympathetic burst frequency (+17±13 versus +7±8 bursts/min, P=0.049), burst incidence (+17±9 versus +6±11 bursts/100 hb, P=0.03), or total activity (+950±660 versus +363±414 arbitrary units, P=0.04). However, neurovascular transduction during peak cold pressor-induced sympathoexcitation remained blunted in pregnant women (0.25±0.11 versus 0.45±0.08 mm Hg/L/min/bursts/min, P<0.001 and 1.9±1.0 versus 3.2±0.9 mm Hg/bursts/min, P=0.006). Therefore, mean arterial pressure (93±21 versus 99±6 mm Hg, P=0.4) and total peripheral resistance (12±3 versus 14±3 mm Hg/L/min) were not different between pregnant and nonpregnant women during peak sympathoexcitation. These data indicate that [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Peak sympathoexcitation was also greater in pregnant than in nonpregnant women, whether expressed as sympathetic burst frequency (+17±13 versus +7±8 bursts/min, P=0.049), burst incidence (+17±9 versus +6±11 bursts/100 hb, P=0.03), or total activity (+950±660 versus +363±414 arbitrary units, P=0.04).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1120, "doc_id": "13907928", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Marmosets have a brain region homologous to Broca's area.\n\nCANDIDATE_PASSAGE:\nDecreased neurogenesis after cholinergic forebrain lesion in the adult rat. Adult neurogenesis has been shown to be regulated by a multitude of extracellular cues, including hormones, growth factors, and neurotransmitters. The cholinergic system of the basal forebrain is one of the key transmitter systems for learning and memory. Because adult neurogenesis has been implicated in cognitive performance, the present work aims at defining the role of cholinergic input for adult neurogenesis by using an immunotoxic lesion approach. The immunotoxin 192IgG-saporin was infused into the lateral ventricle of adult rats to selectively lesion cholinergic neurons of the cholinergic basal forebrain (CBF), which project to the two main regions of adult neurogenesis: the dentate gyrus and the olfactory bulb. Five weeks after lesioning, neurogenesis, defined by the number of cells colocalized for bromodeoxyuridine (BrdU) and the neuronal nuclei marker NeuN, declined significantly in the granule cell layers of the dentate gyrus and olfactory bulb. Furthermore, immunotoxic lesions to the CBF led to increased numbers of apoptotic cells specifically in the subgranular zone, the progenitor region of the dentate gyrus, and within the periglomerular layer of the olfactory bulb. We propose that the cholinergic system plays a survival-promoting role for neuronal progenitors and immature neurons within regions of adult neurogenesis, similar to effects observed previously during brain development. As a working hypothesis, neuronal loss within the CBF system leads not only to cognitive deficits but may also alter on a cellular level the functionality of the dentate gyrus, which in turn may aggravate cognitive deficits.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "758", "doc_id": "22549449", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Type 1 Diabetes is associated with subtle perturbations in T reg development.\n\nCANDIDATE_ABSTRACT:\nTITLE: Large-scale genetic fine mapping and genotype-phenotype associations implicate polymorphism in the IL2RA region in type 1 diabetes\nABSTRACT: Genome-wide association studies are now identifying disease-associated chromosome regions. However, even after convincing replication, the localization of the causal variant(s) requires comprehensive resequencing, extensive genotyping and statistical analyses in large sample sets leading to targeted functional studies. Here, we have localized the type 1 diabetes (T1D) association in the interleukin 2 receptor alpha (IL2RA) gene region to two independent groups of SNPs, spanning overlapping regions of 14 and 40 kb, encompassing IL2RA intron 1 and the 5′ regions of IL2RA and RBM17 (odds ratio = 2.04, 95% confidence interval = 1.70–2.45; P = 1.92 × 10−28; control frequency = 0.635). Furthermore, we have associated IL2RA T1D susceptibility genotypes with lower circulating levels of the biomarker, soluble IL-2RA (P = 6.28 × 10−28), suggesting that an inherited lower immune responsiveness predisposes to T1D.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here, we have localized the type 1 diabetes (T1D) association in the interleukin 2 receptor alpha (IL2RA) gene region to two independent groups of SNPs, spanning overlapping regions of 14 and 40 kb, encompassing IL2RA intron 1 and the 5′ regions of IL2RA and RBM17 (odds ratio = 2.04, 95% confidence interval = 1.70–2.45; P = 1.92 × 10−28; control frequency = 0.635).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1334, "doc_id": "13940200", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: IgA plasma cells that are specific for transglutaminase 2 are scarce in the duodenal mucosa of celiac disease patients when the disease is active.\n\nCANDIDATE_ABSTRACT:\nTITLE: High abundance of plasma cells secreting transglutaminase 2–specific IgA autoantibodies with limited somatic hypermutation in celiac disease intestinal lesions\nABSTRACT: Celiac disease is an immune-mediated disorder in which mucosal autoantibodies to the enzyme transglutaminase 2 (TG2) are generated in response to the exogenous antigen gluten in individuals who express human leukocyte antigen HLA-DQ2 or HLA-DQ8 (ref. 3). We assessed in a comprehensive and nonbiased manner the IgA anti-TG2 response by expression cloning of the antibody repertoire of ex vivo–isolated intestinal antibody-secreting cells (ASCs). We found that TG2-specific plasma cells are markedly expanded within the duodenal mucosa in individuals with active celiac disease. TG2-specific antibodies were of high affinity yet showed little adaptation by somatic mutations. Unlike infection-induced peripheral blood plasmablasts, the TG2-specific ASCs had not recently proliferated and were not short-lived ex vivo. Altogether, these observations demonstrate that there is a germline repertoire with high affinity for TG2 that may favor massive generation of autoreactive B cells. TG2-specific antibodies did not block enzymatic activity and served as substrates for TG2-mediated crosslinking when expressed as IgD or IgM but not as IgA1 or IgG1. This could result in preferential recruitment of plasma cells from naive IgD- and IgM-expressing B cells, thus possibly explaining why the antibody response to TG2 bears signs of a primary immune response despite the disease chronicity.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We found that TG2-specific plasma cells are markedly expanded within the duodenal mucosa in individuals with active celiac disease.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 553, "doc_id": "1471041", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Tuberculosis-induced granulomas express different immune system protein signatures than the surrounding tissue.\n\nCANDIDATE_ABSTRACT:\nTITLE: Inflammatory signaling in human Tuberculosis granulomas is spatially organized\nABSTRACT: Granulomas are the pathological hallmark of tuberculosis (TB). However, their function and mechanisms of formation remain poorly understood. To understand the role of granulomas in TB, we analyzed the proteomes of granulomas from subjects with tuberculosis in an unbiased manner. Using laser-capture microdissection, mass spectrometry and confocal microscopy, we generated detailed molecular maps of human granulomas. We found that the centers of granulomas have a pro-inflammatory environment that is characterized by the presence of antimicrobial peptides, reactive oxygen species and pro-inflammatory eicosanoids. Conversely, the tissue surrounding the caseum has a comparatively anti-inflammatory signature. These findings are consistent across a set of six human subjects and in rabbits. Although the balance between systemic pro- and anti-inflammatory signals is crucial to TB disease outcome, here we find that these signals are physically segregated within each granuloma. From the protein and lipid snapshots of human and rabbit lesions analyzed here, we hypothesize that the pathologic response to TB is shaped by the precise anatomical localization of these inflammatory pathways during the development of the granuloma.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We found that the centers of granulomas have a pro-inflammatory environment that is characterized by the presence of antimicrobial peptides, reactive oxygen species and pro-inflammatory eicosanoids. Conversely, the tissue surrounding the caseum has a comparatively anti-inflammatory signature.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1328, "doc_id": "3475317", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: There is no increased risk of hypospadias with clomiphene.\n\nCANDIDATE_ABSTRACT:\nTITLE: Use of clomifene during early pregnancy and risk of hypospadias: population based case-control study.\nABSTRACT: Clomifene is widely used for inducing ovulation.1 It is structurally related to diethylstilbestrol, which has been linked to vaginal and cervical clear cell adenocarcinoma in women exposed in utero. The adverse effect is less severe in sons, although links to testicular cancer and urogenital anomalies, such as epididymal cysts, have been reported.2 3 A recent study also found an increased risk of hypospadias in the sons of women exposed to diethylstilbestrol in utero.4 Clomifene has a half life of about five days, but its metabolites have been found in blood samples on day 22 of the menstrual cycle and in faeces up to six weeks after administration.5 The occurrence of hypospadias may be increasing. Little is known about the risk of hypospadias in boys born to women who have used clomifene to induce ovulation. ### Methods and results Our case-control study was done in the Danish counties of North Jutland, Aarhus, Viborg, and …", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The adverse effect is less severe in sons, although links to testicular cancer and urogenital anomalies, such as epididymal cysts, have been reported.2 3 A recent study also found an increased risk of hypospadias in the sons of women exposed to diethylstilbestrol in utero.4 Clomifene has a half life of about five days, but its metabolites have been found in blood samples on day 22 of the menstrual cycle and in faeces up to six weeks after administration.5 The occurrence of hypospadias may be increasing.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1293, "doc_id": "43329366", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is Panton-Valentine leucocidin associated with the pathogenesis of Staphylococcus aureus bacteraemia in the UK?\n\nABSTRACT:\nThe morbidity and mortality associated with Panton-Valentine leucocidin (PVL)-positive Staphylococcus aureus suggest that this toxin is a key marker of disease severity. Nevertheless, the importance of PVL in the pathogenesis of primary bacteraemia caused by S. aureus is uncertain. We have determined the prevalence of PVL-encoding genes among isolates of S. aureus from bacteraemic patients. Consecutive bacteraemia isolates of S. aureus (n=244) from patients hospitalized in 25 centres in the UK and Ireland during 2005 were screened for PVL and mecA genes. PVL-positive isolates were characterized by toxin gene profiling, PFGE, spa-typing and MIC determinations for a range of antimicrobials. Four out of 244 isolates (1.6%) were PVL-positive and susceptible to oxacillin [methicillin-susceptible S. aureus (MSSA)]. Eighty-eight out of 244 (36%) were oxacillin-resistant (methicillin-resistant S. aureus), but none was PVL-positive. The four patients (two males: 30 and 33 years; two females: 62 and 80 years) had infection foci of: skin and soft tissue, unknown, indwelling line, and surgical site, and were located at one centre in Wales, one in England and two in Ireland. One of four PVL-positive isolates was resistant to penicillin and fusidic acid, the remainder were susceptible to all antibiotics tested. Genotypic analyses showed that the four isolates represented three distinct strains; the two isolates from Ireland were related.", "output": "{\"label\": \"maybe\", \"rationale\": \"We found that 1.6% of S. aureus (all MSSA) from bacteraemic patients were PVL-positive. This low incidence suggests that PVL-positive S.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 17562682, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The repeat-variable diresidue (RVD) in the loop of Transcription-Activator Like (TAL) effectors specifies the nucleotides-amino acid contact at the target promoter element.\n\nCANDIDATE_ABSTRACT:\nTITLE: Structural basis for sequence-specific recognition of DNA by TAL effectors.\nABSTRACT: TAL (transcription activator-like) effectors, secreted by phytopathogenic bacteria, recognize host DNA sequences through a central domain of tandem repeats. Each repeat comprises 33 to 35 conserved amino acids and targets a specific base pair by using two hypervariable residues [known as repeat variable diresidues (RVDs)] at positions 12 and 13. Here, we report the crystal structures of an 11.5-repeat TAL effector in both DNA-free and DNA-bound states. Each TAL repeat comprises two helices connected by a short RVD-containing loop. The 11.5 repeats form a right-handed, superhelical structure that tracks along the sense strand of DNA duplex, with RVDs contacting the major groove. The 12th residue stabilizes the RVD loop, whereas the 13th residue makes a base-specific contact. Understanding DNA recognition by TAL effectors may facilitate rational design of DNA-binding proteins with biotechnological applications.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"TAL (transcription activator-like) effectors, secreted by phytopathogenic bacteria, recognize host DNA sequences through a central domain of tandem repeats. Each repeat comprises 33 to 35 conserved amino acids and targets a specific base pair by using two hypervariable residues [known as repeat variable diresidues (RVDs)] at positions 12 and 13.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1263, "doc_id": "3981729", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is helicobacter pylori a risk factor for stress ulcer bleeding in polytraumatized patients?\n\nABSTRACT:\nThe pathogenesis of acute stress-related hemorrhage in critically ill polytraumatized patients is uncertain and any role of Helicobacter pylori infection is unknown. The aim of our study was to evaluate the relationship between Helicobacter pylori serological status of patients developing stress-related bleeding and those with no appearance of upper gastrointestinal bleeding. In our single-center prospective cohort study we investigated over a 3-year period all consecutive patients with upper gastrointestinal hemorrhage for Helicobacter pylori infection by serology. Control group comprised 101 such patients with no evidence of hemorrhage. Of 396 assessable patients, stress-related upper gastrointestinal bleeding was observed in 11 (3.1%) patients. Six (55%) of the 11 bleeding patients and 45 (45%) of the 101 control group patients had serological evidence of Helicobacter pylori infection (p=0.5). Bleeding developed significantly more often in patients with more serious injury (for ISS, p=0.04, for TRISS p=0.03). Bleeding patients showed insignificantly higher mortality (36% vs. 15%; p=0.09).", "output": "{\"label\": \"no\", \"rationale\": \"Helicobacter pylori infection was not significantly more prevalent in polytraumatized patients with hemorrhage when compared with control group. Our data suggest that the infection with Helicobacter pylori does not play an important role in bleeding, indicating no causative role for it in upper gastrointestinal hemorrhage of polytraumatized patients. The incidence of bleeding is low and bleeding develops usually later, in the meantime is the Helicobacter pylori infection eradicated with the antibiotics used for another purpose.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 15086186, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Radioiodine treatment of non-toxic multinodular goitre reduces thyroid volume.\n\nCANDIDATE_ABSTRACT:\nTITLE: Radioiodine treatment of multinodular non-toxic goitre.\nABSTRACT: OBJECTIVE To investigate the long term effect of radioactive iodine on thyroid function and size in patients with non-toxic multinodular goitre. DESIGN Consecutive patients with multinodular non-toxic goitre selected for radioactive iodine treatment and followed for a minimum of 12 months (median 48 months) after an intended dose of 3.7 MBq/g thyroid tissue corrected to a 100% uptake of iodine-131 in 24 hours. PATIENTS 69 patients with a growing multinodular non-toxic goitre causing local compression symptoms or cosmetic inconveniences. The treatment was chosen because of a high operative risk, previous thyroidectomy, or refusal to be operated on. MAIN OUTCOME MEASUREMENTS Standard thyroid function variables and ultrasonically determined thyroid volume before treatment as well as 1, 2, 3, 6, and 12 months after treatment and then once a year. RESULTS 56 patients were treated with a single dose of 131I, 12 with two doses, and one with four doses. In 45 patients treated with one dose and remaining euthyroid the median thyroid volume was reduced from 73 (interquartile range 50-106) ml to 29 (23-48) ml at 24 months in the 39 patients in whom this was measured during follow up. The median reduction was 40 (22-48) ml (60% reduction, p < 0.0001), half of which occurred within three months. Patients treated with two doses as well as those developing hypothyroidism and hyperthyroidism had a significant reduction in thyroid volume. Eleven patients developed hypothyroidism (cumulative five year risk 22%, 95% confidence interval 4.8% to 38.4%). Side effects were few: three cases of hyperthyroidism and two cases of radiation thyroiditis. Only one patient was dissatisfied with the result; she was referred for operation six months after treatment. CONCLUSIONS A substantial [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS A substantial reduction in thyroid volume accompanied by a low incidence of hypothyroidism and few side effects makes the use of radioactive iodine an attractive alternative to surgery in selected cases of non-toxic multinodular goitre.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1012, "doc_id": "9745001", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Individuals with Alzheimers who participate in six months of physical activity improve cognitive function for up to 18 months.\n\nCANDIDATE_PASSAGE:\nRadioiodine treatment of multinodular non-toxic goitre. OBJECTIVE To investigate the long term effect of radioactive iodine on thyroid function and size in patients with non-toxic multinodular goitre. DESIGN Consecutive patients with multinodular non-toxic goitre selected for radioactive iodine treatment and followed for a minimum of 12 months (median 48 months) after an intended dose of 3.7 MBq/g thyroid tissue corrected to a 100% uptake of iodine-131 in 24 hours. PATIENTS 69 patients with a growing multinodular non-toxic goitre causing local compression symptoms or cosmetic inconveniences. The treatment was chosen because of a high operative risk, previous thyroidectomy, or refusal to be operated on. MAIN OUTCOME MEASUREMENTS Standard thyroid function variables and ultrasonically determined thyroid volume before treatment as well as 1, 2, 3, 6, and 12 months after treatment and then once a year. RESULTS 56 patients were treated with a single dose of 131I, 12 with two doses, and one with four doses. In 45 patients treated with one dose and remaining euthyroid the median thyroid volume was reduced from 73 (interquartile range 50-106) ml to 29 (23-48) ml at 24 months in the 39 patients in whom this was measured during follow up. The median reduction was 40 (22-48) ml (60% reduction, p < 0.0001), half of which occurred within three months. Patients treated with two doses as well as those developing hypothyroidism and hyperthyroidism had a significant reduction in thyroid volume. Eleven patients developed hypothyroidism (cumulative five year risk 22%, 95% confidence interval 4.8% to 38.4%). Side effects were few: three cases of hyperthyroidism and two cases of radiation thyroiditis. Only one patient was dissatisfied with the result; she was referred for operati [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "621", "doc_id": "9745001", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Leuko-reduced blood reduces infectious complications in red blood cell transfusion.\n\nCANDIDATE_ABSTRACT:\nTITLE: Clinical outcomes following institution of the Canadian universal leukoreduction program for red blood cell transfusions.\nABSTRACT: CONTEXT A number of countries have implemented a policy of universal leukoreduction of their blood supply, but the potential role of leukoreduction in decreasing postoperative mortality and infection is unclear. OBJECTIVE To evaluate clinical outcomes following adoption of a national universal prestorage leukoreduction program for blood transfusions. DESIGN, SETTING, AND POPULATION Retrospective before-and-after cohort study conducted from August 1998 to August 2000 in 23 academic and community hospitals throughout Canada, enrolling 14 786 patients who received red blood cell transfusions following cardiac surgery or repair of hip fracture, or who required intensive care following a surgical intervention or multiple trauma. INTERVENTION Universal prestorage leukoreduction program introduced by 2 Canadian blood agencies. A total of 6982 patients were enrolled during the control period and 7804 patients were enrolled following prestorage leukoreduction. MAIN OUTCOME MEASURES All-cause in-hospital mortality and serious nosocomial infections (pneumonia, bacteremia, septic shock, all surgical site infections) occurring after first transfusion and at least 2 days after index procedure or intensive care unit admission. Secondary outcomes included rates of posttransfusion fever and antibiotic use. RESULTS Unadjusted in-hospital mortality rates were significantly lower following the introduction of leukoreduction compared with the control period (6.19% vs 7.03%, respectively; P =.04). Compared with the control period, the adjusted odds of death following leukoreduction were reduced (odds ratio [OR], 0.87; 95% confidence interval [CI], 0.75-0.99), but serious nosocomial infections did not decrease (adjusted OR, 0.97; 95% CI, 0.87-1.09). The frequency of posttransfusio [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The frequency of posttransfusion fevers decreased significantly following leukoreduction (adjusted OR, 0.86; 95% CI, 0.79-0.94), as did antibiotic use (adjusted OR, 0.90; 95% CI, 0.82-0.99).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 693, "doc_id": "24088502", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does vitamin D supplementation improve human skeletal muscle contractile properties in insufficient young males?\n\nABSTRACT:\nVitamin D may be a regulator of skeletal muscle function, although human trials investigating this hypothesis are limited to predominantly elderly populations. We aimed to assess the effect of oral vitamin D3 in healthy young males upon skeletal muscle function. Participants (n = 29) received an oral dose of 10,000 IU day(-1) vitamin D3 (VITD) or a visually identical placebo (PLB) for 3 months. Serum 25[OH]D and intact parathyroid hormone (iPTH) were measured at baseline and at week 4, 8 and 12. Muscle function was assessed in n = 22 participants by isokinetic dynamometry and percutaneous isometric electromyostimulation at baseline and at week 6 and 12. Baseline mean total serum 25[OH]D was 40 ± 17 and 41 ± 20 nmol L(-1) for PLB and VITD, respectively. VITD showed a significant improvement in total 25[OH]D at week 4 (150 ± 31 nmol L(-1)) that remained elevated throughout the trial (P < 0.005). Contrastingly, PLB showed a significant decrease in 25[OH]D at week 12 (25 ± 15 nmol L(-1)) compared with baseline. Despite marked increases in total serum 25[OH]D in VITD and a decrease in PLB, there were no significant changes in any of the muscle function outcome measures at week 6 or 12 for either group (P > 0.05).", "output": "{\"label\": \"no\", \"rationale\": \"Elevating total serum 25[OH]D to concentrations > 120 nmol L(-1) has no effect on skeletal muscle function. We postulate that skeletal muscle function is only perturbed in conditions of severe deficiency (<12.5 nmol L(-1)).\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 24623067, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: There is no relation between Erythromycin use and hypertrophic pyloric stenosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Use of macrolides in mother and child and risk of infantile hypertrophic pyloric stenosis: nationwide cohort study\nABSTRACT: OBJECTIVE To assess the association between use of macrolide antibiotics in mothers and infants from pregnancy onset until 120 days after birth and infantile hypertrophic pyloric stenosis (IHPS). DESIGN Nationwide register based cohort study. SETTING Denmark, 1996-2011. PARTICIPANTS 999,378 liveborn singletons and linked individual level information on macrolide prescriptions (maternal use during pregnancy, n=30,091; maternal use after birth, n=21,557; use in infants, n=6591), surgery for IHPS, and potential confounders. MAIN OUTCOME MEASURES Surgery for IHPS by three categories of macrolide use: in mothers during pregnancy, in mothers after birth, and in infants after birth. RESULTS 880 infants developed IHPS (0.9 cases per 1000 births). Compared with infants with no use of macrolides, the adjusted rate ratio for IHPS in infants with use of macrolides during days 0 to 13 after birth was 29.8 (95% confidence interval 16.4 to 54.1) and during days 14 to 120 was 3.24 (1.20 to 8.74); the corresponding absolute risk differences were 24.4 (95% confidence interval 13.0 to 44.1) and 0.65 (0.06 to 2.21) cases per 1000 infants exposed to macrolides, respectively. The rate ratio for maternal use of macrolides for days 0 to 13 after birth was 3.49 (1.92 to 6.34) and for days 14 to 120 was 0.70 (0.26 to 1.90); the corresponding absolute risk differences were 2.15 (0.82 to 4.64) and -0.11 (-0.26 to 0.31). The rate ratios for maternal use of macrolides during pregnancy were 1.02 (0.65 to 1.59) for weeks 0 to 27 and 1.77 (0.95 to 3.31) for weeks 28 to birth; the corresponding absolute risk differences were 0.01 (-0.31 to 0.50) and 0.67 (-0.06 to 2.02). CONCLUSIONS Treatment of young infants with macrolide antibiotics was strongly associated with IHPS and should therefore o [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Treatment of young infants with macrolide antibiotics was strongly associated with IHPS and should therefore only be administered if potential treatment benefits outweigh the risk.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1295, "doc_id": "21239672", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Trans-acting factors, such as lncRNAs, influence mRNA translation.\n\nCANDIDATE_ABSTRACT:\nTITLE: LincRNA-p21 suppresses target mRNA translation.\nABSTRACT: Mammalian long intergenic noncoding RNAs (lincRNAs) are best known for modulating transcription. Here we report a posttranscriptional function for lincRNA-p21 as a modulator of translation. Association of the RNA-binding protein HuR with lincRNA-p21 favored the recruitment of let-7/Ago2 to lincRNA-p21, leading to lower lincRNA-p21 stability. Under reduced HuR levels, lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and β-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1311, "doc_id": "13763195", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Stroke patients with prior use of direct oral anticoagulants have a higher risk of in-hospital mortality than stroke patients with prior use of warfarin.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association of Intracerebral Hemorrhage Among Patients Taking Non–Vitamin K Antagonist vs Vitamin K Antagonist Oral Anticoagulants With In-Hospital Mortality\nABSTRACT: Importance Although non–vitamin K antagonist oral anticoagulants (NOACs) are increasingly used to prevent thromboembolic disease, there are limited data on NOAC-related intracerebral hemorrhage (ICH). Objective To assess the association between preceding oral anticoagulant use (warfarin, NOACs, and no oral anticoagulants [OACs]) and in-hospital mortality among patients with ICH. Design, Setting, and Participants Retrospective cohort study of 141 311 patients with ICH admitted from October 2013 to December 2016 to 1662 Get With The Guidelines–Stroke hospitals. Exposures Anticoagulation therapy before ICH, defined as any use of OACs within 7 days prior to hospital arrival. Main Outcomes and Measures In-hospital mortality. Results Among 141 311 patients with ICH (mean [SD] age, 68.3 [15.3] years; 48.1% women), 15 036 (10.6%) were taking warfarin and 4918 (3.5%) were taking NOACs preceding ICH, and 39 585 (28.0%) and 5783 (4.1%) were taking concomitant single and dual antiplatelet agents, respectively. Patients with prior use of warfarin or NOACs were older and had higher prevalence of atrial fibrillation and prior stroke. Acute ICH stroke severity (measured by the National Institutes of Health Stroke Scale) was not significantly different across the 3 groups (median, 9 [interquartile range, 2-21] for warfarin, 8 [2-20] for NOACs, and 8 [2-19] for no OACs). The unadjusted in-hospital mortality rates were 32.6% for warfarin, 26.5% for NOACs, and 22.5% for no OACs. Compared with patients without prior use of OACs, the risk of in-hospital mortality was higher among patients with prior use of warfarin (adjusted risk difference [ARD], 9.0% [97.5% CI, 7.9% to 10.1%]; adjusted odds ratio [AOR], 1.62 [97.5% CI, 1.53 to 1.71]) and higher among patients with prior use of [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Prior use of NOACs, compared with prior use of warfarin, was associated with lower risk of in-hospital mortality.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1103, "doc_id": "3898784", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Sequence conservation in gene regulatory regions between species is a poor predictor of conserved functionality.\n\nCANDIDATE_PASSAGE:\nPrevention of Type 2 Diabetes Mellitus Through Inhibition of the Renin-Angiotensin System Type 2 diabetes mellitus is becoming a major health problem associated with excess morbidity and mortality. As the prevalence of type 2 diabetes is rapidly increasing, prevention of the disease should be considered as a key objective in the near future. Besides lifestyle changes, various pharmacological treatments have proven their efficacy in placebo-controlled clinical trials, including antidiabetic drugs such as metformin, acarbose and troglitazone, or antiobesity agents such as orlistat. Arterial hypertension, a clinical entity in which insulin resistance is common, is strongly associated with type 2 diabetes and may precede the disease by several years. While antihypertensive agents such as diuretics or β-adrenoceptor antagonists may worsen insulin resistance and impair glucose tolerance, newer antihypertensive agents exert neutral or even slightly positive metabolic effects. Numerous clinical trials have investigated the effects of ACE inhibitors or angiotensin II receptor antagonists (ARAs) on insulin sensitivity in hypertensive patients, with or without diabetes, with no consistent results. Almost half of the studies with ACE inhibitors in hypertensive nondiabetic individuals demonstrated a slight but significant increase in insulin sensitivity as assessed by insulin-stimulated glucose disposal during a euglycaemic hyperinsulinaemic clamp, while the other half failed to reveal any significant change. The effects of ARAs on insulin sensitivity are neutral in most studies. Mechanisms of improvement of glucose tolerance and insulin sensitivity through the inhibition of the renin-angiotensin system (RAS) are complex. They may include improvement of blood flow and mi [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1075", "doc_id": "27428509", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: There is an inverse relationship between hip fractures and statin use.\n\nCANDIDATE_ABSTRACT:\nTITLE: HMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients.\nABSTRACT: CONTEXT Recent animal studies have found that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) lipid-lowering drugs (statins) substantially increase bone formation, but whether statin use in humans results in clinically meaningful bone formation or a reduction in the risk of osteoporotic fractures is not known. OBJECTIVE To determine whether the use of statins is associated with reduced hip fracture risk. DESIGN Case-control study. SETTING AND PATIENTS A total of 6110 New Jersey residents aged 65 years or older and enrolled in Medicare and either Medicaid or the Pharmacy Assistance for the Aged and Disabled program. Case patients (n=1222) underwent surgical repair of a hip fracture in 1994. Control patients (n=4888) were identified at a ratio of 4:1 and frequency-matched to case patients for age and sex. MAIN OUTCOME MEASURE Adjusted odds ratio (OR) of hip fracture by statin use in the 180 days and 3 years prior to the index date (the earliest date of admission for surgery), adjusted for demographic and clinical characteristics and health care utilization. RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus. No significant relationship was observed between use of nonstatin lipid-lowering agents and hip fracture risk. Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowe [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS These findings support an association between statin use by elderly patients and reduction in the risk of hip fracture.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1290, "doc_id": "4687948", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: CX3CR1 on the Th2 cells promotes airway inflammation.\n\nCANDIDATE_PASSAGE:\nCX3CR1 is required for airway inflammation by promoting T helper cell survival and maintenance in inflamed lung Allergic asthma is a T helper type 2 (T(H)2)-dominated disease of the lung. In people with asthma, a fraction of CD4(+) T cells express the CX3CL1 receptor, CX3CR1, and CX3CL1 expression is increased in airway smooth muscle, lung endothelium and epithelium upon allergen challenge. Here we found that untreated CX3CR1-deficient mice or wild-type (WT) mice treated with CX3CR1-blocking reagents show reduced lung disease upon allergen sensitization and challenge. Transfer of WT CD4(+) T cells into CX3CR1-deficient mice restored the cardinal features of asthma, and CX3CR1-blocking reagents prevented airway inflammation in CX3CR1-deficient recipients injected with WT T(H)2 cells. We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma. CX3CR1-induced survival was also observed for T(H)1 cells upon airway inflammation but not under homeostatic conditions or upon peripheral inflammation. Therefore, CX3CR1 and CX3CL1 may represent attractive therapeutic targets in asthma.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "218", "doc_id": "21366394", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: HAND2 methylation is a key step in early endometrial carcinogenesis.\n\nCANDIDATE_PASSAGE:\nDownstream of Mutant KRAS, the Transcription Regulator YAP Is Essential for Neoplastic Progression to Pancreatic Ductal Adenocarcinoma Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with poor survival rates and frequently carries oncogenic KRAS mutation. However, KRAS has thus far not been a viable therapeutic target. We found that the abundance of YAP mRNA, which encodes Yes-associated protein (YAP), a protein regulated by the Hippo pathway during tissue development and homeostasis, was increased in human PDAC tissue compared with that in normal pancreatic epithelia. In genetically engineered KrasG12D and KrasG12D:Trp53R172H mouse models, pancreas-specific deletion of Yap halted the progression of early neoplastic lesions to PDAC without affecting normal pancreatic development and endocrine function. Although Yap was dispensable for acinar to ductal metaplasia (ADM), an initial step in the progression to PDAC, Yap was critically required for the proliferation of mutant Kras or Kras:Trp53 neoplastic pancreatic ductal cells in culture and for their growth and progression to invasive PDAC in mice. Yap functioned as a critical transcriptional switch downstream of the oncogenic KRAS–mitogen-activated protein kinase (MAPK) pathway, promoting the expression of genes encoding secretory factors that cumulatively sustained neoplastic proliferation, a tumorigenic stromal response in the tumor microenvironment, and PDAC progression in Kras and Kras:Trp53 mutant pancreas tissue. Together, our findings identified Yap as a critical oncogenic KRAS effector and a promising therapeutic target for PDAC and possibly other types of KRAS-mutant cancers.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "488", "doc_id": "36310858", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Varying expression levels of EBI2 affect the positioning and migration of B cells.\n\nCANDIDATE_PASSAGE:\nType 1 diabetes-associated IL2RA variation lowers IL-2 signaling and contributes to diminished CD4+CD25+ regulatory T cell function. Numerous reports have demonstrated that CD4(+)CD25(+) regulatory T cells (Tregs) from individuals with a range of human autoimmune diseases, including type 1 diabetes, are deficient in their ability to control autologous proinflammatory responses when compared with nondiseased, control individuals. Treg dysfunction could be a primary, causal event or may result from perturbations in the immune system during disease development. Polymorphisms in genes associated with Treg function, such as IL2RA, confer a higher risk of autoimmune disease. Although this suggests a primary role for defective Tregs in autoimmunity, a link between IL2RA gene polymorphisms and Treg function has not been examined. We addressed this by examining the impact of an IL2RA haplotype associated with type 1 diabetes on Treg fitness and suppressive function. Studies were conducted using healthy human subjects to avoid any confounding effects of disease. We demonstrated that the presence of an autoimmune disease-associated IL2RA haplotype correlates with diminished IL-2 responsiveness in Ag-experienced CD4(+) T cells, as measured by phosphorylation of STAT5a, and is associated with lower levels of FOXP3 expression by Tregs and a reduction in their ability to suppress proliferation of autologous effector T cells. These data offer a rationale that contributes to the molecular and cellular mechanisms through which polymorphisms in the IL-2RA gene affect immune regulation, and consequently upon susceptibility to autoimmune and inflammatory diseases.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1361", "doc_id": "11899391", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The binding orientation of the ML-SA1 activator at hTRPML2 is different from the binding orientation of the ML-SA1 activator at hTRPML1.\n\nCANDIDATE_PASSAGE:\nRegulation and effects of hypothalamic galanin: relation to dietary fat, alcohol ingestion, circulating lipids and energy homeostasis. Galanin (GAL) is known to stimulate feeding behavior. This peptide has different properties and functions from other feeding stimulants, e.g., neuropeptide Y and agouti-related protein. Hypothalamic GAL is relatively unresponsive to food deprivation and to changes in corticosterone, glucose utilization, dietary carbohydrate and leptin. This indicates that this peptide is not essential under conditions when food is scarce or low-energy, high-carbohydrate diets are being consumed. In contrast, recent evidence suggests that GAL in the paraventricular nucleus (PVN) functions in close relation to dietary fat and alcohol. In particular, it mediates functions that allow animals to adapt to conditions of positive energy balance involving excess consumption of these nutrients. This peptide in the PVN is stimulated by a high-fat diet and also by alcohol. It is stimulated by an increase in circulating lipids caused by a fat-rich meal or alcohol consumption, and it rises during the middle of the active feeding cycle, when fat consumption and triglycerides naturally rise. When centrally injected, GAL in the PVN increases the consumption of food and alcohol. Moreover, it produces a significantly stronger feeding response in rats maintained on a fat-rich diet, which also promotes alcohol intake. This evidence supports the existence of non-homeostatic, positive feedback circuits between GAL and both dietary fat and alcohol. These circuits are believed to contribute to the large meal size, over-consumption of alcohol, and obesity which are generally associated with fat-rich foods.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1200", "doc_id": "11742219", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Hypothalamic glutamate neurotransmission is unrelated to energy balance.\n\nCANDIDATE_PASSAGE:\nA distinctive DNA damage response in human hematopoietic stem cells reveals an apoptosis-independent role for p53 in self-renewal. Highly regenerative tissues such as blood must possess effective DNA damage responses (DDR) that balance long-term regeneration with protection from leukemogenesis. Hematopoietic stem cells (HSCs) sustain life-long blood production, yet their response to DNA damage remains largely unexplored. We report that human HSCs exhibit delayed DNA double-strand break rejoining, persistent gammaH2AX foci, and enhanced p53- and ASPP1-dependent apoptosis after gamma-radiation compared to progenitors. p53 inactivation or Bcl-2 overexpression reduced radiation-induced apoptosis and preserved in vivo repopulating HSC function. Despite similar protection from irradiation-induced apoptosis, only Bcl-2-overexpressing HSCs showed higher self-renewal capacity, establishing that intact p53 positively regulates self-renewal independently from apoptosis. The reduced self-renewal of HSCs with inactivated p53 was associated with increased spontaneous gammaH2AX foci in secondary transplants of HSCs. Our data reveal distinct physiological roles of p53 that together ensure optimal HSC function: apoptosis regulation and prevention of gammaH2AX foci accumulation upon HSC self-renewal.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "541", "doc_id": "10015292", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: VgrG (Tssl) protein punctures membranes by forming a spike at the tip of the tube apparatus.\n\nCANDIDATE_PASSAGE:\nRegulation of beta catenin signaling and parathyroid hormone anabolic effects in bone by the matricellular protein periostin. Periostin (Postn) is a matricellular protein preferentially expressed by osteocytes and periosteal osteoblasts in response to mechanical stimulation and parathyroid hormone (PTH). Whether and how periostin expression influences bone anabolism, however, remains unknown. We investigated the skeletal response of adult Postn(-/-) and Postn(+/+) mice to intermittent PTH. Compared with Postn(+/+), Postn(-/-) mice had a lower bone mass, cortical bone volume, and strength response to PTH. PTH-stimulated bone-forming indices were all significantly lower in Postn(-/-) mice, particularly at the periosteum. Furthermore, in vivo stimulation of Wnt-β-catenin signaling by PTH, as evaluated in TOPGAL reporter mice, was inhibited in the absence of periostin (TOPGAL;Postn(-/-) mice). PTH stimulated periostin and inhibited MEF2C and sclerostin (Sost) expression in bone and osteoblasts in vitro. Recombinant periostin also suppressed Sost expression, which was mediated through the integrin αVβ3 receptor, whereas periostin-blocking antibody prevented inhibition of MEF2C and Sost by PTH. In turn, administration of a Sost-blocking antiboby partially restored the PTH-mediated increase in bone mass in Postn(-/-) mice. In addition, primary osteoblasts from Postn(-/-) mice showed a lower proliferation, mineralization, and migration, both spontaneously and in response to PTH. Osteoblastic gene expression levels confirmed a defect of Postn(-/-) osteoblast differentiation with and without PTH, as well as an increased osteoblast apoptosis in the absence of periostin. These data elucidate the complex role of periostin on bone anabolism, through the regulation of Sost [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1366", "doc_id": "21564598", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Amitriptyline is an effective treatment for chronic tension-type headaches.\n\nCANDIDATE_PASSAGE:\nMechanisms of astrocytogenesis in the mammalian brain. In the mammalian central nervous system, astrocytes are the most abundant cell type and play crucial roles in brain development and function. Astrocytes are known to be produced from multipotent neural stem cells (NSCs) at the late gestational stage during brain development, and accumulating evidence indicates that this stage-dependent generation of astrocytes from NSCs is achieved by systematic cooperation between environmental cues and cell-intrinsic programs. Exemplifying the former is cytokine signaling through the gp130-Janus kinase/signal transducer and activator of transcription 3 pathway, and exemplifying the latter is epigenetic modification of astrocyte-specific genes. Here, we introduce recent advances in our understanding of the mechanisms that coordinate astrocytogenesis from NSCs by modulating signaling pathways and epigenetic programs, with a particular focus on the developing mammalian forebrain.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "108", "doc_id": "6559201", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Treatment with a protein named FN restores regenerative abilities of aged muscles.\n\nCANDIDATE_PASSAGE:\nLoss of fibronectin from the aged stem cell niche affects the regenerative capacity of skeletal muscle in mice Age-related changes in the niche have long been postulated to impair the function of somatic stem cells. Here we demonstrate that the aged stem cell niche in skeletal muscle contains substantially reduced levels of fibronectin (FN), leading to detrimental consequences for the function and maintenance of muscle stem cells (MuSCs). Deletion of the gene encoding FN from young regenerating muscles replicates the aging phenotype and leads to a loss of MuSC numbers. By using an extracellular matrix (ECM) library screen and pathway profiling, we characterize FN as a preferred adhesion substrate for MuSCs and demonstrate that integrin-mediated signaling through focal adhesion kinase and the p38 mitogen-activated protein kinase pathway is strongly de-regulated in MuSCs from aged mice because of insufficient attachment to the niche. Reconstitution of FN levels in the aged niche remobilizes stem cells and restores youth-like muscle regeneration. Taken together, we identify the loss of stem cell adhesion to FN in the niche ECM as a previously unknown aging mechanism.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1324", "doc_id": "19912367", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Early patent ductus ateriosus (PDA) screening decreases in-hospital mortality.\n\nCANDIDATE_ABSTRACT:\nTITLE: Human T Cell Leukemia Virus Reactivation with Progression of Adult T-Cell Leukemia-Lymphoma\nABSTRACT: BACKGROUND Human T-cell leukemia virus-associated adult T-cell leukemia-lymphoma (ATLL) has a very poor prognosis, despite trials of a variety of different treatment regimens. Virus expression has been reported to be limited or absent when ATLL is diagnosed, and this has suggested that secondary genetic or epigenetic changes are important in disease pathogenesis. METHODS AND FINDINGS We prospectively investigated combination chemotherapy followed by antiretroviral therapy for this disorder. Nineteen patients were prospectively enrolled between 2002 and 2006 at five medical centers in a phase II clinical trial of infusional chemotherapy with etoposide, doxorubicin, and vincristine, daily prednisone, and bolus cyclophosphamide (EPOCH) given for two to six cycles until maximal clinical response, and followed by antiviral therapy with daily zidovudine, lamivudine, and alpha interferon-2a for up to one year. Seven patients were on study for less than one month due to progressive disease or chemotherapy toxicity. Eleven patients achieved an objective response with median duration of response of thirteen months, and two complete remissions. During chemotherapy induction, viral RNA expression increased (median 190-fold), and virus replication occurred, coincident with development of disease progression. CONCLUSIONS EPOCH chemotherapy followed by antiretroviral therapy is an active therapeutic regimen for adult T-cell leukemia-lymphoma, but viral reactivation during induction chemotherapy may contribute to treatment failure. Alternative therapies are sorely needed in this disease that simultaneously prevent virus expression, and are cytocidal for malignant cells.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 367, "doc_id": "601033", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Activation of the Rac1 homolog CED-10 kills viable cells in SRGP-1 mutant Caenorhabditis elegans.\n\nCANDIDATE_ABSTRACT:\nTITLE: Loss of the RhoGAP SRGP-1 promotes the clearance of dead and injured cells in Caenorhabditis elegans\nABSTRACT: Multicellular animals rapidly clear dying cells from their bodies. Many of the pathways that mediate this cell removal are conserved through evolution. Here, we identify srgp-1 as a negative regulator of cell clearance in both Caenorhabditis elegans and mammalian cells. Loss of srgp-1 function results in improved engulfment of apoptotic cells, whereas srgp-1 overexpression inhibits apoptotic cell corpse removal. We show that SRGP-1 functions in engulfing cells and functions as a GTPase activating protein (GAP) for CED-10 (Rac1). Interestingly, loss of srgp-1 function promotes not only the clearance of already dead cells, but also the removal of cells that have been brought to the verge of death through sublethal apoptotic, necrotic or cytotoxic insults. In contrast, impaired engulfment allows damaged cells to escape clearance, which results in increased long-term survival. We propose that C. elegans uses the engulfment machinery as part of a primitive, but evolutionarily conserved, survey mechanism that identifies and removes unfit cells within a tissue.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We show that SRGP-1 functions in engulfing cells and functions as a GTPase activating protein (GAP) for CED-10 (Rac1). Interestingly, loss of srgp-1 function promotes not only the clearance of already dead cells, but also the removal of cells that have been brought to the verge of death through sublethal apoptotic, necrotic or cytotoxic insults.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 71, "doc_id": "1127562", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Including pharmacists in rounding teams does not alter the incidence of adverse drug events (ADEs).\n\nCANDIDATE_ABSTRACT:\nTITLE: Molecular Basis for Target RNA Recognition and Cleavage by Human RISC\nABSTRACT: The RNA-Induced Silencing Complex (RISC) is a ribonucleoprotein particle composed of a single-stranded short interfering RNA (siRNA) and an endonucleolytically active Argonaute protein, capable of cleaving mRNAs complementary to the siRNA. The mechanism by which RISC cleaves a target RNA is well understood, however it remains enigmatic how RISC finds its target RNA. Here, we show, both in vitro and in vivo, that the accessibility of the target site correlates directly with the efficiency of cleavage, demonstrating that RISC is unable to unfold structured RNA. In the course of target recognition, RISC transiently contacts single-stranded RNA nonspecifically and promotes siRNA-target RNA annealing. Furthermore, the 5' part of the siRNA within RISC creates a thermodynamic threshold that determines the stable association of RISC and the target RNA. We therefore provide mechanistic insights by revealing features of RISC and target RNAs that are crucial to achieve efficiency and specificity in RNA interference.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 600, "doc_id": "950306", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Radioiodine treatment of non-toxic multinodular goitre increases thyroid volume.\n\nCANDIDATE_ABSTRACT:\nTITLE: Radioiodine treatment of multinodular non-toxic goitre.\nABSTRACT: OBJECTIVE To investigate the long term effect of radioactive iodine on thyroid function and size in patients with non-toxic multinodular goitre. DESIGN Consecutive patients with multinodular non-toxic goitre selected for radioactive iodine treatment and followed for a minimum of 12 months (median 48 months) after an intended dose of 3.7 MBq/g thyroid tissue corrected to a 100% uptake of iodine-131 in 24 hours. PATIENTS 69 patients with a growing multinodular non-toxic goitre causing local compression symptoms or cosmetic inconveniences. The treatment was chosen because of a high operative risk, previous thyroidectomy, or refusal to be operated on. MAIN OUTCOME MEASUREMENTS Standard thyroid function variables and ultrasonically determined thyroid volume before treatment as well as 1, 2, 3, 6, and 12 months after treatment and then once a year. RESULTS 56 patients were treated with a single dose of 131I, 12 with two doses, and one with four doses. In 45 patients treated with one dose and remaining euthyroid the median thyroid volume was reduced from 73 (interquartile range 50-106) ml to 29 (23-48) ml at 24 months in the 39 patients in whom this was measured during follow up. The median reduction was 40 (22-48) ml (60% reduction, p < 0.0001), half of which occurred within three months. Patients treated with two doses as well as those developing hypothyroidism and hyperthyroidism had a significant reduction in thyroid volume. Eleven patients developed hypothyroidism (cumulative five year risk 22%, 95% confidence interval 4.8% to 38.4%). Side effects were few: three cases of hyperthyroidism and two cases of radiation thyroiditis. Only one patient was dissatisfied with the result; she was referred for operation six months after treatment. CONCLUSIONS A substantial [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In 45 patients treated with one dose and remaining euthyroid the median thyroid volume was reduced from 73 (interquartile range 50-106) ml to 29 (23-48) ml at 24 months in the 39 patients in whom this was measured during follow up.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1011, "doc_id": "9745001", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does maternal obesity have an influence on feeding behavior of obese children?\n\nABSTRACT:\nObese children and adolescents referred to the pediatric endocrinology department were enrolled consecutively. Height and weight of all children and their mothers were measured. Maternal feeding practices were measured using an adapted version of the Child Feeding Questionnaire (CFQ). Answers were compared between obese (Body Mass Index [BMI] ≥ 30 kg/m2) and non-obese mothers. A total of 491 obese subjects (292 girls, mean age 12.0 ± 2.8 years) and their mothers participated in this study. A direct correlation between children's BMI and their mothers' BMI was found (P<0.001) both in girls (r = 0.372) and boys (r = 0.337). While 64.4% of mothers were found obese in the study, only half of them consider themselves as obese. No difference were found in the scores of the subscales \"perceived responsibility\", \"restriction\", \"concern for child's weight\" and \"monitoring\" between obese and non-obese mothers. Child's BMI-SDS positively correlated with mothers' personal weight perception, concern for child's weight and restriction after adjustment for child's age (P<0.001, P = 0.012 and P = 0.002, respectively).", "output": "{\"label\": \"no\", \"rationale\": \"Mothers' BMI highly correlate with children's BMI-z-scores. The degree of child's obesity increases mothers' concern and food restriction behavior. While mothers of obese children have a high prevalence of obesity, maternal obesity was found to have no significant influence on feeding behavior of obese school children.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 25034219, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The cytokine receptor which regulates chemotaxis and formation of lymph nodes is involved in production of myeloperoxidase in the left atrium.\n\nCANDIDATE_ABSTRACT:\nTITLE: Myeloperoxidase acts as a profibrotic mediator of atrial fibrillation\nABSTRACT: Observational clinical and ex vivo studies have established a strong association between atrial fibrillation and inflammation. However, whether inflammation is the cause or the consequence of atrial fibrillation and which specific inflammatory mediators may increase the atria's susceptibility to fibrillation remain elusive. Here we provide experimental and clinical evidence for the mechanistic involvement of myeloperoxidase (MPO), a heme enzyme abundantly expressed by neutrophils, in the pathophysiology of atrial fibrillation. MPO-deficient mice pretreated with angiotensin II (AngII) to provoke leukocyte activation showed lower atrial tissue abundance of the MPO product 3-chlorotyrosine, reduced activity of matrix metalloproteinases and blunted atrial fibrosis as compared to wild-type mice. Upon right atrial electrophysiological stimulation, MPO-deficient mice were protected from atrial fibrillation, which was reversed when MPO was restored. Humans with atrial fibrillation had higher plasma concentrations of MPO and a larger MPO burden in right atrial tissue as compared to individuals devoid of atrial fibrillation. In the atria, MPO colocalized with markedly increased formation of 3-chlorotyrosine. Our data demonstrate that MPO is a crucial prerequisite for structural remodeling of the myocardium, leading to an increased vulnerability to atrial fibrillation.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1208, "doc_id": "10284593", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Human embryonic stem cells give rise to cell types from the outer embryonic germ layer, but not the other two layers.\n\nCANDIDATE_PASSAGE:\nDNA methylation age of human tissues and cell types BACKGROUND It is not yet known whether DNA methylation levels can be used to accurately predict age across a broad spectrum of human tissues and cell types, nor whether the resulting age prediction is a biologically meaningful measure. RESULTS I developed a multi-tissue predictor of age that allows one to estimate the DNA methylation age of most tissues and cell types. The predictor, which is freely available, was developed using 8,000 samples from 82 Illumina DNA methylation array datasets, encompassing 51 healthy tissues and cell types. I found that DNA methylation age has the following properties: first, it is close to zero for embryonic and induced pluripotent stem cells; second, it correlates with cell passage number; third, it gives rise to a highly heritable measure of age acceleration; and, fourth, it is applicable to chimpanzee tissues. Analysis of 6,000 cancer samples from 32 datasets showed that all of the considered 20 cancer types exhibit significant age acceleration, with an average of 36 years. Low age-acceleration of cancer tissue is associated with a high number of somatic mutations and TP53 mutations, while mutations in steroid receptors greatly accelerate DNA methylation age in breast cancer. Finally, I characterize the 353 CpG sites that together form an aging clock in terms of chromatin states and tissue variance. CONCLUSIONS I propose that DNA methylation age measures the cumulative effect of an epigenetic maintenance system. This novel epigenetic clock can be used to address a host of questions in developmental biology, cancer and aging research.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "530", "doc_id": "7808055", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Ultrasound guidance significantly reduces the number of needle insertion attempts necessary for a given procedure.\n\nCANDIDATE_ABSTRACT:\nTITLE: Lymph node T cell responses predict the efficacy of live attenuated SIV vaccines\nABSTRACT: Live attenuated simian immunodeficiency virus (SIV) vaccines (LAVs) remain the most efficacious of all vaccines in nonhuman primate models of HIV and AIDS, yet the basis of their robust protection remains poorly understood. Here we show that the degree of LAV-mediated protection against intravenous wild-type SIVmac239 challenge strongly correlates with the magnitude and function of SIV-specific, effector-differentiated T cells in the lymph node but not with the responses of such T cells in the blood or with other cellular, humoral and innate immune parameters. We found that maintenance of protective T cell responses is associated with persistent LAV replication in the lymph node, which occurs almost exclusively in follicular helper T cells. Thus, effective LAVs maintain lymphoid tissue-based, effector-differentiated, SIV-specific T cells that intercept and suppress early wild-type SIV amplification and, if present in sufficient frequencies, can completely control and perhaps clear infection, an observation that provides a rationale for the development of safe, persistent vectors that can elicit and maintain such responses.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1340, "doc_id": "1071991", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Eilat virus (EILV) produced in mosquitos elicits rapid and long-lasting neutralizing antibodies in nonhuman primates.\n\nCANDIDATE_PASSAGE:\nIsolation from African Sykes' monkeys (Cercopithecus mitis) of a lentivirus related to human and simian immunodeficiency viruses. Analysis of serum samples from 100 wild-caught or colony-born Sykes' monkeys (Cercopithecus mitis) in Kenya revealed that 59 animals had antibodies cross-reactive to human immunodeficiency virus type 2 (HIV-2) and to simian immunodeficiency viruses (SIVs). A lentivirus, designated SIVsyk, was isolated from five of six seropositive asymptomatic Sykes' monkeys, but in four cases isolation was possible only after depletion of CD8+ lymphocytes and cocultivation of the CD4(+)-enriched cell population with peripheral blood mononuclear cells from seronegative Sykes' monkeys. SIVsyk resembled other SIVs and HIVs morphologically, had an Mg2(+)-dependent reverse transcriptase enzyme, and replicated in and was cytopathic for CEMx174 and Sup-T1 cells. SIVsyk differred substantially from other SIVs, however, in that it failed to replicate in normal human, mangabey, and macaque peripheral blood mononuclear cells and serum from seropositive Sykes' monkeys immunoprecipitated env antigens from HIV-1 as well as from HIV-2, SIVsmm, and SIVagm. These data demonstrate a high prevalence of natural infection in Sykes' monkeys in Kenya with a lentivirus that appears to be unique with respect to its host range and antigenic cross-reactivity.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "372", "doc_id": "798152", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Deltex interacts with eIF3. There is no known interaction between Deltex and elF3\n\nCANDIDATE_ABSTRACT:\nTITLE: The Translation Initiation Factor 3f (eIF3f) Exhibits a Deubiquitinase Activity Regulating Notch Activation\nABSTRACT: Activation of the mammalian Notch receptor after ligand binding relies on a succession of events including metalloprotease-cleavage, endocytosis, monoubiquitination, and eventually processing by the gamma-secretase, giving rise to a soluble, transcriptionally active molecule. The Notch1 receptor was proposed to be monoubiquitinated before its gamma-secretase cleavage; the targeted lysine has been localized to its submembrane domain. Investigating how this step might be regulated by a deubiquitinase (DUB) activity will provide new insight for understanding Notch receptor activation and downstream signaling. An immunofluorescence-based screening of an shRNA library allowed us to identify eIF3f, previously known as one of the subunits of the translation initiation factor eIF3, as a DUB targeting the activated Notch receptor. We show that eIF3f has an intrinsic DUB activity. Knocking down eIF3f leads to an accumulation of monoubiquitinated forms of activated Notch, an effect counteracted by murine WT eIF3f but not by a catalytically inactive mutant. We also show that eIF3f is recruited to activated Notch on endocytic vesicles by the putative E3 ubiquitin ligase Deltex1, which serves as a bridging factor. Finally, catalytically inactive forms of eIF3f as well as shRNAs targeting eIF3f repress Notch activation in a coculture assay, showing that eIF3f is a new positive regulator of the Notch pathway. Our results support two new and provocative conclusions: (1) The activated form of Notch needs to be deubiquitinated before being processed by the gamma-secretase activity and entering the nucleus, where it fulfills its transcriptional function. (2) The enzyme accounting for this deubiquitinase activity is eIF3f, known so far as a translation initiation factor. These d [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We also show that eIF3f is recruited to activated Notch on endocytic vesicles by the putative E3 ubiquitin ligase Deltex1, which serves as a bridging factor.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 331, "doc_id": "9505448", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: There is a positive correlation between hip fractures and statin use.\n\nCANDIDATE_PASSAGE:\nThe changing epidemiology of malaria in Ifakara Town, southern Tanzania. Between 1995 and 2000 there were marked changes in the epidemiology of malaria in Ifakara, southern Tanzania. We documented these changes using parasitological and clinical data from a series of community- and hospital-based studies involving children up to the age of 5 years. There was a right shift and lowering in the age-specific parasite prevalence in the community-based cohort studies. The incidence of clinical malaria in placebo-receiving infants in additional study cohorts dropped from 0.8 in 1995 to 0.43 episodes per infant per year in 2000, an incidence rate ratio of 0.53 (95% confidence interval: 0.404, 0.70, P<0.0001). At the same time, there was an increase in the total number of malaria admissions and a marked right shift in the age pattern of these admissions (median age in 1995 1.55 years vs. 2.33 in 2000, P<0.0001). However, the burden of malaria deaths remained in infants. We discuss how these dramatic changes in the epidemiology of malaria may have arisen from the use of currently available malaria control tools. Caution is required in the interpretation of hospital-based data as it is likely to underestimate the impact of anaemia on mortality in the community, where most paediatric deaths occur. Even in low/moderate malaria transmission settings, where older children suffer most malaria episodes, targeting effective malaria control at infants may produce important reductions in infant mortality caused by malaria.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1288", "doc_id": "19824183", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: NFAT4 activation requires IP3R-mediated Ca2+ mobilization.\n\nCANDIDATE_ABSTRACT:\nTITLE: Evidence that the Ipl1-Sli15 (Aurora Kinase-INCENP) Complex Promotes Chromosome Bi-orientation by Altering Kinetochore-Spindle Pole Connections\nABSTRACT: How sister kinetochores attach to microtubules from opposite spindle poles during mitosis (bi-orientation) remains poorly understood. In yeast, the ortholog of the Aurora B-INCENP protein kinase complex (Ipl1-Sli15) may have a role in this crucial process, because it is necessary to prevent attachment of sister kinetochores to microtubules from the same spindle pole. We investigated IPL1 function in cells that cannot replicate their chromosomes but nevertheless duplicate their spindle pole bodies (SPBs). Kinetochores detach from old SPBs and reattach to old and new SPBs with equal frequency in IPL1+ cells, but remain attached to old SPBs in ipl1 mutants. This raises the possibility that Ipl1-Sli15 facilitates bi-orientation by promoting turnover of kinetochore-SPB connections until traction of sister kinetochores toward opposite spindle poles creates tension in the surrounding chromatin.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 832, "doc_id": "493346", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Lice attenuated SIV vaccines induce a stronger antigen-specific T cell response in lymph node cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Control of glutamate clearance and synaptic efficacy by glial coverage of neurons.\nABSTRACT: Analysis of excitatory synaptic transmission in the rat hypothalamic supraoptic nucleus revealed that glutamate clearance and, as a consequence, glutamate concentration and diffusion in the extracellular space, is associated with the degree of astrocytic coverage of its neurons. Reduction in glutamate clearance, whether induced pharmacologically or associated with a relative decrease of glial coverage in the vicinity of synapses, affected transmitter release through modulation of presynaptic metabotropic glutamate receptors. Astrocytic wrapping of neurons, therefore, contributes to the regulation of synaptic efficacy in the central nervous system.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 694, "doc_id": "306311", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Hypothalamic glutamate neurotransmission is unrelated to energy balance.\n\nCANDIDATE_ABSTRACT:\nTITLE: Glutamate mediates the function of melanocortin receptor 4 on Sim1 neurons in body weight regulation.\nABSTRACT: The melanocortin receptor 4 (MC4R) is a well-established mediator of body weight homeostasis. However, the neurotransmitter(s) that mediate MC4R function remain largely unknown; as a result, little is known about the second-order neurons of the MC4R neural pathway. Single-minded 1 (Sim1)-expressing brain regions, which include the paraventricular nucleus of hypothalamus (PVH), represent key brain sites that mediate melanocortin action. We conditionally restored MC4R expression in Sim1 neurons in the background of Mc4r-null mice. The restoration dramatically reduced obesity in Mc4r-null mice. The anti-obesity effect was completely reversed by selective disruption of glutamate release from those same Sim1 neurons. The reversal was caused by lower energy expenditure and hyperphagia. Corroboratively, selective disruption of glutamate release from adult PVH neurons led to rapid obesity development via reduced energy expenditure and hyperphagia. Thus, this study establishes glutamate as the primary neurotransmitter that mediates MC4Rs on Sim1 neurons in body weight regulation.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Thus, this study establishes glutamate as the primary neurotransmitter that mediates MC4Rs on Sim1 neurons in body weight regulation.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 541, "doc_id": "45154987", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Vitamin D deficiency is unrelated to birth weight.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association between maternal serum 25-hydroxyvitamin D level and pregnancy and neonatal outcomes: systematic review and meta-analysis of observational studies.\nABSTRACT: OBJECTIVE To assess the effect of 25-hydroxyvitamin D (25-OHD) levels on pregnancy outcomes and birth variables. DESIGN Systematic review and meta-analysis. DATA SOURCES Medline (1966 to August 2012), PubMed (2008 to August 2012), Embase (1980 to August 2012), CINAHL (1981 to August 2012), the Cochrane database of systematic reviews, and the Cochrane database of registered clinical trials. STUDY SELECTION Studies reporting on the association between serum 25-OHD levels during pregnancy and the outcomes of interest (pre-eclampsia, gestational diabetes, bacterial vaginosis, caesarean section, small for gestational age infants, birth weight, birth length, and head circumference). DATA EXTRACTION Two authors independently extracted data from original research articles, including key indicators of study quality. We pooled the most adjusted odds ratios and weighted mean differences. Associations were tested in subgroups representing different patient characteristics and study quality. RESULTS 3357 studies were identified and reviewed for eligibility. 31 eligible studies were included in the final analysis. Insufficient serum levels of 25-OHD were associated with gestational diabetes (pooled odds ratio 1.49, 95% confidence interval 1.18 to 1.89), pre-eclampsia (1.79, 1.25 to 2.58), and small for gestational age infants (1.85, 1.52 to 2.26). Pregnant women with low serum 25-OHD levels had an increased risk of bacterial vaginosis and low birthweight infants but not delivery by caesarean section. CONCLUSION Vitamin D insufficiency is associated with an increased risk of gestational diabetes, pre-eclampsia, and small for gestational age infants. Pregnant women with low 25-OHD levels had an increased risk of bacterial vaginosis and lower birth weight infants, but not de [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Pregnant women with low serum 25-OHD levels had an increased risk of bacterial vaginosis and low birthweight infants but not delivery by caesarean section.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1370, "doc_id": "2425364", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Autophagy declines in aged organisms.\n\nCANDIDATE_PASSAGE:\nRestoration of chaperone-mediated autophagy in aging liver improves cellular maintenance and hepatic function Chaperone-mediated autophagy (CMA), a selective mechanism for degradation of cytosolic proteins in lysosomes, contributes to the removal of altered proteins as part of the cellular quality-control systems. We have previously found that CMA activity declines in aged organisms and have proposed that this failure in cellular clearance could contribute to the accumulation of altered proteins, the abnormal cellular homeostasis and, eventually, the functional loss characteristic of aged organisms. To determine whether these negative features of aging can be prevented by maintaining efficient autophagic activity until late in life, in this work we have corrected the CMA defect in aged rodents. We have generated a double transgenic mouse model in which the amount of the lysosomal receptor for CMA, previously shown to decrease in abundance with age, can be modulated. We have analyzed in this model the consequences of preventing the age-dependent decrease in receptor abundance in aged rodents at the cellular and organ levels. We show here that CMA activity is maintained until advanced ages if the decrease in the receptor abundance is prevented and that preservation of autophagic activity is associated with lower intracellular accumulation of damaged proteins, better ability to handle protein damage and improved organ function.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "148", "doc_id": "1084345", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: DUSP4 increases apoptosis.\n\nCANDIDATE_PASSAGE:\nInterleukin-33 prevents apoptosis and improves survival after experimental myocardial infarction through ST2 signaling. BACKGROUND ST2 is an interleukin (IL)-1 receptor family member with membrane-bound (ST2L) and soluble (sST2) isoforms, and sST2 is a biomarker for poor outcome in patients with myocardial infarction (MI). IL-33, the recently discovered ligand for ST2, activates nuclear factor kappaB and thus may regulate apoptotic cell death. We tested the hypothesis that IL-33 is cardioprotective after MI through ST2 signaling. METHODS AND RESULTS IL-33 protected cultured cardiomyocytes from hypoxia-induced apoptosis, and this cardioprotection was partially inhibited by sST2. IL-33 induced expression of the antiapoptotic factors XIAP, cIAP1, and survivin. To define the cardioprotective role of IL-33 in vivo, we performed a blinded and randomized study of ischemia/reperfusion in rats. IL-33 reduced cardiomyocyte apoptosis, suppressed caspase-3 activity, and increased expression of IAP family member proteins. IL-33 decreased both infarct and fibrosis volumes at 15 days; furthermore, both echocardiographic and hemodynamic studies revealed that IL-33 improved ventricular function. To determine whether cardioprotection by IL-33 is mediated through ST2 signaling, a randomized and blinded study of ST2(-/-) versus wild-type littermate mice was performed in 98 mice subjected to MI. At 4 weeks after MI, IL-33 reduced ventricular dilation and improved contractile function in wild-type mice but not in ST2(-/-) mice. Finally, IL-33 improved survival after MI in wild-type but not in ST2(-/-) mice. CONCLUSIONS IL-33 prevents cardiomyocyte apoptosis and improves cardiac function and survival after MI through ST2 signaling.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "309", "doc_id": "10576136", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Cyclin A2 destruction is necessary to switch from unstable to stable kt-mt attachments in mitosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cyclin A Regulates Kinetochore-Microtubules to Promote Faithful Chromosome Segregation\nABSTRACT: The most conspicuous event in the cell cycle is the alignment of chromosomes in metaphase. Chromosome alignment fosters faithful segregation through the formation of bi-oriented attachments of kinetochores to spindle microtubules. Notably, numerous kinetochore-microtubule (k-MT) attachment errors are present in early mitosis (prometaphase), and the persistence of those errors is the leading cause of chromosome mis-segregation in aneuploid human tumour cells that continually mis-segregate whole chromosomes and display chromosomal instability. How robust error correction is achieved in prometaphase to ensure error-free mitosis remains unknown. Here we show that k-MT attachments in prometaphase cells are considerably less stable than in metaphase cells. The switch to more stable k-MT attachments in metaphase requires the proteasome-dependent destruction of cyclin A in prometaphase. Persistent cyclin A expression prevents k-MT stabilization even in cells with aligned chromosomes. By contrast, k-MTs are prematurely stabilized in cyclin-A-deficient cells. Consequently, cells lacking cyclin A display higher rates of chromosome mis-segregation. Thus, the stability of k-MT attachments increases decisively in a coordinated fashion among all chromosomes as cells transit from prometaphase to metaphase. Cyclin A creates a cellular environment that promotes microtubule detachment from kinetochores in prometaphase to ensure efficient error correction and faithful chromosome segregation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"By contrast, k-MTs are prematurely stabilized in cyclin-A-deficient cells.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 296, "doc_id": "4398832", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The treatment of cancer patients with co-IR blockade precipitates adverse autoimmune events.\n\nCANDIDATE_PASSAGE:\nCancer Pharmacogenomics and Pharmacoepidemiology: Setting a Research Agenda to Accelerate Translation Recent advances in genomic research have demonstrated a substantial role for genomic factors in predicting response to cancer therapies. Researchers in the fields of cancer pharmacogenomics and pharmacoepidemiology seek to understand why individuals respond differently to drug therapy, in terms of both adverse effects and treatment efficacy. To identify research priorities as well as the resources and infrastructure needed to advance these fields, the National Cancer Institute (NCI) sponsored a workshop titled \"Cancer Pharmacogenomics: Setting a Research Agenda to Accelerate Translation\" on July 21, 2009, in Bethesda, MD. In this commentary, we summarize and discuss five science-based recommendations and four infrastructure-based recommendations that were identified as a result of discussions held during this workshop. Key recommendations include 1) supporting the routine collection of germline and tumor biospecimens in NCI-sponsored clinical trials and in some observational and population-based studies; 2) incorporating pharmacogenomic markers into clinical trials; 3) addressing the ethical, legal, social, and biospecimen- and data-sharing implications of pharmacogenomic and pharmacoepidemiologic research; and 4) establishing partnerships across NCI, with other federal agencies, and with industry. Together, these recommendations will facilitate the discovery and validation of clinical, sociodemographic, lifestyle, and genomic markers related to cancer treatment response and adverse events, and they will improve both the speed and efficiency by which new pharmacogenomic and pharmacoepidemiologic information is translated into clinical practice.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1279", "doc_id": "5855168", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is breast cancer survival improving?\n\nABSTRACT:\nDespite advances in therapies for breast cancer, improvement in survival for patients with recurrent or metastatic breast cancer has been difficult to establish. The objective of the current study was to determine whether the survival of women with recurrent breast cancer has improved from 1974 to 2000. The authors analyzed the survival experience of 834 women who developed recurrent breast cancer between November 1974 and December 2000. All patients had been treated previously with adjuvant anthracycline-based protocols. Patients were divided into five consecutive groups based on year of breast cancer recurrence, and survival was compared across the five groups. Because some prognostic variables were divided unevenly divided among the cohorts, a multivariate model was created to determine the association of year of recurrence and survival after accounting for other prognostic factors. In the unadjusted analysis, there was a statistically significant improvement in survival across the five groups, and the more recent cohorts had longer survival (P<0.001). Other variables that predicted longer survival after breast cancer recurrence included smaller initial tumor size, lower stage of disease, fewer lymph nodes involved, longer disease-free interval, estrogen receptor-positive tumors, and nonvisceral dominant site of disease recurrence. In the multivariate analysis, which adjusted for these prognostic factors, year of recurrence was associated with a trend toward improved survival, with a 1% reduction in risk for each increasing year.", "output": "{\"label\": \"yes\", \"rationale\": \"For these cohorts of patients, the authors present data suggesting that the prognosis for patients with recurrent breast cancer improved between 1974 and 2000.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 14692023, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Primary pro-inflammatory cytokines induce secondary pro- and anti-inflammatory mediators.\n\nCANDIDATE_PASSAGE:\nInter-individual variability and genetic influences on cytokine responses to bacteria and fungi Little is known about the inter-individual variation of cytokine responses to different pathogens in healthy individuals. To systematically describe cytokine responses elicited by distinct pathogens and to determine the effect of genetic variation on cytokine production, we profiled cytokines produced by peripheral blood mononuclear cells from 197 individuals of European origin from the 200 Functional Genomics (200FG) cohort in the Human Functional Genomics Project (http://www.humanfunctionalgenomics.org), obtained over three different years. We compared bacteria- and fungi-induced cytokine profiles and found that most cytokine responses were organized around a physiological response to specific pathogens, rather than around a particular immune pathway or cytokine. We then correlated genome-wide single-nucleotide polymorphism (SNP) genotypes with cytokine abundance and identified six cytokine quantitative trait loci (QTLs). Among them, a cytokine QTL at the NAA35-GOLM1 locus markedly modulated interleukin (IL)-6 production in response to multiple pathogens and was associated with susceptibility to candidemia. Furthermore, the cytokine QTLs that we identified were enriched among SNPs previously associated with infectious diseases and heart diseases. These data reveal and begin to explain the variability in cytokine production by human immune cells in response to pathogens.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "975", "doc_id": "5304891", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Taking anti-depresents is associated with a decrease in the Aβ level in the brain of experimental animals.\n\nCANDIDATE_PASSAGE:\nAn Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice Serotonin signaling suppresses generation of amyloid-β (Aβ) in vitro and in animal models of Alzheimer’s disease (AD). We show that in an aged transgenic AD mouse model (APP/PS1 plaque-bearing mice), the antidepressant citalopram, a selective serotonin reuptake inhibitor, decreased Aβ in brain interstitial fluid in a dose-dependent manner. Growth of individual amyloid plaques was assessed in plaque-bearing mice that were chronically administered citalopram. Citalopram arrested the growth of preexisting plaques and reduced the appearance of new plaques by 78%. In healthy human volunteers, citalopram’s effects on Aβ production and Aβ concentrations in cerebrospinal fluid (CSF) were measured prospectively using stable isotope labeling kinetics, with CSF sampling during acute dosing of citalopram. Aβ production in CSF was slowed by 37% in the citalopram group compared to placebo. This change was associated with a 38% decrease in total CSF Aβ concentrations in the drug-treated group. The ability to safely decrease Aβ concentrations is potentially important as a preventive strategy for AD. This study demonstrates key target engagement for future AD prevention trials.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1142", "doc_id": "5260382", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does extracellular Hsp70 inhibit pro-inflammatory cytokine production by IL-10 driven down-regulation of C/EBPβ and C/EBPδ?\n\nABSTRACT:\nExtracellular Hsp70 has anti-inflammatory potential, demonstrated in different models of inflammatory diseases. We investigated probable mechanisms used by Hsp70 to down-regulate pro-inflammatory cytokines. We analysed cytokine mRNA levels in bone marrow-derived murine dendritic cells treated with Hsp70, lipopolysaccharide (LPS) and peptidoglycan (PGN) or OVA (an irrelevant protein control), hypothesising that this was mediated by C/EBPβ and C/EBPδ transcription factors. We also tested the involvement of TLR2, IL-10, ERK and STAT3, using genetically deficient mice and pharmacological inhibitors. C/EBPβ and C/EBPδ levels were inhibited in bone marrow derived dendritic cells (BMDCs) treated with Hsp70, and that correlated with inhibition of TNF-α, IFN-γ and MCP-1. Such inhibition was not observed in TLR2 or IL-10 knockout mice, and was also abrogated upon pretreatment of cells with ERK and JAK2/STAT3 inhibitors.", "output": "{\"label\": \"yes\", \"rationale\": \"C/EBPβ and C/EBPδ transcription factors are inhibited by Hsp70 treatment, and their inhibition occurs via the TLR2-ERK-STAT3-IL-10 pathway in BMDCs, mediating the anti-inflammatory effects of Hsp70.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 23808579, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Women are more susceptible to death due to pneumonia when compared to men.\n\nCANDIDATE_ABSTRACT:\nTITLE: Gender-dependent differences in outcome after the treatment of infection in hospitalized patients.\nABSTRACT: CONTEXT While it is established that management strategies and outcomes differ by gender for many diseases, its effect on infection has not been adequately studied. OBJECTIVE To investigate the role of gender among hospitalized patients treated for infection. DESIGN Observational cohort study conducted during a 26-month period from December 1996 through January 1999. SETTING University-affiliated hospital. PARTICIPANTS A total of 892 patients in the surgical units of the hospital with 1470 consecutive infectious episodes (782 in men and 688 in women). MAIN OUTCOME MEASURES Mortality during hospitalization by gender for infection episodes overall and for specific infectious sites, including lung, peritoneum, bloodstream, catheter, urine, surgical site, and skin/soft tissue. RESULTS Among all infections, there was no significant difference in mortality based on gender (men, 11.1% vs women, 14.2%; P = .07). After logistic regression analysis, factors independently associated with mortality included higher APACHE (Acute Physiology and Chronic Health Evaluation) II score, older age, malignancy, blood transfusion, and diagnosis of infection more than 7 days after admission, but not gender (female odds ratio [OR] for death, 1.32; 95% confidence interval [CI], 0.90-1.94; P = .16). Mortality was higher in women for lung (men, 18% vs women, 34%; P = .002) and soft tissue (men, 2% vs women, 10%; P < or = .05) infection; for other infectious sites, mortality did not differ by gender. Factors associated with mortality due to pneumonia by logistic regression included higher APACHE II score, malignancy, diabetes mellitus, diagnosis of infection more than 7 days after admission, older age, transplantation, and female gender (OR for death, 2.25; 95% CI, 1.17-4.32; P = .02). [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Although gender may not be predictive of mortality among all infections, women appear to be at increased risk for death from hospital-acquired pneumonia, even after controlling for other comorbidities.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1378, "doc_id": "2488880", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The risk of female prisoners harming themselves is ten times that of male prisoners.\n\nCANDIDATE_ABSTRACT:\nTITLE: Self-harm in prisons in England and Wales: an epidemiological study of prevalence, risk factors, clustering, and subsequent suicide\nABSTRACT: BACKGROUND Self-harm and suicide are common in prisoners, yet robust information on the full extent and characteristics of people at risk of self-harm is scant. Furthermore, understanding how frequently self-harm is followed by suicide, and in which prisoners this progression is most likely to happen, is important. We did a case-control study of all prisoners in England and Wales to ascertain the prevalence of self-harm in this population, associated risk factors, clustering effects, and risk of subsequent suicide after self-harm. METHODS Records of self-harm incidents in all prisons in England and Wales were gathered routinely between January, 2004, and December, 2009. We did a case-control comparison of prisoners who self-harmed and those who did not between January, 2006, and December, 2009. We also used a Bayesian approach to look at clustering of people who self-harmed. Prisoners who self-harmed and subsequently died by suicide in prison were compared with other inmates who self-harmed. FINDINGS 139,195 self-harm incidents were recorded in 26,510 individual prisoners between 2004 and 2009; 5-6% of male prisoners and 20-24% of female inmates self-harmed every year. Self-harm rates were more than ten times higher in female prisoners than in male inmates. Repetition of self-harm was common, particularly in women and teenage girls, in whom a subgroup of 102 prisoners accounted for 17,307 episodes. In both sexes, self-harm was associated with younger age, white ethnic origin, prison type, and a life sentence or being unsentenced; in female inmates, committing a violent offence against an individual was also a factor. Substantial evidence was noted of clustering in time and location of prisoners who self-harmed (adjusted intra-class correlation 0·15, 95% CI 0 [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"FINDINGS 139,195 self-harm incidents were recorded in 26,510 individual prisoners between 2004 and 2009; 5-6% of male prisoners and 20-24% of female inmates self-harmed every year.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1269, "doc_id": "13900610", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Patients with microcytosis and higher erythrocyte count were more resistant to severe malarial anaemia when infected with Plasmodium falciparum.\n\nCANDIDATE_ABSTRACT:\nTITLE: Increased Microerythrocyte Count in Homozygous α+-Thalassaemia Contributes to Protection against Severe Malarial Anaemia\nABSTRACT: BACKGROUND The heritable haemoglobinopathy alpha(+)-thalassaemia is caused by the reduced synthesis of alpha-globin chains that form part of normal adult haemoglobin (Hb). Individuals homozygous for alpha(+)-thalassaemia have microcytosis and an increased erythrocyte count. Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count. We tested the hypothesis that the erythrocyte indices associated with alpha(+)-thalassaemia homozygosity provide a haematological benefit during acute malaria. METHODS AND FINDINGS Data from children living on the north coast of Papua New Guinea who had participated in a case-control study of the protection afforded by alpha(+)-thalassaemia against severe malaria were reanalysed to assess the genotype-specific reduction in erythrocyte count and Hb levels associated with acute malarial disease. We observed a reduction in median erythrocyte count of approximately 1.5 x 10(12)/l in all children with acute falciparum malaria relative to values in community children (p < 0.001). We developed a simple mathematical model of the linear relationship between Hb concentration and erythrocyte count. This model predicted that children homozygous for alpha(+)-thalassaemia lose less Hb than children of normal genotype for a reduction in erythrocyte count of >1.1 x 10(12)/l as a result of the reduced mean cell Hb in homozygous alpha(+)-thalassaemia. In addition, children homozygous for alpha(+)-thalassaemia require a 10% greater reduction in erythrocyte count than children of normal genotype (p = 0.02) for Hb concentration to fall to 50 g/l, the cutoff for SMA. We estimated that the haematological profile in [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We estimated that the haematological profile in children homozygous for alpha(+)-thalassaemia reduces the risk of SMA during acute malaria compared to children of normal genotype (relative risk 0.52; 95% confidence interval [CI] 0.24-1.12, p = 0.09).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 929, "doc_id": "18174210", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Cancer-associated fibroblasts (CAFs) have no known interaction with cancer cells in the formation and activation of CAFs.\n\nCANDIDATE_PASSAGE:\nReplication Fork Stability Confers Chemoresistance in BRCA-deficient Cells Cells deficient in the Brca1 and Brca2 genes have reduced capacity to repair DNA double-strand breaks by homologous recombination and consequently are hypersensitive to DNA-damaging agents, including cisplatin and poly(ADP-ribose) polymerase (PARP) inhibitors. Here we show that loss of the MLL3/4 complex protein, PTIP, protects Brca1/2-deficient cells from DNA damage and rescues the lethality of Brca2-deficient embryonic stem cells. However, PTIP deficiency does not restore homologous recombination activity at double-strand breaks. Instead, its absence inhibits the recruitment of the MRE11 nuclease to stalled replication forks, which in turn protects nascent DNA strands from extensive degradation. More generally, acquisition of PARP inhibitors and cisplatin resistance is associated with replication fork protection in Brca2-deficient tumour cells that do not develop Brca2 reversion mutations. Disruption of multiple proteins, including PARP1 and CHD4, leads to the same end point of replication fork protection, highlighting the complexities by which tumour cells evade chemotherapeutic interventions and acquire drug resistance.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "225", "doc_id": "4444861", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Walking in traffic areas in London improves lung function in elderly adults.\n\nCANDIDATE_ABSTRACT:\nTITLE: Respiratory and cardiovascular responses to walking down a traffic-polluted road compared with walking in a traffic-free area in participants aged 60 years and older with chronic lung or heart disease and age-matched healthy controls: a randomised, crossover study\nABSTRACT: BACKGROUND Long-term exposure to pollution can lead to an increase in the rate of decline of lung function, especially in older individuals and in those with chronic obstructive pulmonary disease (COPD), whereas shorter-term exposure at higher pollution levels has been implicated in causing excess deaths from ischaemic heart disease and exacerbations of COPD. We aimed to assess the effects on respiratory and cardiovascular responses of walking down a busy street with high levels of pollution compared with walking in a traffic-free area with lower pollution levels in older adults. METHODS In this randomised, crossover study, we recruited men and women aged 60 years and older with angiographically proven stable ischaemic heart disease or stage 2 Global initiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable for 6 months, and age-matched healthy volunteers. Individuals with ischaemic heart disease or COPD were recruited from existing databases or outpatient respiratory and cardiology clinics at the Royal Brompton & Harefield NHS Foundation Trust and age-matched healthy volunteers using advertising and existing databases. All participants had abstained from smoking for at least 12 months and medications were taken as recommended by participants' doctors during the study. Participants were randomly assigned by drawing numbered disks at random from a bag to do a 2 h walk either along a commercial street in London (Oxford Street) or in an urban park (Hyde Park). Baseline measurements of participants were taken before the walk in the hospital laboratory. During each walk session, black carbon, particulate matter (PM) concentrations, ultrafine particles, and nitrogen dioxide (NO2) concentrations were measured. FINDINGS Between October, 2012 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Participants with COPD reported more cough (odds ratio [OR] 1·95, 95% CI 0·96-3·95; p<0·1), sputum (3·15, 1·39-7·13; p<0·05), shortness of breath (1·86, 0·97-3·57; p<0·1), and wheeze (4·00, 1·52-10·50; p<0·05) after walking down Oxford Street compared with Hyde Park.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1373, "doc_id": "21003930", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does mild brain ischemia produce bladder hyperactivity without brain damage in rats?\n\nABSTRACT:\nThe influence of brain ischemia without cerebral infarction on voiding function is unknown. To investigate the effects of a reduction in cerebral blood flow on voiding function, the influence of chronic cerebral hypoperfusion (CH) on bladder activity was examined in rats. CH was induced in each of 11 female Sprague-Dawley rats by anastomosis between the right external jugular vein and the right common carotid artery with partial obstruction of the left common carotid artery. Twelve intact animals comprised a control group. Voided volume per micturition was assessed in a metabolic cage for 24 h on weeks 2, 4, and 8. Eight weeks after the operation, the rats were tested in a hippocampus-related learning paradigm, the Morris water maze. Bladder activity was monitored in 13 rats with continuous infusion cystometrography (CMG) at 2 weeks. After evaluation, the rats' brains were stained by perfusion with 2% 2,3,5-triphenyltetrazolium chloride (TTC). Voided volume per micturition was significantly reduced and voiding frequency was significantly increased in CH rats 2 weeks after CH as compared to the control group (p < 0.05). Bladder capacity on CMG of CH rats was significantly reduced 14 days after CH as compared to the controls (p < 0.05). Although TTC staining of the CH rat brain did not show cerebral infarction, CH induced impairment of water maze learning.", "output": "{\"label\": \"yes\", \"rationale\": \"These results indicate that mild forebrain ischemia without infarction results in the development of bladder hyperactivity and impairment of memory. Mild brain ischemia with aging may induce bladder overactivity in humans. Further studies of the nervous system related to bladder hyperactivity using this animal model may lead to pharmacological therapy or prevention of bladder overactivity in the aging individual with an unidentified origin of voiding dysfunction.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 16825817, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Allogeneic mechanical circulatory support is not as effective as autologous mechanical circulatory support for treating acute myocardial infarction.\n\nCANDIDATE_ABSTRACT:\nTITLE: Comparison of allogeneic vs autologous bone marrow–derived mesenchymal stem cells delivered by transendocardial injection in patients with ischemic cardiomyopathy: the POSEIDON randomized trial.\nABSTRACT: CONTEXT Mesenchymal stem cells (MSCs) are under evaluation as a therapy for ischemic cardiomyopathy (ICM). Both autologous and allogeneic MSC therapies are possible; however, their safety and efficacy have not been compared. OBJECTIVE To test whether allogeneic MSCs are as safe and effective as autologous MSCs in patients with left ventricular (LV) dysfunction due to ICM. DESIGN, SETTING, AND PATIENTS A phase 1/2 randomized comparison (POSEIDON study) in a US tertiary-care referral hospital of allogeneic and autologous MSCs in 30 patients with LV dysfunction due to ICM between April 2, 2010, and September 14, 2011, with 13-month follow-up. INTERVENTION Twenty million, 100 million, or 200 million cells (5 patients in each cell type per dose level) were delivered by transendocardial stem cell injection into 10 LV sites. MAIN OUTCOME MEASURES Thirty-day postcatheterization incidence of predefined treatment-emergent serious adverse events (SAEs). Efficacy assessments included 6-minute walk test, exercise peak VO2, Minnesota Living with Heart Failure Questionnaire (MLHFQ), New York Heart Association class, LV volumes, ejection fraction (EF), early enhancement defect (EED; infarct size), and sphericity index. RESULTS Within 30 days, 1 patient in each group (treatment-emergent SAE rate, 6.7%) was hospitalized for heart failure, less than the prespecified stopping event rate of 25%. The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3% (n = 8) in the autologous group (P = .46). At 1 year, there were no ventricular arrhythmia SAEs observed among allogeneic recipients compared with 4 patients (26.7%) in the autologous group (P = .10). Relative to baseline, autologous but not allogeneic MSC therapy was associated with an improvement in the 6- [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Allogeneic and autologous MSCs reduced mean EED by −33.21% (95% CI, −43.61% to −22.81%; P < .001) and sphericity index but did not increase EF.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 104, "doc_id": "40164383", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Tetraspanin-3 is a causative factor in the development of acute myelogenous leukemia\n\nCANDIDATE_PASSAGE:\nHealth and access to care: perspectives of homeless youth in Baltimore City, U.S.A. Homeless youth suffer from high rates of health problems, yet little is known about their perceptions of or context for their own health issues. In this study, a combination of qualitative techniques from participatory rural appraisal and rapid assessment procedures was used to investigate the perceptions of health needs of shelter-based youth in Baltimore, MD in the U.S.A. The most common youth-identified health problems included STDs, HIV/AIDS, pregnancy, depression, drug use and injuries. These correlate well with more objective health status data for the same youth. The youth spoke of environmental safety threats of violence and victimization by adults, as well as racism and sexism in their lives. Youth reported that trusted adult figures such as grandmothers are important sources of health advice. Many homeless youth from less than ideal family situations remain in contact with and continue to seek advice from parents and other family members. Health interventions with urban street youth need to acknowledge the primacy of the social context for these youth, as well as the reality of violence as a daily health threat.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1150", "doc_id": "20334484", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Ethanol stress reduces the expression of SRL in bacteria.\n\nCANDIDATE_ABSTRACT:\nTITLE: Regulatory and metabolic rewiring during laboratory evolution of ethanol tolerance in E. coli\nABSTRACT: Understanding the genetic basis of adaptation is a central problem in biology. However, revealing the underlying molecular mechanisms has been challenging as changes in fitness may result from perturbations to many pathways, any of which may contribute relatively little. We have developed a combined experimental/computational framework to address this problem and used it to understand the genetic basis of ethanol tolerance in Escherichia coli. We used fitness profiling to measure the consequences of single-locus perturbations in the context of ethanol exposure. A module-level computational analysis was then used to reveal the organization of the contributing loci into cellular processes and regulatory pathways (e.g. osmoregulation and cell-wall biogenesis) whose modifications significantly affect ethanol tolerance. Strikingly, we discovered that a dominant component of adaptation involves metabolic rewiring that boosts intracellular ethanol degradation and assimilation. Through phenotypic and metabolomic analysis of laboratory-evolved ethanol-tolerant strains, we investigated naturally accessible pathways of ethanol tolerance. Remarkably, these laboratory-evolved strains, by and large, follow the same adaptive paths as inferred from our coarse-grained search of the fitness landscape.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 393, "doc_id": "1148122", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Blocking the interaction between TDP-43 and respiratory complex I proteins ND3 and ND6 leads to increased TDP-43-induced neuronal loss.\n\nCANDIDATE_PASSAGE:\nEthanol extract of Allium fistulosum inhibits development of non-alcoholic fatty liver disease BACKGROUND/OBJECTIVES Non-alcoholic fatty liver disease (NAFLD) is a leading cause of chronic liver disease and is closely associated with metabolic syndrome. In the present study, we observed the effect of ethanol extract of Allium fistulosum (EAF) on NAFLD and have suggested the possibility of using EAF as a natural product for application in the development of a treatment for NAFLD. MATERIALS/METHODS The preventive effect on hepatic lipid accumulation was estimated by using an oleic acid (OA)-induced NAFLD model in vitro and a Western diet (high-fat high-sucrose; WD)-induced obese mouse model. Animals were divided into three groups (n = 7): normal diet group (ND), WD group, and WD plus 1% EAF group. RESULTS EAF reduced OA-stimulated lipid accumulation in HepG2 cells in the absence of cellular cytotoxicity and significantly blocked transcriptional activation of sterol regulatory element-binding protein 1 and fatty acid synthase genes. Subsequently, we investigated these effects in vivo in mice fed either ND or WD in the presence or absence of EAF supplementation. In comparison to the ND controls, the WD-fed mice exhibited increases in body weight, liver weight, epididymal fat weight, and accumulation of fat in hepatocytes, and these effects were significantly attenuated by EAF supplementation. CONCLUSIONS Allium fistulosum attenuates the development of NAFLD, and EAF elicits anti-lipogenic activity in liver. Therefore, EAF represents a promising candidate for use in the development of novel therapeutic drugs or drug combinations for the prevention and treatment of NAFLD.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "180", "doc_id": "4641348", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does c/EBP homologous protein deficiency aggravate acute pancreatitis and associated lung injury?\n\nABSTRACT:\nTo investigate the pathophysiological role of C/EBP homologous protein (CHOP) in severe acute pancreatitis and associated lung injury. A severe acute pancreatitis model was induced with 6 injections of cerulein (Cn, 50 μg/kg) at 1-h intervals, then intraperitoneal injection of lipopolysaccharide (LPS, 7.5 mg/kg) in CHOP-deficient (Chop(-/-)) mice and wild-type (WT) mice. Animals were sacrificed under anesthesia, 3 h or 18 h after LPS injection. Serum amylase, lipase, and cytokines [interleukin (IL)-6 and tumor necrosis factor (TNF)-α], pathological changes, acute lung injury, and apoptosis in the pancreas were evaluated. Serum amylase and lipase activities were detected using a medical automatic chemical analyzer. Enzyme-linked immunosorbent assay kits were used to evaluate TNF-α and IL-6 levels in mouse serum and lung tissue homogenates. Apoptotic cells in sections of pancreatic tissues were determined by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) analysis. The mouse carotid arteries were cannulated and arterial blood samples were collected for PaO2 analysis. The oxygenation index was expressed as PaO2/FiO2. Administration of Cn and LPS for 9 and 24 h induced severe acute pancreatitis in Chop(-/-) and WT mice. When comparing Chop(-/-) mice and WT mice, we observed that CHOP-deficient mice had greater increases in serum TNF-α (214.40 ± 19.52 pg/mL vs 150.40 ± 16.70 pg/mL; P = 0.037), amylase (4236.40 ± 646.32 U/L vs 2535.30 ± 81.83 U/L; P = 0.041), lipase (1678.20 ± 170.57 U/L vs 1046.21 ± 35.37 U/L; P = 0.008), and IL-6 (2054.44 ± 293.81 pg/mL vs 1316.10 ± 108.74 pg/mL; P = 0.046) than WT mice. The histopathological changes in the pancreases and lungs, decreased PaO2/FiO2 ratio, and increased TNF-α and IL-6 levels i [TRUNCATED]", "output": "{\"label\": \"yes\", \"rationale\": \"These results suggest that CHOP can exert protective effects against acute pancreatitis and limit the spread of inflammatory damage to the lungs.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 24222953, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Varying expression levels of EBI2 affect the positioning and migration of B cells.\n\nCANDIDATE_PASSAGE:\nGuidance of B cells by the orphan G protein-coupled receptor EBI2 shapes humoral immune responses. Humoral immunity depends on both rapid and long-term antibody production against invading pathogens. This is achieved by the generation of spatially distinct extrafollicular plasmablast and follicular germinal center (GC) B cell populations, but the signals that guide responding B cells to these alternative compartments have not been fully elucidated. Here, we show that expression of the orphan G protein-coupled receptor Epstein-Barr virus-induced gene 2 (EBI2, also known as GPR183) by activated B cells was essential for their movement to extrafollicular sites and induction of early plasmablast responses. Conversely, downregulation of EBI2 enabled B cells to access the center of follicles and promoted efficient GC formation. EBI2 therefore provides a previously uncharacterized dimension to B cell migration that is crucial for coordinating rapid versus long-term antibody responses.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1361", "doc_id": "15488881", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is soluble insulin receptor ectodomain elevated in the plasma of patients with diabetes?\n\nABSTRACT:\nInsulin binds to the alpha-subunit of the insulin receptor (IRalpha) and subsequently exerts its effects in the cells. The soluble ectodomains of several receptors have been found to circulate in the plasma. Therefore, we hypothesized that soluble human insulin receptor (hIR) ectodomain (alpha-subunit and a part of beta-subunit) may exist in the plasma of diabetic patients. We identified soluble hIR ectodomain in human plasma by a two-step purification followed by immunoblotting and gel-filtration chromatography. Furthermore, we established an hIRalpha-specific enzyme-linked immunosorbent assay and measured the plasma IRalpha levels in patients with diabetes. We also investigated this phenomenon in streptozotocin-induced diabetic hIR transgenic mice. Soluble hIRalpha, but not intact hIRbeta or whole hIR, exists in human plasma. The plasma IRalpha levels were significantly higher in type 1 (2.00 +/- 0.60 ng/ml; n = 53) and type 2 (2.26 +/- 0.80; n = 473) diabetic patients than in control subjects (1.59 +/- 0.40 ng/ml; n = 123 (P < 0.001 vs. control). Plasma IRalpha level was positively correlated with blood glucose level, and 10-20% of the insulin in plasma bound to hIRalpha. In the in vivo experiments using diabetic hIR transgenic mice, hyperglycemia was confirmed to increase the plasma hIRalpha level and the half-life estimated to be approximately 6 h.", "output": "{\"label\": \"yes\", \"rationale\": \"We propose that the increased soluble IR ectodomain level appears to be a more rapid glycemic marker than A1C or glycoalbumin.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 17563065, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Klf4 is not required for proper myeloid cell differentiation.\n\nCANDIDATE_ABSTRACT:\nTITLE: The myeloid transcription factor KLF2 regulates the host response to polymicrobial infection and endotoxic shock.\nABSTRACT: Precise control of myeloid cell activation is required for optimal host defense. However, this activation process must be under exquisite control to prevent uncontrolled inflammation. Herein, we identify the Kruppel-like transcription factor 2 (KLF2) as a potent regulator of myeloid cell activation in vivo. Exposure of myeloid cells to hypoxia and/or bacterial products reduced KLF2 expression while inducing hypoxia inducible factor-1α (HIF-1α), findings that were recapitulated in human septic patients. Myeloid KLF2 was found to be a potent inhibitor of nuclear factor-kappaB (NF-κB)-dependent HIF-1α transcription and, consequently, a critical determinant of outcome in models of polymicrobial infection and endotoxemia. Collectively, these observations identify KLF2 as a tonic repressor of myeloid cell activation in vivo and an essential regulator of the innate immune system.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 669, "doc_id": "6493422", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Mutant mice lacking SVCT2 have severely reduced ascorbic acid levels in both brain and adrenals.\n\nCANDIDATE_ABSTRACT:\nTITLE: Ascorbic-acid transporter Slc23a1 is essential for vitamin C transport into the brain and for perinatal survival\nABSTRACT: The only proven requirement for ascorbic acid (vitamin C) is in preventing scurvy, presumably because it is a cofactor for hydroxylases required for post-translational modifications that stabilize collagen. We have created mice deficient in the mouse ortholog (solute carrier family 23 member 1 or Slc23a1) of a rat ascorbic-acid transporter, Svct2 (ref. 4). Cultured embryonic fibroblasts from homozygous Slc23a1−/− mice had less than 5% of normal ascorbic-acid uptake. Ascorbic-acid levels were undetectable or markedly reduced in the blood and tissues of Slc23a1−/− mice. Prenatal supplementation of pregnant females did not elevate blood ascorbic acid in Slc23a1−/− fetuses, suggesting Slc23a1 is important in placental ascorbic-acid transport. Slc23a1−/− mice died within a few minutes of birth with respiratory failure and intraparenchymal brain hemorrhage. Lungs showed no postnatal expansion but had normal surfactant protein B levels. Brain hemorrhage was unlikely to be simply a form of scurvy since Slc23a1−/− mice showed no hemorrhage in any other tissues and their skin had normal skin 4-hydroxyproline levels despite low ascorbic-acid content. We conclude that Slc23a1 is required for transport of ascorbic acid into many tissues and across the placenta. Deficiency of the transporter is lethal in newborn mice, thereby revealing a previously unrecognized requirement for ascorbic acid in the perinatal period.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Ascorbic-acid levels were undetectable or markedly reduced in the blood and tissues of Slc23a1−/− mice. Slc23a1−/− mice died within a few minutes of birth with respiratory failure and intraparenchymal brain hemorrhage.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 812, "doc_id": "19799455", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: 7-day-old adult Caenorhabditis elegans exhibit approximately 75% of the learning capacity seen in 1-day old adults.\n\nCANDIDATE_ABSTRACT:\nTITLE: Insulin Signaling and Dietary Restriction Differentially Influence the Decline of Learning and Memory with Age\nABSTRACT: Of all the age-related declines, memory loss is one of the most devastating. While conditions that increase longevity have been identified, the effects of these longevity-promoting factors on learning and memory are unknown. Here we show that the C. elegans Insulin/IGF-1 receptor mutant daf-2 improves memory performance early in adulthood and maintains learning ability better with age but, surprisingly, demonstrates no extension in long-term memory with age. By contrast, eat-2 mutants, a model of Dietary Restriction (DR), exhibit impaired long-term memory in young adulthood but maintain this level of memory longer with age. We find that crh-1, the C. elegans homolog of the CREB transcription factor, is required for long-term associative memory, but not for learning or short-term memory. The expression of crh-1 declines with age and differs in the longevity mutants, and CREB expression and activity correlate with memory performance. Our results suggest that specific longevity treatments have acute and long-term effects on cognitive functions that decline with age through their regulation of rate-limiting genes required for learning and memory.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 20, "doc_id": "3202143", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Charcoal shows no benefit for acute paraquat poisoning.\n\nCANDIDATE_ABSTRACT:\nTITLE: Systematic review of controlled clinical trials of gastric lavage in acute organophosphorus pesticide poisoning.\nABSTRACT: BACKGROUND Organophosphorus pesticide (OP) self-poisoning is a major problem in the developing rural world. There is little clinical trial data to guide therapy, hindering the identification of best therapy. Despite the recognition of adverse effects, gastric lavage is commonly done in Asia. We aimed to identify studies assessing its effectiveness. METHOD We systematically searched the literature for controlled clinical studies that assessed the effect of gastric lavage in OP pesticide self-poisoning. RESULTS All 56 studies identified were Chinese and reported benefit from the intervention studied, including multiple gastric lavages, use of norepinephrine or pralidoxime in the lavage fluid, concurrent treatment with naloxone or scopolamine, insertion of the gastric tube via a laparotomy incision, and lavage later than 12 h post-ingestion. However, only 23 were RCTs and none presented adequate methodology for their quality to be assessed. The patient population and study treatment protocol were not defined - large variation in case fatality in the control arm of the studies (from 4.5 to 93%) suggests marked variation between studies and likely between study arms. No study compared an intervention against a control group receiving no gastric lavage or provided any data to indicate whether a significant quantity of poison was removed. CONCLUSION Despite widespread use of multiple gastric lavages for OP pesticide poisoning across Asia, there is currently no high-quality evidence to support its clinical effectiveness. There is a need for studies to identify in which patients and for what duration gastric lavage is able to remove significant quantities of poison. Following these studies, large clinical trials will be required to address the effectiveness and safet [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 246, "doc_id": "8447873", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Hyperfibrinogenemia decreases rates of femoropopliteal bypass thrombosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Implementing the ESHRE 'poor responder' criteria in research studies: methodological implications.\nABSTRACT: The Bologna criteria for defining poor ovarian response (POR) during IVF provide a useful template for new research in this field of assisted conception. However, designing studies around the European Society for Human Reproduction and Embryology POR criteria can be methodologically challenging, as the new definition includes various POR subpopulations with diverse baseline characteristics and unknown clinical prognosis. When designing RCTs, potential result bias may be introduced if women from each subpopulation are not evenly allocated between intervention groups. In the case of small or moderate-size RCTs, a single-sequence randomization method may not ensure balanced allocation between groups. Stratified randomization methods provide an alternative methodological approach. Depending on the chosen methodology, patient characteristics and outcomes within each intervention group may be better reported according to relevant subpopulations.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 532, "doc_id": "427865", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: COPI coatmer is involved in lipid homeostasis.\n\nCANDIDATE_ABSTRACT:\nTITLE: COPI Complex Is a Regulator of Lipid Homeostasis\nABSTRACT: Lipid droplets are ubiquitous triglyceride and sterol ester storage organelles required for energy storage homeostasis and biosynthesis. Although little is known about lipid droplet formation and regulation, it is clear that members of the PAT (perilipin, adipocyte differentiation related protein, tail interacting protein of 47 kDa) protein family coat the droplet surface and mediate interactions with lipases that remobilize the stored lipids. We identified key Drosophila candidate genes for lipid droplet regulation by RNA interference (RNAi) screening with an image segmentation-based optical read-out system, and show that these regulatory functions are conserved in the mouse. Those include the vesicle-mediated Coat Protein Complex I (COPI) transport complex, which is required for limiting lipid storage. We found that COPI components regulate the PAT protein composition at the lipid droplet surface, and promote the association of adipocyte triglyceride lipase (ATGL) with the lipid droplet surface to mediate lipolysis. Two compounds known to inhibit COPI function, Exo1 and Brefeldin A, phenocopy COPI knockdowns. Furthermore, RNAi inhibition of ATGL and simultaneous drug treatment indicate that COPI and ATGL function in the same pathway. These data indicate that the COPI complex is an evolutionarily conserved regulator of lipid homeostasis, and highlight an interaction between vesicle transport systems and lipid droplets.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We found that COPI components regulate the PAT protein composition at the lipid droplet surface, and promote the association of adipocyte triglyceride lipase (ATGL) with the lipid droplet surface to mediate lipolysis.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 210, "doc_id": "13794374", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does fas labeling status correlate with apoptosis of renal cell carcinoma in vivo?\n\nABSTRACT:\nContribution of the Fas system to apoptosis of renal cell carcinoma (RCC) was investigated in vivo. Tissues from 30 RCC cases were immunostained for Fas and Fas ligand (FasL) to assess associations between Fas labeling status of RCC, indices of FasL-positive tumor-infiltrating mononuclear cells (FasL-TIM) and apoptotic indices (AI) of RCC. In all cases, tumor cells co-expressed Fas and FasL; strongly and diffusely in 13 cases (43%) and weakly in 17 (57%). Despite the constitutive co-expression of Fas and FasL, AI was low in most cases (median, 7 per 1,000 tumor cells; range, 1 to 257). The Fas labeling status did not significantly associate with AI while FasL-TIM index positively correlated with AI.", "output": "{\"label\": \"no\", \"rationale\": \"These results suggest that the Fas system is not the principal mechanism of apoptosis of RCC while activated tumor-infiltrating mononuclear cells induce apoptosis via mechanisms other than the Fas system.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 11848472, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: siRNA knockdown of A20 accelerates tumor progression in an in vivo murine xenograft model.\n\nCANDIDATE_ABSTRACT:\nTITLE: Targeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth\nABSTRACT: Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs). GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets. We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels. To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA). Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis. The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays. The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts. In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival. Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation. Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may funct [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1403, "doc_id": "33370", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: A breast cancer patient's capacity to metabolize tamoxifen influences treatment outcome.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association between CYP2D6 polymorphisms and outcomes among women with early stage breast cancer treated with tamoxifen.\nABSTRACT: CONTEXT The growth inhibitory effect of tamoxifen, which is used for the treatment of hormone receptor-positive breast cancer, is mediated by its metabolites, 4-hydroxytamoxifen and endoxifen. The formation of active metabolites is catalyzed by the polymorphic cytochrome P450 2D6 (CYP2D6) enzyme. OBJECTIVE To determine whether CYP2D6 variation is associated with clinical outcomes in women receiving adjuvant tamoxifen. DESIGN, SETTING, AND PATIENTS Retrospective analysis of German and US cohorts of patients treated with adjuvant tamoxifen for early stage breast cancer. The 1325 patients had diagnoses between 1986 and 2005 of stage I through III breast cancer and were mainly postmenopausal (95.4%). Last follow-up was in December 2008; inclusion criteria were hormone receptor positivity, no metastatic disease at diagnosis, adjuvant tamoxifen therapy, and no chemotherapy. DNA from tumor tissue or blood was genotyped for CYP2D6 variants associated with reduced (*10, *41) or absent (*3, *4, *5) enzyme activity. Women were classified as having an extensive (n=609), heterozygous extensive/intermediate (n=637), or poor (n=79) CYP2D6 metabolism. MAIN OUTCOME MEASURES Time to recurrence, event-free survival, disease-free survival, and overall survival. RESULTS Median follow-up was 6.3 years. At 9 years of follow-up, the recurrence rates were 14.9% for extensive metabolizers, 20.9% for heterozygous extensive/intermediate metabolizers, and 29.0% for poor metabolizers, and all-cause mortality rates were 16.7%, 18.0%, and 22.8%, respectively. Compared with extensive metabolizers, there was a significantly increased risk of recurrence for heterozygous extensive/intermediate metabolizers (time to recurrence adjusted hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.04 [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Compared with extensive metabolizers, there was a significantly increased risk of recurrence for heterozygous extensive/intermediate metabolizers (time to recurrence adjusted hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.04-1.90) and for poor metabolizers (time to recurrence HR, 1.90; 95% CI, 1.10-3.28).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 30, "doc_id": "24341590", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Primary cervical cytology screening with HPV detection has higher longitudinal sensitivity to detect severe cervical intraepithelial neoplasia than conventional cytology.\n\nCANDIDATE_ABSTRACT:\nTITLE: Evidence regarding human papillomavirus testing in secondary prevention of cervical cancer.\nABSTRACT: More than ever, clinicians need regularly updated reviews given the continuously increasing amount of new information regarding innovative cervical cancer prevention methods. A summary is given from recent meta-analyses and systematic reviews on 3 possible clinical applications of human papillomavirus (HPV) testing: triage of women with equivocal or low-grade cytologic abnormalities; prediction of the therapeutic outcome after treatment of cervical intraepithelial neoplasia (CIN) lesions, and last not but not least, primary screening for cervical cancer and pre-cancer. Consistent evidence is available indicating that HPV-triage with the Hybrid Capture(®) 2 assay (Qiagen Gaithersburg, Inc., MD, USA [previously Digene Corp.] (HC2) is more accurate (higher sensitivity, similar specificity) than repeat cytology to triage women with equivocal Pap smear results. Several other tests show at least similar accuracy but mRNA testing with the APTIMA(®) (Gen-Probe Inc., San Diego, CA, USA) test is similarly sensitive but more specific compared to HC2. In triage of low-grade squamous intraepithelial lesions (LSIL), HC2 is more sensitive but its specificity is substantially lower compared to repeat cytology. The APTIMA(®) test is more specific than HC2 without showing a loss in sensitivity. Identification of DNA of HPV types 16 and/or 18, or RNA from the five most carcinogenic HPV types allow selecting women at highest risk for CIN3+ but the sensitivity and negative predictive value of these markers are lower than full-range high-risk HPV (hrHPV) testing. After conservative treatment of cervical pre-cancer, HPV testing picks up more quickly, with higher sensitivity and not lower specificity, residual or recurrent high-grade CIN than follow-up cytology. Primary screening f [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Primary screening for hrHPV generally detects more CIN2, CIN3 or cancer compared to cytology at cut-off atypical squamous cells of undetermined significance (ASC-US) or LSIL, but is less specific.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 973, "doc_id": "28617573", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Gluten tolerance in adult patients with celiac disease 20 years after diagnosis?\n\nABSTRACT:\nCeliac disease (CD) is believed to be a permanent intolerance to gluten. A number of patients, however, discontinue the gluten-free diet (GFD) without developing symptoms or signs. The aim of our study was to investigate whether CD patients are capable of developing tolerance to gluten. All 77 adult patients from our hospital known to have biopsy-proven CD for more than 10 years were invited to participate. We investigated symptoms, gluten consumption, antibodies for CD and other autoimmunity, human leukocyte antigen (HLA)-typing, bone mineral density, and performed small bowel biopsies. Tolerance was defined as no immunological or histological signs of CD while consuming gluten. Sixty-six patients accepted participation, but after review of the diagnostic biopsies 53 were found to have true CD. Twenty-three percent of patients had a gluten-containing diet, 15% admitted gluten transgression and 62% followed the GFD. Patients on a GFD had significantly more osteoporosis. Normal small bowel mucosa was found in four of eight on gluten-containing diet and in four of four with gluten transgression. Two patients were considered to have developed tolerance to gluten. One of them was HLA-DQ2/DQ8 negative.", "output": "{\"label\": \"maybe\", \"rationale\": \"Development of tolerance to gluten seems possible in some patients with CD. Further follow-up will show whether this tolerance is permanent or only a long-term return to latency. This feature may be associated with genetic characteristics, especially with HLA genotypes that differ from DQ2 or DQ8.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 18403944, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: A 100g dose of chloroquine chemoprophylactic regimen results in retinal toxicity after 1 year of weekly intake.\n\nCANDIDATE_ABSTRACT:\nTITLE: Prevention of malaria in long-term travelers.\nABSTRACT: CONTEXT Long-term travelers, defined here as those traveling for periods of 6 months or longer, face particular challenges regarding malaria prevention. Current guidelines for malaria prevention primarily address prevention of Plasmodium falciparum infections in short-term travelers. OBJECTIVES To examine the risk of malaria in long-term travelers, recent developments in personal protective measures, and the safety and tolerability of malaria chemoprophylaxis during long-term use and to consider prevention strategies including continuous chemoprophylaxis, stand-by emergency self-treatment, seasonal prophylaxis, and strategies to prevent primary infection and relapses from P vivax malaria. EVIDENCE ACQUISITION Comprehensive search of scientific publications including MEDLINE via both OVID and PubMED for relevant studies and articles with a cutoff date of July 2006, using the search terms long-term travel and malaria prevention, long-term malaria chemoprophylaxis, and insect repellent and malaria. Additional references were obtained from searching the bibliographies of the selected articles, from dissertations, and from the proceedings of relevant conferences on travel medicine. There were no language restrictions. EVIDENCE SYNTHESIS Long-term travelers have a higher risk of malaria than short-term travelers. Long-term travelers underuse personal protective measures and adhere poorly to continuous chemoprophylaxis regimens. A number of strategies are used during long-term stays: discontinuation of chemoprophylaxis after the initial period, sequential regimens with different medications for chemoprophylaxis, stand-by emergency self-treatment, and seasonal chemoprophylaxis targeting high-incidence periods or locations. All strategies have advantages and drawback [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 26, "doc_id": "32390525", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Genes regulated by Esrrb transcription factor are sensitive to Mbd3 function.\n\nCANDIDATE_ABSTRACT:\nTITLE: An Oct4-Centered Protein Interaction Network in Embryonic Stem Cells\nABSTRACT: Transcription factors, such as Oct4, are critical for establishing and maintaining pluripotent cell identity. Whereas the genomic locations of several pluripotency transcription factors have been reported, the spectrum of their interaction partners is underexplored. Here, we use an improved affinity protocol to purify Oct4-interacting proteins from mouse embryonic stem cells (ESCs). Subsequent purification of Oct4 partners Sall4, Tcfcp2l1, Dax1, and Esrrb resulted in an Oct4 interactome of 166 proteins, including transcription factors and chromatin-modifying complexes with documented roles in self-renewal, but also many factors not previously associated with the ESC network. We find that Esrrb associated with the basal transcription machinery and also detect interactions between transcription factors and components of the TGF-beta, Notch, and Wnt signaling pathways. Acute depletion of Oct4 reduced binding of Tcfcp2l1, Dax1, and Esrrb to several target genes. In conclusion, our purification protocol allowed us to bring greater definition to the circuitry controlling pluripotent cell identity.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 456, "doc_id": "30507607", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: \"Would a man smell a rose then throw it away?\n\nABSTRACT:\nBreast cancer is the most common malignancy afflicting women, and the most common cancer overall in Jordan. A woman's decision to go for screening is influenced by her social support network. This study aims to explore Jordanian men's individual and contextual perspectives on women's breast cancer and their own role in the breast health of the females within their families. An explorative qualitative design was used to purposively recruit 24 married men aged 27 to 65 years (median 43 years) from four governorates in Jordan. Data in the form of interviews transcriptions was subjected to qualitative content analysis. Three themes were identified: a) Supporting one's wife; b) Marital needs and obligations; c) Constrained by a culture of destiny and shame. The first theme was built on men's feelings of responsibility for the family's health and well-being, their experiences of encouraging their wives to seek health care and their providing counselling and instrumental support. The second theme emerged from men's views about other men's rejection of a wife inflicted by breast cancer, their own perceptions of diminished femininity due to mastectomy and their own concerns about protecting the family from the hereditary risk of breast cancer. The third theme was seen in men's perception of breast cancer as an inevitable act of God that is far away from one's own family, in associating breast cancer with improper behaviour and in their readiness to face the culture of Eib (shame).", "output": "{\"label\": \"maybe\", \"rationale\": \"Jordanian men perceive themselves as having a vital role in supporting, guiding and encouraging their wives to follow breast cancer early detection recommendations. Breast health awareness campaigns could involve husbands to capitalize on family support.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 24160268, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is conservation of shh cis-regulatory architecture of the coelacanth consistent with its ancestral phylogenetic position?\n\nABSTRACT:\nThe modern coelacanth (Latimeria) is the extant taxon of a basal sarcopterygian lineage and sister group to tetrapods. Apart from certain apomorphic traits, its morphology is characterized by a high degree of retention of ancestral vertebrate structures and little morphological change. An insight into the molecular evolution that may explain the unchanged character of Latimeria morphology requires the analysis of the expression patterns of developmental regulator genes and their cis-regulatory modules (CRMs). We describe the comparative and functional analysis of the sonic hedgehog (shh) genomic region of Latimeria menadoensis. Several putative enhancers in the Latimeria shh locus have been identified by comparisons to sarcopterygian and actinopterygian extant species. Specific sequence conservation with all known actinopterygian enhancer elements has been detected. However, these elements are selectively missing in more recently diverged actinopterygian and sarcopterygian species. The functionality of the putative Latimeria enhancers was confirmed by reporter gene expression analysis in transient transgenic zebrafish and chick embryos.", "output": "{\"label\": \"yes\", \"rationale\": \"Latimeria shh CRMs represent the ancestral set of enhancers that have emerged before the split of lobe-finned and ray-finned fishes. In contrast to lineage-specific losses and differentiations in more derived lineages, Latimeria shh enhancers reveal low levels of sequence diversification. High overall sequence conservation of shh conserved noncoding elements (CNE) is consistent with the general trend of high levels of conservation of noncoding DNA in the slowly evolving Latimeria genome.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 21047394, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: ATM and Rad3 related protein are critical for sensing DNA damage.\n\nCANDIDATE_PASSAGE:\nDeletion of the developmentally essential gene ATR in adult mice leads to age-related phenotypes and stem cell loss. Developmental abnormalities, cancer, and premature aging each have been linked to defects in the DNA damage response (DDR). Mutations in the ATR checkpoint regulator cause developmental defects in mice (pregastrulation lethality) and humans (Seckel syndrome). Here we show that eliminating ATR in adult mice leads to defects in tissue homeostasis and the rapid appearance of age-related phenotypes, such as hair graying, alopecia, kyphosis, osteoporosis, thymic involution, fibrosis, and other abnormalities. Histological and genetic analyses indicate that ATR deletion causes acute cellular loss in tissues in which continuous cell proliferation is required for maintenance. Importantly, thymic involution, alopecia, and hair graying in ATR knockout mice were associated with dramatic reductions in tissue-specific stem and progenitor cells and exhaustion of tissue renewal and homeostatic capacity. In aggregate, these studies suggest that reduced regenerative capacity in adults via deletion of a developmentally essential DDR gene is sufficient to cause the premature appearance of age-related phenotypes.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "63", "doc_id": "40349336", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cellular differentiation of embryonic stem cells is accompanied by changes in replication timing, transcription and nuclear localization.\n\nCANDIDATE_ABSTRACT:\nTITLE: Aberrant luminal progenitors as the candidate target population for basal tumor development in BRCA1 mutation carriers\nABSTRACT: Basal-like breast cancers arising in women carrying mutations in the BRCA1 gene, encoding the tumor suppressor protein BRCA1, are thought to develop from the mammary stem cell. To explore early cellular changes that occur in BRCA1 mutation carriers, we have prospectively isolated distinct epithelial subpopulations from normal mammary tissue and preneoplastic specimens from individuals heterozygous for a BRCA1 mutation. We describe three epithelial subsets including basal stem/progenitor, luminal progenitor and mature luminal cells. Unexpectedly, we found that breast tissue from BRCA1 mutation carriers harbors an expanded luminal progenitor population that shows factor-independent growth in vitro. Moreover, gene expression profiling revealed that breast tissue heterozygous for a BRCA1 mutation and basal breast tumors were more similar to normal luminal progenitor cells than any other subset, including the stem cell–enriched population. The c-KIT tyrosine kinase receptor (encoded by KIT) emerged as a key marker of luminal progenitor cells and was more highly expressed in BRCA1-associated preneoplastic tissue and tumors. Our findings suggest that an aberrant luminal progenitor population is a target for transformation in BRCA1-associated basal tumors .", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 243, "doc_id": "1866911", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Upregulation of dynein in Drosophila neurons increases the number of microtubule plus-ends growing toward the cell body of each neuron.\n\nCANDIDATE_ABSTRACT:\nTITLE: Dynein is required for polarized dendritic transport and uniform microtubule orientation in axons\nABSTRACT: Axons and dendrites differ in both microtubule organization and in the organelles and proteins they contain. Here we show that the microtubule motor dynein has a crucial role in polarized transport and in controlling the orientation of axonal microtubules in Drosophila melanogaster dendritic arborization (da) neurons. Changes in organelle distribution within the dendritic arbors of dynein mutant neurons correlate with a proximal shift in dendritic branch position. Dynein is also necessary for the dendrite-specific localization of Golgi outposts and the ion channel Pickpocket. Axonal microtubules are normally oriented uniformly plus-end-distal; however, without dynein, axons contain both plus- and minus-end distal microtubules. These data suggest that dynein is required for the distinguishing properties of the axon and dendrites: without dynein, dendritic organelles and proteins enter the axon and the axonal microtubules are no longer uniform in polarity.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Axonal microtubules are normally oriented uniformly plus-end-distal; however, without dynein, axons contain both plus- and minus-end distal microtubules.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1351, "doc_id": "28369117", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Replacement of histone H2A with H2A.Z slows gene activation in yeasts by stabilizing +1 nucleosomes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Nucleosome stability mediated by histone variants H3.3 and H2A.Z.\nABSTRACT: Nucleosomes containing the histone variant H3.3 tend to be clustered in vivo in the neighborhood of transcriptionally active genes and over regulatory elements. It has not been clear, however, whether H3.3-containing nucleosomes possess unique properties that would affect transcription. We report here that H3.3 nucleosomes isolated from vertebrates, regardless of whether they are partnered with H2A or H2A.Z, are unusually sensitive to salt-dependent disruption, losing H2A/H2B or H2A.Z/H2B dimers. Immunoprecipitation studies of nucleosome core particles (NCPs) show that NCPs that contain both H3.3 and H2A.Z are even less stable than NCPs containing H3.3 and H2A. Intriguingly, NCPs containing H3 and H2A.Z are at least as stable as H3/H2A NCPs. These results establish an hierarchy of stabilities for native nucleosomes carrying different complements of variants, and suggest how H2A.Z could play different roles depending on its partners within the NCP. They also are consistent with the idea that H3.3 plays an active role in maintaining accessible chromatin structures in enhancer regions and transcribed regions. Consistent with this idea, promoters and enhancers at transcriptionally active genes and coding regions at highly expressed genes have nucleosomes that simultaneously carry both H3.3 and H2A.Z, and should therefore be extremely sensitive to disruption.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Immunoprecipitation studies of nucleosome core particles (NCPs) show that NCPs that contain both H3.3 and H2A.Z are even less stable than NCPs containing H3.3 and H2A.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1041, "doc_id": "25254425", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: A mutation in HNF4A leads to an increased risk of developing diabetes by the age of 14 years.\n\nCANDIDATE_ABSTRACT:\nTITLE: Macrosomia and Hyperinsulinaemic Hypoglycaemia in Patients with Heterozygous Mutations in the HNF4A Gene\nABSTRACT: Background Macrosomia is associated with considerable neonatal and maternal morbidity. Factors that predict macrosomia are poorly understood. The increased rate of macrosomia in the offspring of pregnant women with diabetes and in congenital hyperinsulinaemia is mediated by increased foetal insulin secretion. We assessed the in utero and neonatal role of two key regulators of pancreatic insulin secretion by studying birthweight and the incidence of neonatal hypoglycaemia in patients with heterozygous mutations in the maturity-onset diabetes of the young (MODY) genes HNF4A (encoding HNF-4α) and HNF1A/TCF1 (encoding HNF-1α), and the effect of pancreatic deletion of Hnf4a on foetal and neonatal insulin secretion in mice.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We assessed the in utero and neonatal role of two key regulators of pancreatic insulin secretion by studying birthweight and the incidence of neonatal hypoglycaemia in patients with heterozygous mutations in the maturity-onset diabetes of the young (MODY) genes HNF4A (encoding HNF-4α) and HNF1A/TCF1 (encoding HNF-1α), and the effect of pancreatic deletion of Hnf4a on foetal and neonatal insulin secretion in mice.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 44, "doc_id": "56893404", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pyridostatin deregulates G2/M progression.\n\nCANDIDATE_ABSTRACT:\nTITLE: Targeting BRCA1 and BRCA2 Deficiencies with G-Quadruplex-Interacting Compounds\nABSTRACT: G-quadruplex (G4)-forming genomic sequences, including telomeres, represent natural replication fork barriers. Stalled replication forks can be stabilized and restarted by homologous recombination (HR), which also repairs DNA double-strand breaks (DSBs) arising at collapsed forks. We have previously shown that HR facilitates telomere replication. Here, we demonstrate that the replication efficiency of guanine-rich (G-rich) telomeric repeats is decreased significantly in cells lacking HR. Treatment with the G4-stabilizing compound pyridostatin (PDS) increases telomere fragility in BRCA2-deficient cells, suggesting that G4 formation drives telomere instability. Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint activation, and deregulated G2/M progression and by enhancing the replication defect intrinsic to HR deficiency. PDS toxicity extends to HR-defective cells that have acquired olaparib resistance through loss of 53BP1 or REV7. Altogether, these results highlight the therapeutic potential of G4-stabilizing drugs to selectively eliminate HR-compromised cells and tumors, including those resistant to PARP inhibition.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint activation, and deregulated G2/M progression and by enhancing the replication defect intrinsic to HR deficiency.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 992, "doc_id": "16472469", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Incidence rates of cervical cancer have decreased.\n\nCANDIDATE_PASSAGE:\nMetabolic shutdown in Escherichia coli cells lacking the outer membrane channel TolC. The outer membrane channel TolC is a key component of multidrug efflux and type I secretion transporters in Escherichia coli. Mutational inactivation of TolC renders cells highly susceptible to antibiotics and leads to defects in secretion of protein toxins. Despite impairment of various transport functions, no growth defects were reported in cells lacking TolC. Unexpectedly, we found that the loss of TolC notably impairs cell division and growth in minimal glucose medium. The TolC-dependent phenotype was further exacerbated by the loss of ygiB and ygiC genes expressed in the same operon as tolC and their homologues yjfM and yjfC located elsewhere on the chromosome. Our results show that this growth deficiency is caused by depletion of the critical metabolite NAD(+) and high NADH/NAD(+) ratios. The increased amounts of PspA and decreased rates of NADH oxidation in Delta tolC membranes indicated stress on the membrane and dissipation of a proton motive force. We conclude that inactivation of TolC triggers metabolic shutdown in E. coli cells grown in minimal glucose medium. The Delta tolC phenotype is partially rescued by YgiBC and YjfMC, which have parallel functions independent from TolC.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "597", "doc_id": "26625002", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Allogeneic mechanical circulatory support is not as effective as autologous mechanical circulatory support for treating acute myocardial infarction.\n\nCANDIDATE_ABSTRACT:\nTITLE: Comparison of allogeneic vs autologous bone marrow–derived mesenchymal stem cells delivered by transendocardial injection in patients with ischemic cardiomyopathy: the POSEIDON randomized trial.\nABSTRACT: CONTEXT Mesenchymal stem cells (MSCs) are under evaluation as a therapy for ischemic cardiomyopathy (ICM). Both autologous and allogeneic MSC therapies are possible; however, their safety and efficacy have not been compared. OBJECTIVE To test whether allogeneic MSCs are as safe and effective as autologous MSCs in patients with left ventricular (LV) dysfunction due to ICM. DESIGN, SETTING, AND PATIENTS A phase 1/2 randomized comparison (POSEIDON study) in a US tertiary-care referral hospital of allogeneic and autologous MSCs in 30 patients with LV dysfunction due to ICM between April 2, 2010, and September 14, 2011, with 13-month follow-up. INTERVENTION Twenty million, 100 million, or 200 million cells (5 patients in each cell type per dose level) were delivered by transendocardial stem cell injection into 10 LV sites. MAIN OUTCOME MEASURES Thirty-day postcatheterization incidence of predefined treatment-emergent serious adverse events (SAEs). Efficacy assessments included 6-minute walk test, exercise peak VO2, Minnesota Living with Heart Failure Questionnaire (MLHFQ), New York Heart Association class, LV volumes, ejection fraction (EF), early enhancement defect (EED; infarct size), and sphericity index. RESULTS Within 30 days, 1 patient in each group (treatment-emergent SAE rate, 6.7%) was hospitalized for heart failure, less than the prespecified stopping event rate of 25%. The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3% (n = 8) in the autologous group (P = .46). At 1 year, there were no ventricular arrhythmia SAEs observed among allogeneic recipients compared with 4 patients (26.7%) in the autologous group (P = .10). Relative to baseline, autologous but not allogeneic MSC therapy was associated with an improvement in the 6- [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3% (n = 8) in the autologous group (P = .46).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 104, "doc_id": "40164383", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Bariatric surgery leads to positive outcomes in mental health.\n\nCANDIDATE_PASSAGE:\nAccumulation of hydroxyethyl starch in human and animal tissues: a systematic review To systematically review clinical and preclinical data on hydroxyethyl starch (HES) tissue storage. MEDLINE (PubMed) was searched and abstracts were screened using defined criteria to identify articles containing original data on HES tissue accumulation. Forty-eight studies were included: 37 human studies with a total of 635 patients and 11 animal studies. The most frequent indication for fluid infusion was surgery accounting for 282 patients (45.9 %). HES localization in skin was shown by 17 studies, in kidney by 12, in liver by 8, and in bone marrow by 5. Additional sites of HES deposition were lymph nodes, spleen, lung, pancreas, intestine, muscle, trophoblast, and placental stroma. Among major organs the highest measured tissue concentration of HES was in the kidney. HES uptake into intracellular vacuoles was observed by 30 min after infusion. Storage was cumulative, increasing in proportion to dose, although in 15 % of patients storage and associated symptoms were demonstrated at the lowest cumulative doses (0.4 g kg−1). Some HES deposits were extremely long-lasting, persisting for 8 years or more in skin and 10 years in kidney. Pruritus associated with HES storage was described in 17 studies and renal dysfunction in ten studies. In one included randomized trial, HES infusion produced osmotic nephrosis-like lesions indicative of HES storage (p = 0.01) and also increased the need for renal replacement therapy (odds ratio, 9.50; 95 % confidence interval, 1.09–82.7; p = 0.02). The tissue distribution of HES was generally similar in animals and humans. Tissue storage of HES is widespread, rapid, cumulative, frequently long-lasting, and potentially harmful.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "167", "doc_id": "24155601", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: TNFAIP3 is a glioblastoma tumor suppressor.\n\nCANDIDATE_ABSTRACT:\nTITLE: Targeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth\nABSTRACT: Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs). GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets. We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels. To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA). Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis. The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays. The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts. In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival. Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation. Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may funct [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may function as a tumor enhancer in glioma through promotion of GSC survival.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1135, "doc_id": "33370", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is postoperative use of hypnotics associated with increased length of stay after uncomplicated surgery for colorectal cancer?\n\nABSTRACT:\nHypnotics are used to treat perioperative sleep disorders. These drugs are associated with a higher risk of adverse effects among patients undergoing surgery. This study aims to quantify the use of hypnotics and factors influencing the administration of hypnotics in relation to colorectal cancer surgery. A retrospective cohort study of 1979 patients undergoing colorectal cancer surgery. In all, 381 patients (19%) received new treatment with hypnotics. Two of the six surgical centres used hypnotics less often (odds ratio (95% confidence interval), 0.24 (0.16-0.38) and 0.20 (0.12-0.35)). Active smokers (odds ratio (95% confidence interval), 1.57 (1.11-2.24)) and patients receiving perioperative blood transfusion (odds ratio (95% confidence interval), 1.58 (1.10-2.26)) had increased likelihood of receiving hypnotics. In the uncomplicated cases, a multivariable linear regression analysis showed that consumption of hypnotics postoperatively was significantly associated with increased length of stay (1.5 (0.9-2.2) days).", "output": "{\"label\": \"yes\", \"rationale\": \"One in five patients began treatment with hypnotics after colorectal cancer surgery. Postoperative use of hypnotics was associated with an increased length of stay for uncomplicated cases of colorectal cancer surgery.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 27660704, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In patients with congenital heart defects, β-blockers significantly improve clinical heart failure outcomes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Carvedilol for children and adolescents with heart failure: a randomized controlled trial.\nABSTRACT: CONTEXT Although beta-blockers improve symptoms and survival in adults with heart failure, little is known about these medications in children and adolescents. OBJECTIVE To prospectively evaluate the effects of carvedilol in children and adolescents with symptomatic systemic ventricular systolic dysfunction. DESIGN, SETTING, AND PARTICIPANTS A multicenter, randomized, double-blind, placebo-controlled study of 161 children and adolescents with symptomatic systolic heart failure from 26 US centers. In addition to treatment with conventional heart failure medications, patients were assigned to receive placebo or carvedilol. Enrollment began in June 2000 and the last dose was given in May 2005 (each patient received medication for 8 months). INTERVENTIONS Patients were randomized in a 1:1:1 ratio to twice-daily dosing with placebo, low-dose carvedilol (0.2 mg/kg per dose if weight <62.5 kg or 12.5 mg per dose if weight > or =62.5 kg), or high-dose carvedilol (0.4 mg/kg per dose if weight <62.5 kg or 25 mg per dose if weight > or =62.5 kg) and were stratified according to whether each patient's systemic ventricle was a left ventricle or not. MAIN OUTCOME MEASURES The primary outcome was a composite measure of heart failure outcomes in patients receiving carvedilol (low- and high-dose combined) vs placebo. Secondary efficacy variables included individual components of this composite, echocardiographic measures, and plasma b-type natriuretic peptide levels. RESULTS There was no statistically significant difference between groups for the composite end point based on the percentage of patients who improved, worsened, or were unchanged. Among 54 patients assigned to placebo, 30 improved (56%), 16 worsened (30%), and 8 were unchanged (15%); among 103 patients assigned [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS These preliminary results suggest that carvedilol does not significantly improve clinical heart failure outcomes in children and adolescents with symptomatic systolic heart failure.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 579, "doc_id": "34139429", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Cataract and trachoma are the primary cause of blindness in Southern Sudan.\n\nCANDIDATE_ABSTRACT:\nTITLE: Prevalence and Causes of Blindness and Low Vision in Southern Sudan \nABSTRACT: Background Blindness and low vision are thought to be common in southern Sudan. However, the magnitude and geographical distribution are largely unknown. We aimed to estimate the prevalence of blindness and low vision, identify the main causes of blindness and low vision, and estimate targets for blindness prevention programs in Mankien payam (district), southern Sudan.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 232, "doc_id": "10536636", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Insulin increases risk of severe kidney failure.\n\nCANDIDATE_PASSAGE:\nCongenital leptin deficiency is associated with severe early-onset obesity in humans. The extreme obesity of the obese (ob/ob) mouse is attributable to mutations in the gene encoding leptin, an adipocyte-specific secreted protein which has profound effects on appetite and energy expenditure. We know of no equivalent evidence regarding leptin's role in the control of fat mass in humans. We have examined two severely obese children who are members of the same highly consanguineous pedigree. Their serum leptin levels were very low despite their markedly elevated fat mass and, in both, a homozygous frame-shift mutation involving the deletion of a single guanine nucleotide in codon 133 of the gene for leptin was found. The severe obesity found in these congenitally leptin-deficient subjects provides the first genetic evidence that leptin is an important regulator of energy balance in humans.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "644", "doc_id": "4353857", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does concerted action of sulfiredoxin and peroxiredoxin I protect against alcohol-induced oxidative injury in mouse liver?\n\nABSTRACT:\nPeroxiredoxins (Prxs) are peroxidases that catalyze the reduction of reactive oxygen species (ROS). The active site cysteine residue of members of the 2-Cys Prx subgroup (Prx I to IV) of Prxs is hyperoxidized to cysteine sulfinic acid (Cys-SO(2) ) during catalysis with concomitant loss of peroxidase activity. Reactivation of the hyperoxidized Prx is catalyzed by sulfiredoxin (Srx). Ethanol consumption induces the accumulation of cytochrome P450 2E1 (CYP2E1), a major contributor to ethanol-induced ROS production in the liver. We now show that chronic ethanol feeding markedly increased the expression of Srx in the liver of mice in a largely Nrf2-dependent manner. Among Prx I to IV, only Prx I was found to be hyperoxidized in the liver of ethanol-fed wildtype mice, and the level of Prx I-SO(2) increased to ≈30% to 50% of total Prx I in the liver of ethanol-fed Srx(-/-) mice. This result suggests that Prx I is the most active 2-Cys Prx in elimination of ROS from the liver of ethanol-fed mice and that, despite the up-regulation of Srx expression by ethanol, the capacity of Srx is not sufficient to counteract the hyperoxidation of Prx I that occurs during ROS reduction. A protease protection assay revealed that a large fraction of Prx I is located together with CYP2E1 at the cytosolic side of the endoplasmic reticulum membrane. The selective role of Prx I in ROS removal is thus likely attributable to the proximity of Prx I and CYP2E1.", "output": "{\"label\": \"yes\", \"rationale\": \"The pivotal functions of Srx and Prx I in protection of the liver in ethanol-fed mice was evident from the severe oxidative damage observed in mice lacking either Srx or Prx I.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 21319188, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The availability of safe places to study is not effective at decreasing homelessness.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mental health problems of homeless children and families: longitudinal study.\nABSTRACT: OBJECTIVE To establish the mental health needs of homeless children and families before and after rehousing. DESIGN Cross sectional, longitudinal study. SETTING City of Birmingham. SUBJECTS 58 rehoused families with 103 children aged 2-16 years and 21 comparison families of low socioeconomic status in stable housing, with 54 children. MAIN OUTCOME MEASURES Children's mental health problems and level of communication; mothers' mental health problems and social support one year after rehousing. RESULTS Mental health problems remained significantly higher in rehoused mothers and their children than in the comparison group (mothers 26% v 5%, P = 0.04; children 39% v 11%, P = 0.0003). Homeless mothers continued to have significantly less social support at follow up. Mothers with a history of abuse and poor social integration were more likely to have children with persistent mental health problems. CONCLUSIONS Homeless families have a high level of complex needs that cannot be met by conventional health services and arrangements. Local strategies for rapid rehousing into permanent accommodation, effective social support and health care for parents and children, and protection from violence and intimidation should be developed and implemented.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1197, "doc_id": "25649714", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Sildenafil worsens erectile function in men who experience sexual dysfunction as a result of the use of SSRI antidepressants.\n\nCANDIDATE_ABSTRACT:\nTITLE: Treatment of antidepressant-associated sexual dysfunction with sildenafil: a randomized controlled trial.\nABSTRACT: CONTEXT Sexual dysfunction is a common adverse effect of antidepressants that frequently results in treatment noncompliance. OBJECTIVE To assess the efficacy of sildenafil citrate in men with sexual dysfunction associated with the use of selective and nonselective serotonin reuptake inhibitor (SRI) antidepressants. DESIGN, SETTING, AND PATIENTS Prospective, parallel-group, randomized, double-blind, placebo-controlled trial conducted between November 1, 2000, and January 1, 2001, at 3 US university medical centers among 90 male outpatients (mean [SD] age, 45 [8] years) with major depression in remission and sexual dysfunction associated with SRI antidepressant treatment. INTERVENTION Patients were randomly assigned to take sildenafil (n = 45) or placebo (n = 45) at a flexible dose starting at 50 mg and adjustable to 100 mg before sexual activity for 6 weeks. MAIN OUTCOME MEASURES The primary outcome measure was score on the Clinical Global Impression-Sexual Function (CGI-SF); secondary measures were scores on the International Index of Erectile Function, Arizona Sexual Experience Scale, Massachusetts General Hospital-Sexual Functioning Questionnaire, and Hamilton Rating Scale for Depression (HAM-D). RESULTS Among the 90 randomized patients, 93% (83/89) of patients treated per protocol took at least 1 dose of study drug and 85% (76/89) completed week 6 end-point assessments with last observation carried forward analyses. At a CGI-SF score of 2 or lower, 54.5% (24/44) of sildenafil compared with 4.4% (2/45) of placebo patients were much or very much improved (P<.001). Erectile function, arousal, ejaculation, orgasm, and overall satisfaction domain measures improved significantly in sildenafil compared with placebo patients. Mean depression scores remained consi [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Erectile function, arousal, ejaculation, orgasm, and overall satisfaction domain measures improved significantly in sildenafil compared with placebo patients.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1087, "doc_id": "39281140", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Patients with common epithelial cancers are more likely to have an emergency event as their first hospital admission if they live in resource-deprived areas.\n\nCANDIDATE_ABSTRACT:\nTITLE: Social variations in access to hospital care for patients with colorectal, breast, and lung cancer between 1999 and 2006: retrospective analysis of hospital episode statistics\nABSTRACT: OBJECTIVES To determine the extent to which type of hospital admission (emergency compared with elective) and surgical procedure varied by socioeconomic circumstances, age, sex, and year of admission for colorectal, breast, and lung cancer. DESIGN Repeated cross sectional study with data from individual patients, 1 April 1999 to 31 March 2006. SETTING Hospital episode statistics (HES) dataset. PARTICIPANTS 564 821 patients aged 50 and over admitted with a diagnosis of colorectal, breast, or lung cancer. MAIN OUTCOME MEASURES Proportion of patients admitted as emergencies, and the proportion receiving the recommended surgical treatment. RESULTS Patients from deprived areas, older people, and women were more likely to be admitted as emergencies. For example, the adjusted odds ratio for patients with breast cancer in the least compared with most deprived fifth of deprivation was 0.63 (95% confidence interval 0.60 to 0.66) and the adjusted odds ratio for patients with lung cancer aged 80-89 compared with those aged 50-59 was 3.13 (2.93 to 3.34). There were some improvements in disparities between age groups but not for patients living in deprived areas over time. Patients from deprived areas were less likely to receive preferred procedures for rectal, breast, and lung cancer. These findings did not improve with time. For example, 67.4% (3529/5237) of patients in the most deprived fifth of deprivation had anterior resection for rectal cancer compared with 75.5% (4497/5959) of patients in the least deprived fifth (1.34, 1.22 to 1.47). Over half (54.0%, 11 256/20 849) of patients in the most deprived fifth of deprivation had breast conserving surgery compared with 63.7% (18 445/28 960) of patients in the least deprived fifth (1.21, 1.16 to 1.26). Men were less like [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"For example, 67.4% (3529/5237) of patients in the most deprived fifth of deprivation had anterior resection for rectal cancer compared with 75.5% (4497/5959) of patients in the least deprived fifth (1.34, 1.22 to 1.47).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 926, "doc_id": "16390264", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Women with a lower birth weight are more likely to develop breast cancer later in life.\n\nCANDIDATE_ABSTRACT:\nTITLE: Intrauterine environments and breast cancer risk: meta-analysis and systematic review\nABSTRACT: INTRODUCTION Various perinatal factors, including birth weight, birth order, maternal age, gestational age, twin status, and parental smoking, have been postulated to affect breast cancer risk in daughters by altering the hormonal environment of the developing fetal mammary glands. Despite ample biologic plausibility, epidemiologic studies to date have yielded conflicting results. We investigated the associations between perinatal factors and subsequent breast cancer risk through meta-analyses. METHODS We reviewed breast cancer studies published from January 1966 to February 2007 that included data on birth weight, birth order, maternal age, gestational age, twin status, and maternal or paternal smoking. Meta-analyses using random effect models were employed to summarize the results. RESULTS We found that heavier birth weights were associated with increased breast cancer risk, with studies involving five categories of birth weight identifying odds ratios (ORs) of 1.24 (95% confidence interval [CI] 1.04 to 1.48) for 4,000 g or more and 1.15 (95% CI 1.04 to 1.26) for 3,500 g to 3,999 g, relative to a birth weight of 2,500 to 2,599 g. These studies provided no support for a J-shaped relationship of birthweight to risk. Support for an association with birthweight was also derived from studies based on three birth weight categories (OR 1.15 [95% CI 1.01 to 1.31] for > or =4,000 g relative to <3,000 g) and two birth weight categories (OR 1.09 [95% CI 1.02 to 1.18] for > or =3,000 g relative to <3,000 g). Women born to older mothers and twins were also at some increased risk, but the results were heterogeneous across studies and publication years. Birth order, prematurity, and maternal smoking were unrelated to breast cancer risk. CONCLUSION Our findings provide so [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"RESULTS We found that heavier birth weights were associated with increased breast cancer risk, with studies involving five categories of birth weight identifying odds ratios (ORs) of 1.24 (95% confidence interval [CI] 1.04 to 1.48) for 4,000 g or more and 1.15 (95% CI 1.04 to 1.26) for 3,500 g to 3,999 g, relative to a birth weight of 2,500 to 2,599 g. These studies provided no support for a J-shaped relationship of birthweight to risk.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1380, "doc_id": "17450673", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Oxidative DNA damage inhibits STING signalling.\n\nCANDIDATE_PASSAGE:\nThe helicase DDX41 senses intracellular DNA mediated by the adaptor STING in dendritic cells The recognition of pathogenic DNA is important to the initiation of antiviral responses. Here we report the identification of DDX41, a member of the DEXDc family of helicases, as an intracellular DNA sensor in myeloid dendritic cells (mDCs). Knockdown of DDX41 expression by short hairpin RNA blocked the ability of mDCs to mount type I interferon and cytokine responses to DNA and DNA viruses. Overexpression of both DDX41 and the membrane-associated adaptor STING together had a synergistic effect in promoting Ifnb promoter activity. DDX41 bound both DNA and STING and localized together with STING in the cytosol. Knockdown of DDX41 expression blocked activation of the mitogen-activated protein kinase TBK1 and the transcription factors NF-κB and IRF3 by B-form DNA. Our results suggest that DDX41 is an additional DNA sensor that depends on STING to sense pathogenic DNA.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "899", "doc_id": "41337677", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Pharmacist attendance at ward rounds increases adverse events in wards.\n\nCANDIDATE_ABSTRACT:\nTITLE: Isolation from African Sykes' monkeys (Cercopithecus mitis) of a lentivirus related to human and simian immunodeficiency viruses.\nABSTRACT: Analysis of serum samples from 100 wild-caught or colony-born Sykes' monkeys (Cercopithecus mitis) in Kenya revealed that 59 animals had antibodies cross-reactive to human immunodeficiency virus type 2 (HIV-2) and to simian immunodeficiency viruses (SIVs). A lentivirus, designated SIVsyk, was isolated from five of six seropositive asymptomatic Sykes' monkeys, but in four cases isolation was possible only after depletion of CD8+ lymphocytes and cocultivation of the CD4(+)-enriched cell population with peripheral blood mononuclear cells from seronegative Sykes' monkeys. SIVsyk resembled other SIVs and HIVs morphologically, had an Mg2(+)-dependent reverse transcriptase enzyme, and replicated in and was cytopathic for CEMx174 and Sup-T1 cells. SIVsyk differred substantially from other SIVs, however, in that it failed to replicate in normal human, mangabey, and macaque peripheral blood mononuclear cells and serum from seropositive Sykes' monkeys immunoprecipitated env antigens from HIV-1 as well as from HIV-2, SIVsmm, and SIVagm. These data demonstrate a high prevalence of natural infection in Sykes' monkeys in Kenya with a lentivirus that appears to be unique with respect to its host range and antigenic cross-reactivity.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 940, "doc_id": "798152", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: A total of 1,000 people in the UK are asymptomatic carriers of vCJD infection.\n\nCANDIDATE_ABSTRACT:\nTITLE: Functional elements within the dynein microtubule-binding domain\nABSTRACT: Dynein interacts with microtubules through an ATP-sensitive linkage mapped to a structurally complex region of the heavy chain following the fourth P-loop motif. Virtually nothing is known regarding how binding affinity is achieved and modulated during ATP hydrolysis. We have performed a detailed dissection of the microtubule contact site, using fragment expression, alanine substitution, and peptide competition. Our work identifies three clusters of amino acids important for the physical contact with microtubules; two of these fall within a region sharing sequence homology with MAP1B, the third in a region just downstream. Amino acid substitutions within any one of these regions can eliminate or weaken microtubule binding (KK3379, 80, E3385, K3387, K3397, KK3410,11, W3414, RKK3418-20, F3426, R3464, S3466, and K3467), suggesting that their activities are highly coordinated. A peptide that actively displaces MAP1B from microtubules perturbs dynein binding, supporting previous evidence for similar sites of interaction. We have also identified four amino acids whose substitutions affect release of the motor from the microtubule (E3413, R3444, E3460, and C3469). These suggest that nucleotide-sensitive affinity may be locally controlled at the site of contact. Our work is the first detailed description of dynein-tubulin interactions and provides a framework for understanding how affinity is achieved and modulated.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 48, "doc_id": "1546650", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Ectopic expression of Sall4, Nanog, Esrrb, and Lin28 generates induced pluripotent stem cells from mouse embryonic fibroblasts more efficiently than other factor combinations.\n\nCANDIDATE_ABSTRACT:\nTITLE: The developmental potential of iPSCs is greatly influenced by reprogramming factor selection.\nABSTRACT: Induced pluripotent stem cells (iPSCs) are commonly generated by transduction of Oct4, Sox2, Klf4, and Myc (OSKM) into cells. Although iPSCs are pluripotent, they frequently exhibit high variation in terms of quality, as measured in mice by chimera contribution and tetraploid complementation. Reliably high-quality iPSCs will be needed for future therapeutic applications. Here, we show that one major determinant of iPSC quality is the combination of reprogramming factors used. Based on tetraploid complementation, we found that ectopic expression of Sall4, Nanog, Esrrb, and Lin28 (SNEL) in mouse embryonic fibroblasts (MEFs) generated high-quality iPSCs more efficiently than other combinations of factors including OSKM. Although differentially methylated regions, transcript number of master regulators, establishment of specific superenhancers, and global aneuploidy were comparable between high- and low-quality lines, aberrant gene expression, trisomy of chromosome 8, and abnormal H2A.X deposition were distinguishing features that could potentially also be applicable to human.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Based on tetraploid complementation, we found that ectopic expression of Sall4, Nanog, Esrrb, and Lin28 (SNEL) in mouse embryonic fibroblasts (MEFs) generated high-quality iPSCs more efficiently than other combinations of factors including OSKM.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 369, "doc_id": "6826100", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: APOE4 expression in iPSC-derived neurons increases AlphaBeta production and tau phosphorylation, delaying GABA neuron degeneration.\n\nCANDIDATE_ABSTRACT:\nTITLE: Gain of toxic Apolipoprotein E4 effects in Human iPSC-Derived Neurons Is Ameliorated by a Small-Molecule Structure Corrector\nABSTRACT: Efforts to develop drugs for Alzheimer's disease (AD) have shown promise in animal studies, only to fail in human trials, suggesting a pressing need to study AD in human model systems. Using human neurons derived from induced pluripotent stem cells that expressed apolipoprotein E4 (ApoE4), a variant of the APOE gene product and the major genetic risk factor for AD, we demonstrated that ApoE4-expressing neurons had higher levels of tau phosphorylation, unrelated to their increased production of amyloid-β (Aβ) peptides, and that they displayed GABAergic neuron degeneration. ApoE4 increased Aβ production in human, but not in mouse, neurons. Converting ApoE4 to ApoE3 by gene editing rescued these phenotypes, indicating the specific effects of ApoE4. Neurons that lacked APOE behaved similarly to those expressing ApoE3, and the introduction of ApoE4 expression recapitulated the pathological phenotypes, suggesting a gain of toxic effects from ApoE4. Treatment of ApoE4-expressing neurons with a small-molecule structure corrector ameliorated the detrimental effects, thus showing that correcting the pathogenic conformation of ApoE4 is a viable therapeutic approach for ApoE4-related AD.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Using human neurons derived from induced pluripotent stem cells that expressed apolipoprotein E4 (ApoE4), a variant of the APOE gene product and the major genetic risk factor for AD, we demonstrated that ApoE4-expressing neurons had higher levels of tau phosphorylation, unrelated to their increased production of amyloid-β (Aβ) peptides, and that they displayed GABAergic neuron degeneration.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 57, "doc_id": "4709641", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Mice lacking Sirt1 in Sf1-expressing neurons are immune to diet-induced obesity and insulin resistance.\n\nCANDIDATE_PASSAGE:\nSIRT1 deacetylase in SF1 neurons protects against metabolic imbalance. Chronic feeding on high-calorie diets causes obesity and type 2 diabetes mellitus (T2DM), illnesses that affect hundreds of millions. Thus, understanding the pathways protecting against diet-induced metabolic imbalance is of paramount medical importance. Here, we show that mice lacking SIRT1 in steroidogenic factor 1 (SF1) neurons are hypersensitive to dietary obesity owing to maladaptive energy expenditure. Also, mutant mice have increased susceptibility to developing dietary T2DM due to insulin resistance in skeletal muscle. Mechanistically, these aberrations arise, in part, from impaired metabolic actions of the neuropeptide orexin-A and the hormone leptin. Conversely, mice overexpressing SIRT1 in SF1 neurons are more resistant to diet-induced obesity and insulin resistance due to increased energy expenditure and enhanced skeletal muscle insulin sensitivity. Our results unveil important protective roles of SIRT1 in SF1 neurons against dietary metabolic imbalance.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "778", "doc_id": "13001323", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Exercise increases cancer mortality rates among Chinese citizens.\n\nCANDIDATE_ABSTRACT:\nTITLE: Combined Impact of Lifestyle-Related Factors on Total and Cause-Specific Mortality among Chinese Women: Prospective Cohort Study\nABSTRACT: BACKGROUND Although cigarette smoking, excessive alcohol drinking, obesity, and several other well-studied unhealthy lifestyle-related factors each have been linked to the risk of multiple chronic diseases and premature death, little is known about the combined impact on mortality outcomes, in particular among Chinese and other non-Western populations. The objective of this study was to quantify the overall impact of lifestyle-related factors beyond that of active cigarette smoking and alcohol consumption on all-cause and cause-specific mortality in Chinese women. METHODS AND FINDINGS We used data from the Shanghai Women's Health Study, an ongoing population-based prospective cohort study in China. Participants included 71,243 women aged 40 to 70 years enrolled during 1996-2000 who never smoked or drank alcohol regularly. A healthy lifestyle score was created on the basis of five lifestyle-related factors shown to be independently associated with mortality outcomes (normal weight, lower waist-hip ratio, daily exercise, never exposed to spouse's smoking, higher daily fruit and vegetable intake). The score ranged from zero (least healthy) to five (most healthy) points. During an average follow-up of 9 years, 2,860 deaths occurred, including 775 from cardiovascular disease (CVD) and 1,351 from cancer. Adjusted hazard ratios for mortality decreased progressively with an increasing number of healthy lifestyle factors. Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality. The inverse association between the healthy lifestyle score and mortality was seen consistently regardless of ch [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 396, "doc_id": "1456068", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Gluten tolerance in adult patients with celiac disease 20 years after diagnosis?\n\nABSTRACT:\nCeliac disease (CD) is believed to be a permanent intolerance to gluten. A number of patients, however, discontinue the gluten-free diet (GFD) without developing symptoms or signs. The aim of our study was to investigate whether CD patients are capable of developing tolerance to gluten. All 77 adult patients from our hospital known to have biopsy-proven CD for more than 10 years were invited to participate. We investigated symptoms, gluten consumption, antibodies for CD and other autoimmunity, human leukocyte antigen (HLA)-typing, bone mineral density, and performed small bowel biopsies. Tolerance was defined as no immunological or histological signs of CD while consuming gluten. Sixty-six patients accepted participation, but after review of the diagnostic biopsies 53 were found to have true CD. Twenty-three percent of patients had a gluten-containing diet, 15% admitted gluten transgression and 62% followed the GFD. Patients on a GFD had significantly more osteoporosis. Normal small bowel mucosa was found in four of eight on gluten-containing diet and in four of four with gluten transgression. Two patients were considered to have developed tolerance to gluten. One of them was HLA-DQ2/DQ8 negative.", "output": "{\"label\": \"maybe\", \"rationale\": \"Development of tolerance to gluten seems possible in some patients with CD. Further follow-up will show whether this tolerance is permanent or only a long-term return to latency. This feature may be associated with genetic characteristics, especially with HLA genotypes that differ from DQ2 or DQ8.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 18403944, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Notch signaling occurs between tumor cells and stromal cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Jagged1-induced Notch signaling drives proliferation of multiple myeloma cells.\nABSTRACT: Notch receptors expressed on hematopoietic stem cells interact with their ligands on bone marrow stromal cells and thereby control cell fate decisions and survival. We recently demonstrated that Notch signaling is involved in proliferation and survival of B cell-derived tumor cells of classic Hodgkin disease and described a novel mechanism for the oncogenic capacity of Notch. In this study we investigated whether Notch signaling is involved in the tight interactions between neoplastic plasma cells and their bone marrow microenvironment, which are essential for tumor cell growth in multiple myeloma (MM). Here we demonstrate that Notch receptors and their ligand Jagged1 are highly expressed in cultured and primary MM cells, whereas nonneoplastic counterparts show low to undetectable levels of Notch. Functional data indicate that ligand-induced Notch signaling is a growth factor for MM cells and suggest that these interactions contribute to myelomagenesis in vivo.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We recently demonstrated that Notch signaling is involved in proliferation and survival of B cell-derived tumor cells of classic Hodgkin disease and described a novel mechanism for the oncogenic capacity of Notch.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 863, "doc_id": "16361581", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Are langerhans cells critical in epicutaneous sensitization with protein antigen via thymic stromal lymphopoietin receptor signaling?\n\nABSTRACT:\nThe clarification of cutaneous dendritic cell subset and the role of thymic stromal lymphopoietin (TSLP) signaling in epicutaneous sensitization with protein antigens, as in the development of atopic dermatitis, is a crucial issue. Because TSLP is highly expressed in the vicinity of Langerhans cells (LCs), we sought to clarify our hypothesis that LCs play an essential role in epicutaneous sensitization with protein antigens through TSLP signaling. By using Langerin-diphtheria toxin receptor knock-in mice and human Langerin-diphtheria toxin A transgenic mice, we prepared mice deficient in LCs. We also prepared mice deficient in TSLP receptors in LCs by using TSLP receptor-deficient mice with bone marrow chimeric technique. We applied these mice to an ovalbumin (OVA)-induced epicutaneous sensitization model. Upon the epicutaneous application of OVA, conditional LC depletion attenuated the development of clinical manifestations as well as serum OVA-specific IgE increase, OVA-specific T-cell proliferation, and IL-4 mRNA expression in the draining lymph nodes. Consistently, even in the steady state, permanent LC depletion resulted in decreased serum IgE levels, suggesting that LCs mediate the T(H)2 local environment. In addition, mice deficient in TSLP receptors on LCs abrogated the induction of OVA-specific IgE levels upon epicutaneous OVA sensitization.", "output": "{\"label\": \"yes\", \"rationale\": \"LCs initiate epicutaneous sensitization with protein antigens and induce T(H)2-type immune responses via TSLP signaling.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 22385635, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: In breast cancer, the loss of myoepithelial cells promotes the transition of ductal carcinoma in situ to invasive carcinoma.\n\nCANDIDATE_ABSTRACT:\nTITLE: Regulation of in situ to invasive breast carcinoma transition.\nABSTRACT: The transition of ductal carcinoma in situ (DCIS) to invasive carcinoma is a poorly understood key event in breast tumor progression. Here, we analyzed the role of myoepithelial cells and fibroblasts in the progression of in situ carcinomas using a model of human DCIS and primary breast tumors. Progression to invasion was promoted by fibroblasts and inhibited by normal myoepithelial cells. Molecular profiles of isolated luminal epithelial and myoepithelial cells identified an intricate interaction network involving TGFbeta, Hedgehog, cell adhesion, and p63 required for myoepithelial cell differentiation, the elimination of which resulted in loss of myoepithelial cells and progression to invasion.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Progression to invasion was promoted by fibroblasts and inhibited by normal myoepithelial cells.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 570, "doc_id": "20333864", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Early patent ductus ateriosus (PDA) screening increases in-hospital mortality.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association Between Early Screening for Patent Ductus Arteriosus and In-Hospital Mortality Among Extremely Preterm Infants.\nABSTRACT: IMPORTANCE There is currently no consensus for the screening and treatment of patent ductus arteriosus (PDA) in extremely preterm infants. Less pharmacological closure and more supportive management have been observed without evidence to support these changes. OBJECTIVE To evaluate the association between early screening echocardiography for PDA and in-hospital mortality. DESIGN, SETTING, AND PARTICIPANTS Comparison of screened and not screened preterm infants enrolled in the EPIPAGE 2 national prospective population-based cohort study that included all preterm infants born at less than 29 weeks of gestation and hospitalized in 68 neonatal intensive care units in France from April through December 2011. Two main analyses were performed to adjust for potential selection bias, one using propensity score matching and one using neonatal unit preference for early screening echocardiography as an instrumental variable. EXPOSURES Early screening echocardiography before day 3 of life. MAIN OUTCOMES AND MEASURES The primary outcome was death between day 3 and discharge. The secondary outcomes were major neonatal morbidities (pulmonary hemorrhage, severe bronchopulmonary dysplasia, severe cerebral lesions, and necrotizing enterocolitis). RESULTS Among the 1513 preterm infants with data available to determine exposure, 847 were screened for PDA and 666 were not; 605 infants from each group could be paired. Exposed infants were treated for PDA more frequently during their hospitalization than nonexposed infants (55.1% vs 43.1%; odds ratio [OR], 1.62 [95% CI, 1.31 to 2.00]; absolute risk reduction [ARR] in events per 100 infants, -12.0 [95% CI, -17.3 to -6.7). Exposed infants had a lower hospital death rate (14.2% vs 18.5% ; OR, 0.73 [95% CI, 0.54 to 0.98]; ARR, 4.3 [95% [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Exposed infants had a lower hospital death rate (14.2% vs 18.5% ; OR, 0.73 [95% CI, 0.54 to 0.98]; ARR, 4.3 [95% CI, 0.3 to 8.3]) and a lower rate of pulmonary hemorrhage (5.6% vs 8.9%; OR, 0.60 [95% CI, 0.38 to 0.95]; ARR, 3.3 [95% CI, 0.4 to 6.3]).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 368, "doc_id": "27099731", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: AMP-activated protein kinase (AMPK) activation increases inflammation-related fibrosis in the lungs.\n\nCANDIDATE_PASSAGE:\nMaternal alloantigens promote the development of tolerogenic fetal regulatory T cells in utero. As the immune system develops, T cells are selected or regulated to become tolerant of self antigens and reactive against foreign antigens. In mice, the induction of such tolerance is thought to be attributable to the deletion of self-reactive cells. Here, we show that the human fetal immune system takes advantage of an additional mechanism: the generation of regulatory T cells (Tregs) that suppress fetal immune responses. We find that substantial numbers of maternal cells cross the placenta to reside in fetal lymph nodes, inducing the development of CD4+CD25highFoxP3+ Tregs that suppress fetal antimaternal immunity and persist at least until early adulthood. These findings reveal a form of antigen-specific tolerance in humans, induced in utero and probably active in regulating immune responses after birth.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "54", "doc_id": "10190778", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: RA activation of DIF2 and NB4 cells induces hallmarks of transcriptionally active promoters.\n\nCANDIDATE_PASSAGE:\nHistone Methylation-Dependent Mechanisms Impose Ligand Dependency for Gene Activation by Nuclear Receptors Nuclear receptors undergo ligand-dependent conformational changes that are required for corepressor-coactivator exchange, but whether there is an actual requirement for specific epigenetic landmarks to impose ligand dependency for gene activation remains unknown. Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases (HMTs) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals. This strategy, based at least in part on an HMT-dependent inhibitory histone code, imposes a requirement for specific histone demethylases, including LSD1, to permit ligand- and signal-dependent activation of regulated gene expression. These events link an inhibitory methylation component of the histone code to a broadly used strategy that circumvents pathological constitutive gene induction by physiologically regulated transcription factors.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1002", "doc_id": "13639330", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does timing of initial surfactant treatment make a difference in rates of chronic lung disease or mortality in premature infants?\n\nABSTRACT:\nTo compare two treatment strategies in preterm infants with or at risk of respiratory distress syndrome: early surfactant administration (within one hour of birth) versus late surfactant administration, in a geographically defined population. The primary outcome was chronic lung disease (CLD) and mortality before/at 36 weeks. Secondary outcomes included: duration of mechanical ventilation and continuous positive airway pressure (CPAP), post-natal steroids for CLD and major neonatal morbidities. Premature infants born at 22-32 weeks' gestation between January 2006 and December 2009. Ten neonatal intensive care units (NICUs) in New South Wales (NSW) and Australian Capital Territory (ACT), Australia. Retrospective analysis of prospectively collected data from the regional NICU database in NSW and ACT. Of the 2170 infants who received surfactant, 1182 (54.5%) and 988 (45.5%) received early and late surfactant, respectively. The early surfactant group was less mature (27.1 ± 2.1 versus 29.4 ± 2.1 weeks) and had more CLD and mortality (40.2% versus 20.0%). The multivariable analysis showed early surfactant to be associated with less duration of ventilation, longer duration of CPAP and longer hospital stay but had little or no impact on CLD/mortality.", "output": "{\"label\": \"maybe\", \"rationale\": \"Early surfactant administration is associated with shorter duration of ventilation but does not appear to be significantly protective against CLD/mortality among premature infants. This may support the growing evidence for consideration of CPAP as an alternative to routine intubation and early surfactant administration. Further investigation from large randomized clinical trials is warranted to confirm these results.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 25394614, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Chinese individuals with TT homozygosity in the MTHFR gene are more vulnerable to strokes caused by low levels of folate intake.\n\nCANDIDATE_PASSAGE:\nSmall-airway obstruction and emphysema in chronic obstructive pulmonary disease. BACKGROUND The major sites of obstruction in chronic obstructive pulmonary disease (COPD) are small airways (<2 mm in diameter). We wanted to determine whether there was a relationship between small-airway obstruction and emphysematous destruction in COPD. METHODS We used multidetector computed tomography (CT) to compare the number of airways measuring 2.0 to 2.5 mm in 78 patients who had various stages of COPD, as judged by scoring on the Global Initiative for Chronic Obstructive Lung Disease (GOLD) scale, in isolated lungs removed from patients with COPD who underwent lung transplantation, and in donor (control) lungs. MicroCT was used to measure the extent of emphysema (mean linear intercept), the number of terminal bronchioles per milliliter of lung volume, and the minimum diameters and cross-sectional areas of terminal bronchioles. RESULTS On multidetector CT, in samples from patients with COPD, as compared with control samples, the number of airways measuring 2.0 to 2.5 mm in diameter was reduced in patients with GOLD stage 1 disease (P=0.001), GOLD stage 2 disease (P=0.02), and GOLD stage 3 or 4 disease (P<0.001). MicroCT of isolated samples of lungs removed from patients with GOLD stage 4 disease showed a reduction of 81 to 99.7% in the total cross-sectional area of terminal bronchioles and a reduction of 72 to 89% in the number of terminal bronchioles (P<0.001). A comparison of the number of terminal bronchioles and dimensions at different levels of emphysematous destruction (i.e., an increasing value for the mean linear intercept) showed that the narrowing and loss of terminal bronchioles preceded emphysematous destruction in COPD (P<0.001). CONCLUSIONS These results s [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "254", "doc_id": "9440748", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Inhibiting HDAC6 increases survival of mice with ARID1A mutated tumors.\n\nCANDIDATE_PASSAGE:\nThe inflammasome component NLRP3 impairs antitumor vaccine by enhancing the accumulation of tumor-associated myeloid-derived suppressor cells. The inflammasome is a proteolysis complex that generates the active forms of the proinflammatory cytokines interleukin (IL)-1β and IL-18. Inflammasome activation is mediated by NLR proteins that respond to microbial and nonmicrobial stimuli. Among NLRs, NLRP3 senses the widest array of stimuli and enhances adaptive immunity. However, its role in antitumor immunity is unknown. Therefore, we evaluated the function of the NLRP3 inflammasome in the immune response using dendritic cell vaccination against the poorly immunogenic melanoma cell line B16-F10. Vaccination of Nlrp3(-/-) mice led to a relative 4-fold improvement in survival relative to control animals. Immunity depended on CD8(+) T cells and exhibited immune specificity and memory. Increased vaccine efficacy in Nlrp3(-/-) hosts did not reflect differences in dendritic cells but rather differences in myeloid-derived suppressor cells (MDSC). Although Nlrp3 was expressed in MDSCs, the absence of Nlrp3 did not alter either their functional capacity to inhibit T cells or their presence in peripheral lymphoid tissues. Instead, the absence of Nlrp3 caused a 5-fold reduction in the number of tumor-associated MDSCs found in host mice. Adoptive transfer experiments also showed that Nlrp3(-/-) MDSCs were less efficient in reaching the tumor site. Depleting MDSCs with an anti-Gr-1 antibody increased the survival of tumor-bearing wild-type mice but not Nlrp3(-/-) mice. We concluded that Nlrp3 was critical for accumulation of MDSCs in tumors and for inhibition of antitumor T-cell immunity after dendritic cell vaccination. Our findings establish an unexpected role for Nlrp3 in [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "631", "doc_id": "15435343", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: CD44v6 is not associated with constitutive and reprogrammed cancer stem cells driving cancer metastasis.\n\nCANDIDATE_ABSTRACT:\nTITLE: CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis.\nABSTRACT: Cancer stem cells drive tumor formation and metastasis, but how they acquire metastatic traits is not well understood. Here, we show that all colorectal cancer stem cells (CR-CSCs) express CD44v6, which is required for their migration and generation of metastatic tumors. CD44v6 expression is low in primary tumors but demarcated clonogenic CR-CSC populations. Cytokines hepatocyte growth factor (HGF), osteopontin (OPN), and stromal-derived factor 1α (SDF-1), secreted from tumor associated cells, increase CD44v6 expression in CR-CSCs by activating the Wnt/β-catenin pathway, which promotes migration and metastasis. CD44v6(-) progenitor cells do not give rise to metastatic lesions but, when treated with cytokines, acquire CD44v6 expression and metastatic capacity. Importantly, phosphatidylinositol 3-kinase (PI3K) inhibition selectively killed CD44v6 CR-CSCs and reduced metastatic growth. In patient cohorts, low levels of CD44v6 predict increased probability of survival. Thus, the metastatic process in colorectal cancer is initiated by CSCs through the expression of CD44v6, which is both a functional biomarker and therapeutic target.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Importantly, phosphatidylinositol 3-kinase (PI3K) inhibition selectively killed CD44v6 CR-CSCs and reduced metastatic growth.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 203, "doc_id": "9558539", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Birth-weight is negatively associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Intrauterine factors and risk of breast cancer: a systematic review and meta-analysis of current evidence.\nABSTRACT: BACKGROUND Emerging evidence suggests an association between female prenatal experience and her subsequent risk of developing breast cancer. Potential underlying mechanisms include variation in amounts of maternal endogenous sex hormones and growth hormones, germ-cell mutations, formation of cancer stem-cells, and other genetic or epigenetic events. We reviewed and summarised quantitatively the available data on intrauterine exposures and risk of breast cancer. METHODS We systematically searched for studies that assessed association between perinatal factors and risk of breast cancer. We reviewed separately each of the perinatal factors, including birthweight, birth length, parental age at delivery, gestational age, intrauterine exposure to diethylstilbestrol, twin membership, maternal pre-eclampsia or eclampsia, and other factors. FINDINGS We identified 57 studies published between Oct 1, 1980, and June 21, 2007. Increased risk of breast cancer was noted with increased birthweight (relative risk [RR] 1.15 [95% CI 1.09-1.21]), birth length (1.28 [1.11-1.48]), higher maternal age (1.13 [1.02-1.25]), and paternal age (1.12 [1.05-1.19]). Decreased risk of breast cancer was noted for maternal pre-eclampsia and eclampsia (0.48 [0.30-0.78]) and twin membership (0.93 [0.87-1.00]). No association was noted between risk of breast cancer and gestational age at birth (0.95 [0.71-1.26]) or maternal diethylstilbestrol treatment (1.40 [0.86-2.28]). INTERPRETATION The intrauterine environment contributes to the predisposition of women to breast cancer in adulthood. The in-utero mechanisms responsible for such predisposition need to be elucidated.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Increased risk of breast cancer was noted with increased birthweight (relative risk [RR] 1.15 [95% CI 1.09-1.21]), birth length (1.28 [1.11-1.48]), higher maternal age (1.13 [1.02-1.25]), and paternal age (1.12 [1.05-1.19]).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 178, "doc_id": "23557241", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Adult tissue-resident macrophages possess a self-renewing capacity.\n\nCANDIDATE_PASSAGE:\nFate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis. Mononuclear phagocytes, including monocytes, macrophages, and dendritic cells, contribute to tissue integrity as well as to innate and adaptive immune defense. Emerging evidence for labor division indicates that manipulation of these cells could bear therapeutic potential. However, specific ontogenies of individual populations and the overall functional organization of this cellular network are not well defined. Here we report a fate-mapping study of the murine monocyte and macrophage compartment taking advantage of constitutive and conditional CX(3)CR1 promoter-driven Cre recombinase expression. We have demonstrated that major tissue-resident macrophage populations, including liver Kupffer cells and lung alveolar, splenic, and peritoneal macrophages, are established prior to birth and maintain themselves subsequently during adulthood independent of replenishment by blood monocytes. Furthermore, we have established that short-lived Ly6C(+) monocytes constitute obligatory steady-state precursors of blood-resident Ly6C(-) cells and that the abundance of Ly6C(+) blood monocytes dynamically controls the circulation lifespan of their progeny.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "88", "doc_id": "7521113", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Mice defective for deoxyribonucleic acid (DNA) polymerase m (polm) fail to reveal increased sensitivity to ionizing radiation (IR).\n\nCANDIDATE_PASSAGE:\nNonoverlapping functions of DNA polymerases mu, lambda, and terminal deoxynucleotidyltransferase during immunoglobulin V(D)J recombination in vivo. DNA polymerases mu (pol mu), lambda (pol lambda), and terminal deoxynucleotidyltransferase (TdT) are enzymes of the pol X family that share homology in sequence and functional domain organization. We showed previously that pol mu participates in light chain but surprisingly not heavy chain gene rearrangement. We show here that immunoglobulin heavy chain junctions from pol lambda-deficient animals have shorter length with normal N-additions, thus indicating that pol lambda is recruited during heavy chain rearrangement at a step that precedes the action of TdT. In contrast to previous in vitro studies, analysis of animals with combined inactivation of these enzymes revealed no overlapping or compensatory activities for V(D)J recombination between pol mu, pol lambda, and TdT. This complex usage of polymerases with distinct catalytic specificities may correspond to the specific function that the third hypervariable region assumes for each immunoglobulin chain, with pol lambda maintaining a large heavy chain junctional heterogeneity and pol mu ensuring a restricted light chain junctional variability.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "776", "doc_id": "32275758", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Approximately 250,000 people are infected with human T-cell lymphotropic virus type 1 in the United Kingdom.\n\nCANDIDATE_ABSTRACT:\nTITLE: HTLV-I/II associated disease in England and Wales, 1993-7: retrospective review of serology requests.\nABSTRACT: Apart from HIV two exogenous retroviruses (human T cell leukaemia viruses type I (HTLV-I) and type II (HTLV-II)) infect humans. HTLV-I infection is endemic in Japan, the Caribbean, Africa, and Melanesia and is found among immigrants from these regions in Europe. HTLV-I infection is associated with a 1-5% lifetime risk of adult T cell leukaemia/lymphoma, 1 a 0.25% lifetime risk of HTLV-I associated myelopathy, 2 and other inflammatory conditions (uveitis, alveolitis, and arthritis).1 HTLV-II infection is endemic in some native American and African peoples and among injecting drug users and has been associated with neurological disease.1 Between 1986 and 1992, 100 cases of HTLV-I associated myelopathy and 44 cases of adult T cell leukaemia/lymphoma were diagnosed in the United Kingdom.3 Adult T cell leukaemia/lymphoma was first described in 1977 and patients with it have a mean life expectancy of only six months, so most of the 44 cases were probably incident cases. …", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 126, "doc_id": "24512064", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Dscam1 acts as a hypervariable pattern-recognition receptor for the immune system.\n\nCANDIDATE_PASSAGE:\nAgDscam, a Hypervariable Immunoglobulin Domain-Containing Receptor of the Anopheles gambiae Innate Immune System Activation of the insect innate immune system is dependent on a limited number of pattern recognition receptors (PRRs) capable of interacting with pathogen-associated molecular pattern. Here we report a novel role of an alternatively spliced hypervariable immunoglobulin domain-encoding gene, Dscam, in generating a broad range of PRRs implicated in immune defense in the malaria vector Anopheles gambiae. The mosquito Down syndrome cell adhesion molecule gene, AgDscam, has a complex genome organization with 101 exons that can produce over 31,000 potential alternative splice forms with different combinations of adhesive domains and interaction specificities. AgDscam responds to infection by producing pathogen challenge-specific splice form repertoires. Transient silencing of AgDscam compromises the mosquito's resistance to infections with bacteria and the malaria parasite Plasmodium. AgDscam is mediating phagocytosis of bacteria with which it can associate and defend against in a splice form–specific manner. AgDscam is a hypervariable PRR of the A. gambiae innate immune system.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "356", "doc_id": "6144337", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does use of hydrophilic guidewires significantly improve technical success rates of peripheral PTA?\n\nABSTRACT:\nTo determine whether the use of hydrophilic guidewires has increased the technical success rate of peripheral percutaneous transluminal angioplasty (PTA).MATERIAL/ We performed 125 procedures and analyzed the technical success rates of PTA using the conventional guidewire first and then if needed, the hydrophilic guidewire for iliac and SFA stenoses or occlusions. Angioplasty was performed on 25 stenosed, 25 occluded iliac arteries and 25 stenosed, 50 occluded femoral arteries. The result was defined as technical success when the lesion was crossed by a guidewire and balloon, then it was dilated with restoration of vessel lumen and less than 30% residual stenosis and the rise in ABI values was at least 0.15 after 24 hours. The technical success rate after PTA of stenosed iliac arteries was achieved in 96% (24/25) using conventional wires and 100% using hydrophilic guidewire; in iliac occlusions, the rates were 60% (15/25) and 96%, respectively; in femoral stenosis - 84% (21/25) and 100%; in occlusions in the first group: lesions<10 cm -64% (16/25) and 96%, in the second group: lesions>10 cm -48% (12/25) and 88%. In the iliac group, there was no significant difference in the success of iliac stenosis PTA. However, there were significant changes in the success rates of PTA performed for SFA stenosis and iliac and SFA occlusions.", "output": "{\"label\": \"maybe\", \"rationale\": \"In summary, we report an overall improvement and high technical success rate for peripherial PTA. The use of hydrophilic guidewires made significant difference to the technical success rate of PTA, especially in occlusion and more complicated lesions.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 16538201, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Inhibiting focal adhesion formation enables cells to convert mechanical strain into eventual scarring.\n\nCANDIDATE_ABSTRACT:\nTITLE: Focal adhesion kinase links mechanical force to skin fibrosis via inflammatory signaling\nABSTRACT: Exuberant fibroproliferation is a common complication after injury for reasons that are not well understood. One key component of wound repair that is often overlooked is mechanical force, which regulates cell-matrix interactions through intracellular focal adhesion components, including focal adhesion kinase (FAK). Here we report that FAK is activated after cutaneous injury and that this process is potentiated by mechanical loading. Fibroblast-specific FAK knockout mice have substantially less inflammation and fibrosis than control mice in a model of hypertrophic scar formation. We show that FAK acts through extracellular-related kinase (ERK) to mechanically trigger the secretion of monocyte chemoattractant protein-1 (MCP-1, also known as CCL2), a potent chemokine that is linked to human fibrotic disorders. Similarly, MCP-1 knockout mice form minimal scars, indicating that inflammatory chemokine pathways are a major mechanism by which FAK mechanotransduction induces fibrosis. Small-molecule inhibition of FAK blocks these effects in human cells and reduces scar formation in vivo through attenuated MCP-1 signaling and inflammatory cell recruitment. These findings collectively indicate that physical force regulates fibrosis through inflammatory FAK–ERK–MCP-1 pathways and that molecular strategies targeting FAK can effectively uncouple mechanical force from pathologic scar formation.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Fibroblast-specific FAK knockout mice have substantially less inflammation and fibrosis than control mice in a model of hypertrophic scar formation.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 632, "doc_id": "5172048", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Teaching hospitals do not provide better care than non-teaching hospitals.\n\nCANDIDATE_ABSTRACT:\nTITLE: Patient Outcomes with Teaching Versus Nonteaching Healthcare: A Systematic Review\nABSTRACT: Background Extensive debate exists in the healthcare community over whether outcomes of medical care at teaching hospitals and other healthcare units are better or worse than those at the respective nonteaching ones. Thus, our goal was to systematically evaluate the evidence pertaining to this question. Methods and Findings We reviewed all studies that compared teaching versus nonteaching healthcare structures for mortality or any other patient outcome, regardless of health condition. Studies were retrieved from PubMed, contact with experts, and literature cross-referencing. Data were extracted on setting, patients, data sources, author affiliations, definition of compared groups, types of diagnoses considered, adjusting covariates, and estimates of effect for mortality and for each other outcome. Overall, 132 eligible studies were identified, including 93 on mortality and 61 on other eligible outcomes (22 addressed both). Synthesis of the available adjusted estimates on mortality yielded a summary relative risk of 0.96 (95% confidence interval [CI], 0.93–1.00) for teaching versus nonteaching healthcare structures and 1.04 (95% CI, 0.99–1.10) for minor teaching versus nonteaching ones. There was considerable heterogeneity between studies (I2 = 72% for the main analysis). Results were similar in studies using clinical and those using administrative databases. No differences were seen in the 14 studies fully adjusting for volume/experience, severity, and comorbidity (relative risk 1.01). Smaller studies did not differ in their results from larger studies. Differences were seen for some diagnoses (e.g., significantly better survival for breast cancer and cerebrovascular accidents in teaching hospitals and significantly better survival from cholecystectomy in no [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Synthesis of the available adjusted estimates on mortality yielded a summary relative risk of 0.96 (95% confidence interval [CI], 0.93–1.00) for teaching versus nonteaching healthcare structures and 1.04 (95% CI, 0.99–1.10) for minor teaching versus nonteaching ones.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1146, "doc_id": "13906581", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Genetic deletion of JAM-A increases gut permeability.\n\nCANDIDATE_ABSTRACT:\nTITLE: Summary\nABSTRACT: Steroid receptor RNA activator (SRA), the only known RNA coactivator, augments transactivation by nuclear receptors (NRs). We identified SLIRP (SRA stem-loop interacting RNA binding protein) binding to a functional substructure of SRA, STR7. SLIRP is expressed in normal and tumor tissues, contains an RNA recognition motif (RRM), represses NR transactivation in a SRA- and RRM-dependent manner, augments the effect of Tamoxifen, and modulates association of SRC-1 with SRA. SHARP, a RRM-containing corepressor, also binds STR7, augmenting repression with SLIRP. SLIRP colocalizes with SKIP (Chr14q24.3), another NR coregulator, and reduces SKIP-potentiated NR signaling. SLIRP is recruited to endogenous promoters (pS2 and metallothionein), the latter in a SRA-dependent manner, while NCoR promoter recruitment is dependent on SLIRP. The majority of the endogenous SLIRP resides in the mitochondria. Our data demonstrate that SLIRP modulates NR transactivation, suggest it may regulate mitochondrial function, and provide mechanistic insight into interactions between SRA, SLIRP, SRC-1, and NCoR.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 461, "doc_id": "885056", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In British Men, haplogroup I increases risk of cardiovascular disease by 50%.\n\nCANDIDATE_ABSTRACT:\nTITLE: Naringenin inhibits allergen-induced airway inflammation and airway responsiveness and inhibits NF-kappaB activity in a murine model of asthma.\nABSTRACT: Naringenin, a flavonoid, has antiinflammatory and immunomodulatory properties. We investigated whether naringenin could attenuate allergen-induced airway inflammation and its possible mechanism in a murine model of asthma. Mice were sensitized and challenged with ovalbumin. Some mice were administered with naringenin before ovalbumin challenge. We evaluated the development of airway inflammation and airway reactivity. Interleukin (IL)4, IL13, chemokine (C-C motif) ligand (CCL)5, and CCL11 in bronchoalveolar lavage fluid and serum total IgE were detected by ELISA. IkappaBalpha degradation and inducible nitric oxide synthase (iNOS) in lungs were measured by Western blot. We also tested NF-kappaB binding activity by electrophoretic mobility shift assay. The mRNA levels of iNOS, CCL5, and CCL11 were detected by real-time PCR. Naringenin attenuated ovalbumin-induced airway inflammation and airway reactivity in experimental mice. The naringenin-treated mice had lower levels of IL4 and IL13 in the bronchoalveolar lavage fluid and lower serum total IgE. Furthermore, naringenin inhibited pulmonary IkappaBalpha degradation and NF-kappaB DNA-binding activity. The levels of CCL5, CCL11, and iNOS were also significantly reduced. The results indicated that naringenin may play protective roles in the asthma process. The inhibition of NF-kappaB and the decreased expression of its target genes may account for this phenomenon.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 564, "doc_id": "888896", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Exposure to fine particulate air pollution is unrelated to anxiety prevalence.\n\nCANDIDATE_ABSTRACT:\nTITLE: The relation between past exposure to fine particulate air pollution and prevalent anxiety: observational cohort study\nABSTRACT: OBJECTIVE To determine whether higher past exposure to particulate air pollution is associated with prevalent high symptoms of anxiety. DESIGN Observational cohort study. SETTING Nurses' Health Study. PARTICIPANTS 71,271 women enrolled in the Nurses' Health Study residing throughout the contiguous United States who had valid estimates on exposure to particulate matter for at least one exposure period of interest and data on anxiety symptoms. MAIN OUTCOME MEASURES Meaningfully high symptoms of anxiety, defined as a score of 6 points or greater on the phobic anxiety subscale of the Crown-Crisp index, administered in 2004. RESULTS The 71,271 eligible women were aged between 57 and 85 years (mean 70 years) at the time of assessment of anxiety symptoms, with a prevalence of high anxiety symptoms of 15%. Exposure to particulate matter was characterized using estimated average exposure to particulate matter <2.5 μm in diameter (PM2.5) and 2.5 to 10 μm in diameter (PM2.5-10) in the one month, three months, six months, one year, and 15 years prior to assessment of anxiety symptoms, and residential distance to the nearest major road two years prior to assessment. Significantly increased odds of high anxiety symptoms were observed with higher exposure to PM2.5 for multiple averaging periods (for example, odds ratio per 10 µg/m(3) increase in prior one month average PM2.5: 1.12, 95% confidence interval 1.06 to 1.19; in prior 12 month average PM2.5: 1.15, 1.06 to 1.26). Models including multiple exposure windows suggested short term averaging periods were more relevant than long term averaging periods. There was no association between anxiety and exposure to PM2.5-10. Residential proximity to major roads was not related to anxiety symptoms in a dose dependent manner. CON [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Significantly increased odds of high anxiety symptoms were observed with higher exposure to PM2.5 for multiple averaging periods (for example, odds ratio per 10 µg/m(3) increase in prior one month average PM2.5: 1.12, 95% confidence interval 1.06 to 1.19; in prior 12 month average PM2.5: 1.15, 1.06 to 1.26).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 400, "doc_id": "791050", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does estrogen administration reduce the rate of recurrence of affective psychosis after childbirth?\n\nABSTRACT:\nHigh rates of postpartum relapse occur in women with histories of bipolar or schizoaffective disorder. These relapses may be triggered by the postdelivery fall in circulating estrogen through alteration of central neurotransmitter (especially dopaminergic) systems. This study tested the hypothesis that estrogen administration after childbirth would prevent postpartum relapse and would alter dopamine receptor sensitivity. Twenty-nine pregnant women with a Research Diagnostic Criteria diagnosis of hypomania (bipolar II), mania (bipolar I), or schizoaffective disorder participated in an open clinical trial. Three transdermal dose regimens of estrogen (17beta-estradiol) were tested. Starting doses were 200 (N = 13), 400 (N = 3), and 800 (N = 13) micro g/day, beginning within 48 hours after delivery and reduced by one half every 4 days for a total of 12 days. On the fourth day after starting estradiol therapy (before relapse occurred), subjects participated in a neuroendocrine challenge test that measured the sensitivity of the central nervous system (tubero-infundibular) dopaminergic system (plasma prolactin and growth hormone responses to apomorphine). Estradiol at all dose regimens did not reduce the rate of relapse. However, of the 12 women who relapsed, those who had taken the highest dose of estradiol (800 micro g/day) needed less subsequent psychotropic medication (fewer chlorpromazine equivalents) and were discharged sooner than those who had taken either of the 2 lower doses. No differences in neuroendocrine responses to apomorphine were detected between women receiving the high-dose and the lower-dose regimens.", "output": "{\"label\": \"no\", \"rationale\": \"The results do not support the hypothesis that a fall in circulating concentrations of estrogens precipitates relapse in subjects at risk of postpartum affective psychosis. The use of prophylactic estrogen in such circumstances is therefore highly questionable.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 12633118, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The C-type lectin receptor (CLEC-2) rearranges the actin cytoskeleton in dendritic cells to promote efficient motility along stromal surfaces.\n\nCANDIDATE_ABSTRACT:\nTITLE: Podoplanin-Rich Stromal Networks Induce Dendritic Cell Motility via Activation of the C-type Lectin Receptor CLEC-2\nABSTRACT: To initiate adaptive immunity, dendritic cells (DCs) move from parenchymal tissues to lymphoid organs by migrating along stromal scaffolds that display the glycoprotein podoplanin (PDPN). PDPN is expressed by lymphatic endothelial and fibroblastic reticular cells and promotes blood-lymph separation during development by activating the C-type lectin receptor, CLEC-2, on platelets. Here, we describe a role for CLEC-2 in the morphodynamic behavior and motility of DCs. CLEC-2 deficiency in DCs impaired their entry into lymphatics and trafficking to and within lymph nodes, thereby reducing T cell priming. CLEC-2 engagement of PDPN was necessary for DCs to spread and migrate along stromal surfaces and sufficient to induce membrane protrusions. CLEC-2 activation triggered cell spreading via downregulation of RhoA activity and myosin light-chain phosphorylation and triggered F-actin-rich protrusions via Vav signaling and Rac1 activation. Thus, activation of CLEC-2 by PDPN rearranges the actin cytoskeleton in DCs to promote efficient motility along stromal surfaces.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Thus, activation of CLEC-2 by PDPN rearranges the actin cytoskeleton in DCs to promote efficient motility along stromal surfaces.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1153, "doc_id": "7370282", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does perspective-taking increase patient satisfaction in medical encounters?\n\nABSTRACT:\nTo assess whether perspective-taking, which researchers in other fields have shown to induce empathy, improves patient satisfaction in encounters between student-clinicians and standardized patients (SPs). In three studies, randomly assigned students (N = 608) received either a perspective-taking instruction or a neutral instruction prior to a clinical skills examination in 2006-2007. SP satisfaction was the main outcome in all three studies. Study 1 involved 245 third-year medical students from two universities. Studies 2 and 3 extended Study 1 to examine generalizability across student and SP subpopulations. Study 2 (105 physician assistant students, one university) explored the effect of perspective-taking on African American SPs' satisfaction. Study 3 (258 third-year medical students, two universities) examined the intervention's effect on students with high and low baseline perspective-taking tendencies. Intervention students outscored controls in patient satisfaction in all studies: Study 1: P = .01, standardized effect size = 0.16; Study 2: P = .001, standardized effect size = 0.31; Study 3: P = .009, standardized effect size = 0.13. In Study 2, perspective-taking improved African American SPs' satisfaction. In Study 3, intervention students with high baseline perspective-taking tendencies outscored controls (P = .0004, standardized effect size = 0.25), whereas those with low perspective-taking tendencies did not (P = .72, standardized effect size = 0.00).", "output": "{\"label\": \"maybe\", \"rationale\": \"Perspective-taking increased patient satisfaction in all three studies, across medical schools, clinical disciplines, and racially diverse students and SPs. Perspective-taking as a means for improving patient satisfaction deserves further exploration in clinical training and practice.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 20736672, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Ultrasound guidance significantly raises the number of traumatic procedures when attempting needle insertion.\n\nCANDIDATE_ABSTRACT:\nTITLE: Ultrasound imaging for lumbar punctures and epidural catheterisations: systematic review and meta-analysis.\nABSTRACT: OBJECTIVE To determine whether ultrasound imaging can reduce the risk of failed lumbar punctures or epidural catheterisations, when compared with standard palpation methods, and whether ultrasound imaging can reduce traumatic procedures, insertion attempts, and needle redirections. DESIGN Systematic review and meta-analysis of randomised controlled trials. DATA SOURCES Ovid Medline, Embase, and Cochrane Central Register of Controlled Trials up to May 2012, without restriction by language or publication status. REVIEW METHODS Randomised trials that compared ultrasound imaging with standard methods (no imaging) in the performance of a lumbar puncture or epidural catheterisation were identified. RESULTS 14 studies with a total of 1334 patients were included (674 patients assigned to the ultrasound group, 660 to the control group). Five studies evaluated lumbar punctures and nine evaluated epidural catheterisations. Six of 624 procedures conducted in the ultrasound group failed; 44 of 610 procedures in the control group failed. Ultrasound imaging reduced the risk of failed procedures (risk ratio 0.21 (95% confidence interval 0.10 to 0.43), P<0.001). Risk reduction was similar when subgroup analysis was performed for lumbar punctures (risk ratio 0.19 (0.07 to 0.56), P=0.002) or epidural catheterisations (0.23 (0.09 to 0.60), P=0.003). Ultrasound imaging also significantly reduced the risk of traumatic procedures (risk ratio 0.27 (0.11 to 0.67), P=0.005), the number of insertion attempts (mean difference -0.44 (-0.64 to -0.24), P<0.001), and the number of needle redirections (mean difference -1.00 (-1.24 to -0.75), P<0.001). CONCLUSIONS Ultrasound imaging can reduce the risk of failed or traumatic lumbar punctures and epidural catheterisations, as well as the numb [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Ultrasound imaging reduced the risk of failed procedures (risk ratio 0.21 (95% confidence interval 0.10 to 0.43), P<0.001). Risk reduction was similar when subgroup analysis was performed for lumbar punctures (risk ratio 0.19 (0.07 to 0.56), P=0.002) or epidural catheterisations (0.23 (0.09 to 0.60), P=0.003).\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1339, "doc_id": "15482274", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Radioiodine treatment of non-toxic multinodular goitre reduces thyroid volume.\n\nCANDIDATE_PASSAGE:\nBody-mass index and risk of 22 specific cancers: a population-based cohort study of 5·24 million UK adults BACKGROUND High body-mass index (BMI) predisposes to several site-specific cancers, but a large-scale systematic and detailed characterisation of patterns of risk across all common cancers adjusted for potential confounders has not previously been undertaken. We aimed to investigate the links between BMI and the most common site-specific cancers. METHODS With primary care data from individuals in the Clinical Practice Research Datalink with BMI data, we fitted Cox models to investigate associations between BMI and 22 of the most common cancers, adjusting for potential confounders. We fitted linear then non-linear (spline) models; investigated effect modification by sex, menopausal status, smoking, and age; and calculated population effects. FINDINGS 5·24 million individuals were included; 166,955 developed cancers of interest. BMI was associated with 17 of 22 cancers, but effects varied substantially by site. Each 5 kg/m(2) increase in BMI was roughly linearly associated with cancers of the uterus (hazard ratio [HR] 1·62, 99% CI 1·56-1·69; p<0·0001), gallbladder (1·31, 1·12-1·52; p<0·0001), kidney (1·25, 1·17-1·33; p<0·0001), cervix (1·10, 1·03-1·17; p=0·00035), thyroid (1·09, 1·00-1·19; p=0·0088), and leukaemia (1·09, 1·05-1·13; p≤0·0001). BMI was positively associated with liver (1·19, 1·12-1·27), colon (1·10, 1·07-1·13), ovarian (1·09, 1.04-1.14), and postmenopausal breast cancers (1·05, 1·03-1·07) overall (all p<0·0001), but these effects varied by underlying BMI or individual-level characteristics. We estimated inverse associations with prostate and premenopausal breast cancer risk, both overall (prostate 0·98, 0·95-1·00; premenopausal breast cance [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1012", "doc_id": "4828631", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: PKG-la does not have a large impact on expression of pain hypersensitivity in PGK-la knockout mice.\n\nCANDIDATE_ABSTRACT:\nTITLE: Presynaptically Localized Cyclic GMP-Dependent Protein Kinase 1 Is a Key Determinant of Spinal Synaptic Potentiation and Pain Hypersensitivity\nABSTRACT: Synaptic long-term potentiation (LTP) at spinal neurons directly communicating pain-specific inputs from the periphery to the brain has been proposed to serve as a trigger for pain hypersensitivity in pathological states. Previous studies have functionally implicated the NMDA receptor-NO pathway and the downstream second messenger, cGMP, in these processes. Because cGMP can broadly influence diverse ion-channels, kinases, and phosphodiesterases, pre- as well as post-synaptically, the precise identity of cGMP targets mediating spinal LTP, their mechanisms of action, and their locus in the spinal circuitry are still unclear. Here, we found that Protein Kinase G1 (PKG-I) localized presynaptically in nociceptor terminals plays an essential role in the expression of spinal LTP. Using the Cre-lox P system, we generated nociceptor-specific knockout mice lacking PKG-I specifically in presynaptic terminals of nociceptors in the spinal cord, but not in post-synaptic neurons or elsewhere (SNS-PKG-I(-/-) mice). Patch clamp recordings showed that activity-induced LTP at identified synapses between nociceptors and spinal neurons projecting to the periaqueductal grey (PAG) was completely abolished in SNS-PKG-I(-/-) mice, although basal synaptic transmission was not affected. Analyses of synaptic failure rates and paired-pulse ratios indicated a role for presynaptic PKG-I in regulating the probability of neurotransmitter release. Inositol 1,4,5-triphosphate receptor 1 and myosin light chain kinase were recruited as key phosphorylation targets of presynaptic PKG-I in nociceptive neurons. Finally, behavioural analyses in vivo showed marked defects in SNS-PKG-I(-/-) mice in several models of activity-induced nociceptive hypersensitivity, and pharmacological studies identified [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Our results thus indicate that presynaptic mechanisms involving an increase in release probability from nociceptors are operational in the expression of synaptic LTP on spinal-PAG projection neurons and that PKG-I localized in presynaptic nociceptor terminals plays an essential role in this process to regulate pain sensitivity.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 909, "doc_id": "11254556", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The M2-phenotype in brown adipose tissue macrophages increases brown adipose tissue thermogenic activity.\n\nCANDIDATE_ABSTRACT:\nTITLE: Alternatively activated macrophages produce catecholamines to sustain adaptive thermogenesis\nABSTRACT: All homeotherms use thermogenesis to maintain their core body temperature, ensuring that cellular functions and physiological processes can continue in cold environments. In the prevailing model of thermogenesis, when the hypothalamus senses cold temperatures it triggers sympathetic discharge, resulting in the release of noradrenaline in brown adipose tissue and white adipose tissue. Acting via the β(3)-adrenergic receptors, noradrenaline induces lipolysis in white adipocytes, whereas it stimulates the expression of thermogenic genes, such as PPAR-γ coactivator 1a (Ppargc1a), uncoupling protein 1 (Ucp1) and acyl-CoA synthetase long-chain family member 1 (Acsl1), in brown adipocytes. However, the precise nature of all the cell types involved in this efferent loop is not well established. Here we report in mice an unexpected requirement for the interleukin-4 (IL-4)-stimulated program of alternative macrophage activation in adaptive thermogenesis. Exposure to cold temperature rapidly promoted alternative activation of adipose tissue macrophages, which secrete catecholamines to induce thermogenic gene expression in brown adipose tissue and lipolysis in white adipose tissue. Absence of alternatively activated macrophages impaired metabolic adaptations to cold, whereas administration of IL-4 increased thermogenic gene expression, fatty acid mobilization and energy expenditure, all in a macrophage-dependent manner. Thus, we have discovered a role for alternatively activated macrophages in the orchestration of an important mammalian stress response, the response to cold.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Absence of alternatively activated macrophages impaired metabolic adaptations to cold, whereas administration of IL-4 increased thermogenic gene expression, fatty acid mobilization and energy expenditure, all in a macrophage-dependent manner.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1169, "doc_id": "4319174", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does lovastatin inhibit the thrombin-induced loss of barrier integrity in bovine corneal endothelium?\n\nABSTRACT:\nIncreased actomyosin contraction of the dense band of actin cytoskeleton at the apical junctional complex (perijunctional actomyosin ring, PAMR) breaks down the barrier integrity of corneal endothelium. This study has investigated the efficacy of statins, which inhibit activation of RhoA, in opposing the thrombin-induced loss of barrier integrity of monolayers of cultured bovine corneal endothelium. Myosin light chain (MLC) phosphorylation, a biochemical measure of actomyosin contraction, was assayed by urea-glycerol gel electrophoresis, followed by western blot analysis. The locus of MLC phosphorylation and changes in the organization of the PAMR were visualized by immunostaining. Phosphorylation of MYPT1, a regulatory subunit of myosin light-chain phosphatase (MLCP), was assessed by Western blot analysis to determine down-regulation of RhoA. The barrier integrity was assessed in terms of trans-endothelial electrical resistance (TER), and further confirmed by determining permeability to FITC dextran (10 kDa) and distribution of ZO-1, a marker of tight junctional assembly. Lovastatin, a prototype of lipophilic statins, induced MLC dephosphorylation under basal conditions. It opposed increase in phosphorylation of MLC and MYPT1 in response to thrombin and nocodazole, agents known to activate RhoA in the endothelium. Pretreatment with the statin opposed the thrombin- and nocodazole-induced disruption of the PAMR and the thrombin-induced decline in TER. Lovastatin also opposed the thrombin- and nocodazole-induced increase in permeability to FITC dextran and redistribution of ZO-1. However, upon supplementation with GGPP (geranylgeranyl pyrophosphate), lovastatin failed to oppose the effects of thrombin and nocodazole on the PAMR, ppMLC, and ZO-1 distribution.", "output": "{\"label\": \"yes\", \"rationale\": \"Lovastatin attenuates RhoA activation in the corneal endothelium presumably by reducing its isoprenylation. This underlies the suppression of the thrombin-induced loss in barrier integrity of the corneal endothelium.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 20148651, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does vaginal intraepithelial neoplasia have the same evolution as cervical intraepithelial neoplasia?\n\nABSTRACT:\nVaginal intraepithelial neoplasia is a little known disease which could be related to risk factors different from simple HPV infections. To ascertain wheter vaginal lesions have a natural history similar to cervical lesions.MATERIALS & A retrospective study to identify patients with vaginal lesions and synchronous cervical lesions through biopsy. The rate of mild cervical lesions (koilocytosis, warts, CIN I with and without koilocytosis) was compared with the rate of severe cervical lesions (CIN II and III, cervical carcinoma) in patients with mild vaginal lesions (warts and koilocytosis, and low-grade VAIN) and in patients with severe vaginal lesions (high-grade VAIN). Using koilocytosis as a marker, the rate of \"active\" cervical lesions was compared with the rate of \"non active\" cervical lesions in patients with \"active\" versus \"non active\" vaginal lesions. Finally, the rates of mild and severe cervical lesions were compared among each group of VAIN (low-grade, high-grade, with or without koilocytosis). In patients with mild vaginal lesions, mild cervical lesions were significantly more frequent than severe cervical lesions. In patients with \"active\" vaginal lesions the rate of \"active\" cervical lesions was significantly higher than \"non active\" cervical lesions. The differences in rates of mild cervical lesions and severe cervical lesions among patients with high-grade VAIN and low-grade VAIN (with and without koilocytosis) were not significant.", "output": "{\"label\": \"maybe\", \"rationale\": \"These data suggest that CIN and VAIN may have some common features in certain cases, i.e., if an HPV infection is proved.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 18714572, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Surgical treatment is not superior to non-surgical in treating adults with displaced fractures of the proximal humerus.\n\nCANDIDATE_ABSTRACT:\nTITLE: Surgical vs nonsurgical treatment of adults with displaced fractures of the proximal humerus: the PROFHER randomized clinical trial.\nABSTRACT: IMPORTANCE The need for surgery for the majority of patients with displaced proximal humeral fractures is unclear, but its use is increasing. OBJECTIVE To evaluate the clinical effectiveness of surgical vs nonsurgical treatment for adults with displaced fractures of the proximal humerus involving the surgical neck. DESIGN, SETTING, AND PARTICIPANTS A pragmatic, multicenter, parallel-group, randomized clinical trial, the Proximal Fracture of the Humerus Evaluation by Randomization (PROFHER) trial, recruited 250 patients aged 16 years or older (mean age, 66 years [range, 24-92 years]; 192 [77%] were female; and 249 [99.6%] were white) who presented at the orthopedic departments of 32 acute UK National Health Service hospitals between September 2008 and April 2011 within 3 weeks after sustaining a displaced fracture of the proximal humerus involving the surgical neck. Patients were followed up for 2 years (up to April 2013) and 215 had complete follow-up data. The data for 231 patients (114 in surgical group and 117 in nonsurgical group) were included in the primary analysis. INTERVENTIONS Fracture fixation or humeral head replacement were performed by surgeons experienced in these techniques. Nonsurgical treatment was sling immobilization. Standardized outpatient and community-based rehabilitation was provided to both groups. MAIN OUTCOMES AND MEASURES Primary outcome was the Oxford Shoulder Score (range, 0-48; higher scores indicate better outcomes) assessed during a 2-year period, with assessment and data collection at 6, 12, and 24 months. Sample size was based on a minimal clinically important difference of 5 points for the Oxford Shoulder Score. Secondary outcomes were the Short-Form 12 (SF-12), complications, subsequent therapy, and mortality. RESULTS Th [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS AND RELEVANCE Among patients with displaced proximal humeral fractures involving the surgical neck, there was no significant difference between surgical treatment compared with nonsurgical treatment in patient-reported clinical outcomes over 2 years following fracture occurrence.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1115, "doc_id": "44048701", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Assembly of invadopodia is triggered by focal generation of phosphatidylinositol-3,4-biphosphate and the activation of the nonreceptor tyrosine kinase Src.\n\nCANDIDATE_PASSAGE:\nDecoding of Cytoplasmic Ca2+ Oscillations through the Spatial Signature Drives Gene Expression Cytoplasmic Ca(2+) oscillations are a universal signaling mode that activates numerous cellular responses [1, 2]. Oscillations are considered the physiological mechanism of Ca(2+) signaling because they occur at low levels of stimulus intensity [3]. Ca(2+) oscillations are proposed to convey information in their amplitude and frequency, leading to activation of specific downstream targets [4-6]. Here, we report that the spatial Ca(2+) gradient within the oscillation is key. Ca(2+) oscillations in mast cells evoked over a range of agonist concentrations in the presence of external Ca(2+) were indistinguishable from those in the absence of Ca(2+) when plasmalemmal Ca(2+) extrusion was suppressed. Nevertheless, only oscillations with accompanying Ca(2+) entry through store-operated CRAC channels triggered gene expression. Increased cytoplasmic Ca(2+) buffering prevented oscillations but not gene activation. Local Ca(2+) influx and not global Ca(2+) oscillations therefore drives gene expression at physiological levels of stimulation. Rather than serving to maintain Ca(2+) oscillations by replenishing stores, we suggest that the role of oscillations might be to activate CRAC channels, thereby ensuring the generation of spatially restricted physiological Ca(2+) signals driving gene activation. Furthermore, we show that the spatial profile of a Ca(2+) oscillation provides a novel mechanism whereby a pleiotropic messenger specifically activates gene expression.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "133", "doc_id": "14719322", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Nonhuman primates are incapable of producing neutralizing antibodies in reponse to the Eilat virus (EILV) produced in mosquitos.\n\nCANDIDATE_PASSAGE:\nTen years' experience with alendronate for osteoporosis in postmenopausal women. BACKGROUND Antiresorptive agents are widely used to treat osteoporosis. We report the results of a multinational randomized, double-blind study, in which postmenopausal women with osteoporosis were treated with alendronate for up to 10 years. METHODS The initial three-year phase of the study compared three daily doses of alendronate with placebo. Women in the original placebo group received alendronate in years 4 and 5 and then were discharged. Women in the original active-treatment groups continued to receive alendronate during the initial extension (years 4 and 5). In two further extensions (years 6 and 7, and 8 through 10), women who had received 5 mg or 10 mg of alendronate daily continued on the same treatment. Women in the discontinuation group received 20 mg of alendronate daily for two years and 5 mg daily in years 3, 4, and 5, followed by five years of placebo. Randomized group assignments and blinding were maintained throughout the 10 years. We report results for the 247 women who participated in all four phases of the study. RESULTS Treatment with 10 mg of alendronate daily for 10 years produced mean increases in bone mineral density of 13.7 percent at the lumbar spine (95 percent confidence interval, 12.0 to 15.5 percent), 10.3 percent at the trochanter (95 percent confidence interval, 8.1 to 12.4 percent), 5.4 percent at the femoral neck (95 percent confidence interval, 3.5 to 7.4 percent), and 6.7 percent at the total proximal femur (95 percent confidence interval, 4.4 to 9.1 percent) as compared with base-line values; smaller gains occurred in the group given 5 mg daily. The discontinuation of alendronate resulted in a gradual loss of effect, as measured by bone d [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "853", "doc_id": "19205326", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: TMEM27 is a marker for beta cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tmem27: a cleaved and shed plasma membrane protein that stimulates pancreatic beta cell proliferation.\nABSTRACT: The signals and molecular mechanisms that regulate the replication of terminally differentiated beta cells are unknown. Here, we report the identification and characterization of transmembrane protein 27 (Tmem27, collectrin) in pancreatic beta cells. Expression of Tmem27 is reduced in Tcf1(-/-) mice and is increased in islets of mouse models with hypertrophy of the endocrine pancreas. Tmem27 forms dimers and its extracellular domain is glycosylated, cleaved and shed from the plasma membrane of beta cells. This cleavage process is beta cell specific and does not occur in other cell types. Overexpression of full-length Tmem27, but not the truncated or soluble protein, leads to increased thymidine incorporation, whereas silencing of Tmem27 using RNAi results in a reduction of cell replication. Furthermore, transgenic mice with increased expression of Tmem27 in pancreatic beta cells exhibit increased beta cell mass. Our results identify a pancreatic beta cell transmembrane protein that regulates cell growth of pancreatic islets.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here, we report the identification and characterization of transmembrane protein 27 (Tmem27, collectrin) in pancreatic beta cells.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1133, "doc_id": "24142891", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Incidence rates of cervical cancer have increased due to nationwide screening programs based primarily on cytology to detect uterine cervical cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mass screening programmes and trends in cervical cancer in Finland and the Netherlands.\nABSTRACT: With respect to cervical cancer management, Finland and the Netherlands are comparable in relevant characteristics, e.g., fertility rate, age-of-mother at first birth and a national screening programme for several years. The aim of this study is to compare trends in incidence of and mortality from cervical cancer in Finland and the Netherlands in relation to the introduction and intensity of the screening programmes. Therefore, incidence and mortality rates were calculated using the Cancer Registries of Finland and the Netherlands. Data on screening intensity were obtained from the Finnish Cancer Registry and the Dutch evaluation centre at ErasmusMC-Rotterdam. Women aged 30-60 have been screened every 5 years, in Finland since 1992 and in the Netherlands since 1996. Screening protocols for smear taking and referral to the gynaecologist are comparable. Incidence and mortality rates have declined more in Finland. In 2003, age-adjusted incidence and mortality in Finland were 4.0 and 0.9 and in the Netherlands 4.9 and 1.4 per 100,000 woman-years, respectively. Excess smear use in the Netherlands was estimated to be 24 per 1,000 women during a 5-year interval compared to 121 in Finland. The decline in mortality in Finland seems to be almost completely related to the screening programme whereas in the Netherlands it was initially considered to be a natural decline. Differences in risk factors might also play a role: the Netherlands has higher population density and higher percentages of immigrants and (female) smokers. The greater excess smear use in Finland might also have affected incidence.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The decline in mortality in Finland seems to be almost completely related to the screening programme whereas in the Netherlands it was initially considered to be a natural decline.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 598, "doc_id": "25742130", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: One in two surgical randomized controlled trials are discontinued early.\n\nCANDIDATE_ABSTRACT:\nTITLE: High abundance of plasma cells secreting transglutaminase 2–specific IgA autoantibodies with limited somatic hypermutation in celiac disease intestinal lesions\nABSTRACT: Celiac disease is an immune-mediated disorder in which mucosal autoantibodies to the enzyme transglutaminase 2 (TG2) are generated in response to the exogenous antigen gluten in individuals who express human leukocyte antigen HLA-DQ2 or HLA-DQ8 (ref. 3). We assessed in a comprehensive and nonbiased manner the IgA anti-TG2 response by expression cloning of the antibody repertoire of ex vivo–isolated intestinal antibody-secreting cells (ASCs). We found that TG2-specific plasma cells are markedly expanded within the duodenal mucosa in individuals with active celiac disease. TG2-specific antibodies were of high affinity yet showed little adaptation by somatic mutations. Unlike infection-induced peripheral blood plasmablasts, the TG2-specific ASCs had not recently proliferated and were not short-lived ex vivo. Altogether, these observations demonstrate that there is a germline repertoire with high affinity for TG2 that may favor massive generation of autoreactive B cells. TG2-specific antibodies did not block enzymatic activity and served as substrates for TG2-mediated crosslinking when expressed as IgD or IgM but not as IgA1 or IgG1. This could result in preferential recruitment of plasma cells from naive IgD- and IgM-expressing B cells, thus possibly explaining why the antibody response to TG2 bears signs of a primary immune response despite the disease chronicity.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 886, "doc_id": "1471041", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is Panton-Valentine leucocidin associated with the pathogenesis of Staphylococcus aureus bacteraemia in the UK?\n\nABSTRACT:\nThe morbidity and mortality associated with Panton-Valentine leucocidin (PVL)-positive Staphylococcus aureus suggest that this toxin is a key marker of disease severity. Nevertheless, the importance of PVL in the pathogenesis of primary bacteraemia caused by S. aureus is uncertain. We have determined the prevalence of PVL-encoding genes among isolates of S. aureus from bacteraemic patients. Consecutive bacteraemia isolates of S. aureus (n=244) from patients hospitalized in 25 centres in the UK and Ireland during 2005 were screened for PVL and mecA genes. PVL-positive isolates were characterized by toxin gene profiling, PFGE, spa-typing and MIC determinations for a range of antimicrobials. Four out of 244 isolates (1.6%) were PVL-positive and susceptible to oxacillin [methicillin-susceptible S. aureus (MSSA)]. Eighty-eight out of 244 (36%) were oxacillin-resistant (methicillin-resistant S. aureus), but none was PVL-positive. The four patients (two males: 30 and 33 years; two females: 62 and 80 years) had infection foci of: skin and soft tissue, unknown, indwelling line, and surgical site, and were located at one centre in Wales, one in England and two in Ireland. One of four PVL-positive isolates was resistant to penicillin and fusidic acid, the remainder were susceptible to all antibiotics tested. Genotypic analyses showed that the four isolates represented three distinct strains; the two isolates from Ireland were related.", "output": "{\"label\": \"maybe\", \"rationale\": \"We found that 1.6% of S. aureus (all MSSA) from bacteraemic patients were PVL-positive. This low incidence suggests that PVL-positive S.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 17562682, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Only a minority of cells survive development after differentiation into stress-resistant spores.\n\nCANDIDATE_PASSAGE:\nCulture of Preimplantation Mouse Embryos Affects Fetal Development and the Expression of Imprinted Genes1 Abstract Culture of preimplantation mammalian embryos and cells can influence their subsequent growth and differentiation. Previously, we reported that culture of mouse embryonic stem cells is associated with deregulation of genomic imprinting and affects the potential for these cells to develop into normal fetuses. The purpose of our current study was to determine whether culture of preimplantation mouse embryos in a chemically defined medium (M16) with or without fetal calf serum (FCS) can affect their subsequent development and imprinted gene expression. Only one third of the blastocysts that had been cultured from two-cell embryos in M16 medium complemented with FCS developed into viable Day 14 fetuses after transfer into recipients. These M16 + FCS fetuses were reduced in weight as compared with controls and M16 fetuses and had decreased expression of the imprinted H19 and insulin-like growth factor 2 genes associated with a gain of DNA methylation at an imprinting control region upstream of H19. They also displayed increased expression of the imprinted gene Grb10. The growth factor receptor binding gene Grb7, in contrast, was strongly reduced in its expression in most of the M16 + FCS fetuses. No alterations were detected for the imprinted gene Mest. Preimplantation culture in the presence of serum can influence the regulation of multiple growth-related imprinted genes, thus leading to aberrant fetal growth and development.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "887", "doc_id": "13441537", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: \"Would a man smell a rose then throw it away?\n\nABSTRACT:\nBreast cancer is the most common malignancy afflicting women, and the most common cancer overall in Jordan. A woman's decision to go for screening is influenced by her social support network. This study aims to explore Jordanian men's individual and contextual perspectives on women's breast cancer and their own role in the breast health of the females within their families. An explorative qualitative design was used to purposively recruit 24 married men aged 27 to 65 years (median 43 years) from four governorates in Jordan. Data in the form of interviews transcriptions was subjected to qualitative content analysis. Three themes were identified: a) Supporting one's wife; b) Marital needs and obligations; c) Constrained by a culture of destiny and shame. The first theme was built on men's feelings of responsibility for the family's health and well-being, their experiences of encouraging their wives to seek health care and their providing counselling and instrumental support. The second theme emerged from men's views about other men's rejection of a wife inflicted by breast cancer, their own perceptions of diminished femininity due to mastectomy and their own concerns about protecting the family from the hereditary risk of breast cancer. The third theme was seen in men's perception of breast cancer as an inevitable act of God that is far away from one's own family, in associating breast cancer with improper behaviour and in their readiness to face the culture of Eib (shame).", "output": "{\"label\": \"maybe\", \"rationale\": \"Jordanian men perceive themselves as having a vital role in supporting, guiding and encouraging their wives to follow breast cancer early detection recommendations. Breast health awareness campaigns could involve husbands to capitalize on family support.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 24160268, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: There is no known interaction between Pioneer factor OCT3/4 and major chromatin remodeling factors.\n\nCANDIDATE_ABSTRACT:\nTITLE: Oct4 links multiple epigenetic pathways to the pluripotency network\nABSTRACT: Oct4 is a well-known transcription factor that plays fundamental roles in stem cell self-renewal, pluripotency, and somatic cell reprogramming. However, limited information is available on Oct4-associated protein complexes and their intrinsic protein-protein interactions that dictate Oct4's critical regulatory activities. Here we employed an improved affinity purification approach combined with mass spectrometry to purify Oct4 protein complexes in mouse embryonic stem cells (mESCs), and discovered many novel Oct4 partners important for self-renewal and pluripotency of mESCs. Notably, we found that Oct4 is associated with multiple chromatin-modifying complexes with documented as well as newly proved functional significance in stem cell maintenance and somatic cell reprogramming. Our study establishes a solid biochemical basis for genetic and epigenetic regulation of stem cell pluripotency and provides a framework for exploring alternative factor-based reprogramming strategies.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Notably, we found that Oct4 is associated with multiple chromatin-modifying complexes with documented as well as newly proved functional significance in stem cell maintenance and somatic cell reprogramming.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1294, "doc_id": "2078658", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Normal granulomas form in the absence of TNF in Zebrafish.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tumor necrosis factor signaling mediates resistance to mycobacteria by inhibiting bacterial growth and macrophage death.\nABSTRACT: Tumor necrosis factor (TNF), a key effector in controlling tuberculosis, is thought to exert protection by directing formation of granulomas, organized aggregates of macrophages and other immune cells. Loss of TNF signaling causes progression of tuberculosis in humans, and the increased mortality of Mycobacterium tuberculosis-infected mice is associated with disorganized necrotic granulomas, although the precise roles of TNF signaling preceding this endpoint remain undefined. We monitored transparent Mycobacterium marinum-infected zebrafish live to conduct a stepwise dissection of how TNF signaling operates in mycobacterial pathogenesis. We found that loss of TNF signaling caused increased mortality even when only innate immunity was operant. In the absence of TNF, intracellular bacterial growth and granuloma formation were accelerated and was followed by necrotic death of overladen macrophages and granuloma breakdown. Thus, TNF is not required for tuberculous granuloma formation, but maintains granuloma integrity indirectly by restricting mycobacterial growth within macrophages and preventing their necrosis.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In the absence of TNF, intracellular bacterial growth and granuloma formation were accelerated and was followed by necrotic death of overladen macrophages and granuloma breakdown.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 860, "doc_id": "16066726", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Cancers that initially benefit from epidermal growth factor receptor targeted therapies later become refractory through several mechanisms.\n\nCANDIDATE_PASSAGE:\nActivation of the estrogen receptor through phosphorylation by mitogen-activated protein kinase. The phosphorylation of the human estrogen receptor (ER) serine residue at position 118 is required for full activity of the ER activation function 1 (AF-1). This Ser118 is phosphorylated by mitogen-activated protein kinase (MAPK) in vitro and in cells treated with epidermal growth factor (EGF) and insulin-like growth factor (IGF) in vivo. Overexpression of MAPK kinase (MAPKK) or of the guanine nucleotide binding protein Ras, both of which activate MAPK, enhanced estrogen-induced and antiestrogen (tamoxifen)-induced transcriptional activity of wild-type ER, but not that of a mutant ER with an alanine in place of Ser118. Thus, the activity of the amino-terminal AF-1 of the ER is modulated by the phosphorylation of Ser118 through the Ras-MAPK cascade of the growth factor signaling pathways.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "227", "doc_id": "4662264", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: 90% of sudden infant death syndrome (SIDS) deaths happen in newborns aged less than 6 months.\n\nCANDIDATE_ABSTRACT:\nTITLE: Sudden infant death syndrome.\nABSTRACT: Despite declines in prevalence during the past two decades, sudden infant death syndrome (SIDS) continues to be the leading cause of death for infants aged between 1 month and 1 year in developed countries. Behavioural risk factors identified in epidemiological studies include prone and side positions for infant sleep, smoke exposure, soft bedding and sleep surfaces, and overheating. Evidence also suggests that pacifier use at sleep time and room sharing without bed sharing are associated with decreased risk of SIDS. Although the cause of SIDS is unknown, immature cardiorespiratory autonomic control and failure of arousal responsiveness from sleep are important factors. Gene polymorphisms relating to serotonin transport and autonomic nervous system development might make affected infants more vulnerable to SIDS. Campaigns for risk reduction have helped to reduce SIDS incidence by 50-90%. However, to reduce the incidence even further, greater strides must be made in reducing prenatal smoke exposure and implementing other recommended infant care practices. Continued research is needed to identify the pathophysiological basis of SIDS.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 25, "doc_id": "2613775", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: CRP is not predictive of postoperative mortality following Coronary Artery Bypass Graft (CABG) surgery.\n\nCANDIDATE_PASSAGE:\nProgression of preclinical diastolic dysfunction to the development of symptoms. BACKGROUND Preclinical diastolic dysfunction (PDD) has been defined as subjects with normal systolic function, diastolic dysfunction but no symptoms of heart failure (HF). The clinical phenotype and natural history of the syndrome remains poorly defined. This study's objective was to determine the clinical phenotype and progression to HF in a group of patients with normal systolic function and moderate or severe diastolic dysfunction as determinate by Doppler criteria without any clinical diagnosis of HF according to the Framingham criteria or any symptoms of HF, specifically dyspnoea, oedema or fatigue at the time of echocardiography. METHODS The authors used resources of the Mayo Clinic echocardiography database to consecutively select among patients who had an echocardiogram in 2005, a cohort with moderate or severe diastolic dysfunction by Doppler criteria and EF >or=50%. Patients could not have a diagnosis of HF, or any HF symptoms-specifically dyspnoea, oedema or fatigue-at the time of echocardiography; nor grade 3 or greater valvular dysfunction (except tricuspid valve). A total of 82 patients had their medical chart reviewed. Primary endpoint was the time to the development of (1) HF according to the Framingham criteria or (2) any symptoms of dyspnoea, oedema or fatigue. RESULTS The mean age of the cohort of PDD subjects was 69+/-10 years with a female (67%) preponderance. Presence of hypertension was 76%, coronary artery disease was 29%, paroxysmal atrial fibrillation was 26%, estimated creatinine clearance <60 ml/min was 51%. The 2-year cumulative probability of development of HF according to the Framingham criteria was 1.9%; however, the 2-year cumulative probability [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "213", "doc_id": "7602348", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: \"Would a man smell a rose then throw it away?\n\nABSTRACT:\nBreast cancer is the most common malignancy afflicting women, and the most common cancer overall in Jordan. A woman's decision to go for screening is influenced by her social support network. This study aims to explore Jordanian men's individual and contextual perspectives on women's breast cancer and their own role in the breast health of the females within their families. An explorative qualitative design was used to purposively recruit 24 married men aged 27 to 65 years (median 43 years) from four governorates in Jordan. Data in the form of interviews transcriptions was subjected to qualitative content analysis. Three themes were identified: a) Supporting one's wife; b) Marital needs and obligations; c) Constrained by a culture of destiny and shame. The first theme was built on men's feelings of responsibility for the family's health and well-being, their experiences of encouraging their wives to seek health care and their providing counselling and instrumental support. The second theme emerged from men's views about other men's rejection of a wife inflicted by breast cancer, their own perceptions of diminished femininity due to mastectomy and their own concerns about protecting the family from the hereditary risk of breast cancer. The third theme was seen in men's perception of breast cancer as an inevitable act of God that is far away from one's own family, in associating breast cancer with improper behaviour and in their readiness to face the culture of Eib (shame).", "output": "{\"label\": \"maybe\", \"rationale\": \"Jordanian men perceive themselves as having a vital role in supporting, guiding and encouraging their wives to follow breast cancer early detection recommendations. Breast health awareness campaigns could involve husbands to capitalize on family support.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 24160268, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does increased conventional chemotherapy improve survival in multiple myeloma : long-term results of two PETHEMA trials including 914 patients?\n\nABSTRACT:\nMelphalan and prednisone (MP) has been the standard treatment for multiple myeloma (MM) for the last 30 years. Combination chemotherapy at conventional doses has not shown a significant prolongation of survival when compared to MP. There are few data comparing conventional chemotherapy at standard doses with conventional treatment at higher doses. We present the long-term outcome of 914 patients from two randomized trials comparing three different dose intensity regimens. From 1 January, 1985 to 31 December, 1989, 487 patients were randomized between MP (melphalan 9 mg/m(2) p.o. and prednisone 60 mg/m(2) days 1-4) and alternating VCMP (vincristine 1 mg i.v. on day 1, cyclophosphamide 500 mg/m(2) i.v. on day 1, melphalan 6 mg/m(2) p.o. on days 1-4, and prednisone 60 mg/m(2) on days 1-4) and VBAP (vincristine 1 mg i.v. on day 1, BCNU and doxorubicin 30 mg/m(2) i.v. each on day 1, and prednisone 60 mg/m(2) on days 1-4). From 1 January, 1990 to 31 May, 1994, 427 patients were randomized between VCMP/VBAP at the above detailed doses (VCMP/VBAP 'SD') and the same regimen increasing the doses of cyclophosphamide and doxorubicin from 500 to 1200 mg/m(2) and from 30 to 50 mg/m(2), respectively (VCMP/VBAP 'HD'). Increasing dose intensity produced a significantly higher partial response rate (31% vs 45% vs 51% for MP, VCMP/VBAP 'SD', and VCMP/VBAP 'HD', respectively; P < 0.01). However, a significantly early death rate was observed in the HD arm (7.7, 7.5 and 12.1% for MP, VCMP/VBAP 'SD', and VCMP/VBAP 'HD', respectively; P = 0.05). Median duration of response (20 vs 18 vs 19 months for MP, VCMP/VBAP 'SD', and VCMP/VBAP 'HD', respectively; P = NS) and median survival (25 vs 31 vs 29 months for MP, VCMP/VBAP 'SD', and VCMP/VBAP 'HD', respectively; P = NS) were similar i [TRUNCATED]", "output": "{\"label\": \"no\", \"rationale\": \"In these trials the response rate significantly correlated with the regimen intensity. However, no significant differences in response duration and survival were found. This highlights the limited role of conventional chemotherapy in MM and the need for further trials, aimed at determining the impact of new treatment approaches such as high-dose therapy/autotransplantation.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 11920260, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Allogeneic mechanical circulatory support is not as effective as autologous mechanical circulatory support for treating acute myocardial infarction.\n\nCANDIDATE_ABSTRACT:\nTITLE: Comparison of allogeneic vs autologous bone marrow–derived mesenchymal stem cells delivered by transendocardial injection in patients with ischemic cardiomyopathy: the POSEIDON randomized trial.\nABSTRACT: CONTEXT Mesenchymal stem cells (MSCs) are under evaluation as a therapy for ischemic cardiomyopathy (ICM). Both autologous and allogeneic MSC therapies are possible; however, their safety and efficacy have not been compared. OBJECTIVE To test whether allogeneic MSCs are as safe and effective as autologous MSCs in patients with left ventricular (LV) dysfunction due to ICM. DESIGN, SETTING, AND PATIENTS A phase 1/2 randomized comparison (POSEIDON study) in a US tertiary-care referral hospital of allogeneic and autologous MSCs in 30 patients with LV dysfunction due to ICM between April 2, 2010, and September 14, 2011, with 13-month follow-up. INTERVENTION Twenty million, 100 million, or 200 million cells (5 patients in each cell type per dose level) were delivered by transendocardial stem cell injection into 10 LV sites. MAIN OUTCOME MEASURES Thirty-day postcatheterization incidence of predefined treatment-emergent serious adverse events (SAEs). Efficacy assessments included 6-minute walk test, exercise peak VO2, Minnesota Living with Heart Failure Questionnaire (MLHFQ), New York Heart Association class, LV volumes, ejection fraction (EF), early enhancement defect (EED; infarct size), and sphericity index. RESULTS Within 30 days, 1 patient in each group (treatment-emergent SAE rate, 6.7%) was hospitalized for heart failure, less than the prespecified stopping event rate of 25%. The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3% (n = 8) in the autologous group (P = .46). At 1 year, there were no ventricular arrhythmia SAEs observed among allogeneic recipients compared with 4 patients (26.7%) in the autologous group (P = .10). Relative to baseline, autologous but not allogeneic MSC therapy was associated with an improvement in the 6- [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Allogeneic and autologous MSCs reduced mean EED by −33.21% (95% CI, −43.61% to −22.81%; P < .001) and sphericity index but did not increase EF.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 104, "doc_id": "40164383", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Reduction of purity of cytoplasmic membranes isolated from overexpressors is indicated by stronger spots for OmpA in 2D BN-PAGE gels.\n\nCANDIDATE_PASSAGE:\nIdentification of a Multicomponent Complex Required for Outer Membrane Biogenesis in Escherichia coli Gram-negative bacteria have an outer membrane (OM) that functions as a barrier to protect the cell from toxic compounds such as antibiotics and detergents. The OM is a highly asymmetric bilayer composed of phospholipids, glycolipids, and proteins. Assembly of this essential organelle occurs outside the cytoplasm in an environment that lacks obvious energy sources such as ATP, and the mechanisms involved are poorly understood. We describe the identification of a multiprotein complex required for the assembly of proteins in the OM of Escherichia coli. We also demonstrate genetic interactions between genes encoding components of this protein assembly complex and imp, which encodes a protein involved in the assembly of lipopolysaccharides (LPS) in the OM. These genetic interactions suggest a role for YfgL, one of the lipoprotein components of the protein assembly complex, in a homeostatic control mechanism that coordinates the overall OM assembly process.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1032", "doc_id": "6836086", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The PRR MDA5 is a sensor of RNA virus infection.\n\nCANDIDATE_ABSTRACT:\nTITLE: Immune signaling by RIG-I-like receptors.\nABSTRACT: The RIG-I-like receptors (RLRs) RIG-I, MDA5, and LGP2 play a major role in pathogen sensing of RNA virus infection to initiate and modulate antiviral immunity. The RLRs detect viral RNA ligands or processed self RNA in the cytoplasm to trigger innate immunity and inflammation and to impart gene expression that serves to control infection. Importantly, RLRs cooperate in signaling crosstalk networks with Toll-like receptors and other factors to impart innate immunity and to modulate the adaptive immune response. RLR regulation occurs at a variety of levels ranging from autoregulation to ligand and cofactor interactions and posttranslational modifications. Abberant RLR signaling or dysregulation of RLR expression is now implicated in the development of autoimmune diseases. Understanding the processes of RLR signaling and response will provide insights to guide RLR-targeted therapeutics for antiviral and immune-modifying applications.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The RIG-I-like receptors (RLRs) RIG-I, MDA5, and LGP2 play a major role in pathogen sensing of RNA virus infection to initiate and modulate antiviral immunity.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1180, "doc_id": "31272411", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Ultrasound guidance significantly reduces the number of traumatic procedures when attempting needle insertion.\n\nCANDIDATE_ABSTRACT:\nTITLE: Rational design of a flavivirus vaccine by abolishing viral RNA 2'-O methylation.\nABSTRACT: Viruses that replicate in the cytoplasm cannot access the host nuclear capping machinery. These viruses have evolved viral methyltransferase(s) to methylate N-7 and 2'-O cap of their RNA; alternatively, they \"snatch\" host mRNA cap to form the 5' end of viral RNA. The function of 2'-O methylation of viral RNA cap is to mimic cellular mRNA and to evade host innate immune restriction. A cytoplasmic virus defective in 2'-O methylation is replicative, but its viral RNA lacks 2'-O methylation and is recognized and eliminated by the host immune response. Such a mutant virus could be rationally designed as a live attenuated vaccine. Here, we use Japanese encephalitis virus (JEV), an important mosquito-borne flavivirus, to prove this novel vaccine concept. We show that JEV methyltransferase is responsible for both N-7 and 2'-O cap methylations as well as evasion of host innate immune response. Recombinant virus completely defective in 2'-O methylation was stable in cell culture after being passaged for >30 days. The mutant virus was attenuated in mice, elicited robust humoral and cellular immune responses, and retained the engineered mutation in vivo. A single dose of immunization induced full protection against lethal challenge with JEV strains in mice. Mechanistically, the attenuation phenotype was attributed to the enhanced sensitivity of the mutant virus to the antiviral effects of interferon and IFIT proteins. Collectively, the results demonstrate the feasibility of using 2'-O methylation-defective virus as a vaccine approach; this vaccine approach should be applicable to other flaviviruses and nonflaviviruses that encode their own viral 2'-O methyltransferases.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1341, "doc_id": "1970884", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does b7-H4 overexpression impair the immune response of T cells in human cervical carcinomas?\n\nABSTRACT:\nTo investigate B7-H4 expression and its correlation with the number of infiltrating T lymphocytes and cytokine production by those lymphocytes in human cervical cancer and to determine the effect of recombinant B7-H4 on the active peripheral blood T cells of the patients in vitro. B7-H4 expression was detected in 67 cases of cervical cancer using immunohistochemical staining. Tumor-infiltrating CD8(+)T, CD4(+)T, and FOXP3(+) (Forkhead Box P3) T lymphocytes and their levels of IFN-γ and TGF-β₁ production were determined by immunofluorescent double-staining. After the peripheral blood T lymphocytes of patients were co-cultured with B7-H4, proliferation, apoptosis, and cell subtypes were analyzed using flow cytometry. Cytokines in the supernatant were detected by ELISA. B7-H4 was expressed in 46% (31/67) of the cases of cervical cancer. The number of infiltrating CD8(+)T lymphocytes and their IFN-γ production in positive B7-H4 expression cervical cancers was significantly lower than in negative B7-H4 cases (P<0.01, P<0.05), but there was no significant difference between cases positive and negative for B7-H4 with respect to infiltrating FOXP3(+)T and CD4(+)T cells or TGF-β1 production. After co-culture with B7-H4 for 48 h, the patients' activated T lymphocytes were arrested at G1/G2 phase. The Ki67 positive rates of CD4(+)T and CD8(+)T cells were 2.13 ± 0.13% and 1.03 ± 1.33%, and they were lower than in the blank group. The proportion of CD4(+)T and CD8(+)T cells decreased, but CD4(+)T/CD8(+)T and the proportion of CD4(+)CD25(+)Foxp3(+)T cells increased. In addition, concentrations of IL-10 and TGF-β1 in the supernatant of co-cultured T cells increased significantly (P<0.05, P<0.05), but that of IFN-γ decreased. B7-H4 had no significant effect on apoptosis of the T cells.", "output": "{\"label\": \"yes\", \"rationale\": \"B7-H4 is overexpressed in human cervical cancers, and it is associated with lower numbers of tumor-infiltrating CD8(+)T lymphocytes and therefore less IFN-γ production. In vitro, B7-H4 inhibits the proliferation of CD4(+)T and CD8(+)T but promotes the proliferation of Tregs and the secretion of IL-10 and TGF-β1. B7-H4 plays an important role in depressing the anti-tumor immunity of CD8(+)T cell in microenvironments of cervical cancer.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25446402, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: High levels of CRP lead to a higher risk of exacerbations in chronic obstructive pulmonary disease (COPD).\n\nCANDIDATE_PASSAGE:\nGlobal, regional, and national disability-adjusted life-years (DALYs) for 315 diseases and injuries and healthy life expectancy (HALE), 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015 BACKGROUND Healthy life expectancy (HALE) and disability-adjusted life-years (DALYs) provide summary measures of health across geographies and time that can inform assessments of epidemiological patterns and health system performance, help to prioritise investments in research and development, and monitor progress toward the Sustainable Development Goals (SDGs). We aimed to provide updated HALE and DALYs for geographies worldwide and evaluate how disease burden changes with development. METHODS We used results from the Global Burden of Diseases, Injuries, and Risk Factors Study 2015 (GBD 2015) for all-cause mortality, cause-specific mortality, and non-fatal disease burden to derive HALE and DALYs by sex for 195 countries and territories from 1990 to 2015. We calculated DALYs by summing years of life lost (YLLs) and years of life lived with disability (YLDs) for each geography, age group, sex, and year. We estimated HALE using the Sullivan method, which draws from age-specific death rates and YLDs per capita. We then assessed how observed levels of DALYs and HALE differed from expected trends calculated with the Socio-demographic Index (SDI), a composite indicator constructed from measures of income per capita, average years of schooling, and total fertility rate. FINDINGS Total global DALYs remained largely unchanged from 1990 to 2015, with decreases in communicable, neonatal, maternal, and nutritional (Group 1) disease DALYs offset by increased DALYs due to non-communicable diseases (NCDs). Much of this epidemiological transition was caused by chan [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "515", "doc_id": "581832", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Transplanted human glial progenitor cells are incapable of forming a neural network with host animals' neurons.\n\nCANDIDATE_PASSAGE:\nDirect isolation of human central nervous system stem cells. Stem cells, which are clonogenic cells with self-renewal and multilineage differentiation properties, have the potential to replace or repair damaged tissue. We have directly isolated clonogenic human central nervous system stem cells (hCNS-SC) from fresh human fetal brain tissue, using antibodies to cell surface markers and fluorescence-activated cell sorting. These hCNS-SC are phenotypically 5F3 (CD133)(+), 5E12(+), CD34(-), CD45(-), and CD24(-/lo). Single CD133(+) CD34(-) CD45(-) sorted cells initiated neurosphere cultures, and the progeny of clonogenic cells could differentiate into both neurons and glial cells. Single cells from neurosphere cultures initiated from CD133(+) CD34(-) CD45(-) cells were again replated as single cells and were able to reestablish neurosphere cultures, demonstrating the self-renewal potential of this highly enriched population. Upon transplantation into brains of immunodeficient neonatal mice, the sorted/expanded hCNS-SC showed potent engraftment, proliferation, migration, and neural differentiation.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1320", "doc_id": "12742164", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Destination container port throughput(CPT) is negatively related to dengue virus (DENV-1) diffusion in air traffic shipments.\n\nCANDIDATE_PASSAGE:\nNrf2 protects human alveolar epithelial cells against injury induced by influenza A virus BACKGROUND Influenza A virus (IAV) infection primarily targets respiratory epithelial cells and produces clinical outcomes ranging from mild upper respiratory infection to severe pneumonia. Recent studies have shown the importance of lung antioxidant defense systems against injury by IAV. Nuclear factor-erythroid 2 related factor 2 (Nrf2) activates the majority of antioxidant genes. METHODS Alveolar type II (ATII) cells and alveolar macrophages (AM) were isolated from human lungs not suitable for transplantation and donated for medical research. In some studies ATII cells were transdifferentiated to alveolar type I-like (ATI-like) cells. Alveolar epithelial cells were infected with A/PR/8/34 (PR8) virus. We analyzed PR8 virus production, influenza A nucleoprotein levels, ROS generation and expression of antiviral genes. Immunocytofluorescence was used to determine Nrf2 translocation and western blotting to detect Nrf2, HO-1 and caspase 1 and 3 cleavage. We also analyzed ingestion of PR8 virus infected apoptotic ATII cells by AM, cytokine levels by ELISA, glutathione levels, necrosis and apoptosis by TUNEL assay. Moreover, we determined the critical importance of Nrf2 using adenovirus Nrf2 (AdNrf2) or Nrf2 siRNA to overexpress or knockdown Nrf2, respectively. RESULTS We found that IAV induced oxidative stress, cytotoxicity and apoptosis in ATI-like and ATII cells. We also found that AM can ingest PR8 virus-induced apoptotic ATII cells (efferocytosis) but not viable cells, whereas ATII cells did not ingest these apoptotic cells. PR8 virus increased ROS production, Nrf2, HO-1, Mx1 and OAS1 expression and Nrf2 translocation to the nucleus. Nrf2 knockdown with siRNA sensitiz [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "336", "doc_id": "6182947", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Stiff substrates encourage mesodermal differentiation by degrading beta-catenin in an integrin-dependent manner.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tissue Mechanics Orchestrate Wnt-Dependent Human Embryonic Stem Cell Differentiation.\nABSTRACT: Regenerative medicine is predicated on understanding the mechanisms regulating development and applying these conditions to direct stem cell fate. Embryogenesis is guided by cell-cell and cell-matrix interactions, but it is unclear how these physical cues influence stem cells in culture. We used human embryonic stem cells (hESCs) to examine whether mechanical features of the extracellular microenvironment could differentially modulate mesoderm specification. We found that, on a hydrogel-based compliant matrix, hESCs accumulate β-catenin at cell-cell adhesions and show enhanced Wnt-dependent mesoderm differentiation. Mechanistically, Src-driven ubiquitination of E-cadherin by Cbl-like ubiquitin ligase releases P120-catenin to facilitate transcriptional activity of β-catenin, which initiates and reinforces mesoderm differentiation. By contrast, on a stiff hydrogel matrix, hESCs show elevated integrin-dependent GSK3 and Src activity that promotes β-catenin degradation and inhibits differentiation. Thus, we found that mechanical features of the microenvironmental matrix influence tissue-specific differentiation of hESCs by altering the cellular response to morphogens.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"By contrast, on a stiff hydrogel matrix, hESCs show elevated integrin-dependent GSK3 and Src activity that promotes β-catenin degradation and inhibits differentiation.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1101, "doc_id": "3874000", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Lysine histone demethylase inhibitor JIB 04 is inactive against KDM5A.\n\nCANDIDATE_PASSAGE:\nHistone methyltransferase activity associated with a human multiprotein complex containing the Enhancer of Zeste protein. Enhancer of Zeste [E(z)] is a Polycomb-group transcriptional repressor and one of the founding members of the family of SET domain-containing proteins. Several SET-domain proteins possess intrinsic histone methyltransferase (HMT) activity. However, recombinant E(z) protein was found to be inactive in a HMT assay. Here we report the isolation of a multiprotein E(z) complex that contains extra sex combs, suppressor of zeste-12 [Su(z)12], and the histone binding proteins RbAp46/RbAp48. This complex, which we termed Polycomb repressive complex (PRC) 2, possesses HMT activity with specificity for Lys 9 (K9) and Lys 27 (K27) of histone H3. The HMT activity of PRC2 is dependent on an intact SET domain in the E(z) protein. We hypothesize that transcriptional repression by the E(z) protein involves methylation-dependent recruitment of PRC1. The presence of Su(z)12, a strong suppressor of position effect variegation, in PRC2 suggests that PRC2 may play a widespread role in heterochromatin-mediated silencing.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "730", "doc_id": "23195302", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\nABSTRACT: Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens. However, signals underlying mTEC development remain largely unclear. Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals. Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment. Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner. These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1004, "doc_id": "2734421", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cytosolic proteins bind to iron-responsive elements on mRNAs coding for DMT1. Cytosolic proteins bind to iron-responsive elements on mRNAs coding for proteins involved in iron uptake.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mitochondrial iron chelation ameliorates cigarette-smoke induced bronchitis and emphysema in mice\nABSTRACT: Chronic obstructive pulmonary disease (COPD) is linked to both cigarette smoking and genetic determinants. We have previously identified iron-responsive element-binding protein 2 (IRP2) as an important COPD susceptibility gene and have shown that IRP2 protein is increased in the lungs of individuals with COPD. Here we demonstrate that mice deficient in Irp2 were protected from cigarette smoke (CS)-induced experimental COPD. By integrating RNA immunoprecipitation followed by sequencing (RIP-seq), RNA sequencing (RNA-seq), and gene expression and functional enrichment clustering analysis, we identified Irp2 as a regulator of mitochondrial function in the lungs of mice. Irp2 increased mitochondrial iron loading and levels of cytochrome c oxidase (COX), which led to mitochondrial dysfunction and subsequent experimental COPD. Frataxin-deficient mice, which had higher mitochondrial iron loading, showed impaired airway mucociliary clearance (MCC) and higher pulmonary inflammation at baseline, whereas mice deficient in the synthesis of cytochrome c oxidase, which have reduced COX, were protected from CS-induced pulmonary inflammation and impairment of MCC. Mice treated with a mitochondrial iron chelator or mice fed a low-iron diet were protected from CS-induced COPD. Mitochondrial iron chelation also alleviated CS-induced impairment of MCC, CS-induced pulmonary inflammation and CS-associated lung injury in mice with established COPD, suggesting a critical functional role and potential therapeutic intervention for the mitochondrial-iron axis in COPD.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 300, "doc_id": "3553087", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Hypothalamic glutamate neurotransmission is unrelated to energy balance.\n\nCANDIDATE_PASSAGE:\nAtaxia, dementia, and hypogonadotropism caused by disordered ubiquitination. BACKGROUND The combination of ataxia and hypogonadism was first described more than a century ago, but its genetic basis has remained elusive. METHODS We performed whole-exome sequencing in a patient with ataxia and hypogonadotropic hypogonadism, followed by targeted sequencing of candidate genes in similarly affected patients. Neurologic and reproductive endocrine phenotypes were characterized in detail. The effects of sequence variants and the presence of an epistatic interaction were tested in a zebrafish model. RESULTS Digenic homozygous mutations in RNF216 and OTUD4, which encode a ubiquitin E3 ligase and a deubiquitinase, respectively, were found in three affected siblings in a consanguineous family. Additional screening identified compound heterozygous truncating mutations in RNF216 in an unrelated patient and single heterozygous deleterious mutations in four other patients. Knockdown of rnf216 or otud4 in zebrafish embryos induced defects in the eye, optic tectum, and cerebellum; combinatorial suppression of both genes exacerbated these phenotypes, which were rescued by nonmutant, but not mutant, human RNF216 or OTUD4 messenger RNA. All patients had progressive ataxia and dementia. Neuronal loss was observed in cerebellar pathways and the hippocampus; surviving hippocampal neurons contained ubiquitin-immunoreactive intranuclear inclusions. Defects were detected at the hypothalamic and pituitary levels of the reproductive endocrine axis. CONCLUSIONS The syndrome of hypogonadotropic hypogonadism, ataxia, and dementia can be caused by inactivating mutations in RNF216 or by the combination of mutations in RNF216 and OTUD4. These findings link disordered ubiquitination to neurode [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "541", "doc_id": "24725136", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Pyridostatin destabilizes the G - quadruplex in the telomeric region.\n\nCANDIDATE_PASSAGE:\nHIV–1 Infects Multipotent Progenitor Cells Causing Cell Death and Establishing Latent Cellular Reservoirs HIV causes a chronic infection characterized by depletion of CD4(+) T lymphocytes and the development of opportunistic infections. Despite drugs that inhibit viral spread, HIV infection has been difficult to cure because of uncharacterized reservoirs of infected cells that are resistant to highly active antiretroviral therapy (HAART) and the immune response. Here we used CD34(+) cells from infected people as well as in vitro studies of wild-type HIV to show infection and killing of CD34(+) multipotent hematopoietic progenitor cells (HPCs). In some HPCs, we detected latent infection that stably persisted in cell culture until viral gene expression was activated by differentiation factors. A unique reporter HIV that directly detects latently infected cells in vitro confirmed the presence of distinct populations of active and latently infected HPCs. These findings have major implications for understanding HIV bone marrow pathology and the mechanisms by which HIV causes persistent infection.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "993", "doc_id": "7224723", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Incidence rates of cervical cancer have decreased.\n\nCANDIDATE_PASSAGE:\nCell cycle, CDKs and cancer: a changing paradigm Tumour-associated cell cycle defects are often mediated by alterations in cyclin-dependent kinase (CDK) activity. Misregulated CDKs induce unscheduled proliferation as well as genomic and chromosomal instability. According to current models, mammalian CDKs are essential for driving each cell cycle phase, so therapeutic strategies that block CDK activity are unlikely to selectively target tumour cells. However, recent genetic evidence has revealed that, whereas CDK1 is required for the cell cycle, interphase CDKs are only essential for proliferation of specialized cells. Emerging evidence suggests that tumour cells may also require specific interphase CDKs for proliferation. Thus, selective CDK inhibition may provide therapeutic benefit against certain human neoplasias.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "597", "doc_id": "2613411", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Mutations in RIM1 raise levels of IME1 RNA.\n\nCANDIDATE_PASSAGE:\nDrosophila MICAL regulates myofilament organization and synaptic structure The overall size and structure of a synaptic terminal is an important determinant of its function. In a large-scale mutagenesis screen, designed to identify Drosophila mutants with abnormally structured neuromuscular junctions (NMJs), we discovered mutations in Drosophila mical, a conserved gene encoding a multi-domain protein with a N-terminal monooxygenase domain. In mical mutants, synaptic boutons do not sprout normally over the muscle surface and tend to form clusters along synaptic branches and at nerve entry sites. Consistent with high expression of MICAL in somatic muscles, immunohistochemical stainings reveal that the subcellular localization and architecture of contractile muscle filaments are dramatically disturbed in mical mutants. Instead of being integrated into a regular sarcomeric pattern, actin and myosin filaments are disorganized and accumulate beneath the plasmamembrane. Whereas contractile elements are strongly deranged, the proposed organizer of sarcomeric structure, D-Titin, is much less affected. Transgenic expression of interfering RNA molecules demonstrates that MICAL is required in muscles for the higher order arrangement of myofilaments. Ultrastructural analysis confirms that myosin-rich thick filaments enter submembranous regions and interfere with synaptic development, indicating that the disorganized myofilaments may cause the synaptic growth phenotype. As a model, we suggest that the filamentous network around synaptic boutons restrains the spreading of synaptic branches.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "816", "doc_id": "16562534", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: ScPif1p has reduced binding ability to G-rich ssDNA compared to non-G-rich ssDNA.\n\nCANDIDATE_PASSAGE:\nLoss of TDP43 inhibits progression of triple-negative breast cancer in coordination with SRSF3 Aberrant alternative splicing has been highlighted as a potential hallmark of cancer. Here, we identify TDP43 (TAR DNA-binding protein 43) as an important splicing regulator responsible for the unique splicing profile in triple-negative breast cancer (TNBC). Clinical data demonstrate that TDP43 is highly expressed in TNBC with poor prognosis. Knockdown of TDP43 inhibits tumor progression, including proliferation and metastasis, and overexpression of TDP43 promotes proliferation and malignancy of mammary epithelial cells. Deep sequencing analysis and functional experiments indicate that TDP43 alters most splicing events with splicing factor SRSF3 (serine/arginine-rich splicing factor 3), in the regulation of TNBC progression. The TDP43/SRSF3 complex controls specific splicing events, including downstream genes PAR3 and NUMB The effect of reduced metastasis and proliferation upon the knockdown of TDP43 or SRSF3 is mediated by the splicing regulation of PAR3 and NUMB exon 12, respectively. The TDP43/SRSF3 complex and downstream PAR3 isoform are potential therapeutic targets for TNBC.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1068", "doc_id": "4889228", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Ca2+ cycling is a UCP1-dependent thermogenic mechanism.\n\nCANDIDATE_ABSTRACT:\nTITLE: UCP1-independent signaling involving SERCA2b-mediated calcium cycling regulates beige fat thermogenesis and systemic glucose homeostasis\nABSTRACT: Uncoupling protein 1 (UCP1) plays a central role in nonshivering thermogenesis in brown fat; however, its role in beige fat remains unclear. Here we report a robust UCP1-independent thermogenic mechanism in beige fat that involves enhanced ATP-dependent Ca2+ cycling by sarco/endoplasmic reticulum Ca2+-ATPase 2b (SERCA2b) and ryanodine receptor 2 (RyR2). Inhibition of SERCA2b impairs UCP1-independent beige fat thermogenesis in humans and mice as well as in pigs, a species that lacks a functional UCP1 protein. Conversely, enhanced Ca2+ cycling by activation of α1- and/or β3-adrenergic receptors or the SERCA2b-RyR2 pathway stimulates UCP1-independent thermogenesis in beige adipocytes. In the absence of UCP1, beige fat dynamically expends glucose through enhanced glycolysis, tricarboxylic acid metabolism and pyruvate dehydrogenase activity for ATP-dependent thermogenesis through the SERCA2b pathway; beige fat thereby functions as a 'glucose sink' and improves glucose tolerance independently of body weight loss. Our study uncovers a noncanonical thermogenic mechanism through which beige fat controls whole-body energy homeostasis via Ca2+ cycling.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Here we report a robust UCP1-independent thermogenic mechanism in beige fat that involves enhanced ATP-dependent Ca2+ cycling by sarco/endoplasmic reticulum Ca2+-ATPase 2b (SERCA2b) and ryanodine receptor 2 (RyR2).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 221, "doc_id": "19205437", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Low expression of miR7a does not repress target genes or exert a biological function in testis.\n\nCANDIDATE_PASSAGE:\nAssessing the ceRNA hypothesis with quantitative measurements of miRNA and target abundance. Recent studies have reported that competitive endogenous RNAs (ceRNAs) can act as sponges for a microRNA (miRNA) through their binding sites and that changes in ceRNA abundances from individual genes can modulate the activity of miRNAs. Consideration of this hypothesis would benefit from knowing the quantitative relationship between a miRNA and its endogenous target sites. Here, we altered intracellular target site abundance through expression of an miR-122 target in hepatocytes and livers and analyzed the effects on miR-122 target genes. Target repression was released in a threshold-like manner at high target site abundance (≥1.5 × 10(5) added target sites per cell), and this threshold was insensitive to the effective levels of the miRNA. Furthermore, in response to extreme metabolic liver disease models, global target site abundance of hepatocytes did not change sufficiently to affect miRNA-mediated repression. Thus, modulation of miRNA target abundance is unlikely to cause significant effects on gene expression and metabolism through a ceRNA effect.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "714", "doc_id": "18421962", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: MICAL redox enzymes regulate actin dynamics.\n\nCANDIDATE_PASSAGE:\nChromatin modifying enzymes as modulators of reprogramming Generation of induced pluripotent stem cells (iPSCs) by somatic cell reprogramming involves global epigenetic remodelling. Whereas several proteins are known to regulate chromatin marks associated with the distinct epigenetic states of cells before and after reprogramming, the role of specific chromatin-modifying enzymes in reprogramming remains to be determined. To address how chromatin-modifying proteins influence reprogramming, we used short hairpin RNAs (shRNAs) to target genes in DNA and histone methylation pathways, and identified positive and negative modulators of iPSC generation. Whereas inhibition of the core components of the polycomb repressive complex 1 and 2, including the histone 3 lysine 27 methyltransferase EZH2, reduced reprogramming efficiency, suppression of SUV39H1, YY1 and DOT1L enhanced reprogramming. Specifically, inhibition of the H3K79 histone methyltransferase DOT1L by shRNA or a small molecule accelerated reprogramming, significantly increased the yield of iPSC colonies, and substituted for KLF4 and c-Myc (also known as MYC). Inhibition of DOT1L early in the reprogramming process is associated with a marked increase in two alternative factors, NANOG and LIN28, which play essential functional roles in the enhancement of reprogramming. Genome-wide analysis of H3K79me2 distribution revealed that fibroblast-specific genes associated with the epithelial to mesenchymal transition lose H3K79me2 in the initial phases of reprogramming. DOT1L inhibition facilitates the loss of this mark from genes that are fated to be repressed in the pluripotent state. These findings implicate specific chromatin-modifying enzymes as barriers to or facilitators of reprogramming, and demonstrate how [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "738", "doc_id": "3669694", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Rapid phosphotransfer rates govern fidelity in two component systems\n\nCANDIDATE_ABSTRACT:\nTITLE: Diversification in the HIV-1 Envelope Hyper-variable Domains V2, V4, and V5 and Higher Probability of Transmitted/Founder Envelope Glycosylation Favor the Development of Heterologous Neutralization Breadth\nABSTRACT: A recent study of plasma neutralization breadth in HIV-1 infected individuals at nine International AIDS Vaccine Initiative (IAVI) sites reported that viral load, HLA-A*03 genotype, and subtype C infection were strongly associated with the development of neutralization breadth. Here, we refine the findings of that study by analyzing the impact of the transmitted/founder (T/F) envelope (Env), early Env diversification, and autologous neutralization on the development of plasma neutralization breadth in 21 participants identified during recent infection at two of those sites: Kigali, Rwanda (n = 9) and Lusaka, Zambia (n = 12). Single-genome analysis of full-length T/F Env sequences revealed that all 21 individuals were infected with a highly homogeneous population of viral variants, which were categorized as subtype C (n = 12), A1 (n = 7), or recombinant AC (n = 2). An extensive amino acid sequence-based analysis of variable loop lengths and glycosylation patterns in the T/F Envs revealed that a lower ratio of NXS to NXT-encoded glycan motifs correlated with neutralization breadth. Further analysis comparing amino acid sequence changes, insertions/deletions, and glycan motif alterations between the T/F Env and autologous early Env variants revealed that extensive diversification focused in the V2, V4, and V5 regions of gp120, accompanied by contemporaneous viral escape, significantly favored the development of breadth. These results suggest that more efficient glycosylation of subtype A and C T/F Envs through fewer NXS-encoded glycan sites is more likely to elicit antibodies that can transition from autologous to heterologous neutralizing activity following exposure to gp120 diversification. This initiates an Env-antibody co-evolution cycle that increases neut [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1019, "doc_id": "2601135", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Chlamydia trachomatis is most prevalent in the UK among individuals in their 50s and 60s.\n\nCANDIDATE_PASSAGE:\nPrevalence, risk factors, and uptake of interventions for sexually transmitted infections in Britain: findings from the National Surveys of Sexual Attitudes and Lifestyles (Natsal) BACKGROUND Population-based estimates of prevalence, risk distribution, and intervention uptake inform delivery of control programmes for sexually transmitted infections (STIs). We undertook the third National Survey of Sexual Attitudes and Lifestyles (Natsal-3) after implementation of national sexual health strategies, and describe the epidemiology of four STIs in Britain (England, Scotland, and Wales) and the uptake of interventions. METHODS Between Sept 6, 2010 and Aug 31, 2012 , we did a probability sample survey of 15,162 women and men aged 16-74 years in Britain. Participants were interviewed with computer-assisted face-to-face and self-completion questionnaires. Urine from a sample of participants aged 16-44 years who reported at least one sexual partner over the lifetime was tested for the presence of Chlamydia trachomatis, type-specific human papillomavirus (HPV), Neisseria gonorrhoeae, and HIV antibody. We describe age-specific and sex-specific prevalences of infection and intervention uptake, in relation to demographic and behavioural factors, and explore changes since Natsal-1 (1990-91) and Natsal-2 (1999-2001). FINDINGS Of 8047 eligible participants invited to provide a urine sample, 4828 (60%) agreed. We excluded 278 samples, leaving 4550 (94%) participants with STI test results. Chlamydia prevalence was 1·5% (95% CI 1·1-2·0) in women and 1·1% (0·7-1·6) in men. Prevalences in individuals aged 16-24 years were 3·1% (2·2-4·3) in women and 2·3% (1·5-3·4) in men. Area-level deprivation and higher numbers of partners, especially without use of condoms, were risk factors. [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "255", "doc_id": "5850219", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Medications to treat obesity do not have side effects.\n\nCANDIDATE_PASSAGE:\nAdjustable gastric banding and conventional therapy for type 2 diabetes: a randomized controlled trial. CONTEXT Observational studies suggest that surgically induced loss of weight may be effective therapy for type 2 diabetes. OBJECTIVE To determine if surgically induced weight loss results in better glycemic control and less need for diabetes medications than conventional approaches to weight loss and diabetes control. DESIGN, SETTING, AND PARTICIPANTS Unblinded randomized controlled trial conducted from December 2002 through December 2006 at the University Obesity Research Center in Australia, with general community recruitment to established treatment programs. Participants were 60 obese patients (BMI >30 and <40) with recently diagnosed (<2 years) type 2 diabetes. INTERVENTIONS Conventional diabetes therapy with a focus on weight loss by lifestyle change vs laparoscopic adjustable gastric banding with conventional diabetes care. MAIN OUTCOME MEASURES Remission of type 2 diabetes (fasting glucose level <126 mg/dL [7.0 mmol/L] and glycated hemoglobin [HbA1c] value <6.2% while taking no glycemic therapy). Secondary measures included weight and components of the metabolic syndrome. Analysis was by intention-to-treat. RESULTS Of the 60 patients enrolled, 55 (92%) completed the 2-year follow-up. Remission of type 2 diabetes was achieved by 22 (73%) in the surgical group and 4 (13%) in the conventional-therapy group. Relative risk of remission for the surgical group was 5.5 (95% confidence interval, 2.2-14.0). Surgical and conventional-therapy groups lost a mean (SD) of 20.7% (8.6%) and 1.7% (5.2%) of weight, respectively, at 2 years (P < .001). Remission of type 2 diabetes was related to weight loss (R2 = 0.46, P < .001) and lower baseline HbA1c levels (combin [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "765", "doc_id": "7098463", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The density of cytokine receptor bearing cells has no effect on the distance over which cytokines act.\n\nCANDIDATE_PASSAGE:\nTAA1-Mediated Auxin Biosynthesis Is Essential for Hormone Crosstalk and Plant Development Plants have evolved a tremendous ability to respond to environmental changes by adapting their growth and development. The interaction between hormonal and developmental signals is a critical mechanism in the generation of this enormous plasticity. A good example is the response to the hormone ethylene that depends on tissue type, developmental stage, and environmental conditions. By characterizing the Arabidopsis wei8 mutant, we have found that a small family of genes mediates tissue-specific responses to ethylene. Biochemical studies revealed that WEI8 encodes a long-anticipated tryptophan aminotransferase, TAA1, in the essential, yet genetically uncharacterized, indole-3-pyruvic acid (IPA) branch of the auxin biosynthetic pathway. Analysis of TAA1 and its paralogues revealed a link between local auxin production, tissue-specific ethylene effects, and organ development. Thus, the IPA route of auxin production is key to generating robust auxin gradients in response to environmental and developmental cues.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1211", "doc_id": "10504681", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Activated Cdk5 phosphorylates the ATM protein in response to DNA damage.\n\nCANDIDATE_PASSAGE:\nGlutathione and glutathione-dependent enzymes represent a co-ordinately regulated defence against oxidative stress. Increases in the intracellular levels of reactive oxygen species (ROS), frequently referred to as oxidative stress, represents a potentially toxic insult which if not counteracted will lead to membrane dysfunction, DNA damage and inactivation of proteins. Chronic oxidative stress has numerous pathological consequences including cancer, arthritis and neurodegenerative disease. Glutathione-associated metabolism is a major mechanism for cellular protection against agents which generate oxidative stress. It is becoming increasingly apparent that the glutathione tripeptide is central to a complex multifaceted detoxification system, where there is substantial inter-dependence between separate component members. Glutathione participates in detoxification at several different levels, and may scavenge free radicals, reduce peroxides or be conjugated with electrophilic compounds. Thus, glutathione provides the cell with multiple defences not only against ROS but also against their toxic products. This article discusses how glutathione biosynthesis, glutathione peroxidases, glutathione S-transferases and glutathione S-conjugate efflux pumps function in an integrated fashion to allow cellular adaption to oxidative stress. Co-ordination of this response is achieved, at least in part, through the antioxidant responsive element (ARE) which is found in the promoters of many of the genes that are inducible by oxidative and chemical stress. Transcriptional activation through this enhancer appears to be mediated by basic leucine zipper transcription factors such as Nrf and small Maf proteins. The nature of the intracellular sensor(s) for ROS and thiol-active chem [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "67", "doc_id": "25488034", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Adult tissue-resident macrophages are seeded before birth.\n\nCANDIDATE_PASSAGE:\nSkeletal Myogenic Progenitors Originating from Embryonic Dorsal Aorta Coexpress Endothelial and Myogenic Markers and Contribute to Postnatal Muscle Growth and Regeneration Skeletal muscle in vertebrates is derived from somites, epithelial structures of the paraxial mesoderm, yet many unrelated reports describe the occasional appearance of myogenic cells from tissues of nonsomite origin, suggesting either transdifferentiation or the persistence of a multipotent progenitor. Here, we show that clonable skeletal myogenic cells are present in the embryonic dorsal aorta of mouse embryos. This finding is based on a detailed clonal analysis of different tissue anlagen at various developmental stages. In vitro, these myogenic cells show the same morphology as satellite cells derived from adult skeletal muscle, and express a number of myogenic and endothelial markers. Surprisingly, the latter are also expressed by adult satellite cells. Furthermore, it is possible to clone myogenic cells from limbs of mutant c-Met-/- embryos, which lack appendicular muscles, but have a normal vascular system. Upon transplantation, aorta-derived myogenic cells participate in postnatal muscle growth and regeneration, and fuse with resident satellite cells. The potential of the vascular system to generate skeletal muscle cells may explain observations of nonsomite skeletal myogenesis and raises the possibility that a subset of satellite cells may derive from the vascular system.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "86", "doc_id": "12411274", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Sudden death can occur in patients with complex ventricular arrhythmias.\n\nCANDIDATE_PASSAGE:\nTranscriptional integration of mitochondrial biogenesis. Gene regulatory factors encoded by the nuclear genome are essential for mitochondrial biogenesis and function. Some of these factors act exclusively within the mitochondria to regulate the control of mitochondrial transcription, translation, and other functions. Others govern the expression of nuclear genes required for mitochondrial metabolism and organelle biogenesis. The peroxisome proliferator-activated receptor γ coactivator-1 (PGC-1) family of transcriptional coactivators play a major role in transducing and integrating physiological signals governing metabolism, differentiation, and cell growth to the transcriptional machinery controlling mitochondrial functional capacity. Thus, the PGC-1 coactivators serve as a central component of the transcriptional regulatory circuitry that coordinately controls the energy-generating functions of mitochondria in accordance with the metabolic demands imposed by changing physiological conditions, senescence, and disease.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1111", "doc_id": "27693891", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Thigh-length graduated compression stockings (GCS) did not reduce deep vein thrombosis in patients admitted to hospital who are immobile because of acute stroke.\n\nCANDIDATE_PASSAGE:\nAdverse Events Associated With the Treatment of Multidrug-Resistant Tuberculosis: A Systematic Review and Meta-analysis. Multidrug-resistant tuberculosis (MDR-TB) is a growing public health problem. Due to long duration of therapy and concurrent use of multiple second-line drugs, adverse drug events (ADEs) are regarded as the most important clinical consideration in patients undergoing anti-MDR-TB treatment. To evaluate the frequency and type of treatment-related ADEs owing to MDR-TB therapy. The Cochrane Library, MEDLINE, and EMBASE were searched from inception through October 1, 2012, with additional manual search of International Journal of Tuberculosis and Lung Disease. Studies with available ADEs were selected if MDR-TB patients were treated with regimen including second-line drugs. Pooled estimations of incidence for each specific type of ADEs were calculated with 95% confidence intervals using random-effects model. Of the 5346 patients included, 2602 (57.3%) experienced at least 1 kind of ADE. The 3 most common side effects were gastrointestinal disorders (32.1%), ototoxicity (14.6%), and psychiatric disorders (13.2%). Subgroup analyses based on each characteristic (study population, previous tuberculosis treated, human immunodeficiency virus prevalence, and length of treatment) did not show any significant difference between groups. Additionally, among 1519 patients who developed ADEs with available data of impact on MDR-TB therapy, 70.4% required change of MDR-TB treatment. Adverse events were common among MDR-TB cases, occurring in more than half of the cases, with over two-thirds requiring change of anti-MDR-TB treatment. MDR-TB patients should be monitored closely and managed aggressively for side effects during therapy, especially for ototoxicit [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1298", "doc_id": "11254040", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The risk of breast cancer among parous women increases with placental weight of pregnancies, and this association is strongest for premenopausal breast cancer.\n\nCANDIDATE_PASSAGE:\nCancer treatment and survivorship statistics, 2014. The number of cancer survivors continues to increase due to the aging and growth of the population and improvements in early detection and treatment. In order for the public health community to better serve these survivors, the American Cancer Society and the National Cancer Institute collaborated to estimate the number of current and future cancer survivors using data from the Surveillance, Epidemiology, and End Results (SEER) program registries. In addition, current treatment patterns for the most common cancer types are described based on information in the National Cancer Data Base and the SEER and SEER-Medicare linked databases; treatment-related side effects are also briefly described. Nearly 14.5 million Americans with a history of cancer were alive on January 1, 2014; by January 1, 2024, that number will increase to nearly 19 million. The 3 most common prevalent cancers among males are prostate cancer (43%), colorectal cancer (9%), and melanoma (8%), and those among females are cancers of the breast (41%), uterine corpus (8%), and colon and rectum (8%). The age distribution of survivors varies substantially by cancer type. For example, the majority of prostate cancer survivors (62%) are aged 70 years or older, whereas less than one-third (32%) of melanoma survivors are in this older age group. It is important for clinicians to understand the unique medical and psychosocial needs of cancer survivors and to proactively assess and manage these issues. There are a growing number of resources that can assist patients, caregivers, and health care providers in navigating the various phases of cancer survivorship.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1266", "doc_id": "25121903", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Autologous transplantation of mesenchymal stem cells has lower rates of rejection than induction therapy with anti-interleukin-2 receptor antibodies.\n\nCANDIDATE_PASSAGE:\nInduction of cell cycle entry eliminates human leukemia stem cells in a mouse model of AML Cancer stem cells have been proposed to be important for initiation, maintenance and recurrence of various malignancies, including acute myeloid leukemia (AML). We have previously reported that CD34+CD38− human primary AML stem cells residing in the endosteal region of the bone marrow are relatively chemotherapy resistant. Using a NOD/SCID/IL2rγnull mouse model of human AML, we now show that the AML stem cells in the endosteal region are cell cycle quiescent and that these stem cells can be induced to enter the cell cycle by treatment with granulocyte colony-stimulating factor (G-CSF). In combination with cell cycle-dependent chemotherapy, G-CSF treatment significantly enhances induction of apoptosis and elimination of human primary AML stem cells in vivo. The combination therapy leads to significantly increased survival of secondary recipients after transplantation of leukemia cells compared with chemotherapy alone.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "146", "doc_id": "19510470", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Helminths interfere with immune system control of coinfections by microbial pathogens 16.\n\nCANDIDATE_ABSTRACT:\nTITLE: Preexisting helminth infection induces inhibition of innate pulmonary anti-tuberculosis defense by engaging the IL-4 receptor pathway\nABSTRACT: Tuberculosis and helminthic infections coexist in many parts of the world, yet the impact of helminth-elicited Th2 responses on the ability of the host to control Mycobacterium tuberculosis (Mtb) infection has not been fully explored. We show that mice infected with the intestinal helminth Nippostrongylus brasiliensis (Nb) exhibit a transitory impairment of resistance to airborne Mtb infection. Furthermore, a second dose of Nb infection substantially increases the bacterial burden in the lungs of co-infected mice. Interestingly, the Th2 response in the co-infected animals did not impair the onset and development of the protective Mtb-specific Th1 cellular immune responses. However, the helminth-induced Th2 environment resulted in the accumulation of alternatively activated macrophages (AAMs) in the lung. Co-infected mice lacking interleukin (IL) 4Rα exhibited improved ability to control Mtb infection, which was accompanied by significantly reduced accumulation of AAMs. Moreover, IL-4Rα(-/-) mice adoptively transferred with wild-type macrophages had a significantly higher Mtb load in their lungs compared with those that received IL-4Rα(-/-) macrophages, suggesting a direct contribution for the IL-4R pathway to the heightened susceptibility of co-infected animals. The Th2 response can thus enhance the intracellular persistence of Mtb, in part by mediating the alternative activation of macrophages via the IL-4Rα signaling pathway.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Furthermore, a second dose of Nb infection substantially increases the bacterial burden in the lungs of co-infected mice.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 506, "doc_id": "7433668", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The US health care system can save up to $750 million if 7% of patients waiting for kidney transplants participate in the optimized national kidney paired donation program.\n\nCANDIDATE_PASSAGE:\nComparisons of patient and physician expectations for cancer survivorship care. PURPOSE To compare expectations for cancer survivorship care between patients and their physicians and between primary care providers (PCPs) and oncologists. METHODS Survivors and their physicians were surveyed to evaluate for expectations regarding physician participation in primary cancer follow-up, screening for other cancers, general preventive health, and management of comorbidities. RESULTS Of 992 eligible survivors and 607 physicians surveyed, 535 (54%) and 378 (62%) were assessable, respectively. Among physician respondents, 255 (67%) were PCPs and 123 (33%) were oncologists. Comparing patients with their oncologists, expectations were highly discrepant for screening for cancers other than the index one (agreement rate, 29%), with patients anticipating significantly more oncologist involvement. Between patients and their PCPs, expectations were most incongruent for primary cancer follow-up (agreement rate, 35%), with PCPs indicating they should contribute a much greater part to this aspect of care. Expectations between patients and their PCPs were generally more concordant than between patients and their oncologists. PCPs and oncologists showed high discordances in perceptions of their own roles for primary cancer follow-up, cancer screening, and general preventive health (agreement rates of 3%, 44%, and 51%, respectively). In the case of primary cancer follow-up, both PCPs and oncologists indicated they should carry substantial responsibility for this task. CONCLUSION Patients and physicians have discordant expectations with respect to the roles of PCPs and oncologists in cancer survivorship care. Uncertainties around physician roles and responsibilities can lead to defi [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1185", "doc_id": "9274291", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Nonhuman primates are incapable of producing neutralizing antibodies in reponse to the Eilat virus (EILV) produced in mosquitos.\n\nCANDIDATE_PASSAGE:\nTen years' experience with alendronate for osteoporosis in postmenopausal women. BACKGROUND Antiresorptive agents are widely used to treat osteoporosis. We report the results of a multinational randomized, double-blind study, in which postmenopausal women with osteoporosis were treated with alendronate for up to 10 years. METHODS The initial three-year phase of the study compared three daily doses of alendronate with placebo. Women in the original placebo group received alendronate in years 4 and 5 and then were discharged. Women in the original active-treatment groups continued to receive alendronate during the initial extension (years 4 and 5). In two further extensions (years 6 and 7, and 8 through 10), women who had received 5 mg or 10 mg of alendronate daily continued on the same treatment. Women in the discontinuation group received 20 mg of alendronate daily for two years and 5 mg daily in years 3, 4, and 5, followed by five years of placebo. Randomized group assignments and blinding were maintained throughout the 10 years. We report results for the 247 women who participated in all four phases of the study. RESULTS Treatment with 10 mg of alendronate daily for 10 years produced mean increases in bone mineral density of 13.7 percent at the lumbar spine (95 percent confidence interval, 12.0 to 15.5 percent), 10.3 percent at the trochanter (95 percent confidence interval, 8.1 to 12.4 percent), 5.4 percent at the femoral neck (95 percent confidence interval, 3.5 to 7.4 percent), and 6.7 percent at the total proximal femur (95 percent confidence interval, 4.4 to 9.1 percent) as compared with base-line values; smaller gains occurred in the group given 5 mg daily. The discontinuation of alendronate resulted in a gradual loss of effect, as measured by bone d [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "853", "doc_id": "19205326", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Mitochondria are uninvolved in apoptosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mitochondria: Dynamic Organelles in Disease, Aging, and Development\nABSTRACT: Mitochondria are the primary energy-generating system in most eukaryotic cells. Additionally, they participate in intermediary metabolism, calcium signaling, and apoptosis. Given these well-established functions, it might be expected that mitochondrial dysfunction would give rise to a simple and predictable set of defects in all tissues. However, mitochondrial dysfunction has pleiotropic effects in multicellular organisms. Clearly, much about the basic biology of mitochondria remains to be understood. Here we discuss recent work that suggests that the dynamics (fusion and fission) of these organelles is important in development and disease.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Additionally, they participate in intermediary metabolism, calcium signaling, and apoptosis.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 793, "doc_id": "8551160", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Normal granulomas form in the absence of TNF in Zebrafish.\n\nCANDIDATE_ABSTRACT:\nTITLE: Dynamic capsule restructuring by the main pneumococcal autolysin LytA in response to the epithelium\nABSTRACT: Bacterial pathogens produce complex carbohydrate capsules to protect against bactericidal immune molecules. Paradoxically, the pneumococcal capsule sensitizes the bacterium to antimicrobial peptides found on epithelial surfaces. Here we show that upon interaction with antimicrobial peptides, encapsulated pneumococci survive by removing capsule from the cell surface within minutes in a process dependent on the suicidal amidase autolysin LytA. In contrast to classical bacterial autolysis, during capsule shedding, LytA promotes bacterial survival and is dispersed circumferentially around the cell. However, both autolysis and capsule shedding depend on the cell wall hydrolytic activity of LytA. Capsule shedding drastically increases invasion of epithelial cells and is the main pathway by which pneumococci reduce surface bound capsule during early acute lung infection of mice. The previously unrecognized role of LytA in removing capsule to combat antimicrobial peptides may explain why nearly all clinical isolates of pneumococci conserve this enzyme despite the lethal selective pressure of antibiotics.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 860, "doc_id": "1234098", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Ethanol stress reduces the expression of SRL in bacteria.\n\nCANDIDATE_ABSTRACT:\nTITLE: Regulatory and metabolic rewiring during laboratory evolution of ethanol tolerance in E. coli\nABSTRACT: Understanding the genetic basis of adaptation is a central problem in biology. However, revealing the underlying molecular mechanisms has been challenging as changes in fitness may result from perturbations to many pathways, any of which may contribute relatively little. We have developed a combined experimental/computational framework to address this problem and used it to understand the genetic basis of ethanol tolerance in Escherichia coli. We used fitness profiling to measure the consequences of single-locus perturbations in the context of ethanol exposure. A module-level computational analysis was then used to reveal the organization of the contributing loci into cellular processes and regulatory pathways (e.g. osmoregulation and cell-wall biogenesis) whose modifications significantly affect ethanol tolerance. Strikingly, we discovered that a dominant component of adaptation involves metabolic rewiring that boosts intracellular ethanol degradation and assimilation. Through phenotypic and metabolomic analysis of laboratory-evolved ethanol-tolerant strains, we investigated naturally accessible pathways of ethanol tolerance. Remarkably, these laboratory-evolved strains, by and large, follow the same adaptive paths as inferred from our coarse-grained search of the fitness landscape.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 393, "doc_id": "1148122", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Suboptimal nutrition is a leading cause of premature death\n\nCANDIDATE_ABSTRACT:\nTITLE: The state of US health, 1990-2010: burden of diseases, injuries, and risk factors.\nABSTRACT: IMPORTANCE Understanding the major health problems in the United States and how they are changing over time is critical for informing national health policy. OBJECTIVES To measure the burden of diseases, injuries, and leading risk factors in the United States from 1990 to 2010 and to compare these measurements with those of the 34 countries in the Organisation for Economic Co-operation and Development (OECD) countries. DESIGN We used the systematic analysis of descriptive epidemiology of 291 diseases and injuries, 1160 sequelae of these diseases and injuries, and 67 risk factors or clusters of risk factors from 1990 to 2010 for 187 countries developed for the Global Burden of Disease 2010 Study to describe the health status of the United States and to compare US health outcomes with those of 34 OECD countries. Years of life lost due to premature mortality (YLLs) were computed by multiplying the number of deaths at each age by a reference life expectancy at that age. Years lived with disability (YLDs) were calculated by multiplying prevalence (based on systematic reviews) by the disability weight (based on population-based surveys) for each sequela; disability in this study refers to any short- or long-term loss of health. Disability-adjusted life-years (DALYs) were estimated as the sum of YLDs and YLLs. Deaths and DALYs related to risk factors were based on systematic reviews and meta-analyses of exposure data and relative risks for risk-outcome pairs. Healthy life expectancy (HALE) was used to summarize overall population health, accounting for both length of life and levels of ill health experienced at different ages. RESULTS US life expectancy for both sexes combined increased from 75.2 years in 1990 to 78.2 years in 2010; during the same period, HALE inc [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The leading risk factors related to DALYs were dietary risks, tobacco smoking, high body mass index, high blood pressure, high fasting plasma glucose, physical inactivity, and alcohol use.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1109, "doc_id": "8582337", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Diabetic patients with acute coronary syndrome experience increased short-term and long-term risk for bleeding events.\n\nCANDIDATE_ABSTRACT:\nTITLE: Platelet glycoprotein IIb/IIIa inhibitors reduce mortality in diabetic patients with non-ST-segment-elevation acute coronary syndromes.\nABSTRACT: BACKGROUND Diabetes mellitus is a major risk factor for adverse outcomes after acute coronary syndromes (ACS). Because this disease may be associated with increased platelet aggregation, we investigated whether diabetic patients with ACS derive particular benefit from platelet glycoprotein (GP) IIb/IIIa receptor inhibition. METHODS AND RESULTS We performed a meta-analysis of the diabetic populations enrolled in the 6 large-scale platelet GP IIb/IIIa inhibitor ACS trials: PRISM, PRISM-PLUS, PARAGON A, PARAGON B, PURSUIT, and GUSTO IV. Among 6458 diabetic patients, platelet GP IIb/IIIa inhibition was associated with a significant mortality reduction at 30 days, from 6.2% to 4.6% (OR 0.74; 95% CI 0.59 to 0.92; P=0.007). Conversely, 23 072 nondiabetic patients had no survival benefit (3.0% versus 3.0%). The interaction between platelet GP IIb/IIIa inhibition and diabetic status was statistically significant (P=0.036). Among 1279 diabetic patients undergoing percutaneous coronary intervention (PCI) during index hospitalization, the use of these agents was associated with a mortality reduction at 30 days from 4.0% to 1.2% (OR 0.30; 95% CI 0.14 to 0.69; P=0.002). CONCLUSIONS This meta-analysis, including the entire large-scale trial experience of intravenous platelet GP IIb/IIIa inhibitors for the medical management of non-ST-segment-elevation ACS, shows that these agents may significantly reduce mortality at 30 days in diabetic patients. Although not based on a randomized assessment, the survival benefit appears to be of greater magnitude in patients undergoing PCI. Therefore, the use of platelet GP IIb/IIIa inhibitors should be strongly considered in diabetic patients with ACS.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 343, "doc_id": "7873737", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Toll-like receptor (TLR) signaling is involved in the pathogenesis of human MDS.\n\nCANDIDATE_PASSAGE:\nA KEY ROLE FOR OREXIN IN PANIC ANXIETY Panic disorder is a severe anxiety disorder with recurrent, debilitating panic attacks. In individuals with panic disorder there is evidence of decreased central gamma-aminobutyric acid (GABA) activity as well as marked increases in autonomic and respiratory responses after intravenous infusions of hypertonic sodium lactate. In a rat model of panic disorder, chronic inhibition of GABA synthesis in the dorsomedial-perifornical hypothalamus of rats produces anxiety-like states and a similar vulnerability to sodium lactate-induced cardioexcitatory responses. The dorsomedial-perifornical hypothalamus is enriched in neurons containing orexin (ORX, also known as hypocretin), which have a crucial role in arousal, vigilance and central autonomic mobilization, all of which are key components of panic. Here we show that activation of ORX-synthesizing neurons is necessary for developing a panic-prone state in the rat panic model, and either silencing of the hypothalamic gene encoding ORX (Hcrt) with RNAi or systemic ORX-1 receptor antagonists blocks the panic responses. Moreover, we show that human subjects with panic anxiety have elevated levels of ORX in the cerebrospinal fluid compared to subjects without panic anxiety. Taken together, our results suggest that the ORX system may be involved in the pathophysiology of panic anxiety and that ORX antagonists constitute a potential new treatment strategy for panic disorder.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1306", "doc_id": "16056514", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does liver transplantation prevent the development of life-threatening arrhythmia in familial amyloidotic polyneuropathy , Portuguese-type ( ATTR Val30Met ) patients?\n\nABSTRACT:\nOrthotopic liver transplantation (OLT) is today the only available treatment to halt the progress of familial amyloidotic polyneuropathy (FAP). Because heart arrhythmia and conduction disturbances are well-known manifestations of FAP, the aim of this study was to investigate the occurrence and development of heart conduction and rhythm disturbances in Swedish FAP patients who underwent liver transplantation. Ambulatory 24-hour electrocardiography (ECG) recordings (Holter-ECGs) were available from 30 patients, who had been investigated before and reexamined after OLT. RESULTS.: The number of patients with abnormalities on their ECG recordings increased after OLT. Four patients developed serious arrhythmia after transplantation that necessitated the insertion of a pacemaker 40 months or longer after OLT.", "output": "{\"label\": \"no\", \"rationale\": \"The development of cardiac conduction disturbances and arrhythmias appear not to be halted by liver transplantation, indicating that the physician should be aware of the potential risk for FAP patients receiving transplants to develop fatal arrhythmia. The follow-up after liver transplantation should include Holter-ECG recordings.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 15257048, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Omnivores produce less trimethylamine N-oxide from dietary I-carnitine than vegans.\n\nCANDIDATE_PASSAGE:\nCardiorespiratory adaptation during sleep in infants and children. The cardiorespiratory control system undergoes functional maturation after birth. Until this process is completed, the cardiorespiratory system is unstable, placing infants at risk for cardiorespiratory disturbances, especially during sleep. The profound influence of states of alertness on respiratory and cardiac control has been the focus of intense scrutiny during the last decade. The effects of rapid-eye movement (REM) sleep on various mechanisms involved in cardiorespiratory control are of particular significance during the postnatal period since newborns spend much of their time in this sleep state. In fullterm newborns, REM sleep occupies more than 50% of total sleep time, and this percentage is even greater in preterm newborns. From term to six months of age, the proportion of REM sleep decreases. Since respiratory and cardiac disturbances are known to occur selectively during REM sleep, the predominance of REM sleep may be a risk factor for abnormal sleep-related events during early infancy. Awareness of these developmental changes in sleep patterns is important for clinicians dealing with problems such as apparent life-threatening events (ALTE), sudden infant death syndrome (SIDS), and/or cardiorespiratory responses to respiratory disorders. Our current understanding of respiratory and cardiac control rests mainly on studies conducted during the first months of life. There is a paucity of data on late infancy and early childhood. The present paper will review available data on how sleep affects 1) ventilatory mechanics, in particular of the upper airways and the chest wall; ventilation and apnea; gas exchange; chemoreceptor function; and arousal responses; 2) changes in heart rate an [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "881", "doc_id": "35521287", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Increased conversion of PGE 2 to PPARy ligand 15-ket-PGE 2 causes accumulation of PGE.\n\nCANDIDATE_PASSAGE:\nPharmacological correction of a defect in PPARγ signaling ameliorates disease severity in Cftr-deficient mice Cystic fibrosis is caused by mutations in the cystic fibrosis transmembrane conductance regulator (encoded by Cftr) that impair its role as an apical chloride channel that supports bicarbonate transport. Individuals with cystic fibrosis show retained, thickened mucus that plugs airways and obstructs luminal organs as well as numerous other abnormalities that include inflammation of affected organs, alterations in lipid metabolism and insulin resistance. Here we show that colonic epithelial cells and whole lung tissue from Cftr-deficient mice show a defect in peroxisome proliferator-activated receptor-gamma (PPAR-gamma, encoded by Pparg) function that contributes to a pathological program of gene expression. Lipidomic analysis of colonic epithelial cells suggests that this defect results in part from reduced amounts of the endogenous PPAR-gamma ligand 15-keto-prostaglandin E(2) (15-keto-PGE(2)). Treatment of Cftr-deficient mice with the synthetic PPAR-gamma ligand rosiglitazone partially normalizes the altered gene expression pattern associated with Cftr deficiency and reduces disease severity. Rosiglitazone has no effect on chloride secretion in the colon, but it increases expression of the genes encoding carbonic anhydrases 4 and 2 (Car4 and Car2), increases bicarbonate secretion and reduces mucus retention. These studies reveal a reversible defect in PPAR-gamma signaling in Cftr-deficient cells that can be pharmacologically corrected to ameliorate the severity of the cystic fibrosis phenotype in mice.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "606", "doc_id": "712078", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Walking in traffic areas in London improves lung function in elderly adults.\n\nCANDIDATE_ABSTRACT:\nTITLE: Respiratory and cardiovascular responses to walking down a traffic-polluted road compared with walking in a traffic-free area in participants aged 60 years and older with chronic lung or heart disease and age-matched healthy controls: a randomised, crossover study\nABSTRACT: BACKGROUND Long-term exposure to pollution can lead to an increase in the rate of decline of lung function, especially in older individuals and in those with chronic obstructive pulmonary disease (COPD), whereas shorter-term exposure at higher pollution levels has been implicated in causing excess deaths from ischaemic heart disease and exacerbations of COPD. We aimed to assess the effects on respiratory and cardiovascular responses of walking down a busy street with high levels of pollution compared with walking in a traffic-free area with lower pollution levels in older adults. METHODS In this randomised, crossover study, we recruited men and women aged 60 years and older with angiographically proven stable ischaemic heart disease or stage 2 Global initiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable for 6 months, and age-matched healthy volunteers. Individuals with ischaemic heart disease or COPD were recruited from existing databases or outpatient respiratory and cardiology clinics at the Royal Brompton & Harefield NHS Foundation Trust and age-matched healthy volunteers using advertising and existing databases. All participants had abstained from smoking for at least 12 months and medications were taken as recommended by participants' doctors during the study. Participants were randomly assigned by drawing numbered disks at random from a bag to do a 2 h walk either along a commercial street in London (Oxford Street) or in an urban park (Hyde Park). Baseline measurements of participants were taken before the walk in the hospital laboratory. During each walk session, black carbon, particulate matter (PM) concentrations, ultrafine particles, and nitrogen dioxide (NO2) concentrations were measured. FINDINGS Between October, 2012 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In all participants, irrespective of their disease status, walking in Hyde Park led to an increase in lung function (forced expiratory volume in the first second [FEV1] and forced vital capacity [FVC]) and a decrease in pulse wave velocity (PWV) and augmentation index up to 26 h after the walk. By contrast, these beneficial responses were attenuated after walking on Oxford Street.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1373, "doc_id": "21003930", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Normal expression of RUNX1 causes tumorsupressing effects.\n\nCANDIDATE_PASSAGE:\nFunctional inhibition of osteoblastic cells in an in vivo mouse model of myeloid leukemia. Pancytopenia is a major cause of morbidity in acute myeloid leukemia (AML), yet its cause is unclear. Normal osteoblastic cells have been shown to support hematopoiesis. To define the effects of leukemia on osteoblastic cells, we used an immunocompetent murine model of AML. Leukemic mice had inhibition of osteoblastic cells, with decreased serum levels of the bone formation marker osteocalcin. Osteoprogenitor cells and endosteal-lining osteopontin(+) cells were reduced, and osteocalcin mRNA in CD45(-) marrow cells was diminished. This resulted in severe loss of mineralized bone. Osteoclasts were only transiently increased without significant increases in bone resorption, and their inhibition only partially rescued leukemia-induced bone loss. In vitro data suggested that a leukemia-derived secreted factor inhibited osteoblastic cells. Because the chemokine CCL-3 was recently reported to inhibit osteoblastic function in myeloma, we tested its expression in our model and in AML patients. Consistent with its potential novel role in leukemic-dependent bone loss, CCL-3 mRNA was significantly increased in malignant marrow cells from leukemic mice and from samples from AML patients. Based on these results, we propose that therapeutic mitigation of leukemia-induced uncoupling of osteoblastic and osteoclastic cells may represent a novel approach to promote normal hematopoiesis in patients with myeloid neoplasms.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "858", "doc_id": "10795340", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does oxybutynin hydrochloride cause arrhythmia in children with bladder dysfunction?\n\nABSTRACT:\nThis study represents a subset of a complete data set, considering only those children aged admitted to the Pediatric Surgery and Pediatric Nephrology Clinics during the period January 2011 to July 2012. In this study, we have determined that the QT interval changes significantly depending on the use of oxybutynin. The QT changes increased cardiac arrhythmia in children.", "output": "{\"label\": \"yes\", \"rationale\": \"For this reason, children using such drugs should be closely monitored for cardiac arrhythmia.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 23848044, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Tirasemtiv has no effect on fast-twitch muscle.\n\nCANDIDATE_PASSAGE:\nBlood pressure and incidence of twelve cardiovascular diseases: lifetime risks, healthy life-years lost, and age-specific associations in 1·25 million people BACKGROUND The associations of blood pressure with the different manifestations of incident cardiovascular disease in a contemporary population have not been compared. In this study, we aimed to analyse the associations of blood pressure with 12 different presentations of cardiovascular disease. METHODS We used linked electronic health records from 1997 to 2010 in the CALIBER (CArdiovascular research using LInked Bespoke studies and Electronic health Records) programme to assemble a cohort of 1·25 million patients, 30 years of age or older and initially free from cardiovascular disease, a fifth of whom received blood pressure-lowering treatments. We studied the heterogeneity in the age-specific associations of clinically measured blood pressure with 12 acute and chronic cardiovascular diseases, and estimated the lifetime risks (up to 95 years of age) and cardiovascular disease-free life-years lost adjusted for other risk factors at index ages 30, 60, and 80 years. This study is registered at ClinicalTrials.gov, number NCT01164371. FINDINGS During 5·2 years median follow-up, we recorded 83,098 initial cardiovascular disease presentations. In each age group, the lowest risk for cardiovascular disease was in people with systolic blood pressure of 90-114 mm Hg and diastolic blood pressure of 60-74 mm Hg, with no evidence of a J-shaped increased risk at lower blood pressures. The effect of high blood pressure varied by cardiovascular disease endpoint, from strongly positive to no effect. Associations with high systolic blood pressure were strongest for intracerebral haemorrhage (hazard ratio 1·44 [95% CI 1·3 [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1303", "doc_id": "4506414", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: COPI coatmer is involved in lipid homeostasis.\n\nCANDIDATE_PASSAGE:\nCOPI Complex Is a Regulator of Lipid Homeostasis Lipid droplets are ubiquitous triglyceride and sterol ester storage organelles required for energy storage homeostasis and biosynthesis. Although little is known about lipid droplet formation and regulation, it is clear that members of the PAT (perilipin, adipocyte differentiation related protein, tail interacting protein of 47 kDa) protein family coat the droplet surface and mediate interactions with lipases that remobilize the stored lipids. We identified key Drosophila candidate genes for lipid droplet regulation by RNA interference (RNAi) screening with an image segmentation-based optical read-out system, and show that these regulatory functions are conserved in the mouse. Those include the vesicle-mediated Coat Protein Complex I (COPI) transport complex, which is required for limiting lipid storage. We found that COPI components regulate the PAT protein composition at the lipid droplet surface, and promote the association of adipocyte triglyceride lipase (ATGL) with the lipid droplet surface to mediate lipolysis. Two compounds known to inhibit COPI function, Exo1 and Brefeldin A, phenocopy COPI knockdowns. Furthermore, RNAi inhibition of ATGL and simultaneous drug treatment indicate that COPI and ATGL function in the same pathway. These data indicate that the COPI complex is an evolutionarily conserved regulator of lipid homeostasis, and highlight an interaction between vesicle transport systems and lipid droplets.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "210", "doc_id": "13794374", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Hematopoietic Stem Cell purification reaches purity rate of up to 50%.\n\nCANDIDATE_PASSAGE:\nCombined Single-Cell Functional and Gene Expression Analysis Resolves Heterogeneity within Stem Cell Populations Heterogeneity within the self-renewal durability of adult hematopoietic stem cells (HSCs) challenges our understanding of the molecular framework underlying HSC function. Gene expression studies have been hampered by the presence of multiple HSC subtypes and contaminating non-HSCs in bulk HSC populations. To gain deeper insight into the gene expression program of murine HSCs, we combined single-cell functional assays with flow cytometric index sorting and single-cell gene expression assays. Through bioinformatic integration of these datasets, we designed an unbiased sorting strategy that separates non-HSCs away from HSCs, and single-cell transplantation experiments using the enriched population were combined with RNA-seq data to identify key molecules that associate with long-term durable self-renewal, producing a single-cell molecular dataset that is linked to functional stem cell activity. Finally, we demonstrated the broader applicability of this approach for linking key molecules with defined cellular functions in another stem cell system.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "508", "doc_id": "13980338", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: PDPN promotes efficient motility along stromal surfaces by activating the C-type lectin receptor to rearrange the actin cytoskeleton in dendritic cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Diminished performance on neuropsychological testing in late life depression is correlated with microstructural white matter abnormalities.\nABSTRACT: BACKGROUND Traditional T2 weighted MR imaging results are non-specific for the extent of underlying white matter structural abnormalities present in late life depression (LLD). Diffusion tensor imaging provides a unique opportunity to investigate the extent and nature of structural injury, but has been limited by examining only a subset of regions of interest (ROI) and by confounds common to the study of an elderly population, including comorbid vascular pathology. Furthermore, comprehensive correlation of diffusion tensor imaging (DTI) measurements, including axial and radial diffusivity measurements, has not been demonstrated in the late life depression population. METHODS 51 depressed and 16 non-depressed, age- and cerebrovascular risk factor-matched elderly subjects underwent traditional anatomic T1 and T2 weight imaging, as well as DTI. The DTI data were skeletonized using tract based spatial statistics (TBSS), and both regional and global analyses were performed. RESULTS Widespread structural abnormalities within white matter were detected in the LLD group, accounting for age, gender and education and matched for cerebrovascular risk factors and global T2 white matter hyperintensities (T2WMH). Regional differences were most prominent in uncinate and cingulate white matter and were generally characterized by an increase in radial diffusivity. Age-related changes particularly in the cingulate bundle were more advanced in individuals with LLD relative to controls. Regression analysis demonstrated significant correlations of regional fractional anisotropy and radial diffusivity with five different neuropsychological factor scores. TBSS analysis demonstrated a greater extent of white matter abnormalities in LLD not responsive to treatment, as compared to co [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 904, "doc_id": "1412089", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: AMP-activated protein kinase (AMPK) activation increases inflammation-related fibrosis in the lungs.\n\nCANDIDATE_ABSTRACT:\nTITLE: Prognostic importance of 6-mercaptopurine dose intensity in acute lymphoblastic leukemia.\nABSTRACT: 6-Mercaptopurine (6MP) and methotrexate are the backbone of continuation therapy for childhood acute lymphoblastic leukemia (ALL). In studies of oral 6MP and methotrexate, indices of chronic systemic exposure to active metabolites of these agents, namely, red blood cell (RBC) concentrations of methotrexate polyglutamates (MTXPGs) and thioguanine nucleotides (TGNs) have positively correlated with event-free survival (EFS). Our objective was to evaluate whether MTXPGs, TGNs, and the dose intensity of administered methotrexate and 6MP were prognostic in the setting of a treatment protocol in which all treatment was coordinated through a single center, and the weekly doses of methotrexate were given parenterally. On protocol Total XII, 182 children achieved remission and received weekly methotrexate 40 mg/m2 parenterally and daily oral 6MP, interrupted every 6 weeks during the first year by pulse chemotherapy. A total of 709 TGN, 418 MTX-PG, and 267 thiopurine methyltransferase (TPMT) measurements, along with complete dose intensity information (dose received divided by protocol dose per week) for 19,046 weeks of 6MP and methotrexate, were analyzed. In univariate analyses, only higher dose intensity of 6MP and of weekly methotrexate were significant predictors of overall EFS (P =.006 and. 039, respectively). The occurrence of neutropenia was associated with worse outcome (P =.040). In a multivariate analysis, only higher dose intensity of 6MP (P =.020) was a significant predictor of EFS, with lower TPMT activity (P =.096) tending to associate with better outcome. 6MP dose intensity was also associated (P =.007) with EFS among patients with homozygous wild-type TPMT phenotype. Lower 6MP dose intensity was primarily due to missed weeks of therapy and not to reduct [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 54, "doc_id": "1373287", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Upon viral challenge, influenza-specific memory CD4+ T cells greatly diminish the early production of inflammatory chemokines in the lung.\n\nCANDIDATE_ABSTRACT:\nTITLE: Memory CD4+ T cells induce innate responses independently of pathogen\nABSTRACT: Inflammation induced by recognition of pathogen-associated molecular patterns markedly affects subsequent adaptive responses. We asked whether the adaptive immune system can also affect the character and magnitude of innate inflammatory responses. We found that the response of memory, but not naive, CD4+ T cells enhances production of multiple innate inflammatory cytokines and chemokines (IICs) in the lung and that, during influenza infection, this leads to early control of virus. Memory CD4+ T cell–induced IICs and viral control require cognate antigen recognition and are optimal when memory cells are either T helper type 1 (TH1) or TH17 polarized but are independent of interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) production and do not require activation of conserved pathogen recognition pathways. This represents a previously undescribed mechanism by which memory CD4+ T cells induce an early innate response that enhances immune protection against pathogens.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We found that the response of memory, but not naive, CD4+ T cells enhances production of multiple innate inflammatory cytokines and chemokines (IICs) in the lung and that, during influenza infection, this leads to early control of virus.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1347, "doc_id": "19005293", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: In breast cancer, the loss of myoepithelial cells slows the transition of ductal carcinoma in situ to invasive carcinoma.\n\nCANDIDATE_PASSAGE:\nRegulation of in situ to invasive breast carcinoma transition. The transition of ductal carcinoma in situ (DCIS) to invasive carcinoma is a poorly understood key event in breast tumor progression. Here, we analyzed the role of myoepithelial cells and fibroblasts in the progression of in situ carcinomas using a model of human DCIS and primary breast tumors. Progression to invasion was promoted by fibroblasts and inhibited by normal myoepithelial cells. Molecular profiles of isolated luminal epithelial and myoepithelial cells identified an intricate interaction network involving TGFbeta, Hedgehog, cell adhesion, and p63 required for myoepithelial cell differentiation, the elimination of which resulted in loss of myoepithelial cells and progression to invasion.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "571", "doc_id": "20333864", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Tonic signaling from the scFv is amplified by MyD88/CD40.\n\nCANDIDATE_PASSAGE:\nTie2/Angiopoietin-1 Signaling Regulates Hematopoietic Stem Cell Quiescence in the Bone Marrow Niche The quiescent state is thought to be an indispensable property for the maintenance of hematopoietic stem cells (HSCs). Interaction of HSCs with their particular microenvironments, known as the stem cell niches, is critical for adult hematopoiesis in the bone marrow (BM). Here, we demonstrate that HSCs expressing the receptor tyrosine kinase Tie2 are quiescent and antiapoptotic, and comprise a side-population (SP) of HSCs, which adhere to osteoblasts (OBs) in the BM niche. The interaction of Tie2 with its ligand Angiopoietin-1 (Ang-1) induced cobblestone formation of HSCs in vitro and maintained in vivo long-term repopulating activity of HSCs. Furthermore, Ang-1 enhanced the ability of HSCs to become quiescent and induced adhesion to bone, resulting in protection of the HSC compartment from myelosuppressive stress. These data suggest that the Tie2/Ang-1 signaling pathway plays a critical role in the maintenance of HSCs in a quiescent state in the BM niche.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1308", "doc_id": "17271462", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Do emergency medical services professionals think they should participate in disease prevention?\n\nABSTRACT:\nThe primary objective of the study was to determine emergency medical services (EMS) professionals' opinions regarding participation in disease and injury prevention programs. A secondary objective was to determine the proportion of EMS professionals who had participated in disease prevention programs. As part of the National Registry of Emergency Medical Technicians' biennial reregistration process, EMS professionals reregistering in 2006 were asked to complete an optional survey regarding their opinions on and participation in disease and injury prevention. Demographic characteristics were also collected. Data were analyzed using descriptive statistics and 99% confidence intervals (CIs). The chi-square test was used to compare differences by responder demographics (alpha = 0.01). A 10% difference between groups was determined to be clinically significant. The survey was completed by 27,233 EMS professionals. Of these responders, 82.7% (99% CI: 82.1-83.3) felt that EMS professionals should participate in disease prevention, with those working 20 to 29 hours per week being the least likely to think they should participate (67.4%, p<0.001). About a third, 33.8% (99% CI: 33.1-34.6), of the respondents reported having provided prevention services, with those having a graduate degree (43.5%, p<0.001), those working in EMS for more than 21 years (44%, p<0.001), those working for the military (57%, p<0.001), those working 60 to 69 hours per week (41%, p<0.001), and those responding to zero emergency calls in a typical week (43%, p<0.001) being the most likely to report having provided prevention services. About half, 51.1% (99% CI: 50.4-51.9), of the respondents agreed that prevention services should be provided during emergency calls, and 7.7% (99% CI: 7.3-8.1) o [TRUNCATED]", "output": "{\"label\": \"maybe\", \"rationale\": \"The majority of EMS professionals thought that they should participate in disease and injury prevention programs. The respondents were mixed as to whether prevention services should be provided while on emergency calls, but those with experience providing these services were more likely to agree with providing them during emergency calls.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 19145527, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The M2-phenotype in brown adipose tissue macrophages increases brown adipose tissue thermogenic activity.\n\nCANDIDATE_PASSAGE:\nAlternatively activated macrophages produce catecholamines to sustain adaptive thermogenesis All homeotherms use thermogenesis to maintain their core body temperature, ensuring that cellular functions and physiological processes can continue in cold environments. In the prevailing model of thermogenesis, when the hypothalamus senses cold temperatures it triggers sympathetic discharge, resulting in the release of noradrenaline in brown adipose tissue and white adipose tissue. Acting via the β(3)-adrenergic receptors, noradrenaline induces lipolysis in white adipocytes, whereas it stimulates the expression of thermogenic genes, such as PPAR-γ coactivator 1a (Ppargc1a), uncoupling protein 1 (Ucp1) and acyl-CoA synthetase long-chain family member 1 (Acsl1), in brown adipocytes. However, the precise nature of all the cell types involved in this efferent loop is not well established. Here we report in mice an unexpected requirement for the interleukin-4 (IL-4)-stimulated program of alternative macrophage activation in adaptive thermogenesis. Exposure to cold temperature rapidly promoted alternative activation of adipose tissue macrophages, which secrete catecholamines to induce thermogenic gene expression in brown adipose tissue and lipolysis in white adipose tissue. Absence of alternatively activated macrophages impaired metabolic adaptations to cold, whereas administration of IL-4 increased thermogenic gene expression, fatty acid mobilization and energy expenditure, all in a macrophage-dependent manner. Thus, we have discovered a role for alternatively activated macrophages in the orchestration of an important mammalian stress response, the response to cold.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1169", "doc_id": "4319174", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Medications to treat obesity have unwanted side effects.\n\nCANDIDATE_PASSAGE:\nThe S. cerevisiae Rrm3p DNA helicase moves with the replication fork and affects replication of all yeast chromosomes. The Saccharomyces cerevisiae DNA helicase Rrm3p is needed for normal fork progression through >1000 discrete sites scattered throughout the genome. Here we show that replication of all yeast chromosomes was markedly delayed in rrm3 cells. Delayed replication was seen even in a region that lacks any predicted Rrm3p-dependent sites. Based on the pattern of replication intermediates in two-dimensional gels, the rate of fork movement in rrm3 cells appeared similar to wild-type except at known Rrm3p-dependent sites. These data suggest that although Rrm3p has a global role in DNA replication, its activity is needed only or primarily at specific, difficult-to-replicate sites. By the criterion of chromatin immunoprecipitation, Rrm3p was associated with both Rrm3p-dependent and -independent sites, and moved with the replication fork through both. In addition, Rrm3p interacted with Pol2p, the catalytic subunit of DNA polymerase epsilon, in vivo. Thus, rather than being recruited to its sites of action when replication forks stall at these sites, Rrm3p is likely a component of the replication fork apparatus.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "766", "doc_id": "26083387", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Hematopoietic Stem Cell purification reaches purity rates above 90%.\n\nCANDIDATE_PASSAGE:\nCombined Single-Cell Functional and Gene Expression Analysis Resolves Heterogeneity within Stem Cell Populations Heterogeneity within the self-renewal durability of adult hematopoietic stem cells (HSCs) challenges our understanding of the molecular framework underlying HSC function. Gene expression studies have been hampered by the presence of multiple HSC subtypes and contaminating non-HSCs in bulk HSC populations. To gain deeper insight into the gene expression program of murine HSCs, we combined single-cell functional assays with flow cytometric index sorting and single-cell gene expression assays. Through bioinformatic integration of these datasets, we designed an unbiased sorting strategy that separates non-HSCs away from HSCs, and single-cell transplantation experiments using the enriched population were combined with RNA-seq data to identify key molecules that associate with long-term durable self-renewal, producing a single-cell molecular dataset that is linked to functional stem cell activity. Finally, we demonstrated the broader applicability of this approach for linking key molecules with defined cellular functions in another stem cell system.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "509", "doc_id": "13980338", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Converting apoE4 to apoE3 by gene editing worsens the pathology associated with apoE4 in human iPSCderived neurons.\n\nCANDIDATE_ABSTRACT:\nTITLE: Gain of toxic Apolipoprotein E4 effects in Human iPSC-Derived Neurons Is Ameliorated by a Small-Molecule Structure Corrector\nABSTRACT: Efforts to develop drugs for Alzheimer's disease (AD) have shown promise in animal studies, only to fail in human trials, suggesting a pressing need to study AD in human model systems. Using human neurons derived from induced pluripotent stem cells that expressed apolipoprotein E4 (ApoE4), a variant of the APOE gene product and the major genetic risk factor for AD, we demonstrated that ApoE4-expressing neurons had higher levels of tau phosphorylation, unrelated to their increased production of amyloid-β (Aβ) peptides, and that they displayed GABAergic neuron degeneration. ApoE4 increased Aβ production in human, but not in mouse, neurons. Converting ApoE4 to ApoE3 by gene editing rescued these phenotypes, indicating the specific effects of ApoE4. Neurons that lacked APOE behaved similarly to those expressing ApoE3, and the introduction of ApoE4 expression recapitulated the pathological phenotypes, suggesting a gain of toxic effects from ApoE4. Treatment of ApoE4-expressing neurons with a small-molecule structure corrector ameliorated the detrimental effects, thus showing that correcting the pathogenic conformation of ApoE4 is a viable therapeutic approach for ApoE4-related AD.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Converting ApoE4 to ApoE3 by gene editing rescued these phenotypes, indicating the specific effects of ApoE4.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 287, "doc_id": "4709641", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Cyclin A2 destruction is necessary to switch from unstable to stable kt-mt attachments in mitosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cyclin A Regulates Kinetochore-Microtubules to Promote Faithful Chromosome Segregation\nABSTRACT: The most conspicuous event in the cell cycle is the alignment of chromosomes in metaphase. Chromosome alignment fosters faithful segregation through the formation of bi-oriented attachments of kinetochores to spindle microtubules. Notably, numerous kinetochore-microtubule (k-MT) attachment errors are present in early mitosis (prometaphase), and the persistence of those errors is the leading cause of chromosome mis-segregation in aneuploid human tumour cells that continually mis-segregate whole chromosomes and display chromosomal instability. How robust error correction is achieved in prometaphase to ensure error-free mitosis remains unknown. Here we show that k-MT attachments in prometaphase cells are considerably less stable than in metaphase cells. The switch to more stable k-MT attachments in metaphase requires the proteasome-dependent destruction of cyclin A in prometaphase. Persistent cyclin A expression prevents k-MT stabilization even in cells with aligned chromosomes. By contrast, k-MTs are prematurely stabilized in cyclin-A-deficient cells. Consequently, cells lacking cyclin A display higher rates of chromosome mis-segregation. Thus, the stability of k-MT attachments increases decisively in a coordinated fashion among all chromosomes as cells transit from prometaphase to metaphase. Cyclin A creates a cellular environment that promotes microtubule detachment from kinetochores in prometaphase to ensure efficient error correction and faithful chromosome segregation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Persistent cyclin A expression prevents k-MT stabilization even in cells with aligned chromosomes.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 296, "doc_id": "4398832", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: 53% of perinatal mortality is due to low birth weight.\n\nCANDIDATE_ABSTRACT:\nTITLE: Estimates of global prevalence of childhood underweight in 1990 and 2015.\nABSTRACT: CONTEXT One key target of the United Nations Millennium Development goals is to reduce the prevalence of underweight among children younger than 5 years by half between 1990 and 2015. OBJECTIVE To estimate trends in childhood underweight by geographic regions of the world. DESIGN, SETTING, AND PARTICIPANTS Time series study of prevalence of underweight, defined as weight 2 SDs below the mean weight for age of the National Center for Health Statistics and World Health Organization (WHO) reference population. National prevalence rates derived from the WHO Global Database on Child Growth and Malnutrition, which includes data on approximately 31 million children younger than 5 years who participated in 419 national nutritional surveys in 139 countries from 1965 through 2002. MAIN OUTCOME MEASURES Linear mixed-effects modeling was used to estimate prevalence rates and numbers of underweight children by region in 1990 and 2015 and to calculate the changes (ie, increase or decrease) to these values between 1990 and 2015. RESULTS Worldwide, underweight prevalence was projected to decline from 26.5% in 1990 to 17.6% in 2015, a change of -34% (95% confidence interval [CI], -43% to -23%). In developed countries, the prevalence was estimated to decrease from 1.6% to 0.9%, a change of -41% (95% CI, -92% to 343%). In developing regions, the prevalence was forecasted to decline from 30.2% to 19.3%, a change of -36% (95% CI, -45% to -26%). In Africa, the prevalence of underweight was forecasted to increase from 24.0% to 26.8%, a change of 12% (95% CI, 8%-16%). In Asia, the prevalence was estimated to decrease from 35.1% to 18.5%, a change of -47% (95% CI, -58% to -34%). Worldwide, the number of underweight children was projected to decline from 163.8 million in 1990 to 113. [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 17, "doc_id": "1606628", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Only a minority of cells survive development after differentiation into stress-resistant spores.\n\nCANDIDATE_PASSAGE:\nConditional Kif3a ablation causes abnormal hedgehog signaling topography, growth plate dysfunction, and excessive bone and cartilage formation during mouse skeletogenesis. The motor protein Kif3a and primary cilia regulate important developmental processes, but their roles in skeletogenesis remain ill-defined. Here we created mice deficient in Kif3a in cartilage and focused on the cranial base and synchondroses. Kif3a deficiency caused cranial base growth retardation and dysmorphogenesis, which were evident in neonatal animals by anatomical and micro-computed tomography (microCT) inspection. Kif3a deficiency also changed synchondrosis growth plate organization and function, and the severity of these changes increased over time. By postnatal day (P)7, mutant growth plates lacked typical zones of chondrocyte proliferation and hypertrophy, and were instead composed of chondrocytes with an unusual phenotype characterized by strong collagen II (Col2a1) gene expression but barely detectable expression of Indian hedgehog (Ihh), collagen X (Col10a1), Vegf (Vegfa), MMP-13 (Mmp13) and osterix (Sp7). Concurrently, unexpected developmental events occurred in perichondrial tissues, including excessive intramembranous ossification all along the perichondrial border and the formation of ectopic cartilage masses. Looking for possible culprits for these latter processes, we analyzed hedgehog signalling topography and intensity by monitoring the expression of the hedgehog effectors Patched 1 and Gli1, and of the hedgehog-binding cell-surface component syndecan 3. Compared with controls, hedgehog signaling was quite feeble within mutant growth plates as early as P0, but was actually higher and was widespread all along mutant perichondrial tissues. Lastly, we studied postnatal [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "887", "doc_id": "15365719", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Including pharmacists in rounding teams does not alter the incidence of adverse drug events (ADEs).\n\nCANDIDATE_ABSTRACT:\nTITLE: CD28 and ITK signals regulate autoreactive T cell trafficking\nABSTRACT: Activation of self-reactive T cells and their trafficking to target tissues leads to autoimmune organ destruction. Mice lacking the co-inhibitory receptor cytotoxic T lymphocyte antigen-4 (CTLA-4) develop fatal autoimmunity characterized by lymphocytic infiltration into nonlymphoid tissues. Here, we demonstrate that the CD28 co-stimulatory pathway regulates the trafficking of self-reactive Ctla4(-/-) T cells to tissues. Concurrent ablation of the CD28-activated Tec family kinase ITK does not block spontaneous T cell activation but instead causes self-reactive Ctla4(-/-) T cells to accumulate in secondary lymphoid organs. Despite excessive spontaneous T cell activation and proliferation in lymphoid organs, Itk(-/-); Ctla4(-/-) mice are otherwise healthy, mount antiviral immune responses and exhibit a long lifespan. We propose that ITK specifically licenses autoreactive T cells to enter tissues to mount destructive immune responses. Notably, ITK inhibitors mimic the null mutant phenotype and also prevent pancreatic islet infiltration by diabetogenic T cells in mouse models of type 1 diabetes, highlighting their potential utility for the treatment of human autoimmune disorders.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 600, "doc_id": "2462673", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Pharmacist attendance at ward rounds reduces adverse events in wards.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pharmacist participation on physician rounds and adverse drug events in the intensive care unit.\nABSTRACT: CONTEXT Pharmacist review of medication orders in the intensive care unit (ICU) has been shown to prevent errors, and pharmacist consultation has reduced drug costs. However, whether pharmacist participation in the ICU at the time of drug prescribing reduces adverse events has not been studied. OBJECTIVE To measure the effect of pharmacist participation on medical rounds in the ICU on the rate of preventable adverse drug events (ADEs) caused by ordering errors. DESIGN Before-after comparison between phase 1 (baseline) and phase 2 (after intervention implemented) and phase 2 comparison with a control unit that did not receive the intervention. SETTING A medical ICU (study unit) and a coronary care unit (control unit) in a large urban teaching hospital. PATIENTS Seventy-five patients randomly selected from each of 3 groups: all admissions to the study unit from February 1, 1993, through July 31, 1993 (baseline) and all admissions to the study unit (postintervention) and control unit from October 1, 1994, through July 7, 1995. In addition, 50 patients were selected at random from the control unit during the baseline period. INTERVENTION A senior pharmacist made rounds with the ICU team and remained in the ICU for consultation in the morning, and was available on call throughout the day. MAIN OUTCOME MEASURES Preventable ADEs due to ordering (prescribing) errors and the number, type, and acceptance of interventions made by the pharmacist. Preventable ADEs were identified by review of medical records of the randomly selected patients during both preintervention and postintervention phases. Pharmacists recorded all recommendations, which were then analyzed by type and acceptance. RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 pat [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS The presence of a pharmacist on rounds as a full member of the patient care team in a medical ICU was associated with a substantially lower rate of ADEs caused by prescribing errors.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 941, "doc_id": "12258338", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Primary cervical cancer screening with HPV detection has higher longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_PASSAGE:\nInfluence of smoking cessation after diagnosis of early stage lung cancer on prognosis: systematic review of observational studies with meta-analysis OBJECTIVE To systematically review the evidence that smoking cessation after diagnosis of a primary lung tumour affects prognosis. DESIGN Systematic review with meta-analysis. DATA SOURCES CINAHL (from 1981), Embase (from 1980), Medline (from 1966), Web of Science (from 1966), CENTRAL (from 1977) to December 2008, and reference lists of included studies. STUDY SELECTION Randomised controlled trials or observational longitudinal studies that measured the effect of quitting smoking after diagnosis of lung cancer on prognostic outcomes, regardless of stage at presentation or tumour histology, were included. DATA EXTRACTION Two researchers independently identified studies for inclusion and extracted data. Estimates were combined by using a random effects model, and the I(2) statistic was used to examine heterogeneity. Life tables were used to model five year survival for early stage non-small cell lung cancer and limited stage small cell lung cancer, using death rates for continuing smokers and quitters obtained from this review. RESULTS In 9/10 included studies, most patients studied were diagnosed as having an early stage lung tumour. Continued smoking was associated with a significantly increased risk of all cause mortality (hazard ratio 2.94, 95% confidence interval 1.15 to 7.54) and recurrence (1.86, 1.01 to 3.41) in early stage non-small cell lung cancer and of all cause mortality (1.86, 1.33 to 2.59), development of a second primary tumour (4.31, 1.09 to 16.98), and recurrence (1.26, 1.06 to 1.50) in limited stage small cell lung cancer. No study contained data on the effect of quitting smoking on cancer spe [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "971", "doc_id": "7639744", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Long chain polyunsaturated fatty acids supplementation is associated with lower rates of atopic eczema at 1 year.\n\nCANDIDATE_PASSAGE:\nLong-term effects of continuing adjuvant tamoxifen to 10 years versus stopping at 5 years after diagnosis of oestrogen receptor-positive breast cancer: ATLAS, a randomised trial BACKGROUND For women with oestrogen receptor (ER)-positive early breast cancer, treatment with tamoxifen for 5 years substantially reduces the breast cancer mortality rate throughout the first 15 years after diagnosis. We aimed to assess the further effects of continuing tamoxifen to 10 years instead of stopping at 5 years. METHODS In the worldwide Adjuvant Tamoxifen: Longer Against Shorter (ATLAS) trial, 12,894 women with early breast cancer who had completed 5 years of treatment with tamoxifen were randomly allocated to continue tamoxifen to 10 years or stop at 5 years (open control). Allocation (1:1) was by central computer, using minimisation. After entry (between 1996 and 2005), yearly follow-up forms recorded any recurrence, second cancer, hospital admission, or death. We report effects on breast cancer outcomes among the 6846 women with ER-positive disease, and side-effects among all women (with positive, negative, or unknown ER status). Long-term follow-up still continues. This study is registered, number ISRCTN19652633. FINDINGS Among women with ER-positive disease, allocation to continue tamoxifen reduced the risk of breast cancer recurrence (617 recurrences in 3428 women allocated to continue vs 711 in 3418 controls, p=0·002), reduced breast cancer mortality (331 deaths vs 397 deaths, p=0·01), and reduced overall mortality (639 deaths vs 722 deaths, p=0·01). The reductions in adverse breast cancer outcomes appeared to be less extreme before than after year 10 (recurrence rate ratio [RR] 0·90 [95% CI 0·79–1·02] during years 5–9 and 0·75 [0·62–0·90] in later years; breast ca [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "709", "doc_id": "12438901", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does limb-salvage surgery offer patients better quality of life and functional capacity than amputation?\n\nABSTRACT:\nPatients with aggressive lower extremity musculoskeletal tumors may be candidates for either above-knee amputation or limb-salvage surgery. However, the subjective and objective benefits of limb-salvage surgery compared with amputation are not fully clear.QUESTIONS/ We therefore compared functional status and quality of life for patients treated with above-knee amputation versus limb-salvage surgery. We reviewed 20 of 51 patients aged 15 years and older treated with above-knee amputation or limb-salvage surgery for aggressive musculoskeletal tumors around the knee between 1994 and 2004 as a retrospective cohort study. At last followup we obtained the Physiological Cost Index, the Reintegration to Normal Living Index, SF-36, and the Toronto Extremity Salvage Score questionnaires. The minimum followup was 12 months (median, 56 months; range, 12-108 months). Compared with patients having above-knee amputation, patients undergoing limb-salvage surgery had superior Physiological Cost Index scores and Reintegration to Normal Living Index. The Toronto Extremity Salvage scores and SF-36 scores were similar in the two groups.", "output": "{\"label\": \"maybe\", \"rationale\": \"These data suggest that limb-salvage surgery offers better gait efficiency and return to normal living compared with above-knee amputation, but does not improve the patient's perception of quality of life.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 22302658, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Major vault protein (MVP) leads to more aggressive tumors by regulating the sorting of tumor suppressive miR-193a into extracellular vesicles (EVs).\n\nCANDIDATE_PASSAGE:\nMVP-mediated exosomal sorting of miR-193a promotes colon cancer progression Exosomes are emerging mediators of intercellular communication; whether the release of exosomes has an effect on the exosome donor cells in addition to the recipient cells has not been investigated to any extent. Here, we examine different exosomal miRNA expression profiles in primary mouse colon tumour, liver metastasis of colon cancer and naive colon tissues. In more advanced disease, higher levels of tumour suppressor miRNAs are encapsulated in the exosomes. miR-193a interacts with major vault protein (MVP). Knockout of MVP leads to miR-193a accumulation in the exosomal donor cells instead of exosomes, inhibiting tumour progression. Furthermore, miR-193a causes cell cycle G1 arrest and cell proliferation repression through targeting of Caprin1, which upregulates Ccnd2 and c-Myc. Human colon cancer patients with more advanced disease show higher levels of circulating exosomal miR-193a. In summary, our data demonstrate that MVP-mediated selective sorting of tumour suppressor miRNA into exosomes promotes tumour progression.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "751", "doc_id": "19800147", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The combination of physical examinations with C-reactive protein values do not improve the accuracy of radiographic verified pneumonia predictions.\n\nCANDIDATE_PASSAGE:\nTyrosine-Phosphorylated Caveolin-1 Blocks Bacterial Uptake by Inducing Vav2-RhoA-Mediated Cytoskeletal Rearrangements Certain bacterial adhesins appear to promote a pathogen's extracellular lifestyle rather than its entry into host cells. However, little is known about the stimuli elicited upon such pathogen host-cell interactions. Here, we report that type IV pili (Tfp)-producing Neisseria gonorrhoeae (P(+)GC) induces an immediate recruitment of caveolin-1 (Cav1) in the host cell, which subsequently prevents bacterial internalization by triggering cytoskeletal rearrangements via downstream phosphotyrosine signaling. A broad and unbiased analysis of potential interaction partners for tyrosine-phosphorylated Cav1 revealed a direct interaction with the Rho-family guanine nucleotide exchange factor Vav2. Both Vav2 and its substrate, the small GTPase RhoA, were found to play a direct role in the Cav1-mediated prevention of bacterial uptake. Our findings, which have been extended to enteropathogenic Escherichia coli, highlight how Tfp-producing bacteria avoid host cell uptake. Further, our data establish a mechanistic link between Cav1 phosphorylation and pathogen-induced cytoskeleton reorganization and advance our understanding of caveolin function.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1205", "doc_id": "14461101", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is flow cytometric DNA analysis useful in detecting multiple genetic alterations in squamous cell carcinoma of the esophagus?\n\nABSTRACT:\nAlthough flow cytometric DNA analysis has been recognized to be a useful prognostic indicator for patients with squamous cell carcinoma of the esophagus, the biologic significance of DNA aneuploidy remains to be elucidated. Twenty-five patients with squamous cell carcinoma of the esophagus who underwent a curative subtotal esophagectomy were divided into 2 groups according to the DNA ploidy pattern. Multiple genetic changes, including the gene amplification of bcl-1, epidermal growth factor receptor, and c-myc, and the loss of heterozygosity of multiple tumor suppressor genes, including retinoblastoma, mutated in colorectal carcinoma, adenomatous polyposis coli, and deleted in colorectal carcinoma, in each case were investigated and the frequency of genetic alterations compared between both groups. In addition, the clinical outcome of these patients was also investigated. Eleven of 15 cases in the aneuploid group demonstrated at least 1 genetic change (73.3%) whereas only 2 of 10 cases in the diploid group did so (20.0%) (P<0.05). Both cases in the diploid group with genetic alterations had only 1 genetic change of 7 tested genes whereas 9 of 11 cases in the aneuploid group had multiple genetic alterations. Patients in the aneuploid group also showed a more unfavorable prognosis than patients in the diploid group.", "output": "{\"label\": \"yes\", \"rationale\": \"Based on the findings of the current study, flow cytometric DNA analysis is considered to be useful for both detecting multiple genetic alterations and predicting the prognosis of patients with carcinoma of the esophagus.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 10357400, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Autologous transplantation of mesenchymal stem cells causes a higher rate of opportunistic infections than induction therapy with anti-interleukin-2 receptor antibodies.\n\nCANDIDATE_ABSTRACT:\nTITLE: Histone deacetylase 5 interacts with Krüppel-like factor 2 and inhibits its transcriptional activity in endothelium.\nABSTRACT: AIMS Vascular endothelial dysfunction and inflammation are hallmarks of atherosclerosis. Krüppel-like factor 2 (KLF2) is a key mediator of anti-inflammatory and anti-atherosclerotic properties of the endothelium. However, little is known of the molecular mechanisms for regulating KLF2 transcriptional activation. METHODS AND RESULTS Here, we found that histone deacetylase 5 (HDAC5) associates with KLF2 and represses KLF2 transcriptional activation. HDAC5 resided with KLF2 in the nuclei of human umbilical cord vein endothelial cells (HUVECs). Steady laminar flow attenuated the association of HDAC5 with KLF2 via stimulating HDAC5 phosphorylation-dependent nuclear export in HUVEC. We also mapped the KLF2-HDAC5-interacting domains and found that the N-terminal region of HDAC5 interacts with the C-terminal domain of KLF2. Chromatin immunoprecipitation and luciferase reporter assays showed that HDAC5 through a direct association with KLF2 suppressed KLF2 transcriptional activation. HDAC5 overexpression inhibited KLF2-dependent endothelial nitric oxide synthesis (eNOS) promoter activity in COS7 cell and gene expression in both HUVECs and bovine aortic endothelial cells (BAECs). Conversely, HDAC5 silencing enhanced KLF2 transcription and hence eNOS expression in HUVEC. Moreover, we observed that the level of eNOS protein in the thoracic aorta isolated from HDAC5 knockout mice was higher, whereas expression of pro-inflammatory vascular cell adhesion molecule 1 was lower, compared with those of HDAC5 wild-type mice. CONCLUSIONS We reveal a novel role of HDAC5 in modulating the KLF2 transcriptional activation and eNOS expression. These findings suggest that HDAC5, a binding partner and modulator of KLF2, could be a new therapeutic target to prevent vascular endothelial [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 142, "doc_id": "2316374", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The risk of male prisoners harming themselves is ten times that of female prisoners.\n\nCANDIDATE_ABSTRACT:\nTITLE: Self-harm in prisons in England and Wales: an epidemiological study of prevalence, risk factors, clustering, and subsequent suicide\nABSTRACT: BACKGROUND Self-harm and suicide are common in prisoners, yet robust information on the full extent and characteristics of people at risk of self-harm is scant. Furthermore, understanding how frequently self-harm is followed by suicide, and in which prisoners this progression is most likely to happen, is important. We did a case-control study of all prisoners in England and Wales to ascertain the prevalence of self-harm in this population, associated risk factors, clustering effects, and risk of subsequent suicide after self-harm. METHODS Records of self-harm incidents in all prisons in England and Wales were gathered routinely between January, 2004, and December, 2009. We did a case-control comparison of prisoners who self-harmed and those who did not between January, 2006, and December, 2009. We also used a Bayesian approach to look at clustering of people who self-harmed. Prisoners who self-harmed and subsequently died by suicide in prison were compared with other inmates who self-harmed. FINDINGS 139,195 self-harm incidents were recorded in 26,510 individual prisoners between 2004 and 2009; 5-6% of male prisoners and 20-24% of female inmates self-harmed every year. Self-harm rates were more than ten times higher in female prisoners than in male inmates. Repetition of self-harm was common, particularly in women and teenage girls, in whom a subgroup of 102 prisoners accounted for 17,307 episodes. In both sexes, self-harm was associated with younger age, white ethnic origin, prison type, and a life sentence or being unsentenced; in female inmates, committing a violent offence against an individual was also a factor. Substantial evidence was noted of clustering in time and location of prisoners who self-harmed (adjusted intra-class correlation 0·15, 95% CI 0 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"FINDINGS 139,195 self-harm incidents were recorded in 26,510 individual prisoners between 2004 and 2009; 5-6% of male prisoners and 20-24% of female inmates self-harmed every year.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1270, "doc_id": "13900610", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cost effectiveness evaluations based on cRCT data lack external validity.\n\nCANDIDATE_ABSTRACT:\nTITLE: A Comparison of Cost Effectiveness Using Data from Randomized Trials or Actual Clinical Practice: Selective Cox-2 Inhibitors as an Example\nABSTRACT: BACKGROUND Data on absolute risks of outcomes and patterns of drug use in cost-effectiveness analyses are often based on randomised clinical trials (RCTs). The objective of this study was to evaluate the external validity of published cost-effectiveness studies by comparing the data used in these studies (typically based on RCTs) to observational data from actual clinical practice. Selective Cox-2 inhibitors (coxibs) were used as an example. METHODS AND FINDINGS The UK General Practice Research Database (GPRD) was used to estimate the exposure characteristics and individual probabilities of upper gastrointestinal (GI) events during current exposure to nonsteroidal anti-inflammatory drugs (NSAIDs) or coxibs. A basic cost-effectiveness model was developed evaluating two alternative strategies: prescription of a conventional NSAID or coxib. Outcomes included upper GI events as recorded in GPRD and hospitalisation for upper GI events recorded in the national registry of hospitalisations (Hospital Episode Statistics) linked to GPRD. Prescription costs were based on the prescribed number of tables as recorded in GPRD and the 2006 cost data from the British National Formulary. The study population included over 1 million patients prescribed conventional NSAIDs or coxibs. Only a minority of patients used the drugs long-term and daily (34.5% of conventional NSAIDs and 44.2% of coxibs), whereas coxib RCTs required daily use for at least 6-9 months. The mean cost of preventing one upper GI event as recorded in GPRD was US$104k (ranging from US$64k with long-term daily use to US$182k with intermittent use) and US$298k for hospitalizations. The mean costs (for GPRD events) over calendar time were US$58k during 1990-1993 and US$174k during 2002-2005. Using RCT data rather [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Only a minority of patients used the drugs long-term and daily (34.5% of conventional NSAIDs and 44.2% of coxibs), whereas coxib RCTs required daily use for at least 6-9 months.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 292, "doc_id": "15048300", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Crossover hot spots are not found within gene promoters in Saccharomyces cerevisiae.\n\nCANDIDATE_PASSAGE:\nCoordinate regulation of the IL-4, IL-13, and IL-5 cytokine cluster in Th2 clones revealed by allelic expression patterns. The cytokines IL-4, IL-13, and IL-5 are markers for the Th2 subset of effector T cells and are often expressed together. These cytokine genes are organized within 140 kb of orthologous DNA in both mouse and human. Using IL-4-expressing CD4+ T cell clones derived from F1 mice, we identified allelic polymorphisms for each of these cytokines and assessed the parental identity of the cytokine mRNAs. Both monoallelic and biallelic expression occurred for each gene and for an additional gene, IL-3, that lies with GM-CSF over 450 kb telomeric on the same chromosome. When coexpressed in T cell clones, IL-4 was expressed from the same allele as IL-13 or IL-5 in 81% of instances. In contrast, there was only 52% concordance of these three cytokines at the allelic level among clones that expressed IL-3. Independent expression of the cytokine alleles occurs commonly in T cells, but the clustered locus encompassing IL-4, IL-13, and IL-5 is subject to coordinate regulation.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "294", "doc_id": "36242796", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Converting apoE4 to apoE3 by gene editing worsens the pathology associated with apoE4 in human iPSCderived neurons.\n\nCANDIDATE_ABSTRACT:\nTITLE: The behaviour change wheel: A new method for characterising and designing behaviour change interventions\nABSTRACT: BACKGROUND Improving the design and implementation of evidence-based practice depends on successful behaviour change interventions. This requires an appropriate method for characterising interventions and linking them to an analysis of the targeted behaviour. There exists a plethora of frameworks of behaviour change interventions, but it is not clear how well they serve this purpose. This paper evaluates these frameworks, and develops and evaluates a new framework aimed at overcoming their limitations. METHODS A systematic search of electronic databases and consultation with behaviour change experts were used to identify frameworks of behaviour change interventions. These were evaluated according to three criteria: comprehensiveness, coherence, and a clear link to an overarching model of behaviour. A new framework was developed to meet these criteria. The reliability with which it could be applied was examined in two domains of behaviour change: tobacco control and obesity. RESULTS Nineteen frameworks were identified covering nine intervention functions and seven policy categories that could enable those interventions. None of the frameworks reviewed covered the full range of intervention functions or policies, and only a minority met the criteria of coherence or linkage to a model of behaviour. At the centre of a proposed new framework is a 'behaviour system' involving three essential conditions: capability, opportunity, and motivation (what we term the 'COM-B system'). This forms the hub of a 'behaviour change wheel' (BCW) around which are positioned the nine intervention functions aimed at addressing deficits in one or more of these conditions; around this are placed seven categories of policy that could enable those interventions to occur. The BCW was us [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 287, "doc_id": "704526", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Beta-band coherence is diminished for visible stimuli over invisible stimuli.\n\nCANDIDATE_PASSAGE:\nA transition in brain state during propofol-induced unconsciousness. Rhythmic oscillations shape cortical dynamics during active behavior, sleep, and general anesthesia. Cross-frequency phase-amplitude coupling is a prominent feature of cortical oscillations, but its role in organizing conscious and unconscious brain states is poorly understood. Using high-density EEG and intracranial electrocorticography during gradual induction of propofol general anesthesia in humans, we discovered a rapid drug-induced transition between distinct states with opposite phase-amplitude coupling and different cortical source distributions. One state occurs during unconsciousness and may be similar to sleep slow oscillations. A second state occurs at the loss or recovery of consciousness and resembles an enhanced slow cortical potential. These results provide objective electrophysiological landmarks of distinct unconscious brain states, and could be used to help improve EEG-based monitoring for general anesthesia.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "174", "doc_id": "8734695", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Mutations in G-Beta protein GNB1 are present in many cancers, resulting in loss of interaction with G-alpha subunits and concomitant activation of AKT pathway.\n\nCANDIDATE_PASSAGE:\nMutations in G protein beta subunits promote transformation and kinase inhibitor resistance Activating mutations in genes encoding G protein α (Gα) subunits occur in 4-5% of all human cancers, but oncogenic alterations in Gβ subunits have not been defined. Here we demonstrate that recurrent mutations in the Gβ proteins GNB1 and GNB2 confer cytokine-independent growth and activate canonical G protein signaling. Multiple mutations in GNB1 affect the protein interface that binds Gα subunits as well as downstream effectors and disrupt Gα interactions with the Gβγ dimer. Different mutations in Gβ proteins clustered partly on the basis of lineage; for example, all 11 GNB1 K57 mutations were in myeloid neoplasms, and seven of eight GNB1 I80 mutations were in B cell neoplasms. Expression of patient-derived GNB1 variants in Cdkn2a-deficient mouse bone marrow followed by transplantation resulted in either myeloid or B cell malignancies. In vivo treatment with the dual PI3K-mTOR inhibitor BEZ235 suppressed GNB1-induced signaling and markedly increased survival. In several human tumors, mutations in the gene encoding GNB1 co-occurred with oncogenic kinase alterations, including the BCR-ABL fusion protein, the V617F substitution in JAK2 and the V600K substitution in BRAF. Coexpression of patient-derived GNB1 variants with these mutant kinases resulted in inhibitor resistance in each context. Thus, GNB1 and GNB2 alterations confer transformed and resistance phenotypes across a range of human tumors and may be targetable with inhibitors of G protein signaling.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "813", "doc_id": "33387953", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: YAP/TAZ is required in intestinal regeneration in mouse models of ulcerative colitis.\n\nCANDIDATE_PASSAGE:\nYAP/TAZ-Dependent Reprogramming of Colonic Epithelium Links ECM Remodeling to Tissue Regeneration Tissue regeneration requires dynamic cellular adaptation to the wound environment. It is currently unclear how this is orchestrated at the cellular level and how cell fate is affected by severe tissue damage. Here we dissect cell fate transitions during colonic regeneration in a mouse dextran sulfate sodium (DSS) colitis model, and we demonstrate that the epithelium is transiently reprogrammed into a primitive state. This is characterized by de novo expression of fetal markers as well as suppression of markers for adult stem and differentiated cells. The fate change is orchestrated by remodeling the extracellular matrix (ECM), increased FAK/Src signaling, and ultimately YAP/TAZ activation. In a defined cell culture system recapitulating the extracellular matrix remodeling observed in vivo, we show that a collagen 3D matrix supplemented with Wnt ligands is sufficient to sustain endogenous YAP/TAZ and induce conversion of cell fate. This provides a simple model for tissue regeneration, implicating cellular reprogramming as an essential element.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1381", "doc_id": "13481880", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Helminths interfere with immune system control of coinfections by microbial pathogens 16.\n\nCANDIDATE_PASSAGE:\nAge-structured red blood cell susceptibility and the dynamics of malaria infections. Malaria parasites and immune responses in an infected human interact on a dynamic landscape, in which a population of replicating parasites depletes a population of replenishing red blood cells (RBCs). These underlying dynamics receive relatively little attention, but they offer unique insights into the processes that control most malaria infections. Here, we focus on the observation that three of the four malaria-parasite species that infect humans are restricted to particular age classes of RBC. We explicitly incorporate this observation in models of infection dynamics to distinguish common from species-specific pressures on host immune responses, and we find that age structuring has profound effects on the course of infection. For all four species conditions exist under which the parasites may persist at low densities, or may clear, even in the absence of an immune response. Catastrophic anemia can occur even with the two species that attack only the youngest RBCs, although only a small fraction of cells are parasitized at any point. Furthermore, with these two, compensatory erythropoetic responses in the host accelerate parasite population growth. A \"basic reproduction rate\" characterizes these differences in outcomes.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "506", "doc_id": "26474812", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Lack of FGF21 in mice increases life expectancy.\n\nCANDIDATE_PASSAGE:\nFibroblast Growth Factor 21 Prevents Atherosclerosis by Suppression of Hepatic Sterol Regulatory Element-Binding Protein-2 and Induction of Adiponectin in Mice BACKGROUND Fibroblast growth factor 21 (FGF21) is a metabolic hormone with pleiotropic effects on glucose and lipid metabolism and insulin sensitivity. It acts as a key downstream target of both peroxisome proliferator-activated receptor α and γ, the agonists of which have been used for lipid lowering and insulin sensitization, respectively. However, the role of FGF21 in the cardiovascular system remains elusive. METHODS AND RESULTS The roles of FGF21 in atherosclerosis were investigated by evaluating the impact of FGF21 deficiency and replenishment with recombinant FGF21 in apolipoprotein E(-/-) mice. FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia. Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia. Chronic treatment with adiponectin partially reverses atherosclerosis without obvious effects on hypercholesterolemia in FGF21-deficient apolipoprotein E(-/-) mice. By contrast, the cholesterol-lowering effects of FGF21 are abrogated by hepatic expression of sterol regulatory element-binding protein-2. CONCLUSIONS FGF21 protects against at [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "680", "doc_id": "9315213", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Having a main partner improves HIV outcomes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\nABSTRACT: OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART). DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study). SETTING Seven outpatient clinics throughout Switzerland. PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years). MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound. RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion. When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership. In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without. Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression. CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 495, "doc_id": "17077004", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Obesity is determined solely by environmental factors.\n\nCANDIDATE_ABSTRACT:\nTITLE: Genetic analysis of human obesity in an Italian sample.\nABSTRACT: An analysis of the genetic factors in obesity has been carried out on a sample of nuclear families from Aosta (N. Italy). The families consisted of the parents and sibs of all elementary school children considered to be obese during a preliminary screening and a similar sample of non-obese children and their nuclear families. The numbers of such families were 67 and 112, respectively. Several tests were applied in order to examine the genetic contribution to obesity, and in particular to investigate the presence of a dominant major gene. Our conclusions are that genetic factors are certainly present. Several analyses suggest the presence of a dominant major gene with weak effect.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Our conclusions are that genetic factors are certainly present.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 873, "doc_id": "3315558", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Differentiated E2f-1, -2, -3 TKO cells in the intestine do not exhibit apoptosis.\n\nCANDIDATE_PASSAGE:\nE2F1-3 Switch from Activators in Progenitor Cells to Repressors in Differentiating Cells In the established model of mammalian cell cycle control, the retinoblastoma protein (Rb) functions to restrict cells from entering S phase by binding and sequestering E2f activators (E2f1, E2f2 and E2f3), which are invariably portrayed as the ultimate effectors of a transcriptional program that commit cells to enter and progress through S phase. Using a panel of tissue-specific cre-transgenic mice and conditional E2f alleles we examined the effects of E2f1, E2f2 and E2f3 triple deficiency in murine embryonic stem cells, embryos and small intestines. We show that in normal dividing progenitor cells E2f1-3 function as transcriptional activators, but contrary to the current view, are dispensable for cell division and instead are necessary for cell survival. In differentiating cells E2f1-3 function in a complex with Rb as repressors to silence E2f targets and facilitate exit from the cell cycle. The inactivation of Rb in differentiating cells resulted in a switch of E2f1-3 from repressors to activators, leading to the superactivation of E2f responsive targets and ectopic cell divisions. Loss of E2f1-3 completely suppressed these phenotypes caused by Rb deficiency. This work contextualizes the activator versus repressor functions of E2f1-3 in vivo, revealing distinct roles in dividing versus differentiating cells and in normal versus cancer-like cell cycles.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "345", "doc_id": "4394817", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The innate immune response struggles to remove small numbers of parasites.\n\nCANDIDATE_PASSAGE:\nMice deficient in CD4 T cells have only transiently diminished levels of IFN-gamma, yet succumb to tuberculosis. CD4 T cells are important in the protective immune response against tuberculosis. Two mouse models deficient in CD4 T cells were used to examine the mechanism by which these cells participate in protection against Mycobacterium tuberculosis challenge. Transgenic mice deficient in either MHC class II or CD4 molecules demonstrated increased susceptibility to M. tuberculosis, compared with wild-type mice. MHC class II-/- mice were more susceptible than CD4-/- mice, as measured by survival following M. tuberculosis challenge, but the relative resistance of CD4-/- mice did not appear to be due to increased numbers of CD4-8- (double-negative) T cells. Analysis of in vivo IFN-gamma production in the lungs of infected mice revealed that both mutant mouse strains were only transiently impaired in their ability to produce IFN-gamma following infection. At 2 wk postinfection, IFN-gamma production, assessed by RT-PCR and intracellular cytokine staining, in the mutant mice was reduced by >50% compared with that in wild-type mice. However, by 4 wk postinfection, both mutant and wild-type mice had similar levels of IFN-gamma mRNA and protein production. In CD4 T cell-deficient mice, IFN-gamma production was due to CD8 T cells. Thus, the importance of IFN-gamma production by CD4 T cells appears to be early in infection, lending support to the hypothesis that early events in M. tuberculosis infection are crucial determinants of the course of infection.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1223", "doc_id": "21878751", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does vaginal intraepithelial neoplasia have the same evolution as cervical intraepithelial neoplasia?\n\nABSTRACT:\nVaginal intraepithelial neoplasia is a little known disease which could be related to risk factors different from simple HPV infections. To ascertain wheter vaginal lesions have a natural history similar to cervical lesions.MATERIALS & A retrospective study to identify patients with vaginal lesions and synchronous cervical lesions through biopsy. The rate of mild cervical lesions (koilocytosis, warts, CIN I with and without koilocytosis) was compared with the rate of severe cervical lesions (CIN II and III, cervical carcinoma) in patients with mild vaginal lesions (warts and koilocytosis, and low-grade VAIN) and in patients with severe vaginal lesions (high-grade VAIN). Using koilocytosis as a marker, the rate of \"active\" cervical lesions was compared with the rate of \"non active\" cervical lesions in patients with \"active\" versus \"non active\" vaginal lesions. Finally, the rates of mild and severe cervical lesions were compared among each group of VAIN (low-grade, high-grade, with or without koilocytosis). In patients with mild vaginal lesions, mild cervical lesions were significantly more frequent than severe cervical lesions. In patients with \"active\" vaginal lesions the rate of \"active\" cervical lesions was significantly higher than \"non active\" cervical lesions. The differences in rates of mild cervical lesions and severe cervical lesions among patients with high-grade VAIN and low-grade VAIN (with and without koilocytosis) were not significant.", "output": "{\"label\": \"maybe\", \"rationale\": \"These data suggest that CIN and VAIN may have some common features in certain cases, i.e., if an HPV infection is proved.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 18714572, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Ribosomopathies have a low degree of cell and tissue specific pathology.\n\nCANDIDATE_PASSAGE:\nFinding the right niche: B-cell migration in the early phases of T-dependent antibody responses. Humoral immune responses depend on B cells encountering antigen, interacting with helper T cells, proliferating and differentiating into low-affinity plasma cells or, after organizing into a germinal center (GC), high-affinity plasma cells and memory B cells. Remarkably, each of these events occurs in association with distinct stromal cells in separate subcompartments of the lymphoid tissue. B cells must migrate from niche to niche in a rapid and highly regulated manner to successfully mount a response. The chemokine, CXCL13, plays a central role in guiding B cells to follicles whereas T-zone chemokines guide activated B cells to the T zone. Sphingosine-1-phosphate (S1P) promotes cell egress from the tissue, as well as marginal-zone B-cell positioning in the spleen. Recent studies have identified a role for the orphan receptor, EBV-induced molecule 2 (EBI2; GPR183), in guiding activated B cells to inter and outer follicular niche(s) and down-regulation of this receptor is essential for organizing cells into GCs. In this review, we discuss current understanding of the roles played by chemokines, S1P and EBI2 in the migration events that underlie humoral immune responses.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1049", "doc_id": "38587347", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Utility of unenhanced fat-suppressed T1-weighted MRI in children with sickle cell disease -- can it differentiate bone infarcts from acute osteomyelitis?\n\nABSTRACT:\nChildren with sickle cell disease (SCD) are at risk of bone infarcts and acute osteomyelitis. The clinical differentiation between a bone infarct and acute osteomyelitis is a diagnostic challenge. Unenhanced T1-W fat-saturated MR images have been proposed as a potential tool to differentiate bone infarcts from osteomyelitis. To evaluate the reliability of unenhanced T1-W fat-saturated MRI for differentiation between bone infarcts and acute osteomyelitis in children with SCD. We retrospectively reviewed the records of 31 children (20 boys, 11 girls; mean age 10.6 years, range 1.1-17.9 years) with SCD and acute bone pain who underwent MR imaging including unenhanced T1-W fat-saturated images from 2005 to 2010. Complete clinical charts were reviewed by a pediatric hematologist with training in infectious diseases to determine a clinical standard to define the presence or absence of osteomyelitis. A pediatric radiologist reviewed all MR imaging and was blinded to clinical information. Based on the signal intensity in T1-W fat-saturated images, the children were further classified as positive for osteomyelitis (low bone marrow signal intensity) or positive for bone infarct (high bone marrow signal intensity). Based on the clinical standard, 5 children were classified as positive for osteomyelitis and 26 children as positive for bone infarct (negative for osteomyelitis). The bone marrow signal intensity on T1-W fat-saturated imaging was not significant for the differentiation between bone infarct and osteomyelitis (P = 0.56). None of the additional evaluated imaging parameters on unenhanced MRI proved reliable in differentiating these diagnoses.", "output": "{\"label\": \"no\", \"rationale\": \"The bone marrow signal intensity on unenhanced T1-W fat-saturated MR images is not a reliable criterion to differentiate bone infarcts from osteomyelitis in children.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 26209118, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: V-9302 inhibits antitumor responses by decreasing cell death and oxidative stress.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pharmacological Blockade of ASCT2-dependent Glutamine Transport Leads To Anti-tumor Efficacy in Preclinical Models\nABSTRACT: The unique metabolic demands of cancer cells underscore potentially fruitful opportunities for drug discovery in the era of precision medicine. However, therapeutic targeting of cancer metabolism has led to surprisingly few new drugs to date. The neutral amino acid glutamine serves as a key intermediate in numerous metabolic processes leveraged by cancer cells, including biosynthesis, cell signaling, and oxidative protection. Herein we report the preclinical development of V-9302, a competitive small molecule antagonist of transmembrane glutamine flux that selectively and potently targets the amino acid transporter ASCT2. Pharmacological blockade of ASCT2 with V-9302 resulted in attenuated cancer cell growth and proliferation, increased cell death, and increased oxidative stress, which collectively contributed to antitumor responses in vitro and in vivo. This is the first study, to our knowledge, to demonstrate the utility of a pharmacological inhibitor of glutamine transport in oncology, representing a new class of targeted therapy and laying a framework for paradigm-shifting therapies targeting cancer cell metabolism.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Pharmacological blockade of ASCT2 with V-9302 resulted in attenuated cancer cell growth and proliferation, increased cell death, and increased oxidative stress, which collectively contributed to antitumor responses in vitro and in vivo.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1355, "doc_id": "5256564", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Gastric infection with Helicobacter pylori decreases risk of gastric cancer in humans.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association between infection with Helicobacter pylori and risk of gastric cancer: evidence from a prospective investigation.\nABSTRACT: OBJECTIVE To investigate the association between gastric cancer and prior infection with Helicobacter pylori. DESIGN Case-control comparison of prevalence of IgG antibodies to H pylori in blood samples collected prospectively, before diagnosis of gastric cancer in the cases. Presence of H pylori antibody (greater than 10 micrograms IgG/ml) determined by enzyme linked immunosorbent assay (ELISA). SUBJECTS 29 men with a subsequent diagnosis of gastric cancer and 116 aged matched controls selected from over 22,000 middle aged men participating in two ongoing cohort studies (the British United Provident Association study and the Caerphilly collaborative heart disease study), who had provided blood samples during 1975-1982. RESULTS 20 of the 29 cases (69%) and 54 of the 116 controls (47%) were positive for H pylori specific antibody. The median specific IgG concentration was significantly higher in the cases than controls (90 micrograms/ml v 3.6 micrograms/ml, p less than 0.01). The estimated odds ratio for the risk of gastric cancer in those with a history of infection with H pylori was 2.77 (95% confidence interval 1.04 to 7.97, 2p = 0.039). CONCLUSIONS H pylori infection may be an important cause of gastric cancer; between 35% and 55% of all cases may be associated with such an infection.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS H pylori infection may be an important cause of gastric cancer; between 35% and 55% of all cases may be associated with such an infection.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 447, "doc_id": "2052720", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: DRD1 proteins enable Pol V transcription in vivo.\n\nCANDIDATE_PASSAGE:\nA Conserved MST-FOXO Signaling Pathway Mediates Oxidative-Stress Responses and Extends Life Span Oxidative stress influences cell survival and homeostasis, but the mechanisms underlying the biological effects of oxidative stress remain to be elucidated. Here, we demonstrate that the protein kinase MST1 mediates oxidative-stress-induced cell death in primary mammalian neurons by directly activating the FOXO transcription factors. MST1 phosphorylates FOXO proteins at a conserved site within the forkhead domain that disrupts their interaction with 14-3-3 proteins, promotes FOXO nuclear translocation, and thereby induces cell death in neurons. We also extend the MST-FOXO signaling link to nematodes. Knockdown of the C. elegans MST1 ortholog CST-1 shortens life span and accelerates tissue aging, while overexpression of cst-1 promotes life span and delays aging. The cst-1-induced life-span extension occurs in a daf-16-dependent manner. The identification of the FOXO transcription factors as major and evolutionarily conserved targets of MST1 suggests that MST kinases play important roles in diverse biological processes including cellular responses to oxidative stress and longevity.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "305", "doc_id": "14496749", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is elevated miR-29a expression correlated with disease activity index in PBMCs of patients with ankylosing spondylitis?\n\nABSTRACT:\nAnkylosing spondylitis (AS) is a chronic inflammatory disease characterized by new bone formation. Recent evidence suggests that new bone formation in AS may be due to upregulation of Wnt signaling in the osteoblastic pathway secondary to low serum Dickkopf homolog 1 (Dkk-1) levels. And miR-29a orchestrates osteoblast differentiation through direct targeting and negative regulation of Dkk-1. We initially validated the expression levels of miR-29a in the peripheral blood mononuclear cells (PBMCs) of AS patients (n = 30), rheumatoid arthritis (RA) patients (n = 30) and healthy controls (n = 30) using real-time quantitative reverse transcription PCR (qRT-PCR). Correlation analysis was assessed between miR-29a level in PBMCs of AS patients and disease activity indexes, including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), Bath ankylosing spondylitis disease activity index (BASDAI), Bath ankylosing spondylitis function index (BASFI) and modified Stoke ankylosing spondylitis spinal score (mSASSS). Significantly higher expression of miR-29a was observed in PBMCs of AS patients (Ct 9.18 ± 1.96) compared with that in RA patients (10.97 ± 0.70, p < 0.001) and healthy controls (Ct 11.45 ± 1.23, p < 0.001). There was no significant difference between RA patients and healthy controls in miR-29a expression (p > 0.05). Elevated miR-29a expression is not correlated with disease activity index (p > 0.05). A weak correlation was found between elevated miR-29a expression and mSASSS (r = -0.393, p = 0.032).", "output": "{\"label\": \"no\", \"rationale\": \"We report for the first time elevated miR-29a expression in PBMCs of patients with ankylosing spondylitis, and miR-29a might be used as a useful diagnostic marker in new bone formation but cannot reflect disease activity.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 24593209, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Varenicline monotherapy is more effective after 26 weeks of treatment compared to combination nicotine replacement therapies with varenicline or bupropion.\n\nCANDIDATE_ABSTRACT:\nTITLE: Investigating survival prognosis of glioblastoma using evolutional properties of gene networks\nABSTRACT: In recent years, there has been widespread interest and a large number of publications on the application of graph theory techniques into constructing and analyzing biologically-informed gene networks from cancer cell line data sets. Current research efforts have predominantly looked at an overall static, topological, representation of the network, and have not investigated the application of graph theoretical techniques to evolutionary investigations of cancer. A number of these studies have used graph theory metrics, such as degree, betweenness, and closeness centrality, to identify important hub genes in these networks. However, these have not fully investigated the importance of genes across the different stages of the disease. Previous human glioblastoma publications have identified four subtypes of glioblastoma in adults, based on signature genes. In one such publication, Verhaak et al. found that the subtypes correspond to a narrow median survival range, from 11.3 months for the most aggressive subtype, to 13.1 months for the least aggressive one. In this work, we present an evolutionary graph theory study of glioblastoma based on survival data categorization, confirming genes associated with different survival times identified using established graph theory metrics. The work is extending the application of graph theory approaches to evolutionary studies of cancer cell line data.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1360, "doc_id": "831167", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Energy balance requires hypothalamic glutamate neurotransmission.\n\nCANDIDATE_PASSAGE:\nControl of glutamate clearance and synaptic efficacy by glial coverage of neurons. Analysis of excitatory synaptic transmission in the rat hypothalamic supraoptic nucleus revealed that glutamate clearance and, as a consequence, glutamate concentration and diffusion in the extracellular space, is associated with the degree of astrocytic coverage of its neurons. Reduction in glutamate clearance, whether induced pharmacologically or associated with a relative decrease of glial coverage in the vicinity of synapses, affected transmitter release through modulation of presynaptic metabotropic glutamate receptors. Astrocytic wrapping of neurons, therefore, contributes to the regulation of synaptic efficacy in the central nervous system.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "378", "doc_id": "306311", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Intramembrane cleavage by signal peptide peptidase aids in the degradation of proteins with a complex membrane orientation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Ubiquitin-dependent intramembrane rhomboid protease promotes ERAD of membrane proteins.\nABSTRACT: The ER-associated degradation (ERAD) pathway serves as an important cellular safeguard by directing incorrectly folded and unassembled proteins from the ER to the proteasome. Still, however, little is known about the components mediating ERAD of membrane proteins. Here we show that the evolutionary conserved rhomboid family protein RHBDL4 is a ubiquitin-dependent ER-resident intramembrane protease that is upregulated upon ER stress. RHBDL4 cleaves single-spanning and polytopic membrane proteins with unstable transmembrane helices, leading to their degradation by the canonical ERAD machinery. RHBDL4 specifically binds the AAA+-ATPase p97, suggesting that proteolytic processing and dislocation into the cytosol are functionally linked. The phylogenetic relationship between rhomboids and the ERAD factor derlin suggests that substrates for intramembrane proteolysis and protein dislocation are recruited by a shared mechanism.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here we show that the evolutionary conserved rhomboid family protein RHBDL4 is a ubiquitin-dependent ER-resident intramembrane protease that is upregulated upon ER stress. RHBDL4 cleaves single-spanning and polytopic membrane proteins with unstable transmembrane helices, leading to their degradation by the canonical ERAD machinery.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 657, "doc_id": "8533245", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: aPKCz causes tumour suppression by affecting glutamine metabolism.\n\nCANDIDATE_ABSTRACT:\nTITLE: Control of Nutrient Stress-Induced Metabolic Reprogramming by PKCζ in Tumorigenesis\nABSTRACT: Tumor cells have high-energetic and anabolic needs and are known to adapt their metabolism to be able to survive and keep proliferating under conditions of nutrient stress. We show that PKCζ deficiency promotes the plasticity necessary for cancer cells to reprogram their metabolism to utilize glutamine through the serine biosynthetic pathway in the absence of glucose. PKCζ represses the expression of two key enzymes of the pathway, PHGDH and PSAT1, and phosphorylates PHGDH at key residues to inhibit its enzymatic activity. Interestingly, the loss of PKCζ in mice results in enhanced intestinal tumorigenesis and increased levels of these two metabolic enzymes, whereas patients with low levels of PKCζ have a poor prognosis. Furthermore, PKCζ and caspase-3 activities are correlated with PHGDH levels in human intestinal tumors. Taken together, this demonstrates that PKCζ is a critical metabolic tumor suppressor in mouse and human cancer.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Interestingly, the loss of PKCζ in mice results in enhanced intestinal tumorigenesis and increased levels of these two metabolic enzymes, whereas patients with low levels of PKCζ have a poor prognosis.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1383, "doc_id": "17755060", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: APOE4 expression in iPSC-derived neurons increases AlphaBeta production and tau phosphorylation causing GABA neuron degeneration.\n\nCANDIDATE_ABSTRACT:\nTITLE: Primary cilia and coordination of receptor tyrosine kinase (RTK) signalling.\nABSTRACT: Primary cilia are microtubule-based sensory organelles that coordinate signalling pathways in cell-cycle control, migration, differentiation and other cellular processes critical during development and for tissue homeostasis. Accordingly, defects in assembly or function of primary cilia lead to a plethora of developmental disorders and pathological conditions now known as ciliopathies. In this review, we summarize the current status of the role of primary cilia in coordinating receptor tyrosine kinase (RTK) signalling pathways. Further, we present potential mechanisms of signalling crosstalk and networking in the primary cilium and discuss how defects in ciliary RTK signalling are linked to human diseases and disorders.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 56, "doc_id": "1917068", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Diabetic patients with acute coronary syndrome experience increased short-term and long-term risk for bleeding events.\n\nCANDIDATE_PASSAGE:\nPlatelet glycoprotein IIb/IIIa inhibitors reduce mortality in diabetic patients with non-ST-segment-elevation acute coronary syndromes. BACKGROUND Diabetes mellitus is a major risk factor for adverse outcomes after acute coronary syndromes (ACS). Because this disease may be associated with increased platelet aggregation, we investigated whether diabetic patients with ACS derive particular benefit from platelet glycoprotein (GP) IIb/IIIa receptor inhibition. METHODS AND RESULTS We performed a meta-analysis of the diabetic populations enrolled in the 6 large-scale platelet GP IIb/IIIa inhibitor ACS trials: PRISM, PRISM-PLUS, PARAGON A, PARAGON B, PURSUIT, and GUSTO IV. Among 6458 diabetic patients, platelet GP IIb/IIIa inhibition was associated with a significant mortality reduction at 30 days, from 6.2% to 4.6% (OR 0.74; 95% CI 0.59 to 0.92; P=0.007). Conversely, 23 072 nondiabetic patients had no survival benefit (3.0% versus 3.0%). The interaction between platelet GP IIb/IIIa inhibition and diabetic status was statistically significant (P=0.036). Among 1279 diabetic patients undergoing percutaneous coronary intervention (PCI) during index hospitalization, the use of these agents was associated with a mortality reduction at 30 days from 4.0% to 1.2% (OR 0.30; 95% CI 0.14 to 0.69; P=0.002). CONCLUSIONS This meta-analysis, including the entire large-scale trial experience of intravenous platelet GP IIb/IIIa inhibitors for the medical management of non-ST-segment-elevation ACS, shows that these agents may significantly reduce mortality at 30 days in diabetic patients. Although not based on a randomized assessment, the survival benefit appears to be of greater magnitude in patients undergoing PCI. Therefore, the use of platelet GP IIb/IIIa inhibitors should be s [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "343", "doc_id": "7873737", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: MICAL redox enzymes regulate actin dynamics.\n\nCANDIDATE_ABSTRACT:\nTITLE: Differential regulation of actin microfilaments by human MICAL proteins.\nABSTRACT: The Drosophila melanogaster MICAL protein is essential for the neuronal growth cone machinery that functions through plexin- and semaphorin-mediated axonal signaling. Drosophila MICAL is also involved in regulating myofilament organization and synaptic structures, and serves as an actin disassembly factor downstream of plexin-mediated axonal repulsion. In mammalian cells there are three known isoforms, MICAL1, MICAL2 and MICAL3, as well as the MICAL-like proteins MICAL-L1 and MICAL-L2, but little is known of their function, and information comes almost exclusively from neural cells. In this study we show that in non-neural cells human MICALs are required for normal actin organization, and all three MICALs regulate actin stress fibers. Moreover, we provide evidence that the generation of reactive oxygen species by MICAL proteins is crucial for their actin-regulatory function. However, although MICAL1 is auto-inhibited by its C-terminal coiled-coil region, MICAL2 remains constitutively active and affects stress fibers. These data suggest differential but complementary roles for MICAL1 and MICAL2 in actin microfilament regulation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In this study we show that in non-neural cells human MICALs are required for normal actin organization, and all three MICALs regulate actin stress fibers.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 738, "doc_id": "6609935", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Oxidative phosphorylation is one of the primary glycometabolic pathways in cells.\n\nCANDIDATE_PASSAGE:\nGender, age, and heart failure with preserved left ventricular systolic function. OBJECTIVES This study was designed to determine if women are more likely than men to have heart failure (HF) with preserved systolic function after adjustment for potential confounders, including age. BACKGROUND Although prior evidence suggests an independent association between female gender and preserved left ventricular systolic function (LVSF) in patients with HF, existing studies are limited by referral biases, small sample sizes, or the inability to adjust for a wide range of potential confounding variables. METHODS This is a cross-sectional study using data from retrospective medical chart abstraction of a national sample of Medicare beneficiaries hospitalized with the principal discharge diagnosis of HF in acute-care nongovernmental hospitals in the U.S. between April 1998 and March 1999. Patients were eligible for this analysis if they were age 65 years or older, had documentation of LVSF, and corroboration of the diagnosis of HF. We used multivariable logistic regression to identify the correlates of preserved LVSF, which was defined as qualitatively normal function or quantitatively reported ejection fraction > or =0.50. Stratified regressions by gender were performed to identify significant interactions. RESULTS Of the 19,710 patients in the analysis, preserved LVSF was present in 6,700 (35%), 79% of whom were women. In contrast, among the 12,956 patients with impaired LVSF, only 49% were women. Patients with preserved LVSF were 1.5 years older than those with impaired LVSF. After adjustment for age and other patient factors, female gender remained strongly associated with preserved LVSF (calculated risk ratio = 1.71; 95% confidence interval 1.63 to 1.78). The assoc [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "900", "doc_id": "13481731", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\nABSTRACT: Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens. However, signals underlying mTEC development remain largely unclear. Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals. Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment. Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner. These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1004, "doc_id": "2734421", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The morphology change from large white adipocytes to small brown adipocytes is a sign of increased energy expenditure potential in white adipose tissue.\n\nCANDIDATE_ABSTRACT:\nTITLE: Human ‘brite / beige’ adipocytes develop from capillary networks and their implantation improves metabolic homeostasis in mice\nABSTRACT: Uncoupling protein 1 (UCP1) is highly expressed in brown adipose tissue, where it generates heat by uncoupling electron transport from ATP production. UCP1 is also found outside classical brown adipose tissue depots, in adipocytes that are termed 'brite' (brown-in-white) or 'beige'. In humans, the presence of brite or beige (brite/beige) adipocytes is correlated with a lean, metabolically healthy phenotype, but whether a causal relationship exists is not clear. Here we report that human brite/beige adipocyte progenitors proliferate in response to pro-angiogenic factors, in association with expanding capillary networks. Adipocytes formed from these progenitors transform in response to adenylate cyclase activation from being UCP1 negative to being UCP1 positive, which is a defining feature of the beige/brite phenotype, while displaying uncoupled respiration. When implanted into normal chow-fed, or into high-fat diet (HFD)-fed, glucose-intolerant NOD-scid IL2rg(null) (NSG) mice, brite/beige adipocytes activated in vitro enhance systemic glucose tolerance. These adipocytes express neuroendocrine and secreted factors, including the pro-protein convertase PCSK1, which is strongly associated with human obesity. Pro-angiogenic conditions therefore drive the proliferation of human beige/brite adipocyte progenitors, and activated beige/brite adipocytes can affect systemic glucose homeostasis, potentially through a neuroendocrine mechanism.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1236, "doc_id": "17973161", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: PKG-la plays an essential role in expression of spinal long term potentiation in PGK-la knockout mice.\n\nCANDIDATE_PASSAGE:\nPresynaptically Localized Cyclic GMP-Dependent Protein Kinase 1 Is a Key Determinant of Spinal Synaptic Potentiation and Pain Hypersensitivity Synaptic long-term potentiation (LTP) at spinal neurons directly communicating pain-specific inputs from the periphery to the brain has been proposed to serve as a trigger for pain hypersensitivity in pathological states. Previous studies have functionally implicated the NMDA receptor-NO pathway and the downstream second messenger, cGMP, in these processes. Because cGMP can broadly influence diverse ion-channels, kinases, and phosphodiesterases, pre- as well as post-synaptically, the precise identity of cGMP targets mediating spinal LTP, their mechanisms of action, and their locus in the spinal circuitry are still unclear. Here, we found that Protein Kinase G1 (PKG-I) localized presynaptically in nociceptor terminals plays an essential role in the expression of spinal LTP. Using the Cre-lox P system, we generated nociceptor-specific knockout mice lacking PKG-I specifically in presynaptic terminals of nociceptors in the spinal cord, but not in post-synaptic neurons or elsewhere (SNS-PKG-I(-/-) mice). Patch clamp recordings showed that activity-induced LTP at identified synapses between nociceptors and spinal neurons projecting to the periaqueductal grey (PAG) was completely abolished in SNS-PKG-I(-/-) mice, although basal synaptic transmission was not affected. Analyses of synaptic failure rates and paired-pulse ratios indicated a role for presynaptic PKG-I in regulating the probability of neurotransmitter release. Inositol 1,4,5-triphosphate receptor 1 and myosin light chain kinase were recruited as key phosphorylation targets of presynaptic PKG-I in nociceptive neurons. Finally, behavioural analyses in vivo showed ma [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "912", "doc_id": "11254556", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The risk of male prisoners harming themselves is ten times that of female prisoners.\n\nCANDIDATE_ABSTRACT:\nTITLE: Self-harm in prisons in England and Wales: an epidemiological study of prevalence, risk factors, clustering, and subsequent suicide\nABSTRACT: BACKGROUND Self-harm and suicide are common in prisoners, yet robust information on the full extent and characteristics of people at risk of self-harm is scant. Furthermore, understanding how frequently self-harm is followed by suicide, and in which prisoners this progression is most likely to happen, is important. We did a case-control study of all prisoners in England and Wales to ascertain the prevalence of self-harm in this population, associated risk factors, clustering effects, and risk of subsequent suicide after self-harm. METHODS Records of self-harm incidents in all prisons in England and Wales were gathered routinely between January, 2004, and December, 2009. We did a case-control comparison of prisoners who self-harmed and those who did not between January, 2006, and December, 2009. We also used a Bayesian approach to look at clustering of people who self-harmed. Prisoners who self-harmed and subsequently died by suicide in prison were compared with other inmates who self-harmed. FINDINGS 139,195 self-harm incidents were recorded in 26,510 individual prisoners between 2004 and 2009; 5-6% of male prisoners and 20-24% of female inmates self-harmed every year. Self-harm rates were more than ten times higher in female prisoners than in male inmates. Repetition of self-harm was common, particularly in women and teenage girls, in whom a subgroup of 102 prisoners accounted for 17,307 episodes. In both sexes, self-harm was associated with younger age, white ethnic origin, prison type, and a life sentence or being unsentenced; in female inmates, committing a violent offence against an individual was also a factor. Substantial evidence was noted of clustering in time and location of prisoners who self-harmed (adjusted intra-class correlation 0·15, 95% CI 0 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Self-harm rates were more than ten times higher in female prisoners than in male inmates.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1270, "doc_id": "13900610", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: NF2 (Merlin) prevents phosphorylation and subsequent cytoplasmic sequestration of YAP in Drosophila.\n\nCANDIDATE_PASSAGE:\nDelta–Notch—and then? Protein interactions and proposed modes of repression by Hes and Hey bHLH factors Hes and Hey genes are the mammalian counterparts of the Hairy and Enhancer-of-split type of genes in Drosophila and they represent the primary targets of the Delta-Notch signaling pathway. Hairy-related factors control multiple steps of embryonic development and misregulation is associated with various defects. Hes and Hey genes (also called Hesr, Chf, Hrt, Herp or gridlock) encode transcriptional regulators of the basic helix-loop-helix class that mainly act as repressors. The molecular details of how Hes and Hey proteins control transcription are still poorly understood, however. Proposed modes of action include direct binding to N- or E-box DNA sequences of target promoters as well as indirect binding through other sequence-specific transcription factors or sequestration of transcriptional activators. Repression may rely on recruitment of corepressors and induction of histone modifications, or even interference with the general transcriptional machinery. All of these models require extensive protein-protein interactions. Here we review data published on protein-protein and protein-DNA interactions of Hairy-related factors and discuss their implications for transcriptional regulation. In addition, we summarize recent progress on the identification of potential target genes and the analysis of mouse models.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "831", "doc_id": "51817902", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Formation of N-terminal pyroglutamate by glutamine cyclase (GC) competes with NTAQ1 for Nt-Gln substrates.\n\nCANDIDATE_ABSTRACT:\nTITLE: Glutamine-specific N-terminal amidase, a component of the N-end rule pathway.\nABSTRACT: Deamidation of N-terminal Gln by Nt(Q)-amidase, an N-terminal amidohydrolase, is a part of the N-end rule pathway of protein degradation. We detected the activity of Nt(Q)-amidase, termed Ntaq1, in mouse tissues, purified Ntaq1 from bovine brains, identified its gene, and began analyzing this enzyme. Ntaq1 is highly conserved among animals, plants, and some fungi, but its sequence is dissimilar to sequences of other amidases. An earlier mutant in the Drosophila Cg8253 gene that we show here to encode Nt(Q)-amidase has defective long-term memory. Other studies identified protein ligands of the uncharacterized human C8orf32 protein that we show here to be the Ntaq1 Nt(Q)-amidase. Remarkably, \"high-throughput\" studies have recently solved the crystal structure of C8orf32 (Ntaq1). Our site-directed mutagenesis of Ntaq1 and its crystal structure indicate that the active site and catalytic mechanism of Nt(Q)-amidase are similar to those of transglutaminases.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 429, "doc_id": "36540079", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The PDPN gene deactivates the C-type lectin receptor (CLEC-2).\n\nCANDIDATE_ABSTRACT:\nTITLE: Podoplanin-Rich Stromal Networks Induce Dendritic Cell Motility via Activation of the C-type Lectin Receptor CLEC-2\nABSTRACT: To initiate adaptive immunity, dendritic cells (DCs) move from parenchymal tissues to lymphoid organs by migrating along stromal scaffolds that display the glycoprotein podoplanin (PDPN). PDPN is expressed by lymphatic endothelial and fibroblastic reticular cells and promotes blood-lymph separation during development by activating the C-type lectin receptor, CLEC-2, on platelets. Here, we describe a role for CLEC-2 in the morphodynamic behavior and motility of DCs. CLEC-2 deficiency in DCs impaired their entry into lymphatics and trafficking to and within lymph nodes, thereby reducing T cell priming. CLEC-2 engagement of PDPN was necessary for DCs to spread and migrate along stromal surfaces and sufficient to induce membrane protrusions. CLEC-2 activation triggered cell spreading via downregulation of RhoA activity and myosin light-chain phosphorylation and triggered F-actin-rich protrusions via Vav signaling and Rac1 activation. Thus, activation of CLEC-2 by PDPN rearranges the actin cytoskeleton in DCs to promote efficient motility along stromal surfaces.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Thus, activation of CLEC-2 by PDPN rearranges the actin cytoskeleton in DCs to promote efficient motility along stromal surfaces.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1173, "doc_id": "7370282", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Diabetic patients with acute coronary syndrome experience decreased short-term and long-term risk for bleeding events.\n\nCANDIDATE_PASSAGE:\nMarkers of myocardial damage and inflammation in relation to long-term mortality in unstable coronary artery disease. FRISC Study Group. Fragmin during Instability in Coronary Artery Disease. BACKGROUND In patients with unstable coronary artery disease, there is a relation between the short-term risk of death and blood levels of troponin T (a marker of myocardial damage) and C-reactive protein and fibrinogen (markers of inflammation). Using information obtained during an extension of the follow-up period in the Fragmin during Instability in Coronary Artery Disease trial, we evaluated the usefulness of troponin T, C-reactive protein, and fibrinogen levels and other indicators of risk as predictors of the long-term risk of death from cardiac causes. METHODS Levels of C-reactive protein and fibrinogen at enrollment and the maximal level of troponin T during the first 24 hours after enrollment were analyzed in 917 patients included in a clinical trial of low-molecular-weight heparin in unstable coronary artery disease. The patients were followed for a mean of 37.0 months (range, 1.6 to 50.6). RESULTS During follow-up, 1.2 percent of the 173 patients with maximal blood troponin T levels of less than 0.06 microg per liter died of cardiac causes, as compared with 8.7 percent of the 367 patients with levels of 0.06 to 0.59 microg per liter and 15.4 percent of the 377 patients with levels of at least 0.60 microg per liter (P=0.007 and P=0.001, respectively). The rates of death from cardiac causes were 5.7 percent among the 314 patients with blood C-reactive protein levels of less than 2 mg per liter, 7.8 percent among the 294 with levels of 2 to 10 mg per liter, and 16.5 percent among the 309 with levels of more than 10 mg per liter (P=0.29 and P=0.001, respectively) [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "342", "doc_id": "25028913", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: In rhesus macaques, daily subcutaneous injections of tenofovir protects against rectally transmitted simian-human immunodeficiency virus.\n\nCANDIDATE_PASSAGE:\nVariations in the quality and sustainability of long-term glycaemic control with continuous subcutaneous insulin infusion. AIMS To investigate the pattern of changes in HbA1c in people with Type 1 diabetes managed by long-term Continuous subcutaneous insulin infusion. METHODS We studied HbA1c changes using computerized clinic records in 35 adult people with Type 1 diabetes and an elevated HbA1c (≥ 64 mmol/mol, 8.0%) on multiple daily insulin injections, who were then switched to continuous subcutaneous insulin infusion for at least 5 years. RESULTS We identified three subgroups with similar baseline HbA1c but different long-term responses to pump therapy: group A--those with improvement followed by deterioration (57%); group B--those with improvement that was sustained throughout the 5 years (31%); and group C-those where HbA1c did not change significantly from baseline (12%). The patients in group C had a higher BMI: 31.0 ± 5.2 vs. 25.9 ± 3.3 vs. 25.2 ± 3.1 kg/m² (group C vs. group A and group B; P = 0.02). CONCLUSIONS Improved glycaemic control with continuous subcutaneous insulin infusion was maintained over 5 years by 88% of people with Type 1 diabetes in this study, but there were variations in the long-term efficacy, with some people improving and worsening, others maintaining strict control and a few subcutaneous insulin infusion 'non-responders'.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "584", "doc_id": "5262240", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Integrated care is successful at tackling multiple comorbidities.\n\nCANDIDATE_ABSTRACT:\nTITLE: Functional outcomes of multi-condition collaborative care and successful ageing: results of randomised trial\nABSTRACT: OBJECTIVE To evaluate the effectiveness of integrated care for chronic physical diseases and depression in reducing disability and improving quality of life. DESIGN A randomised controlled trial of multi-condition collaborative care for depression and poorly controlled diabetes and/or risk factors for coronary heart disease compared with usual care among middle aged and elderly people SETTING Fourteen primary care clinics in Seattle, Washington. PARTICIPANTS Patients with diabetes or coronary heart disease, or both, and blood pressure above 140/90 mm Hg, low density lipoprotein concentration >3.37 mmol/L, or glycated haemoglobin 8.5% or higher, and PHQ-9 depression scores of ≥ 10. INTERVENTION A 12 month intervention to improve depression, glycaemic control, blood pressure, and lipid control by integrating a \"treat to target\" programme for diabetes and risk factors for coronary heart disease with collaborative care for depression. The intervention combined self management support, monitoring of disease control, and pharmacotherapy to control depression, hyperglycaemia, hypertension, and hyperlipidaemia. MAIN OUTCOME MEASURES Social role disability (Sheehan disability scale), global quality of life rating, and World Health Organization disability assessment schedule (WHODAS-2) scales to measure disabilities in activities of daily living (mobility, self care, household maintenance). RESULTS Of 214 patients enrolled (106 intervention and 108 usual care), disability and quality of life measures were obtained for 97 intervention patients at six months (92%) and 92 at 12 months (87%), and for 96 usual care patients at six months (89%) and 92 at 12 months (85%). Improvements from baseline on the Sheehan disability scale (-0.9, 95% confidence interval -1.5 to -0.2; [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"There was a trend toward greater improvement in disabilities in activities of daily living (-1.5, -3.3 to 0.4; P = 0.10).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 648, "doc_id": "15041758", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The risk of female prisoners harming themselves is ten times that of male prisoners.\n\nCANDIDATE_ABSTRACT:\nTITLE: Self-harm in prisons in England and Wales: an epidemiological study of prevalence, risk factors, clustering, and subsequent suicide\nABSTRACT: BACKGROUND Self-harm and suicide are common in prisoners, yet robust information on the full extent and characteristics of people at risk of self-harm is scant. Furthermore, understanding how frequently self-harm is followed by suicide, and in which prisoners this progression is most likely to happen, is important. We did a case-control study of all prisoners in England and Wales to ascertain the prevalence of self-harm in this population, associated risk factors, clustering effects, and risk of subsequent suicide after self-harm. METHODS Records of self-harm incidents in all prisons in England and Wales were gathered routinely between January, 2004, and December, 2009. We did a case-control comparison of prisoners who self-harmed and those who did not between January, 2006, and December, 2009. We also used a Bayesian approach to look at clustering of people who self-harmed. Prisoners who self-harmed and subsequently died by suicide in prison were compared with other inmates who self-harmed. FINDINGS 139,195 self-harm incidents were recorded in 26,510 individual prisoners between 2004 and 2009; 5-6% of male prisoners and 20-24% of female inmates self-harmed every year. Self-harm rates were more than ten times higher in female prisoners than in male inmates. Repetition of self-harm was common, particularly in women and teenage girls, in whom a subgroup of 102 prisoners accounted for 17,307 episodes. In both sexes, self-harm was associated with younger age, white ethnic origin, prison type, and a life sentence or being unsentenced; in female inmates, committing a violent offence against an individual was also a factor. Substantial evidence was noted of clustering in time and location of prisoners who self-harmed (adjusted intra-class correlation 0·15, 95% CI 0 [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Self-harm rates were more than ten times higher in female prisoners than in male inmates.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1269, "doc_id": "13900610", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: General exercise therapy is more effective than scapular stabilizer exercises in reducing pain and improving function of the shoulder.\n\nCANDIDATE_ABSTRACT:\nTITLE: Arteriolar function in visceral adipose tissue is impaired in human obesity.\nABSTRACT: OBJECTIVE The purpose of this study was to characterize the relationship between adipose tissue phenotype and depot-specific microvascular function in fat. METHODS AND RESULTS In 30 obese subjects (age 42±11 years, body mass index 46±11 kg/m(2)) undergoing bariatric surgery, we intraoperatively collected visceral and subcutaneous adipose tissue and characterized depot-specific adipose phenotypes. We assessed vasomotor function of the adipose microvasculature using videomicroscopy of small arterioles (75-250 μm) isolated from different fat compartments. Endothelium-dependent, acetylcholine-mediated vasodilation was severely impaired in visceral arterioles, compared to the subcutaneous depot (P<0.001 by ANOVA). Nonendothelium dependent responses to papaverine and nitroprusside were similar. Endothelial nitric oxide synthase inhibition with N(ω)-nitro-l-arginine methyl ester reduced subcutaneous vasodilation but had no effect on severely blunted visceral arteriolar responses. Visceral fat exhibited greater expression of proinflammatory, oxidative stress-related, hypoxia-induced, and proangiogenic genes; increased activated macrophage populations; and had a higher capacity for cytokine production ex vivo. CONCLUSIONS Our findings provide clinical evidence that the visceral microenvironment may be intrinsically toxic to arterial health providing a potential mechanism by which visceral adiposity burden is linked to atherosclerotic vascular disease. Our findings also support the evolving concept that both adipose tissue quality and quantity may play significant roles in shaping cardiovascular phenotypes in human obesity.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 454, "doc_id": "79447", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does low-intensity resistance exercise affect cardiac autonomic modulation in patients with peripheral artery disease?\n\nABSTRACT:\nTo analyze the effect of a single bout of resistance exercise on cardiac autonomic modulation in patients with peripheral artery disease. Fifteen patients with peripheral artery disease (age: 58.3±4.0 years) underwent the following sessions in a random order: resistance exercise (three sets of 10 repetitions of the six resistance exercises with a workload of 5-7 in the OMNI-RES scale) and control (similar to the resistance session; however, the resistance exercises were performed with no load). The frequency domain (low frequency, high frequency and sympathovagal balance) and symbolic analysis (0V, 1V and 2V patterns) of heart rate variability were obtained before and until one hour after the interventions. After the resistance exercise and control sessions, similar increases were observed in the consecutive heartbeat intervals (control: 720.8±28.6 vs. 790.9±34.4 ms; resistance exercise: 712.9±30.1 vs. 756.8±37.9 ms; p<0.05) and in the pattern of the symbolic analysis with no variation (0V) (control: 25.1±3.5 vs. 33.4±4.1%; resistance exercise: 26.1±3.2 vs. 29.7±3.5%; p<0.05) until 50 min after both interventions. The pattern of two variations (2V) decreased similarly (control: 11.2±2.1 vs. 8.3±2.1%; resistance exercise: 9.5±1.7 vs. 7.8±1.7%; p<0.05). In contrast, the pattern of one variation (1V), the low and high frequency bands and sympathovagal balance did not change after the interventions (p>0.05).", "output": "{\"label\": \"no\", \"rationale\": \"A single bout of resistance exercise did not alter cardiac autonomic modulation in patients with peripheral artery disease.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 23778414, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\nABSTRACT: Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens. However, signals underlying mTEC development remain largely unclear. Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals. Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment. Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner. These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1004, "doc_id": "2734421", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: High levels of CRP reduces the risk of exacerbations in chronic obstructive pulmonary disease (COPD).\n\nCANDIDATE_PASSAGE:\nRedox regulation of cell migration and adhesion. Reactive oxygen species (ROS), particularly hydrogen peroxide, and the proteins that regulate them play important roles in the migration and adhesion of cells. Stimulation of cell surface receptors with growth factors and chemoattractants generates ROS, which relay signals from the cell surface to key signaling proteins inside the cell. ROS act within cells to promote migration and also in nonmigrating cells to influence the behavior of migrating cells. Hydrogen peroxide has also been suggested to act as a chemoattractant in its own right, drawing immune cells to wounds. We discuss recent progress made towards understanding how organisms use ROS, and to what degree they depend on them, during the related processes of cell migration and adhesion.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "516", "doc_id": "26297042", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Podocytes are motile and migrate in the presence of injury.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tracking the fate of glomerular epithelial cells in vivo using serial multiphoton imaging in novel mouse models with fluorescent lineage tags\nABSTRACT: Podocytes are critical in the maintenance of a healthy glomerular filter; however, they have been difficult to study in the intact kidney because of technical limitations. Here we report the development of serial multiphoton microscopy (MPM) of the same glomeruli over several days to visualize the motility of podocytes and parietal epithelial cells (PECs) in vivo. In podocin-GFP mice, podocytes formed sporadic multicellular clusters after unilateral ureteral ligation and migrated into the parietal Bowman's capsule. The tracking of single cells in podocin-confetti mice featuring cell-specific expression of CFP, GFP, YFP or RFP revealed the simultaneous migration of multiple podocytes. In phosphoenolpyruvate carboxykinase (PEPCK)-GFP mice, serial MPM found PEC-to-podocyte migration and nanotubule connections. Our data support a highly dynamic rather than a static nature of the glomerular environment and cellular composition. Future application of this new approach should advance our understanding of the mechanisms of glomerular injury and regeneration.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In podocin-GFP mice, podocytes formed sporadic multicellular clusters after unilateral ureteral ligation and migrated into the parietal Bowman's capsule.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 957, "doc_id": "123859", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: p16INK4A degradation is encoded by CDKN2A.\n\nCANDIDATE_PASSAGE:\nReduced NF1 expression confers resistance to EGFR inhibition in lung cancer. Activating mutations in the EGF receptor (EGFR) are associated with clinical responsiveness to EGFR tyrosine kinase inhibitors (TKI), such as erlotinib and gefitinib. However, resistance eventually arises, often due to a second EGFR mutation, most commonly T790M. Through a genome-wide siRNA screen in a human lung cancer cell line and analyses of murine mutant EGFR-driven lung adenocarcinomas, we found that erlotinib resistance was associated with reduced expression of neurofibromin, the RAS GTPase-activating protein encoded by the NF1 gene. Erlotinib failed to fully inhibit RAS-ERK signaling when neurofibromin levels were reduced. Treatment of neurofibromin-deficient lung cancers with a MAP-ERK kinase (MEK) inhibitor restored sensitivity to erlotinib. Low levels of NF1 expression were associated with primary and acquired resistance of lung adenocarcinomas to EGFR TKIs in patients. These findings identify a subgroup of patients with EGFR-mutant lung adenocarcinoma who might benefit from combination therapy with EGFR and MEK inhibitors.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1398", "doc_id": "2272614", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: H4 G94P proteins induce chromatin assembly, which increases free histones.\n\nCANDIDATE_PASSAGE:\nAutonomic neuropathy, QT interval lengthening, and unexpected deaths in male diabetic patients QT intervals were measured over RR intervals ranging from 500 ms to 1000 ms in 13 normal male subjects, 13 male diabetic subjects without and 13 with autonomic neuropathy. There was a close linear relationship between QT and RR in all subjects. The slope of the regression line was significantly greater in the autonomic neuropathy group than the normal group. Thirty-two male diabetic subjects with varying degrees of autonomic dysfunction had repeat QT measurements 3 (range 2–6) years later. QT and QTC lengthened significantly at the second visit, unrelated to age or time between recordings, but which corresponded with changes in autonomic function. Of 71 male diabetic subjects under 60 years followed for 3 years, 13 had died, 8 unexpectedly. Of those with autonomic neuropathy, QT and QTC were significantly longer in those who subsequently died, despite similar ages and duration of diabetes. We conclude that QT/RR interval relationships are altered in diabetic autonomic neuropathy, and that changes in QT length with time parallel changese in autonomic function. There may be an association between QT interval prolongation and the risk of dying unexpectedly in diabetic autonomic neuropathy.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "484", "doc_id": "9047718", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: HIF1A as a major vascular endothelial growth factor regulator: do its polymorphisms have an association with age-related macular degeneration?\n\nABSTRACT:\nTo investigate the association between age-related macular degeneration (AMD) and the polymorphisms of HIF1A, a major vascular epithelial growth factor regulator under hypoxic conditions. The associations of AMD and polymorphisms of genes CFH, SKIV2L and MYRIP were also studied. Prospective study. Eighty-seven AMD patients and 80 healthy subjects admitted to the Department of Ophthalmology at Pamukkale University Hospital, Denizli, Turkey, were included: 45 (52%) had wet type AMD, and 42 (48%) had dry type AMD. Polymorphisms rs1061170 (CFH), rs429608 (SKIV2L), rs2679798 (MYRIP) and both rs11549465 and rs11549467 (HIF1A) were investigated in DNA isolated from peripheral blood samples of the cases and controls by dye-termination DNA sequencing. Genotype distribution of rs1061170 (CFH), rs429608 (SKIV2L), rs2679798 (MYRIP) and both rs11549465 and rs11549467 (HIF1A) in AMD cases and healthy controls; association between genotypes and AMD subtypes. Given the significant difference between the mean age of case and control groups (72.13 ± 5.77 vs. 62.80 ± 5.22, respectively) (P = .000), subsequent analyses were adjusted for age. We found that having at least one C allele for polymorphism rs1061170 increases AMD risk independent of age (OR = 2.42, 95% confidence interval [CI], 1.22-4.81). The ancestral T allele for polymorphism rs1061170 has a protective effect for AMD (OR = 0.53, 95% CI, 0.34-0.83). No statistically significant difference for distributions of other single nucleotide polymorphisms (SNPs) emerged between patients and healthy subjects.", "output": "{\"label\": \"maybe\", \"rationale\": \"No associations appeared between HIF1A SNPs and AMD, which were studied here for the first time; however, polymorphism rs1061170 of the CFH gene is associated with AMD in our population.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 24995509, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: HSCT-T dosage may not be diagnostic if the onset of symptoms occurs less than 3 hours before AMI.\n\nCANDIDATE_PASSAGE:\nAging, habitual exercise, and dynamic arterial compliance. BACKGROUND A reduction in compliance of the large-sized cardiothoracic (central) arteries is an independent risk factor for the development of cardiovascular disease with advancing age. METHODS AND RESULTS We determined the role of habitual exercise on the age-related decrease in central arterial compliance by using both cross-sectional and interventional approaches. First, we studied 151 healthy men aged 18 to 77 years: 54 were sedentary, 45 were recreationally active, and 53 were endurance exercise-trained. Central arterial compliance (simultaneous B-mode ultrasound and arterial applanation tonometry on the common carotid artery) was lower (P:<0.05) in middle-aged and older men than in young men in all 3 groups. There were no significant differences between sedentary and recreationally active men at any age. However, arterial compliance in the endurance-trained middle-aged and older men was 20% to 35% higher than in the 2 less active groups (P:<0.01). As such, age-related differences in central arterial compliance were smaller in the endurance-trained men than in the sedentary and recreationally active men. Second, we studied 20 middle-aged and older (53+/-2 years) sedentary healthy men before and after a 3-month aerobic exercise intervention (primarily walking). Regular exercise increased central arterial compliance (P:<0.01) to levels similar to those of the middle-aged and older endurance-trained men. These effects were independent of changes in body mass, adiposity, arterial blood pressure, or maximal oxygen consumption. CONCLUSIONS Regular aerobic-endurance exercise attenuates age-related reductions in central arterial compliance and restores levels in previously sedentary healthy middle-aged [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "494", "doc_id": "752423", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Medications to treat obesity are highly effective.\n\nCANDIDATE_ABSTRACT:\nTITLE: Long term pharmacotherapy for obesity and overweight: updated meta-analysis.\nABSTRACT: OBJECTIVE To summarise the long term efficacy of anti-obesity drugs in reducing weight and improving health status. DESIGN Updated meta-analysis of randomised trials. DATA SOURCES Medline, Embase, the Cochrane controlled trials register, the Current Science meta-register of controlled trials, and reference lists of identified articles. All data sources were searched from December 2002 (end date of last search) to December 2006. STUDIES REVIEWED Double blind randomised placebo controlled trials of approved anti-obesity drugs used in adults (age over 18) for one year or longer. RESULTS 30 trials of one to four years' duration met the inclusion criteria: 16 orlistat (n=10 631 participants), 10 sibutramine (n=2623), and four rimonabant (n=6365). Of these, 14 trials were new and 16 had previously been identified. Attrition rates averaged 30-40%. Compared with placebo, orlistat reduced weight by 2.9 kg (95% confidence interval 2.5 kg to 3.2 kg), sibutramine by 4.2 kg (3.6 kg to 4.7 kg), and rimonabant by 4.7 kg (4.1 kg to 5.3 kg). Patients receiving active drug treatment were significantly more likely to achieve 5% and 10% weight loss thresholds. Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein. Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorde [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Orlistat, sibutramine, and rimonabant modestly reduce weight, have differing effects on cardiovascular risk profiles, and have specific adverse effects.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 764, "doc_id": "7552215", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: AMP-activated protein kinase (AMPK) activation increases inflammation-related fibrosis in the lungs.\n\nCANDIDATE_ABSTRACT:\nTITLE: Metformin reverses established lung fibrosis in a bleomycin model\nABSTRACT: Fibrosis is a pathological result of a dysfunctional repair response to tissue injury and occurs in a number of organs, including the lungs1. Cellular metabolism regulates tissue repair and remodelling responses to injury2-4. AMPK is a critical sensor of cellular bioenergetics and controls the switch from anabolic to catabolic metabolism5. However, the role of AMPK in fibrosis is not well understood. Here, we demonstrate that in humans with idiopathic pulmonary fibrosis (IPF) and in an experimental mouse model of lung fibrosis, AMPK activity is lower in fibrotic regions associated with metabolically active and apoptosis-resistant myofibroblasts. Pharmacological activation of AMPK in myofibroblasts from lungs of humans with IPF display lower fibrotic activity, along with enhanced mitochondrial biogenesis and normalization of sensitivity to apoptosis. In a bleomycin model of lung fibrosis in mice, metformin therapeutically accelerates the resolution of well-established fibrosis in an AMPK-dependent manner. These studies implicate deficient AMPK activation in non-resolving, pathologic fibrotic processes, and support a role for metformin (or other AMPK activators) to reverse established fibrosis by facilitating deactivation and apoptosis of myofibroblasts.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Pharmacological activation of AMPK in myofibroblasts from lungs of humans with IPF display lower fibrotic activity, along with enhanced mitochondrial biogenesis and normalization of sensitivity to apoptosis.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 54, "doc_id": "49556906", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Sildenafil improves erectile function in men who experience sexual dysfunction as a result of the use of SSRI antidepressants.\n\nCANDIDATE_ABSTRACT:\nTITLE: Treatment of antidepressant-associated sexual dysfunction with sildenafil: a randomized controlled trial.\nABSTRACT: CONTEXT Sexual dysfunction is a common adverse effect of antidepressants that frequently results in treatment noncompliance. OBJECTIVE To assess the efficacy of sildenafil citrate in men with sexual dysfunction associated with the use of selective and nonselective serotonin reuptake inhibitor (SRI) antidepressants. DESIGN, SETTING, AND PATIENTS Prospective, parallel-group, randomized, double-blind, placebo-controlled trial conducted between November 1, 2000, and January 1, 2001, at 3 US university medical centers among 90 male outpatients (mean [SD] age, 45 [8] years) with major depression in remission and sexual dysfunction associated with SRI antidepressant treatment. INTERVENTION Patients were randomly assigned to take sildenafil (n = 45) or placebo (n = 45) at a flexible dose starting at 50 mg and adjustable to 100 mg before sexual activity for 6 weeks. MAIN OUTCOME MEASURES The primary outcome measure was score on the Clinical Global Impression-Sexual Function (CGI-SF); secondary measures were scores on the International Index of Erectile Function, Arizona Sexual Experience Scale, Massachusetts General Hospital-Sexual Functioning Questionnaire, and Hamilton Rating Scale for Depression (HAM-D). RESULTS Among the 90 randomized patients, 93% (83/89) of patients treated per protocol took at least 1 dose of study drug and 85% (76/89) completed week 6 end-point assessments with last observation carried forward analyses. At a CGI-SF score of 2 or lower, 54.5% (24/44) of sildenafil compared with 4.4% (2/45) of placebo patients were much or very much improved (P<.001). Erectile function, arousal, ejaculation, orgasm, and overall satisfaction domain measures improved significantly in sildenafil compared with placebo patients. Mean depression scores remained consi [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Erectile function, arousal, ejaculation, orgasm, and overall satisfaction domain measures improved significantly in sildenafil compared with placebo patients.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1086, "doc_id": "39281140", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Active Ly49Q prevents neutrophil polarization.\n\nCANDIDATE_ABSTRACT:\nTITLE: A nuclear Argonaute promotes multi-generational epigenetic inheritance and germline immortality\nABSTRACT: Epigenetic information is frequently erased near the start of each new generation. In some cases, however, epigenetic information can be transmitted from parent to progeny (multigenerational epigenetic inheritance). A particularly notable example of this type of epigenetic inheritance is double-stranded RNA-mediated gene silencing in Caenorhabditis elegans. This RNA-mediated interference (RNAi) can be inherited for more than five generations. To understand this process, here we conduct a genetic screen for nematodes defective in transmitting RNAi silencing signals to future generations. This screen identified the heritable RNAi defective 1 (hrde-1) gene. hrde-1 encodes an Argonaute protein that associates with small interfering RNAs in the germ cells of progeny of animals exposed to double-stranded RNA. In the nuclei of these germ cells, HRDE-1 engages the nuclear RNAi defective pathway to direct the trimethylation of histone H3 at Lys 9 (H3K9me3) at RNAi-targeted genomic loci and promote RNAi inheritance. Under normal growth conditions, HRDE-1 associates with endogenously expressed short interfering RNAs, which direct nuclear gene silencing in germ cells. In hrde-1- or nuclear RNAi-deficient animals, germline silencing is lost over generational time. Concurrently, these animals exhibit steadily worsening defects in gamete formation and function that ultimately lead to sterility. These results establish that the Argonaute protein HRDE-1 directs gene-silencing events in germ-cell nuclei that drive multigenerational RNAi inheritance and promote immortality of the germ-cell lineage. We propose that C. elegans use the RNAi inheritance machinery to transmit epigenetic information, accrued by past generations, into future generations to regulate important biologic [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 77, "doc_id": "2541699", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is a HindIII polymorphism of fibronectin gene associated with nephrolithiasis?\n\nABSTRACT:\nTo evaluate the association between fibronectin gene (FN1) polymorphisms and calcium oxalate nephrolithiasis as a genetic risk factor. Genomic DNA of 143 patients with calcium oxalate nephrolithiasis and 154 healthy controls were screened for polymorphisms (HaeIII b, MspI, and HindIII) of the FN1 gene, using polymerase chain reaction-restriction fragments length polymorphism method. Allele and genotype frequencies were compared between the groups. Although the observed differences between distribution of genotypes of AA, AB, and BB (for HaeIII b), as well as CC, CD, and DD (MspI) were not significant, FF genotype for HindIII showed significant difference when compared with both EF and EE + EF genotype (P = .00202 and P = .00203, respectively).", "output": "{\"label\": \"yes\", \"rationale\": \"The results of our study revealed that HindIII polymorphism of the FN1 gene is highly associated with calcium oxalate stone disease. This association makes FN a good candidate for further studies about the etiology of stone disease, and in the future it could be a candidate marker for evaluating the genetic risks in patients with nephrolithiasis.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 19616291, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Excess gestational weight gain is associated with obesity-related pregnancy outcomes.\n\nCANDIDATE_PASSAGE:\nLife course breast cancer risk factors and adult breast density (United Kingdom) Objective To determine whether risk factors in childhood and early adulthood affect later mammographic breast density. Methods: Subjects were 628 women who attended a medical examination at the University of Glasgow Student Health Service (1948–1968), responded to a questionnaire (2001) and had a screening mammogram in Scotland (1989–2002). Mammograms (median age of 59years) were classified using a six category classification (SCC) of breast density percent. Logistic regression was used to determine associations between risk factors and having a high-risk mammogram (≥25 dense). Results: In multi-variable analyses, high-risk mammograms were associated with parity (adjusted odds ratio (OR) per child: 0.77 (95 confidence interval (CI) 0.61–0.99)), age at first birth, OR per year: 1.05 (0.99–1.11), smoking at university, OR smokers versus non-smokers: 0.58 (0.36–0.92) and body mass index (BMI) while at university, OR per 1kg/m20.75 (0.69–0.82). No associations with SCC were found for age at menarche, birth weight, oral contraceptive (OC) use, height, leg length or exercise at age 20. Conclusions: We confirm previous findings that breast density is affected by reproductive events and some anthropometric measures, however most of the risk factors acting throughout the life course which we examined were not closely related to adult breast density.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "394", "doc_id": "38784540", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: PKG-la plays an essential role in expression of spinal long term potentiation in PGK-la knockout mice.\n\nCANDIDATE_ABSTRACT:\nTITLE: Presynaptically Localized Cyclic GMP-Dependent Protein Kinase 1 Is a Key Determinant of Spinal Synaptic Potentiation and Pain Hypersensitivity\nABSTRACT: Synaptic long-term potentiation (LTP) at spinal neurons directly communicating pain-specific inputs from the periphery to the brain has been proposed to serve as a trigger for pain hypersensitivity in pathological states. Previous studies have functionally implicated the NMDA receptor-NO pathway and the downstream second messenger, cGMP, in these processes. Because cGMP can broadly influence diverse ion-channels, kinases, and phosphodiesterases, pre- as well as post-synaptically, the precise identity of cGMP targets mediating spinal LTP, their mechanisms of action, and their locus in the spinal circuitry are still unclear. Here, we found that Protein Kinase G1 (PKG-I) localized presynaptically in nociceptor terminals plays an essential role in the expression of spinal LTP. Using the Cre-lox P system, we generated nociceptor-specific knockout mice lacking PKG-I specifically in presynaptic terminals of nociceptors in the spinal cord, but not in post-synaptic neurons or elsewhere (SNS-PKG-I(-/-) mice). Patch clamp recordings showed that activity-induced LTP at identified synapses between nociceptors and spinal neurons projecting to the periaqueductal grey (PAG) was completely abolished in SNS-PKG-I(-/-) mice, although basal synaptic transmission was not affected. Analyses of synaptic failure rates and paired-pulse ratios indicated a role for presynaptic PKG-I in regulating the probability of neurotransmitter release. Inositol 1,4,5-triphosphate receptor 1 and myosin light chain kinase were recruited as key phosphorylation targets of presynaptic PKG-I in nociceptive neurons. Finally, behavioural analyses in vivo showed marked defects in SNS-PKG-I(-/-) mice in several models of activity-induced nociceptive hypersensitivity, and pharmacological studies identified [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Patch clamp recordings showed that activity-induced LTP at identified synapses between nociceptors and spinal neurons projecting to the periaqueductal grey (PAG) was completely abolished in SNS-PKG-I(-/-) mice, although basal synaptic transmission was not affected.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 912, "doc_id": "11254556", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Ten percent (10%) of kidney cancers in the UK are attributable to excess weight.\n\nCANDIDATE_PASSAGE:\nCongruent Visual Speech Enhances Cortical Entrainment to Continuous Auditory Speech in Noise-Free Conditions. UNLABELLED Congruent audiovisual speech enhances our ability to comprehend a speaker, even in noise-free conditions. When incongruent auditory and visual information is presented concurrently, it can hinder a listener's perception and even cause him or her to perceive information that was not presented in either modality. Efforts to investigate the neural basis of these effects have often focused on the special case of discrete audiovisual syllables that are spatially and temporally congruent, with less work done on the case of natural, continuous speech. Recent electrophysiological studies have demonstrated that cortical response measures to continuous auditory speech can be easily obtained using multivariate analysis methods. Here, we apply such methods to the case of audiovisual speech and, importantly, present a novel framework for indexing multisensory integration in the context of continuous speech. Specifically, we examine how the temporal and contextual congruency of ongoing audiovisual speech affects the cortical encoding of the speech envelope in humans using electroencephalography. We demonstrate that the cortical representation of the speech envelope is enhanced by the presentation of congruent audiovisual speech in noise-free conditions. Furthermore, we show that this is likely attributable to the contribution of neural generators that are not particularly active during unimodal stimulation and that it is most prominent at the temporal scale corresponding to syllabic rate (2-6 Hz). Finally, our data suggest that neural entrainment to the speech envelope is inhibited when the auditory and visual streams are incongruent both temporally and [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1148", "doc_id": "14437255", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Low expression of miR7a does represses target genes and exerts a biological function in ovaries.\n\nCANDIDATE_PASSAGE:\nParathyroid hormone-induced E4BP4/NFIL3 down-regulates transcription in osteoblasts. Parathyroid hormone (PTH), a major regulator of bone metabolism, activates the PTHR1 receptor on the osteoblast plasma membrane to initiate signaling and induce transcription of primary response genes. Subsequently, primary genes with transcriptional activity regulate expression of downstream PTH targets. We have identified the adenovirus E4 promoter-binding protein/nuclear factor regulated by IL-3 (E4bp4) as a PTH-induced primary gene in osteoblasts. E4BP4 is a basic leucine zipper (bZIP) transcription factor that represses or activates transcription in non-osteoblastic cells. We report here that PTH rapidly and transiently induced E4bp4 mRNA in osteoblastic cells and that this induction did not require protein synthesis. PTH also induced E4BP4 protein synthesis and E4BP4 binding to a consensus but not to a mutant E4BP4 response element (EBPRE). E4BP4 overexpression inhibited an EBPRE-containing promoter-reporter construct, whereas PTH treatment attenuated activity of the same construct in primary mouse osteoblasts. Finally, E4BP4 overexpression inhibited PTH-induced activity of a cyclooxygenase-2 promoter-reporter construct. Our data suggest a role for E4BP4 in attenuation of PTH target gene transcription in osteoblasts.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "715", "doc_id": "9301606", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Do baseline depression levels affect efficacy of cognitive-behavioral self-help treatment for insomnia?\n\nABSTRACT:\nCognitive-behavioral therapy can effectively treat insomnia (CBT-I). Randomized controlled trials have shown efficacy of self-help CBT-I, but unclear is whether excluding depressive patients boosted treatment effects. We administered unsupported self-help CBT-I to insomnia patients with low and high depression levels. Based on the validated Centre of Epidemiological Studies-Depression (CES-D) scale, the internet-recruited sample (N = 479) was divided into three groups: low depression scores (n = 198), mild depression scores (n = 182), and high depression scores (n = 99). Follow-ups were 4 and 18 weeks after completion of the treatment. At 4-week follow-up, all groups had a similar amelioration on the primary sleep measures (d = 0.1-0.7; P < 0.05) and the secondary insomnia ratings (d = 1.2; P < 0.001). The only difference was that the high/mild depression groups had a steeper reduction in depression (d = 1.0-1.1; P < 0.001) and anxiety scores (d = 0.7-0.8; P < 0.001) than the low depression group (depression and anxiety: d = 0.3; P < 0.01), possibly due to floor effects in the latter group. The observed effects were sustained at the 18-week follow-up.", "output": "{\"label\": \"no\", \"rationale\": \"This study showed that CBT-I is effective regardless of baseline depression levels. Treating the combination of insomnia and depression is an extra challenge since it is associated with increased sleep problems. These data may help us understand the relationship between insomnia and depression and indicate that self-help CBT-I may be a promising addition to regular depression treatment.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 23080373, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: B cells go though plasmablast differentiation and antibody production by continuous expression of EBI2.\n\nCANDIDATE_PASSAGE:\nGuidance of B cells by the orphan G protein-coupled receptor EBI2 shapes humoral immune responses. Humoral immunity depends on both rapid and long-term antibody production against invading pathogens. This is achieved by the generation of spatially distinct extrafollicular plasmablast and follicular germinal center (GC) B cell populations, but the signals that guide responding B cells to these alternative compartments have not been fully elucidated. Here, we show that expression of the orphan G protein-coupled receptor Epstein-Barr virus-induced gene 2 (EBI2, also known as GPR183) by activated B cells was essential for their movement to extrafollicular sites and induction of early plasmablast responses. Conversely, downregulation of EBI2 enabled B cells to access the center of follicles and promoted efficient GC formation. EBI2 therefore provides a previously uncharacterized dimension to B cell migration that is crucial for coordinating rapid versus long-term antibody responses.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "152", "doc_id": "15488881", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Rising temperatures caused by global warming lowers the risk of dengue fever transmission.\n\nCANDIDATE_PASSAGE:\nSpatial and Temporal Clustering of Dengue Virus Transmission in Thai Villages BACKGROUND Transmission of dengue viruses (DENV), the leading cause of arboviral disease worldwide, is known to vary through time and space, likely owing to a combination of factors related to the human host, virus, mosquito vector, and environment. An improved understanding of variation in transmission patterns is fundamental to conducting surveillance and implementing disease prevention strategies. To test the hypothesis that DENV transmission is spatially and temporally focal, we compared geographic and temporal characteristics within Thai villages where DENV are and are not being actively transmitted. METHODS AND FINDINGS Cluster investigations were conducted within 100 m of homes where febrile index children with (positive clusters) and without (negative clusters) acute dengue lived during two seasons of peak DENV transmission. Data on human infection and mosquito infection/density were examined to precisely (1) define the spatial and temporal dimensions of DENV transmission, (2) correlate these factors with variation in DENV transmission, and (3) determine the burden of inapparent and symptomatic infections. Among 556 village children enrolled as neighbors of 12 dengue-positive and 22 dengue-negative index cases, all 27 DENV infections (4.9% of enrollees) occurred in positive clusters (p < 0.01; attributable risk [AR] = 10.4 per 100; 95% confidence interval 1-19.8 per 100]. In positive clusters, 12.4% of enrollees became infected in a 15-d period and DENV infections were aggregated centrally near homes of index cases. As only 1 of 217 pairs of serologic specimens tested in positive clusters revealed a recent DENV infection that occurred prior to cluster initiation, we attribu [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1053", "doc_id": "18816720", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Low expression of miR7a does represses target genes and exerts a biological function in ovaries.\n\nCANDIDATE_ABSTRACT:\nTITLE: Assessing the ceRNA hypothesis with quantitative measurements of miRNA and target abundance.\nABSTRACT: Recent studies have reported that competitive endogenous RNAs (ceRNAs) can act as sponges for a microRNA (miRNA) through their binding sites and that changes in ceRNA abundances from individual genes can modulate the activity of miRNAs. Consideration of this hypothesis would benefit from knowing the quantitative relationship between a miRNA and its endogenous target sites. Here, we altered intracellular target site abundance through expression of an miR-122 target in hepatocytes and livers and analyzed the effects on miR-122 target genes. Target repression was released in a threshold-like manner at high target site abundance (≥1.5 × 10(5) added target sites per cell), and this threshold was insensitive to the effective levels of the miRNA. Furthermore, in response to extreme metabolic liver disease models, global target site abundance of hepatocytes did not change sufficiently to affect miRNA-mediated repression. Thus, modulation of miRNA target abundance is unlikely to cause significant effects on gene expression and metabolism through a ceRNA effect.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 715, "doc_id": "18421962", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The minor G allele of FOXO3 up-regulates IL-10.\n\nCANDIDATE_ABSTRACT:\nTITLE: Human SNP Links Differential Outcomes in Inflammatory and Infectious Disease to a FOXO3-Regulated Pathway\nABSTRACT: The clinical course and eventual outcome, or prognosis, of complex diseases varies enormously between affected individuals. This variability critically determines the impact a disease has on a patient's life but is very poorly understood. Here, we exploit existing genome-wide association study data to gain insight into the role of genetics in prognosis. We identify a noncoding polymorphism in FOXO3A (rs12212067: T > G) at which the minor (G) allele, despite not being associated with disease susceptibility, is associated with a milder course of Crohn's disease and rheumatoid arthritis and with increased risk of severe malaria. Minor allele carriage is shown to limit inflammatory responses in monocytes via a FOXO3-driven pathway, which through TGFβ1 reduces production of proinflammatory cytokines, including TNFα, and increases production of anti-inflammatory cytokines, including IL-10. Thus, we uncover a shared genetic contribution to prognosis in distinct diseases that operates via a FOXO3-driven pathway modulating inflammatory responses.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Minor allele carriage is shown to limit inflammatory responses in monocytes via a FOXO3-driven pathway, which through TGFβ1 reduces production of proinflammatory cytokines, including TNFα, and increases production of anti-inflammatory cytokines, including IL-10.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1234, "doc_id": "13905670", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\nABSTRACT: Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens. However, signals underlying mTEC development remain largely unclear. Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals. Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment. Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner. These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1004, "doc_id": "2734421", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Rising temperatures caused by global warming lowers the risk of dengue fever transmission.\n\nCANDIDATE_PASSAGE:\nSpatial and Temporal Clustering of Dengue Virus Transmission in Thai Villages BACKGROUND Transmission of dengue viruses (DENV), the leading cause of arboviral disease worldwide, is known to vary through time and space, likely owing to a combination of factors related to the human host, virus, mosquito vector, and environment. An improved understanding of variation in transmission patterns is fundamental to conducting surveillance and implementing disease prevention strategies. To test the hypothesis that DENV transmission is spatially and temporally focal, we compared geographic and temporal characteristics within Thai villages where DENV are and are not being actively transmitted. METHODS AND FINDINGS Cluster investigations were conducted within 100 m of homes where febrile index children with (positive clusters) and without (negative clusters) acute dengue lived during two seasons of peak DENV transmission. Data on human infection and mosquito infection/density were examined to precisely (1) define the spatial and temporal dimensions of DENV transmission, (2) correlate these factors with variation in DENV transmission, and (3) determine the burden of inapparent and symptomatic infections. Among 556 village children enrolled as neighbors of 12 dengue-positive and 22 dengue-negative index cases, all 27 DENV infections (4.9% of enrollees) occurred in positive clusters (p < 0.01; attributable risk [AR] = 10.4 per 100; 95% confidence interval 1-19.8 per 100]. In positive clusters, 12.4% of enrollees became infected in a 15-d period and DENV infections were aggregated centrally near homes of index cases. As only 1 of 217 pairs of serologic specimens tested in positive clusters revealed a recent DENV infection that occurred prior to cluster initiation, we attribu [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1053", "doc_id": "18816720", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Destination container port throughput(CPT) is positively related to dengue virus (DENV-1) diffusion in air traffic shipments.\n\nCANDIDATE_PASSAGE:\nPopulation Density, Water Supply, and the Risk of Dengue Fever in Vietnam: Cohort Study and Spatial Analysis BACKGROUND Aedes aegypti, the major vector of dengue viruses, often breeds in water storage containers used by households without tap water supply, and occurs in high numbers even in dense urban areas. We analysed the interaction between human population density and lack of tap water as a cause of dengue fever outbreaks with the aim of identifying geographic areas at highest risk. METHODS AND FINDINGS We conducted an individual-level cohort study in a population of 75,000 geo-referenced households in Vietnam over the course of two epidemics, on the basis of dengue hospital admissions (n = 3,013). We applied space-time scan statistics and mathematical models to confirm the findings. We identified a surprisingly narrow range of critical human population densities between around 3,000 to 7,000 people/km² prone to dengue outbreaks. In the study area, this population density was typical of villages and some peri-urban areas. Scan statistics showed that areas with a high population density or adequate water supply did not experience severe outbreaks. The risk of dengue was higher in rural than in urban areas, largely explained by lack of piped water supply, and in human population densities more often falling within the critical range. Mathematical modeling suggests that simple assumptions regarding area-level vector/host ratios may explain the occurrence of outbreaks. CONCLUSIONS Rural areas may contribute at least as much to the dissemination of dengue fever as cities. Improving water supply and vector control in areas with a human population density critical for dengue transmission could increase the efficiency of control efforts. Please see later in the [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "337", "doc_id": "2097256", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Activation of the Rac1 homolog CED-10 kills viable cells in SRGP-1 mutant Caenorhabditis elegans.\n\nCANDIDATE_PASSAGE:\nE-cadherin engagement stimulates proliferation via Rac1 E-cadherin has been linked to the suppression of tumor growth and the inhibition of cell proliferation in culture. We observed that progressively decreasing the seeding density of normal rat kidney-52E (NRK-52E) or MCF-10A epithelial cells from confluence, indeed, released cells from growth arrest. Unexpectedly, a further decrease in seeding density so that cells were isolated from neighboring cells decreased proliferation. Experiments using microengineered substrates showed that E-cadherin engagement stimulated the peak in proliferation at intermediate seeding densities, and that the proliferation arrest at high densities did not involve E-cadherin, but rather resulted from a crowding-dependent decrease in cell spreading against the underlying substrate. Rac1 activity, which was induced by E-cadherin engagement specifically at intermediate seeding densities, was required for the cadherin-stimulated proliferation, and the control of Rac1 activation by E-cadherin was mediated by p120-catenin. Together, these findings demonstrate a stimulatory role for E-cadherin in proliferative regulation, and identify a simple mechanism by which cell–cell contact may trigger or inhibit epithelial cell proliferation in different settings.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "71", "doc_id": "14149065", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does a family meetings intervention prevent depression and anxiety in family caregivers of dementia patients?\n\nABSTRACT:\nFamily caregivers of dementia patients are at increased risk of developing depression or anxiety. A multi-component program designed to mobilize support of family networks demonstrated effectiveness in decreasing depressive symptoms in caregivers. However, the impact of an intervention consisting solely of family meetings on depression and anxiety has not yet been evaluated. This study examines the preventive effects of family meetings for primary caregivers of community-dwelling dementia patients. A randomized multicenter trial was conducted among 192 primary caregivers of community dwelling dementia patients. Caregivers did not meet the diagnostic criteria for depressive or anxiety disorder at baseline. Participants were randomized to the family meetings intervention (n = 96) or usual care (n = 96) condition. The intervention consisted of two individual sessions and four family meetings which occurred once every 2 to 3 months for a year. Outcome measures after 12 months were the incidence of a clinical depressive or anxiety disorder and change in depressive and anxiety symptoms (primary outcomes), caregiver burden and quality of life (secondary outcomes). Intention-to-treat as well as per protocol analyses were performed. A substantial number of caregivers (72/192) developed a depressive or anxiety disorder within 12 months. The intervention was not superior to usual care either in reducing the risk of disorder onset (adjusted IRR 0.98; 95% CI 0.69 to 1.38) or in reducing depressive (randomization-by-time interaction coefficient = -1.40; 95% CI -3.91 to 1.10) or anxiety symptoms (randomization-by-time interaction coefficient = -0.55; 95% CI -1.59 to 0.49). The intervention did not reduce caregiver burden or their health related quality of life.", "output": "{\"label\": \"no\", \"rationale\": \"This study did not demonstrate preventive effects of family meetings on the mental health of family caregivers. Further research should determine whether this intervention might be more beneficial if provided in a more concentrated dose, when applied for therapeutic purposes or targeted towards subgroups of caregivers.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 22303473, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Toll-like receptor (TLR) signaling is involved in the pathogenesis of human MDS.\n\nCANDIDATE_PASSAGE:\nInduction of myelodysplasia by myeloid-derived suppressor cells. Myelodysplastic syndromes (MDS) are age-dependent stem cell malignancies that share biological features of activated adaptive immune response and ineffective hematopoiesis. Here we report that myeloid-derived suppressor cells (MDSC), which are classically linked to immunosuppression, inflammation, and cancer, were markedly expanded in the bone marrow of MDS patients and played a pathogenetic role in the development of ineffective hematopoiesis. These clonally distinct MDSC overproduce hematopoietic suppressive cytokines and function as potent apoptotic effectors targeting autologous hematopoietic progenitors. Using multiple transfected cell models, we found that MDSC expansion is driven by the interaction of the proinflammatory molecule S100A9 with CD33. These 2 proteins formed a functional ligand/receptor pair that recruited components to CD33’s immunoreceptor tyrosine-based inhibition motif (ITIM), inducing secretion of the suppressive cytokines IL-10 and TGF-β by immature myeloid cells. S100A9 transgenic mice displayed bone marrow accumulation of MDSC accompanied by development of progressive multilineage cytopenias and cytological dysplasia. Importantly, early forced maturation of MDSC by either all-trans-retinoic acid treatment or active immunoreceptor tyrosine-based activation motif–bearing (ITAM-bearing) adapter protein (DAP12) interruption of CD33 signaling rescued the hematologic phenotype. These findings indicate that primary bone marrow expansion of MDSC driven by the S100A9/CD33 pathway perturbs hematopoiesis and contributes to the development of MDS.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1306", "doc_id": "5836", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Primary cervical cancer screening with HPV detection has higher longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_PASSAGE:\nEvidence regarding human papillomavirus testing in secondary prevention of cervical cancer. More than ever, clinicians need regularly updated reviews given the continuously increasing amount of new information regarding innovative cervical cancer prevention methods. A summary is given from recent meta-analyses and systematic reviews on 3 possible clinical applications of human papillomavirus (HPV) testing: triage of women with equivocal or low-grade cytologic abnormalities; prediction of the therapeutic outcome after treatment of cervical intraepithelial neoplasia (CIN) lesions, and last not but not least, primary screening for cervical cancer and pre-cancer. Consistent evidence is available indicating that HPV-triage with the Hybrid Capture(®) 2 assay (Qiagen Gaithersburg, Inc., MD, USA [previously Digene Corp.] (HC2) is more accurate (higher sensitivity, similar specificity) than repeat cytology to triage women with equivocal Pap smear results. Several other tests show at least similar accuracy but mRNA testing with the APTIMA(®) (Gen-Probe Inc., San Diego, CA, USA) test is similarly sensitive but more specific compared to HC2. In triage of low-grade squamous intraepithelial lesions (LSIL), HC2 is more sensitive but its specificity is substantially lower compared to repeat cytology. The APTIMA(®) test is more specific than HC2 without showing a loss in sensitivity. Identification of DNA of HPV types 16 and/or 18, or RNA from the five most carcinogenic HPV types allow selecting women at highest risk for CIN3+ but the sensitivity and negative predictive value of these markers are lower than full-range high-risk HPV (hrHPV) testing. After conservative treatment of cervical pre-cancer, HPV testing picks up more quickly, with higher sensitivity and not lower sp [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "971", "doc_id": "28617573", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pioglitazone use is not associated with an increased risk of prostate cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Vaccines against malaria\nABSTRACT: There is no licenced vaccine against any human parasitic disease and Plasmodium falciparum malaria, a major cause of infectious mortality, presents a great challenge to vaccine developers. This has led to the assessment of a wide variety of approaches to malaria vaccine design and development, assisted by the availability of a safe challenge model for small-scale efficacy testing of vaccine candidates. Malaria vaccine development has been at the forefront of assessing many new vaccine technologies including novel adjuvants, vectored prime-boost regimes and the concept of community vaccination to block malaria transmission. Most current vaccine candidates target a single stage of the parasite's life cycle and vaccines against the early pre-erythrocytic stages have shown most success. A protein in adjuvant vaccine, working through antibodies against sporozoites, and viral vector vaccines targeting the intracellular liver-stage parasite with cellular immunity show partial efficacy in humans, and the anti-sporozoite vaccine is currently in phase III trials. However, a more effective malaria vaccine suitable for widespread cost-effective deployment is likely to require a multi-component vaccine targeting more than one life cycle stage. The most attractive near-term approach to develop such a product is to combine existing partially effective pre-erythrocytic vaccine candidates.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 952, "doc_id": "2264455", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Long chain polyunsaturated fatty acids supplementation reduces wheezing and asthma.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effect of n-3 long chain polyunsaturated fatty acid supplementation in pregnancy on infants’ allergies in first year of life: randomised controlled trial\nABSTRACT: OBJECTIVE To determine whether dietary n-3 long chain polyunsaturated fatty acid (LCPUFA) supplementation of pregnant women with a fetus at high risk of allergic disease reduces immunoglobulin E associated eczema or food allergy at 1 year of age. DESIGN Follow-up of infants at high hereditary risk of allergic disease in the Docosahexaenoic Acid to Optimise Mother Infant Outcome (DOMInO) randomised controlled trial. SETTING Adelaide, South Australia. PARTICIPANTS 706 infants at high hereditary risk of developing allergic disease whose mothers were participating in the DOMInO trial. INTERVENTIONS The intervention group (n=368) was randomly allocated to receive fish oil capsules (providing 900 mg of n-3 LCPUFA daily) from 21 weeks' gestation until birth; the control group (n=338) received matched vegetable oil capsules without n-3 LCPUFA. MAIN OUTCOME MEASURE Immunoglobulin E associated allergic disease (eczema or food allergy with sensitisation) at 1 year of age. RESULTS No differences were seen in the overall percentage of infants with immunoglobulin E associated allergic disease between the n-3 LCPUFA and control groups (32/368 (9%) v 43/338 (13%); unadjusted relative risk 0.68, 95% confidence interval 0.43 to 1.05, P=0.08; adjusted relative risk 0.70, 0.45 to 1.09, P=0.12), although the percentage of infants diagnosed as having atopic eczema (that is, eczema with associated sensitisation) was lower in the n-3 LCPUFA group (26/368 (7%) v 39/338 (12%); unadjusted relative risk 0.61, 0.38 to 0.98, P=0.04; adjusted relative risk 0.64, 0.40 to 1.02, P=0.06). Fewer infants were sensitised to egg in the n-3 LCPUFA group (34/368 (9%) v 52/338 (15%); unadjusted relative risk 0.61, 0.40 to 0.91, P=0.02; adjusted relative risk 0.62, 0.41 to 0.93, P=0.02), but no diffe [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 710, "doc_id": "22442133", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: HNF4A mutations can cause diabetes in mutant carriers by the age of 14 years\n\nCANDIDATE_PASSAGE:\nMacrosomia and Hyperinsulinaemic Hypoglycaemia in Patients with Heterozygous Mutations in the HNF4A Gene Background Macrosomia is associated with considerable neonatal and maternal morbidity. Factors that predict macrosomia are poorly understood. The increased rate of macrosomia in the offspring of pregnant women with diabetes and in congenital hyperinsulinaemia is mediated by increased foetal insulin secretion. We assessed the in utero and neonatal role of two key regulators of pancreatic insulin secretion by studying birthweight and the incidence of neonatal hypoglycaemia in patients with heterozygous mutations in the maturity-onset diabetes of the young (MODY) genes HNF4A (encoding HNF-4α) and HNF1A/TCF1 (encoding HNF-1α), and the effect of pancreatic deletion of Hnf4a on foetal and neonatal insulin secretion in mice.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "491", "doc_id": "56893404", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Increased microtubule acetylation worsens interference of axonal transport caused by LRRK2 Roc-COR domain mutations.\n\nCANDIDATE_PASSAGE:\nIncreasing microtubule acetylation rescues axonal transport and locomotor deficits caused by LRRK2 Roc-COR domain mutations Leucine-rich repeat kinase 2 (LRRK2) mutations are the most common genetic cause of Parkinson's disease. LRRK2 is a multifunctional protein affecting many cellular processes and has been described to bind microtubules. Defective microtubule-based axonal transport is hypothesized to contribute to Parkinson's disease, but whether LRRK2 mutations affect this process to mediate pathogenesis is not known. Here we find that LRRK2 containing pathogenic Roc-COR domain mutations (R1441C, Y1699C) preferentially associates with deacetylated microtubules, and inhibits axonal transport in primary neurons and in Drosophila, causing locomotor deficits in vivo. In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport. In vivo knockdown of the deacetylases HDAC6 and Sirt2, or administration of TSA rescues both axonal transport and locomotor behavior. Thus, this study reveals a pathogenic mechanism and a potential intervention for Parkinson's disease.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "615", "doc_id": "9638032", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Many proteins in human cells can be post-translationally modified at lysine residues via acetylation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cold Exposure Promotes Atherosclerotic Plaque Growth and Instability via UCP1-Dependent Lipolysis\nABSTRACT: Molecular mechanisms underlying the cold-associated high cardiovascular risk remain unknown. Here, we show that the cold-triggered food-intake-independent lipolysis significantly increased plasma levels of small low-density lipoprotein (LDL) remnants, leading to accelerated development of atherosclerotic lesions in mice. In two genetic mouse knockout models (apolipoprotein E(-/-) [ApoE(-/-)] and LDL receptor(-/-) [Ldlr(-/-)] mice), persistent cold exposure stimulated atherosclerotic plaque growth by increasing lipid deposition. Furthermore, marked increase of inflammatory cells and plaque-associated microvessels were detected in the cold-acclimated ApoE(-/-) and Ldlr(-/-) mice, leading to plaque instability. Deletion of uncoupling protein 1 (UCP1), a key mitochondrial protein involved in thermogenesis in brown adipose tissue (BAT), in the ApoE(-/-) strain completely protected mice from the cold-induced atherosclerotic lesions. Cold acclimation markedly reduced plasma levels of adiponectin, and systemic delivery of adiponectin protected ApoE(-/-) mice from plaque development. These findings provide mechanistic insights on low-temperature-associated cardiovascular risks.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 756, "doc_id": "970012", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Combination nicotine replacement therapies with varenicline or bupropion are more effective after 12 weeks of reatment compared to varenicline monotherapy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Combination varenicline and bupropion SR for tobacco-dependence treatment in cigarette smokers: a randomized trial.\nABSTRACT: IMPORTANCE Combining pharmacotherapies for tobacco-dependence treatment may increase smoking abstinence. OBJECTIVE To determine efficacy and safety of varenicline and bupropion sustained-release (SR; combination therapy) compared with varenicline (monotherapy) in cigarette smokers. DESIGN, SETTING, AND PARTICIPANTS Randomized, blinded, placebo-controlled multicenter clinical trial with a 12-week treatment period and follow-up through week 52 conducted between October 2009 and April 2013 at 3 midwestern clinical research sites. Five hundred six adult (≥18 years) cigarette smokers were randomly assigned and 315 (62%) completed the study. INTERVENTIONS Twelve weeks of varenicline and bupropion SR or varenicline and placebo. MAIN OUTCOMES AND MEASURES Primary outcome was abstinence rates at week 12, defined as prolonged (no smoking from 2 weeks after the target quit date) abstinence and 7-day point-prevalence (no smoking past 7 days) abstinence. Secondary outcomes were prolonged and point-prevalence smoking abstinence rates at weeks 26 and 52. Outcomes were biochemically confirmed. RESULTS At 12 weeks, 53.0% of the combination therapy group achieved prolonged smoking abstinence and 56.2% achieved 7-day point-prevalence smoking abstinence compared with 43.2% and 48.6% in varenicline monotherapy (odds ratio [OR], 1.49; 95% CI, 1.05-2.12; P = .03 and OR, 1.36; 95% CI, 0.95-1.93; P = .09, respectively). At 26 weeks, 36.6% of the combination therapy group achieved prolonged and 38.2% achieved 7-day point-prevalence smoking abstinence compared with 27.6% and 31.9% in varenicline monotherapy (OR, 1.52; 95% CI, 1.04-2.22; P = .03 and OR, 1.32; 95% CI, 0.91-1.91; P = .14, respectively). At 52 weeks, 30.9% of the combination therapy group achieved prolonged and 36.6% achi [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"RESULTS At 12 weeks, 53.0% of the combination therapy group achieved prolonged smoking abstinence and 56.2% achieved 7-day point-prevalence smoking abstinence compared with 43.2% and 48.6% in varenicline monotherapy (odds ratio [OR], 1.49; 95% CI, 1.05-2.12; P = .03 and OR, 1.36; 95% CI, 0.95-1.93; P = .09, respectively).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 272, "doc_id": "11614737", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does minocycline inhibit glial proliferation in the H-Tx rat model of congenital hydrocephalus?\n\nABSTRACT:\nReactive astrocytosis and microgliosis are important features of the pathophysiology of hydrocephalus, and persistent glial \"scars\" that form could exacerbate neuroinflammation, impair cerebral perfusion, impede neuronal regeneration, and alter biomechanical properties. The purpose of this study was to determine the efficacy of minocycline, an antibiotic known for its anti-inflammatory properties, to reduce gliosis in the H-Tx rat model of congenital hydrocephalus. Minocycline (45 mg/kg/day i.p. in 5% sucrose at a concentration of 5-10 mg/ml) was administered to hydrocephalic H-Tx rats from postnatal day 15 to day 21, when ventriculomegaly had reached moderate to severe stages. Treated animals were compared to age-matched non-hydrocephalic and untreated hydrocephalic littermates. The cerebral cortex (both gray matter laminae and white matter) was processed for immunohistochemistry (glial fibrillary acidic protein, GFAP, for astrocytes and ionized calcium binding adaptor molecule, Iba-1, for microglia) and analyzed by qualitative and quantitative light microscopy. The mean number of GFAP-immunoreactive astrocytes was significantly higher in untreated hydrocephalic animals compared to both types of controls (p < 0.001). Minocycline treatment of hydrocephalic animals reduced the number of GFAP immunoreactive cells significantly (p < 0.001). Likewise, the mean number of Iba-1 immunoreactive microglia was significantly higher in untreated hydrocephalic animals compared to both types of controls (p < 0.001). Furthermore, no differences in the numbers of GFAP-positive astrocytes or Iba-1-positive microglia were noted between control animals receiving no minocycline and control animals receiving minocycline, suggesting that minocycline does not produce an effect und [TRUNCATED]", "output": "{\"label\": \"yes\", \"rationale\": \"Overall, these data suggest that minocycline treatment is effective in reducing the gliosis that accompanies hydrocephalus, and thus may provide an added benefit when used as a supplement to ventricular shunting.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 20507614, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does limb-salvage surgery offer patients better quality of life and functional capacity than amputation?\n\nABSTRACT:\nPatients with aggressive lower extremity musculoskeletal tumors may be candidates for either above-knee amputation or limb-salvage surgery. However, the subjective and objective benefits of limb-salvage surgery compared with amputation are not fully clear.QUESTIONS/ We therefore compared functional status and quality of life for patients treated with above-knee amputation versus limb-salvage surgery. We reviewed 20 of 51 patients aged 15 years and older treated with above-knee amputation or limb-salvage surgery for aggressive musculoskeletal tumors around the knee between 1994 and 2004 as a retrospective cohort study. At last followup we obtained the Physiological Cost Index, the Reintegration to Normal Living Index, SF-36, and the Toronto Extremity Salvage Score questionnaires. The minimum followup was 12 months (median, 56 months; range, 12-108 months). Compared with patients having above-knee amputation, patients undergoing limb-salvage surgery had superior Physiological Cost Index scores and Reintegration to Normal Living Index. The Toronto Extremity Salvage scores and SF-36 scores were similar in the two groups.", "output": "{\"label\": \"maybe\", \"rationale\": \"These data suggest that limb-salvage surgery offers better gait efficiency and return to normal living compared with above-knee amputation, but does not improve the patient's perception of quality of life.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 22302658, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: GATA3 regulates self-renewal capacity in bone marrow hematopoietic stem cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Dynamic capsule restructuring by the main pneumococcal autolysin LytA in response to the epithelium\nABSTRACT: Bacterial pathogens produce complex carbohydrate capsules to protect against bactericidal immune molecules. Paradoxically, the pneumococcal capsule sensitizes the bacterium to antimicrobial peptides found on epithelial surfaces. Here we show that upon interaction with antimicrobial peptides, encapsulated pneumococci survive by removing capsule from the cell surface within minutes in a process dependent on the suicidal amidase autolysin LytA. In contrast to classical bacterial autolysis, during capsule shedding, LytA promotes bacterial survival and is dispersed circumferentially around the cell. However, both autolysis and capsule shedding depend on the cell wall hydrolytic activity of LytA. Capsule shedding drastically increases invasion of epithelial cells and is the main pathway by which pneumococci reduce surface bound capsule during early acute lung infection of mice. The previously unrecognized role of LytA in removing capsule to combat antimicrobial peptides may explain why nearly all clinical isolates of pneumococci conserve this enzyme despite the lethal selective pressure of antibiotics.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 445, "doc_id": "1234098", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: T regulatory cells (tTregs) lacking αvβ8 are more adept at suppressing pathogenic T-cell responses during active inflammation.\n\nCANDIDATE_PASSAGE:\nLocal, Efflux-Dependent Auxin Gradients as a Common Module for Plant Organ Formation Plants, compared to animals, exhibit an amazing adaptability and plasticity in their development. This is largely dependent on the ability of plants to form new organs, such as lateral roots, leaves, and flowers during postembryonic development. Organ primordia develop from founder cell populations into organs by coordinated cell division and differentiation. Here, we show that organ formation in Arabidopsis involves dynamic gradients of the signaling molecule auxin with maxima at the primordia tips. These gradients are mediated by cellular efflux requiring asymmetrically localized PIN proteins, which represent a functionally redundant network for auxin distribution in both aerial and underground organs. PIN1 polar localization undergoes a dynamic rearrangement, which correlates with establishment of auxin gradients and primordium development. Our results suggest that PIN-dependent, local auxin gradients represent a common module for formation of all plant organs, regardless of their mature morphology or developmental origin.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1130", "doc_id": "16557565", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Crossover hot spots are not found within gene promoters in Saccharomyces cerevisiae.\n\nCANDIDATE_PASSAGE:\nMapping Meiotic Single-Strand DNA Reveals a New Landscape of DNA Double-Strand Breaks in Saccharomyces cerevisiae DNA double-strand breaks (DSBs), which are formed by the Spo11 protein, initiate meiotic recombination. Previous DSB-mapping studies have used rad50S or sae2Δ mutants, which are defective in break processing, to accumulate Spo11-linked DSBs, and report large (≥ 50 kb) “DSB-hot” regions that are separated by “DSB-cold” domains of similar size. Substantial recombination occurs in some DSB-cold regions, suggesting that DSB patterns are not normal in rad50S or sae2Δ mutants. We therefore developed a novel method to map genome-wide, single-strand DNA (ssDNA)–associated DSBs that accumulate in processing-capable, repair-defective dmc1Δ and dmc1Δ rad51Δ mutants. DSBs were observed at known hot spots, but also in most previously identified “DSB-cold” regions, including near centromeres and telomeres. Although approximately 40% of the genome is DSB-cold in rad50S mutants, analysis of meiotic ssDNA from dmc1Δ shows that most of these regions have substantial DSB activity. Southern blot assays of DSBs in selected regions in dmc1Δ, rad50S, and wild-type cells confirm these findings. Thus, DSBs are distributed much more uniformly than was previously believed. Comparisons of DSB signals in dmc1, dmc1 rad51, and dmc1 spo11 mutant strains identify Dmc1 as a critical strand-exchange activity genome-wide, and confirm previous conclusions that Spo11-induced lesions initiate all meiotic recombination.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "294", "doc_id": "10874408", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Incidence of 10/66 dementia is higher than the incidence of DSM-IV dementia.\n\nCANDIDATE_ABSTRACT:\nTITLE: Dementia incidence and mortality in middle-income countries, and associations with indicators of cognitive reserve: a 10/66 Dementia Research Group population-based cohort study\nABSTRACT: BACKGROUND Results of the few cohort studies from countries with low incomes or middle incomes suggest a lower incidence of dementia than in high-income countries. We assessed incidence of dementia according to criteria from the 10/66 Dementia Research Group and Diagnostic and Statistical Manual of Mental Disorders (DSM) IV, the effect of dementia at baseline on mortality, and the independent effects of age, sex, socioeconomic position, and indicators of cognitive reserve. METHODS We did a population-based cohort study of all people aged 65 years and older living in urban sites in Cuba, the Dominican Republic, and Venezuela, and rural and urban sites in Peru, Mexico, and China, with ascertainment of incident 10/66 and DSM-IV dementia 3-5 years after cohort inception. We used questionnaires to obtain information about age in years, sex, educational level, literacy, occupational attainment, and number of household assets. We obtained information about mortality from all sites. For participants who had died, we interviewed a friend or relative to ascertain the likelihood that they had dementia before death. FINDINGS 12,887 participants were interviewed at baseline. 11,718 were free of dementia, of whom 8137 (69%) were reinterviewed, contributing 34,718 person-years of follow-up. Incidence for 10/66 dementia varied between 18·2 and 30·4 per 1000 person-years, and were 1·4-2·7 times higher than were those for DSM-IV dementia (9·9-15·7 per 1000 person-years). Mortality hazards were 1·56-5·69 times higher in individuals with dementia at baseline than in those who were dementia-free. Informant reports suggested a high incidence of dementia before death; overall incidence might be 4-19% higher if these data were included. 10/66 dementia incidence was independently as [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Incidence for 10/66 dementia varied between 18·2 and 30·4 per 1000 person-years, and were 1·4-2·7 times higher than were those for DSM-IV dementia (9·9-15·7 per 1000 person-years).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 591, "doc_id": "14682243", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Inhibiting glucose-6-phospate dehydrogenase improves lipogenesis by deactivating LKB1-AMPK signaling.\n\nCANDIDATE_PASSAGE:\nPKD1 Inhibits AMPKα2 through Phosphorylation of Serine 491 and Impairs Insulin Signaling in Skeletal Muscle Cells. AMP-activated protein kinase (AMPK) is an energy-sensing enzyme whose activity is inhibited in settings of insulin resistance. Exposure to a high glucose concentration has recently been shown to increase phosphorylation of AMPK at Ser(485/491) of its α1/α2 subunit; however, the mechanism by which it does so is not known. Diacylglycerol (DAG), which is also increased in muscle exposed to high glucose, activates a number of signaling molecules including protein kinase (PK)C and PKD1. We sought to determine whether PKC or PKD1 is involved in inhibition of AMPK by causing Ser(485/491) phosphorylation in skeletal muscle cells. C2C12 myotubes were treated with the PKC/D1 activator phorbol 12-myristate 13-acetate (PMA), which acts as a DAG mimetic. This caused dose- and time-dependent increases in AMPK Ser(485/491) phosphorylation, which was associated with a ∼60% decrease in AMPKα2 activity. Expression of a phosphodefective AMPKα2 mutant (S491A) prevented the PMA-induced reduction in AMPK activity. Serine phosphorylation and inhibition of AMPK activity were partially prevented by the broad PKC inhibitor Gö6983 and fully prevented by the specific PKD1 inhibitor CRT0066101. Genetic knockdown of PKD1 also prevented Ser(485/491) phosphorylation of AMPK. Inhibition of previously identified kinases that phosphorylate AMPK at this site (Akt, S6K, and ERK) did not prevent these events. PMA treatment also caused impairments in insulin-signaling through Akt, which were prevented by PKD1 inhibition. Finally, recombinant PKD1 phosphorylated AMPKα2 at Ser(491) in cell-free conditions. These results identify PKD1 as a novel upstream kinase of AMPKα2 Ser(491) that p [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "635", "doc_id": "23974474", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Charcoal shows no benefit for acute paraquat poisoning.\n\nCANDIDATE_PASSAGE:\nEffect of activated charcoal hemoperfusion on renal function in patients with paraquat poisoning. The present study retrospectively analyzed 19 patients diagnosed with paraquat (PQ) poisoning with the aim to investigate the effect of activated charcoal hemoperfusion on renal function and PQ elimination. The results indicated that 7 patients died and 12 survived. Non-oliguric renal failure occurred in all of the 7 patients who died. Among the 12 surviving patients, 10 had normal renal function and 2 developed non-oliguric renal failure. There was a linear correlation between plasma and urine paraquat concentration prior to and during activated charcoal hemoperfusion. The equation parameters together with the correlation coefficient on admission were as follows: Y=0.5820+1.7348X (R2=0.678; F=35.768; P<0.0001). The equation parameters together with the correlation coefficient were as follows during activated charcoal hemoperfusion: Y=0.6827+1.2649X (R2=0.626; F=50.308; P<0.0001). Therefore, it was concluded that in patients with normal renal function, the elimination kinetics of PQ by the kidneys were only associated with the plasma PQ concentration. Activated charcoal hemoperfusion had little effect on avoiding acute kidney injury in patients with severe PQ poisoning.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "246", "doc_id": "3430789", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Incidence of 10/66 dementia is lower than the incidence of DSM-IV dementia.\n\nCANDIDATE_PASSAGE:\nThe SIR2/3/4 complex and SIR2 alone promote longevity in Saccharomyces cerevisiae by two different mechanisms. Genes Dev 13 The SIR genes are determinants of life span in yeast mother cells. Here we show that life span regulation by the Sir proteins is independent of their role in nonhomologous end joining. The short life span of a sir3 or sir4 mutant is due to the simultaneous expression of a and alpha mating-type information, which indirectly causes an increase in rDNA recombination and likely increases the production of extrachromosomal rDNA circles. The short life span of a sir2 mutant also reveals a direct failure to repress recombination generated by the Fob1p-mediated replication block in the rDNA. Sir2p is a limiting component in promoting yeast longevity, and increasing the gene dosage extends the life span in wild-type cells. A possible role of the conserved SIR2 in mammalian aging is discussed.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "592", "doc_id": "11527822", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Women with a higher birth weight are more likely to develop breast cancer later in life.\n\nCANDIDATE_PASSAGE:\nGenome-Wide Profiling of H3K56 Acetylation and Transcription Factor Binding Sites in Human Adipocytes The growing epidemic of obesity and metabolic diseases calls for a better understanding of adipocyte biology. The regulation of transcription in adipocytes is particularly important, as it is a target for several therapeutic approaches. Transcriptional outcomes are influenced by both histone modifications and transcription factor binding. Although the epigenetic states and binding sites of several important transcription factors have been profiled in the mouse 3T3-L1 cell line, such data are lacking in human adipocytes. In this study, we identified H3K56 acetylation sites in human adipocytes derived from mesenchymal stem cells. H3K56 is acetylated by CBP and p300, and deacetylated by SIRT1, all are proteins with important roles in diabetes and insulin signaling. We found that while almost half of the genome shows signs of H3K56 acetylation, the highest level of H3K56 acetylation is associated with transcription factors and proteins in the adipokine signaling and Type II Diabetes pathways. In order to discover the transcription factors that recruit acetyltransferases and deacetylases to sites of H3K56 acetylation, we analyzed DNA sequences near H3K56 acetylated regions and found that the E2F recognition sequence was enriched. Using chromatin immunoprecipitation followed by high-throughput sequencing, we confirmed that genes bound by E2F4, as well as those by HSF-1 and C/EBPα, have higher than expected levels of H3K56 acetylation, and that the transcription factor binding sites and acetylation sites are often adjacent but rarely overlap. We also discovered a significant difference between bound targets of C/EBPα in 3T3-L1 and human adipocytes, highlighting the [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1379", "doc_id": "3052213", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Bariatric surgery reduces postmenopausal breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Bariatric Surgery in the United Kingdom: A Cohort Study of Weight Loss and Clinical Outcomes in Routine Clinical Care.\nABSTRACT: BACKGROUND Bariatric surgery is becoming a more widespread treatment for obesity. Comprehensive evidence of the long-term effects of contemporary surgery on a broad range of clinical outcomes in large populations treated in routine clinical practice is lacking. The objective of this study was to measure the association between bariatric surgery, weight, body mass index, and obesity-related co-morbidities. METHODS AND FINDINGS This was an observational retrospective cohort study using data from the United Kingdom Clinical Practice Research Datalink. All 3,882 patients registered in the database and with bariatric surgery on or before 31 December 2014 were included and matched by propensity score to 3,882 obese patients without surgery. The main outcome measures were change in weight and body mass index over 4 y; incident diagnoses of type 2 diabetes mellitus (T2DM), hypertension, angina, myocardial infarction (MI), stroke, fractures, obstructive sleep apnoea, and cancer; mortality; and resolution of hypertension and T2DM. Weight measures were available for 3,847 patients between 1 and 4 mo, 2,884 patients between 5 and 12 mo, and 2,258 patients between 13 and 48 mo post-procedure. Bariatric surgery patients exhibited rapid weight loss for the first four postoperative months, at a rate of 4.98 kg/mo (95% CI 4.88-5.08). Slower weight loss was sustained to the end of 4 y. Gastric bypass (6.56 kg/mo) and sleeve gastrectomy (6.29 kg/mo) were associated with greater initial weight reduction than gastric banding (2.77 kg/mo). Protective hazard ratios (HRs) were detected for bariatric surgery for incident T2DM, 0.68 (95% CI 0.55-0.83); hypertension, 0.35 (95% CI 0.27-0.45); angina, 0.59 (95% CI 0.40-0.87);MI, 0.28 (95% CI 0.10-0.74); and obstructive sleep apnoea, 0.5 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"No association was detected between bariatric surgery and fractures, cancer, or stroke.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 169, "doc_id": "5824985", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: TMEM27 is a marker for beta cells.\n\nCANDIDATE_PASSAGE:\nMetabolic phenotyping of human blood plasma: a powerful tool to discriminate between cancer types? BACKGROUND Accumulating evidence has shown that cancer cell metabolism differs from that of normal cells. However, up to now it is not clear whether different cancer types are characterized by a specific metabolite profile. Therefore, this study aims to evaluate whether the plasma metabolic phenotype allows to discriminate between lung and breast cancer. PATIENTS AND METHODS The proton nuclear magnetic resonance spectrum of plasma is divided into 110 integration regions, representing the metabolic phenotype. These integration regions reflect the relative metabolite concentrations and were used to train a classification model in discriminating between 80 female breast cancer patients and 54 female lung cancer patients, all with an adenocarcinoma. The validity of the model was examined by permutation testing and by classifying an independent validation cohort of 60 female breast cancer patients and 81 male lung cancer patients, all with an adenocarcinoma. RESULTS The model allows to classify 99% of the breast cancer patients and 93% of the lung cancer patients correctly with an area under the curve (AUC) of 0.96 and can be validated in the independent cohort with a sensitivity of 89%, a specificity of 82% and an AUC of 0.94. Decreased levels of sphingomyelin and phosphatidylcholine (phospholipids with choline head group) and phospholipids with short, unsaturated fatty acid chains next to increased levels of phospholipids with long, saturated fatty acid chains seem to indicate that cell membranes of lung tumors are more rigid and less sensitive to lipid peroxidation. The other discriminating metabolites are pointing to a more pronounced response of the body to the [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1133", "doc_id": "17163294", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Splenomegaly is observed in knockin mouse lacking the SHP-2 MAPK pathway.\n\nCANDIDATE_PASSAGE:\nToll-like receptor 7 agonist GS-9620 induces prolonged inhibition of HBV via a type I interferon-dependent mechanism. BACKGROUND & AIMS GS-9620, an oral agonist of toll-like receptor 7 (TLR7), is in clinical development for the treatment of chronic hepatitis B (CHB). GS-9620 was previously shown to induce prolonged suppression of serum viral DNA and antigens in the woodchuck and chimpanzee models of CHB. Herein, we investigated the molecular mechanisms that contribute to the antiviral response to GS-9620 using in vitro models of hepatitis B virus (HBV) infection. METHODS Cryopreserved primary human hepatocytes (PHH) and differentiated HepaRG (dHepaRG) cells were infected with HBV and treated with GS-9620, conditioned media from human peripheral blood mononuclear cells treated with GS-9620 (GS-9620 conditioned media [GS-9620-CM]), or other innate immune stimuli. The antiviral and transcriptional response to these agents was determined. RESULTS GS-9620 had no antiviral activity in HBV-infected PHH, consistent with low level TLR7 mRNA expression in human hepatocytes. In contrast, GS-9620-CM induced prolonged reduction of HBV DNA, RNA, and antigen levels in PHH and dHepaRG cells via a type I interferon (IFN)-dependent mechanism. GS-9620-CM did not reduce covalently closed circular DNA (cccDNA) levels in either cell type. Transcriptional profiling demonstrated that GS-9620-CM strongly induced various HBV restriction factors - although not APOBEC3A or the Smc5/6 complex - and indicated that established HBV infection does not modulate innate immune sensing or signaling in cryopreserved PHH. GS-9620-CM also induced expression of immunoproteasome subunits and enhanced presentation of an immunodominant viral peptide in HBV-infected PHH. CONCLUSIONS Type I IFN induced [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1097", "doc_id": "20960682", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Radioiodine treatment of non-toxic multinodular goitre increases thyroid volume.\n\nCANDIDATE_PASSAGE:\nExercise-induced asthma: a practical guide to definitions, diagnosis, prevalence, and treatment. Exercise-induced asthma is defined as an intermittent narrowing of the airways, demonstrated by a decrease in some measure of flow, that the patient experiences as wheezing, chest tightness, coughing, and difficulty breathing that is triggered by exercise. Exercise will trigger asthma in most individuals who have chronic asthma, as well as in some who do not otherwise have asthma. Definitive diagnosis requires demonstration of a drop in flow rate, typically > or = 13-15% for forced expiratory volume in one second (FEV1) and > or = 15-20% for peak expiratory flow rate (PEFR), after exercise, associated with symptoms. Prevalence data indicate that this disorder is very common in those who participate in recreational sports as well as in highly competitive athletes, with at least 12-15% of unselected athletes having positive exercise challenges. Treatment of exercise induced asthma involves use of nonpharmacological measures (such as the use of the refractory period after exercise and prewarming air) as well as use of medications (beta-agonists, cromolyn, and nedocromil). With treatment, those who suffer from exercise-induced asthma may be able to participate and compete at the highest levels of performance.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1011", "doc_id": "25761154", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Pre-mRNAs associated with spliceosomal components are less stable than unassociated splicing substrates.\n\nCANDIDATE_ABSTRACT:\nTITLE: Linking Splicing to Pol II Transcription Stabilizes Pre-mRNAs and Influences Splicing Patterns\nABSTRACT: RNA processing is carried out in close proximity to the site of transcription, suggesting a regulatory link between transcription and pre-mRNA splicing. Using an in vitro transcription/splicing assay, we demonstrate that an association of RNA polymerase II (Pol II) transcription and pre-mRNA splicing is required for efficient gene expression. Pol II-synthesized RNAs containing functional splice sites are protected from nuclear degradation, presumably because the local concentration of the splicing machinery is sufficiently high to ensure its association over interactions with nucleases. Furthermore, the process of transcription influences alternative splicing of newly synthesized pre-mRNAs. Because other RNA polymerases do not provide similar protection from nucleases, and their RNA products display altered splicing patterns, the link between transcription and RNA processing is RNA Pol II-specific. We propose that the connection between transcription by Pol II and pre-mRNA splicing guarantees an extended half-life and proper processing of nascent pre-mRNAs.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We propose that the connection between transcription by Pol II and pre-mRNA splicing guarantees an extended half-life and proper processing of nascent pre-mRNAs.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 963, "doc_id": "4162857", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: PD-1 triggering on monocytes reduces IL-10 production by monocytes.\n\nCANDIDATE_PASSAGE:\nProgrammed death-1–induced interleukin-10 production by monocytes impairs CD4+ T cell activation during HIV infection Viral replication and microbial translocation from the gut to the blood during HIV infection lead to hyperimmune activation, which contributes to the decline in CD4+ T cell numbers during HIV infection. Programmed death-1 (PD-1) and interleukin-10 (IL-10) are both upregulated during HIV infection. Blocking interactions between PD-1 and programmed death ligand-1 (PD-L1) and between IL-10 and IL-10 receptor (IL-10R) results in viral clearance and improves T cell function in animal models of chronic viral infections. Here we show that high amounts of microbial products and inflammatory cytokines in the plasma of HIV-infected subjects lead to upregulation of PD-1 expression on monocytes that correlates with high plasma concentrations of IL-10. Triggering of PD-1 expressed on monocytes by PD-L1 expressed on various cell types induced IL-10 production and led to reversible CD4+ T cell dysfunction. We describe a new function for PD-1 whereby microbial products inhibit T cell expansion and function by upregulating PD-1 levels and IL-10 production by monocytes after binding of PD-1 by PD-L1.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "903", "doc_id": "10648422", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Sn is present on mature DCs during inflammation in vivo.\n\nCANDIDATE_PASSAGE:\nSiglec-1 Is a Novel Dendritic Cell Receptor That Mediates HIV-1 Trans-Infection Through Recognition of Viral Membrane Gangliosides Dendritic cells (DCs) are essential antigen-presenting cells for the induction of immunity against pathogens. However, HIV-1 spread is strongly enhanced in clusters of DCs and CD4(+) T cells. Uninfected DCs capture HIV-1 and mediate viral transfer to bystander CD4(+) T cells through a process termed trans-infection. Initial studies identified the C-type lectin DC-SIGN as the HIV-1 binding factor on DCs, which interacts with the viral envelope glycoproteins. Upon DC maturation, however, DC-SIGN is down-regulated, while HIV-1 capture and trans-infection is strongly enhanced via a glycoprotein-independent capture pathway that recognizes sialyllactose-containing membrane gangliosides. Here we show that the sialic acid-binding Ig-like lectin 1 (Siglec-1, CD169), which is highly expressed on mature DCs, specifically binds HIV-1 and vesicles carrying sialyllactose. Furthermore, Siglec-1 is essential for trans-infection by mature DCs. These findings identify Siglec-1 as a key factor for HIV-1 spread via infectious DC/T-cell synapses, highlighting a novel mechanism that mediates HIV-1 dissemination in activated tissues.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1091", "doc_id": "2603304", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: N348I mutations cause resistance to nevirapine.\n\nCANDIDATE_ABSTRACT:\nTITLE: Scaling of Dorsal-Ventral Patterning by Embryo Size-Dependent Degradation of Spemann’s Organizer Signals\nABSTRACT: Spemann's organizer plays a key role in dorsal-ventral (DV) patterning in the amphibian embryo by secreting diffusible proteins such as Chordin, an antagonist to ventralizing bone morphogenetic proteins (BMPs). The DV patterning is so robust that an amphibian embryo with its ventral half surgically removed can develop into a smaller but proportionally patterned larva. Here, we show that this robust patterning depends on facilitated Chordin degradation and requires the expression of the Chordin-proteinase inhibitor Sizzled on the opposite side. Sizzled, which is stable and diffuses widely along the DV axis, stabilizes Chordin and expands its distribution in the ventral direction. This expanded Chordin distribution, in turn, limits BMP-dependent Sizzled production, forming an axis-wide feedback loop for shaping Chordin's activity. Using bisection assays, we demonstrate that Chordin degradation is dynamically controlled by embryo-size-coupled Sizzled accumulation. We propose a scaling model that enables the DV pattern to adjust proportionally to embryonic axis size.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 822, "doc_id": "1031534", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: HOXB4 facilitates HSC expansion when co-cultured with HSCs.\n\nCANDIDATE_PASSAGE:\nReprogramming factor stoichiometry influences the epigenetic state and biological properties of induced pluripotent stem cells. We compared two genetically highly defined transgenic systems to identify parameters affecting reprogramming of somatic cells to a pluripotent state. Our results demonstrate that the level and stoichiometry of reprogramming factors during the reprogramming process strongly influence the resulting pluripotency of iPS cells. High expression of Oct4 and Klf4 combined with lower expression of c-Myc and Sox2 produced iPS cells that efficiently generated \"all-iPSC mice\" by tetraploid (4n) complementation, maintained normal imprinting at the Dlk1-Dio3 locus, and did not create mice with tumors. Loss of imprinting (LOI) at the Dlk1-Dio3 locus did not strictly correlate with reduced pluripotency though the efficiency of generating \"all-iPSC mice\" was diminished. Our data indicate that stoichiometry of reprogramming factors can influence epigenetic and biological properties of iPS cells. This concept complicates efforts to define a \"generic\" epigenetic state of iPSCs and ESCs and should be considered when comparing different iPS and ES cell lines.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "492", "doc_id": "16541762", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Patients in stable partnerships progress from HIV to death at the same rate as patients not in partnerships.\n\nCANDIDATE_ABSTRACT:\nTITLE: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\nABSTRACT: OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART). DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study). SETTING Seven outpatient clinics throughout Switzerland. PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years). MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound. RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion. When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership. In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without. Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression. CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 925, "doc_id": "17077004", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: PKG-la plays an essential role in expression of spinal long term potentiation in PGK-la knockout mice.\n\nCANDIDATE_ABSTRACT:\nTITLE: Presynaptically Localized Cyclic GMP-Dependent Protein Kinase 1 Is a Key Determinant of Spinal Synaptic Potentiation and Pain Hypersensitivity\nABSTRACT: Synaptic long-term potentiation (LTP) at spinal neurons directly communicating pain-specific inputs from the periphery to the brain has been proposed to serve as a trigger for pain hypersensitivity in pathological states. Previous studies have functionally implicated the NMDA receptor-NO pathway and the downstream second messenger, cGMP, in these processes. Because cGMP can broadly influence diverse ion-channels, kinases, and phosphodiesterases, pre- as well as post-synaptically, the precise identity of cGMP targets mediating spinal LTP, their mechanisms of action, and their locus in the spinal circuitry are still unclear. Here, we found that Protein Kinase G1 (PKG-I) localized presynaptically in nociceptor terminals plays an essential role in the expression of spinal LTP. Using the Cre-lox P system, we generated nociceptor-specific knockout mice lacking PKG-I specifically in presynaptic terminals of nociceptors in the spinal cord, but not in post-synaptic neurons or elsewhere (SNS-PKG-I(-/-) mice). Patch clamp recordings showed that activity-induced LTP at identified synapses between nociceptors and spinal neurons projecting to the periaqueductal grey (PAG) was completely abolished in SNS-PKG-I(-/-) mice, although basal synaptic transmission was not affected. Analyses of synaptic failure rates and paired-pulse ratios indicated a role for presynaptic PKG-I in regulating the probability of neurotransmitter release. Inositol 1,4,5-triphosphate receptor 1 and myosin light chain kinase were recruited as key phosphorylation targets of presynaptic PKG-I in nociceptive neurons. Finally, behavioural analyses in vivo showed marked defects in SNS-PKG-I(-/-) mice in several models of activity-induced nociceptive hypersensitivity, and pharmacological studies identified [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Patch clamp recordings showed that activity-induced LTP at identified synapses between nociceptors and spinal neurons projecting to the periaqueductal grey (PAG) was completely abolished in SNS-PKG-I(-/-) mice, although basal synaptic transmission was not affected.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 912, "doc_id": "11254556", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: ScPif1p has reduced binding ability to G-rich ssDNA compared to non-G-rich ssDNA.\n\nCANDIDATE_PASSAGE:\nIntracellular transport of fat-soluble vitamins A and E. Vitamins are compounds that are essential for the normal growth, reproduction and functioning of the human body. Of the 13 known vitamins, vitamins A, D, E and K are lipophilic compounds and are therefore called fat-soluble vitamins. Because of their lipophilicity, fat-soluble vitamins are solubilized and transported by intracellular carrier proteins to exert their actions and to be metabolized properly. Vitamin A and its derivatives, collectively called retinoids, are solubilized by intracellular retinoid-binding proteins such as cellular retinol-binding protein (CRBP), cellular retinoic acid-binding protein (CRABP) and cellular retinal-binding protein (CRALBP). These proteins act as chaperones that regulate the metabolism, signaling and transport of retinoids. CRALBP-mediated intracellular retinoid transport is essential for vision in human. α-Tocopherol, the main form of vitamin E found in the body, is transported by α-tocopherol transfer protein (α-TTP) in hepatic cells. Defects of α-TTP cause vitamin E deficiency and neurological disorders in humans. Recently, it has been shown that the interaction of α-TTP with phosphoinositides plays a critical role in the intracellular transport of α-tocopherol and is associated with familial vitamin E deficiency. In this review, we summarize the mechanisms and biological significance of the intracellular transport of vitamins A and E.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1068", "doc_id": "21380348", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Autologous transplantation of mesenchymal stem cells has lower rates of rejection than induction therapy with anti-interleukin-2 receptor antibodies.\n\nCANDIDATE_ABSTRACT:\nTITLE: Induction therapy with autologous mesenchymal stem cells in living-related kidney transplants: a randomized controlled trial.\nABSTRACT: CONTEXT Antibody-based induction therapy plus calcineurin inhibitors (CNIs) reduce acute rejection rates in kidney recipients; however, opportunistic infections and toxic CNI effects remain challenging. Reportedly, mesenchymal stem cells (MSCs) have successfully treated graft-vs-host disease. OBJECTIVE To assess autologous MSCs as replacement of antibody induction for patients with end-stage renal disease who undergo ABO-compatible, cross-match-negative kidney transplants from a living-related donor. DESIGN, SETTING, AND PATIENTS One hundred fifty-nine patients were enrolled in this single-site, prospective, open-label, randomized study from February 2008-May 2009, when recruitment was completed. INTERVENTION Patients were inoculated with marrow-derived autologous MSC (1-2 x 10(6)/kg) at kidney reperfusion and two weeks later. Fifty-three patients received standard-dose and 52 patients received low-dose CNIs (80% of standard); 51 patients in the control group received anti-IL-2 receptor antibody plus standard-dose CNIs. MAIN OUTCOME MEASURES The primary measure was 1-year incidence of acute rejection and renal function (estimated glomerular filtration rate [eGFR]); the secondary measure was patient and graft survival and incidence of adverse events. RESULTS Patient and graft survival at 13 to 30 months was similar in all groups. After 6 months, 4 of 53 patients (7.5%) in the autologous MSC plus standard-dose CNI group (95% CI, 0.4%-14.7%; P = .04) and 4 of 52 patients (7.7%) in the low-dose group (95% CI, 0.5%-14.9%; P = .046) compared with 11 of 51 controls (21.6%; 95% CI, 10.5%-32.6%) had biopsy-confirmed acute rejection. None of the patients in either autologous MSC group had glucorticoid-resistant rejection, whereas 4 patients (7.8%) in the control group [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Also, during the 1-year follow-up, combined analysis of MSC-treated groups revealed significantly decreased risk of opportunistic infections than the control group (hazard ratio, 0.42; 95% CI, 0.20-0.85, P=.02) CONCLUSION Among patients undergoing renal transplant, the use of autologous MSCs compared with anti-IL-2 receptor antibody induction therapy resulted in lower incidence of acute rejection, decreased risk of opportunistic infection, and better estimated renal function at 1 year.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 146, "doc_id": "10582939", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Depletion of T-helper 17 (Th17) cells during simian immunodeficiency virus (SIV) infection decreases dissemination of Salmonella Typhimurium from the gut.\n\nCANDIDATE_ABSTRACT:\nTITLE: Age‐associated microRNA expression in human peripheral blood is associated with all‐cause mortality and age‐related traits\nABSTRACT: Recent studies provide evidence of correlations of DNA methylation and expression of protein-coding genes with human aging. The relations of microRNA expression with age and age-related clinical outcomes have not been characterized thoroughly. We explored associations of age with whole-blood microRNA expression in 5221 adults and identified 127 microRNAs that were differentially expressed by age at P < 3.3 × 10-4 (Bonferroni-corrected). Most microRNAs were underexpressed in older individuals. Integrative analysis of microRNA and mRNA expression revealed changes in age-associated mRNA expression possibly driven by age-associated microRNAs in pathways that involve RNA processing, translation, and immune function. We fitted a linear model to predict 'microRNA age' that incorporated expression levels of 80 microRNAs. MicroRNA age correlated modestly with predicted age from DNA methylation (r = 0.3) and mRNA expression (r = 0.2), suggesting that microRNA age may complement mRNA and epigenetic age prediction models. We used the difference between microRNA age and chronological age as a biomarker of accelerated aging (Δage) and found that Δage was associated with all-cause mortality (hazards ratio 1.1 per year difference, P = 4.2 × 10-5 adjusted for sex and chronological age). Additionally, Δage was associated with coronary heart disease, hypertension, blood pressure, and glucose levels. In conclusion, we constructed a microRNA age prediction model based on whole-blood microRNA expression profiling. Age-associated microRNAs and their targets have potential utility to detect accelerated aging and to predict risks for age-related diseases.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 332, "doc_id": "663464", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In melanoma, anti-CTLA-4 treatment reinvigorates exhausted PD-1+Eomes+CD8 T cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Manslaughter by Fake Artesunate in Asia—Will Africa Be Next?\nABSTRACT: Falciparum malaria kills, and it particularly kills the rural poor. Artemisinin derivatives, such as artesunate, are a vital component of Plasmodium falciparum malaria treatment and control in the face of globally increasing antimalarial drug resistance. Since 1998 a worsening epidemic of sophisticated counterfeit “artesunate” tablets (containing no artesunate) has plagued mainland Southeast Asia (see Figure S1). In some countries, most of the available artesunate is fake [ 1–5]. Artemisinin derivatives are remarkably rapid in their antimalarial effects, and they are very well tolerated. So where these medicines are available, they are sought after. But as they are relatively expensive, a demand is created for cheaper versions amongst the poorest and most vulnerable people, upon whom the counterfeiters have preyed–with fatal results.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 576, "doc_id": "2526777", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Deltex interacts with eIF3. There is no known interaction between Deltex and elF3\n\nCANDIDATE_PASSAGE:\nChromatin remodelling at promoters suppresses antisense transcription Chromatin allows the eukaryotic cell to package its DNA efficiently. To understand how chromatin structure is controlled across the Saccharomyces cerevisiae genome, we have investigated the role of the ATP-dependent chromatin remodelling complex Isw2 in positioning nucleosomes. We find that Isw2 functions adjacent to promoter regions where it repositions nucleosomes at the interface between genic and intergenic sequences. Nucleosome repositioning by Isw2 is directional and results in increased nucleosome occupancy of the intergenic region. Loss of Isw2 activity leads to inappropriate transcription, resulting in the generation of both coding and noncoding transcripts. Here we show that Isw2 repositions nucleosomes to enforce directionality on transcription by preventing transcription initiation from cryptic sites. Our analyses reveal how chromatin is organized on a global scale and advance our understanding of how transcription is regulated.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "331", "doc_id": "4305576", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Interleukin-18 plays an important role in the pathogenesis of atherosclerosis.\n\nCANDIDATE_PASSAGE:\nTex10 Coordinates Epigenetic Control of Super-Enhancer Activity in Pluripotency and Reprogramming. Super-enhancers (SEs) are large clusters of transcriptional enhancers that are co-occupied by multiple lineage-specific transcription factors driving expression of genes that define cell identity. In embryonic stem cells (ESCs), SEs are highly enriched for the core pluripotency factors Oct4, Sox2, and Nanog. In this study, we sought to dissect the molecular control mechanism of SE activity in pluripotency and reprogramming. Starting from a protein interaction network surrounding Sox2, we identified Tex10 as a key pluripotency factor that plays a functionally significant role in ESC self-renewal, early embryo development, and reprogramming. Tex10 is enriched at SEs in a Sox2-dependent manner and coordinates histone acetylation and DNA demethylation at SEs. Tex10 activity is also important for pluripotency and reprogramming in human cells. Our study therefore highlights Tex10 as a core component of the pluripotency network and sheds light on its role in epigenetic control of SE activity for cell fate determination.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "653", "doc_id": "19384430", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Citrullinated proteins externalized in neutrophil extracellular traps act indirectly to disrupt the inflammatory cycle.\n\nCANDIDATE_ABSTRACT:\nTITLE: Neutrophil extracellular chromatin traps connect innate immune response to autoimmunity\nABSTRACT: Autoantibodies to DNA and histones (chromatin) are the defining antigen specificity in systemic lupus erythematosus (SLE) and related musculoskeletal disorders but the mechanisms responsible for their induction remain mysterious. That situation rapidly changed once neutrophil extracellular chromatin traps (NETs) were discovered and observed to play a conserved role in innate immune responses to a broad variety of microbial pathogens. At the center of an infectious process, neutrophils exert various antimicrobial defenses, including the release of nuclear chromatin into the extracellular space. The externalized NETs, a complex meshwork of nuclear chromatin and antimicrobial proteins, serve to immobilize and degrade microbial pathogens. Here, we critically evaluate the evidence supporting NETs versus apoptotic bodies as a source for nuclear antigens in autoimmunity. We also discuss the possibility that NET chromatin forms an essential component of immune deposits in the pathogenesis of glomerulonephritis in SLE and other autoimmune immune complex diseases.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 263, "doc_id": "14853989", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Hyperfibrinogenemia increases rates of femoropopliteal bypass thrombosis.\n\nCANDIDATE_PASSAGE:\nGlobal, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015 BACKGROUND The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. METHODS We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors-the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "533", "doc_id": "13770184", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Upregulation of dynein in Drosophila neurons increases the number of microtubule plus-ends growing toward the cell body of each neuron.\n\nCANDIDATE_PASSAGE:\nDynein is required for polarized dendritic transport and uniform microtubule orientation in axons Axons and dendrites differ in both microtubule organization and in the organelles and proteins they contain. Here we show that the microtubule motor dynein has a crucial role in polarized transport and in controlling the orientation of axonal microtubules in Drosophila melanogaster dendritic arborization (da) neurons. Changes in organelle distribution within the dendritic arbors of dynein mutant neurons correlate with a proximal shift in dendritic branch position. Dynein is also necessary for the dendrite-specific localization of Golgi outposts and the ion channel Pickpocket. Axonal microtubules are normally oriented uniformly plus-end-distal; however, without dynein, axons contain both plus- and minus-end distal microtubules. These data suggest that dynein is required for the distinguishing properties of the axon and dendrites: without dynein, dendritic organelles and proteins enter the axon and the axonal microtubules are no longer uniform in polarity.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1351", "doc_id": "28369117", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does solar ultraviolet radiation exposure appear to exacerbate HIV infection in homosexual men . The Multicenter AIDS Cohort Study?\n\nABSTRACT:\nTo determine the effect of sun exposure on HIV progression. Cross-sectional survey nested within a longitudinal cohort study. The Multicenter AIDS Cohort Study. A total of 1155 white HIV-seronegative and 496 white HIV-seropositive homosexual men, of whom 142 seroconverted during the study. T-helper lymphocyte decline and AIDS. No positive correlation was found between the development of AIDS or loss of T-helper lymphocytes and (i) phenotypic characteristics associated with enhanced ultraviolet radiation (UVR) sensitivity (hair or eye color, skin type), or (ii) reported UVR exposure (sun lamp/tanning bed use, frequency of beach vacations, sunscreen use), or (iii) composite score of UVR sensitivity and exposure history. The composite scores and individual measures of risk were not correlated with rate of T-helper lymphocyte decline (slope) based upon rank correlation (correlation coefficient, 0.04; P = 0.32). In fact, individuals purposefully seeking the sun had slower T-helper lymphocyte declines. Sensitivity to UVR was also not significantly associated with AIDS [odds ratio (OR), 1.11 per unit of higher composite score; 95% confidence interval (CI), 0.66-1.88; P = 0.63]. Among individuals who were HIV-infected at baseline, those who have been purposely seeking sun exposure were less likely to have AIDS (OR, 0.67; 95% CI, 0.39-1.11; P = 0.12).", "output": "{\"label\": \"no\", \"rationale\": \"These data suggest that phenotypic characteristics of high UVR sensitivity and exposure are not highly correlated with decline in T-helper lymphocyte count or with progression to AIDS.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 9386813, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Golli-deficient T-cells prefer to differentiate into an anergic phenotype in the adaptive immune response when there are increased levels of Ca2+ in the cytosol.\n\nCANDIDATE_PASSAGE:\nIsolated liver perfusion for non-resectable liver tumours: a review. Many treatments have been proposed for non-resectable primary or secondary hepatic cancer but the results have generally been disappointing. Isolated Hepatic Perfusion (IHP) was first attempted four decades ago but it gained acceptance only recently, after spectacular tumour responses were obtained by isolated limb perfusion with melphalan and tumour necrosis factor (TNF) for melanomas and sarcomas. Surgical isolation of the liver is a technically demanding operation that allows the safe administration of high doses of chemotherapeutics and TNF. Percutaneous techniques using balloon occlusion catheters are simpler but result in higher leakage rates from the perfusion circuit into the systemic circulation. Several phase I-II trials indicate that IHP can yield high tumour response rates, even when there is resistance to systemic chemotherapy. However, no significant advantage in overall survival has been demonstrated so far. IHP offers unique pharmacokinetic advantages for locoregional chemotherapy and biotherapy. It might also allow gene therapy with limited systemic exposure and toxicity. At present, IHP nevertheless remains an experimental treatment modality which should therefore be used in controlled trials only.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "478", "doc_id": "13380980", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Depletion of nitric oxide is responsible for vasospasm.\n\nCANDIDATE_PASSAGE:\nAngiopoietin-2 is increased in sepsis and inversely associated with nitric oxide-dependent microvascular reactivity INTRODUCTION Angiopoietin-2 (ang-2), an angiogenic peptide released by endothelial cell Weibel-Palade bodies (WPBs), increases endothelial activation and vascular permeability. Ang-2 is raised in severe sepsis but the mechanisms underlying this are not known. Nitric oxide (NO) inhibits WPB exocytosis, and bioavailability of endothelial NO is decreased in sepsis. We hypothesized that endothelial NO bioavailability would be inversely correlated with ang-2 concentrations in sepsis. METHODS Plasma ang-2, vascular endothelial growth factor (VEGF) and endothelial-active cytokines were assessed in 83 patients with early sepsis and 41 hospital controls, and related to reactive hyperaemia-peripheral arterial tonometry, RH-PAT, a measure of endothelial NO bioavailability. RESULTS Plasma Ang-2 was elevated in sepsis (median [interquartile range (IQR)], ng/ml: severe sepsis 12.4 [8.5-33.4], sepsis without organ failure 6.1 [5.0-10.4], controls 2.7 [2.2-3.6], P < 0.0001). It correlated inversely with RH-PAT (r = -0.38, P < 0.0001) and positively with IL-6 (r = 0.57, P < 0.0001) and degree of organ failure (sequential organ function assessment score) (r = 0.58, P < 0.0001). The correlation of ang-2 with RH-PAT persisted after controlling for sepsis severity. In a longitudinal mixed-effects model, recovery of RH-PAT over time was associated with decline in ang-2. CONCLUSIONS Ang-2 is elevated in proportion to sepsis severity, and inversely correlated with NO-dependent microvascular reactivity. Impaired endothelial NO bioavailability may contribute to increased endothelial cell release of ang-2, endothelial activation and capillary leak. Agents that increase e [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "334", "doc_id": "11459139", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: In mice, P. chabaudi parasites are able to proliferate faster early in infection when inoculated at lower numbers than when inoculated at high numbers.\n\nCANDIDATE_PASSAGE:\nDecreased proteasomal activity causes age-related phenotypes and promotes the development of metabolic abnormalities. The proteasome is a multicatalytic enzyme complex responsible for the degradation of both normal and damaged proteins. An age-related decline in proteasomal activity has been implicated in various age-related pathologies. The relevance of decreased proteasomal activity to aging and age-related diseases remains unclear, however, because suitable animal models are not available. In the present study, we established a transgenic (Tg) mouse model with decreased proteasomal chymotrypsin-like activity. Tg mice exhibited a shortened life span and developed age-related phenotypes. In Tg mice, polyubiquitinated and oxidized proteins accumulated, and the expression levels of cellular proteins such as Bcl-xL and RNase L were altered. When Tg mice were fed a high-fat diet, they developed more pronounced obesity and hepatic steatosis than did wild-type mice. Consistent with its role in lipid droplet formation, the expression of adipose differentiation-related protein (ADRP) was elevated in the livers of Tg mice. Of note, obesity and hepatic steatosis induced by a high-fat diet were more pronounced in aged than in young wild-type mice, and aged wild-type mice had elevated levels of ADRP, suggesting that the metabolic abnormalities present in Tg mice mimic those in aged mice. Our results provide the first in vivo evidence that decreased proteasomal chymotrypsin-like activity affects longevity and aggravates age-related metabolic disorders, such as obesity and hepatic steatosis.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "577", "doc_id": "24347647", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Long chain polyunsaturated fatty acids supplementation reduces wheezing and asthma.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effect of n-3 long chain polyunsaturated fatty acid supplementation in pregnancy on infants’ allergies in first year of life: randomised controlled trial\nABSTRACT: OBJECTIVE To determine whether dietary n-3 long chain polyunsaturated fatty acid (LCPUFA) supplementation of pregnant women with a fetus at high risk of allergic disease reduces immunoglobulin E associated eczema or food allergy at 1 year of age. DESIGN Follow-up of infants at high hereditary risk of allergic disease in the Docosahexaenoic Acid to Optimise Mother Infant Outcome (DOMInO) randomised controlled trial. SETTING Adelaide, South Australia. PARTICIPANTS 706 infants at high hereditary risk of developing allergic disease whose mothers were participating in the DOMInO trial. INTERVENTIONS The intervention group (n=368) was randomly allocated to receive fish oil capsules (providing 900 mg of n-3 LCPUFA daily) from 21 weeks' gestation until birth; the control group (n=338) received matched vegetable oil capsules without n-3 LCPUFA. MAIN OUTCOME MEASURE Immunoglobulin E associated allergic disease (eczema or food allergy with sensitisation) at 1 year of age. RESULTS No differences were seen in the overall percentage of infants with immunoglobulin E associated allergic disease between the n-3 LCPUFA and control groups (32/368 (9%) v 43/338 (13%); unadjusted relative risk 0.68, 95% confidence interval 0.43 to 1.05, P=0.08; adjusted relative risk 0.70, 0.45 to 1.09, P=0.12), although the percentage of infants diagnosed as having atopic eczema (that is, eczema with associated sensitisation) was lower in the n-3 LCPUFA group (26/368 (7%) v 39/338 (12%); unadjusted relative risk 0.61, 0.38 to 0.98, P=0.04; adjusted relative risk 0.64, 0.40 to 1.02, P=0.06). Fewer infants were sensitised to egg in the n-3 LCPUFA group (34/368 (9%) v 52/338 (15%); unadjusted relative risk 0.61, 0.40 to 0.91, P=0.02; adjusted relative risk 0.62, 0.41 to 0.93, P=0.02), but no diffe [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 710, "doc_id": "22442133", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is dopamine an independent risk factor for reduced amikacin clearance in extremely low-birth-weight infants?\n\nABSTRACT:\nImportant inter-individual variability in amikacin clearance was observed in preterm infants, only in part explained by gestational age (GA), birth weight, or coadministration of nonselective cyclo-oxygenase (COX) inhibitor. We therefore evaluated whether dopamine had an additional effect on amikacin clearance. Clinical characteristics (GA, weight, COX inhibitor, dopamine, prenatal betamethasone) and amikacin pharmacokinetics were retrospectively collected in a cohort of preterm infants (GA of <31 wks, early neonatal life on respiratory support, between January 1, 1999 and January 6, 2005). Pharmacokinetics were calculated by assuming a one-compartment model with instantaneous input and first-order output based on paired samples collected for therapeutic drug monitoring before and following second administration. Monovariate analysis (Spearman, Mann-Whitney U test) was used to study the impact of clinical characteristics on amikacin clearance, and logistic regression was used to assess their potential independent effect. Paired amikacin samples were available for 240 neonates (mean GA, 28 wks; birth weight, 1042 g). Amikacin clearance was 0.46 (range, 0.09-2.33) mL/kg/min and distribution volume was 0.54 (range, 0.17-2.31) L/kg. GA, birth weight, COX inhibitor, and dopamine had a significant effect on amikacin clearance. In a logistic regression model, dopamine was no longer a significant variable when GA, birth weight, or cotreatment of a nonselective COX inhibitor was entered as second variable.", "output": "{\"label\": \"no\", \"rationale\": \"Dopamine is an indicator but not an independent marker of reduced amikacin clearance in early neonatal life in extremely low-birth-weight infants. Therefore, neither dose nor interval should be adapted when dopamine is prescribed, if GA and coadministration of nonselective COX inhibitors already have been taken into account.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 16446602, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: CX3CR1 on the Th2 cells suppresses airway inflammation.\n\nCANDIDATE_PASSAGE:\nBlood pressure and incidence of twelve cardiovascular diseases: lifetime risks, healthy life-years lost, and age-specific associations in 1·25 million people BACKGROUND The associations of blood pressure with the different manifestations of incident cardiovascular disease in a contemporary population have not been compared. In this study, we aimed to analyse the associations of blood pressure with 12 different presentations of cardiovascular disease. METHODS We used linked electronic health records from 1997 to 2010 in the CALIBER (CArdiovascular research using LInked Bespoke studies and Electronic health Records) programme to assemble a cohort of 1·25 million patients, 30 years of age or older and initially free from cardiovascular disease, a fifth of whom received blood pressure-lowering treatments. We studied the heterogeneity in the age-specific associations of clinically measured blood pressure with 12 acute and chronic cardiovascular diseases, and estimated the lifetime risks (up to 95 years of age) and cardiovascular disease-free life-years lost adjusted for other risk factors at index ages 30, 60, and 80 years. This study is registered at ClinicalTrials.gov, number NCT01164371. FINDINGS During 5·2 years median follow-up, we recorded 83,098 initial cardiovascular disease presentations. In each age group, the lowest risk for cardiovascular disease was in people with systolic blood pressure of 90-114 mm Hg and diastolic blood pressure of 60-74 mm Hg, with no evidence of a J-shaped increased risk at lower blood pressures. The effect of high blood pressure varied by cardiovascular disease endpoint, from strongly positive to no effect. Associations with high systolic blood pressure were strongest for intracerebral haemorrhage (hazard ratio 1·44 [95% CI 1·3 [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "219", "doc_id": "4506414", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Bariatric surgery leads to negative outcomes in mental health.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mental Health Conditions Among Patients Seeking and Undergoing Bariatric Surgery: A Meta-analysis.\nABSTRACT: IMPORTANCE Bariatric surgery is associated with sustained weight loss and improved physical health status for severely obese individuals. Mental health conditions may be common among patients seeking bariatric surgery; however, the prevalence of these conditions and whether they are associated with postoperative outcomes remains unknown. OBJECTIVE To determine the prevalence of mental health conditions among bariatric surgery candidates and recipients, to evaluate the association between preoperative mental health conditions and health outcomes following bariatric surgery, and to evaluate the association between surgery and the clinical course of mental health conditions. DATA SOURCES We searched PubMed, MEDLINE on OVID, and PsycINFO for studies published between January 1988 and November 2015. Study quality was assessed using an adapted tool for risk of bias; quality of evidence was rated based on GRADE (Grading of Recommendations Assessment, Development and Evaluation) criteria. FINDINGS We identified 68 publications meeting inclusion criteria: 59 reporting the prevalence of preoperative mental health conditions (65,363 patients) and 27 reporting associations between preoperative mental health conditions and postoperative outcomes (50,182 patients). Among patients seeking and undergoing bariatric surgery, the most common mental health conditions, based on random-effects estimates of prevalence, were depression (19% [95% CI, 14%-25%]) and binge eating disorder (17% [95% CI, 13%-21%]). There was conflicting evidence regarding the association between preoperative mental health conditions and postoperative weight loss. Neither depression nor binge eating disorder was consistently associated with differences in weight outcomes. Bariatric surgery was, however, c [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Bariatric surgery was, however, consistently associated with postoperative decreases in the prevalence of depression (7 studies; 8%-74% decrease) and the severity of depressive symptoms (6 studies; 40%-70% decrease).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 166, "doc_id": "18872233", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The Snf1 complex regulates carbon and energy metabolism in baker's yeast (Saccharomyces cerevisiae).\n\nCANDIDATE_PASSAGE:\nKRAS gene amplification and overexpression but not mutation associates with aggressive and metastatic endometrial cancer BACKGROUND Three quarter of endometrial carcinomas are treated at early stage. Still, 15 to 20% of these patients experience recurrence, with little effect from systemic therapies. Homo sapiens v-Ki-ras2 Kirsten rat sarcoma viral oncogenes homologue (KRAS) mutations have been reported to have an important role in tumorigenesis for human cancers, but there is limited knowledge regarding clinical relevance of KRAS status in endometrial carcinomas. METHODS We have performed a comprehensive and integrated characterisation of genome-wide expression related to KRAS mutations and copy-number alterations in primary- and metastatic endometrial carcinoma lesions in relation to clinical and histopathological data. A primary investigation set and clinical validation set was applied, consisting of 414 primary tumours and 61 metastatic lesions totally. RESULTS Amplification and gain of KRAS present in 3% of the primary lesions and 18% of metastatic lesions correlated significantly with poor outcome, high International Federation of Gynaecology and Obstetrics stage, non-endometrioid subtype, high grade, aneuploidy, receptor loss and high KRAS mRNA levels, also found to be associated with aggressive phenotype. In contrast, KRAS mutations were present in 14.7% of primary lesions with no increase in metastatic lesions, and did not influence outcome, but was significantly associated with endometrioid subtype, low grade and obesity. CONCLUSION These results support that KRAS amplification and KRAS mRNA expression, both increasing from primary to metastatic lesions, are relevant for endometrial carcinoma disease progression.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1182", "doc_id": "3210545", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Reduced phosphorylation of PP2A suppresses HDAC4 dephosphorylation.\n\nCANDIDATE_PASSAGE:\nNuclear accumulation of HDAC4 in ATM deficiency promotes neurodegeneration in ataxia-telangiectasia Ataxia telangiectasia is a neurodegenerative disease caused by mutation of the Atm gene. Here we report that ataxia telangiectasia mutated (ATM) deficiency causes nuclear accumulation of histone deacetylase 4 (HDAC4) in neurons and promotes neurodegeneration. Nuclear HDAC4 binds to chromatin, as well as to myocyte enhancer factor 2A (MEF2A) and cAMP-responsive element binding protein (CREB), leading to histone deacetylation and altered neuronal gene expression. Blocking either HDAC4 activity or its nuclear accumulation blunts these neurodegenerative changes and rescues several behavioral abnormalities of ATM-deficient mice. Full rescue of the neurodegeneration, however, also requires the presence of HDAC4 in the cytoplasm, suggesting that the ataxia telangiectasia phenotype results both from a loss of cytoplasmic HDAC4 as well as its nuclear accumulation. To remain cytoplasmic, HDAC4 must be phosphorylated. The activity of the HDAC4 phosphatase, protein phosphatase 2A (PP2A), is downregulated by ATM-mediated phosphorylation. In ATM deficiency, enhanced PP2A activity leads to HDAC4 dephosphorylation and the nuclear accumulation of HDAC4. Our results define a crucial role of the cellular localization of HDAC4 in the events leading to ataxia telangiectasia neurodegeneration.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1027", "doc_id": "3113630", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Smc5/6 engagment halts the activation of SUMO E3 ligase Mms21 by ATP-dependent remolding.\n\nCANDIDATE_PASSAGE:\nAnother Barrier to Regeneration in the CNS: Activated Macrophages Induce Extensive Retraction of Dystrophic Axons through Direct Physical Interactions Injured axons of the adult CNS undergo lengthy retraction from the initial site of axotomy after spinal cord injury. Macrophage infiltration correlates spatiotemporally with this deleterious phenomenon, but the direct involvement of these inflammatory cells has not been demonstrated. In the present study, we examined the role of macrophages in axonal retraction within the dorsal columns after spinal cord injury in vivo and found that retraction occurred between days 2 and 28 after lesion and that the ends of injured axons were associated with ED-1+ cells. Clodronate liposome-mediated depletion of infiltrating macrophages resulted in a significant reduction in axonal retraction; however, we saw no evidence of regeneration. We used time-lapse imaging of adult dorsal root ganglion neurons in an in vitro model of the glial scar to examine macrophage-axon interactions and observed that adhesive contacts and considerable physical interplay between macrophages and dystrophic axons led to extensive axonal retraction. The induction of retraction was dependent on both the growth state of the axon and the activation state of the macrophage. Only dystrophic adult axons were susceptible to macrophage \"attack. \" Unlike intrinsically active cell line macrophages, both primary macrophages and microglia required activation to induce axonal retraction. Contact with astrocytes had no deleterious effect on adult dystrophic axons, suggesting that the induction of extensive retraction was specific to phagocytic cells. Our data are the first to indicate a direct role of activated macrophages in axonal retraction by physical cell-cel [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1090", "doc_id": "16905344", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Febrile seizures reduce the threshold for development of epilepsy.\n\nCANDIDATE_PASSAGE:\nHusbands' involvement in delivery care utilization in rural Bangladesh: A qualitative study BACKGROUND A primary cause of high maternal mortality in Bangladesh is lack of access to professional delivery care. Examining the role of the family, particularly the husband, during pregnancy and childbirth is important to understanding women's access to and utilization of professional maternal health services that can prevent maternal mortality. This qualitative study examines husbands' involvement during childbirth and professional delivery care utilization in a rural sub-district of Netrokona district, Bangladesh. METHODS Using purposive sampling, ten households utilizing a skilled attendant during the birth of the youngest child were selected and matched with ten households utilizing an untrained traditional birth attendant, or dhatri. Households were selected based on a set of inclusion criteria, such as approximate household income, ethnicity, and distance to the nearest hospital. Twenty semi-structured interviews were conducted in Bangla with husbands in these households in June 2010. Interviews were transcribed, translated into English, and analyzed using NVivo 9.0. RESULTS By purposefully selecting households that differed on the type of provider utilized during delivery, common themes--high costs, poor transportation, and long distances to health facilities--were eliminated as sufficient barriers to the utilization of professional delivery care. Divergent themes, namely husbands' social support and perceived social norms, were identified as underlying factors associated with delivery care utilization. We found that husbands whose wives utilized professional delivery care provided emotional, instrumental and informational support to their wives during deliv [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "411", "doc_id": "10854174", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Taking 400mg of α-tocopheryl acetate in combination with vitamin C reduces the risk of prostate cancer.\n\nCANDIDATE_PASSAGE:\nLiraglutide improves hippocampal synaptic plasticity associated with increased expression of Mash1 in ob/ob mice Objective:Consumption of high-fat diet exerts adverse effects on learning and memory formation, which is linked to impaired hippocampal function. Activation of glucagon-like peptide-1 (GLP-1) signalling ameliorates detrimental effects of obesity-diabetes on cognitive function; however, mechanisms underlying these beneficial actions remain unclear. This study examined effects of daily subcutaneous treatment with GLP-1 mimetic, Liraglutide, on synaptic plasticity, hippocampal gene expression and metabolic control in adult obese diabetic (ob/ob) mice. Results:Long-term potentiation (LTP) induced by area CA1 was completely abolished in ob/ob mice compared with lean controls. Deleterious effects on LTP were rescued (P<0.001) with Liraglutide. Indeed, Liraglutide-treated mice exhibited superior LTP profile compared with lean controls (P<0.01). Expression of hippocampal brain-derived neurotropic factor and neurotrophic tyrosine kinase receptor-type 2 were not significantly different, but synaptophysin and Mash1 were decreased in ob/ob mice. Treatment with Liraglutide over 21 days increased expression of Mash1 in ob/ob mice (2.0-fold; P<0.01). These changes were associated with significantly reduced plasma glucose (21% reduction; P<0.05) and markedly improved plasma insulin concentrations (2.1- to 3.3-fold; P<0.05 to P<0.01). Liraglutide also significantly reduced the glycaemic excursion following an intraperitonal glucose load (area under curve (AUC) values: 22%; P<0.05) and markedly enhanced the insulin response to glucose (AUC values: 1.6-fold; P<0.05). O2 consumption, CO2 production, respiratory exchange ratio and energy expenditure were not altered b [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1141", "doc_id": "23601616", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Varenicline monotherapy is more effective after 26 weeks of treatment compared to combination nicotine replacement therapies with varenicline or bupropion.\n\nCANDIDATE_PASSAGE:\nThe Combination of Exercise and Respiratory Training Improves Respiratory Muscle Function in Pulmonary Hypertension Increased dyspnea and reduced exercise capacity in pulmonary arterial hypertension (PAH) can be partly attributed to impaired respiratory muscle function. This prospective study was designed to assess the impact of exercise and respiratory training on respiratory muscle strength and 6-min walking distance (6MWD) in PAH patients. Patients with invasively confirmed PAH underwent 3 weeks of in-hospital exercise and respiratory training, which was continued at home for another 12 weeks. Medication remained constant during the study period. Blinded observers assessed efficacy parameters at baseline (I) and after 3 (II) and 15 weeks (III). Respiratory muscle function was assessed by twitch mouth pressure (TwPmo) during nonvolitional supramaximal magnetic phrenic nerve stimulation. Seven PAH patients (4 women; mean pulmonary artery pressure 45 ± 11 mmHg, median WHO functional class 3.1 ± 0.4, idiopathic/associated PAH n = 5/2) were included. The training program was feasible and well tolerated by all patients with excellent compliance. TwPmo was I: 0.86 ± 0.37 kPa, II: 1.04 ± 0.29 kPa, and III: 1.27 ± 0.44 kPa, respectively. 6MWD was I: 417 ± 51 m, II: 509 ± 39 m, and III: 498 ± 39 m, respectively. Both TwPmo (+0.41 ± 0.34 kPa, +56 ± 39 %) and 6MWD (+81 ± 30 m, +20 ± 9 %) increased significantly in the period between baseline and the final assessment (pairwise comparison: p = 0.012/<0.001; RM-ANOVA considering I, II, III: p = 0.037/<0.001). Exercise and respiratory training as an adjunct to medical therapy may be effective in patients with PAH to improve respiratory muscle strength and exercise capacity. Future, randomized, controlled trials should be [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1360", "doc_id": "40631095", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Androgenetic haploid mouse embryonic stem cells (ESCs) can be derived and genetically manipulated in vitro.\n\nCANDIDATE_PASSAGE:\nGeneration of Genetically Modified Mice by Oocyte Injection of Androgenetic Haploid Embryonic Stem Cells Haploid cells are amenable for genetic analysis. Recent success in the derivation of mouse haploid embryonic stem cells (haESCs) via parthenogenesis has enabled genetic screening in mammalian cells. However, successful generation of live animals from these haESCs, which is needed to extend the genetic analysis to the organism level, has not been achieved. Here, we report the derivation of haESCs from androgenetic blastocysts. These cells, designated as AG-haESCs, partially maintain paternal imprints, express classical ESC pluripotency markers, and contribute to various tissues, including the germline, upon injection into diploid blastocysts. Strikingly, live mice can be obtained upon injection of AG-haESCs into MII oocytes, and these mice bear haESC-carried genetic traits and develop into fertile adults. Furthermore, gene targeting via homologous recombination is feasible in the AG-haESCs. Our results demonstrate that AG-haESCs can be used as a genetically tractable fertilization agent for the production of live animals via injection into oocytes.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "111", "doc_id": "13513790", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Bariatric surgery leads to positive outcomes in mental health.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mental Health Conditions Among Patients Seeking and Undergoing Bariatric Surgery: A Meta-analysis.\nABSTRACT: IMPORTANCE Bariatric surgery is associated with sustained weight loss and improved physical health status for severely obese individuals. Mental health conditions may be common among patients seeking bariatric surgery; however, the prevalence of these conditions and whether they are associated with postoperative outcomes remains unknown. OBJECTIVE To determine the prevalence of mental health conditions among bariatric surgery candidates and recipients, to evaluate the association between preoperative mental health conditions and health outcomes following bariatric surgery, and to evaluate the association between surgery and the clinical course of mental health conditions. DATA SOURCES We searched PubMed, MEDLINE on OVID, and PsycINFO for studies published between January 1988 and November 2015. Study quality was assessed using an adapted tool for risk of bias; quality of evidence was rated based on GRADE (Grading of Recommendations Assessment, Development and Evaluation) criteria. FINDINGS We identified 68 publications meeting inclusion criteria: 59 reporting the prevalence of preoperative mental health conditions (65,363 patients) and 27 reporting associations between preoperative mental health conditions and postoperative outcomes (50,182 patients). Among patients seeking and undergoing bariatric surgery, the most common mental health conditions, based on random-effects estimates of prevalence, were depression (19% [95% CI, 14%-25%]) and binge eating disorder (17% [95% CI, 13%-21%]). There was conflicting evidence regarding the association between preoperative mental health conditions and postoperative weight loss. Neither depression nor binge eating disorder was consistently associated with differences in weight outcomes. Bariatric surgery was, however, c [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Moderate-quality evidence supports an association between bariatric surgery and lower rates of depression postoperatively.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 167, "doc_id": "18872233", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Fibroblast Growth Factor is a ligand which signals through receptor tyrosine kinases.\n\nCANDIDATE_PASSAGE:\nSprouty1 Regulates Reversible Quiescence of a Self-Renewing Adult Muscle Stem Cell Pool during Regeneration Satellite cells are skeletal muscle stem cells capable of self-renewal and differentiation after transplantation, but whether they contribute to endogenous muscle fiber repair has been unclear. The transcription factor Pax7 marks satellite cells and is critical for establishing the adult satellite cell pool. By using a lineage tracing approach, we show that after injury, quiescent adult Pax7(+) cells enter the cell cycle; a subpopulation returns to quiescence to replenish the satellite cell compartment, while others contribute to muscle fiber formation. We demonstrate that Sprouty1 (Spry1), a receptor tyrosine kinase signaling inhibitor, is expressed in quiescent Pax7(+) satellite cells in uninjured muscle, downregulated in proliferating myogenic cells after injury, and reinduced as Pax7(+) cells re-enter quiescence. We show that Spry1 is required for the return to quiescence and homeostasis of the satellite cell pool during repair. Our results therefore define a role for Spry1 in adult muscle stem cell biology and tissue repair.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "418", "doc_id": "16660256", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is interval-force relation unaffected by the presence of cardiomyopathy or coronary artery disease in patients with atrial fibrillation?\n\nABSTRACT:\nWe tested the hypothesis that cycle length-dependent cardiac contractility in atrial fibrillation is primarily governed by the negative interval-force relation in patients with normal and depressed systolic function. We performed two-dimensional guided M-mode echocardiography in 41 patients (mean age, 69 +/- 4 years; range, 48 to 92 years; 19 men, 11 women). Twelve patients had objective evidence of left ventricular systolic dysfunction (CMP; mean ejection fraction, 37% +/- 7%) in the absence of coronary artery disease (CAD), 13 patients had documented CAD (mean ejection fraction, 43% +/- 6%), and 16 patients had normal resting left ventricular systolic function (mean ejection fraction, 58% +/- 7%). Simultaneous beat-to-beat blood pressure, end-systolic and end-diastolic dimension, circumferential velocity of fiber shortening (Vcf), and end-systolic wall stress (ESWS) were calculated for all patients. All three groups showed a significant linear relation between beat-to-beat Vcf and Vcf corrected for afterload (represented as the Vcf/ESWS ratio) and preceding cycle length. There was, however, no significant difference in the relation between either of these variables and cycle length among the three groups. There was also no difference in the rate of change in either Vcf or Vcf corrected for afterload (Vcf/ESWS ratio) from beat-to-beat among the three groups. Control patients with normal systolic function showed greater Vcf at any given cycle length compared with patients with CMP or CAD.", "output": "{\"label\": \"yes\", \"rationale\": \"Our data show that, for each beat in atrial fibrillation, Vcf and Vcf/ESWS ratio are decreased after shorter cycle lengths and increased after long cycles, but there is no significant attenuation of this effect in patients with systolic dysfunction with or without coronary disease compared with controls. Thus, the negative interval-force relation, the predominant determinant of beat-to-beat variation in contractility in atrial fibrillation, is preserved in patients with CAD or reduced left ventricular systolic function.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 10404349, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: β1/Ketel is able to bind microtubules.\n\nCANDIDATE_PASSAGE:\nStructural features of the interaction of the 3'-untranslated region of mRNA containing exosomal RNA-specific motifs with YB-1, a potential mediator of mRNA sorting. We have previously shown that YB-1 is the only protein of the HEK293 cell cytoplasmic (S100) extract that specifically interacts with RNA hairpins each containing one of the motifs ACCAGCCU (1), CAGUGAGC (2) and UAAUCCCA (3), which had been identified as often found in exosomal RNA and proposed as potential cis-acting elements targeting RNAs into exosomes. Here we explored the interactions of YB-1 with a fragment of the 3'-untranslated region (UTR) of septin 14 mRNA (SEPT14 RNA), which contains all three motifs. We demonstrated the occurrence of YB-1 among proteins pulled down from the HEK293 S100 extract using biotinylated SEPT14 RNA. With recombinant YB-1, it was found that SEPT14 RNA can bind up to 5 moles of protein per mole of RNA in a cooperative manner, which was shown to be mainly facilitated by the presence of the above motifs. RNA hairpins with motifs 1 and 2 competed with SEPT14 RNA for binding to the protein, whereas that with motif 3 was less competitive, in accordance with the affinity of YB-1 for these RNA hairpins. With YB-1-bound RNA, nucleotides protected from attack by hydroxyl radicals were revealed in all three motifs, although hairpins with motif 2 and especially with motif 1 contained many protected nucleotides outside the motifs, suggesting that the specific environments of these motifs contribute significantly to the YB-1 binding. An analysis of the environments of motifs 1-3 in the HEK293 cell mRNA 3' UTRs gained from RNA-seq data led us to conclude that the primary binding sites of YB-1 in the 3' UTRs are hairpins containing some part of the motif along with its specif [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1407", "doc_id": "40721190", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Ubiquitin ligase UBC13 generates a K63-linked polyubiquitin moiety at PCNA K164.\n\nCANDIDATE_PASSAGE:\nPhosphorylation of the autophagy receptor optineurin restricts Salmonella growth. Selective autophagy can be mediated via receptor molecules that link specific cargoes to the autophagosomal membranes decorated by ubiquitin-like microtubule-associated protein light chain 3 (LC3) modifiers. Although several autophagy receptors have been identified, little is known about mechanisms controlling their functions in vivo. In this work, we found that phosphorylation of an autophagy receptor, optineurin, promoted selective autophagy of ubiquitin-coated cytosolic Salmonella enterica. The protein kinase TANK binding kinase 1 (TBK1) phosphorylated optineurin on serine-177, enhancing LC3 binding affinity and autophagic clearance of cytosolic Salmonella. Conversely, ubiquitin- or LC3-binding optineurin mutants and silencing of optineurin or TBK1 impaired Salmonella autophagy, resulting in increased intracellular bacterial proliferation. We propose that phosphorylation of autophagy receptors might be a general mechanism for regulation of cargo-selective autophagy.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1337", "doc_id": "23972114", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Many proteins in human cells can be post-translationally modified at lysine residues via acetylation.\n\nCANDIDATE_PASSAGE:\nProtein Lysine Acetylated/Deacetylated Enzymes and the Metabolism-Related Diseases Lysine acetylation is a reversible posttranslational modifcation, an epigenetic phenomenon, referred to as transfer of an acetyl group from acetyl CoA to lysine e- amino group of targeted protein, which is modulated by acetyltransferases (histone/ lysine (K) acetyltransferases, HATs/KATs) and deacetylases (histone/lysine (K) deacetylases, HDACs/KDACs). Lysine acetylation regulates various metabolic processes, such as fatty acid oxidation, Krebs cycle, oxidative phosphorylation, angiogenesis and so on. Thus disorders of lysine acetylation may be correlated with obesity, diabetes and cardiovascular disease, which are termed as the metabolic complication. With accumulating studies on proteomic acetylation, lysine acetylation also involves in cell immune status and degenerative diseases, for example, Alzheimer’s disease and Huntington’s disease. This review primarily summarizes the current studies of lysine acetylation in metabolism modulation and in metabolism-related diseases, such as cardiovascular disease and fat metabolism disorder.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "756", "doc_id": "2831620", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Patients in stable partnerships progress from HIV to death at the same rate as patients not in partnerships.\n\nCANDIDATE_ABSTRACT:\nTITLE: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\nABSTRACT: OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART). DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study). SETTING Seven outpatient clinics throughout Switzerland. PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years). MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound. RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion. When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership. In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without. Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression. CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 925, "doc_id": "17077004", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Neutrophil extracellular traps (NETs) are released by ANCA-stimulated neutrophils.\n\nCANDIDATE_PASSAGE:\nHow reliable are light traps in estimating biting rates of adult Anopheles gambiae s.l. (Diptera: Culicidae) in the presence of treated bed nets? The sampling efficiency of light trap catches relative to human bait catches in estimating biting rates of the mosquito Anopheles gambiae Giles was investigated in two types of community in southern Sierra Leone: (i) where most of the inhabitants slept under treated bed nets; and (ii) where most of the inhabitants slept without bed nets. The number of female A. gambiae mosquitoes caught in these communities by light trap was strongly correlated (r > or = 0.72) with those from corresponding human biting catches performed either on the same or adjacent nights. It was found that the relative sampling efficiency of light traps varied slightly but significantly with mosquito abundance in villages with treated bed nets, but not in those without them. Nevertheless, the relationship between relative sampling efficiency and mosquito abundance did not differ significantly between the two types of village. Overall, there was insufficient evidence to show that the presence of treated nets altered the relative efficiency of light traps and any bias was only slight, and unlikely to be of any practical importance. Hence, it was concluded that light traps can be used as a surrogate for human bait catches in estimating biting rates of A. gambiae mosquitoes in the two communities.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "845", "doc_id": "18592108", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Patients with common epithelial cancers are less likely to have an emergency event as their first hospital admission if they live in resource-deprived areas.\n\nCANDIDATE_ABSTRACT:\nTITLE: Social variations in access to hospital care for patients with colorectal, breast, and lung cancer between 1999 and 2006: retrospective analysis of hospital episode statistics\nABSTRACT: OBJECTIVES To determine the extent to which type of hospital admission (emergency compared with elective) and surgical procedure varied by socioeconomic circumstances, age, sex, and year of admission for colorectal, breast, and lung cancer. DESIGN Repeated cross sectional study with data from individual patients, 1 April 1999 to 31 March 2006. SETTING Hospital episode statistics (HES) dataset. PARTICIPANTS 564 821 patients aged 50 and over admitted with a diagnosis of colorectal, breast, or lung cancer. MAIN OUTCOME MEASURES Proportion of patients admitted as emergencies, and the proportion receiving the recommended surgical treatment. RESULTS Patients from deprived areas, older people, and women were more likely to be admitted as emergencies. For example, the adjusted odds ratio for patients with breast cancer in the least compared with most deprived fifth of deprivation was 0.63 (95% confidence interval 0.60 to 0.66) and the adjusted odds ratio for patients with lung cancer aged 80-89 compared with those aged 50-59 was 3.13 (2.93 to 3.34). There were some improvements in disparities between age groups but not for patients living in deprived areas over time. Patients from deprived areas were less likely to receive preferred procedures for rectal, breast, and lung cancer. These findings did not improve with time. For example, 67.4% (3529/5237) of patients in the most deprived fifth of deprivation had anterior resection for rectal cancer compared with 75.5% (4497/5959) of patients in the least deprived fifth (1.34, 1.22 to 1.47). Over half (54.0%, 11 256/20 849) of patients in the most deprived fifth of deprivation had breast conserving surgery compared with 63.7% (18 445/28 960) of patients in the least deprived fifth (1.21, 1.16 to 1.26). Men were less like [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"For example, the adjusted odds ratio for patients with breast cancer in the least compared with most deprived fifth of deprivation was 0.63 (95% confidence interval 0.60 to 0.66) and the adjusted odds ratio for patients with lung cancer aged 80-89 compared with those aged 50-59 was 3.13 (2.93 to 3.34). There were some improvements in disparities between age groups but not for patients living in deprived areas over time.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 927, "doc_id": "16390264", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The mean suicide rate in women is lower after miscarriage than live birth.\n\nCANDIDATE_ABSTRACT:\nTITLE: Suicides after pregnancy in Finland, 1987-94: register linkage study.\nABSTRACT: OBJECTIVE To determine rates of suicide associated with pregnancy by the type of pregnancy. DESIGN Register linkage study. Information on suicides in women of reproductive age was linked with the Finnish birth, abortion, and hospital discharge registers to find out how many women who committed suicide had had a completed pregnancy during her last year of life. SETTING Nationwide data from Finland. SUBJECTS Women who committed suicide in 1987-94. RESULTS There were 73 suicides associated with pregnancy, representing 5.4% of all suicides in women in this age group. The mean annual suicide rate was 11.3 per 100,000. The suicide rate associated with birth was significantly lower (5.9) and the rates associated with miscarriage (18.1) and induced abortion (34.7) were significantly higher than in the population. The risk associated with birth was higher among teenagers and that associated with abortion was increased in all age groups. Women who had committed a suicide tended to come from lower social classes and were more likely to be unmarried than other women who had had a completed pregnancy. CONCLUSIONS The increased risk of suicide after an induced abortion indicates either common risk factors for both or harmful effects of induced abortion on mental health.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The suicide rate associated with birth was significantly lower (5.9) and the rates associated with miscarriage (18.1) and induced abortion (34.7) were significantly higher than in the population.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1228, "doc_id": "25641414", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Ambulatory blood pressure monitoring is inaccurate at diagnosing hypertension.\n\nCANDIDATE_ABSTRACT:\nTITLE: Relative effectiveness of clinic and home blood pressure monitoring compared with ambulatory blood pressure monitoring in diagnosis of hypertension: systematic review\nABSTRACT: OBJECTIVE To determine the relative accuracy of clinic measurements and home blood pressure monitoring compared with ambulatory blood pressure monitoring as a reference standard for the diagnosis of hypertension. DESIGN Systematic review with meta-analysis with hierarchical summary receiver operating characteristic models. Methodological quality was appraised, including evidence of validation of blood pressure measurement equipment. DATA SOURCES Medline (from 1966), Embase (from 1980), Cochrane Database of Systematic Reviews, DARE, Medion, ARIF, and TRIP up to May 2010. Eligibility criteria for selecting studies Eligible studies examined diagnosis of hypertension in adults of all ages using home and/or clinic blood pressure measurement compared with those made using ambulatory monitoring that clearly defined thresholds to diagnose hypertension. RESULTS The 20 eligible studies used various thresholds for the diagnosis of hypertension, and only seven studies (clinic) and three studies (home) could be directly compared with ambulatory monitoring. Compared with ambulatory monitoring thresholds of 135/85 mm Hg, clinic measurements over 140/90 mm Hg had mean sensitivity and specificity of 74.6% (95% confidence interval 60.7% to 84.8%) and 74.6% (47.9% to 90.4%), respectively, whereas home measurements over 135/85 mm Hg had mean sensitivity and specificity of 85.7% (78.0% to 91.0%) and 62.4% (48.0% to 75.0%). CONCLUSIONS Neither clinic nor home measurement had sufficient sensitivity or specificity to be recommended as a single diagnostic test. If ambulatory monitoring is taken as the reference standard, then treatment decisions based on clinic or home blood pressure alone might result in substantial overdiagnosis. Ambulatory monitoring before the start of lifelong [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Ambulatory monitoring before the start of lifelong drug treatment might lead to more appropriate targeting of treatment, particularly around the diagnostic threshold.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 106, "doc_id": "25515907", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The repeat-variable diresidue (RVD) in the loop of Transcription-Activator Like (TAL) effectors specifies the nucleotides-amino acid contact at the target promoter element.\n\nCANDIDATE_ABSTRACT:\nTITLE: Structural basis for sequence-specific recognition of DNA by TAL effectors.\nABSTRACT: TAL (transcription activator-like) effectors, secreted by phytopathogenic bacteria, recognize host DNA sequences through a central domain of tandem repeats. Each repeat comprises 33 to 35 conserved amino acids and targets a specific base pair by using two hypervariable residues [known as repeat variable diresidues (RVDs)] at positions 12 and 13. Here, we report the crystal structures of an 11.5-repeat TAL effector in both DNA-free and DNA-bound states. Each TAL repeat comprises two helices connected by a short RVD-containing loop. The 11.5 repeats form a right-handed, superhelical structure that tracks along the sense strand of DNA duplex, with RVDs contacting the major groove. The 12th residue stabilizes the RVD loop, whereas the 13th residue makes a base-specific contact. Understanding DNA recognition by TAL effectors may facilitate rational design of DNA-binding proteins with biotechnological applications.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"TAL (transcription activator-like) effectors, secreted by phytopathogenic bacteria, recognize host DNA sequences through a central domain of tandem repeats. Each repeat comprises 33 to 35 conserved amino acids and targets a specific base pair by using two hypervariable residues [known as repeat variable diresidues (RVDs)] at positions 12 and 13.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1263, "doc_id": "3981729", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Up-regulation of the p53 pathway and related molecular events casues cancer resistance and results in a significantly shortened lifespan marked by senescent cells and accelerated organismal aging.\n\nCANDIDATE_ABSTRACT:\nTITLE: Senescent Cells, Tumor Suppression, and Organismal Aging: Good Citizens, Bad Neighbors\nABSTRACT: Cells from organisms with renewable tissues can permanently withdraw from the cell cycle in response to diverse stress, including dysfunctional telomeres, DNA damage, strong mitogenic signals, and disrupted chromatin. This response, termed cellular senescence, is controlled by the p53 and RB tumor suppressor proteins and constitutes a potent anticancer mechanism. Nonetheless, senescent cells acquire phenotypic changes that may contribute to aging and certain age-related diseases, including late-life cancer. Thus, the senescence response may be antagonistically pleiotropic, promoting early-life survival by curtailing the development of cancer but eventually limiting longevity as dysfunctional senescent cells accumulate.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1344, "doc_id": "9559146", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Pharmacist attendance at ward rounds reduces adverse events in wards.\n\nCANDIDATE_PASSAGE:\nSpread of chloroquine resistance in Plasmodium falciparum. Malaria resistant to chloroquine has now been confirmed in more than 40 countries. The drug was introduced in 1934, but was not in large-scale use until the early 1950s. Anecdotal reports suggest that resistance emerged as early as 1957 both in Colombia and along the then Cambodia-Thailand border area. But by 1960, resistance in these areas was confirmed - and may represent two separate events. Resistance spread rapidly, with a new focus of resistance confirmed in East Africa by 1977. Chloroquine resistance represents a severe problem both for prophylaxis and treatment of malaria. In this aricle, David Payne traces the spread of resistance and discusses some of its implications.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "941", "doc_id": "37205685", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does perioperative influenza vaccination reduce postoperative metastatic disease by reversing surgery-induced dysfunction in natural killer cells?\n\nABSTRACT:\nSurgical removal of solid primary tumors is an essential component of cancer treatment. Surgery-induced dysfunction in natural killer (NK) cells has been linked to the development of metastases in animal models and patients with cancer. We investigated the activation of NK cells using influenza vaccine in the perioperative period to eradicate micrometastatic disease. Both the B16lacZ and 4T1 tumor models in immunocompetent mice were used to assess the in vivo efficacy of perioperative influenza vaccine administration. In healthy human donors and cancer surgery patients, we assessed NK cell function pre- and post-influenza vaccination using both in vivo and ex vivo assays. Using the TLR3 agonist poly(I:C), we showed as proof-of-principle that perioperative administration of a nonspecific innate immune stimulant can inhibit surgery-induced dysfunction in NK cells and attenuate metastases. Next, we assessed a panel of prophylactic vaccines for NK cell activation and determined that inactivated influenza vaccine was the best candidate for perioperative administration. Perioperative influenza vaccine significantly reduced tumor metastases and improved NK cytotoxicity in preclinical tumor models. Significantly, IFNα is the main cytokine mediator for the therapeutic effect of influenza vaccination. In human studies, influenza vaccine significantly enhanced NK cell activity in healthy human donors and cancer surgery patients.", "output": "{\"label\": \"yes\", \"rationale\": \"These results provide the preclinical rationale to pursue future clinical trials of perioperative NK cell activation, using vaccination in cancer surgery patients. Research into perioperative immune therapy is warranted to prevent immune dysfunction following surgery and eradicate metastatic disease.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 23881927, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The G34R/V mutation creates a hypomethylated phenotype at the H3K36 histone.\n\nCANDIDATE_ABSTRACT:\nTITLE: ZMYND11 links histone H3.3K36me3 to transcription elongation and tumour suppression\nABSTRACT: Recognition of modified histones by ‘reader’ proteins plays a critical role in the regulation of chromatin. H3K36 trimethylation (H3K36me3) is deposited onto the nucleosomes in the transcribed regions after RNA polymerase II elongation. In yeast, this mark in turn recruits epigenetic regulators to reset the chromatin to a relatively repressive state, thus suppressing cryptic transcription. However, much less is known about the role of H3K36me3 in transcription regulation in mammals. This is further complicated by the transcription-coupled incorporation of the histone variant H3.3 in gene bodies. Here we show that the candidate tumour suppressor ZMYND11 specifically recognizes H3K36me3 on H3.3 (H3.3K36me3) and regulates RNA polymerase II elongation. Structural studies show that in addition to the trimethyl-lysine binding by an aromatic cage within the PWWP domain, the H3.3-dependent recognition is mediated by the encapsulation of the H3.3-specific ‘Ser 31’ residue in a composite pocket formed by the tandem bromo–PWWP domains of ZMYND11. Chromatin immunoprecipitation followed by sequencing shows a genome-wide co-localization of ZMYND11 with H3K36me3 and H3.3 in gene bodies, and its occupancy requires the pre-deposition of H3.3K36me3. Although ZMYND11 is associated with highly expressed genes, it functions as an unconventional transcription co-repressor by modulating RNA polymerase II at the elongation stage. ZMYND11 is critical for the repression of a transcriptional program that is essential for tumour cell growth; low expression levels of ZMYND11 in breast cancer patients correlate with worse prognosis. Consistently, overexpression of ZMYND11 suppresses cancer cell growth in vitro and tumour formation in mice. Together, this study identifies ZMYND11 as an H3 [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1164, "doc_id": "4455466", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: PDPN promotes efficient motility along stromal surfaces by activating the C-type lectin receptor to rearrange the actin cytoskeleton in dendritic cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: A Candidate Gene Approach Identifies the TRAF1/C5 Region as a Risk Factor for Rheumatoid Arthritis\nABSTRACT: Correction for: Kurreeman FAS, Padyukov L, Marques RB, Schrodi SJ, Seddighzadeh M, et al. (2007) A Candidate Gene Approach Identifies the TRAF1/C5 Region as a Risk Factor for Rheumatoid Arthritis. PLoS Med 4(9): e278. doi:10.1371/journal.pmed.0040278 In Table 1, the allele ratio in column eight (Allele Ratiosb: Cases, Controls) refers to allele A: allele B and not allele1:allele2 as described in footnote b, with Allele A being the Susceptibility Allele as denoted in column seven. The footnote should read: bNumber of alleles were compared in cases versus controls: allele A: allele B cases, allele A: allele B controls. Allele A refers to the susceptibility alleles as given in column seven.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 904, "doc_id": "1967017", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Most termination events in Okazaki fragments are dictated by initiation patterns.\n\nCANDIDATE_ABSTRACT:\nTITLE: Quantitative, genome-wide analysis of eukaryotic replication initiation and termination.\nABSTRACT: Many fundamental aspects of DNA replication, such as the exact locations where DNA synthesis is initiated and terminated, how frequently origins are used, and how fork progression is influenced by transcription, are poorly understood. Via the deep sequencing of Okazaki fragments, we comprehensively document replication fork directionality throughout the S. cerevisiae genome, which permits the systematic analysis of initiation, origin efficiency, fork progression, and termination. We show that leading-strand initiation preferentially occurs within a nucleosome-free region at replication origins. Using a strain in which late origins can be induced to fire early, we show that replication termination is a largely passive phenomenon that does not rely on cis-acting sequences or replication fork pausing. The replication profile is predominantly determined by the kinetics of origin firing, allowing us to reconstruct chromosome-wide timing profiles from an asynchronous culture.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The replication profile is predominantly determined by the kinetics of origin firing, allowing us to reconstruct chromosome-wide timing profiles from an asynchronous culture.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 807, "doc_id": "36606083", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Distant CREs are important for transcriptional regulation.\n\nCANDIDATE_PASSAGE:\nMonitoring starvation-induced reactive oxygen species formation. Reactive oxygen species (ROS) are potentially harmful to cells because of their ability to oxidize cell constituents such as DNA, proteins, and lipids. However, at low levels, and under tight control, this feature makes them excellent modifiers in a variety of signal transduction pathways, including autophagy. Autophagy was traditionally associated with oxidative stress, acting in the degradation of oxidized proteins and organelles. Recently, a signaling role was suggested for ROS in the regulation of autophagy, leading, under different circumstances, either to survival or to death. To study the effects of ROS on this pathway, one must determine the localization, intensity, kinetics, and essentiality of the oxidative signal in autophagy. Moreover, once characterized, detection and manipulation of ROS formation could be used to monitor and control autophagic activity. In this chapter we discuss methods to examine ROS in the context of autophagy.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "351", "doc_id": "19922508", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does 362 Priming of the Brain Tumor Microenvironment enable Improved Nanomedicine Delivery?\n\nABSTRACT:\nA major challenge in cancer nanotechnology is the efficient delivery of nanomedicines into solid tumors. Nanomedicine relies on a functional vascular network and minimal tissue resistance to achieve homogeneous transport and distribution in solid tumor via convection- and diffusion-based mechanisms. This is especially true for brain tumors, where the presence of specialized blood-brain barrier further impedes transport of nanomedicine from the systemic circulation into the central nervous system. Unlike blood vessels within healthy tissues, tumor vessels are often morphologically pathological and functionally impaired, due to an imbalance of pro- and antiangiogenic growth factor production within the tumor microenvironment. Furthermore, within the tumor stroma, excessive and heterogeneous productions of collagen and other matrix proteins further restrict nanomedicine distribution. We characterized in real-time, perfusion and diffusion parameters of luminescent nanoparticles using syngeneic GL261 and the spontaneous RCAS-hPDGFb-HA/nestin Tv-a; Ink4a/Arf-/- brain tumor model with multiphoton imaging in vivo. We demonstrate that tumor vasculature exhibits increased permeability and decreased perfusion capacity compared with normal vessels. As a result, transport of nanomedicine across the vessel wall into the tumor stroma is strongly dependent on particle size and surface polarity. Intratumoral mapping of nanomedicine distribution reveals that once gaining entry into tumors, nanoparticles often experience perivascular clumping and are unable to reach tumor tissue beyond 20 µm from the nearest vessels. Finally, with therapeutic modulation of the tumor microenvironment using anti-VEGFr or anti-TGFβ1 antibody treatments to remodel the tumor vasculature and collage [TRUNCATED]", "output": "{\"label\": \"yes\", \"rationale\": \"The successful implementation of this combined therapeutic approach can have significant implications in developing effective targeted nanomedicines for brain tumors. These findings suggest that optimized delivery of nanomedicine for brain tumors may be possible through the modulation of both the tumor vasculature and extracellular matrix.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 27399559, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: PRC1-bound plasmids sediment at a slower rate in unbound plasmids than in sucrose gradients.\n\nCANDIDATE_PASSAGE:\nPolycomb Proteins Remain Bound to Chromatin and DNA during DNA Replication In Vitro The transcriptional status of a gene can be maintained through multiple rounds of cell division during development. This epigenetic effect is believed to reflect heritable changes in chromatin folding and histone modifications or variants at target genes, but little is known about how these chromatin features are inherited through cell division. A particular challenge for maintaining transcription states is DNA replication, which disrupts or dilutes chromatin-associated proteins and histone modifications. PRC1-class Polycomb group protein complexes are essential for development and are thought to heritably silence transcription by altering chromatin folding and histone modifications. It is not known whether these complexes and their effects are maintained during DNA replication or subsequently re-established. We find that when PRC1-class Polycomb complex-bound chromatin or DNA is replicated in vitro, Polycomb complexes remain bound to replicated templates. Retention of Polycomb proteins through DNA replication may contribute to maintenance of transcriptional silencing through cell division.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "916", "doc_id": "18037805", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: PKG-la does not have a large impact on expression of pain hypersensitivity in PGK-la knockout mice.\n\nCANDIDATE_PASSAGE:\nGeneration of large numbers of dendritic cells from mouse bone marrow cultures supplemented with granulocyte/macrophage colony-stimulating factor Antigen-presenting, major histocompatibility complex (MHC) class II-rich dendritic cells are known to arise from bone marrow. However, marrow lacks mature dendritic cells, and substantial numbers of proliferating less-mature cells have yet to be identified. The methodology for inducing dendritic cell growth that was recently described for mouse blood now has been modified to MHC class II-negative precursors in marrow. A key step is to remove the majority of nonadherent, newly formed granulocytes by gentle washes during the first 2-4 d of culture. This leaves behind proliferating clusters that are loosely attached to a more firmly adherent \"stroma. \" At days 4-6 the clusters can be dislodged, isolated by 1-g sedimentation, and upon reculture, large numbers of dendritic cells are released. The latter are readily identified on the basis of their distinct cell shape, ultrastructure, and repertoire of antigens, as detected with a panel of monoclonal antibodies. The dendritic cells express high levels of MHC class II products and act as powerful accessory cells for initiating the mixed leukocyte reaction. Neither the clusters nor mature dendritic cells are generated if macrophage colony-stimulating factor rather than granulocyte/macrophage colony-stimulating factor (GM-CSF) is applied. Therefore, GM-CSF generates all three lineages of myeloid cells (granulocytes, macrophages, and dendritic cells). Since > 5 x 10(6) dendritic cells develop in 1 wk from precursors within the large hind limb bones of a single animal, marrow progenitors can act as a major source of dendritic cells. This feature should prove useful for future [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "909", "doc_id": "188911", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: One in two surgical randomized controlled trials are discontinued early.\n\nCANDIDATE_PASSAGE:\nWhat is the best way to help caregivers in cancer and palliative care? A systematic literature review of interventions and their effectiveness. Informal carers in cancer and palliative care are known to have high needs and psychological morbidity, yet a literature review identified few targeted interventions. This systematic review of interventions for carers of patients using home cancer and palliative care services searched Medline, CancerLit, Psycinfo and Cinahl databases. The terms used were carer(s), caregiver(s), palliative and cancer. Papers that reported interventions for adults actively providing informal care for noninstitutionalized cancer and palliative care patients were reviewed. Twenty-two interventions were identified, comprising home nursing care (four), respite services (three), social networks and activity enhancement (two), problem solving and education (three) and group work (10). Of these, nine were delivered solely to carers (i.e., were targeted services). Only six of the carers' interventions had been evaluated, two of these had used a randomized control trial (RCT; grades IB), three employed a single group methodology (two prospective grades IIIC and one retrospective grade IIIC) and one was evaluated using facilitator feedback. There was a lack of outcome evaluation designs, small sample sizes and a reliance on intervention descriptions and formative evaluations. Methodological challenges may mean alternatives to 'pure' RCTs should be considered. The current evidence contributes more to understanding feasibility and acceptability than to effectiveness. Practitioners and evaluators must prioritize the further development of intervention studies.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "886", "doc_id": "22446093", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: EGR2 is important to myelination of the peripheral nervous system.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Transcription Factors Egr2 and Egr3 Are Essential for the Control of Inflammation and Antigen-Induced Proliferation of B and T Cells\nABSTRACT: Lymphocytes provide optimal responses against pathogens with minimal inflammatory pathology. However, the intrinsic mechanisms regulating these responses are unknown. Here, we report that deletion of both transcription factors Egr2 and Egr3 in lymphocytes resulted in a lethal autoimmune syndrome with excessive serum proinflammatory cytokines but also impaired antigen receptor-induced proliferation of B and T cells. Egr2- and Egr3-defective B and T cells had hyperactive signal transducer and activator of transcription-1 (STAT1) and STAT3 while antigen receptor-induced activation of transcription factor AP-1 was severely impaired. We discovered that Egr2 and/or Egr3 directly induced expression of suppressor of cytokine signaling-1 (SOCS1) and SOCS3, inhibitors of STAT1 and STAT3, and also blocked the function of Batf, an AP-1 inhibitor, in B and T cells. Thus, Egr2 and Egr3 regulate B and T cell function in adaptive immune responses and homeostasis by promoting antigen receptor signaling and controlling inflammation.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 364, "doc_id": "1550937", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: MICAL redox enzymes regulate actin dynamics.\n\nCANDIDATE_PASSAGE:\nDrosophila MICAL regulates myofilament organization and synaptic structure The overall size and structure of a synaptic terminal is an important determinant of its function. In a large-scale mutagenesis screen, designed to identify Drosophila mutants with abnormally structured neuromuscular junctions (NMJs), we discovered mutations in Drosophila mical, a conserved gene encoding a multi-domain protein with a N-terminal monooxygenase domain. In mical mutants, synaptic boutons do not sprout normally over the muscle surface and tend to form clusters along synaptic branches and at nerve entry sites. Consistent with high expression of MICAL in somatic muscles, immunohistochemical stainings reveal that the subcellular localization and architecture of contractile muscle filaments are dramatically disturbed in mical mutants. Instead of being integrated into a regular sarcomeric pattern, actin and myosin filaments are disorganized and accumulate beneath the plasmamembrane. Whereas contractile elements are strongly deranged, the proposed organizer of sarcomeric structure, D-Titin, is much less affected. Transgenic expression of interfering RNA molecules demonstrates that MICAL is required in muscles for the higher order arrangement of myofilaments. Ultrastructural analysis confirms that myosin-rich thick filaments enter submembranous regions and interfere with synaptic development, indicating that the disorganized myofilaments may cause the synaptic growth phenotype. As a model, we suggest that the filamentous network around synaptic boutons restrains the spreading of synaptic branches.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "738", "doc_id": "16562534", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does long-term changes in serum cholesterol level influence the progression of coronary calcification?\n\nABSTRACT:\nA number of reports controversially describe the influence of cholesterol level and lipid-lowering treatment (LLT) on the progression of coronary calcium (CC). We tested the hypothesis that long-term changes in serum cholesterol (CL) would affect the progression of CC. The study population comprised 510 patients with stable angina pectoris, mean age of 63 ± 9 years. At baseline 372 patients received statin and/or fibrate (LLT group) while 138 patients did not (No-LLT at baseline group). Spiral CT every 24 months was used to track the progression of CC over a median 5.6 year follow-up. CL decreased during follow-up in both groups, but more pronouncedly in patients with LLT. The changes in total calcium score (TCS) were similar in both groups (p=0.3). Changes in CL during follow-up were not associated with CC: TCS increased by 501 ± 63 from baseline in the 1st (upper) quartile, and by 350 ± 44, 403 ± 41 and 480 ± 56 in the 2nd, 3rd, and 4th quartiles of CL longitudinal changes (p = 0.2), respectively. Baseline TCS and its changes were not correlated with baseline CL and its changes. New calcified lesions were diagnosed in 132 (28.2%) out of the 467 patients available for this analysis, without significant difference between groups (p=0.4). Multivariate analysis demonstrated that only baseline TCS (p < 0.001), body mass index (p = 0.007) and age (p = 0.006) were independent predictors for the TCS changes.", "output": "{\"label\": \"no\", \"rationale\": \"Longitudinal CL changes do not seem to have a measurable effect on the rate of progression of CC.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 20350769, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Progerin induces premature aging in stem cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Human iPSC-based modeling of late-onset disease via progerin-induced aging.\nABSTRACT: Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) resets their identity back to an embryonic age and, thus, presents a significant hurdle for modeling late-onset disorders. In this study, we describe a strategy for inducing aging-related features in human iPSC-derived lineages and apply it to the modeling of Parkinson's disease (PD). Our approach involves expression of progerin, a truncated form of lamin A associated with premature aging. We found that expression of progerin in iPSC-derived fibroblasts and neurons induces multiple aging-related markers and characteristics, including dopamine-specific phenotypes such as neuromelanin accumulation. Induced aging in PD iPSC-derived dopamine neurons revealed disease phenotypes that require both aging and genetic susceptibility, such as pronounced dendrite degeneration, progressive loss of tyrosine hydroxylase (TH) expression, and enlarged mitochondria or Lewy-body-precursor inclusions. Thus, our study suggests that progerin-induced aging can be used to reveal late-onset age-related disease features in hiPSC-based disease models.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Thus, our study suggests that progerin-induced aging can be used to reveal late-onset age-related disease features in hiPSC-based disease models.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 979, "doc_id": "11659421", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Reduction of Rpl38 alters the composition of the Hox gene mRNAs translation in mice without lowering overall protein synthesis.\n\nCANDIDATE_PASSAGE:\nThe effect of folate fortification on folic acid-based homocysteine-lowering intervention and stroke risk: a meta-analysis. OBJECTIVE Folate and vitamin B12 are two vital regulators in the metabolic process of homocysteine, which is a risk factor of atherothrombotic events. Low folate intake or low plasma folate concentration is associated with increased stroke risk. Previous randomized controlled trials presented discordant findings in the effect of folic acid supplementation-based homocysteine lowering on stroke risk. The aim of the present review was to perform a meta-analysis of relevant randomized controlled trials to check the how different folate fortification status might affect the effects of folic acid supplementation in lowering homocysteine and reducing stroke risk. DESIGN Relevant randomized controlled trials were identified through formal literature search. Homocysteine reduction was compared in subgroups stratified by folate fortification status. Relative risks with 95 % confidence intervals were used as a measure to assess the association between folic acid supplementation and stroke risk. SETTING The meta-analysis included fourteen randomized controlled trials, SUBJECTS A total of 39 420 patients. RESULTS Homocysteine reductions were 26·99 (sd 1·91) %, 18·38 (sd 3·82) % and 21·30 (sd 1·98) %, respectively, in the subgroups without folate fortification, with folate fortification and with partial folate fortification. Significant difference was observed between the subgroups with folate fortification and without folate fortification (P=0·05). The relative risk of stroke was 0·88 (95 % CI 0·77, 1·00, P=0·05) in the subgroup without folate fortification, 0·94 (95 % CI 0·58, 1·54, P=0·82) in the subgroup with folate fortification and 0·91 (95 % C [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1031", "doc_id": "37424881", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Women with a higher birth weight are more likely to develop breast cancer later in life.\n\nCANDIDATE_ABSTRACT:\nTITLE: Birth Size and Breast Cancer Risk: Re-analysis of Individual Participant Data from 32 Studies\nABSTRACT: BACKGROUND Birth size, perhaps a proxy for prenatal environment, might be a correlate of subsequent breast cancer risk, but findings from epidemiological studies have been inconsistent. We re-analysed individual participant data from published and unpublished studies to obtain more precise estimates of the magnitude and shape of the birth size-breast cancer association. METHODS AND FINDINGS Studies were identified through computer-assisted and manual searches, and personal communication with investigators. Individual participant data from 32 studies, comprising 22,058 breast cancer cases, were obtained. Random effect models were used, if appropriate, to combine study-specific estimates of effect. Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003). Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data. Birth length and head circumference from birth records were also positively associated with breast cancer risk (pooled RR per one SD increment: 1.06 [95% CI 1.03-1.10] and 1.09 [95% CI 1.03-1.15], respectively). Simultaneous adjustment for these three birth size variables showed that length was the strongest independent predictor of risk. The birth size effec [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1379, "doc_id": "16322674", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does juvenile ferric iron prevent microbiota dysbiosis and colitis in adult rodents?\n\nABSTRACT:\nTo assess whether juvenile chronic ferric iron ingestion limit colitis and dysbiosis at adulthood in rats and mice. Two sets of experiments were designed. In the first set, recently weaned mice were either orally administered ferrous (Fe²⁺) iron salt or ferric (Fe³⁺) microencapsulated iron for 6 wk. The last week of experiments trinitrobenzene sulfonic acid (TNBS) colitis was induced. In the second set, juvenile rats received the microencapsulated ferric iron for 6 wk and were also submitted to TNBS colitis during the last week of experiments. In both sets of experiments, animals were sacrificed 7 d after TNBS instillation. Severity of the inflammation was assessed by scoring macroscopic lesions and quantifying colonic myeloperoxidase (MPO) activity. Alteration of the microflora profile was estimated using quantitative polymerase chain reaction (qPCR) by measuring the evolution of total caecal microflora, Bacteroidetes, Firmicutes and enterobacteria. Neither ferrous nor ferric iron daily exposures at the juvenile period result in any effect in control animals at adulthood although ferrous iron repeated administration in infancy limited weight gain. Ferrous iron was unable to limit the experimental colitis (1.71 ± 0.27 MPO U/mg protein vs 2.47 ± 0.22 MPO U/mg protein in colitic mice). In contrast, ferric iron significantly prevented the increase of MPO activity (1.64 ± 0.14 MPO U/mg protein) in TNBS-induced colitis. Moreover, this positive effect was observed at both the doses of ferric iron used (75 and 150 mg/kg per day po--6 wk). In the study we also compared, in both rats and mice, the consequences of chronic repeated low level exposure to ferric iron (75 mg/kg per day po--6 wk) on TNBS-induced colitis and its related dysbiosis. We confirmed that ferric i [TRUNCATED]", "output": "{\"label\": \"yes\", \"rationale\": \"Rats and mice juvenile chronic ferric iron ingestion prevents colitis and dysbiosis at adulthood as assessed by the first interspecies comparison.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 22690070, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: In S. cerevisiae, the absence of RNA surveillance pathways causes sensitivity to high iron conditions.\n\nCANDIDATE_PASSAGE:\nMultiple RNA surveillance pathways limit aberrant expression of iron uptake mRNAs and prevent iron toxicity in S. cerevisiae. Tight regulation of the expression of mRNAs encoding iron uptake proteins is essential to control iron homeostasis and avoid intracellular iron toxicity. We show that many mRNAs encoding iron uptake or iron mobilization proteins are expressed in iron-replete conditions in the absence of the S. cerevisiae RNase III ortholog Rnt1p or of the nuclear exosome component Rrp6p. Extended forms of these mRNAs accumulate in the absence of Rnt1p or of the 5'-->3' exonucleases Xrn1p and Rat1p, showing that multiple degradative pathways contribute to the surveillance of aberrant forms of these transcripts. RNase III-deficient cells are hypersensitive to high iron concentrations, suggesting that Rnt1p-mediated RNA surveillance is required to prevent iron toxicity. These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "565", "doc_id": "16120395", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Energy balance requires hypothalamic glutamate neurotransmission.\n\nCANDIDATE_PASSAGE:\nInflammatory cytokines in depression: neurobiological mechanisms and therapeutic implications. Mounting evidence indicates that inflammatory cytokines contribute to the development of depression in both medically ill and medically healthy individuals. Cytokines are important for development and normal brain function, and have the ability to influence neurocircuitry and neurotransmitter systems to produce behavioral alterations. Acutely, inflammatory cytokine administration or activation of the innate immune system produces adaptive behavioral responses that promote conservation of energy to combat infection or recovery from injury. However, chronic exposure to elevated inflammatory cytokines and persistent alterations in neurotransmitter systems can lead to neuropsychiatric disorders and depression. Mechanisms of cytokine behavioral effects involve activation of inflammatory signaling pathways in the brain that results in changes in monoamine, glutamate, and neuropeptide systems, and decreases in growth factors, such as brain-derived neurotrophic factor. Furthermore, inflammatory cytokines may serve as mediators of both environmental (e.g. childhood trauma, obesity, stress, and poor sleep) and genetic (functional gene polymorphisms) factors that contribute to depression's development. This review explores the idea that specific gene polymorphisms and neurotransmitter systems can confer protection from or vulnerability to specific symptom dimensions of cytokine-related depression. Additionally, potential therapeutic strategies that target inflammatory cytokine signaling or the consequences of cytokines on neurotransmitter systems in the brain to prevent or reverse cytokine effects on behavior are discussed.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "378", "doc_id": "25315295", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does guselkumab ( an IL-23-specific mAb ) demonstrate clinical and molecular response in patients with moderate-to-severe psoriasis?\n\nABSTRACT:\nIL-23 expression is increased in psoriatic lesions and might regulate TH17 T-cell counts in patients with psoriasis. We sought to test a novel IL-23-specific therapeutic agent for the treatment of psoriasis. In this randomized, double-blind, placebo-controlled study the safety, tolerability, and clinical response of guselkumab, an anti-IL-23-specific mAb, were evaluated in patients with moderate-to-severe plaque psoriasis. A total of 24 patients were randomized to receive a single dose of placebo or 10, 30, 100, or 300 mg of guselkumab. Clinical response was assessed by using the Psoriasis Area and Severity Index (PASI). Additionally, histologic analysis and gene expression in skin biopsy specimens from guselkumab-treated patients were compared with those from placebo-treated patients. At week 12, 50% (10 mg), 60% (30 and 100 mg), and 100% (300 mg) of guselkumab-treated patients, respectively, achieved a 75% improvement in PASI scores from baseline compared with 0% of placebo-treated patients. Improvements in PASI scores were generally maintained through week 24 in all guselkumab-treated patients. The proportion of patients experiencing an adverse event was comparable between the combined guselkumab (13/20 [65.0%]) and placebo (2/4 [50.0%]) groups through week 24. Analysis of lesional and nonlesional skin biopsy specimens demonstrated decreases in epidermal thickness and T-cell and dendritic cell expression in guselkumab-treated patients compared with values seen in placebo-treated patients. At week 12, significant reductions in psoriasis gene expression and serum IL-17A levels were observed in guselkumab-treated patients.", "output": "{\"label\": \"yes\", \"rationale\": \"IL-23 inhibition with a single dose of guselkumab results in clinical responses in patients with moderate-to-severe psoriasis, suggesting that neutralization of IL-23 alone is a promising therapy for psoriasis.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 24679469, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: RUNX1 is downregulated or mutated in TLX1 T-ALL.\n\nCANDIDATE_PASSAGE:\nBias in meta-analysis detected by a simple, graphical test. OBJECTIVE Funnel plots (plots of effect estimates against sample size) may be useful to detect bias in meta-analyses that were later contradicted by large trials. We examined whether a simple test of asymmetry of funnel plots predicts discordance of results when meta-analyses are compared to large trials, and we assessed the prevalence of bias in published meta-analyses. DESIGN Medline search to identify pairs consisting of a meta-analysis and a single large trial (concordance of results was assumed if effects were in the same direction and the meta-analytic estimate was within 30% of the trial); analysis of funnel plots from 37 meta-analyses identified from a hand search of four leading general medicine journals 1993-6 and 38 meta-analyses from the second 1996 issue of the Cochrane Database of Systematic Reviews. MAIN OUTCOME MEASURE Degree of funnel plot asymmetry as measured by the intercept from regression of standard normal deviates against precision. RESULTS In the eight pairs of meta-analysis and large trial that were identified (five from cardiovascular medicine, one from diabetic medicine, one from geriatric medicine, one from perinatal medicine) there were four concordant and four discordant pairs. In all cases discordance was due to meta-analyses showing larger effects. Funnel plot asymmetry was present in three out of four discordant pairs but in none of concordant pairs. In 14 (38%) journal meta-analyses and 5 (13%) Cochrane reviews, funnel plot asymmetry indicated that there was bias. CONCLUSIONS A simple analysis of funnel plots provides a useful test for the likely presence of bias in meta-analyses, but as the capacity to detect bias will be limited when meta-analyses are based on a [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1009", "doc_id": "22711954", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Noninvasive positive pressure ventilation is not predictive of acute respiratory failure after solid organ transplantation.\n\nCANDIDATE_PASSAGE:\nHealth-related quality of life among children with acute lymphoblastic leukemia. BACKGROUND The objective was to quantify the health-related quality of life (HRQL) of children treated for acute lymphoblastic leukemia (ALL) and identify specific disabilities for remediation. PROCEDURE Two types of subjects were included: ALL patients 5 plus years old in a multi-center clinical trial and general population control groups. Patients were assessed during all four major phases of active treatment and approximately 2 years after treatment. Health status and HRQL were measured using HEALTH UTILITIES INDEX® (HUI®) Mark 2 (HUI2) and Mark 3 (HUI3). HRQL scores were used to calculate quality-adjusted life years (QALYs). Excess disability rates identified attributes for remediation. RESULTS HUI assessments (n = 749) were collected during the five phases. Mean HRQL increased from induction through the post-treatment phase (P < 0.001). There were no significant demographic or treatment effects on HRQL, except for type of asparaginase during continuation therapy (P = 0.005 for HUI2 and P = 0.007 for HUI3). Differences in mean HRQL scores between patients and controls were important (P < 0.001) during the active treatment phases but not during the post-treatment phase. Relative to controls, patients lost approximately 0.2 QALYs during active treatment. Disability was evident in mobility/ambulation, emotion, self-care and pain, and declined over time. CONCLUSIONS Patients with ALL experienced important but declining deficits in HRQL during active treatment phases: Equivalent to losing approximately 2 months of life in perfect health. HRQL within the 2-years post-treatment phase was similar to controls. The policy challenge is to develop new treatment protocols producing fewer [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "855", "doc_id": "42913391", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Sweet taste receptors on the tongue are deactivated by between 1 and 10 mM glucose.\n\nCANDIDATE_ABSTRACT:\nTITLE: Detection of sweet and umami taste in the absence of taste receptor T1r3.\nABSTRACT: The tastes of sugars (sweet) and glutamate (umami) are thought to be detected by T1r receptors expressed in taste cells. Molecular genetics and heterologous expression implicate T1r2 plus T1r3 as a sweet-responsive receptor,and T1r1 plus T1r3,as well as a truncated form of the type 4 metabotropic glutamate receptor (taste-mGluR4),as umami-responsive receptors. Here,we show that mice lacking T1r3 showed no preference for artificial sweeteners and had diminished but not abolished behavioral and nerve responses to sugars and umami compounds. These results indicate that T1r3-independent sweet- and umami-responsive receptors and/or pathways exist in taste cells.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1118, "doc_id": "23351136", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: A strong bias in the phage genome locations where the spacers were derived has been observed in many CRISPR subtypes that confer the immunity to phage.\n\nCANDIDATE_PASSAGE:\nIAP antagonists induce anti-tumor immunity in multiple myeloma The cellular inhibitors of apoptosis (cIAP) 1 and 2 are amplified in about 3% of cancers and have been identified in multiple malignancies as being potential therapeutic targets as a result of their role in the evasion of apoptosis. Consequently, small-molecule IAP antagonists, such as LCL161, have entered clinical trials for their ability to induce tumor necrosis factor (TNF)-mediated apoptosis of cancer cells. However, cIAP1 and cIAP2 are recurrently homozygously deleted in multiple myeloma (MM), resulting in constitutive activation of the noncanonical nuclear factor (NF)-κB pathway. To our surprise, we observed robust in vivo anti-myeloma activity of LCL161 in a transgenic myeloma mouse model and in patients with relapsed-refractory MM, where the addition of cyclophosphamide resulted in a median progression-free-survival of 10 months. This effect was not a result of direct induction of tumor cell death, but rather of upregulation of tumor-cell-autonomous type I interferon (IFN) signaling and a strong inflammatory response that resulted in the activation of macrophages and dendritic cells, leading to phagocytosis of tumor cells. Treatment of a MM mouse model with LCL161 established long-term anti-tumor protection and induced regression in a fraction of the mice. Notably, combination of LCL161 with the immune-checkpoint inhibitor anti-PD1 was curative in all of the treated mice.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "47", "doc_id": "3981033", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: In breast cancer, the loss of myoepithelial cells slows the transition of ductal carcinoma in situ to invasive carcinoma.\n\nCANDIDATE_PASSAGE:\nOf lineage and legacy: the development of mammalian hematopoietic stem cells The hematopoietic system is one of the first complex tissues to develop in the mammalian conceptus. Of particular interest in the field of developmental hematopoiesis is the origin of adult bone marrow hematopoietic stem cells. Tracing their origin is complicated because blood is a mobile tissue and because hematopoietic cells emerge from many embryonic sites. The origin of the adult mammalian blood system remains a topic of lively discussion and intense research. Interest is also focused on developmental signals that induce the adult hematopoietic stem cell program, as these may prove useful for generating and expanding these clinically important cell populations ex vivo. This review presents a historical overview of and the most recent data on the developmental origins of hematopoiesis.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "571", "doc_id": "34982259", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Transcription factor EB induces transcription of pro-inflammatory cytokines in macrophages infected with Staphylococcus aureus.\n\nCANDIDATE_ABSTRACT:\nTITLE: Innate host defense requires TFEB-mediated transcription of cytoprotective and antimicrobial genes.\nABSTRACT: Animal host defense against infection requires the expression of defense genes at the right place and the right time. Understanding such tight control of host defense requires the elucidation of the transcription factors involved. By using an unbiased approach in the model Caenorhabditis elegans, we discovered that HLH-30 (known as TFEB in mammals) is a key transcription factor for host defense. HLH-30 was activated shortly after Staphylococcus aureus infection, and drove the expression of close to 80% of the host response, including antimicrobial and autophagy genes that were essential for host tolerance of infection. TFEB was also rapidly activated in murine macrophages upon S. aureus infection and was required for proper transcriptional induction of several proinflammatory cytokines and chemokines. Thus, our data suggest that TFEB is a previously unappreciated, evolutionarily ancient transcription factor in the host response to infection.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"TFEB was also rapidly activated in murine macrophages upon S. aureus infection and was required for proper transcriptional induction of several proinflammatory cytokines and chemokines.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1312, "doc_id": "24177706", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Reduced responsiveness to interleukin-2 in regulatory T cells is associated with greater resistance to autoimmune diseases such as Type 1 Diabetes.\n\nCANDIDATE_PASSAGE:\nLarge-scale genetic fine mapping and genotype-phenotype associations implicate polymorphism in the IL2RA region in type 1 diabetes Genome-wide association studies are now identifying disease-associated chromosome regions. However, even after convincing replication, the localization of the causal variant(s) requires comprehensive resequencing, extensive genotyping and statistical analyses in large sample sets leading to targeted functional studies. Here, we have localized the type 1 diabetes (T1D) association in the interleukin 2 receptor alpha (IL2RA) gene region to two independent groups of SNPs, spanning overlapping regions of 14 and 40 kb, encompassing IL2RA intron 1 and the 5′ regions of IL2RA and RBM17 (odds ratio = 2.04, 95% confidence interval = 1.70–2.45; P = 1.92 × 10−28; control frequency = 0.635). Furthermore, we have associated IL2RA T1D susceptibility genotypes with lower circulating levels of the biomarker, soluble IL-2RA (P = 6.28 × 10−28), suggesting that an inherited lower immune responsiveness predisposes to T1D.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1029", "doc_id": "13940200", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Assembly of invadopodia is triggered by focal generation of phosphatidylinositol-3,4-biphosphate and the activation of the nonreceptor tyrosine kinase Src.\n\nCANDIDATE_PASSAGE:\nDecoding of Cytoplasmic Ca2+ Oscillations through the Spatial Signature Drives Gene Expression Cytoplasmic Ca(2+) oscillations are a universal signaling mode that activates numerous cellular responses [1, 2]. Oscillations are considered the physiological mechanism of Ca(2+) signaling because they occur at low levels of stimulus intensity [3]. Ca(2+) oscillations are proposed to convey information in their amplitude and frequency, leading to activation of specific downstream targets [4-6]. Here, we report that the spatial Ca(2+) gradient within the oscillation is key. Ca(2+) oscillations in mast cells evoked over a range of agonist concentrations in the presence of external Ca(2+) were indistinguishable from those in the absence of Ca(2+) when plasmalemmal Ca(2+) extrusion was suppressed. Nevertheless, only oscillations with accompanying Ca(2+) entry through store-operated CRAC channels triggered gene expression. Increased cytoplasmic Ca(2+) buffering prevented oscillations but not gene activation. Local Ca(2+) influx and not global Ca(2+) oscillations therefore drives gene expression at physiological levels of stimulation. Rather than serving to maintain Ca(2+) oscillations by replenishing stores, we suggest that the role of oscillations might be to activate CRAC channels, thereby ensuring the generation of spatially restricted physiological Ca(2+) signals driving gene activation. Furthermore, we show that the spatial profile of a Ca(2+) oscillation provides a novel mechanism whereby a pleiotropic messenger specifically activates gene expression.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "133", "doc_id": "14719322", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Gastric lavage is an effective treatment for acute paraquat poisoning.\n\nCANDIDATE_PASSAGE:\nEffect of activated charcoal hemoperfusion on renal function in patients with paraquat poisoning. The present study retrospectively analyzed 19 patients diagnosed with paraquat (PQ) poisoning with the aim to investigate the effect of activated charcoal hemoperfusion on renal function and PQ elimination. The results indicated that 7 patients died and 12 survived. Non-oliguric renal failure occurred in all of the 7 patients who died. Among the 12 surviving patients, 10 had normal renal function and 2 developed non-oliguric renal failure. There was a linear correlation between plasma and urine paraquat concentration prior to and during activated charcoal hemoperfusion. The equation parameters together with the correlation coefficient on admission were as follows: Y=0.5820+1.7348X (R2=0.678; F=35.768; P<0.0001). The equation parameters together with the correlation coefficient were as follows during activated charcoal hemoperfusion: Y=0.6827+1.2649X (R2=0.626; F=50.308; P<0.0001). Therefore, it was concluded that in patients with normal renal function, the elimination kinetics of PQ by the kidneys were only associated with the plasma PQ concentration. Activated charcoal hemoperfusion had little effect on avoiding acute kidney injury in patients with severe PQ poisoning.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "449", "doc_id": "3430789", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does avoidance of cellular blood product transfusions in LVAD recipients prevent HLA allosensitization?\n\nABSTRACT:\nTransfusion of cellular blood products during left ventricular assist device (LVAD) implantation has been associated with HLA allosensitization, resulting in the need for a negative prospective cross-match and prolonged transplant waiting times. In order to prevent this risk, we developed a protocol to avoid transfusion of cellular blood products. The protocol included preoperative patient stabilization, perioperative recombinant erythropoietin and blood conservation strategies, and postoperative monitoring of mixed venous oxygen saturation (SVO2) to assure adequate peripheral oxygen delivery. Panel reactive antibody (PRA) was measured in all patients pre and post LVAD placement to assess HLA sensitization. Seven consecutive patients underwent LVAD implantation without transfusion of blood or platelets, one of whom expired perioperatively. Mean hematocrit was 35.2% preoperatively, and 21.8% postoperatively, reaching a nadir of 20.2%. Postoperative SVO2 was >60% in all patients. In the six survivors, mean hematocrit reach 24.3%, 27.3%, and 33.0% by postoperative day seven, fourteen, and thirty, respectively. PRA in three patients was 0% preoperatively and remained 0% until transplantation after 33, 34, and 50 days of support. In two patients, preoperative PRA was 7% and 17%, dropped to 3% and 0% after thirty days, then progressively rose to 96% and 100% after 60 and 90 days, respectively. In one other patient, preoperative PRA was 0%, remained at 0% after thirty days, then rose to 96% by 60 days.", "output": "{\"label\": \"no\", \"rationale\": \"Avoiding transfusion of cellular blood products in LVAD recipients is safe and well tolerated, but does not universally protect from HLA allosensitization. Other factors may also produce sensitization, such as immunogenic components of the LVAD, soluble antigen in fresh frozen plasma, or latent sensitization which is not initially evident in critically ill and possibly anergic patients.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 10194040, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: In breast cancer, the loss of myoepithelial cells promotes the transition of ductal carcinoma in situ to invasive carcinoma.\n\nCANDIDATE_ABSTRACT:\nTITLE: Regulation of in situ to invasive breast carcinoma transition.\nABSTRACT: The transition of ductal carcinoma in situ (DCIS) to invasive carcinoma is a poorly understood key event in breast tumor progression. Here, we analyzed the role of myoepithelial cells and fibroblasts in the progression of in situ carcinomas using a model of human DCIS and primary breast tumors. Progression to invasion was promoted by fibroblasts and inhibited by normal myoepithelial cells. Molecular profiles of isolated luminal epithelial and myoepithelial cells identified an intricate interaction network involving TGFbeta, Hedgehog, cell adhesion, and p63 required for myoepithelial cell differentiation, the elimination of which resulted in loss of myoepithelial cells and progression to invasion.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Molecular profiles of isolated luminal epithelial and myoepithelial cells identified an intricate interaction network involving TGFbeta, Hedgehog, cell adhesion, and p63 required for myoepithelial cell differentiation, the elimination of which resulted in loss of myoepithelial cells and progression to invasion.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 570, "doc_id": "20333864", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Helminths interfere with immune system control of coinfections by microbial pathogens 16.\n\nCANDIDATE_ABSTRACT:\nTITLE: DNA Deamination Mediates Innate Immunity to Retroviral Infection\nABSTRACT: CEM15/APOBEC3G is a cellular protein required for resistance to infection by virion infectivity factor (Vif)-deficient human immunodeficiency virus (HIV). Here, using a murine leukemia virus (MLV)-based system, we provide evidence that CEM15/APOBEC3G is a DNA deaminase that is incorporated into virions during viral production and subsequently triggers massive deamination of deoxycytidine to deoxyuridine within the retroviral minus (first)-strand cDNA, thus providing a probable trigger for viral destruction. Furthermore, HIV Vif can protect MLV from this CEM15/APOBEC3G-dependent restriction. These findings imply that targeted DNA deamination is a major strategy of innate immunity to retroviruses and likely also contributes to the sequence variation observed in many viruses (including HIV).", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 506, "doc_id": "544971", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: HbA1c consistently overestimates glycemic control in black individuals with Sickle cell trait (SCT).\n\nCANDIDATE_ABSTRACT:\nTITLE: Association of Sickle Cell Trait With Hemoglobin A1c in African Americans\nABSTRACT: Importance Hemoglobin A1c (HbA1c) reflects past glucose concentrations, but this relationship may differ between those with sickle cell trait (SCT) and those without it. Objective To evaluate the association between SCT and HbA1c for given levels of fasting or 2-hour glucose levels among African Americans. Design, Setting, and Participants Retrospective cohort study using data collected from 7938 participants in 2 community-based cohorts, the Coronary Artery Risk Development in Young Adults (CARDIA) study and the Jackson Heart Study (JHS). From the CARDIA study, 2637 patients contributed a maximum of 2 visits (2005-2011); from the JHS, 5301 participants contributed a maximum of 3 visits (2000-2013). All visits were scheduled at approximately 5-year intervals. Participants without SCT data, those without any concurrent HbA1c and glucose measurements, and those with hemoglobin variants HbSS, HbCC, or HbAC were excluded. Analysis of the primary outcome was conducted using generalized estimating equations (GEE) to examine the association of SCT with HbA1c levels, controlling for fasting or 2-hour glucose measures. Exposures Presence of SCT. Main Outcomes and Measures Hemoglobin A1c stratified by the presence or absence of SCT was the primary outcome measure. Results The analytic sample included 4620 participants (mean age, 52.3 [SD, 11.8] years; 2835 women [61.3%]; 367 [7.9%] with SCT) with 9062 concurrent measures of fasting glucose and HbA1c levels. In unadjusted GEE analyses, for a given fasting glucose, HbA1c values were statistically significantly lower in those with (5.72%) vs those without (6.01%) SCT (mean HbA1c difference, −0.29%; 95% CI, −0.35% to −0.23%). Findings were similar in models adjusted for key risk factors and in analyses using 2001 concurre [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"These findings suggest that HbA1c may systematically underestimate past glycemia in black patients with SCT and may require further evaluation.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 499, "doc_id": "26064662", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Type 1 Diabetes is associated with subtle perturbations in T reg development.\n\nCANDIDATE_PASSAGE:\nAlphavbeta6-Fyn signaling promotes oral cancer progression. We have previously shown that the integrin beta6 is neo-expressed in invasive oral squamous cell carcinoma (SCC) and is correlated with oral tumor progression. However, the mechanism by which the integrin beta6 promotes oral tumor progression is not well understood. The purpose of the present study was to determine whether integrin beta6 signaling activates Fyn and thus promotes oral squamous cell carcinoma progression. We analyzed the integrin beta6 signaling complex and investigated the function of these signaling molecules in oral SCC cells. We found that, upon ligation of the integrin beta6 with fibronectin, beta6 complexed with Fyn and activated it. The activation of Fyn recruited and activated focal adhesion kinase to this complex. This complex was necessary to activate Shc and to couple beta6 signaling to the Raf-ERK/MAPK pathway. This pathway transcriptionally activated the matrix metalloproteinase-3 gene and promoted oral SCC cell proliferation and experimental metastasis in vivo. These findings indicate that integrin beta6 signaling activates Fyn and thus promotes oral cancer progression.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1334", "doc_id": "12650610", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Recurrent mutations occur frequently within CTCF anchor sites adjacent to oncogenes.\n\nCANDIDATE_PASSAGE:\nSpecific sites in the C terminus of CTCF interact with the SA2 subunit of the cohesin complex and are required for cohesin-dependent insulation activity. Recent studies have shown that the protein CTCF, which plays an important role in insulation and in large-scale organization of chromatin within the eukaryotic nucleus, depends for both activities on recruitment of the cohesin complex. We show here that the interaction of CTCF with the cohesin complex involves direct contacts between the cohesin subunit SA2 and specific regions of the C-terminal tail of CTCF. All other cohesin components are recruited through their interaction with SA2. Expression in vivo of CTCF mutants lacking the C-terminal domain, or with mutations at sites within it required for SA2 binding, disrupts the normal expression profile of the imprinted genes IGF2-H19 and also results in a loss of insulation activity. Taken together, our results demonstrate that specific sites on the C terminus of CTCF are essential for cohesin binding and insulator function. The only direct interaction between CTCF and cohesin involves contact with SA2, which is external to the cohesin ring. This suggests that in recruiting cohesin to CTCF, SA2 could bind first and the ring could assemble subsequently.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1024", "doc_id": "24995939", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Mice lacking Sirt1 in Sf1-expressing neurons have increased susceptibility to diet-induced obesity and insulin resistance.\n\nCANDIDATE_PASSAGE:\nEffects of a high-fat diet exposure in utero on the metabolic syndrome-like phenomenon in mouse offspring through epigenetic changes in adipocytokine gene expression. The links between obesity in parents and their offspring and the role of genes and a shared environment are not completely understood. Adipocytokines such as leptin and adiponectin play important roles in glucose and lipid metabolism. Therefore, we examined whether the offspring from dams exposed to a high-fat diet during pregnancy (OH mice) exhibited hypertension, insulin resistance, and hyperlipidemia along with epigenetic changes in the expression of adipocytokine genes. OH mice were significantly heavier than the offspring of dams exposed to a control diet during pregnancy (OC mice) from 14 wk of age after an increased caloric intake from 8 wk. OH mice exhibited higher blood pressure and worse glucose tolerance than the OC mice at 24 wk. Total triglyceride and leptin levels were significantly higher and the adiponectin level was significantly lower in OH compared with OC mice at 12 wk of age. This was associated with changes in leptin and adiponectin expression in white adipose tissue. There were lower acetylation and higher methylation levels of histone H3 at lysine 9 of the promoter of adiponectin in adipose tissues of OH mice at 2 wk of age as well as at 12 and 24 wk of age compared with OC mice. In contrast, methylation of histone 4 at lysine 20 in the leptin promoter was significantly higher in OH compared with OC mice. Thus, exposure to a high-fat diet in utero might cause a metabolic syndrome-like phenomenon through epigenetic modifications of adipocytokine, adiponectin, and leptin gene expression.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "779", "doc_id": "6042706", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Increased microtubule acetylation repairs LRRK2 Roc-COR domain mutation induced locomotor deficits.\n\nCANDIDATE_ABSTRACT:\nTITLE: Increasing microtubule acetylation rescues axonal transport and locomotor deficits caused by LRRK2 Roc-COR domain mutations\nABSTRACT: Leucine-rich repeat kinase 2 (LRRK2) mutations are the most common genetic cause of Parkinson's disease. LRRK2 is a multifunctional protein affecting many cellular processes and has been described to bind microtubules. Defective microtubule-based axonal transport is hypothesized to contribute to Parkinson's disease, but whether LRRK2 mutations affect this process to mediate pathogenesis is not known. Here we find that LRRK2 containing pathogenic Roc-COR domain mutations (R1441C, Y1699C) preferentially associates with deacetylated microtubules, and inhibits axonal transport in primary neurons and in Drosophila, causing locomotor deficits in vivo. In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport. In vivo knockdown of the deacetylases HDAC6 and Sirt2, or administration of TSA rescues both axonal transport and locomotor behavior. Thus, this study reveals a pathogenic mechanism and a potential intervention for Parkinson's disease.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 613, "doc_id": "9638032", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Lack of FGF21 in mice leads to atherosclerotic plaque formation.\n\nCANDIDATE_ABSTRACT:\nTITLE: De novo assembly of a PML nuclear subcompartment occurs through multiple pathways and induces telomere elongation.\nABSTRACT: Telomerase-negative tumor cells use an alternative lengthening of telomeres (ALT) pathway that involves DNA recombination and repair to maintain their proliferative potential. The cytological hallmark of this process is the accumulation of promyelocytic leukemia (PML) nuclear protein at telomeric DNA to form ALT-associated PML bodies (APBs). Here, the de novo formation of a telomeric PML nuclear subcompartment was investigated by recruiting APB protein components. We show that functionally distinct proteins were able to initiate the formation of bona fide APBs with high efficiency in a self-organizing and self-propagating manner. These included: (1) PML and Sp100 as the constituting components of PML nuclear bodies, (2) telomere repeat binding factors 1 and 2 (TRF1 and TRF2, respectively), (3) the DNA repair protein NBS1 and (4) the SUMO E3 ligase MMS21, as well as the isolated SUMO1 domain, through an interacting domain of another protein factor. By contrast, the repair factors Rad9, Rad17 and Rad51 were less efficient in APB nucleation but were recruited to preassembled APBs. The artificially created APBs induced telomeric extension through a DNA repair mechanism, as inferred from their colocalization with sites of non-replicative DNA synthesis and histone H2A.X phosphorylation, and an increase of the telomere repeat length. These activities were absent after recruitment of the APB factors to a pericentric locus and establish APBs as functional intermediates of the ALT pathway.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 681, "doc_id": "143251", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Peroxynitrite is required for induction of T cell tolerance.\n\nCANDIDATE_ABSTRACT:\nTITLE: Altered recognition of antigen is a mechanism of CD8+ T cell tolerance in cancer\nABSTRACT: Antigen-specific CD8+ T-cell tolerance, induced by myeloid-derived suppressor cells (MDSCs), is one of the main mechanisms of tumor escape. Using in vivo models, we show here that MDSCs directly disrupt the binding of specific peptide–major histocompatibility complex (pMHC) dimers to CD8-expressing T cells through nitration of tyrosines in a T-cell receptor (TCR)-CD8 complex. This process makes CD8-expressing T cells unable to bind pMHC and to respond to the specific peptide, although they retain their ability to respond to nonspecific stimulation. Nitration of TCR-CD8 is induced by MDSCs through hyperproduction of reactive oxygen species and peroxynitrite during direct cell-cell contact. Molecular modeling suggests specific sites of nitration that might affect the conformational flexibility of TCR-CD8 and its interaction with pMHC. These data identify a previously unknown mechanism of T-cell tolerance in cancer that is also pertinent to many pathological conditions associated with accumulation of MDSCs.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Nitration of TCR-CD8 is induced by MDSCs through hyperproduction of reactive oxygen species and peroxynitrite during direct cell-cell contact. These data identify a previously unknown mechanism of T-cell tolerance in cancer that is also pertinent to many pathological conditions associated with accumulation of MDSCs.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 935, "doc_id": "5483793", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does alteration in emergency theatre prioritisation alter outcome for acute appendicitis : comparative cohort study?\n\nABSTRACT:\nDespite dedicated emergency theatre, emergency surgery can be often delayed due to competing urgencies, suggesting a need for innovative theatre time management. To investigate if a change in the emergency theatre prioritisation affects outcomes for a common urgent operation such as appendicectomy. We prospectively recorded data from 67 patients undergoing appendicectomy, for two cohorts of patients: before and after change in theatre prioritisation: Group 1 (Jan-Mar) and 2 (Aug-Oct) respectively. Demographic and peri-operative data, time from admission to surgery, postoperative length of stay and total length of stay and complications were compared. The two groups were comparable with regards to gender, age, time of admission and histological confirmation of appendicitis. No differences between the two groups were found regarding time from admission to surgery (24.4 (95% CI 11.2;27.6) hours versus 16.1 (95% CI 10.4;21.7) hours, Mann-Whitney U test, p = 0.35), postoperative length of stay (90.8 (95% CI 61.4;120.1) hours versus 70 (95% CI 48.3;91.6) hours, Mann-Whitney U test, p = 0.25) and total length of stay (115.2 (95% CI 84.6;145.7) hours versus 86 (95% CI 61.6;110.4) hours, Mann-Whitney U test, p = 0.07) as well as complication or re-admission rates.", "output": "{\"label\": \"no\", \"rationale\": \"A change in the emergency theatre prioritisation does not affect outcome for appendicectomy. Provision of a second emergency theatre could be a solution to reduce the delays in acute surgical operations.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 19505298, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: General exercise therapy is more effective than scapular stabilizer exercises in reducing pain and improving function of the shoulder.\n\nCANDIDATE_PASSAGE:\nLinkage with methadone treatment upon release from incarceration: a promising opportunity. Injection drug users (IDUs) are at increased risk for HIV, viral hepatitis, and tuberculosis, and making up more than a quarter of the incarcerated population in the United States. Methadone maintenance treatment of opiate addiction is highly effective at reducing drug use, drug-related criminal activity, and risk of HIV transmission. Recently released inmates are at particularly high risk for overdose and disease transmission. Linkage to methadone treatment immediately upon release from incarceration is a promising opportunity to combat disease transmission, facilitate reentry into the community, and reduce recidivism.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "454", "doc_id": "24700152", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cell autonomous sex determination in somatic cells occurs in Passeriformes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Somatic sex identity is cell-autonomous in the chicken\nABSTRACT: In the mammalian model of sex determination, embryos are considered to be sexually indifferent until the transient action of a sex-determining gene initiates gonadal differentiation. Although this model is thought to apply to all vertebrates, this has yet to be established. Here we have examined three lateral gynandromorph chickens (a rare, naturally occurring phenomenon in which one side of the animal appears male and the other female) to investigate the sex-determining mechanism in birds. These studies demonstrated that gynandromorph birds are genuine male:female chimaeras, and indicated that male and female avian somatic cells may have an inherent sex identity. To test this hypothesis, we transplanted presumptive mesoderm between embryos of reciprocal sexes to generate embryos containing male:female chimaeric gonads. In contrast to the outcome for mammalian mixed-sex chimaeras, in chicken mixed-sex chimaeras the donor cells were excluded from the functional structures of the host gonad. In an example where female tissue was transplanted into a male host, donor cells contributing to the developing testis retained a female identity and expressed a marker of female function. Our study demonstrates that avian somatic cells possess an inherent sex identity and that, in birds, sexual differentiation is substantively cell autonomous.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"These studies demonstrated that gynandromorph birds are genuine male:female chimaeras, and indicated that male and female avian somatic cells may have an inherent sex identity.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 236, "doc_id": "4388470", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Many cytokines that are produced by cancer cells also contribute to carcinogenesis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Autocrine VEGF Signaling Synergizes with EGFR in Tumor Cells to Promote Epithelial Cancer Development\nABSTRACT: It is established that tumor cell-derived VEGF acts on endothelial cells to promote angiogenesis and tumor growth. Here, we demonstrate that in K5-SOS-dependent mouse skin tumors, autocrine VEGF is required for tumor cell proliferation in a cell-autonomous and angiogenesis-independent manner. VEGF is upregulated in SOS-expressing tumors, and its deletion in epidermal cells delays tumorigenesis by suppressing angiogenesis and tumor cell proliferation. Epidermis-specific Flt1 deletion also impairs tumorigenesis and proliferation. Surprisingly, complete tumor inhibition occurs in the absence of VEGF in EGFR mutant mice, demonstrating that VEGFR and EGFR synergize in neoplastic cells to promote tumor growth. Mechanistically, K5-SOS upregulates VEGF, Flt1, and Neuropilin-1 in an Erk-dependent manner, thereby activating an autocrine proliferation loop, whereas EGFR prevents tumor cells from apoptosis. Moreover, Flt1 is upregulated in human SCC, and its inhibition in SCC cells impairs proliferation. Thus, in addition to regulating angiogenesis, VEGF has to be considered as a potent growth factor for epidermal tumors.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 755, "doc_id": "17844478", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Eliminating the last sporadic cases of malaria requires considerable funding.\n\nCANDIDATE_PASSAGE:\nStages of the pathologic process in Alzheimer disease: age categories from 1 to 100 years. Two thousand three hundred and thirty two nonselected brains from 1- to 100-year-old individuals were examined using immunocytochemistry (AT8) and Gallyas silver staining for abnormal tau; immunocytochemistry (4G8) and Campbell-Switzer staining were used for the detection ofβ-amyloid. A total of 342 cases was negative in the Gallyas stain but when restaged for AT8 only 10 were immunonegative. Fifty-eight cases had subcortical tau predominantly in the locus coeruleus, but there was no abnormal cortical tau (subcortical Stages a-c). Cortical involvement (abnormal tau in neurites) was identified first in the transentorhinal region (Stage 1a, 38 cases). Transentorhinal pyramidal cells displayed pretangle material (Stage 1b, 236 cases). Pretangles gradually became argyrophilic neurofibrillary tangles (NFTs) that progressed in parallel with NFT Stages I to VI. Pretangles restricted to subcortical sites were seen chiefly at younger ages. Of the total cases, 1,031 (44.2%) had β-amyloid plaques. The first plaques occurred in the neocortex after the onset of tauopathy in the brainstem. Plaques generally developed in the 40s in 4% of all cases, culminating in their tenth decade (75%). β-amyloid plaques and NFTs were significantly correlated (p < 0.0001). These data suggest that tauopathy associated with sporadic Alzheimer disease may begin earlier than previously thought and possibly in the lower brainstem rather than in the transentorhinal region.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "376", "doc_id": "739734", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Enhanced early production of inflammatory chemokines improves viral control in the lung.\n\nCANDIDATE_PASSAGE:\nBCL-6 represses genes that function in lymphocyte differentiation, inflammation, and cell cycle control. BCL-6, a transcriptional repressor frequently translocated in lymphomas, regulates germinal center B cell differentiation and inflammation. DNA microarray screening identified genes repressed by BCL-6, including many lymphocyte activation genes, suggesting that BCL-6 modulates B cell receptor signals. BCL-6 repression of two chemokine genes, MIP-1alpha and IP-10, may also attenuate inflammatory responses. Blimp-1, another BCL-6 target, is important for plasmacytic differentiation. Since BCL-6 expression is silenced in plasma cells, repression of blimp-1 by BCL-6 may control plasmacytic differentiation. Indeed, inhibition of BCL-6 function initiated changes indicative of plasmacytic differentiation, including decreased expression of c-Myc and increased expression of the cell cycle inhibitor p27kip1. These data suggest that malignant transformation by BCL-6 involves inhibition of differentiation and enhanced proliferation.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "380", "doc_id": "16550075", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Destination container port throughput(CPT) is positively related to dengue virus (DENV-1) diffusion in air traffic shipments.\n\nCANDIDATE_ABSTRACT:\nTITLE: Population Density, Water Supply, and the Risk of Dengue Fever in Vietnam: Cohort Study and Spatial Analysis\nABSTRACT: BACKGROUND Aedes aegypti, the major vector of dengue viruses, often breeds in water storage containers used by households without tap water supply, and occurs in high numbers even in dense urban areas. We analysed the interaction between human population density and lack of tap water as a cause of dengue fever outbreaks with the aim of identifying geographic areas at highest risk. METHODS AND FINDINGS We conducted an individual-level cohort study in a population of 75,000 geo-referenced households in Vietnam over the course of two epidemics, on the basis of dengue hospital admissions (n = 3,013). We applied space-time scan statistics and mathematical models to confirm the findings. We identified a surprisingly narrow range of critical human population densities between around 3,000 to 7,000 people/km² prone to dengue outbreaks. In the study area, this population density was typical of villages and some peri-urban areas. Scan statistics showed that areas with a high population density or adequate water supply did not experience severe outbreaks. The risk of dengue was higher in rural than in urban areas, largely explained by lack of piped water supply, and in human population densities more often falling within the critical range. Mathematical modeling suggests that simple assumptions regarding area-level vector/host ratios may explain the occurrence of outbreaks. CONCLUSIONS Rural areas may contribute at least as much to the dissemination of dengue fever as cities. Improving water supply and vector control in areas with a human population density critical for dengue transmission could increase the efficiency of control efforts. Please see later in the article for the Editors' Summary.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 337, "doc_id": "2097256", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: A 100g dose of chloroquine chemoprophylactic regimen results in retinal toxicity after 1 year of weekly intake.\n\nCANDIDATE_ABSTRACT:\nTITLE: Prevention of malaria in long-term travelers.\nABSTRACT: CONTEXT Long-term travelers, defined here as those traveling for periods of 6 months or longer, face particular challenges regarding malaria prevention. Current guidelines for malaria prevention primarily address prevention of Plasmodium falciparum infections in short-term travelers. OBJECTIVES To examine the risk of malaria in long-term travelers, recent developments in personal protective measures, and the safety and tolerability of malaria chemoprophylaxis during long-term use and to consider prevention strategies including continuous chemoprophylaxis, stand-by emergency self-treatment, seasonal prophylaxis, and strategies to prevent primary infection and relapses from P vivax malaria. EVIDENCE ACQUISITION Comprehensive search of scientific publications including MEDLINE via both OVID and PubMED for relevant studies and articles with a cutoff date of July 2006, using the search terms long-term travel and malaria prevention, long-term malaria chemoprophylaxis, and insect repellent and malaria. Additional references were obtained from searching the bibliographies of the selected articles, from dissertations, and from the proceedings of relevant conferences on travel medicine. There were no language restrictions. EVIDENCE SYNTHESIS Long-term travelers have a higher risk of malaria than short-term travelers. Long-term travelers underuse personal protective measures and adhere poorly to continuous chemoprophylaxis regimens. A number of strategies are used during long-term stays: discontinuation of chemoprophylaxis after the initial period, sequential regimens with different medications for chemoprophylaxis, stand-by emergency self-treatment, and seasonal chemoprophylaxis targeting high-incidence periods or locations. All strategies have advantages and drawback [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 26, "doc_id": "32390525", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Inositol lipid 3-phosphatase PTEN converts Ptdlns(3,4)P 2 into phosphatidylinositol 4-phosphate.\n\nCANDIDATE_ABSTRACT:\nTITLE: A Triple-Stain Flow Cytometric Method to Assess Plasma- and Acrosome-Membrane Integrity of Cryopreserved Bovine Sperm Immediately after Thawing in Presence of Egg-Yolk Particles1\nABSTRACT: Abstract Simultaneously evaluating postthaw viability and acrosome integrity of spermatozoa by flow cytometry would provide a valuable testing tool in both research and routine work. In the present study, a new triple-stain combination was developed for the simultaneous evaluation of viability and acrosome integrity of bovine sperm processed in egg yolk-based extender by flow cytometer. SYBR-14 and propidium iodide (PI) enabled the discrimination of sperm cells from egg yolk and debris particles, which was instrumental for the flow cytometric analyses of frozen-thawed bovine sperm, because it implied that washing steps to remove egg yolk were no longer required. In addition, phycoerythrin-conjugated peanut agglutinin (PE-PNA) was used to discriminate acrosome-damaged/reacted sperm cells from acrosome-intact cells. Repeatability was calculated using two processed ejaculates of 10 bulls. Three straws per batch were analyzed in duplicate measurements. Method-agreement analysis between the SYBR-14/PE-PNA/PI and fluorescein isothiocyanate (FITC)-conjugated PNA was performed, with FITC-PNA/PI staining being carried out on 14 frozen-thawed semen samples immediately after thawing and after a 3-h incubation at 37°C. The British Standards Institution repeatability index of the SYBR-14/PE-PNA/PI combination was 2.6%. On average, the FITC-PNA/PI method showed a 6.3% overestimation of the live and acrosome-intact sperm cell subpopulation. In conclusion, the new triple-stain combination is highly repeatable and easy to use in routine application, and it provides a more precise estimate for the rate of sperm cells with intact head membrane and acrosome compared to the generally used and validated FITC-PNA/PI staining.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 636, "doc_id": "371289", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Ten percent (10%) of kidney cancers in the UK are attributable to excess weight.\n\nCANDIDATE_PASSAGE:\nCongruent Visual Speech Enhances Cortical Entrainment to Continuous Auditory Speech in Noise-Free Conditions. UNLABELLED Congruent audiovisual speech enhances our ability to comprehend a speaker, even in noise-free conditions. When incongruent auditory and visual information is presented concurrently, it can hinder a listener's perception and even cause him or her to perceive information that was not presented in either modality. Efforts to investigate the neural basis of these effects have often focused on the special case of discrete audiovisual syllables that are spatially and temporally congruent, with less work done on the case of natural, continuous speech. Recent electrophysiological studies have demonstrated that cortical response measures to continuous auditory speech can be easily obtained using multivariate analysis methods. Here, we apply such methods to the case of audiovisual speech and, importantly, present a novel framework for indexing multisensory integration in the context of continuous speech. Specifically, we examine how the temporal and contextual congruency of ongoing audiovisual speech affects the cortical encoding of the speech envelope in humans using electroencephalography. We demonstrate that the cortical representation of the speech envelope is enhanced by the presentation of congruent audiovisual speech in noise-free conditions. Furthermore, we show that this is likely attributable to the contribution of neural generators that are not particularly active during unimodal stimulation and that it is most prominent at the temporal scale corresponding to syllabic rate (2-6 Hz). Finally, our data suggest that neural entrainment to the speech envelope is inhibited when the auditory and visual streams are incongruent both temporally and [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1148", "doc_id": "14437255", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Ca2+ cycling is a UCP1-independent thermogenic mechanism.\n\nCANDIDATE_PASSAGE:\nCXCR2 mediates NADPH oxidase–independent neutrophil extracellular trap formation in cystic fibrosis airway inflammation Upon activation, neutrophils release DNA fibers decorated with antimicrobial proteins, forming neutrophil extracellular traps (NETs). Although NETs are bactericidal and contribute to innate host defense, excessive NET formation has been linked to the pathogenesis of autoinflammatory diseases. However, the mechanisms regulating NET formation, particularly during chronic inflammation, are poorly understood. Here we show that the G protein–coupled receptor (GPCR) CXCR2 mediates NET formation. Downstream analyses showed that CXCR2-mediated NET formation was independent of NADPH oxidase and involved Src family kinases. We show the pathophysiological relevance of this mechanism in cystic fibrosis lung disease, characterized by chronic neutrophilic inflammation. We found abundant NETs in airway fluids of individuals with cystic fibrosis and mouse cystic fibrosis lung disease, and NET amounts correlated with impaired obstructive lung function. Pulmonary blockade of CXCR2 by intra-airway delivery of small-molecule antagonists inhibited NET formation and improved lung function in vivo without affecting neutrophil recruitment, proteolytic activity or antibacterial host defense. These studies establish CXCR2 as a receptor mediating NADPH oxidase–independent NET formation and provide evidence that this GPCR pathway is operative and druggable in cystic fibrosis lung disease.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "222", "doc_id": "1800734", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: B cells go though plasmablast differentiation and antibody production by continuous expression of EBI2.\n\nCANDIDATE_ABSTRACT:\nTITLE: Guidance of B cells by the orphan G protein-coupled receptor EBI2 shapes humoral immune responses.\nABSTRACT: Humoral immunity depends on both rapid and long-term antibody production against invading pathogens. This is achieved by the generation of spatially distinct extrafollicular plasmablast and follicular germinal center (GC) B cell populations, but the signals that guide responding B cells to these alternative compartments have not been fully elucidated. Here, we show that expression of the orphan G protein-coupled receptor Epstein-Barr virus-induced gene 2 (EBI2, also known as GPR183) by activated B cells was essential for their movement to extrafollicular sites and induction of early plasmablast responses. Conversely, downregulation of EBI2 enabled B cells to access the center of follicles and promoted efficient GC formation. EBI2 therefore provides a previously uncharacterized dimension to B cell migration that is crucial for coordinating rapid versus long-term antibody responses.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here, we show that expression of the orphan G protein-coupled receptor Epstein-Barr virus-induced gene 2 (EBI2, also known as GPR183) by activated B cells was essential for their movement to extrafollicular sites and induction of early plasmablast responses.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 152, "doc_id": "15488881", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Incidence of 10/66 dementia is higher than the incidence of DSM-IV dementia.\n\nCANDIDATE_PASSAGE:\nAssociation between smoking and risk of bladder cancer among men and women. CONTEXT Previous studies indicate that the population attributable risk (PAR) of bladder cancer for tobacco smoking is 50% to 65% in men and 20% to 30% in women and that current cigarette smoking triples bladder cancer risk relative to never smoking. During the last 30 years, incidence rates have remained stable in the United States in men (123.8 per 100,000 person-years to 142.2 per 100,000 person-years) and women (32.5 per 100,000 person-years to 33.2 per 100,000 person-years); however, changing smoking prevalence and cigarette composition warrant revisiting risk estimates for smoking and bladder cancer. OBJECTIVE To evaluate the association between tobacco smoking and bladder cancer. DESIGN, SETTING, AND PARTICIPANTS Men (n = 281,394) and women (n = 186,134) of the National Institutes of Health-AARP (NIH-AARP) Diet and Health Study cohort completed a lifestyle questionnaire and were followed up between October 25, 1995, and December 31, 2006. Previous prospective cohort studies of smoking and incident bladder cancer were identified by systematic review and relative risks were estimated from fixed-effects models with heterogeneity assessed by the I(2) statistic. MAIN OUTCOME MEASURES Hazard ratios (HRs), PARs, and number needed to harm (NNH). RESULTS During 4,518,941 person-years of follow-up, incident bladder cancer occurred in 3896 men (144.0 per 100,000 person-years) and 627 women (34.5 per 100,000 person-years). Former smokers (119.8 per 100,000 person-years; HR, 2.22; 95% confidence interval [CI], 2.03-2.44; NNH, 1250) and current smokers (177.3 per 100,000 person-years; HR, 4.06; 95% CI, 3.66-4.50; NNH, 727) had higher risks of bladder cancer than never smokers (39.8 per 100, [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "591", "doc_id": "17124832", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does perspective-taking increase patient satisfaction in medical encounters?\n\nABSTRACT:\nTo assess whether perspective-taking, which researchers in other fields have shown to induce empathy, improves patient satisfaction in encounters between student-clinicians and standardized patients (SPs). In three studies, randomly assigned students (N = 608) received either a perspective-taking instruction or a neutral instruction prior to a clinical skills examination in 2006-2007. SP satisfaction was the main outcome in all three studies. Study 1 involved 245 third-year medical students from two universities. Studies 2 and 3 extended Study 1 to examine generalizability across student and SP subpopulations. Study 2 (105 physician assistant students, one university) explored the effect of perspective-taking on African American SPs' satisfaction. Study 3 (258 third-year medical students, two universities) examined the intervention's effect on students with high and low baseline perspective-taking tendencies. Intervention students outscored controls in patient satisfaction in all studies: Study 1: P = .01, standardized effect size = 0.16; Study 2: P = .001, standardized effect size = 0.31; Study 3: P = .009, standardized effect size = 0.13. In Study 2, perspective-taking improved African American SPs' satisfaction. In Study 3, intervention students with high baseline perspective-taking tendencies outscored controls (P = .0004, standardized effect size = 0.25), whereas those with low perspective-taking tendencies did not (P = .72, standardized effect size = 0.00).", "output": "{\"label\": \"maybe\", \"rationale\": \"Perspective-taking increased patient satisfaction in all three studies, across medical schools, clinical disciplines, and racially diverse students and SPs. Perspective-taking as a means for improving patient satisfaction deserves further exploration in clinical training and practice.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 20736672, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Pyridostatin destabilizes the G - quadruplex in the telomeric region.\n\nCANDIDATE_PASSAGE:\nExpression of a human cytomegalovirus latency-associated homolog of interleukin-10 during the productive phase of infection. The human cytomegalovirus UL111A region is active during both productive and latent phases of infection. During productive infection, the virus expresses ORF79, a protein with oncogenic properties, and cmvIL-10, a functional homolog of human IL-10. During latent infection of myeloid progenitor cells, an alternately spliced variant of cmvIL-10, termed latency-associated (LA) cmvIL-10 has previously been identified. To determine whether LAcmvIL-10 transcription occurs during productive infection, we performed 5' and 3' RACE to map UL111A-region transcripts in productively infected human foreskin fibroblasts (HFFs). This analysis revealed the presence of a singly spliced UL111A-region transcript predicted to encode LAcmvIL-10. This transcript was expressed in HFFs with early (beta) kinetics, a temporal class that differs from that of ORF79 (alpha kinetics) and cmvIL-10 (gamma kinetics). These data identify and map a transcript encoding a latency-associated homolog of IL-10 which is expressed by the virus during the productive phase of infection.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "993", "doc_id": "25141908", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Nuclear transfer from adult human fibroblasts to human oocytes can give rise to blastocysts containing expandable pluripotent cells.\n\nCANDIDATE_PASSAGE:\nMetabolic rescue in pluripotent cells from patients with mtDNA disease Mitochondria have a major role in energy production via oxidative phosphorylation, which is dependent on the expression of critical genes encoded by mitochondrial (mt)DNA. Mutations in mtDNA can cause fatal or severely debilitating disorders with limited treatment options. Clinical manifestations vary based on mutation type and heteroplasmy (that is, the relative levels of mutant and wild-type mtDNA within each cell). Here we generated genetically corrected pluripotent stem cells (PSCs) from patients with mtDNA disease. Multiple induced pluripotent stem (iPS) cell lines were derived from patients with common heteroplasmic mutations including 3243A>G, causing mitochondrial encephalomyopathy and stroke-like episodes (MELAS), and 8993T>G and 13513G>A, implicated in Leigh syndrome. Isogenic MELAS and Leigh syndrome iPS cell lines were generated containing exclusively wild-type or mutant mtDNA through spontaneous segregation of heteroplasmic mtDNA in proliferating fibroblasts. Furthermore, somatic cell nuclear transfer (SCNT) enabled replacement of mutant mtDNA from homoplasmic 8993T>G fibroblasts to generate corrected Leigh-NT1 PSCs. Although Leigh-NT1 PSCs contained donor oocyte wild-type mtDNA (human haplotype D4a) that differed from Leigh syndrome patient haplotype (F1a) at a total of 47 nucleotide sites, Leigh-NT1 cells displayed transcriptomic profiles similar to those in embryo-derived PSCs carrying wild-type mtDNA, indicative of normal nuclear-to-mitochondrial interactions. Moreover, genetically rescued patient PSCs displayed normal metabolic function compared to impaired oxygen consumption and ATP production observed in mutant cells. We conclude that both reprogramming approaches offe [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "866", "doc_id": "4410181", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Microcin J25 encourages nucleoside triphosphate (NTP) binding.\n\nCANDIDATE_ABSTRACT:\nTITLE: Microenvironment rigidity modulates responses to the HER2 receptor tyrosine kinase inhibitor lapatinib via YAP and TAZ transcription factors.\nABSTRACT: Stiffness is a biophysical property of the extracellular matrix that modulates cellular functions, including proliferation, invasion, and differentiation, and it also may affect therapeutic responses. Therapeutic durability in cancer treatments remains a problem for both chemotherapies and pathway-targeted drugs, but the reasons for this are not well understood. Tumor progression is accompanied by changes in the biophysical properties of the tissue, and we asked whether matrix rigidity modulated the sensitive versus resistant states in HER2-amplified breast cancer cell responses to the HER2-targeted kinase inhibitor lapatinib. The antiproliferative effect of lapatinib was inversely proportional to the elastic modulus of the adhesive substrata. Down-regulation of the mechanosensitive transcription coactivators YAP and TAZ, either by siRNA or with the small-molecule YAP/TEAD inhibitor verteporfin, eliminated modulus-dependent lapatinib resistance. Reduction of YAP in vivo in mice also slowed the growth of implanted HER2-amplified tumors, showing a trend of increasing sensitivity to lapatinib as YAP decreased. Thus we address the role of stiffness in resistance to and efficacy of a HER2 pathway-targeted therapeutic via the mechanotransduction arm of the Hippo pathway.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 787, "doc_id": "1065627", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Tumor development occurs in conjunction with upregulation of pro-inflammatory cytokines.\n\nCANDIDATE_PASSAGE:\nCell-mediated immunity and antibody responses elicited by attenuated Salmonella enterica Serovar Typhi strains used as live oral vaccines in humans. The development of improved typhoid vaccines is a high global public health priority. However, their development has been hampered by a lack of information regarding the specific determinants of protective immunity to Salmonella enterica serovar Typhi (S. Typhi) infection in humans. Although antibodies to S. Typhi O, H, and Vi appear to be involved in protection against S. Typhi infection, it is unknown whether such antibodies mediate protection, act in conjunction with other adaptive responses, or serve as a surrogate for the presence of other, more dominant protective immune responses (e.g., cell-mediated immunity [CMI]). CMI responses elicited by immunization of subjects with attenuated S. Typhi oral vaccines include lymphoproliferation; production of type 1 cytokines (e.g., interferon- gamma and tumor necrosis factor- alpha ); and classical major histocompatibility complex (MHC) class Ia-restricted and novel, nonclassical MHC class Ib (human leukocyte antigen [HLA]-E)-restricted CD8(+) cytotoxic T cell responses. In sum, human immunity to S. Typhi elicited by immunization is unexpectedly broad and complex. However, the immunologic correlates of protection remain largely undefined.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1331", "doc_id": "18275697", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Bactericidal activity of 3 cutaneous/mucosal antiseptic solutions in the presence of interfering substances: Improvement of the NF EN 13727 European Standard?\n\nABSTRACT:\nThere is no standard protocol for the evaluation of antiseptics used for skin and mucous membranes in the presence of interfering substances. Our objective was to suggest trial conditions adapted from the NF EN 13727 standard, for the evaluation of antiseptics used in gynecology and dermatology. Three antiseptic solutions were tested in vitro: a chlorhexidine-benzalkonium (CB) combination, a hexamidine-chlorhexidine-chlorocresol (HCC) combination, and povidone iodine (P). The adaptation of trial conditions to the standard involved choosing dilutions, solvent, and interfering substances. The activity of solutions was assessed on the recommended strains at concentrations of 97% (pure solution), 50%, and 10% (diluted solution), and 1%. A logarithmic reduction ≥ 5 was expected after 60seconds of contact, to meet requirements of bactericidal activity. HCC did not present any bactericidal activity except on P. aeruginosa at a concentration of 97%. P was not bactericidal on E. hirae at any concentration and on S. aureus at 97%. CB had the most homogeneous bactericidal activity with a reduction>5 log on the 4 bacterial strains at concentrations of 97%, 50% and 10%.", "output": "{\"label\": \"maybe\", \"rationale\": \"Adapting the NF EN 13727 standard allowed assessing the 3 tested solutions: only CB was bactericidal in dirty conditions. This study proved the possibility of validating antiseptic choice in vitro, in current practice conditions, for adjunctive treatment of skin and mucous membranes disorders, primarily of bacterial origin or with a potential of superinfection.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 25779009, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Epigenetic modulating agents (EMAs) modulate antitumor immune response in a cancer model system.\n\nCANDIDATE_ABSTRACT:\nTITLE: Epigenetic therapy activates type I interferon signaling in murine ovarian cancer to reduce immunosuppression and tumor burden.\nABSTRACT: Ovarian cancer is the most lethal of all gynecological cancers, and there is an urgent unmet need to develop new therapies. Epithelial ovarian cancer (EOC) is characterized by an immune suppressive microenvironment, and response of ovarian cancers to immune therapies has thus far been disappointing. We now find, in a mouse model of EOC, that clinically relevant doses of DNA methyltransferase and histone deacetylase inhibitors (DNMTi and HDACi, respectively) reduce the immune suppressive microenvironment through type I IFN signaling and improve response to immune checkpoint therapy. These data indicate that the type I IFN response is required for effective in vivo antitumorigenic actions of the DNMTi 5-azacytidine (AZA). Through type I IFN signaling, AZA increases the numbers of CD45+ immune cells and the percentage of active CD8+ T and natural killer (NK) cells in the tumor microenvironment, while reducing tumor burden and extending survival. AZA also increases viral defense gene expression in both tumor and immune cells, and reduces the percentage of macrophages and myeloid-derived suppressor cells in the tumor microenvironment. The addition of an HDACi to AZA enhances the modulation of the immune microenvironment, specifically increasing T and NK cell activation and reducing macrophages over AZA treatment alone, while further increasing the survival of the mice. Finally, a triple combination of DNMTi/HDACi plus the immune checkpoint inhibitor α-PD-1 provides the best antitumor effect and longest overall survival, and may be an attractive candidate for future clinical trials in ovarian cancer.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 385, "doc_id": "9767444", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Higher plasma levels of I-carnitine, when associated with trimethylamine N-oxide, are negatively correlated with cardiovascular events in humans.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Arabidopsis Chromatin-Modifying Nuclear siRNA Pathway Involves a Nucleolar RNA Processing Center\nABSTRACT: In Arabidopsis thaliana, small interfering RNAs (siRNAs) direct cytosine methylation at endogenous DNA repeats in a pathway involving two forms of nuclear RNA polymerase IV (Pol IVa and Pol IVb), RNA-DEPENDENT RNA POLYMERASE 2 (RDR2), DICER-LIKE 3 (DCL3), ARGONAUTE4 (AGO4), the chromatin remodeler DRD1, and the de novo cytosine methyltransferase DRM2. We show that RDR2, DCL3, AGO4, and NRPD1b (the largest subunit of Pol IVb) colocalize with siRNAs within the nucleolus. By contrast, Pol IVa and DRD1 are external to the nucleolus and colocalize with endogenous repeat loci. Mutation-induced loss of pathway proteins causes downstream proteins to mislocalize, revealing their order of action. Pol IVa acts first, and its localization is RNA dependent, suggesting an RNA template. We hypothesize that maintenance of the heterochromatic state involves locus-specific Pol IVa transcription followed by siRNA production and assembly of AGO4- and NRPD1b-containing silencing complexes within nucleolar processing centers.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 523, "doc_id": "1354567", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Do islet-like cell aggregates generated from human adipose tissue derived stem cells ameliorate experimental diabetes in mice?\n\nABSTRACT:\nType 1 Diabetes Mellitus is caused by auto immune destruction of insulin producing beta cells in the pancreas. Currently available treatments include transplantation of isolated islets from donor pancreas to the patient. However, this method is limited by inadequate means of immuno-suppression to prevent islet rejection and importantly, limited supply of islets for transplantation. Autologous adult stem cells are now considered for cell replacement therapy in diabetes as it has the potential to generate neo-islets which are genetically part of the treated individual. Adopting methods of islet encapsulation in immuno-isolatory devices would eliminate the need for immuno-suppressants. In the present study we explore the potential of human adipose tissue derived adult stem cells (h-ASCs) to differentiate into functional islet like cell aggregates (ICAs). Our stage specific differentiation protocol permit the conversion of mesodermic h-ASCs to definitive endoderm (Hnf3β, TCF2 and Sox17) and to PDX1, Ngn3, NeuroD, Pax4 positive pancreatic endoderm which further matures in vitro to secrete insulin. These ICAs are shown to produce human C-peptide in a glucose dependent manner exhibiting in-vitro functionality. Transplantation of mature ICAs, packed in immuno-isolatory biocompatible capsules to STZ induced diabetic mice restored near normoglycemia within 3-4 weeks. The detection of human C-peptide, 1155±165 pM in blood serum of experimental mice demonstrate the efficacy of our differentiation approach.", "output": "{\"label\": \"yes\", \"rationale\": \"h-ASC is an ideal population of personal stem cells for cell replacement therapy, given that they are abundant, easily available and autologous in origin. Our findings present evidence that h-ASCs could be induced to differentiate into physiologically competent functional islet like cell aggregates, which may provide as a source of alternative islets for cell replacement therapy in type 1 diabetes.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 21687731, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Epigenetic modulating agents (EMAs) modulate antitumor immune response in a cancer model system.\n\nCANDIDATE_PASSAGE:\nTh2-mediated host protective immunity to intestinal nematode infections. Despite many years of study, relatively little is known about the effector mechanisms that operate against intestine-dwelling nematodes. Most of the current understanding comes from studies of laboratory model systems in rodents. It is clear that when an intestinal helminth infection takes place the immune system generates a strong Th2-mediated response, which regulates a variety of responses characteristic of helminth infections such as eosinophilia, intestinal mastocytosis and elevated IgE production. The ability to modulate the host's immune response in vivo with cytokine-specific monoclonal antibodies and recombinant cytokines, together with the use of animals with disruption of key genes involved in the immune response, have provided powerful tools with which to dissect the potential effector mechanisms operating. In the absence of a T-cell compartment the host is unable to expel the parasite. If a Th1-dominated response is generated, protective immunity is almost universally compromised. Thus, it it would appear that some aspect of a Th2-mediated response controls effector mechanisms. Although it is clear that for some infections the mast cell appears to be involved in protection, probably through the generation of a non-specific inflammatory response, how these cells become activated remains unclear. Data from infections in transgenic animals suggest that activation is not through the high-affinity receptor for IgE. Such studies also call into doubt the importance of conventional interactions between effector leucocytes and antibody. There is little evidence to support a protective role for eosinophilia in any system. New data also imply that, although interleukin 4 (IL-4) is gen [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "385", "doc_id": "23801039", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Antiretroviral therapy increases rates of tuberculosis across a broad range of CD4 strata.\n\nCANDIDATE_ABSTRACT:\nTITLE: Antiretroviral Therapy for Prevention of Tuberculosis in Adults with HIV: A Systematic Review and Meta-Analysis\nABSTRACT: BACKGROUND Human immunodeficiency virus (HIV) infection is the strongest risk factor for developing tuberculosis and has fuelled its resurgence, especially in sub-Saharan Africa. In 2010, there were an estimated 1.1 million incident cases of tuberculosis among the 34 million people living with HIV worldwide. Antiretroviral therapy has substantial potential to prevent HIV-associated tuberculosis. We conducted a systematic review of studies that analysed the impact of antiretroviral therapy on the incidence of tuberculosis in adults with HIV infection. METHODS AND FINDINGS PubMed, Embase, African Index Medicus, LILACS, and clinical trial registries were systematically searched. Randomised controlled trials, prospective cohort studies, and retrospective cohort studies were included if they compared tuberculosis incidence by antiretroviral therapy status in HIV-infected adults for a median of over 6 mo in developing countries. For the meta-analyses there were four categories based on CD4 counts at antiretroviral therapy initiation: (1) less than 200 cells/µl, (2) 200 to 350 cells/µl, (3) greater than 350 cells/µl, and (4) any CD4 count. Eleven studies met the inclusion criteria. Antiretroviral therapy is strongly associated with a reduction in the incidence of tuberculosis in all baseline CD4 count categories: (1) less than 200 cells/µl (hazard ratio [HR] 0.16, 95% confidence interval [CI] 0.07 to 0.36), (2) 200 to 350 cells/µl (HR 0.34, 95% CI 0.19 to 0.60), (3) greater than 350 cells/µl (HR 0.43, 95% CI 0.30 to 0.63), and (4) any CD4 count (HR 0.35, 95% CI 0.28 to 0.44). There was no evidence of hazard ratio modification with respect to baseline CD4 count category (p = 0.20). CONCLUSIONS Antiretroviral therapy is strongly associated with a reduction in the inc [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Antiretroviral therapy is strongly associated with a reduction in the incidence of tuberculosis across all CD4 count strata.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 123, "doc_id": "4883040", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Increased vessel density along with a reduction in fibrosis improves the efficacy of chemotherapy treatments.\n\nCANDIDATE_PASSAGE:\nPhase II study of panobinostat in combination with bevacizumab for recurrent glioblastoma and anaplastic glioma. BACKGROUND Panobinostat is a histone deacetylase inhibitor with antineoplastic and antiangiogenic effects in glioma that may work synergistically with bevacizumab. We conducted a multicenter phase II trial of panobinostat combined with bevacizumab in patients with recurrent high-grade glioma (HGG). METHODS Patients with recurrent HGG were treated with oral panobinostat 30 mg 3 times per week, every other week, in combination with bevacizumab 10 mg/kg every other week. The primary endpoint was a 6-month progression-fee survival (PFS6) rate for participants with recurrent glioblastoma (GBM). Patients with recurrent anaplastic glioma (AG) were evaluated as an exploratory arm of the study. RESULTS At interim analysis, the GBM arm did not meet criteria for continued accrual, and the GBM arm was closed. A total of 24 patients with GBM were accrued prior to closure. The PFS6 rate was 30.4% (95%, CI 12.4%-50.7%), median PFS was 5 months (range, 3-9 months), and median overall survival (OS) was 9 months (range, 6-19 months). Accrual in the AG arm continued to completion, and a total of 15 patients were enrolled. The PFS6 rate was 46.7% (range, 21%-73%), median PFS was 7 months (range, 2-10 months), and median OS was 17 months (range, 5 months-27 months). CONCLUSIONS This phase II study of panobinostat and bevacizumab in participants with recurrent GBM did not meet criteria for continued accrual, and the GBM cohort of the study was closed. Although it was reasonably well tolerated, the addition of panobinostat to bevacizumab did not significantly improve PFS6 compared with historical controls of bevacizumab monotherapy in either cohort.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "620", "doc_id": "14482051", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: FACT and other histone chaperone(s) compensate for Histone 2A (H2A)-histone 2B (H2B) dimer eviction during the histone exchange process.\n\nCANDIDATE_PASSAGE:\nFACT Disrupts Nucleosome Structure by Binding H2A-H2B with Conserved Peptide Motifs. FACT, a heterodimer of Spt16 and Pob3, is an essential histone chaperone. We show that the H2A-H2B binding activity that is central to FACT function resides in short acidic regions near the C termini of each subunit. Mutations throughout these regions affect binding and cause correlated phenotypes that range from mild to lethal, with the largest individual contributions unexpectedly coming from an aromatic residue and a nearby carboxylate residue within each domain. Spt16 and Pob3 bind overlapping sites on H2A-H2B, and Spt16-Pob3 heterodimers simultaneously bind two H2A-H2B dimers, the same stoichiometry as the components of a nucleosome. An Spt16:H2A-H2B crystal structure explains the biochemical and genetic data, provides a model for Pob3 binding, and implies a mechanism for FACT reorganization that we confirm biochemically. Moreover, unexpected similarity to binding of ANP32E and Swr1 with H2A.Z-H2B reveals that diverse H2A-H2B chaperones use common mechanisms of histone binding and regulating nucleosome functions.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "407", "doc_id": "9889151", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: CDK6 shows improved binding to loss-of-function variants of p18 INK4C.\n\nCANDIDATE_PASSAGE:\nThe p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases. The cyclin-dependent kinase Cdk2 associates with cyclins A, D, and E and has been implicated in the control of the G1 to S phase transition in mammals. To identify potential Cdk2 regulators, we have employed an improved two-hybrid system to isolate human genes encoding Cdk-interacting proteins (Cips). CIP1 encodes a novel 21 kd protein that is found in cyclin A, cyclin D1, cyclin E, and Cdk2 immunoprecipitates. p21CIP1 is a potent, tight-binding inhibitor of Cdks and can inhibit the phosphorylation of Rb by cyclin A-Cdk2, cyclin E-Cdk2, cyclin D1-Cdk4, and cyclin D2-Cdk4 complexes. Cotransfection experiments indicate that CIP1 and SV40 T antigen function in a mutually antagonistic manner to control cell cycle progression.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "205", "doc_id": "13614794", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: NF2 (Merlin) causes phosphorylation and subsequent cytoplasmic sequestration of YAP in Drosophila by activating LATS1/2 kinases.\n\nCANDIDATE_PASSAGE:\nA genetic screen identifies an LKB1–MARK signalling axis controlling the Hippo–YAP pathway The Hippo–YAP pathway is an emerging signalling cascade involved in the regulation of stem cell activity and organ size. To identify components of this pathway, we performed an RNAi-based kinome screen in human cells. Our screen identified several kinases not previously associated with Hippo signalling that control multiple cellular processes. One of the hits, LKB1, is a common tumour suppressor whose mechanism of action is only partially understood. We demonstrate that LKB1 acts through its substrates of the microtubule affinity-regulating kinase family to regulate the localization of the polarity determinant Scribble and the activity of the core Hippo kinases. Our data also indicate that YAP is functionally important for the tumour suppressive effects of LKB1. Our results identify a signalling axis that links YAP activation with LKB1 mutations, and have implications for the treatment of LKB1-mutant human malignancies. In addition, our findings provide insight into upstream signals of the Hippo–YAP signalling cascade.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "830", "doc_id": "1897324", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The myocardial cell lineage originally develops from cardiac progenitors of exclusively endodermal origin.\n\nCANDIDATE_PASSAGE:\nElectron microscopic studies of macrophages in early human yolk sacs. Distribution and fine structure of macrophages were studied in 10 human embryos in the 6th and 7th week of gestation, 5.5 to 12 mm in crown-rump length. The yolk sac macrophages were found in the extravascular mesenchymal tissues and intravascular spaces long before the first appearance of bone marrow and lymphatic tissues in the embryos. In addition to the macrophages, the fibroblastic cells and the cells of erythropoietic series were also present in the extravascular space. The macrophages showed a variety of cellular structures suggesting transition from immature cell type with no heterophagolysosomes to mature cell type in phagocytosis. The mature macrophages avidly phagocytized the primitive erythroblasts and occasionally platelets. They were positively stained for lysosomal enzymes and were characterized by numerous pleomorphic heterophagolysosomes which exhibited various stages of digestion of phagocytized blood cells. The origin of intravascular macrophages may be in either migrated extravascular macrophages or phagocytic endothelial cells. The phagocytosis and degradation of erythroblasts appear to be one of the main functions of yolk sac macrophages. The presence of the macrophages in mitosis indicates their proliferation in situ.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1239", "doc_id": "25068298", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: ALDH1 expression is associated with poorer prognosis in breast cancer.\n\nCANDIDATE_PASSAGE:\nFascin protein is critical for transforming growth factor β protein-induced invasion and filopodia formation in spindle-shaped tumor cells. Fascin, an actin-bundling protein overexpressed in all carcinomas, has been associated with poor prognosis, shorter survival, and more metastatic diseases. It is believed that fascin facilitates tumor metastasis by promoting the formation of invasive membrane protrusions. However, the mechanisms by which fascin is overexpressed in tumors are not clear. TGFβ is a cytokine secreted by tumor and mesenchymal cells and promotes metastasis in many late stage tumors. The pro-metastasis mechanisms of TGFβ remain to be fully elucidated. Here we demonstrated that TGFβ induced fascin expression in spindle-shaped tumor cells through the canonical Smad-dependent pathway. Fascin was critical for TGFβ-promoted filopodia formation, migration, and invasion in spindle tumor cells. More importantly, fascin expression significantly correlates with TGFβ1 and TGFβ receptor I levels in a cohort of primary breast tumor samples. Our results indicate that elevated TGFβ level in the tumor microenvironment may be responsible for fascin overexpression in some of the metastatic tumors. Our data also suggest that fascin could play a central role in TGFβ-promoted tumor metastasis.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "53", "doc_id": "7795952", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Beta-band coherence is enhanced for visible stimuli over invisible stimuli.\n\nCANDIDATE_PASSAGE:\nConverging Intracranial Markers of Conscious Access We compared conscious and nonconscious processing of briefly flashed words using a visual masking procedure while recording intracranial electroencephalogram (iEEG) in ten patients. Nonconscious processing of masked words was observed in multiple cortical areas, mostly within an early time window (<300 ms), accompanied by induced gamma-band activity, but without coherent long-distance neural activity, suggesting a quickly dissipating feedforward wave. In contrast, conscious processing of unmasked words was characterized by the convergence of four distinct neurophysiological markers: sustained voltage changes, particularly in prefrontal cortex, large increases in spectral power in the gamma band, increases in long-distance phase synchrony in the beta range, and increases in long-range Granger causality. We argue that all of those measures provide distinct windows into the same distributed state of conscious processing. These results have a direct impact on current theoretical discussions concerning the neural correlates of conscious access.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "175", "doc_id": "1710116", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Leuko-increased blood increases infectious complications in red blood cell transfusion.\n\nCANDIDATE_ABSTRACT:\nTITLE: Clinical outcomes following institution of the Canadian universal leukoreduction program for red blood cell transfusions.\nABSTRACT: CONTEXT A number of countries have implemented a policy of universal leukoreduction of their blood supply, but the potential role of leukoreduction in decreasing postoperative mortality and infection is unclear. OBJECTIVE To evaluate clinical outcomes following adoption of a national universal prestorage leukoreduction program for blood transfusions. DESIGN, SETTING, AND POPULATION Retrospective before-and-after cohort study conducted from August 1998 to August 2000 in 23 academic and community hospitals throughout Canada, enrolling 14 786 patients who received red blood cell transfusions following cardiac surgery or repair of hip fracture, or who required intensive care following a surgical intervention or multiple trauma. INTERVENTION Universal prestorage leukoreduction program introduced by 2 Canadian blood agencies. A total of 6982 patients were enrolled during the control period and 7804 patients were enrolled following prestorage leukoreduction. MAIN OUTCOME MEASURES All-cause in-hospital mortality and serious nosocomial infections (pneumonia, bacteremia, septic shock, all surgical site infections) occurring after first transfusion and at least 2 days after index procedure or intensive care unit admission. Secondary outcomes included rates of posttransfusion fever and antibiotic use. RESULTS Unadjusted in-hospital mortality rates were significantly lower following the introduction of leukoreduction compared with the control period (6.19% vs 7.03%, respectively; P =.04). Compared with the control period, the adjusted odds of death following leukoreduction were reduced (odds ratio [OR], 0.87; 95% confidence interval [CI], 0.75-0.99), but serious nosocomial infections did not decrease (adjusted OR, 0.97; 95% CI, 0.87-1.09). The frequency of posttransfusio [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The frequency of posttransfusion fevers decreased significantly following leukoreduction (adjusted OR, 0.86; 95% CI, 0.79-0.94), as did antibiotic use (adjusted OR, 0.90; 95% CI, 0.82-0.99).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 692, "doc_id": "24088502", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: RUNX1 is downregulated or mutated in TLX1 T-ALL.\n\nCANDIDATE_ABSTRACT:\nTITLE: Integrated molecular genetic profiling of pediatric high-grade gliomas reveals key differences with the adult disease.\nABSTRACT: PURPOSE To define copy number alterations and gene expression signatures underlying pediatric high-grade glioma (HGG). PATIENTS AND METHODS We conducted a high-resolution analysis of genomic imbalances in 78 de novo pediatric HGGs, including seven diffuse intrinsic pontine gliomas, and 10 HGGs arising in children who received cranial irradiation for a previous cancer using single nucleotide polymorphism microarray analysis. Gene expression was analyzed with gene expression microarrays for 53 tumors. Results were compared with publicly available data from adult tumors. RESULTS Significant differences in copy number alterations distinguish childhood and adult glioblastoma. PDGFRA was the predominant target of focal amplification in childhood HGG, including diffuse intrinsic pontine gliomas, and gene expression analyses supported an important role for deregulated PDGFRalpha signaling in pediatric HGG. No IDH1 hotspot mutations were found in pediatric tumors, highlighting molecular differences with adult secondary glioblastoma. Pediatric and adult glioblastomas were clearly distinguished by frequent gain of chromosome 1q (30% v 9%, respectively) and lower frequency of chromosome 7 gain (13% v 74%, respectively) and 10q loss (35% v 80%, respectively). PDGFRA amplification and 1q gain occurred at significantly higher frequency in irradiation-induced tumors, suggesting that these are initiating events in childhood gliomagenesis. A subset of pediatric HGGs showed minimal copy number changes. CONCLUSION Integrated molecular profiling showed substantial differences in the molecular features underlying pediatric and adult HGG, indicating that findings in adult tumors cannot be simply extrapolated to younger patients. PDGFRalpha may be a useful target for pediatric HGG, [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1009, "doc_id": "2360905", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Tumor necrosis factor alpha (TNF-α) and interleukin-1 (IL-1) are pro-inflammatory cytokines that inhibit IL-6 and IL-10.\n\nCANDIDATE_PASSAGE:\nThe Snf1 kinase controls glucose repression in yeast by modulating interactions between the Mig1 repressor and the Cyc8-Tup1 co-repressor. Among lower eukaryotes, glucose repression is a conserved, widely spread mechanism regulating carbon catabolism. The yeast Snf1 kinase, the Mig1 DNA-binding repressor and the Mig1-interacting co-repressor complex Cyc8(Ssn6)-Tup1 are central components of this pathway. Previous experiments suggested that cytoplasmic translocation of Mig1, upon its phosphorylation by Snf1 in the nucleus, is the key regulatory step for releasing glucose repression. In this report we re-evaluate this model. We establish the coordinated repressive action of Mig1 and Cyc8-Tup1 on GAL1 transcription, but we find that Cyc8-Tup1 is not tethered by Mig1 to the promoter DNA. We demonstrate that both negative regulators occupy GAL1 continuously under either repression or activation conditions, although the majority of the Mig1 is redistributed to the cytoplasm upon activation. We show that Snf1-dependent phosphorylation of Mig1 abolishes interaction with Cyc8-Tup1, and we propose that regulation of this interaction, not the Mig1 cytoplasmic localization, is the molecular switch that controls transcriptional repression/de-repression.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1332", "doc_id": "9199796", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Chenodeosycholic acid treatment increases whole-body energy expenditure.\n\nCANDIDATE_PASSAGE:\nLXRS and FXR: the yin and yang of cholesterol and fat metabolism. Liver X receptors (LXRs) and farnesoid X receptor (FXR) are nuclear receptors that function as intracellular sensors for sterols and bile acids, respectively. In response to their ligands, these receptors induce transcriptional responses that maintain a balanced, finely tuned regulation of cholesterol and bile acid metabolism. LXRs also permit the efficient storage of carbohydrate- and fat-derived energy, whereas FXR activation results in an overall decrease in triglyceride levels and modulation of glucose metabolism. The elegant, dual interplay between these two receptor systems suggests that they coevolved to constitute a highly sensitive and efficient system for the maintenance of total body fat and cholesterol homeostasis. Emerging evidence suggests that the tissue-specific action of these receptors is also crucial for the proper function of the cardiovascular, immune, reproductive, endocrine pancreas, renal, and central nervous systems. Together, LXRs and FXR represent potential therapeutic targets for the treatment and prevention of numerous metabolic and lipid-related diseases.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "248", "doc_id": "11238784", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Deltex interacts with eIF3. There is no known interaction between Deltex and elF3\n\nCANDIDATE_ABSTRACT:\nTITLE: CD169+ MACROPHAGES PRESENT LIPID ANTIGENS TO MEDIATE EARLY ACTIVATION OF INVARIANT NKT CELLS IN LYMPH NODES\nABSTRACT: Invariant natural killer T cells (iNKT cells) are involved in the host defense against microbial infection. Although it is known that iNKT cells recognize glycolipids presented by CD1d, how and where they encounter antigen in vivo remains unclear. Here we used multiphoton microscopy to visualize the dynamics and activation of iNKT cells in lymph nodes. After antigen administration, iNKT cells became confined in a CD1d-dependent manner in close proximity to subcapsular sinus CD169(+) macrophages. These macrophages retained, internalized and presented lipid antigen and were required for iNKT cell activation, cytokine production and population expansion. Thus, CD169(+) macrophages can act as true antigen-presenting cells controlling early iNKT cell activation and favoring the fast initiation of immune responses.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 331, "doc_id": "1933281", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The mean suicide rate in women is lower after miscarriage than live birth.\n\nCANDIDATE_PASSAGE:\nStructural basis for the activation of microtubule assembly by the EB1 and p150Glued complex. Plus-end tracking proteins, such as EB1 and the dynein/dynactin complex, regulate microtubule dynamics. These proteins are thought to stabilize microtubules by forming a plus-end complex at microtubule growing ends with ill-defined mechanisms. Here we report the crystal structure of two plus-end complex components, the carboxy-terminal dimerization domain of EB1 and the microtubule binding (CAP-Gly) domain of the dynactin subunit p150Glued. Each molecule of the EB1 dimer contains two helices forming a conserved four-helix bundle, while also providing p150Glued binding sites in its flexible tail region. Combining crystallography, NMR, and mutational analyses, our studies reveal the critical interacting elements of both EB1 and p150Glued, whose mutation alters microtubule polymerization activity. Moreover, removal of the key flexible tail from EB1 activates microtubule assembly by EB1 alone, suggesting that the flexible tail negatively regulates EB1 activity. We, therefore, propose that EB1 possesses an auto-inhibited conformation, which is relieved by p150Glued as an allosteric activator.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1228", "doc_id": "21598000", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Allogeneic mechanical circulatory support is not as effective as autologous mechanical circulatory support for treating acute myocardial infarction.\n\nCANDIDATE_ABSTRACT:\nTITLE: Comparison of allogeneic vs autologous bone marrow–derived mesenchymal stem cells delivered by transendocardial injection in patients with ischemic cardiomyopathy: the POSEIDON randomized trial.\nABSTRACT: CONTEXT Mesenchymal stem cells (MSCs) are under evaluation as a therapy for ischemic cardiomyopathy (ICM). Both autologous and allogeneic MSC therapies are possible; however, their safety and efficacy have not been compared. OBJECTIVE To test whether allogeneic MSCs are as safe and effective as autologous MSCs in patients with left ventricular (LV) dysfunction due to ICM. DESIGN, SETTING, AND PATIENTS A phase 1/2 randomized comparison (POSEIDON study) in a US tertiary-care referral hospital of allogeneic and autologous MSCs in 30 patients with LV dysfunction due to ICM between April 2, 2010, and September 14, 2011, with 13-month follow-up. INTERVENTION Twenty million, 100 million, or 200 million cells (5 patients in each cell type per dose level) were delivered by transendocardial stem cell injection into 10 LV sites. MAIN OUTCOME MEASURES Thirty-day postcatheterization incidence of predefined treatment-emergent serious adverse events (SAEs). Efficacy assessments included 6-minute walk test, exercise peak VO2, Minnesota Living with Heart Failure Questionnaire (MLHFQ), New York Heart Association class, LV volumes, ejection fraction (EF), early enhancement defect (EED; infarct size), and sphericity index. RESULTS Within 30 days, 1 patient in each group (treatment-emergent SAE rate, 6.7%) was hospitalized for heart failure, less than the prespecified stopping event rate of 25%. The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3% (n = 8) in the autologous group (P = .46). At 1 year, there were no ventricular arrhythmia SAEs observed among allogeneic recipients compared with 4 patients (26.7%) in the autologous group (P = .10). Relative to baseline, autologous but not allogeneic MSC therapy was associated with an improvement in the 6- [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3% (n = 8) in the autologous group (P = .46).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 104, "doc_id": "40164383", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Basophils promote disease development in patients with systemic lupus erythematosus (SLE).\n\nCANDIDATE_ABSTRACT:\nTITLE: BASOPHILS AND THE T HELPER 2 ENVIRONMENT CAN PROMOTE THE DEVELOPMENT OF LUPUS NEPHRITIS\nABSTRACT: In systemic lupus erythematosus (SLE), self-reactive antibodies can target the kidney (lupus nephritis), leading to functional failure and possible mortality. We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice). Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis. Basophils were also present in the lymph nodes and spleen of subjects with SLE. Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 172, "doc_id": "12670680", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Suboptimal nutrition is not predictive of chronic disease\n\nCANDIDATE_ABSTRACT:\nTITLE: Specific inhibition of cyclin-dependent kinase 4/6 by PD 0332991 and associated antitumor activity in human tumor xenografts.\nABSTRACT: PD 0332991 is a highly specific inhibitor of cyclin-dependent kinase 4 (Cdk4) (IC50, 0.011 micromol/L) and Cdk6 (IC50, 0.016 micromol/L), having no activity against a panel of 36 additional protein kinases. It is a potent antiproliferative agent against retinoblastoma (Rb)-positive tumor cells in vitro, inducing an exclusive G1 arrest, with a concomitant reduction of phospho-Ser780/Ser795 on the Rb protein. Oral administration of PD 0332991 to mice bearing the Colo-205 human colon carcinoma produces marked tumor regression. Therapeutic doses of PD 0332991 cause elimination of phospho-Rb and the proliferative marker Ki-67 in tumor tissue and down-regulation of genes under the transcriptional control of E2F. The results indicate that inhibition of Cdk4/6 alone is sufficient to cause tumor regression and a net reduction in tumor burden in some tumors.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1110, "doc_id": "864491", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The arm density of TatAd complexes is due to structural rearrangements within Class1 TatAd complexes such as the 'charge zipper mechanism'.\n\nCANDIDATE_PASSAGE:\nXRCC4's interaction with XLF is required for coding (but not signal) end joining XRCC4 and XLF are structurally related proteins important for DNA Ligase IV function. XRCC4 forms a tight complex with DNA Ligase IV while XLF interacts directly with XRCC4. Both XRCC4 and XLF form homodimers that can polymerize as heterotypic filaments independently of DNA Ligase IV. Emerging structural and in vitro biochemical data suggest that XRCC4 and XLF together generate a filamentous structure that promotes bridging between DNA molecules. Here, we show that ablating XRCC4's affinity for XLF results in DNA repair deficits including a surprising deficit in VDJ coding, but not signal end joining. These data are consistent with a model whereby XRCC4/XLF complexes hold DNA ends together--stringently required for coding end joining, but dispensable for signal end joining. Finally, DNA-PK phosphorylation of XRCC4/XLF complexes disrupt DNA bridging in vitro, suggesting a regulatory role for DNA-PK's phosphorylation of XRCC4/XLF complexes.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1194", "doc_id": "17768946", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Anthrax spores can be disposed of easily after they are dispersed.\n\nCANDIDATE_ABSTRACT:\nTITLE: Secondary aerosolization of viable Bacillus anthracis spores in a contaminated US Senate Office.\nABSTRACT: CONTEXT Bioterrorist attacks involving letters and mail-handling systems in Washington, DC, resulted in Bacillus anthracis (anthrax) spore contamination in the Hart Senate Office Building and other facilities in the US Capitol's vicinity. OBJECTIVE To provide information about the nature and extent of indoor secondary aerosolization of B anthracis spores. DESIGN Stationary and personal air samples, surface dust, and swab samples were collected under semiquiescent (minimal activities) and then simulated active office conditions to estimate secondary aerosolization of B anthracis spores. Nominal size characteristics, airborne concentrations, and surface contamination of B anthracis particles (colony-forming units) were evaluated. RESULTS Viable B anthracis spores reaerosolized under semiquiescent conditions, with a marked increase in reaerosolization during simulated active office conditions. Increases were observed for B anthracis collected on open sheep blood agar plates (P<.001) and personal air monitors (P =.01) during active office conditions. More than 80% of the B anthracis particles collected on stationary monitors were within an alveolar respirable size range of 0.95 to 3.5 micro m. CONCLUSIONS Bacillus anthracis spores used in a recent terrorist incident reaerosolized under common office activities. These findings have important implications for appropriate respiratory protection, remediation, and reoccupancy of contaminated office environments.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"More than 80% of the B anthracis particles collected on stationary monitors were within an alveolar respirable size range of 0.95 to 3.5 micro m. CONCLUSIONS Bacillus anthracis spores used in a recent terrorist incident reaerosolized under common office activities.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 115, "doc_id": "33872649", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Klf4 is not required for proper myeloid cell differentiation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Kruppel-like factor 4 is essential for inflammatory monocyte differentiation in vivo.\nABSTRACT: Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types. We demonstrate in this study that hematopoietic cells from KLF4(-/-) fetal livers (FL) contained normal numbers of functional hematopoietic progenitor cells, were radioprotective, and performed as well as KLF4(+/+) cells in competitive repopulation assays. However, hematopoietic \"KLF4(-/-) chimeras\" generated by transplantation of KLF4(-/-) fetal livers cells into lethally irradiated wild-type mice completely lacked circulating inflammatory (CD115(+)Gr1(+)) monocytes, and had reduced numbers of resident (CD115(+)Gr1(-)) monocytes. Although the numbers and function of peritoneal macrophages were normal in KLF4(-/-) chimeras, bone marrow monocytic cells from KLF4(-/-) chimeras expressed lower levels of key trafficking molecules and were more apoptotic. Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes. In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells. The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 669, "doc_id": "25148216", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Tumor necrosis factor alpha (TNF-α) and interleukin-1 (IL-1) are pro-inflammatory cytokines that inhibit IL-6 and IL-10.\n\nCANDIDATE_ABSTRACT:\nTITLE: Inter-individual variability and genetic influences on cytokine responses to bacteria and fungi\nABSTRACT: Little is known about the inter-individual variation of cytokine responses to different pathogens in healthy individuals. To systematically describe cytokine responses elicited by distinct pathogens and to determine the effect of genetic variation on cytokine production, we profiled cytokines produced by peripheral blood mononuclear cells from 197 individuals of European origin from the 200 Functional Genomics (200FG) cohort in the Human Functional Genomics Project (http://www.humanfunctionalgenomics.org), obtained over three different years. We compared bacteria- and fungi-induced cytokine profiles and found that most cytokine responses were organized around a physiological response to specific pathogens, rather than around a particular immune pathway or cytokine. We then correlated genome-wide single-nucleotide polymorphism (SNP) genotypes with cytokine abundance and identified six cytokine quantitative trait loci (QTLs). Among them, a cytokine QTL at the NAA35-GOLM1 locus markedly modulated interleukin (IL)-6 production in response to multiple pathogens and was associated with susceptibility to candidemia. Furthermore, the cytokine QTLs that we identified were enriched among SNPs previously associated with infectious diseases and heart diseases. These data reveal and begin to explain the variability in cytokine production by human immune cells in response to pathogens.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1332, "doc_id": "5304891", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Neutrophil extracellular traps (NETs) are released by ANCA-stimulated neutrophils.\n\nCANDIDATE_PASSAGE:\nNeuronal replacement from endogenous precursors in the adult brain after stroke In the adult brain, new neurons are continuously generated in the subventricular zone and dentate gyrus, but it is unknown whether these neurons can replace those lost following damage or disease. Here we show that stroke, caused by transient middle cerebral artery occlusion in adult rats, leads to a marked increase of cell proliferation in the subventricular zone. Stroke-generated new neurons, as well as neuroblasts probably already formed before the insult, migrate into the severely damaged area of the striatum, where they express markers of developing and mature, striatal medium-sized spiny neurons. Thus, stroke induces differentiation of new neurons into the phenotype of most of the neurons destroyed by the ischemic lesion. Here we show that the adult brain has the capacity for self-repair after insults causing extensive neuronal death. If the new neurons are functional and their formation can be stimulated, a novel therapeutic strategy might be developed for stroke in humans.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "845", "doc_id": "7157436", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Assessing treatment adherence is more beneficial to clinical practice than measuring routine outcomes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Anxiety\nABSTRACT: OBJECTIVES To examine the effect of routinely administered psychiatric questionnaires on the recognition, management, and outcome of psychiatric disorders in non-psychiatric settings. DATA SOURCES Embase, Medline, PsycLIT, Cinahl, Cochrane Controlled Trials Register, and hand searches of key journals. METHODS A systematic review of randomised controlled trials of the administration and routine feedback of psychiatric screening and outcome questionnaires to clinicians in non-psychiatric settings. Narrative overview of key design features and end points, together with a random effects quantitative synthesis of comparable studies. MAIN OUTCOME MEASURES Recognition of psychiatric disorders after feedback of questionnaire results; interventions for psychiatric disorders; and outcome of psychiatric disorders. RESULTS Nine randomised studies were identified that examined the use of common psychiatric instruments in primary care and general hospital settings. Studies compared the effect of the administration of these instruments followed by the feedback of the results to clinicians, with administration with no feedback. Meta-analytic pooling was possible for four of these studies (2457 participants), which measured the effect of feedback on the recognition of depressive disorders. Routine administration and feedback of scores for all patients (irrespective of score) did not increase the overall rate of recognition of mental disorders such as anxiety and depression (relative risk of detection of depression by clinician after feedback 0.95, 95% confidence interval 0.83 to 1.09). Two studies showed that routine administration followed by selective feedback for only high scorers increased the rate of recognition of depression (relative risk of detection of depression af [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 134, "doc_id": "4695046", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Inositol lipid 3-phosphatase PTEN converts Ptdlns(3,4)P 2 into phosphatidylinositol 4-phosphate.\n\nCANDIDATE_PASSAGE:\nAutophagic programmed cell death by selective catalase degradation. Autophagy plays a central role in regulating important cellular functions such as cell survival during starvation and control of infectious pathogens. Recently, it has been shown that autophagy can induce cells to die; however, the mechanism of the autophagic cell death program is unclear. We now show that caspase inhibition leading to cell death by means of autophagy involves reactive oxygen species (ROS) accumulation, membrane lipid oxidation, and loss of plasma membrane integrity. Inhibition of autophagy by chemical compounds or knocking down the expression of key autophagy proteins such as ATG7, ATG8, and receptor interacting protein (RIP) blocks ROS accumulation and cell death. The cause of abnormal ROS accumulation is the selective autophagic degradation of the major enzymatic ROS scavenger, catalase. Caspase inhibition directly induces catalase degradation and ROS accumulation, which can be blocked by autophagy inhibitors. These findings unveil a molecular mechanism for the role of autophagy in cell death and provide insight into the complex relationship between ROS and nonapoptotic programmed cell death.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "636", "doc_id": "2543135", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: De novo assembly of sequence data has shorter contigs than unassembled sequence data.\n\nCANDIDATE_ABSTRACT:\nTITLE: A culture-independent sequence-based metagenomics approach to the investigation of an outbreak of Shiga-toxigenic Escherichia coli O104:H4.\nABSTRACT: IMPORTANCE Identification of the bacterium responsible for an outbreak can aid in disease management. However, traditional culture-based diagnosis can be difficult, particularly if no specific diagnostic test is available for an outbreak strain. OBJECTIVE To explore the potential of metagenomics, which is the direct sequencing of DNA extracted from microbiologically complex samples, as an open-ended clinical discovery platform capable of identifying and characterizing bacterial strains from an outbreak without laboratory culture. DESIGN, SETTING, AND PATIENTS In a retrospective investigation, 45 samples were selected from fecal specimens obtained from patients with diarrhea during the 2011 outbreak of Shiga-toxigenic Escherichia coli (STEC) O104:H4 in Germany. Samples were subjected to high-throughput sequencing (August-September 2012), followed by a 3-phase analysis (November 2012-February 2013). In phase 1, a de novo assembly approach was developed to obtain a draft genome of the outbreak strain. In phase 2, the depth of coverage of the outbreak strain genome was determined in each sample. In phase 3, sequences from each sample were compared with sequences from known bacteria to identify pathogens other than the outbreak strain. MAIN OUTCOMES AND MEASURES The recovery of genome sequence data for the purposes of identification and characterization of the outbreak strain and other pathogens from fecal samples. RESULTS During phase 1, a draft genome of the STEC outbreak strain was obtained. During phase 2, the outbreak strain genome was recovered from 10 samples at greater than 10-fold coverage and from 26 samples at greater than 1-fold coverage. Sequences from the Shiga-toxin genes were detected in 27 of 40 STEC-positive samples (67%). In phase 3, sequences [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 313, "doc_id": "6173523", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is perforation of the appendix a risk factor for tubal infertility and ectopic pregnancy?\n\nABSTRACT:\nTo critically assess the evidence that appendiceal perforation is a risk factor for subsequent tubal infertility or ectopic pregnancy. Epidemiologic studies investigating the relationship between appendectomy and infertility or ectopic pregnancy were identified by searching the MEDLINE database from 1966 to 1997. Appropriate citations were also extracted from a manual search of the bibliographies of selected papers. Twenty-three articles were retrieved. Only 4 presented original data including comparisons to a nonexposed control group and they form the basis for this study. Because the raw data or specific techniques of data analysis were not always explicitly described, indices of risk for exposure were extracted from the data as presented and were analysed without attempting to convert them to a common measure. Articles were assessed according to the criteria of the Evidence-Based Medicine Working Group for evaluating articles on harm. Review of the literature yielded estimates of the risk of adverse fertility outcomes ranging from 1.6 (95% confidence interval [CI] 1.1 to 2.5) for ectopic pregnancy after an appendectomy to 4.8 (95% CI 1.5 to 14.9) for tubal infertility from perforation of the appendix. Recall bias, and poor adjustment for confounding variables in some reports, weakened the validity of the studies.", "output": "{\"label\": \"maybe\", \"rationale\": \"The methodologic weaknesses of the studies do not permit acceptance of increased risk of tubal pregnancy or infertility as a consequence of perforation of the appendix, so a causal relationship cannot be supported by the data currently available. Only a well-designed case-control study with unbiased ascertainment of exposure and adjustment for confounding variables will provide a definitive answer.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 10223070, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Histone demethylase recruitment and a transient decrease in histone methylation is necessary for ligand-dependent induction of transcription by nuclear receptors.\n\nCANDIDATE_PASSAGE:\nMolecular mechanisms of ribosomal protein gene coregulation. The 137 ribosomal protein genes (RPGs) of Saccharomyces provide a model for gene coregulation. We examined the positional and functional organization of their regulators (Rap1 [repressor activator protein 1], Fhl1, Ifh1, Sfp1, and Hmo1), the transcription machinery (TFIIB, TFIID, and RNA polymerase II), and chromatin at near-base-pair resolution using ChIP-exo, as RPGs are coordinately reprogrammed. Where Hmo1 is enriched, Fhl1, Ifh1, Sfp1, and Hmo1 cross-linked broadly to promoter DNA in an RPG-specific manner and demarcated by general minor groove widening. Importantly, Hmo1 extended 20-50 base pairs (bp) downstream from Fhl1. Upon RPG repression, Fhl1 remained in place. Hmo1 dissociated, which was coupled to an upstream shift of the +1 nucleosome, as reflected by the Hmo1 extension and core promoter region. Fhl1 and Hmo1 may create two regulatable and positionally distinct barriers, against which chromatin remodelers position the +1 nucleosome into either an activating or a repressive state. Consistent with in vitro studies, we found that specific TFIID subunits, in addition to cross-linking at the core promoter, made precise cross-links at Rap1 sites, which we interpret to reflect native Rap1-TFIID interactions. Our findings suggest how sequence-specific DNA binding regulates nucleosome positioning and transcription complex assembly >300 bp away and how coregulation coevolved with coding sequences.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "525", "doc_id": "11420613", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: High dietary calcium intakes are unnecessary for prevention of secondary hyperparathyroidism in subjects with 25(OH)D levels above 75 nmol/liter.\n\nCANDIDATE_ABSTRACT:\nTITLE: Relationship between serum parathyroid hormone levels, vitamin D sufficiency, and calcium intake.\nABSTRACT: CONTEXT Adequate vitamin D status for optimum bone health has received increased recognition in recent years; however, the ideal intake is not known. Serum 25-hydroxyvitamin D is the generally accepted indicator of vitamin D status, but no universal reference level has been reached. OBJECTIVE To investigate the relative importance of high calcium intake and serum 25-hydroxyvitamin D for calcium homeostasis, as determined by serum intact parathyroid hormone (PTH). DESIGN, SETTING, AND PARTICIPANTS Cross-sectional study of 2310 healthy Icelandic adults who were divided equally into 3 age groups (30-45 years, 50-65 years, or 70-85 years) and recruited from February 2001 to January 2003. They were administered a semi-quantitative food frequency questionnaire, which assessed vitamin D and calcium intake. Participants were further divided into groups according to calcium intake (<800 mg/d, 800-1200 mg/d, and >1200 mg/d) and serum 25-hydroxyvitamin D level (<10 ng/mL, 10-18 ng/mL, and >18 ng/mL). MAIN OUTCOME MEASURE Serum intact PTH as determined by calcium intake and vitamin D. RESULTS A total of 944 healthy participants completed all parts of the study. After adjusting for relevant factors, serum PTH was lowest in the group with a serum 25-hydroxyvitamin D level of more than 18 ng/mL but highest in the group with a serum 25-hydroxyvitamin D level of less than 10 ng/mL. At the low serum 25-hydroxyvitamin D level (<10 ng/mL), calcium intake of less than 800 mg/d vs more than 1200 mg/d was significantly associated with higher serum PTH (P = .04); and at a calcium intake of more than 1200 mg/d, there was a significant difference between the lowest and highest vitamin D groups (P = .04). CONCLUSIONS As long as vitamin D status is ensured, calcium intake levels of mor [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 514, "doc_id": "16256507", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: 53% of perinatal mortality is due to low birth weight.\n\nCANDIDATE_PASSAGE:\nAntidepressant fluoxetine enhances glucocorticoid receptor function in vitro by modulating membrane steroid transporters. 1. Incubation of LMCAT fibroblast cells with antidepressants potentiates glucocorticoid receptor (GR)-mediated gene transcription in the presence of dexamethasone and cortisol, but not of corticosterone. We have shown that antidepressants do so by inhibiting the LMCAT cell membrane steroid transporter (which is virtually identical to the multidrug resistance P-glycoprotein) and thus by increasing dexamethasone or cortisol intracellular concentrations. However, previous experiments with the antidepressant fluoxetine in the presence of dexamethasone have produced negative results (Pariante et al. (2001). Br. J. Pharmacol., 134, 1335-1343). 2. We have since re-examined the effects of fluoxetine on GR-mediated gene transcription in the presence of dexamethasone. Moreover, we have examined the effects of fluoxetine on GR-mediated gene transcription in the presence of cortisol and corticosterone, and on the intracellular accumulation of radioactive cortisol and corticosterone. Finally, we have examined the effects of fluoxetine on inhibition of P-glycoprotein activity in Caco-2 cells. 3. We now find that fluoxetine (1-10 micro M) enhances GR-mediated gene transcription in the presence of dexamethasone and cortisol (+140-170%), but not of corticosterone, and increases the intracellular accumulation of (3)H-cortisol (+5-15%), but not of (3)H-corticosterone. Moreover, fluoxetine (10 micro M) induces approximately 30% inhibition of PGP activity in Caco-2 cells. 4. Our results show that fluoxetine, like other antidepressants, inhibits membrane steroid transporters.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "17", "doc_id": "6083952", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: AMP-activated protein kinase (AMPK) activation reduces inflammation-related fibrosis in the lungs.\n\nCANDIDATE_PASSAGE:\nCDX2 inhibits the proliferation and tumor formation of colon cancer cells by suppressing Wnt/β-catenin signaling via transactivation of GSK-3β and Axin2 expression Caudal-related homeobox transcription factor 2 (CDX2), an intestine-specific nuclear transcription factor, has been strongly implicated in the tumourigenesis of various human cancers. However, the functional role of CDX2 in the development and progression of colorectal cancer (CRC) is not well known. In this study, CDX2 knockdown in colon cancer cells promoted cell proliferation in vitro, accelerated tumor formation in vivo, and induced a cell cycle transition from G0/G1 to S phase, whereas CDX2 overexpression inhibited cell proliferation. TOP/FOP-Flash reporter assay showed that CDX2 knockdown or CDX2 overexpression significantly increased or decreased Wnt signaling activity. Western blot assay showed that downstream targets of Wnt signaling, including β-catenin, cyclin D1 and c-myc, were up-regulated or down-regulated in CDX2-knockdown or CDX2-overexpressing colon cancer cells. In addition, suppression of Wnt signaling by XAV-939 led to a marked suppression of the cell proliferation enhanced by CDX2 knockdown, whereas activation of this signaling by CHIR-99021 significantly enhanced the cell proliferation inhibited by CDX2 overexpression. Dual-luciferase reporter and quantitative chromatin immunoprecipitation (qChIP) assays further confirmed that CDX2 transcriptionally activates glycogen synthase kinase-3β (GSK-3β) and axis inhibition protein 2 (Axin2) expression by directly binding to the promoter of GSK-3β and the upstream enhancer of Axin2. In conclusion, these results indicated that CDX2 inhibits the proliferation and tumor formation of colon cancer cells by suppressing Wnt/β-catenin signaling.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "55", "doc_id": "57783564", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Immune responses in immune cells are geographically segregated.\n\nCANDIDATE_ABSTRACT:\nTITLE: Oncostatin M and leukemia inhibitory factor do not use the same functional receptor in mice.\nABSTRACT: Oncostatin M (OSM) and leukemia inhibitory factor (LIF) are members of the interleukin-6 (IL-6) subfamily of cytokines that use a common signal transducer gp130. Human OSM (hOSM) and LIF share a functional high-affinity receptor that is composed of gp130 and LIF receptor beta subunit (LIFRbeta). A second high-affinity receptor for hOSM was recently found to be formed by gp130 and the hOSM receptor beta subunit. However, the nature of murine OSM (mOSM) and its receptors has remained unknown. Using the recently cloned mOSM cDNA, we produced recombinant mOSM and studied its biological activity and receptor structure. Murine hematopoietic cell lines M1 and DA1.a, an embryonic stem cell line CCE, and Ba/F3 transfectants expressing gp130 and LIFRbeta responded to murine LIF (mLIF) and hOSM equally well, while these cells responded to mOSM only at a 30-fold to 100-fold higher concentration than those of mLIF and hOSM. In contrast, NIH3T3 cells responded to mOSM, but not to mLIF and hOSM. Scatchard plot analyses showed that mOSM bound to gp130 with low-affinity (kd = 2.8 to 4.2 nmol/L) and that the binding affinity did not increase in the presence of LIFRbeta. However, mOSM bound to NIH3T3 cells with high-affinity (kd = 660 pmol/L), whereas mLIF did not bind to NIH3T3 cells at all. These results indicate that unlike hOSM, mOSM and mLIF do not share the same functional receptor, and mOSM delivers signals only through its specific receptor complex. Further studies in mice will define the physiological roles of OSM.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 559, "doc_id": "2053540", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Intake of folic acid (FA) and vitamin B6 (VB6) reduces levels of homocysteine.\n\nCANDIDATE_PASSAGE:\nFolate and vitamin B6 from diet and supplements in relation to risk of coronary heart disease among women. CONTEXT Hyperhomocysteinemia is caused by genetic and lifestyle influences, including low intakes of folate and vitamin B6. However, prospective data relating intake of these vitamins to risk of coronary heart disease (CHD) are not available. OBJECTIVE To examine intakes of folate and vitamin B6 in relation to the incidence of nonfatal myocardial infarction (MI) and fatal CHD. DESIGN Prospective cohort study. SETTING AND PATIENTS In 1980, a total of 80082 women from the Nurses' Health Study with no previous history of cardiovascular disease, cancer, hypercholesterolemia, or diabetes completed a detailed food frequency questionnaire from which we derived usual intake of folate and vitamin B6. MAIN OUTCOME MEASURE Nonfatal MI and fatal CHD confirmed by World Health Organization criteria. RESULTS During 14 years of follow-up, we documented 658 incident cases of nonfatal MI and 281 cases of fatal CHD. After controlling for cardiovascular risk factors, including smoking and hypertension and intake of alcohol, fiber, vitamin E, and saturated, polyunsaturated, and trans fat, the relative risks (RRs) of CHD between extreme quintiles were 0.69 (95% confidence interval [CI], 0.55-0.87) for folate (median intake, 696 microg/d vs 158 microg/d) and 0.67 (95% CI, 0.53-0.85) for vitamin B6 (median intake, 4.6 mg/d vs 1.1 mg/d). Controlling for the same variables, the RR was 0.55 (95% CI, 0.41-0.74) among women in the highest quintile of both folate and vitamin B6 intake compared with the opposite extreme. Risk of CHD was reduced among women who regularly used multiple vitamins (RR=0.76; 95% CI, 0.65-0.90), the major source of folate and vitamin B6, and after excluding [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "646", "doc_id": "12810152", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Forkhead 0 (fox0) transcription factors are involved in cellular differentiation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cell Stem Cell Review FoxO Transcription Factors and Stem Cell Homeostasis: Insights from the Hematopoietic System\nABSTRACT: The forkhead O (FoxO) family of transcription factors participates in diverse physiologic processes, including induction of cell-cycle arrest, stress resistance, differentiation, apoptosis, and metabolism. Several recent studies indicate that FoxO-dependent signaling is required for long-term regenerative potential of the hematopoietic stem cell (HSC) compartment through regulation of HSC response to physiologic oxidative stress, quiescence, and survival. These observations link FoxO function in mammalian systems with the evolutionarily conserved role of FoxO in promotion of stress resistance and longevity in lower phylogenetic systems. Furthermore, these findings have implications for aging in higher organisms and in malignant stem cell biology, and suggest that FoxOs may play an important role in the maintenance and integrity of stem cell compartments in a broad spectrum of tissues.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The forkhead O (FoxO) family of transcription factors participates in diverse physiologic processes, including induction of cell-cycle arrest, stress resistance, differentiation, apoptosis, and metabolism.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 428, "doc_id": "16728949", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Taxation of sugar-sweetened beverages had no effect on the incidence rate of type II diabetes in India.\n\nCANDIDATE_ABSTRACT:\nTITLE: Averting Obesity and Type 2 Diabetes in India through Sugar-Sweetened Beverage Taxation: An Economic-Epidemiologic Modeling Study\nABSTRACT: BACKGROUND Taxing sugar-sweetened beverages (SSBs) has been proposed in high-income countries to reduce obesity and type 2 diabetes. We sought to estimate the potential health effects of such a fiscal strategy in the middle-income country of India, where there is heterogeneity in SSB consumption, patterns of substitution between SSBs and other beverages after tax increases, and vast differences in chronic disease risk within the population. METHODS AND FINDINGS Using consumption and price variations data from a nationally representative survey of 100,855 Indian households, we first calculated how changes in SSB price alter per capita consumption of SSBs and substitution with other beverages. We then incorporated SSB sales trends, body mass index (BMI), and diabetes incidence data stratified by age, sex, income, and urban/rural residence into a validated microsimulation of caloric consumption, glycemic load, overweight/obesity prevalence, and type 2 diabetes incidence among Indian subpopulations facing a 20% SSB excise tax. The 20% SSB tax was anticipated to reduce overweight and obesity prevalence by 3.0% (95% CI 1.6%-5.9%) and type 2 diabetes incidence by 1.6% (95% CI 1.2%-1.9%) among various Indian subpopulations over the period 2014-2023, if SSB consumption continued to increase linearly in accordance with secular trends. However, acceleration in SSB consumption trends consistent with industry marketing models would be expected to increase the impact efficacy of taxation, averting 4.2% of prevalent overweight/obesity (95% CI 2.5-10.0%) and 2.5% (95% CI 1.0-2.8%) of incident type 2 diabetes from 2014-2023. Given current consumption and BMI distributions, our results suggest the largest relative effect would be expected among young rural men, refuting our a [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSION Sustained SSB taxation at a high tax rate could mitigate rising obesity and type 2 diabetes in India among both urban and rural subpopulations.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1144, "doc_id": "10071552", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Upon developing tyrosine-kinase inhibitor resistance, new mutations in epidermal growth factor receptors emerge and cause treatment failure.\n\nCANDIDATE_PASSAGE:\nSubsequent chemotherapy reverses acquired tyrosine kinase inhibitor resistance and restores response to tyrosine kinase inhibitor in advanced non-small-cell lung cancer BACKGROUND Patients with advanced or metastatic non-small cell lung cancer (NSCLC) can develop acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors (TKIs) erlotinib and gefitinib. Here, we report the successful treatment with alternating chemotherapy and TKIs of two cases of advanced NSCLC who developed resistance to TKI. CASE PRESENTATION Two patients with advanced or metastatic NSCLC were treated with palliative chemotherapy followed by erlotinib/gefitinib. When TKI therapy failed, two cycles of chemotherapy were provided, which were followed by re-challenge with erlotinib or gefitinib. CONCLUSION NSCLC patients with acquired TKI resistance should be managed aggressively whenever possible. Subsequent chemotherapy and target treatment is one of the reasonable choices for those with an initial dramatic clinical response with erlotinib/gefitinib treatment. Further studies are warranted to substantiate the association of erlotinib /gefitinib treatment with the efficacy of NSCLC patients with acquired TKI failure.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1346", "doc_id": "9929089", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: TRAP+ osteoclasts regulate mature osteoblast maintenance.\n\nCANDIDATE_ABSTRACT:\nTITLE: PDGF-BB secreted by preosteoclasts induces angiogenesis during coupling with osteogenesis\nABSTRACT: Osteogenesis during bone modeling and remodeling is coupled with angiogenesis. A recent study showed that a specific vessel subtype, strongly positive for CD31 and endomucin (CD31hiEmcnhi), couples angiogenesis and osteogenesis. Here, we found that platelet-derived growth factor-BB (PDGF-BB) secreted by preosteoclasts induces CD31hiEmcnhi vessel formation during bone modeling and remodeling. Mice with depletion of PDGF-BB in the tartrate-resistant acid phosphatase–positive cell lineage show significantly lower trabecular and cortical bone mass, serum and bone marrow PDGF-BB concentrations, and fewer CD31hiEmcnhi vessels compared to wild-type mice. In the ovariectomy (OVX)-induced osteoporotic mouse model, serum and bone marrow levels of PDGF-BB and numbers of CD31hiEmcnhi vessels are significantly lower compared to sham-operated controls. Treatment with exogenous PDGF-BB or inhibition of cathepsin K to increase the number of preosteoclasts, and thus the endogenous levels of PDGF-BB, increases CD31hiEmcnhi vessel number and stimulates bone formation in OVX mice. Thus, pharmacotherapies that increase PDGF-BB secretion from preosteoclasts offer a new therapeutic target for treating osteoporosis by promoting angiogenesis and thus bone formation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Mice with depletion of PDGF-BB in the tartrate-resistant acid phosphatase–positive cell lineage show significantly lower trabecular and cortical bone mass, serum and bone marrow PDGF-BB concentrations, and fewer CD31hiEmcnhi vessels compared to wild-type mice.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1138, "doc_id": "6796297", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The tip of the inner tube of the toxic type VI secretion system (T6SS) antibacterial effector in Escherichia coli (E. coli) carries toxic effector proteins.\n\nCANDIDATE_PASSAGE:\nA view to a kill: the bacterial type VI secretion system. The bacterial type VI secretion system (T6SS) is an organelle that is structurally and mechanistically analogous to an intracellular membrane-attached contractile phage tail. Recent studies determined that a rapid conformational change in the structure of a sheath protein complex propels T6SS spike and tube components along with antibacterial and antieukaryotic effectors out of predatory T6SS(+) cells and into prey cells. The contracted organelle is then recycled in an ATP-dependent process. T6SS is regulated at transcriptional and posttranslational levels, the latter involving detection of membrane perturbation in some species. In addition to directly targeting eukaryotic cells, the T6SS can also target other bacteria coinfecting a mammalian host, highlighting the importance of the T6SS not only for bacterial survival in environmental ecosystems, but also in the context of infection and disease. This review highlights these and other advances in our understanding of the structure, mechanical function, assembly, and regulation of the T6SS.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1274", "doc_id": "27731651", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Lack of FGF21 in mice slows the rate of atherosclerotic plaque formation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Fibroblast Growth Factor 21 Prevents Atherosclerosis by Suppression of Hepatic Sterol Regulatory Element-Binding Protein-2 and Induction of Adiponectin in Mice\nABSTRACT: BACKGROUND Fibroblast growth factor 21 (FGF21) is a metabolic hormone with pleiotropic effects on glucose and lipid metabolism and insulin sensitivity. It acts as a key downstream target of both peroxisome proliferator-activated receptor α and γ, the agonists of which have been used for lipid lowering and insulin sensitization, respectively. However, the role of FGF21 in the cardiovascular system remains elusive. METHODS AND RESULTS The roles of FGF21 in atherosclerosis were investigated by evaluating the impact of FGF21 deficiency and replenishment with recombinant FGF21 in apolipoprotein E(-/-) mice. FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia. Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia. Chronic treatment with adiponectin partially reverses atherosclerosis without obvious effects on hypercholesterolemia in FGF21-deficient apolipoprotein E(-/-) mice. By contrast, the cholesterol-lowering effects of FGF21 are abrogated by hepatic expression of sterol regulatory element-binding protein-2. CONCLUSIONS FGF21 protects against atherosclerosis via fine tuning the multiorgan crosstalk among liver, adipose tissue, and blood vessels.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 683, "doc_id": "9315213", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: TNFAIP3 is a glioblastoma tumor enhancer.\n\nCANDIDATE_PASSAGE:\nSATB1 Expression Governs Epigenetic Repression of PD‐1 in Tumor‐Reactive T Cells &NA; Despite the importance of programmed cell death‐1 (PD‐1) in inhibiting T cell effector activity, the mechanisms regulating its expression remain poorly defined. We found that the chromatin organizer special AT‐rich sequence‐binding protein‐1 (Satb1) restrains PD‐1 expression induced upon T cell activation by recruiting a nucleosome remodeling deacetylase (NuRD) complex to Pdcd1 regulatory regions. Satb1 deficienct T cells exhibited a 40‐fold increase in PD‐1 expression. Tumor‐derived transforming growth factor &bgr; (Tgf‐&bgr;) decreased Satb1 expression through binding of Smad proteins to the Satb1 promoter. Smad proteins also competed with the Satb1‐NuRD complex for binding to Pdcd1 enhancers, releasing Pdcd1 expression from Satb1‐mediated repression, Satb1‐deficient tumor‐reactive T cells lost effector activity more rapidly than wild‐type lymphocytes at tumor beds expressing PD‐1 ligand (CD274), and these differences were abrogated by sustained CD274 blockade. Our findings suggest that Satb1 functions to prevent premature T cell exhaustion by regulating Pdcd1 expression upon T cell activation. Dysregulation of this pathway in tumor‐infiltrating T cells results in diminished anti‐tumor immunity. Graphical Abstract Figure. No caption available. HighlightsT cell activation increased the expression of Satb1 in mature CD8+ and CD4+ T cellsRecruitment of the NuRD repression complex by Satb1 inhibits expression of Pdcd1In tumors, TGF‐&bgr; inhibits Satb1 expression in T cells, increasing Pdcd1 expressionSatb1−/− T cells express high amounts of PD‐1 and have decreased anti‐tumor activity &NA; Stephen et al. show that the chromatin organizer Satb1 controls expression levels of PD [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1134", "doc_id": "5377642", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The genomic aberrations found in matasteses are very similar to those found in the primary tumor.\n\nCANDIDATE_ABSTRACT:\nTITLE: Evolution of metastasis revealed by mutational landscapes of chemically induced skin cancers\nABSTRACT: Human tumors show a high level of genetic heterogeneity, but the processes that influence the timing and route of metastatic dissemination of the subclones are unknown. Here we have used whole-exome sequencing of 103 matched benign, malignant and metastatic skin tumors from genetically heterogeneous mice to demonstrate that most metastases disseminate synchronously from the primary tumor, supporting parallel rather than linear evolution as the predominant model of metastasis. Shared mutations between primary carcinomas and their matched metastases have the distinct A-to-T signature of the initiating carcinogen dimethylbenzanthracene, but non-shared mutations are primarily G-to-T, a signature associated with oxidative stress. The existence of carcinomas that either did or did not metastasize in the same host animal suggests that there are tumor-intrinsic factors that influence metastatic seeding. We also demonstrate the importance of germline polymorphisms in determining allele-specific mutations, and we identify somatic genetic alterations that are specifically related to initiation of carcinogenesis by Hras or Kras mutations. Mouse tumors that mimic the genetic heterogeneity of human cancers can aid our understanding of the clonal evolution of metastasis and provide a realistic model for the testing of novel therapies.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Shared mutations between primary carcinomas and their matched metastases have the distinct A-to-T signature of the initiating carcinogen dimethylbenzanthracene, but non-shared mutations are primarily G-to-T, a signature associated with oxidative stress.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1221, "doc_id": "19736671", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does preoperative dilatation affect the surgical outcome of laparoscopic Heller myotomy and Dor fundoplication for esophageal achalasia?\n\nABSTRACT:\nLaparoscopic Heller myotomy and Dor fundoplication are now widely performed for achalasia. In patients who have had dilatation in the past, inflammation between the esophageal mucosal and muscular layers may make it difficult to perform myotomy. We investigated the effects of preoperative dilatation on the surgical outcomes. : One hundred and twelve patients were divided into 2 groups: 37 patients with a past history of preoperative dilatation and 75 patients who had no history of preoperative dilatation. The operating time, intraoperative blood loss, days required to resume postoperative oral intake, postoperative hospital stay, improvement in dysphagia, and incidence of postoperative esophagitis were compared. The operating time, intraoperative blood loss, postoperative hospital stay, and improvement of dysphagia were no significant differences between these groups. Furthermore, there were no significant differences in the incidence of postoperative esophagitis.", "output": "{\"label\": \"no\", \"rationale\": \"The therapeutic outcome of laparoscopic Heller myotomy and Dor fundoplication is not affected by preoperative pneumatic dilatation.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 19390272, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: CD28 signals regulate trafficking of murine auto-reactive T cells into target tissues.\n\nCANDIDATE_PASSAGE:\nPrison health care: a review of the literature. The prison population is increasing and the health problems of prisoners are considerable. Prison is designed with punishment, correction and rehabilitation to the community in mind and these goals may conflict with the aims of health care. A literature review showed that the main issues in prison health care are mental health, substance abuse and communicable diseases. Women prisoners and older prisoners have needs which are distinct from other prisoners. Health promotion and the health of the community outside prisons are desirable aims of prison health care. The delivery of effective health care to prisoners is dependent upon partnership between health and prison services and telemedicine is one possible mode of delivery.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "201", "doc_id": "20491205", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Overexpressing Cnp1 N-tail variants rescues the temperature-sensitive growth defect of scm3-139.\n\nCANDIDATE_ABSTRACT:\nTITLE: Fission Yeast Scm3: A CENP-A Receptor Required for Integrity of Subkinetochore Chromatin\nABSTRACT: The mechanisms ensuring specific incorporation of CENP-A at centromeres are poorly understood. Mis16 and Mis18 are required for CENP-A localization at centromeres and form a complex that is conserved from fission yeast to human. Fission yeast sim1 mutants that alleviate kinetochore domain silencing are defective in Scm3(Sp), the ortholog of budding yeast Scm3(Sc). Scm3(Sp) depends on Mis16/18 for its centromere localization and like them is recruited to centromeres in late anaphase. Importantly, Scm3(Sp) coaffinity purifies with CENP-A(Cnp1) and associates with CENP-A(Cnp1) in vitro, yet localizes independently of intact CENP-A(Cnp1) chromatin and is differentially released from chromatin. While Scm3(Sc) has been proposed to form a unique hexameric nucleosome with CENP-A(Cse4) and histone H4 at budding yeast point centromeres, we favor a model in which Scm3(Sp) acts as a CENP-A(Cnp1) receptor/assembly factor, cooperating with Mis16 and Mis18 to receive CENP-A(Cnp1) from the Sim3 escort and mediate assembly of CENP-A(Cnp1) into subkinetochore chromatin.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 897, "doc_id": "14338915", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: IRG1 has antiviral effects against neurotropic viruses.\n\nCANDIDATE_PASSAGE:\nDifferential innate immune response programs in neuronal subtypes determine susceptibility to infection in the brain by positive stranded RNA viruses Although susceptibility of neurons in the brain to microbial infection is a major determinant of clinical outcome, little is known about the molecular factors governing this vulnerability. Here we show that two types of neurons from distinct brain regions showed differential permissivity to replication of several positive-stranded RNA viruses. Granule cell neurons of the cerebellum and cortical neurons from the cerebral cortex have unique innate immune programs that confer differential susceptibility to viral infection ex vivo and in vivo. By transducing cortical neurons with genes that were expressed more highly in granule cell neurons, we identified three interferon-stimulated genes (ISGs; Ifi27, Irg1 and Rsad2 (also known as Viperin)) that mediated the antiviral effects against different neurotropic viruses. Moreover, we found that the epigenetic state and microRNA (miRNA)-mediated regulation of ISGs correlates with enhanced antiviral response in granule cell neurons. Thus, neurons from evolutionarily distinct brain regions have unique innate immune signatures, which probably contribute to their relative permissiveness to infection.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "549", "doc_id": "9433958", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pioglitazone use is significantly associated with an increased risk of prostate cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pioglitazone Use and Risk of Bladder Cancer and Other Common Cancers in Persons With Diabetes.\nABSTRACT: IMPORTANCE Studies suggest pioglitazone use may increase risk of cancers. OBJECTIVE To examine whether pioglitazone use for diabetes is associated with risk of bladder and 10 additional cancers. DESIGN, SETTING, AND PARTICIPANTS Cohort and nested case-control analyses among persons with diabetes. A bladder cancer cohort followed 193,099 persons aged 40 years or older in 1997-2002 until December 2012; 464 case patients and 464 matched controls were surveyed about additional confounders. A cohort analysis of 10 additional cancers included 236,507 persons aged 40 years or older in 1997-2005 and followed until June 2012. Cohorts were from Kaiser Permanente Northern California. EXPOSURES Ever use, duration, cumulative dose, and time since initiation of pioglitazone as time dependent. MAIN OUTCOMES AND MEASURES Incident cancer, including bladder, prostate, female breast, lung/bronchus, endometrial, colon, non-Hodgkin lymphoma, pancreas, kidney/renal pelvis, rectum, and melanoma. RESULTS Among 193,099 persons in the bladder cancer cohort, 34,181 (18%) received pioglitazone (median duration, 2.8 years; range, 0.2-13.2 years) and 1261 had incident bladder cancer. Crude incidences of bladder cancer in pioglitazone users and nonusers were 89.8 and 75.9 per 100,000 person-years, respectively. Ever use of pioglitazone was not associated with bladder cancer risk (adjusted hazard ratio [HR], 1.06; 95% CI, 0.89-1.26). Results were similar in case-control analyses (pioglitazone use: 19.6% among case patients and 17.5% among controls; adjusted odds ratio, 1.18; 95% CI, 0.78-1.80). In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95% CI, 1.02-1.26) and p [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95% CI, 1.02-1.26) and pancreatic cancer (HR, 1.41; 95% CI, 1.16-1.71).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 954, "doc_id": "3355397", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: 7-day-old adult Caenorhabditis elegans exhibit approximately 5% of the learning capacity seen in 1-day old adults.\n\nCANDIDATE_PASSAGE:\nRequirement for the ERI/DICER complex in endogenous RNA interference and sperm development in Caenorhabditis elegans. Small regulatory RNAs are key regulators of gene expression. One class of small regulatory RNAs, termed the endogenous small interfering RNAs (endo siRNAs), is thought to negatively regulate cellular transcripts via an RNA interference (RNAi)-like mechanism termed endogenous RNAi (endo RNAi). A complex of proteins composed of ERI-1/3/5, RRF-3, and DICER (the ERI/DICER complex) mediates endo RNAi processes in Caenorhabditis elegans. We conducted a genetic screen to identify additional components of the endo RNAi machinery. Our screen recovered alleles of eri-9, which encodes a novel DICER-interacting protein, and a missense mutation within the helicase domain of DICER [DCR-1(G492R)]. ERI-9(-) and DCR-1(G492) animals exhibit defects in endo siRNA expression and a concomitant failure to regulate mRNAs that exhibit sequence homology to these endo siRNAs, indicating that ERI-9 and the DCR-1 helicase domain function in the C. elegans endo RNAi pathway. We define a subset of Eri mutant animals (including eri-1, rrf-3, eri-3, and dcr-1, but not eri-9 or ergo-1) that exhibit temperature-sensitive, sperm-specific sterility and defects in X chromosome segregation. Among these mutants we find multiple aberrations in sperm development beginning with cytokinesis and extending through terminal differentiation. These results identify novel components of the endo RNAi machinery, demonstrate differential requirements for the Eri factors in the sperm-producing germline, and begin to delineate the functional requirement for the ERI/DICER complex in sperm development.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "19", "doc_id": "22362025", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does perspective-taking increase patient satisfaction in medical encounters?\n\nABSTRACT:\nTo assess whether perspective-taking, which researchers in other fields have shown to induce empathy, improves patient satisfaction in encounters between student-clinicians and standardized patients (SPs). In three studies, randomly assigned students (N = 608) received either a perspective-taking instruction or a neutral instruction prior to a clinical skills examination in 2006-2007. SP satisfaction was the main outcome in all three studies. Study 1 involved 245 third-year medical students from two universities. Studies 2 and 3 extended Study 1 to examine generalizability across student and SP subpopulations. Study 2 (105 physician assistant students, one university) explored the effect of perspective-taking on African American SPs' satisfaction. Study 3 (258 third-year medical students, two universities) examined the intervention's effect on students with high and low baseline perspective-taking tendencies. Intervention students outscored controls in patient satisfaction in all studies: Study 1: P = .01, standardized effect size = 0.16; Study 2: P = .001, standardized effect size = 0.31; Study 3: P = .009, standardized effect size = 0.13. In Study 2, perspective-taking improved African American SPs' satisfaction. In Study 3, intervention students with high baseline perspective-taking tendencies outscored controls (P = .0004, standardized effect size = 0.25), whereas those with low perspective-taking tendencies did not (P = .72, standardized effect size = 0.00).", "output": "{\"label\": \"maybe\", \"rationale\": \"Perspective-taking increased patient satisfaction in all three studies, across medical schools, clinical disciplines, and racially diverse students and SPs. Perspective-taking as a means for improving patient satisfaction deserves further exploration in clinical training and practice.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 20736672, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Side effects associated with antidepressants increases risk of stroke.\n\nCANDIDATE_ABSTRACT:\nTITLE: Quantitative Detection of Hepatitis C Virus RNA by Light Cycler PCR and Comparison with Two Different PCR Assays\nABSTRACT: The new Light Cycler technology was adapted to the detection of hepatitis C virus (HCV) RNA in clinical samples. Sera from 81 patients were tested by Light Cycler PCR, AMPLICOR HCV Monitor assay, and in-house PCR. Our data demonstrate that Light Cycler is a fast and reliable method for the detection and quantitation of HCV RNA.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1084, "doc_id": "285794", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Treatment with the EC uptake inhibitor AM404 resulted in a dose-dependent decrease in the expression of immobility.\n\nCANDIDATE_ABSTRACT:\nTITLE: Functional role of high-affinity anandamide transport, as revealed by selective inhibition.\nABSTRACT: Anandamide, an endogenous ligand for central cannabinoid receptors, is released from neurons on depolarization and rapidly inactivated. Anandamide inactivation is not completely understood, but it may occur by transport into cells or by enzymatic hydrolysis. The compound N-(4-hydroxyphenyl)arachidonylamide (AM404) was shown to inhibit high-affinity anandamide accumulation in rat neurons and astrocytes in vitro, an indication that this accumulation resulted from carrier-mediated transport. Although AM404 did not activate cannabinoid receptors or inhibit anandamide hydrolysis, it enhanced receptor-mediated anandamide responses in vitro and in vivo. The data indicate that carrier-mediated transport may be essential for termination of the biological effects of anandamide, and may represent a potential drug target.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1325, "doc_id": "40476126", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Type 1 Diabetes is associated with subtle perturbations in T reg development.\n\nCANDIDATE_PASSAGE:\nArray-based Comparative Genomic Hybridization for Genome-Wide Screening of DNA Copy Number in Bladder Tumors Genome-wide copy number profiles were characterized in 41 primary bladder tumors using array-based comparative genomic hybridization (array CGH). In addition to previously identified alterations in large chromosomal regions, alterations were identified in many small genomic regions, some with high-level amplifications or homozygous deletions. High-level amplifications were detected for 192 genomic clones, most frequently at 6p22.3 (E2F3), 8p12 (FGFR1), 8q22.2 (CMYC), 11q13 (CCND1, EMS1, INT2), and 19q13.1 (CCNE). Homozygous deletions were detected in 51 genomic clones, with four showing deletions in more than one case: two clones mapping to 9p21.3 (CDKN2A/p16, in nine cases), one at 8p23.1 (three cases), and one at 11p13 (two cases). Significant correlations were observed between copy number gain of clones containing CCNE1 and gain of ERBB2, and between gain of CCND1 and deletion of TP53. In addition, there was a significant complementary association between gain of CCND1 and gain of E2F3. Although there was no significant relationship between copy number changes and tumor stage or grade, the linked behavior among genomic loci suggests that array CGH will be increasingly important in understanding pathways critical to bladder tumor biology.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1334", "doc_id": "2402323", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Sildenafil improves erectile function in men who experience sexual dysfunction as a result of the use of SSRI antidepressants.\n\nCANDIDATE_ABSTRACT:\nTITLE: Treatment of antidepressant-associated sexual dysfunction with sildenafil: a randomized controlled trial.\nABSTRACT: CONTEXT Sexual dysfunction is a common adverse effect of antidepressants that frequently results in treatment noncompliance. OBJECTIVE To assess the efficacy of sildenafil citrate in men with sexual dysfunction associated with the use of selective and nonselective serotonin reuptake inhibitor (SRI) antidepressants. DESIGN, SETTING, AND PATIENTS Prospective, parallel-group, randomized, double-blind, placebo-controlled trial conducted between November 1, 2000, and January 1, 2001, at 3 US university medical centers among 90 male outpatients (mean [SD] age, 45 [8] years) with major depression in remission and sexual dysfunction associated with SRI antidepressant treatment. INTERVENTION Patients were randomly assigned to take sildenafil (n = 45) or placebo (n = 45) at a flexible dose starting at 50 mg and adjustable to 100 mg before sexual activity for 6 weeks. MAIN OUTCOME MEASURES The primary outcome measure was score on the Clinical Global Impression-Sexual Function (CGI-SF); secondary measures were scores on the International Index of Erectile Function, Arizona Sexual Experience Scale, Massachusetts General Hospital-Sexual Functioning Questionnaire, and Hamilton Rating Scale for Depression (HAM-D). RESULTS Among the 90 randomized patients, 93% (83/89) of patients treated per protocol took at least 1 dose of study drug and 85% (76/89) completed week 6 end-point assessments with last observation carried forward analyses. At a CGI-SF score of 2 or lower, 54.5% (24/44) of sildenafil compared with 4.4% (2/45) of placebo patients were much or very much improved (P<.001). Erectile function, arousal, ejaculation, orgasm, and overall satisfaction domain measures improved significantly in sildenafil compared with placebo patients. Mean depression scores remained consi [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"At a CGI-SF score of 2 or lower, 54.5% (24/44) of sildenafil compared with 4.4% (2/45) of placebo patients were much or very much improved (P<.001).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1086, "doc_id": "39281140", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Mice that lack Interferon-γ or its receptor exhibit high resistance to experimental autoimmune myocarditis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Autosomal dominant immune dysregulation syndrome in humans with CTLA4 mutations\nABSTRACT: The protein cytotoxic T lymphocyte antigen-4 (CTLA-4) is an essential negative regulator of immune responses, and its loss causes fatal autoimmunity in mice. We studied a large family in which five individuals presented with a complex, autosomal dominant immune dysregulation syndrome characterized by hypogammaglobulinemia, recurrent infections and multiple autoimmune clinical features. We identified a heterozygous nonsense mutation in exon 1 of CTLA4. Screening of 71 unrelated patients with comparable clinical phenotypes identified five additional families (nine individuals) with previously undescribed splice site and missense mutations in CTLA4. Clinical penetrance was incomplete (eight adults of a total of 19 genetically proven CTLA4 mutation carriers were considered unaffected). However, CTLA-4 protein expression was decreased in regulatory T cells (Treg cells) in both patients and carriers with CTLA4 mutations. Whereas Treg cells were generally present at elevated numbers in these individuals, their suppressive function, CTLA-4 ligand binding and transendocytosis of CD80 were impaired. Mutations in CTLA4 were also associated with decreased circulating B cell numbers. Taken together, mutations in CTLA4 resulting in CTLA-4 haploinsufficiency or impaired ligand binding result in disrupted T and B cell homeostasis and a complex immune dysregulation syndrome.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 781, "doc_id": "857189", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Vitamin D deficiency effects birth weight.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association between maternal serum 25-hydroxyvitamin D level and pregnancy and neonatal outcomes: systematic review and meta-analysis of observational studies.\nABSTRACT: OBJECTIVE To assess the effect of 25-hydroxyvitamin D (25-OHD) levels on pregnancy outcomes and birth variables. DESIGN Systematic review and meta-analysis. DATA SOURCES Medline (1966 to August 2012), PubMed (2008 to August 2012), Embase (1980 to August 2012), CINAHL (1981 to August 2012), the Cochrane database of systematic reviews, and the Cochrane database of registered clinical trials. STUDY SELECTION Studies reporting on the association between serum 25-OHD levels during pregnancy and the outcomes of interest (pre-eclampsia, gestational diabetes, bacterial vaginosis, caesarean section, small for gestational age infants, birth weight, birth length, and head circumference). DATA EXTRACTION Two authors independently extracted data from original research articles, including key indicators of study quality. We pooled the most adjusted odds ratios and weighted mean differences. Associations were tested in subgroups representing different patient characteristics and study quality. RESULTS 3357 studies were identified and reviewed for eligibility. 31 eligible studies were included in the final analysis. Insufficient serum levels of 25-OHD were associated with gestational diabetes (pooled odds ratio 1.49, 95% confidence interval 1.18 to 1.89), pre-eclampsia (1.79, 1.25 to 2.58), and small for gestational age infants (1.85, 1.52 to 2.26). Pregnant women with low serum 25-OHD levels had an increased risk of bacterial vaginosis and low birthweight infants but not delivery by caesarean section. CONCLUSION Vitamin D insufficiency is associated with an increased risk of gestational diabetes, pre-eclampsia, and small for gestational age infants. Pregnant women with low 25-OHD levels had an increased risk of bacterial vaginosis and lower birth weight infants, but not de [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Pregnant women with low 25-OHD levels had an increased risk of bacterial vaginosis and lower birth weight infants, but not delivery by caesarean section.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1367, "doc_id": "2425364", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Citrullinated proteins externalized in neutrophil extracellular traps act indirectly to disrupt the inflammatory cycle.\n\nCANDIDATE_ABSTRACT:\nTITLE: NETs are a source of citrullinated autoantigens and stimulate inflammatory responses in rheumatoid arthritis.\nABSTRACT: The early events leading to the development of rheumatoid arthritis (RA) remain unclear, but formation of autoantibodies to citrullinated protein antigens (ACPAs) is considered a key pathogenic event. Neutrophils isolated from patients with various autoimmune diseases display enhanced neutrophil extracellular trap (NET) formation, a phenomenon that exposes autoantigens in the context of immunostimulatory molecules. We investigated whether aberrant NETosis occurs in RA, determined its triggers, and examined its deleterious inflammatory consequences. Enhanced NETosis was observed in circulating and RA synovial fluid neutrophils compared to neutrophils from healthy controls and from patients with osteoarthritis (OA). Further, netting neutrophils infiltrated RA synovial tissue, rheumatoid nodules, and skin. NETosis correlated with ACPA presence and levels and with systemic inflammatory markers. RA sera and immunoglobulin fractions from RA patients with high levels of ACPA and/or rheumatoid factor significantly enhanced NETosis, and the NETs induced by these autoantibodies displayed distinct protein content. Indeed, during NETosis, neutrophils externalized the citrullinated autoantigens implicated in RA pathogenesis, and anti-citrullinated vimentin antibodies potently induced NET formation. Moreover, the inflammatory cytokines interleukin-17A (IL-17A) and tumor necrosis factor-α (TNF-α) induced NETosis in RA neutrophils. In turn, NETs significantly augmented inflammatory responses in RA and OA synovial fibroblasts, including induction of IL-6, IL-8, chemokines, and adhesion molecules. These observations implicate accelerated NETosis in RA pathogenesis, through externalization of citrullinated autoantigens and immunostimulatory molecules that may promote aberrant [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Indeed, during NETosis, neutrophils externalized the citrullinated autoantigens implicated in RA pathogenesis, and anti-citrullinated vimentin antibodies potently induced NET formation. In turn, NETs significantly augmented inflammatory responses in RA and OA synovial fibroblasts, including induction of IL-6, IL-8, chemokines, and adhesion molecules.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 263, "doc_id": "11328820", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Bariatric surgery increases rates of colorectal cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Yeast sirtuins and the regulation of aging.\nABSTRACT: The sirtuins are a phylogenetically conserved family of NAD(+) -dependent protein deacetylases that consume one molecule of NAD(+) for every deacetylated lysine side chain. Their requirement for NAD(+) potentially makes them prone to regulation by fluctuations in NAD(+) or biosynthesis intermediates, thus linking them to cellular metabolism. The Sir2 protein from Saccharomyces cerevisiae is the founding sirtuin family member and has been well characterized as a histone deacetylase that functions in transcriptional silencing of heterochromatin domains and as a pro-longevity factor for replicative life span (RLS), defined as the number of times a mother cell divides (buds) before senescing. Deleting SIR2 shortens RLS, while increased gene dosage causes extension. Furthermore, Sir2 has been implicated in mediating the beneficial effects of caloric restriction (CR) on life span, not only in yeast, but also in higher eukaryotes. While this paradigm has had its share of disagreements and debate, it has also helped rapidly drive the aging research field forward. S. cerevisiae has four additional sirtuins, Hst1, Hst2, Hst3, and Hst4. This review discusses the function of Sir2 and the Hst homologs in replicative aging and chronological aging, and also addresses how the sirtuins are regulated in response to environmental stresses such as CR.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 164, "doc_id": "1754001", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The tissue surrounding the granuloma in an immune cell induces an anti-inflammatory immune response.\n\nCANDIDATE_ABSTRACT:\nTITLE: Inflammatory signaling in human Tuberculosis granulomas is spatially organized\nABSTRACT: Granulomas are the pathological hallmark of tuberculosis (TB). However, their function and mechanisms of formation remain poorly understood. To understand the role of granulomas in TB, we analyzed the proteomes of granulomas from subjects with tuberculosis in an unbiased manner. Using laser-capture microdissection, mass spectrometry and confocal microscopy, we generated detailed molecular maps of human granulomas. We found that the centers of granulomas have a pro-inflammatory environment that is characterized by the presence of antimicrobial peptides, reactive oxygen species and pro-inflammatory eicosanoids. Conversely, the tissue surrounding the caseum has a comparatively anti-inflammatory signature. These findings are consistent across a set of six human subjects and in rabbits. Although the balance between systemic pro- and anti-inflammatory signals is crucial to TB disease outcome, here we find that these signals are physically segregated within each granuloma. From the protein and lipid snapshots of human and rabbit lesions analyzed here, we hypothesize that the pathologic response to TB is shaped by the precise anatomical localization of these inflammatory pathways during the development of the granuloma.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Conversely, the tissue surrounding the caseum has a comparatively anti-inflammatory signature.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1276, "doc_id": "3475317", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Chenodeoxycholic acid treatment decreases brown adipose tissue activity.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Bile Acid Chenodeoxycholic Acid Increases Human Brown Adipose Tissue Activity.\nABSTRACT: The interest in brown adipose tissue (BAT) as a target to combat metabolic disease has recently been renewed with the discovery of functional BAT in humans. In rodents, BAT can be activated by bile acids, which activate type 2 iodothyronine deiodinase (D2) in BAT via the G-coupled protein receptor TGR5, resulting in increased oxygen consumption and energy expenditure. Here we examined the effects of oral supplementation of the bile acid chenodeoxycholic acid (CDCA) on human BAT activity. Treatment of 12 healthy female subjects with CDCA for 2 days resulted in increased BAT activity. Whole-body energy expenditure was also increased upon CDCA treatment. In vitro treatment of primary human brown adipocytes derived with CDCA or specific TGR5 agonists increased mitochondrial uncoupling and D2 expression, an effect that was absent in human primary white adipocytes. These findings identify bile acids as a target to activate BAT in humans.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Treatment of 12 healthy female subjects with CDCA for 2 days resulted in increased BAT activity.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 250, "doc_id": "1568684", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Clathrin stabilizes the spindle fiber apparatus during mitosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Clathrin is required for the function of the mitotic spindle\nABSTRACT: Clathrin has an established function in the generation of vesicles that transfer membrane and proteins around the cell. The formation of clathrin-coated vesicles occurs continuously in non-dividing cells, but is shut down during mitosis, when clathrin concentrates at the spindle apparatus. Here, we show that clathrin stabilizes fibres of the mitotic spindle to aid congression of chromosomes. Clathrin bound to the spindle directly by the amino-terminal domain of clathrin heavy chain. Depletion of clathrin heavy chain using RNA interference prolonged mitosis; kinetochore fibres were destabilized, leading to defective congression of chromosomes to the metaphase plate and persistent activation of the spindle checkpoint. Normal mitosis was rescued by clathrin triskelia but not the N-terminal domain of clathrin heavy chain, indicating that stabilization of kinetochore fibres was dependent on the unique structure of clathrin. The importance of clathrin for normal mitosis may be relevant to understanding human cancers that involve gene fusions of clathrin heavy chain.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Normal mitosis was rescued by clathrin triskelia but not the N-terminal domain of clathrin heavy chain, indicating that stabilization of kinetochore fibres was dependent on the unique structure of clathrin.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 265, "doc_id": "2033917", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Up-regulation of the p53 pathway and related molecular events speeds cancer progression.\n\nCANDIDATE_ABSTRACT:\nTITLE: Senescent Cells, Tumor Suppression, and Organismal Aging: Good Citizens, Bad Neighbors\nABSTRACT: Cells from organisms with renewable tissues can permanently withdraw from the cell cycle in response to diverse stress, including dysfunctional telomeres, DNA damage, strong mitogenic signals, and disrupted chromatin. This response, termed cellular senescence, is controlled by the p53 and RB tumor suppressor proteins and constitutes a potent anticancer mechanism. Nonetheless, senescent cells acquire phenotypic changes that may contribute to aging and certain age-related diseases, including late-life cancer. Thus, the senescence response may be antagonistically pleiotropic, promoting early-life survival by curtailing the development of cancer but eventually limiting longevity as dysfunctional senescent cells accumulate.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1345, "doc_id": "9559146", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Taking 400mg of α-tocopheryl acetate does not prevent prostate cancer.\n\nCANDIDATE_PASSAGE:\nPoor prognosis in carcinoma is associated with a gene expression signature of aberrant PTEN tumor suppressor pathway activity. Pathway-specific therapy is the future of cancer management. The oncogenic phosphatidylinositol 3-kinase (PI3K) pathway is frequently activated in solid tumors; however, currently, no reliable test for PI3K pathway activation exists for human tumors. Taking advantage of the observation that loss of PTEN, the negative regulator of PI3K, results in robust activation of this pathway, we developed and validated a microarray gene expression signature for immunohistochemistry (IHC)-detectable PTEN loss in breast cancer (BC). The most significant signature gene was PTEN itself, indicating that PTEN mRNA levels are the primary determinant of PTEN protein levels in BC. Some PTEN IHC-positive BCs exhibited the signature of PTEN loss, which was associated to moderately reduced PTEN mRNA levels cooperating with specific types of PIK3CA mutations and/or amplification of HER2. This demonstrates that the signature is more sensitive than PTEN IHC for identifying tumors with pathway activation. In independent data sets of breast, prostate, and bladder carcinoma, prediction of pathway activity by the signature correlated significantly to poor patient outcome. Stathmin, encoded by the signature gene STMN1, was an accurate IHC marker of the signature and had prognostic significance in BC. Stathmin was also pathway-pharmacodynamic in vitro and in vivo. Thus, the signature or its components such as stathmin may be clinically useful tests for stratification of patients for anti-PI3K pathway therapy and monitoring therapeutic efficacy. This study indicates that aberrant PI3K pathway signaling is strongly associated with metastasis and poor survival across c [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1139", "doc_id": "15113221", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Misunderstandings between doctors and patients can lead to non-adherence.\n\nCANDIDATE_ABSTRACT:\nTITLE: CpG island methylation in premalignant stages of gastric carcinoma.\nABSTRACT: There are limited reports on methylation analysis of the premalignant lesions of gastric carcinoma thus far. This is despite the fact that gastric carcinoma is one of the tumors with a high frequency of CpG island hypermethylation. To determine the frequency and timing of hypermethylation during multistep gastric carcinogenesis, non-neoplastic gastric mucosa (n = 118), adenomas (n = 61), and carcinomas (n = 64) were analyzed for their p16, human Mut L homologue 1 (hMLH1), death-associated protein (DAP)-kinase, thromobospondin-1 (THBS1), and tissue inhibitor of metalloproteinase 3 (TIMP-3) methylation status using methylation-specific PCR. Three different classes of methylation behaviors were found in the five tested genes. DAP-kinase was methylated at a similar frequency in all four stages, whereas hMLH1 and p16 were methylated in cancer samples (20.3% and 42.2%, respectively) more frequently than in intestinal metaplasia (6.3% and 2.1%, respectively) or adenomas (9.8% and 11.5%, respectively). However, hMLH1 and p16 were not methylated in chronic gastritis. THBS-1 and TIMP-3 were methylated in all stages but showed a marked increase in hypermethylation frequency from chronic gastritis (10.1% and 14.5%, respectively) to intestinal metaplasia (34.7% and 36.7%, respectively; P < 0.05) and from adenomas (28.3% and 26.7%, respectively) to carcinomas (48.4% and 57.4%, respectively: P < 0.05). The hMLH1, THBS1, and TIMP-3 hypermethylation frequencies were similar in both intestinal metaplasia and adenomas, but the p16 hypermethylation frequency tended to be higher in adenomas (11.5%) than in intestinal metaplasia (2.1%; P = 0.073). The average number of methylated genes was 0.6, 1.1, 1.1, and 2.0 per five genes per sample in chronic gastritis, intestinal metaplasi [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 792, "doc_id": "2494748", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Integrated care is successful at tackling multiple comorbidities.\n\nCANDIDATE_PASSAGE:\nSystematic review of role of bisphosphonates on skeletal morbidity in metastatic cancer. OBJECTIVE To review the evidence for the use of bisphosphonates to reduce skeletal morbidity in cancer patients with bone metastases. DATA SOURCES Electronic databases, scanning reference lists, and consultation with experts and pharmaceutical companies. Foreign language papers were included. STUDY SELECTION Included trials were randomised controlled trials of patients with malignant disease and bone metastases who were treated with oral or intravenous bisphosphonate compared with another bisphosphonate, placebo, or standard care. All trials measured at least one outcome of skeletal morbidity. RESULTS 95 articles were identified; 30 studies fulfilled inclusion criteria. In studies that lasted > or = 6 months, compared with placebo bisphosphonates significantly reduced the odds ratio for fractures (vertebral 0.69, 95% confidence interval 0.57 to 0.84, P < 0.0001; non-vertebral 0.65, 0.54 to 0.79, P < 0.0001; combined 0.65, 0.55 to 0.78, P < 0.0001), radiotherapy (0.67, 0.57 to 0.79, P < 0.0001), and hypercalcaemia (0.54, 0.36 to 0.81, P = 0.003) but not for orthopaedic surgery (0.70, 0.46 to 1.05, P = 0.086) or spinal cord compression (0.71, 0.47 to 1.08, P = 0.113). The reduction in orthopaedic surgery was significant in studies that lasted over a year (0.59, 0.39 to 0.88, P = 0.009). Use of bisphosphonates significantly increased time to first skeletal related event but did not increase survival. Subanalyses showed that most evidence supports use of intravenous aminobisphosphonates. CONCLUSIONS In people with metastatic bone disease bisphosphonates significantly decrease skeletal morbidity, except for spinal cord compression and increased time to first skeletal related [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "648", "doc_id": "17482507", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Genomic aberrations of metastases provide information for targeted therapy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Evolution of metastasis revealed by mutational landscapes of chemically induced skin cancers\nABSTRACT: Human tumors show a high level of genetic heterogeneity, but the processes that influence the timing and route of metastatic dissemination of the subclones are unknown. Here we have used whole-exome sequencing of 103 matched benign, malignant and metastatic skin tumors from genetically heterogeneous mice to demonstrate that most metastases disseminate synchronously from the primary tumor, supporting parallel rather than linear evolution as the predominant model of metastasis. Shared mutations between primary carcinomas and their matched metastases have the distinct A-to-T signature of the initiating carcinogen dimethylbenzanthracene, but non-shared mutations are primarily G-to-T, a signature associated with oxidative stress. The existence of carcinomas that either did or did not metastasize in the same host animal suggests that there are tumor-intrinsic factors that influence metastatic seeding. We also demonstrate the importance of germline polymorphisms in determining allele-specific mutations, and we identify somatic genetic alterations that are specifically related to initiation of carcinogenesis by Hras or Kras mutations. Mouse tumors that mimic the genetic heterogeneity of human cancers can aid our understanding of the clonal evolution of metastasis and provide a realistic model for the testing of novel therapies.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Mouse tumors that mimic the genetic heterogeneity of human cancers can aid our understanding of the clonal evolution of metastasis and provide a realistic model for the testing of novel therapies.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 463, "doc_id": "19736671", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Monoclonal antibody targeting of N-cadherin encourages castration resistance.\n\nCANDIDATE_ABSTRACT:\nTITLE: Increased gene expression of brown fat uncoupling protein (UCP)1 and skeletal muscle UCP2 and UCP3 in MAC16-induced cancer cachexia.\nABSTRACT: Weight loss in cancer cachexia is attributable to decreased food intake and/or enhanced energy expenditure. We investigated the roles of the uncoupling proteins (UCPs) UCPI, -2, and -3 in a murine model of cachexia, the MAC16 adenocarcinoma. Weight fell to 24% below that of non-tumor-bearing controls (P < 0.01) 18 days after MAC16 inoculation, with significant reductions in fat-pad mass (-67%; P < 0.01) and muscle mass (-20%; P < 0.01). Food intake was 26-60% lower (P < 0.01) than in controls on days 17-18. Non-tumor-bearing mice, pair-fed to match MAC16-induced hypophagia, showed less weight loss (10% below controls, P < 0.01; 16% above MAC-16, P < 0.01) and smaller decreases in fat-pad mass (21% below controls, P < 0.01). Core temperature in MAC16 mice was significantly lower (-2.4 degrees C, P < 0.01) than in controls, and pair-feeding had no effect. MAC16 mice showed significantly higher UCP1 mRNA levels in brown adipose tissue (BAT) than in controls (+63%, P < 0.01), and pair-feeding had no effect. UCP2 and -3 expression in BAT did not differ significantly between groups. By contrast, UCP2 mRNA levels in skeletal muscle were comparably increased in both MAC16 and pair-fed groups (respectively, 183 and 163% above controls; both, P < 0.05), with no significant difference between these two groups. Similarly, UCP3 mRNA was significantly higher than controls in both MAC16 (+163%, P < 0.05) and pair-fed (+253%, P < 0.01) groups, with no significant difference between the two experimental groups. Overexpression of UCP1 in BAT in MAC16-bearing mice may be an adaptive response to hypothermia, which is apparently induced by tumor products; increased thermogenesis in BAT could increase total energy expenditure and, thus, contribute to tissue wasting. Increased UCP [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 801, "doc_id": "1507222", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Nonhypertensive people who are 55 years old have a 90% chance of developing hypertension during their lifetime.\n\nCANDIDATE_ABSTRACT:\nTITLE: Residual lifetime risk for developing hypertension in middle-aged women and men: The Framingham Heart Study.\nABSTRACT: CONTEXT The long-term risk for developing hypertension is best described by the lifetime risk statistic. The lifetime risk for hypertension and trends in this risk over time are unknown. OBJECTIVES To estimate the residual lifetime risk for hypertension in older US adults and to evaluate temporal trends in this risk. DESIGN, SETTING, AND PARTICIPANTS Community-based prospective cohort study of 1298 participants from the Framingham Heart Study who were aged 55 to 65 years and free of hypertension at baseline (1976-1998). MAIN OUTCOME MEASURES Residual lifetime risk (lifetime cumulative incidence not adjusted for competing causes of mortality) for hypertension, defined as blood pressure of 140/90 mm Hg or greater or use of antihypertensive medications. RESULTS The residual lifetime risks for developing hypertension and stage 1 high blood pressure or higher (greater-than-or-equal to 140/90 mm Hg regardless of treatment) were 90% in both 55- and 65-year-old participants. The lifetime probability of receiving antihypertensive medication was 60%. The risk for hypertension remained unchanged for women, but it was approximately 60% higher for men in the contemporary 1976-1998 period compared with an earlier 1952-1975 period. In contrast, the residual lifetime risk for stage 2 high blood pressure or higher (greater-than-or-equal to 160/100 mm Hg regardless of treatment) was considerably lower in both sexes in the recent period (35%-57% in 1952-1975 vs 35%-44% in 1976-1998), likely due to a marked increase in treatment of individuals with substantially elevated blood pressure. CONCLUSION The residual lifetime risk for hypertension for middle-aged and elderly individuals is 90%, indicating a huge public health burden. Although the decline in lifetime risk for stage 2 h [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSION The residual lifetime risk for hypertension for middle-aged and elderly individuals is 90%, indicating a huge public health burden.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 854, "doc_id": "12206390", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Active Ly49Q prevents neutrophil polarization.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Ly49Q receptor plays a crucial role in neutrophil polarization and migration by regulating raft trafficking.\nABSTRACT: Neutrophils rapidly undergo polarization and directional movement to infiltrate the sites of infection and inflammation. Here, we show that an inhibitory MHC I receptor, Ly49Q, was crucial for the swift polarization of and tissue infiltration by neutrophils. During the steady state, Ly49Q inhibited neutrophil adhesion by preventing focal-complex formation, likely by inhibiting Src and PI3 kinases. However, in the presence of inflammatory stimuli, Ly49Q mediated rapid neutrophil polarization and tissue infiltration in an ITIM-domain-dependent manner. These opposite functions appeared to be mediated by distinct use of effector phosphatase SHP-1 and SHP-2. Ly49Q-dependent polarization and migration were affected by Ly49Q regulation of membrane raft functions. We propose that Ly49Q is pivotal in switching neutrophils to their polarized morphology and rapid migration upon inflammation, through its spatiotemporal regulation of membrane rafts and raft-associated signaling molecules.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Here, we show that an inhibitory MHC I receptor, Ly49Q, was crucial for the swift polarization of and tissue infiltration by neutrophils.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 77, "doc_id": "5531479", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cancers that initially benefit from epidermal growth factor receptor targeted therapies later become refractory through several mechanisms.\n\nCANDIDATE_ABSTRACT:\nTITLE: The quest to overcome resistance to EGFR-targeted therapies in cancer\nABSTRACT: All patients with metastatic lung, colorectal, pancreatic or head and neck cancers who initially benefit from epidermal growth factor receptor (EGFR)-targeted therapies eventually develop resistance. An increasing understanding of the number and complexity of resistance mechanisms highlights the Herculean challenge of killing tumors that are resistant to EGFR inhibitors. Our growing knowledge of resistance pathways provides an opportunity to develop new mechanism-based inhibitors and combination therapies to prevent or overcome therapeutic resistance in tumors. We present a comprehensive review of resistance pathways to EGFR-targeted therapies in lung, colorectal and head and neck cancers and discuss therapeutic strategies that are designed to circumvent resistance.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"All patients with metastatic lung, colorectal, pancreatic or head and neck cancers who initially benefit from epidermal growth factor receptor (EGFR)-targeted therapies eventually develop resistance.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 227, "doc_id": "26973393", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Cancer-associated fibroblasts (CAFs) interact with cancer cells to mediate formation and activation of CAFs.\n\nCANDIDATE_PASSAGE:\nAll dosage compensation is local: Gene-by-gene regulation of sex-biased expression on the chicken Z chromosome Recent reports have suggested that birds lack a mechanism of wholesale dosage compensation for the Z sex chromosome. This discovery was rather unexpected, as all other animals investigated with chromosomal mechanisms of sex determination have some method to counteract the effects of gene dosage of the dominant sex chromosome in males and females. Despite the lack of a global mechanism of avian dosage compensation, the pattern of gene expression difference between males and females varies a great deal for individual Z-linked genes. This suggests that some genes may be individually dosage compensated, and that some less-than-global pattern of dosage compensation, such as local or temporal, exists on the avian Z chromosome. We used global gene expression profiling in males and females for both somatic and gonadal tissue at several time points in the life cycle of the chicken to assess the pattern of sex-biased gene expression on the Z chromosome. Average fold-change between males and females varied somewhat among tissue time-point combinations, with embryonic brain samples having the smallest gene dosage effects, and adult gonadal tissue having the largest degree of male bias. Overall, there were no neighborhoods of overall dosage compensation along the Z. Taken together, this suggests that dosage compensation is regulated on the Z chromosome entirely on a gene-by-gene level, and can vary during the life cycle and by tissue type. This regulation may be an indication of how critical a given gene's functionality is, as the expression level for essential genes will be tightly regulated in order to avoid perturbing important pathways and networks with diff [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "226", "doc_id": "12232678", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Increased vessel density along with a reduction in fibrosis improves the efficacy of chemotherapy treatments.\n\nCANDIDATE_PASSAGE:\nHyaluronan impairs vascular function and drug delivery in a mouse model of pancreatic cancer OBJECTIVE Pancreatic ductal adenocarcinoma (PDA) is characterised by stromal desmoplasia and vascular dysfunction, which critically impair drug delivery. This study examines the role of an abundant extracellular matrix component, the megadalton glycosaminoglycan hyaluronan (HA), as a novel therapeutic target in PDA. METHODS Using a genetically engineered mouse model of PDA, the authors enzymatically depleted HA by a clinically formulated PEGylated human recombinant PH20 hyaluronidase (PEGPH20) and examined tumour perfusion, vascular permeability and drug delivery. The preclinical utility of PEGPH20 in combination with gemcitabine was assessed by short-term and survival studies. RESULTS PEGPH20 rapidly and sustainably depleted HA, inducing the re-expansion of PDA blood vessels and increasing the intratumoral delivery of two chemotherapeutic agents, doxorubicin and gemcitabine. Moreover, PEGPH20 triggered fenestrations and interendothelial junctional gaps in PDA tumour endothelia and promoted a tumour-specific increase in macromolecular permeability. Finally, combination therapy with PEGPH20 and gemcitabine led to inhibition of PDA tumour growth and prolonged survival over gemcitabine monotherapy, suggesting immediate clinical utility. CONCLUSIONS The authors demonstrate that HA impedes the intratumoral vasculature in PDA and propose that its enzymatic depletion be explored as a means to improve drug delivery and response in patients with pancreatic cancer.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "620", "doc_id": "2565138", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Phase information is useful for predicting donor-recipient matches in organ transplantation.\n\nCANDIDATE_ABSTRACT:\nTITLE: MHC Haplotype Matching for Unrelated Hematopoietic Cell Transplantation\nABSTRACT: Background Current criteria for the selection of unrelated donors for hematopoietic cell transplantation (HCT) include matching for the alleles of each human leukocyte antigen (HLA) locus within the major histocompatibility complex (MHC). Graft-versus-host disease (GVHD), however, remains a significant and potentially life-threatening complication even after HLA-identical unrelated HCT. The MHC harbors more than 400 genes, but the total number of transplantation antigens is unknown. Genes that influence transplantation outcome could be identified by using linkage disequilibrium (LD)-mapping approaches, if the extended MHC haplotypes of the unrelated donor and recipient could be defined.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Genes that influence transplantation outcome could be identified by using linkage disequilibrium (LD)-mapping approaches, if the extended MHC haplotypes of the unrelated donor and recipient could be defined.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 942, "doc_id": "11527199", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Articles published in open access format are less likely to be cited than traditional journals.\n\nCANDIDATE_PASSAGE:\nOpen Access Increases Citation Rate PLoS Biology publishes today a research article by Gunther Eysenbach that is not about biology. It is about citations. It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles. As such, it adds objective support to the belief we have always held that open-access publication speeds up scientific dialog between researchers and, consequently, should be extended to the whole scientific literature as quickly as possible. It is therefore fitting that we publish such a paper. We have long argued that papers freely available in a journal will be more often read and cited than those behind a subscription barrier. However, solid evidence to support or refute such a claim has been surprisingly hard to find. Since most open-access journals are new, comparisons of the effects of open access with established subscription-based journals are easily confounded by age and reputation. In the current study, Eysenbach compared citations compiled by Thomson Scientific (formerly Thomson ISI) to individual articles published between June 2004 and December 2004 in the same journal—namely, Proceedings of the National Academy of Sciences (PNAS), which announced its open-access option for authors on June 8 of that year, with an associated publication charge of US$1,000. Non-OA articles in PNAS are subject to a six-month “toll-access” delay before the article becomes publicly available. The results of this natural experiment are clear: in the 4 to 16 months following publication, OA articles gained a significant citation advantage over non-OA articles during the same period. They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely be [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "129", "doc_id": "27768226", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Early patent ductus ateriosus (PDA) screening decreases in-hospital mortality.\n\nCANDIDATE_PASSAGE:\nClinical benefits and considerations of bisphosphonate treatment in metastatic bone disease. Patients with metastatic bone disease are at risk for developing skeletal-related events that can negatively influence quality of life, contributing to loss of autonomy and functional capabilities. Bisphosphonates have become an important component in the treatment of patients with bone metastases as they delay the onset and reduce the risk of skeletal-related events and also palliate or control bone pain in multiple cancer types, thus preserving quality of life. Zoledronic acid has proven efficacy and safety in patients with bone lesions from breast cancer, prostate cancer, lung cancer, and other solid tumors, as well as in patients with multiple myeloma. Current data suggest that early treatment with zoledronic acid (before the onset of bone pain) may provide additional clinical benefits and also positive effects on survival in subsets of patients who have elevated levels of N-telopeptide of type I collagen (NTX), a biochemical marker of bone resorption. Studies have shown that in patients with breast cancer, prostate cancer, lung cancer, or other solid tumors, normalization of elevated levels of NTX was observed in the majority of patients who received zoledronic acid. Furthermore, normalization of NTX values correlated with extended survival.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "367", "doc_id": "24873253", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Enhanced early production of inflammatory chemokines damages viral control in the lung.\n\nCANDIDATE_ABSTRACT:\nTITLE: Memory CD4+ T cells induce innate responses independently of pathogen\nABSTRACT: Inflammation induced by recognition of pathogen-associated molecular patterns markedly affects subsequent adaptive responses. We asked whether the adaptive immune system can also affect the character and magnitude of innate inflammatory responses. We found that the response of memory, but not naive, CD4+ T cells enhances production of multiple innate inflammatory cytokines and chemokines (IICs) in the lung and that, during influenza infection, this leads to early control of virus. Memory CD4+ T cell–induced IICs and viral control require cognate antigen recognition and are optimal when memory cells are either T helper type 1 (TH1) or TH17 polarized but are independent of interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) production and do not require activation of conserved pathogen recognition pathways. This represents a previously undescribed mechanism by which memory CD4+ T cells induce an early innate response that enhances immune protection against pathogens.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We found that the response of memory, but not naive, CD4+ T cells enhances production of multiple innate inflammatory cytokines and chemokines (IICs) in the lung and that, during influenza infection, this leads to early control of virus.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 379, "doc_id": "19005293", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In breast cancer, the loss of myoepithelial cells slows the transition of ductal carcinoma in situ to invasive carcinoma.\n\nCANDIDATE_ABSTRACT:\nTITLE: Bayesian measures of model complexity and fit\nABSTRACT: Summary. We consider the problem of comparing complex hierarchical models in which the number of parameters is not clearly defined. Using an information theoretic argument we derive a measure pD for the effective number of parameters in a model as the difference between the posterior mean of the deviance and the deviance at the posterior means of the parameters of interest. In general pD approximately corresponds to the trace of the product of Fisher's information and the posterior covariance, which in normal models is the trace of the ‘hat’ matrix projecting observations onto fitted values. Its properties in exponential families are explored. The posterior mean deviance is suggested as a Bayesian measure of fit or adequacy, and the contributions of individual observations to the fit and complexity can give rise to a diagnostic plot of deviance residuals against leverages. Adding pD to the posterior mean deviance gives a deviance information criterion for comparing models, which is related to other information criteria and has an approximate decision theoretic justification. The procedure is illustrated in some examples, and comparisons are drawn with alternative Bayesian and classical proposals. Throughout it is emphasized that the quantities required are trivial to compute in a Markov chain Monte Carlo analysis.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 571, "doc_id": "70115", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: RUNX is not expressed in skin tissue.\n\nCANDIDATE_PASSAGE:\nProduction of cloned mice and ES cells from adult somatic cells by nuclear transfer: how to improve cloning efficiency? Although it has now been 10 years since the first cloned mammals were generated from somatic cells using nuclear transfer (NT), most cloned embryos usually undergo developmental arrest prior to or soon after implantation, and the success rate for producing live offspring by cloning remains below 5%. The low success rate is believed to be associated with epigenetic errors, including abnormal DNA hypermethylation, but the mechanism of \"reprogramming\" is unclear. We have been able to develop a stable NT method in the mouse in which donor nuclei are directly injected into the oocyte using a piezo-actuated micromanipulator. Especially in the mouse, only a few laboratories can make clones from adult somatic cells, and cloned mice are never successfully produced from most mouse strains. However, this technique promises to be an important tool for future research in basic biology. For example, NT can be used to generate embryonic stem (NT-ES) cell lines from a patient's own somatic cells. We have shown that NT-ES cells are equivalent to ES cells derived from fertilized embryos and that they can be generated relatively easily from a variety of mouse genotypes and cell types of both sexes, even though it may be more difficult to generate clones directly. In general, NT-ES cell techniques are expected to be applied to regenerative medicine; however, this technique can also be applied to the preservation of genetic resources of mouse strain instead of embryos, oocytes and spermatozoa. This review describes how to improve cloning efficiency and NT-ES cell establishment and further applications.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1008", "doc_id": "22490293", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Smc5/6 engagment halts the activation of SUMO E3 ligase Mms21 by ATP-dependent remolding.\n\nCANDIDATE_ABSTRACT:\nTITLE: The atypical antipsychotic olanzapine causes weight gain by targeting serotonin receptor 2C.\nABSTRACT: Atypical antipsychotics such as olanzapine often induce excessive weight gain and type 2 diabetes. However, the mechanisms underlying these drug-induced metabolic perturbations remain poorly understood. Here, we used an experimental model that reproduces olanzapine-induced hyperphagia and obesity in female C57BL/6 mice. We found that olanzapine treatment acutely increased food intake, impaired glucose tolerance, and altered physical activity and energy expenditure in mice. Furthermore, olanzapine-induced hyperphagia and weight gain were blunted in mice lacking the serotonin 2C receptor (HTR2C). Finally, we showed that treatment with the HTR2C-specific agonist lorcaserin suppressed olanzapine-induced hyperphagia and weight gain. Lorcaserin treatment also improved glucose tolerance in olanzapine-fed mice. Collectively, our studies suggest that olanzapine exerts some of its untoward metabolic effects via antagonism of HTR2C.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1090, "doc_id": "1428830", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: ITAM phosphorylation allows for the transfer of the T cell receptor (TCR) signal from the echo-domain to the cytoplasmic tail of the T cell receptor (TCR).\n\nCANDIDATE_ABSTRACT:\nTITLE: Full activation of the T cell receptor requires both clustering and conformational changes at CD3.\nABSTRACT: T cell receptor (TCR-CD3) triggering involves both receptor clustering and conformational changes at the cytoplasmic tails of the CD3 subunits. The mechanism by which TCRalphabeta ligand binding confers conformational changes to CD3 is unknown. By using well-defined ligands, we showed that induction of the conformational change requires both multivalent engagement and the mobility restriction of the TCR-CD3 imposed by the plasma membrane. The conformational change is elicited by cooperative rearrangements of two TCR-CD3 complexes and does not require accompanying changes in the structure of the TCRalphabeta ectodomains. This conformational change at CD3 reverts upon ligand dissociation and is required for T cell activation. Thus, our permissive geometry model provides a molecular mechanism that rationalizes how the information of ligand binding to TCRalphabeta is transmitted to the CD3 subunits and to the intracellular signaling machinery.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 550, "doc_id": "33499189", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Long chain polyunsaturated fatty acids supplementation is associated with lower rates of atopic eczema at 1 year.\n\nCANDIDATE_PASSAGE:\nLong-term effects of continuing adjuvant tamoxifen to 10 years versus stopping at 5 years after diagnosis of oestrogen receptor-positive breast cancer: ATLAS, a randomised trial BACKGROUND For women with oestrogen receptor (ER)-positive early breast cancer, treatment with tamoxifen for 5 years substantially reduces the breast cancer mortality rate throughout the first 15 years after diagnosis. We aimed to assess the further effects of continuing tamoxifen to 10 years instead of stopping at 5 years. METHODS In the worldwide Adjuvant Tamoxifen: Longer Against Shorter (ATLAS) trial, 12,894 women with early breast cancer who had completed 5 years of treatment with tamoxifen were randomly allocated to continue tamoxifen to 10 years or stop at 5 years (open control). Allocation (1:1) was by central computer, using minimisation. After entry (between 1996 and 2005), yearly follow-up forms recorded any recurrence, second cancer, hospital admission, or death. We report effects on breast cancer outcomes among the 6846 women with ER-positive disease, and side-effects among all women (with positive, negative, or unknown ER status). Long-term follow-up still continues. This study is registered, number ISRCTN19652633. FINDINGS Among women with ER-positive disease, allocation to continue tamoxifen reduced the risk of breast cancer recurrence (617 recurrences in 3428 women allocated to continue vs 711 in 3418 controls, p=0·002), reduced breast cancer mortality (331 deaths vs 397 deaths, p=0·01), and reduced overall mortality (639 deaths vs 722 deaths, p=0·01). The reductions in adverse breast cancer outcomes appeared to be less extreme before than after year 10 (recurrence rate ratio [RR] 0·90 [95% CI 0·79–1·02] during years 5–9 and 0·75 [0·62–0·90] in later years; breast ca [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "709", "doc_id": "12438901", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Men are more susceptible to death due to pneumonia when compared to women.\n\nCANDIDATE_PASSAGE:\nSpecificity of the dRP/AP lyase of Ku promotes nonhomologous end joining (NHEJ) fidelity at damaged ends. Nonhomologous end joining (NHEJ) is essential for efficient repair of chromosome breaks. However, the NHEJ ligation step is often obstructed by break-associated nucleotide damage, including base loss (abasic site or 5'-dRP/AP sites). Ku, a 5'-dRP/AP lyase, can excise such damage at ends in preparation for the ligation step. We show here that this activity is greatest if the abasic site is within a short 5' overhang, when this activity is necessary and sufficient to prepare such termini for ligation. In contrast, Ku is less active near 3' strand termini, where excision would leave a ligation-blocking α,β-unsaturated aldehyde. The Ku AP lyase activity is also strongly suppressed by as little as two paired bases 5' of the abasic site. Importantly, in vitro end joining experiments show that abasic sites significantly embedded in double-stranded DNA do not block the NHEJ ligation step. Suppression of the excision activity of Ku in this context therefore is not essential for ligation and further helps NHEJ retain terminal sequence in junctions. We show that the DNA between the 5' terminus and the abasic site can also be retained in junctions formed by cellular NHEJ, indicating that these sites are at least partly resistant to other abasic site-cleaving activities as well. High levels of the 5'-dRP/AP lyase activity of Ku are thus restricted to substrates where excision of an abasic site is required for ligation, a degree of specificity that promotes more accurate joining.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "767", "doc_id": "20821402", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Diminished ovarian reserve is a reliable indicator of infertility in a non-infertile population.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\nABSTRACT: Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential. Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age. Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area. Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH. Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle). Conception was defined as a positive pregnancy test result. Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis. After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively). Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cy [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 349, "doc_id": "13497630", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Diabetes remission occurs more in people treated with conventional therapy than in people treated with laparoscopic adjustable gastric banding surgery.\n\nCANDIDATE_ABSTRACT:\nTITLE: Adjustable gastric banding and conventional therapy for type 2 diabetes: a randomized controlled trial.\nABSTRACT: CONTEXT Observational studies suggest that surgically induced loss of weight may be effective therapy for type 2 diabetes. OBJECTIVE To determine if surgically induced weight loss results in better glycemic control and less need for diabetes medications than conventional approaches to weight loss and diabetes control. DESIGN, SETTING, AND PARTICIPANTS Unblinded randomized controlled trial conducted from December 2002 through December 2006 at the University Obesity Research Center in Australia, with general community recruitment to established treatment programs. Participants were 60 obese patients (BMI >30 and <40) with recently diagnosed (<2 years) type 2 diabetes. INTERVENTIONS Conventional diabetes therapy with a focus on weight loss by lifestyle change vs laparoscopic adjustable gastric banding with conventional diabetes care. MAIN OUTCOME MEASURES Remission of type 2 diabetes (fasting glucose level <126 mg/dL [7.0 mmol/L] and glycated hemoglobin [HbA1c] value <6.2% while taking no glycemic therapy). Secondary measures included weight and components of the metabolic syndrome. Analysis was by intention-to-treat. RESULTS Of the 60 patients enrolled, 55 (92%) completed the 2-year follow-up. Remission of type 2 diabetes was achieved by 22 (73%) in the surgical group and 4 (13%) in the conventional-therapy group. Relative risk of remission for the surgical group was 5.5 (95% confidence interval, 2.2-14.0). Surgical and conventional-therapy groups lost a mean (SD) of 20.7% (8.6%) and 1.7% (5.2%) of weight, respectively, at 2 years (P < .001). Remission of type 2 diabetes was related to weight loss (R2 = 0.46, P < .001) and lower baseline HbA1c levels (combined R2 = 0.52, P < .001). There were no serious complications in either group. CONCLUSIONS Participants r [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Remission of type 2 diabetes was achieved by 22 (73%) in the surgical group and 4 (13%) in the conventional-therapy group.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 341, "doc_id": "7098463", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: There is a positive correlation between hip fractures and statin use.\n\nCANDIDATE_ABSTRACT:\nTITLE: HMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients.\nABSTRACT: CONTEXT Recent animal studies have found that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) lipid-lowering drugs (statins) substantially increase bone formation, but whether statin use in humans results in clinically meaningful bone formation or a reduction in the risk of osteoporotic fractures is not known. OBJECTIVE To determine whether the use of statins is associated with reduced hip fracture risk. DESIGN Case-control study. SETTING AND PATIENTS A total of 6110 New Jersey residents aged 65 years or older and enrolled in Medicare and either Medicaid or the Pharmacy Assistance for the Aged and Disabled program. Case patients (n=1222) underwent surgical repair of a hip fracture in 1994. Control patients (n=4888) were identified at a ratio of 4:1 and frequency-matched to case patients for age and sex. MAIN OUTCOME MEASURE Adjusted odds ratio (OR) of hip fracture by statin use in the 180 days and 3 years prior to the index date (the earliest date of admission for surgery), adjusted for demographic and clinical characteristics and health care utilization. RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus. No significant relationship was observed between use of nonstatin lipid-lowering agents and hip fracture risk. Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowe [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowering agents.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1288, "doc_id": "4687948", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: M. stadtmanae induces ASC speck formation in BlaER1 monocytes.\n\nCANDIDATE_PASSAGE:\nT cell receptor ligation induces the formation of dynamically regulated signaling assemblies Tcell antigen receptor (TCR) ligation initiates tyrosine kinase activation, signaling complex assembly, and immune synapse formation. Here, we studied the kinetics and mechanics of signaling complex formation in live Jurkat leukemic T cells using signaling proteins fluorescently tagged with variants of enhanced GFP (EGFP). Within seconds of contacting coverslips coated with stimulatory antibodies, T cells developed small, dynamically regulated clusters which were enriched in the TCR, phosphotyrosine, ZAP-70, LAT, Grb2, Gads, and SLP-76, excluded the lipid raft marker enhanced yellow fluorescent protein–GPI, and were competent to induce calcium elevations. LAT, Grb2, and Gads were transiently associated with the TCR. Although ZAP-70–containing clusters persisted for more than 20 min, photobleaching studies revealed that ZAP-70 continuously dissociated from and returned to these complexes. Strikingly, SLP-76 translocated to a perinuclear structure after clustering with the TCR. Our results emphasize the dynamically changing composition of signaling complexes and indicate that these complexes can form within seconds of TCR engagement, in the absence of either lipid raft aggregation or the formation of a central TCR-rich cluster.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "733", "doc_id": "2825380", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: There is no known interaction between Pioneer factor OCT3/4 and major chromatin remodeling factors.\n\nCANDIDATE_ABSTRACT:\nTITLE: An Oct4-Centered Protein Interaction Network in Embryonic Stem Cells\nABSTRACT: Transcription factors, such as Oct4, are critical for establishing and maintaining pluripotent cell identity. Whereas the genomic locations of several pluripotency transcription factors have been reported, the spectrum of their interaction partners is underexplored. Here, we use an improved affinity protocol to purify Oct4-interacting proteins from mouse embryonic stem cells (ESCs). Subsequent purification of Oct4 partners Sall4, Tcfcp2l1, Dax1, and Esrrb resulted in an Oct4 interactome of 166 proteins, including transcription factors and chromatin-modifying complexes with documented roles in self-renewal, but also many factors not previously associated with the ESC network. We find that Esrrb associated with the basal transcription machinery and also detect interactions between transcription factors and components of the TGF-beta, Notch, and Wnt signaling pathways. Acute depletion of Oct4 reduced binding of Tcfcp2l1, Dax1, and Esrrb to several target genes. In conclusion, our purification protocol allowed us to bring greater definition to the circuitry controlling pluripotent cell identity.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Subsequent purification of Oct4 partners Sall4, Tcfcp2l1, Dax1, and Esrrb resulted in an Oct4 interactome of 166 proteins, including transcription factors and chromatin-modifying complexes with documented roles in self-renewal, but also many factors not previously associated with the ESC network.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1294, "doc_id": "30507607", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: In mouse models, the loss of CSF1R facilitates MOZ-TIF2-induced leuekmogenesis.\n\nCANDIDATE_ABSTRACT:\nTITLE: PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2\nABSTRACT: Leukemias and other cancers possess self-renewing stem cells that help to maintain the cancer. Cancer stem cell eradication is thought to be crucial for successful anticancer therapy. Using an acute myeloid leukemia (AML) model induced by the leukemia-associated monocytic leukemia zinc finger (MOZ)-TIF2 fusion protein, we show here that AML can be cured by the ablation of leukemia stem cells. The MOZ fusion proteins MOZ-TIF2 and MOZ-CBP interacted with the transcription factor PU.1 to stimulate the expression of macrophage colony–stimulating factor receptor (CSF1R, also known as M-CSFR, c-FMS or CD115). Studies using PU.1-deficient mice showed that PU.1 is essential for the ability of MOZ-TIF2 to establish and maintain AML stem cells. Cells expressing high amounts of CSF1R (CSF1Rhigh cells), but not those expressing low amounts of CSF1R (CSF1Rlow cells), showed potent leukemia-initiating activity. Using transgenic mice expressing a drug-inducible suicide gene controlled by the CSF1R promoter, we cured AML by ablation of CSF1Rhigh cells. Moreover, induction of AML was suppressed in CSF1R-deficient mice and CSF1R inhibitors slowed the progression of MOZ-TIF2–induced leukemia. Thus, in this subtype of AML, leukemia stem cells are contained within the CSF1Rhigh cell population, and we suggest that targeting of PU.1-mediated upregulation of CSF1R expression might be a useful therapeutic approach.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Moreover, induction of AML was suppressed in CSF1R-deficient mice and CSF1R inhibitors slowed the progression of MOZ-TIF2–induced leukemia.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 578, "doc_id": "8764879", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Pretreatment with the Arp2/3 inhibitor CK-666 affects lamelliopodia formation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Characterization of two classes of small molecule inhibitors of Arp2/3 complex\nABSTRACT: Polymerization of actin filaments directed by the actin-related protein (Arp)2/3 complex supports many types of cellular movements. However, questions remain regarding the relative contributions of Arp2/3 complex versus other mechanisms of actin filament nucleation to processes such as path finding by neuronal growth cones; this is because of the lack of simple methods to inhibit Arp2/3 complex reversibly in living cells. Here we describe two classes of small molecules that bind to different sites on the Arp2/3 complex and inhibit its ability to nucleate actin filaments. CK-0944636 binds between Arp2 and Arp3, where it appears to block movement of Arp2 and Arp3 into their active conformation. CK-0993548 inserts into the hydrophobic core of Arp3 and alters its conformation. Both classes of compounds inhibit formation of actin filament comet tails by Listeria and podosomes by monocytes. Two inhibitors with different mechanisms of action provide a powerful approach for studying the Arp2/3 complex in living cells.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 967, "doc_id": "2119889", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Sn is present on mature DCs during inflammation in vivo.\n\nCANDIDATE_PASSAGE:\nQuercetin attenuates vascular calcification by inhibiting oxidative stress and mitochondrial fission. Vascular calcification is a strong independent predictor of increased cardiovascular morbidity and mortality and has a high prevalence among patients with chronic kidney disease. The present study investigated the effects of quercetin on vascular calcification caused by oxidative stress and abnormal mitochondrial dynamics both in vitro and in vivo. Calcifying vascular smooth muscle cells (VSMCs) treated with inorganic phosphate (Pi) exhibited mitochondrial dysfunction, as demonstrated by decreased mitochondrial potential and ATP production. Disruption of mitochondrial structural integrity was also observed in a rat model of adenine-induced aortic calcification. Increased production of reactive oxygen species, enhanced expression and phosphorylation of Drp1, and excessive mitochondrial fragmentation were also observed in Pi-treated VSMCs. These effects were accompanied by mitochondria-dependent apoptotic events, including release of cytochrome c from the mitochondria into the cytosol and subsequent activation of caspase-3. Quercetin was shown to block Pi-induced apoptosis and calcification of VSMCs by inhibiting oxidative stress and decreasing mitochondrial fission by inhibiting the expression and phosphorylation of Drp1. Quercetin also significantly ameliorated adenine-induced aortic calcification in rats. In summary, our findings suggest that quercetin attenuates calcification by reducing apoptosis of VSMCs by blocking oxidative stress and inhibiting mitochondrial fission.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1091", "doc_id": "9588931", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: RAD52 is involved in break-induced DNA replication (BIR).\n\nCANDIDATE_PASSAGE:\nHuman cancer cells utilize mitotic DNA synthesis to resist replication stress at telomeres regardless of their telomere maintenance mechanism Telomeres resemble common fragile sites (CFSs) in that they are difficult-to-replicate and exhibit fragility in mitosis in response to DNA replication stress. At CFSs, this fragility is associated with a delay in the completion of DNA replication until early mitosis, whereupon cells are proposed to switch to a RAD52-dependent form of break-induced replication. Here, we show that this mitotic DNA synthesis (MiDAS) is also a feature of human telomeres. Telomeric MiDAS is not restricted to those telomeres displaying overt fragility, and is a feature of a wide range of cell lines irrespective of whether their telomeres are maintained by telomerase or by the alternative lengthening of telomeres (ALT) mechanism. MiDAS at telomeres requires RAD52, and is mechanistically similar to CFS-associated MiDAS, with the notable exception that telomeric MiDAS does not require the MUS81-EME1 endonuclease. We propose a model whereby replication stress initiates a RAD52-dependent form of break-induced replication that bypasses a requirement for MUS81-EME1 to complete DNA synthesis in mitosis.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1003", "doc_id": "4899981", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: CD28 initiates tonic signaling in conventional T cells, which causes an exhaustion phenotype and limited efficiency.\n\nCANDIDATE_ABSTRACT:\nTITLE: 4-1BB Costimulation Ameliorates T Cell Exhaustion Induced by Tonic Signaling of Chimeric Antigen Receptors\nABSTRACT: Chimeric antigen receptors (CARs) targeting CD19 have mediated dramatic antitumor responses in hematologic malignancies, but tumor regression has rarely occurred using CARs targeting other antigens. It remains unknown whether the impressive effects of CD19 CARs relate to greater susceptibility of hematologic malignancies to CAR therapies, or superior functionality of the CD19 CAR itself. We show that tonic CAR CD3-ζ phosphorylation, triggered by antigen-independent clustering of CAR single-chain variable fragments, can induce early exhaustion of CAR T cells that limits antitumor efficacy. Such activation is present to varying degrees in all CARs studied, except the highly effective CD19 CAR. We further determine that CD28 costimulation augments, whereas 4-1BB costimulation reduces, exhaustion induced by persistent CAR signaling. Our results provide biological explanations for the antitumor effects of CD19 CARs and for the observations that CD19 CAR T cells incorporating the 4-1BB costimulatory domain are more persistent than those incorporating CD28 in clinical trials.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We further determine that CD28 costimulation augments, whereas 4-1BB costimulation reduces, exhaustion induced by persistent CAR signaling.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 200, "doc_id": "18231807", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Intra-cerebroventricular infusion of amyloid-β oligomers increases expression of fibronectin type-III domain-containing protein 5 mRNA in mice hippocampi.\n\nCANDIDATE_ABSTRACT:\nTITLE: Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models\nABSTRACT: Defective brain hormonal signaling has been associated with Alzheimer's disease (AD), a disorder characterized by synapse and memory failure. Irisin is an exercise-induced myokine released on cleavage of the membrane-bound precursor protein fibronectin type III domain-containing protein 5 (FNDC5), also expressed in the hippocampus. Here we show that FNDC5/irisin levels are reduced in AD hippocampi and cerebrospinal fluid, and in experimental AD models. Knockdown of brain FNDC5/irisin impairs long-term potentiation and novel object recognition memory in mice. Conversely, boosting brain levels of FNDC5/irisin rescues synaptic plasticity and memory in AD mouse models. Peripheral overexpression of FNDC5/irisin rescues memory impairment, whereas blockade of either peripheral or brain FNDC5/irisin attenuates the neuroprotective actions of physical exercise on synaptic plasticity and memory in AD mice. By showing that FNDC5/irisin is an important mediator of the beneficial effects of exercise in AD models, our findings place FNDC5/irisin as a novel agent capable of opposing synapse failure and memory impairment in AD.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 654, "doc_id": "57574395", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The minor G allele of FOXO3 up-regulates IL-10.\n\nCANDIDATE_ABSTRACT:\nTITLE: Human SNP Links Differential Outcomes in Inflammatory and Infectious Disease to a FOXO3-Regulated Pathway\nABSTRACT: The clinical course and eventual outcome, or prognosis, of complex diseases varies enormously between affected individuals. This variability critically determines the impact a disease has on a patient's life but is very poorly understood. Here, we exploit existing genome-wide association study data to gain insight into the role of genetics in prognosis. We identify a noncoding polymorphism in FOXO3A (rs12212067: T > G) at which the minor (G) allele, despite not being associated with disease susceptibility, is associated with a milder course of Crohn's disease and rheumatoid arthritis and with increased risk of severe malaria. Minor allele carriage is shown to limit inflammatory responses in monocytes via a FOXO3-driven pathway, which through TGFβ1 reduces production of proinflammatory cytokines, including TNFα, and increases production of anti-inflammatory cytokines, including IL-10. Thus, we uncover a shared genetic contribution to prognosis in distinct diseases that operates via a FOXO3-driven pathway modulating inflammatory responses.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Minor allele carriage is shown to limit inflammatory responses in monocytes via a FOXO3-driven pathway, which through TGFβ1 reduces production of proinflammatory cytokines, including TNFα, and increases production of anti-inflammatory cytokines, including IL-10.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1234, "doc_id": "13905670", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Xanthogranulomatous cholecystitis: a premalignant condition?\n\nABSTRACT:\nXanthogranulomatous cholecystitis (XGC) is an uncommon variant of chronic cholecystitis, characterized by marked thickening of the gallbladder wall and dense local adhesions. It often mimics a gallbladder carcinoma (GBC), and may coexist with GBC, leading to a diagnostic dilemma. Furthermore, the premalignant nature of this entity is not known. This study was undertaken to assess the p53, PCNA and beta-catenin expression in XGC in comparison to GBC and chronic inflammation. Sections from paraffin-embedded blocks of surgically resected specimens of GBC (69 cases), XGC (65), chronic cholecystitis (18) and control gallbladder (10) were stained with the monoclonal antibodies to p53 and PCNA, and a polyclonal antibody to beta-catenin. p53 expression was scored as the percentage of nuclei stained. PCNA expression was scored as the product of the percentage of nuclei stained and the intensity of the staining (1-3). A cut-off value of 80 for this score was taken as a positive result. Beta-catenin expression was scored as type of expression-membranous, cytoplasmic or nuclear staining. p53 mutation was positive in 52% of GBC cases and 3% of XGC, but was not expressed in chronic cholecystitis and control gallbladders. p53 expression was lower in XGC than in GBC (P<0.0001). PCNA expression was seen in 65% of GBC cases and 11% of XGC, but not in chronic cholecystitis and control gallbladders. PCNA expression was higher in GBC than XGC (P=0.0001), but there was no significant difference between the XGC, chronic cholecystitis and control gallbladder groups. Beta-catenin expression was positive in the GBC, XGC, chronic cholecystitis and control gallbladder groups. But the expression pattern in XGC, chronic cholecystitis and control gallbladders was homogenously membranous, [TRUNCATED]", "output": "{\"label\": \"no\", \"rationale\": \"The expression of p53, PCNA and beta-catenin in XGC was significantly different from GBC and similar to chronic cholecystitis, thus indicating the inflammatory nature of XGC and may not support a premalignant nature of the lesion.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 21459725, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Cnn1 recruitment varies with cell cycle timing.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cnn1 inhibits the interactions between the KMN complexes of the yeast kinetochore\nABSTRACT: Kinetochores attach the replicated chromosomes to the mitotic spindle and orchestrate their transmission to the daughter cells. Kinetochore–spindle binding and chromosome segregation are mediated by the multi-copy KNL1Spc105, MIS12Mtw1 and NDC80Ndc80 complexes that form the so-called KMN network. KMN–spindle attachment is regulated by the Aurora BIpl1 and MPS1Mps1 kinases. It is unclear whether other mechanisms exist that support KMN activity during the cell cycle. Using budding yeast, we show that kinetochore protein Cnn1 localizes to the base of the Ndc80 complex and promotes a functionally competent configuration of the KMN network. Cnn1 regulates KMN activity in a spatiotemporal manner by inhibiting the interaction between its complexes. Cnn1 activity peaks in anaphase and is driven by the Cdc28, Mps1 and Ipl1 kinases.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Cnn1 activity peaks in anaphase and is driven by the Cdc28, Mps1 and Ipl1 kinases.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 266, "doc_id": "22405338", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: CCL19 is a ligand for CCR7.\n\nCANDIDATE_PASSAGE:\nGenetic Interaction between Mutations in c-Myb and the KIX Domains of CBP and p300 Affects Multiple Blood Cell Lineages and Influences Both Gene Activation and Repression Adult blood cell production or definitive hematopoiesis requires the transcription factor c-Myb. The closely related KAT3 histone acetyltransferases CBP (CREBBP) and p300 (EP300) bind c-Myb through their KIX domains and mice homozygous for a p300 KIX domain mutation exhibit multiple blood defects. Perplexingly, mice homozygous for the same KIX domain mutation in CBP have normal blood. Here we test the hypothesis that the CBP KIX domain contributes subordinately to hematopoiesis via a genetic interaction with c-Myb. We assessed hematopoiesis in mice bearing compound mutations of c-Myb and/or the KIX domains of CBP and p300, and measured the effect of KIX domain mutations on c-Myb-dependent gene expression. We found that in the context of a p300 KIX mutation, the CBP KIX domain mutation affects platelets, B cells, T cells, and red cells. Gene interaction (epistasis) analysis provides mechanistic evidence that blood defects in KIX mutant mice are consistent with reduced c-Myb and KIX interaction. Lastly, we demonstrated that the CBP and p300 KIX domains contribute to both c-Myb-dependent gene activation and repression. Together these results suggest that the KIX domains of CBP, and especially p300, are principal mediators of c-Myb-dependent gene activation and repression that is required for definitive hematopoiesis.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "197", "doc_id": "16745747", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Lysine histone demethylase inhibitor JIB 04 is inactive against KDM5A.\n\nCANDIDATE_PASSAGE:\nHistone methyltransferase activity associated with a human multiprotein complex containing the Enhancer of Zeste protein. Enhancer of Zeste [E(z)] is a Polycomb-group transcriptional repressor and one of the founding members of the family of SET domain-containing proteins. Several SET-domain proteins possess intrinsic histone methyltransferase (HMT) activity. However, recombinant E(z) protein was found to be inactive in a HMT assay. Here we report the isolation of a multiprotein E(z) complex that contains extra sex combs, suppressor of zeste-12 [Su(z)12], and the histone binding proteins RbAp46/RbAp48. This complex, which we termed Polycomb repressive complex (PRC) 2, possesses HMT activity with specificity for Lys 9 (K9) and Lys 27 (K27) of histone H3. The HMT activity of PRC2 is dependent on an intact SET domain in the E(z) protein. We hypothesize that transcriptional repression by the E(z) protein involves methylation-dependent recruitment of PRC1. The presence of Su(z)12, a strong suppressor of position effect variegation, in PRC2 suggests that PRC2 may play a widespread role in heterochromatin-mediated silencing.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "730", "doc_id": "23195302", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is clinically significant anemia in HIV-infected pregnant women in India a major barrier to zidovudine use for prevention of maternal-to-child transmission?\n\nABSTRACT:\nTo determine the prevalence of anemia (serum hemoglobin <10 g/dL) and assess zidovudine use and toxicity in HIV-positive pregnant women in India. From 2002 through 2006, 24,105 pregnant women in Pune were screened for HIV and anemia. As part of an infant prevention of mother-to-child transmission (PMTCT) trial, enrolled HIV-positive women (n = 467) were assessed for anemia and associated outcomes, comparing women receiving zidovudine for >or=2 weeks versus no zidovudine. The prevalence of anemia was 38.7% in HIV-positive women. Anemic women were as likely as nonanemic women to receive zidovudine. At delivery, regardless of anemia status at enrollment, women receiving >or=2 weeks of zidovudine were 70% less likely to be anemic compared with women receiving no zidovudine (odds ratio = 0.28, 95% confidence interval: 0.14 to 0.57; P < 0.01), received iron and folic acid supplements for longer periods, and had no increased adverse delivery or newborn birth outcomes.", "output": "{\"label\": \"no\", \"rationale\": \"A significant proportion of HIV-positive pregnant women in India present for antenatal care with anemia. With concurrent iron and folic acid supplementation, however, zidovudine use is not associated with persistent or worsening anemia or associated adverse outcomes. In Indian community settings, all pregnant HIV-positive women should receive early anemia treatment.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 17414927, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Women with a higher birth weight are more likely to develop breast cancer later in life.\n\nCANDIDATE_PASSAGE:\nGenome-Wide Profiling of H3K56 Acetylation and Transcription Factor Binding Sites in Human Adipocytes The growing epidemic of obesity and metabolic diseases calls for a better understanding of adipocyte biology. The regulation of transcription in adipocytes is particularly important, as it is a target for several therapeutic approaches. Transcriptional outcomes are influenced by both histone modifications and transcription factor binding. Although the epigenetic states and binding sites of several important transcription factors have been profiled in the mouse 3T3-L1 cell line, such data are lacking in human adipocytes. In this study, we identified H3K56 acetylation sites in human adipocytes derived from mesenchymal stem cells. H3K56 is acetylated by CBP and p300, and deacetylated by SIRT1, all are proteins with important roles in diabetes and insulin signaling. We found that while almost half of the genome shows signs of H3K56 acetylation, the highest level of H3K56 acetylation is associated with transcription factors and proteins in the adipokine signaling and Type II Diabetes pathways. In order to discover the transcription factors that recruit acetyltransferases and deacetylases to sites of H3K56 acetylation, we analyzed DNA sequences near H3K56 acetylated regions and found that the E2F recognition sequence was enriched. Using chromatin immunoprecipitation followed by high-throughput sequencing, we confirmed that genes bound by E2F4, as well as those by HSF-1 and C/EBPα, have higher than expected levels of H3K56 acetylation, and that the transcription factor binding sites and acetylation sites are often adjacent but rarely overlap. We also discovered a significant difference between bound targets of C/EBPα in 3T3-L1 and human adipocytes, highlighting the [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1379", "doc_id": "3052213", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Lysine histone demethylase inhibitor JIB 04 is inactive against KDM5A.\n\nCANDIDATE_PASSAGE:\nExosomes in Plasma of Patients with Ovarian Carcinoma: Potential Biomarkers of Tumor Progression and Response to Therapy. BACKGROUND In patients with Ovarian Cancer (OvCa) exosomes released by tumor cells are present in the plasma and could be involved in tumor progression. This study examines the association between the exosome presence/protein content in plasma of OvCa patients and disease outcome, response to standard therapy and/or tumorresistance to therapies in patients studied at diagnosis and also serially during and after therapy. DESIGN AND METHODS Exosomes were purified from OvCa patients' plasma (n=22), patients with benign tumors (n=10) or (n=10) healthy controls (NC) using ultracentrifugation. Exosomes were visualized by scanning electron microscopy. Their protein content was measured. The presence of MAGE 3/6 and TGF-β1 in exosomes was evaluated in Western blots. RESULTS The OvCa patients' plasma contained higher levels of exosomal proteins (p<0.05) compared to those isolated from plasma of patients with benign tumors or NC. Exosomes isolated from OvCa patients's plasma carried TGF-β1 and MAGE3/6, which distinguished OvCa patients from those with benign tumors and NC. High protein levels of exosomes were seen in newly diagnosed patients; however in advanced stages of OvCa patients the protein content of isolated exosomes was significantly higher than that of early stages. The exosome levels variably changed during/after chemotherapy, and correlations between the changes in exosomal protein levels and clinical data suggested that the protein content of exosomes might be useful in predicting responses to therapy and prognosis in OvCa patients. CONCLUSION Analysis of plasma exosomes levels offers a novel approach to diagnosis and monitoring respo [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "730", "doc_id": "9095943", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: High levels of CRP reduces the risk of exacerbations in chronic obstructive pulmonary disease (COPD).\n\nCANDIDATE_ABSTRACT:\nTITLE: Getting started with yeast.\nABSTRACT: Publisher Summary The yeast Saccharomyces cerevisiae is now recognized as a model system representing a simple eukaryote whose genome can be easily manipulated. Yeast has only a slightly greater genetic complexity than bacteria and shares many of the technical advantages that permitted rapid progress in the molecular genetics of prokaryotes and their viruses. Some of the properties that make yeast particularly suitable for biological studies include rapid growth, dispersed cells, the ease of replica plating and mutant isolation, a well-defined genetic system, and most important, a highly versatile DNA transformation system. Being nonpathogenic, yeast can be handled with little precautions. Large quantities of normal baker's yeast are commercially available and can provide a cheap source for biochemical studies. The development of DNA transformation has made yeast particularly accessible to gene cloning and genetic engineering techniques. Structural genes corresponding to virtually any genetic trait can be identified by complementation from plasmid libraries. Plasmids can be introduced into yeast cells either as replicating molecules or by integration into the genome. In contrast to most other organisms, integrative recombination of transforming DNA in yeast proceeds exclusively via homologous recombination. Cloned yeast sequences, accompanied by foreign sequences on plasmids, can therefore be directed at will to specific locations in the genome.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 516, "doc_id": "1631583", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Vitamin D deficiency is unrelated to birth weight.\n\nCANDIDATE_PASSAGE:\nRelationship between serum parathyroid hormone levels, vitamin D sufficiency, and calcium intake. CONTEXT Adequate vitamin D status for optimum bone health has received increased recognition in recent years; however, the ideal intake is not known. Serum 25-hydroxyvitamin D is the generally accepted indicator of vitamin D status, but no universal reference level has been reached. OBJECTIVE To investigate the relative importance of high calcium intake and serum 25-hydroxyvitamin D for calcium homeostasis, as determined by serum intact parathyroid hormone (PTH). DESIGN, SETTING, AND PARTICIPANTS Cross-sectional study of 2310 healthy Icelandic adults who were divided equally into 3 age groups (30-45 years, 50-65 years, or 70-85 years) and recruited from February 2001 to January 2003. They were administered a semi-quantitative food frequency questionnaire, which assessed vitamin D and calcium intake. Participants were further divided into groups according to calcium intake (<800 mg/d, 800-1200 mg/d, and >1200 mg/d) and serum 25-hydroxyvitamin D level (<10 ng/mL, 10-18 ng/mL, and >18 ng/mL). MAIN OUTCOME MEASURE Serum intact PTH as determined by calcium intake and vitamin D. RESULTS A total of 944 healthy participants completed all parts of the study. After adjusting for relevant factors, serum PTH was lowest in the group with a serum 25-hydroxyvitamin D level of more than 18 ng/mL but highest in the group with a serum 25-hydroxyvitamin D level of less than 10 ng/mL. At the low serum 25-hydroxyvitamin D level (<10 ng/mL), calcium intake of less than 800 mg/d vs more than 1200 mg/d was significantly associated with higher serum PTH (P = .04); and at a calcium intake of more than 1200 mg/d, there was a significant difference between the lowest and highest vitamin D [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1370", "doc_id": "16256507", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Osteocytes have an essential role in G-CSF induced HSPC mobilization.\n\nCANDIDATE_ABSTRACT:\nTITLE: Matrix-embedded osteocytes regulate mobilization of hematopoietic stem/progenitor cells.\nABSTRACT: The bone marrow (BM) niche comprises multiple cell types that regulate hematopoietic stem/progenitor cell (HSPC) migration out of the niche and into the circulation. Here, we demonstrate that osteocytes, the major cellular component of mature bone, are regulators of HSPC egress. Granulocyte colony-stimulating factor (G-CSF), used clinically to mobilize HSPCs, induces changes in the morphology and gene expression of the osteocytic network that precedes changes in osteoblasts. This rapid response is likely under control of the sympathetic nervous system, since osteocytes express the β2-adrenergic receptor and surgical sympathectomy prevents it. Mice with targeted ablation of osteocytes or a disrupted osteocyte network have comparable numbers of HSPCs in the BM but fail to mobilize HSPCs in response to G-CSF. Taken together, these results indicate that the BM/bone niche interface is critically controlled from inside of the bone matrix and establish an important physiological role for skeletal tissues in hematopoietic function.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Mice with targeted ablation of osteocytes or a disrupted osteocyte network have comparable numbers of HSPCs in the BM but fail to mobilize HSPCs in response to G-CSF.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 893, "doc_id": "13509809", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Reduced responsiveness to interleukin-2 in regulatory T cells is associated with greater resistance to autoimmune diseases such as Type 1 Diabetes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Type 1 diabetes-associated IL2RA variation lowers IL-2 signaling and contributes to diminished CD4+CD25+ regulatory T cell function.\nABSTRACT: Numerous reports have demonstrated that CD4(+)CD25(+) regulatory T cells (Tregs) from individuals with a range of human autoimmune diseases, including type 1 diabetes, are deficient in their ability to control autologous proinflammatory responses when compared with nondiseased, control individuals. Treg dysfunction could be a primary, causal event or may result from perturbations in the immune system during disease development. Polymorphisms in genes associated with Treg function, such as IL2RA, confer a higher risk of autoimmune disease. Although this suggests a primary role for defective Tregs in autoimmunity, a link between IL2RA gene polymorphisms and Treg function has not been examined. We addressed this by examining the impact of an IL2RA haplotype associated with type 1 diabetes on Treg fitness and suppressive function. Studies were conducted using healthy human subjects to avoid any confounding effects of disease. We demonstrated that the presence of an autoimmune disease-associated IL2RA haplotype correlates with diminished IL-2 responsiveness in Ag-experienced CD4(+) T cells, as measured by phosphorylation of STAT5a, and is associated with lower levels of FOXP3 expression by Tregs and a reduction in their ability to suppress proliferation of autologous effector T cells. These data offer a rationale that contributes to the molecular and cellular mechanisms through which polymorphisms in the IL-2RA gene affect immune regulation, and consequently upon susceptibility to autoimmune and inflammatory diseases.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We demonstrated that the presence of an autoimmune disease-associated IL2RA haplotype correlates with diminished IL-2 responsiveness in Ag-experienced CD4(+) T cells, as measured by phosphorylation of STAT5a, and is associated with lower levels of FOXP3 expression by Tregs and a reduction in their ability to suppress proliferation of autologous effector T cells.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1029, "doc_id": "11899391", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Noninvasive positive pressure ventilation is not predictive of acute respiratory failure after solid organ transplantation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Noninvasive ventilation for treatment of acute respiratory failure in patients undergoing solid organ transplantation: a randomized trial.\nABSTRACT: CONTEXT Noninvasive ventilation (NIV) has been associated with lower rates of endotracheal intubation in populations of patients with acute respiratory failure. OBJECTIVE To compare NIV with standard treatment using supplemental oxygen administration to avoid endotracheal intubation in recipients of solid organ transplantation with acute hypoxemic respiratory failure. DESIGN AND SETTING Prospective randomized study conducted at a 14-bed, general intensive care unit of a university hospital. PATIENTS Of 238 patients who underwent solid organ transplantation from December 1995 to October 1997, 51 were treated for acute respiratory failure. Of these, 40 were eligible and 20 were randomized to each group. INTERVENTION Noninvasive ventilation vs standard treatment with supplemental oxygen administration. MAIN OUTCOME MEASURES The need for endotracheal intubation and mechanical ventilation at any time during the study, complications not present on admission, duration of ventilatory assistance, length of hospital stay, and intensive care unit mortality. RESULTS The 2 groups were similar at study entry. Within the first hour of treatment, 14 patients (70%) in the NIV group, and 5 patients (25%) in the standard treatment group improved their ratio of the PaO2 to the fraction of inspired oxygen (FIO2). Over time, a sustained improvement in PaO2 to FIO2 was noted in 12 patients (60%) in the NIV group, and in 5 patients (25%) randomized to standard treatment (P = .03). The use of NIV was associated with a significant reduction in the rate of endotracheal intubation (20% vs 70%; P = .002), rate of fatal complications (20% vs 50%; P = .05), length of stay in the intensive care unit by survivors (mean [SD] days, 5.5 [3] vs 9 [4]; P = .03), and intensive care unit mortality [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Over time, a sustained improvement in PaO2 to FIO2 was noted in 12 patients (60%) in the NIV group, and in 5 patients (25%) randomized to standard treatment (P = .03).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 855, "doc_id": "8190282", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: LSD1-positive promoters are associated with RNA polymerase II\n\nCANDIDATE_ABSTRACT:\nTITLE: Histone Methylation-Dependent Mechanisms Impose Ligand Dependency for Gene Activation by Nuclear Receptors\nABSTRACT: Nuclear receptors undergo ligand-dependent conformational changes that are required for corepressor-coactivator exchange, but whether there is an actual requirement for specific epigenetic landmarks to impose ligand dependency for gene activation remains unknown. Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases (HMTs) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals. This strategy, based at least in part on an HMT-dependent inhibitory histone code, imposes a requirement for specific histone demethylases, including LSD1, to permit ligand- and signal-dependent activation of regulated gene expression. These events link an inhibitory methylation component of the histone code to a broadly used strategy that circumvents pathological constitutive gene induction by physiologically regulated transcription factors.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 679, "doc_id": "13639330", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: CX3CR1 on the Th2 cells suppresses airway inflammation.\n\nCANDIDATE_PASSAGE:\nCD4+ T cell help guides formation of CD103+ lung-resident memory CD8+ T cells during influenza viral infection. Tissue-resident memory T (Trm) cells provide enhanced protection against infection at mucosal sites. Here we found that CD4(+) T cells are important for the formation of functional lung-resident CD8(+) T cells after influenza virus infection. In the absence of CD4(+) T cells, CD8(+) T cells displayed reduced expression of CD103 (Itgae), were mislocalized away from airway epithelia, and demonstrated an impaired ability to recruit CD8(+) T cells to the lung airways upon heterosubtypic challenge. CD4(+) T cell-derived interferon-γ was necessary for generating lung-resident CD103(+) CD8(+) Trm cells. Furthermore, expression of the transcription factor T-bet was increased in \"unhelped\" lung Trm cells, and a reduction in T-bet rescued CD103 expression in the absence of CD4(+) T cell help. Thus, CD4(+) T cell-dependent signals are important to limit expression of T-bet and allow for the development of CD103(+) CD8(+) Trm cells in the lung airways following respiratory infection.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "219", "doc_id": "3835423", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: LDL cholesterol has no involvement in the development of cardiovascular disease.\n\nCANDIDATE_ABSTRACT:\nTITLE: LDL-cholesterol concentrations: a genome-wide association study\nABSTRACT: BACKGROUND LDL cholesterol has a causal role in the development of cardiovascular disease. Improved understanding of the biological mechanisms that underlie the metabolism and regulation of LDL cholesterol might help to identify novel therapeutic targets. We therefore did a genome-wide association study of LDL-cholesterol concentrations. METHODS We used genome-wide association data from up to 11,685 participants with measures of circulating LDL-cholesterol concentrations across five studies, including data for 293 461 autosomal single nucleotide polymorphisms (SNPs) with a minor allele frequency of 5% or more that passed our quality control criteria. We also used data from a second genome-wide array in up to 4337 participants from three of these five studies, with data for 290,140 SNPs. We did replication studies in two independent populations consisting of up to 4979 participants. Statistical approaches, including meta-analysis and linkage disequilibrium plots, were used to refine association signals; we analysed pooled data from all seven populations to determine the effect of each SNP on variations in circulating LDL-cholesterol concentrations. FINDINGS In our initial scan, we found two SNPs (rs599839 [p=1.7x10(-15)] and rs4970834 [p=3.0x10(-11)]) that showed genome-wide statistical association with LDL cholesterol at chromosomal locus 1p13.3. The second genome screen found a third statistically associated SNP at the same locus (rs646776 [p=4.3x10(-9)]). Meta-analysis of data from all studies showed an association of SNPs rs599839 (combined p=1.2x10(-33)) and rs646776 (p=4.8x10(-20)) with LDL-cholesterol concentrations. SNPs rs599839 and rs646776 both explained around 1% of the variation in circulating LDL-cholesterol concentrations and were associated wi [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"BACKGROUND LDL cholesterol has a causal role in the development of cardiovascular disease.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 674, "doc_id": "2095573", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_ABSTRACT:\nTITLE: Evidence regarding human papillomavirus testing in secondary prevention of cervical cancer.\nABSTRACT: More than ever, clinicians need regularly updated reviews given the continuously increasing amount of new information regarding innovative cervical cancer prevention methods. A summary is given from recent meta-analyses and systematic reviews on 3 possible clinical applications of human papillomavirus (HPV) testing: triage of women with equivocal or low-grade cytologic abnormalities; prediction of the therapeutic outcome after treatment of cervical intraepithelial neoplasia (CIN) lesions, and last not but not least, primary screening for cervical cancer and pre-cancer. Consistent evidence is available indicating that HPV-triage with the Hybrid Capture(®) 2 assay (Qiagen Gaithersburg, Inc., MD, USA [previously Digene Corp.] (HC2) is more accurate (higher sensitivity, similar specificity) than repeat cytology to triage women with equivocal Pap smear results. Several other tests show at least similar accuracy but mRNA testing with the APTIMA(®) (Gen-Probe Inc., San Diego, CA, USA) test is similarly sensitive but more specific compared to HC2. In triage of low-grade squamous intraepithelial lesions (LSIL), HC2 is more sensitive but its specificity is substantially lower compared to repeat cytology. The APTIMA(®) test is more specific than HC2 without showing a loss in sensitivity. Identification of DNA of HPV types 16 and/or 18, or RNA from the five most carcinogenic HPV types allow selecting women at highest risk for CIN3+ but the sensitivity and negative predictive value of these markers are lower than full-range high-risk HPV (hrHPV) testing. After conservative treatment of cervical pre-cancer, HPV testing picks up more quickly, with higher sensitivity and not lower specificity, residual or recurrent high-grade CIN than follow-up cytology. Primary screening f [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Primary screening for hrHPV generally detects more CIN2, CIN3 or cancer compared to cytology at cut-off atypical squamous cells of undetermined significance (ASC-US) or LSIL, but is less specific.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 972, "doc_id": "28617573", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Many transmembrane receptors transmit signals by long-range conformational changes in the association of alpha-helices across the plasma membrane.\n\nCANDIDATE_ABSTRACT:\nTITLE: Dynamic Helix Interactions in Transmembrane Signaling\nABSTRACT: Studying how protein transmembrane domains transmit signals across membranes is beset by unique challenges. Here, we discuss the circumstances that have led to success and reflect on what has been learned from these examples. Such efforts suggest that some of the most interesting properties of transmembrane helix interactions may be the least amenable to study by current techniques.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 757, "doc_id": "17123657", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Misunderstandings between doctors and patients can lead to non-adherence.\n\nCANDIDATE_PASSAGE:\nAlterations of white matter integrity in adults with major depressive disorder: a magnetic resonance imaging study. OBJECTIVE The purpose of our study was to investigate alterations of white matter integrity in adults with major depressive disorder (MDD) using magnetic resonance imaging (MRI). METHODS We performed diffusion tensor imaging with a 3T MRI scanner on 45 patients with major depression and 45 healthy controls matched for age, sex and education. Using a voxel-based analysis, we measured the fractional anisotropy (FA), and we investigated the differences between the patient and control groups. We examined the correlations between the microstructure abnormalities of white matter and symptom severity, age of illness onset and cumulative illness duration, respectively. RESULTS We found a significant decrease in FA in the left hemisphere, including the anterior limb of the internal capsule and the inferior parietal portion of the superior longitudinal fasciculus, in patients with MDD compared with healthy controls. Diffusion tensor imaging measures in the left anterior limb of the internal capsule were negatively related to the severity of depressive symptoms, even after we controlled for age and sex. CONCLUSION Our findings provide new evidence of microstructural changes of white matter in non-late-onset adult depression. Our results complement those observed in late-life depression and support the hypothesis that the disruption of cortical- subcortical circuit integrity may be involved in the etiology of major depressive disorder.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "792", "doc_id": "1472815", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Lice attenuated SIV vaccines induce a stronger antigen-specific T cell response in lymph node cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Robustness of Random Forest-based gene selection methods\nABSTRACT: Gene selection is an important part of microarray data analysis because it provides information that can lead to a better mechanistic understanding of an investigated phenomenon. At the same time, gene selection is very difficult because of the noisy nature of microarray data. As a consequence, gene selection is often performed with machine learning methods. The Random Forest method is particularly well suited for this purpose. In this work, four state-of-the-art Random Forest-based feature selection methods were compared in a gene selection context. The analysis focused on the stability of selection because, although it is necessary for determining the significance of results, it is often ignored in similar studies. The comparison of post-selection accuracy in the validation of Random Forest classifiers revealed that all investigated methods were equivalent in this context. However, the methods substantially differed with respect to the number of selected genes and the stability of selection. Of the analysed methods, the Boruta algorithm predicted the most genes as potentially important. The post-selection classifier error rate, which is a frequently used measure, was found to be a potentially deceptive measure of gene selection quality. When the number of consistently selected genes was considered, the Boruta algorithm was clearly the best. Although it was also the most computationally intensive method, the Boruta algorithm's computational demands could be reduced to levels comparable to those of other algorithms by replacing the Random Forest importance with a comparable measure from Random Ferns (a similar but simplified classifier). Despite their design assumptions, the minimal optimal selection methods, were found to select a high fraction of false positives.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 694, "doc_id": "1542437", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Anthrax spores can be disposed of easily after they are dispersed.\n\nCANDIDATE_PASSAGE:\nSecondary aerosolization of viable Bacillus anthracis spores in a contaminated US Senate Office. CONTEXT Bioterrorist attacks involving letters and mail-handling systems in Washington, DC, resulted in Bacillus anthracis (anthrax) spore contamination in the Hart Senate Office Building and other facilities in the US Capitol's vicinity. OBJECTIVE To provide information about the nature and extent of indoor secondary aerosolization of B anthracis spores. DESIGN Stationary and personal air samples, surface dust, and swab samples were collected under semiquiescent (minimal activities) and then simulated active office conditions to estimate secondary aerosolization of B anthracis spores. Nominal size characteristics, airborne concentrations, and surface contamination of B anthracis particles (colony-forming units) were evaluated. RESULTS Viable B anthracis spores reaerosolized under semiquiescent conditions, with a marked increase in reaerosolization during simulated active office conditions. Increases were observed for B anthracis collected on open sheep blood agar plates (P<.001) and personal air monitors (P =.01) during active office conditions. More than 80% of the B anthracis particles collected on stationary monitors were within an alveolar respirable size range of 0.95 to 3.5 micro m. CONCLUSIONS Bacillus anthracis spores used in a recent terrorist incident reaerosolized under common office activities. These findings have important implications for appropriate respiratory protection, remediation, and reoccupancy of contaminated office environments.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "115", "doc_id": "33872649", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does wasting or obesity at time of transplant predict pediatric heart transplant outcomes : analysis of ISHLT pediatric heart transplant registry?\n\nABSTRACT:\nBody mass index (BMI) both before and after heart transplant (HT) is used to risk stratify in adult HT. Single-center studies identify BMI as a potential predictor of outcome after HT in children; large-scale analyses in pediatric HT have not been performed. The ISHLT pediatric heart transplant registry was queried for HT recipients >2 years old between 1996 and 2006 with data for BMI percentile (BMI%ile) at HT. Survival and morbidity rates post-HT were compared between BMI%ile cohorts defined as: wasted, <5th BMI%ile; normal, 5th to 95th BMI%ile; and obese, >95th BMI%ile at HT. Data from 2,333 pediatric HT patients were available for analysis. Incidence of abnormal BMI%ile at HT was: wasted = 23% and obese = 8%. Wasting and obesity were similar in patients with congenital or cardiomyopathic diagnoses. Wasted or obese patients at HT did not differ from patients with normal BMI in survival on Kaplan-Meier or multivariate analyses. There were no significant differences in pre-, peri- or post-operative adverse events between patients with wasting or obesity and those with normal BMI%ile at HT.", "output": "{\"label\": \"no\", \"rationale\": \"In contrast to adults, abnormal body mass at time of transplant was not associated with decreased survival in pediatric HT recipients. Potential pediatric transplant candidates should not be excluded based on the perception that wasting or obesity will increase the risk of adverse outcomes.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 19783177, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Removal of H3K9me3 improves reprogramming efficiency in human somatic cell nuclear transfer experiments.\n\nCANDIDATE_PASSAGE:\nComparison of Maximal Oxygen Consumption Between Black and White Prepubertal and Pubertal Children The purpose of this investigation was to determine whether maximal oxygen consumption (VO2max) differed between two selected groups of black and white children and whether a difference existed to determine whether it was related to hematologic profiles, body composition, and/or physical activity/inactivity level. Forty-five prepubertal and 42 pubertal, clinically normal black and white children participated. Dual-energy x-ray absorptiometry was used to determine body composition. A computed tomography scan of the abdomen was used to determine visceral adipose tissue and s.c. adipose tissue. Daily physical activity/inactivity was assessed by questionnaire. Black prepubertal and pubertal children had lower VO2max values when compared with white children (28.8 ± 7.8 versus 35.0 ± 6.5 mL · kg−1 · min−1, p < 0.01; 33.7 ± 6.4 versus 40.4 ± 10.2 mL · kg−1 · min−1, p < 0.05; respectively). Black prepubertal and pubertal children had lower Hb concentrations ([Hb]) and hematocrits than white children (prepubertal: 12.1 ± 0.5 versus 12.8 ± 0.9 g/dL, p < 0.001; 35.6 ± 1.4 versus 37.4 ± 2.3%, p < 0.01, respectively; pubertal: 13.0 ± 0.9 versus 13.6 ± 0.7 g/dL, p < 0.05; 37.7 ± 2.5 versus 39.5 ± 2.1%, p < 0.05, respectively). In conclusion, these findings indicate that black prepubertal and pubertal children had lower VO2max when compared with their white peers matched for age, pubertal stage, and body mass index. This difference in VO2max could be attributed at least in part to comparatively lower [Hb] and more sedentary lifestyle in the black children. Further investigations should study Hb flow rate (a function of [Hb] × maximal cardiac output) in black and white children [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1036", "doc_id": "18537148", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: There is an inverse relationship between hip fractures and statin use.\n\nCANDIDATE_ABSTRACT:\nTITLE: HMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients.\nABSTRACT: CONTEXT Recent animal studies have found that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) lipid-lowering drugs (statins) substantially increase bone formation, but whether statin use in humans results in clinically meaningful bone formation or a reduction in the risk of osteoporotic fractures is not known. OBJECTIVE To determine whether the use of statins is associated with reduced hip fracture risk. DESIGN Case-control study. SETTING AND PATIENTS A total of 6110 New Jersey residents aged 65 years or older and enrolled in Medicare and either Medicaid or the Pharmacy Assistance for the Aged and Disabled program. Case patients (n=1222) underwent surgical repair of a hip fracture in 1994. Control patients (n=4888) were identified at a ratio of 4:1 and frequency-matched to case patients for age and sex. MAIN OUTCOME MEASURE Adjusted odds ratio (OR) of hip fracture by statin use in the 180 days and 3 years prior to the index date (the earliest date of admission for surgery), adjusted for demographic and clinical characteristics and health care utilization. RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus. No significant relationship was observed between use of nonstatin lipid-lowering agents and hip fracture risk. Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowe [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1290, "doc_id": "4687948", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: COPI coatmer is involved in viral replication.\n\nCANDIDATE_PASSAGE:\nA map of human circular RNAs in clinically relevant tissues Cellular circular RNAs (circRNAs) are generated by head-to-tail splicing and are present in all multicellular organisms studied so far. Recently, circRNAs have emerged as a large class of RNA which can function as post-transcriptional regulators. It has also been shown that many circRNAs are tissue- and stage-specifically expressed. Moreover, the unusual stability and expression specificity make circRNAs important candidates for clinical biomarker research. Here, we present a circRNA expression resource of 20 human tissues highly relevant to disease-related research: vascular smooth muscle cells (VSMCs), human umbilical vein cells (HUVECs), artery endothelial cells (HUAECs), atrium, vena cava, neutrophils, platelets, cerebral cortex, placenta, and samples from mesenchymal stem cell differentiation. In eight different samples from a single donor, we found highly tissue-specific circRNA expression. Circular-to-linear RNA ratios revealed that many circRNAs were expressed higher than their linear host transcripts. Among the 71 validated circRNAs, we noticed potential biomarkers. In adenosine deaminase-deficient, severe combined immunodeficiency (ADA-SCID) patients and in Wiskott-Aldrich-Syndrome (WAS) patients' samples, we found evidence for differential circRNA expression of genes that are involved in the molecular pathogenesis of both phenotypes. Our findings underscore the need to assess circRNAs in mechanisms of human disease. KEY MESSAGES: circRNA resource catalog of 20 clinically relevant tissues. circRNA expression is highly tissue-specific. circRNA transcripts are often more abundant than their linear host RNAs. circRNAs can be differentially expressed in disease-associated genes.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "211", "doc_id": "8995263", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Do urinary citrate levels correlate with urinary pH in patients with urinary stone formation?\n\nABSTRACT:\nUrinary excretion of citrate is dependent on glomerular filtration, tubular reabsorption, and excretion. Acid base status is thought to play a significant role in urinary citrate excretion. It has been assumed that increased urinary citrate will increase urinary pH. The aim of this study was to confirm the association of increased urinary citrate levels with increased urinary pH. The 24-hour urine collections of all patients with stones referred to our clinic in the past 4 years were reviewed. The samples were collected and analyzed for routine stone risk profiles by a commercial laboratory (Litholink, Chicago, Ill). The Student t test and analysis of variance were used to compare the mean values as applicable. Pearson's correlations were also calculated for each variable. A total of 572 patients had at least one 24-hour urine sample from the past 4 years. The mean urinary citrate was 305 mg/day. The mean urinary pH of all patients was 6.14. Statistical evaluation of all patients showed no correlation between urinary citrate and pH (r = -0.04, P = 0.36). In a subset of patients with urinary potassium greater than 100 mEq/day (n = 100), urinary citrate and urinary pH were both increased; however, there was still no correlation between the two (r = 0.011, P = 0.806).", "output": "{\"label\": \"no\", \"rationale\": \"Despite the current dogma that increasing urinary citrate increases urinary pH, in a cohort of patients with urinary stone formation who provided 24-hour urine specimens, no correlation was found between urinary citrate and urinary pH levels.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 17991528, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Normal granulomas form in the presence of TNF in Zebrafish.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tumor necrosis factor signaling mediates resistance to mycobacteria by inhibiting bacterial growth and macrophage death.\nABSTRACT: Tumor necrosis factor (TNF), a key effector in controlling tuberculosis, is thought to exert protection by directing formation of granulomas, organized aggregates of macrophages and other immune cells. Loss of TNF signaling causes progression of tuberculosis in humans, and the increased mortality of Mycobacterium tuberculosis-infected mice is associated with disorganized necrotic granulomas, although the precise roles of TNF signaling preceding this endpoint remain undefined. We monitored transparent Mycobacterium marinum-infected zebrafish live to conduct a stepwise dissection of how TNF signaling operates in mycobacterial pathogenesis. We found that loss of TNF signaling caused increased mortality even when only innate immunity was operant. In the absence of TNF, intracellular bacterial growth and granuloma formation were accelerated and was followed by necrotic death of overladen macrophages and granuloma breakdown. Thus, TNF is not required for tuberculous granuloma formation, but maintains granuloma integrity indirectly by restricting mycobacterial growth within macrophages and preventing their necrosis.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Thus, TNF is not required for tuberculous granuloma formation, but maintains granuloma integrity indirectly by restricting mycobacterial growth within macrophages and preventing their necrosis.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 861, "doc_id": "16066726", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: A diminished ovarian reserve is a very strong indicator of infertility, even in an a priori non-infertile population.\n\nCANDIDATE_PASSAGE:\nThe VTI family of SNARE proteins is necessary for plant viability and mediates different protein transport pathways. The Arabidopsis genome contains a family of v-SNAREs: VTI11, VTI12, and VTI13. Only VTI11 and VTI12 are expressed at appreciable levels. Although these two proteins are 60% identical, they complement different transport pathways when expressed in the yeast vti1 mutant. VTI11 was identified recently as the mutated gene in the shoot gravitropic mutant zig. Here, we show that the vti11 zig mutant has defects in vascular patterning and auxin transport. An Arabidopsis T-DNA insertion mutant, vti12, had a normal phenotype under nutrient-rich growth conditions. However, under nutrient-poor conditions, vti12 showed an accelerated senescence phenotype, suggesting that VTI12 may play a role in the plant autophagy pathway. VTI11 and VTI12 also were able to substitute for each other in their respective SNARE complexes, and a double-mutant cross between zig and vti12 was embryo lethal. These results suggest that some VTI1 protein was necessary for plant viability and that the two proteins were partially functionally redundant.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "40", "doc_id": "1669173", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is Panton-Valentine leucocidin associated with the pathogenesis of Staphylococcus aureus bacteraemia in the UK?\n\nABSTRACT:\nThe morbidity and mortality associated with Panton-Valentine leucocidin (PVL)-positive Staphylococcus aureus suggest that this toxin is a key marker of disease severity. Nevertheless, the importance of PVL in the pathogenesis of primary bacteraemia caused by S. aureus is uncertain. We have determined the prevalence of PVL-encoding genes among isolates of S. aureus from bacteraemic patients. Consecutive bacteraemia isolates of S. aureus (n=244) from patients hospitalized in 25 centres in the UK and Ireland during 2005 were screened for PVL and mecA genes. PVL-positive isolates were characterized by toxin gene profiling, PFGE, spa-typing and MIC determinations for a range of antimicrobials. Four out of 244 isolates (1.6%) were PVL-positive and susceptible to oxacillin [methicillin-susceptible S. aureus (MSSA)]. Eighty-eight out of 244 (36%) were oxacillin-resistant (methicillin-resistant S. aureus), but none was PVL-positive. The four patients (two males: 30 and 33 years; two females: 62 and 80 years) had infection foci of: skin and soft tissue, unknown, indwelling line, and surgical site, and were located at one centre in Wales, one in England and two in Ireland. One of four PVL-positive isolates was resistant to penicillin and fusidic acid, the remainder were susceptible to all antibiotics tested. Genotypic analyses showed that the four isolates represented three distinct strains; the two isolates from Ireland were related.", "output": "{\"label\": \"maybe\", \"rationale\": \"We found that 1.6% of S. aureus (all MSSA) from bacteraemic patients were PVL-positive. This low incidence suggests that PVL-positive S.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 17562682, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Lmna knock-in models are appropriate for testing therapeutic approaches against Hutchinson-Gilford progeria syndrome (HGPS).\n\nCANDIDATE_PASSAGE:\nOptimal therapy for reduction of lipoprotein(a). WHAT IS KNOWN AND OBJECTIVE There is a growing body of experimental and clinical evidence for the atherogenic and pro-thrombotic potential of Lipoprotein(a) [Lp(a)], as well as for its causative role in coronary heart disease and stroke. We comment on novel strategies for reducing Lp(a) levels. COMMENT Irrespective of the underlying biological mechanisms explaining the athero-thrombotic potential of this lipoprotein, most work has focused on the identification of suitable therapies for hyperlipoproteinemia(a). These include apheresis techniques, nicotinic acid and statins. None of these strategies have been shown to be definitely effective or convenient for the patient and new strategies are being attempted. Promising results are emerging with therapeutic interventions targeting the 'inflammatory pathways' by inhibition of Interleukin-6 (IL-6) signalling with natural compounds (e.g., Ginko biloba) or the IL-6 receptor antibody Tocilizumab. These may both lower Lp(a) and cardiovascular risk of the patients. Besides inhibiting platelet function, antiplatelet therapy with aspirin may also decrease the plasma concentration of Lp(a) and modulate its influence on platelets. WHAT IS NEW AND CONCLUSION We highlight the inadequacy of current approaches for lowering Lp(a) and draw attention to novel insights that may lead to better treatment.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "698", "doc_id": "33118292", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: In S. cerevisiae, the absence of RNA surveillance pathways reduces sensitivity to high iron conditions.\n\nCANDIDATE_PASSAGE:\nMultiple RNA surveillance pathways limit aberrant expression of iron uptake mRNAs and prevent iron toxicity in S. cerevisiae. Tight regulation of the expression of mRNAs encoding iron uptake proteins is essential to control iron homeostasis and avoid intracellular iron toxicity. We show that many mRNAs encoding iron uptake or iron mobilization proteins are expressed in iron-replete conditions in the absence of the S. cerevisiae RNase III ortholog Rnt1p or of the nuclear exosome component Rrp6p. Extended forms of these mRNAs accumulate in the absence of Rnt1p or of the 5'-->3' exonucleases Xrn1p and Rat1p, showing that multiple degradative pathways contribute to the surveillance of aberrant forms of these transcripts. RNase III-deficient cells are hypersensitive to high iron concentrations, suggesting that Rnt1p-mediated RNA surveillance is required to prevent iron toxicity. These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "566", "doc_id": "16120395", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does use of hydrophilic guidewires significantly improve technical success rates of peripheral PTA?\n\nABSTRACT:\nTo determine whether the use of hydrophilic guidewires has increased the technical success rate of peripheral percutaneous transluminal angioplasty (PTA).MATERIAL/ We performed 125 procedures and analyzed the technical success rates of PTA using the conventional guidewire first and then if needed, the hydrophilic guidewire for iliac and SFA stenoses or occlusions. Angioplasty was performed on 25 stenosed, 25 occluded iliac arteries and 25 stenosed, 50 occluded femoral arteries. The result was defined as technical success when the lesion was crossed by a guidewire and balloon, then it was dilated with restoration of vessel lumen and less than 30% residual stenosis and the rise in ABI values was at least 0.15 after 24 hours. The technical success rate after PTA of stenosed iliac arteries was achieved in 96% (24/25) using conventional wires and 100% using hydrophilic guidewire; in iliac occlusions, the rates were 60% (15/25) and 96%, respectively; in femoral stenosis - 84% (21/25) and 100%; in occlusions in the first group: lesions<10 cm -64% (16/25) and 96%, in the second group: lesions>10 cm -48% (12/25) and 88%. In the iliac group, there was no significant difference in the success of iliac stenosis PTA. However, there were significant changes in the success rates of PTA performed for SFA stenosis and iliac and SFA occlusions.", "output": "{\"label\": \"maybe\", \"rationale\": \"In summary, we report an overall improvement and high technical success rate for peripherial PTA. The use of hydrophilic guidewires made significant difference to the technical success rate of PTA, especially in occlusion and more complicated lesions.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 16538201, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Lice attenuated SIV vaccines induce a stronger antigen-specific T cell response in lymph node cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Lymph node T cell responses predict the efficacy of live attenuated SIV vaccines\nABSTRACT: Live attenuated simian immunodeficiency virus (SIV) vaccines (LAVs) remain the most efficacious of all vaccines in nonhuman primate models of HIV and AIDS, yet the basis of their robust protection remains poorly understood. Here we show that the degree of LAV-mediated protection against intravenous wild-type SIVmac239 challenge strongly correlates with the magnitude and function of SIV-specific, effector-differentiated T cells in the lymph node but not with the responses of such T cells in the blood or with other cellular, humoral and innate immune parameters. We found that maintenance of protective T cell responses is associated with persistent LAV replication in the lymph node, which occurs almost exclusively in follicular helper T cells. Thus, effective LAVs maintain lymphoid tissue-based, effector-differentiated, SIV-specific T cells that intercept and suppress early wild-type SIV amplification and, if present in sufficient frequencies, can completely control and perhaps clear infection, an observation that provides a rationale for the development of safe, persistent vectors that can elicit and maintain such responses.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here we show that the degree of LAV-mediated protection against intravenous wild-type SIVmac239 challenge strongly correlates with the magnitude and function of SIV-specific, effector-differentiated T cells in the lymph node but not with the responses of such T cells in the blood or with other cellular, humoral and innate immune parameters.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 694, "doc_id": "1071991", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Podocytes are motile and migrate in the presence of injury.\n\nCANDIDATE_PASSAGE:\nAmitriptyline is effective in chronic but not in episodic tension-type headache: pathogenetic implications. The tricyclic antidepressant, amitriptyline, is an effective drug for the treatment of chronic tension-type headache and for other chronic pain syndromes, but it is also effective in the prophylaxis of an episodic type of headache such as migraine. However, its efficacy in episodic tension-type headache has not yet been clarified. We compared the efficacy of amitriptyline (25 mg/day) in 82 nondepressed patients with either chronic or episodic tension-type headache in an open-label study. Amitriptyline significantly reduced (P < 0.05) frequency and duration of headache as well as analgesic consumption in chronic, but not in episodic, tension-type headache. Further placebo-controlled trials, possibly with higher doses of amitriptyline, might confirm if the different pattern of response to amitriptyline can be explained in terms of different involvement of central nociception and of peripheral myofascial factors in the chronic and in the episodic forms of tension-type headache.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "957", "doc_id": "22995579", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Beta-band coherence is enhanced for visible stimuli over invisible stimuli.\n\nCANDIDATE_ABSTRACT:\nTITLE: Converging Intracranial Markers of Conscious Access\nABSTRACT: We compared conscious and nonconscious processing of briefly flashed words using a visual masking procedure while recording intracranial electroencephalogram (iEEG) in ten patients. Nonconscious processing of masked words was observed in multiple cortical areas, mostly within an early time window (<300 ms), accompanied by induced gamma-band activity, but without coherent long-distance neural activity, suggesting a quickly dissipating feedforward wave. In contrast, conscious processing of unmasked words was characterized by the convergence of four distinct neurophysiological markers: sustained voltage changes, particularly in prefrontal cortex, large increases in spectral power in the gamma band, increases in long-distance phase synchrony in the beta range, and increases in long-range Granger causality. We argue that all of those measures provide distinct windows into the same distributed state of conscious processing. These results have a direct impact on current theoretical discussions concerning the neural correlates of conscious access.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 175, "doc_id": "1710116", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Increased LDL receptors plays a role in the reduction of plasma Lp(a).\n\nCANDIDATE_PASSAGE:\nEffects of PCSK9 Inhibition With Alirocumab on Lipoprotein Metabolism in Healthy Humans BACKGROUND Alirocumab, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), lowers plasma low-density lipoprotein (LDL) cholesterol and apolipoprotein B100 (apoB). Although studies in mice and cells have identified increased hepatic LDL receptors as the basis for LDL lowering by PCSK9 inhibitors, there have been no human studies characterizing the effects of PCSK9 inhibitors on lipoprotein metabolism. In particular, it is not known whether inhibition of PCSK9 has any effects on very low-density lipoprotein or intermediate-density lipoprotein (IDL) metabolism. Inhibition of PCSK9 also results in reductions of plasma lipoprotein (a) levels. The regulation of plasma Lp(a) levels, including the role of LDL receptors in the clearance of Lp(a), is poorly defined, and no mechanistic studies of the Lp(a) lowering by alirocumab in humans have been published to date. METHODS Eighteen (10 F, 8 mol/L) participants completed a placebo-controlled, 2-period study. They received 2 doses of placebo, 2 weeks apart, followed by 5 doses of 150 mg of alirocumab, 2 weeks apart. At the end of each period, fractional clearance rates (FCRs) and production rates (PRs) of apoB and apo(a) were determined. In 10 participants, postprandial triglycerides and apoB48 levels were measured. RESULTS Alirocumab reduced ultracentrifugally isolated LDL-C by 55.1%, LDL-apoB by 56.3%, and plasma Lp(a) by 18.7%. The fall in LDL-apoB was caused by an 80.4% increase in LDL-apoB FCR and a 23.9% reduction in LDL-apoB PR. The latter was due to a 46.1% increase in IDL-apoB FCR coupled with a 27.2% decrease in conversion of IDL to LDL. The FCR of apo(a) tended to increase (24.6%) without any c [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "603", "doc_id": "6540064", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Ultrasound guidance significantly reduces the number of traumatic procedures when attempting needle insertion.\n\nCANDIDATE_PASSAGE:\nN348I in the Connection Domain of HIV-1 Reverse Transcriptase Confers Zidovudine and Nevirapine Resistance Background The catalytically active 66-kDa subunit of the human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) consists of DNA polymerase, connection, and ribonuclease H (RNase H) domains. Almost all known RT inhibitor resistance mutations identified to date map to the polymerase domain of the enzyme. However, the connection and RNase H domains are not routinely analysed in clinical samples and none of the genotyping assays available for patient management sequence the entire RT coding region. The British Columbia Centre for Excellence in HIV/AIDS (the Centre) genotypes clinical isolates up to codon 400 in RT, and our retrospective statistical analyses of the Centre’s database have identified an N348I mutation in the RT connection domain in treatment-experienced individuals. The objective of this multidisciplinary study was to establish the in vivo relevance of this mutation and its role in drug resistance. Methods and Findings The prevalence of N348I in clinical isolates, the time taken for it to emerge under selective drug pressure, and its association with changes in viral load, specific drug treatment, and known drug resistance mutations was analysed from genotypes, viral loads, and treatment histories from the Centre’s database. N348I increased in prevalence from below 1% in 368 treatmentnao ¨ve individuals to 12.1% in 1,009 treatment-experienced patients (p ¼ 7.7 3 10 � 12 ). N348I appeared early in therapy and was highly associated with thymidine analogue mutations (TAMs) M41L and T215Y/F (p , 0.001), the lamivudine resistance mutations M184V/I (p , 0.001), and non-nucleoside RTI (NNRTI) resistance mutations K103N and Y181C/I (p [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1341", "doc_id": "15319019", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Mice without IFN-γ or its receptor are highly susceptible to EAM induced with α-MyHC/CFA.\n\nCANDIDATE_ABSTRACT:\nTITLE: the Development of Autoimmune Myocarditis in Mice by an\nABSTRACT: BACKGROUND Interleukin (IL)-12 exerts a potent proinflammatory effect by stimulating T-helper (Th) 1 responses. This effect is believed to be mediated primarily through the activation of STAT4 and subsequent production of interferon (IFN)-gamma. Methods and Results- We examined the role of IL-12 receptor (IL-12R) signaling in the development of murine experimental autoimmune myocarditis (EAM) induced by cardiac myosin immunization. Both IL-12Rbeta1-deficient mice and STAT4-deficient mice were resistant to the induction of myocarditis. Treatment with exogenous IL-12 exacerbated disease. We questioned whether IFN-gamma is required for the disease-promoting activity of IL-12. On the contrary, we found that IFN-gamma suppresses EAM. Lack of IFN-gamma due to either depletion with an antibody or a genetic deficiency exacerbated myocarditis. Spleens from IFN-gamma-deficient mice immunized with cardiac myosin showed increased cellularity; greater numbers of CD3+, CD4+, CD8+, and IL-2-producing cells; and heightened ability to produce cytokines on stimulation in vitro. Treatment of mice with recombinant IFN-gamma suppressed the development of myocarditis. CONCLUSIONS IL-12/IL-12R/STAT4 signaling promotes the development of EAM. In contrast, IFN-gamma plays a protective role. The disease-limiting effects of IFN-gamma might be explained by its ability to control the expansion of activated T lymphocytes.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In contrast, IFN-gamma plays a protective role.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 782, "doc_id": "8246922", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Mutations in G-Beta protein GNB1 are present in many cancers, resulting in loss of interaction with G-alpha subunits and concomitant activation of AKT pathway.\n\nCANDIDATE_PASSAGE:\nThe Self-Incompatibility Genes of Brassica: Expression and Use in Genetic Ablation of Floral Tissues INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 394 POLLINATION AND POLLEN TUBE GROWTH . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 395 Interaction s between the M ale G ameto phyte and Pistil . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 395 SelfIncom patibili ty Systems: Gameto phytic and S poro phyti c Determin ation of Pollen Phenoty pe . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 397 DEVELOPMENTAL S TUDIES OF REPRODUCTIVE STRUCTURES . . . . . . . . .. . . ... . . . . 398 Tissues of the Pistil with Special Reference to Pollination Functions 398 The Male Gametophyte . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 399 MOLECULAR ANALYSIS OF SELF-INCOMPATIBILITY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40 1 The S-M ultigene F amily o j Brassica. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . 402 Allelism at the S-Lo cus and the SLG Gene\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\" 402 The S-Locus Related (SLR) Genes 405 Molecular Complexity oj the S-Locus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 407 EXPRESSION OF THE SLG GENE IN PIS TILS AND ANTHERS . . . . . . . . . . . . . . . . . . . . . . . 409 Expression in Cruc ifers . . . . . . . . . . . . . . . . . . . . . . . . . [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "813", "doc_id": "86217760", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Crossover hot spots are not found within gene promoters in Saccharomyces cerevisiae.\n\nCANDIDATE_PASSAGE:\nCoordinate regulation of the IL-4, IL-13, and IL-5 cytokine cluster in Th2 clones revealed by allelic expression patterns. The cytokines IL-4, IL-13, and IL-5 are markers for the Th2 subset of effector T cells and are often expressed together. These cytokine genes are organized within 140 kb of orthologous DNA in both mouse and human. Using IL-4-expressing CD4+ T cell clones derived from F1 mice, we identified allelic polymorphisms for each of these cytokines and assessed the parental identity of the cytokine mRNAs. Both monoallelic and biallelic expression occurred for each gene and for an additional gene, IL-3, that lies with GM-CSF over 450 kb telomeric on the same chromosome. When coexpressed in T cell clones, IL-4 was expressed from the same allele as IL-13 or IL-5 in 81% of instances. In contrast, there was only 52% concordance of these three cytokines at the allelic level among clones that expressed IL-3. Independent expression of the cytokine alleles occurs commonly in T cells, but the clustered locus encompassing IL-4, IL-13, and IL-5 is subject to coordinate regulation.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "294", "doc_id": "36242796", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is Panton-Valentine leucocidin associated with the pathogenesis of Staphylococcus aureus bacteraemia in the UK?\n\nABSTRACT:\nThe morbidity and mortality associated with Panton-Valentine leucocidin (PVL)-positive Staphylococcus aureus suggest that this toxin is a key marker of disease severity. Nevertheless, the importance of PVL in the pathogenesis of primary bacteraemia caused by S. aureus is uncertain. We have determined the prevalence of PVL-encoding genes among isolates of S. aureus from bacteraemic patients. Consecutive bacteraemia isolates of S. aureus (n=244) from patients hospitalized in 25 centres in the UK and Ireland during 2005 were screened for PVL and mecA genes. PVL-positive isolates were characterized by toxin gene profiling, PFGE, spa-typing and MIC determinations for a range of antimicrobials. Four out of 244 isolates (1.6%) were PVL-positive and susceptible to oxacillin [methicillin-susceptible S. aureus (MSSA)]. Eighty-eight out of 244 (36%) were oxacillin-resistant (methicillin-resistant S. aureus), but none was PVL-positive. The four patients (two males: 30 and 33 years; two females: 62 and 80 years) had infection foci of: skin and soft tissue, unknown, indwelling line, and surgical site, and were located at one centre in Wales, one in England and two in Ireland. One of four PVL-positive isolates was resistant to penicillin and fusidic acid, the remainder were susceptible to all antibiotics tested. Genotypic analyses showed that the four isolates represented three distinct strains; the two isolates from Ireland were related.", "output": "{\"label\": \"maybe\", \"rationale\": \"We found that 1.6% of S. aureus (all MSSA) from bacteraemic patients were PVL-positive. This low incidence suggests that PVL-positive S.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 17562682, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Drosophila supracellular actomyosin structures are found at boundaries in wing imaginal discs.\n\nCANDIDATE_PASSAGE:\nIn vitro differentiation of transplantable neural precursors from human embryonic stem cells The remarkable developmental potential and replicative capacity of human embryonic stem (ES) cells promise an almost unlimited supply of specific cell types for transplantation therapies. Here we describe the in vitro differentiation, enrichment, and transplantation of neural precursor cells from human ES cells. Upon aggregation to embryoid bodies, differentiating ES cells formed large numbers of neural tube–like structures in the presence of fibroblast growth factor 2 (FGF-2). Neural precursors within these formations were isolated by selective enzymatic digestion and further purified on the basis of differential adhesion. Following withdrawal of FGF-2, they differentiated into neurons, astrocytes, and oligodendrocytes. After transplantation into the neonatal mouse brain, human ES cell–derived neural precursors were incorporated into a variety of brain regions, where they differentiated into both neurons and astrocytes. No teratoma formation was observed in the transplant recipients. These results depict human ES cells as a source of transplantable neural precursors for possible nervous system repair.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "355", "doc_id": "2437807", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: ATM and Rad3 related protein have no role in sensing DNA damage.\n\nCANDIDATE_PASSAGE:\nAssociation Between Early Screening for Patent Ductus Arteriosus and In-Hospital Mortality Among Extremely Preterm Infants. IMPORTANCE There is currently no consensus for the screening and treatment of patent ductus arteriosus (PDA) in extremely preterm infants. Less pharmacological closure and more supportive management have been observed without evidence to support these changes. OBJECTIVE To evaluate the association between early screening echocardiography for PDA and in-hospital mortality. DESIGN, SETTING, AND PARTICIPANTS Comparison of screened and not screened preterm infants enrolled in the EPIPAGE 2 national prospective population-based cohort study that included all preterm infants born at less than 29 weeks of gestation and hospitalized in 68 neonatal intensive care units in France from April through December 2011. Two main analyses were performed to adjust for potential selection bias, one using propensity score matching and one using neonatal unit preference for early screening echocardiography as an instrumental variable. EXPOSURES Early screening echocardiography before day 3 of life. MAIN OUTCOMES AND MEASURES The primary outcome was death between day 3 and discharge. The secondary outcomes were major neonatal morbidities (pulmonary hemorrhage, severe bronchopulmonary dysplasia, severe cerebral lesions, and necrotizing enterocolitis). RESULTS Among the 1513 preterm infants with data available to determine exposure, 847 were screened for PDA and 666 were not; 605 infants from each group could be paired. Exposed infants were treated for PDA more frequently during their hospitalization than nonexposed infants (55.1% vs 43.1%; odds ratio [OR], 1.62 [95% CI, 1.31 to 2.00]; absolute risk reduction [ARR] in events per 100 infants, -12.0 [95% CI, -17. [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "64", "doc_id": "27099731", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: A diminished ovarian reserve is a very strong indicator of infertility, even in an a priori non-infertile population.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\nABSTRACT: Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential. Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age. Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area. Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH. Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle). Conception was defined as a positive pregnancy test result. Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis. After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively). Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cy [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 40, "doc_id": "13497630", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Artefacts in 24-h pharyngeal and oesophageal pH monitoring: is simplification of pH data analysis feasible?\n\nABSTRACT:\nAmbulatory 24-h dual-channel pharyngeal and oesophageal pH monitoring is the standard test for measuring gastro-oesophageal and gastropharyngeal reflux. Artefacts caused by the intake of food may result in falsely positive gastropharyngeal reflux, which necessitates a manual review of 24-h pH data. The purpose of the study was to investigate the influence of meals and whether leaving out meals affected the reliability of the test. Patients referred for otolaryngological complaints, suspected to have been caused by gastro-oesophageal reflux, underwent 24-h dual-channel pH monitoring. The raw unprocessed pH data were corrected by visual inspection of the 24-h tracings (corrected data), by leaving out meals or meals plus a 2-h postprandrial period. The raw pH data were substantially influenced by artefacts of food intake and pseudoreflux. Data obtained by leaving out meals agreed best with manually corrected data. Many of the falsely positive reflux episodes could be removed, thereby inducing a 9%-18% chance of undetected reflux. When examining the fraction of time supine, manually corrected data and data leaving out meals were fully concordant and detected 79% of patients with gastropharyngeal reflux. However, leaving out meals plus a 2-h postprandrial period resulted in 21%-50% falsely negative tests.", "output": "{\"label\": \"maybe\", \"rationale\": \"Leaving out the period of intake of meals and beverages from the raw pH data might be the second best test after the time-consuming visual correction with a small chance of undetected gastropharyngeal reflux. For scientific purposes and when in doubt, it remains necessary to review the computer-generated data manually to discover every gastropharyngeal reflux event.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 14992556, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: MICAL redox enzymes regulate actin dynamics in many cell types.\n\nCANDIDATE_ABSTRACT:\nTITLE: The behaviour change wheel: A new method for characterising and designing behaviour change interventions\nABSTRACT: BACKGROUND Improving the design and implementation of evidence-based practice depends on successful behaviour change interventions. This requires an appropriate method for characterising interventions and linking them to an analysis of the targeted behaviour. There exists a plethora of frameworks of behaviour change interventions, but it is not clear how well they serve this purpose. This paper evaluates these frameworks, and develops and evaluates a new framework aimed at overcoming their limitations. METHODS A systematic search of electronic databases and consultation with behaviour change experts were used to identify frameworks of behaviour change interventions. These were evaluated according to three criteria: comprehensiveness, coherence, and a clear link to an overarching model of behaviour. A new framework was developed to meet these criteria. The reliability with which it could be applied was examined in two domains of behaviour change: tobacco control and obesity. RESULTS Nineteen frameworks were identified covering nine intervention functions and seven policy categories that could enable those interventions. None of the frameworks reviewed covered the full range of intervention functions or policies, and only a minority met the criteria of coherence or linkage to a model of behaviour. At the centre of a proposed new framework is a 'behaviour system' involving three essential conditions: capability, opportunity, and motivation (what we term the 'COM-B system'). This forms the hub of a 'behaviour change wheel' (BCW) around which are positioned the nine intervention functions aimed at addressing deficits in one or more of these conditions; around this are placed seven categories of policy that could enable those interventions to occur. The BCW was us [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 737, "doc_id": "704526", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: 1 in 5 million in UK have abnormal PrP positivity.\n\nCANDIDATE_PASSAGE:\nPrevalent abnormal prion protein in human appendixes after bovine spongiform encephalopathy epizootic: large scale survey OBJECTIVES To carry out a further survey of archived appendix samples to understand better the differences between existing estimates of the prevalence of subclinical infection with prions after the bovine spongiform encephalopathy epizootic and to see whether a broader birth cohort was affected, and to understand better the implications for the management of blood and blood products and for the handling of surgical instruments. DESIGN Irreversibly unlinked and anonymised large scale survey of archived appendix samples. SETTING Archived appendix samples from the pathology departments of 41 UK hospitals participating in the earlier survey, and additional hospitals in regions with lower levels of participation in that survey. SAMPLE 32,441 archived appendix samples fixed in formalin and embedded in paraffin and tested for the presence of abnormal prion protein (PrP). RESULTS Of the 32,441 appendix samples 16 were positive for abnormal PrP, indicating an overall prevalence of 493 per million population (95% confidence interval 282 to 801 per million). The prevalence in those born in 1941-60 (733 per million, 269 to 1596 per million) did not differ significantly from those born between 1961 and 1985 (412 per million, 198 to 758 per million) and was similar in both sexes and across the three broad geographical areas sampled. Genetic testing of the positive specimens for the genotype at PRNP codon 129 revealed a high proportion that were valine homozygous compared with the frequency in the normal population, and in stark contrast with confirmed clinical cases of vCJD, all of which were methionine homozygous at PRNP codon 129. CONCLUSIONS This s [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "2", "doc_id": "13734012", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Pyridostatin deregulates G2/M progression.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tet2 is required to resolve inflammation by recruiting Hdac2 to specifically repress IL-6\nABSTRACT: Epigenetic modifiers have fundamental roles in defining unique cellular identity through the establishment and maintenance of lineage-specific chromatin and methylation status. Several DNA modifications such as 5-hydroxymethylcytosine (5hmC) are catalysed by the ten eleven translocation (Tet) methylcytosine dioxygenase family members, and the roles of Tet proteins in regulating chromatin architecture and gene transcription independently of DNA methylation have been gradually uncovered. However, the regulation of immunity and inflammation by Tet proteins independent of their role in modulating DNA methylation remains largely unknown. Here we show that Tet2 selectively mediates active repression of interleukin-6 (IL-6) transcription during inflammation resolution in innate myeloid cells, including dendritic cells and macrophages. Loss of Tet2 resulted in the upregulation of several inflammatory mediators, including IL-6, at late phase during the response to lipopolysaccharide challenge. Tet2-deficient mice were more susceptible to endotoxin shock and dextran-sulfate-sodium-induced colitis, displaying a more severe inflammatory phenotype and increased IL-6 production compared to wild-type mice. IκBζ, an IL-6-specific transcription factor, mediated specific targeting of Tet2 to the Il6 promoter, further indicating opposite regulatory roles of IκBζ at initial and resolution phases of inflammation. For the repression mechanism, independent of DNA methylation and hydroxymethylation, Tet2 recruited Hdac2 and repressed transcription of Il6 via histone deacetylation. We provide mechanistic evidence for the gene-specific transcription repression activity of Tet2 via histone deacetylation and for the prevention of constant transcription activation at the chromatin level [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 992, "doc_id": "2405259", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Incidence of heart failure increased by 10% in women since 1979.\n\nCANDIDATE_PASSAGE:\nThioredoxin mediates oxidation-dependent phosphorylation of CRMP2 and growth cone collapse. Semaphorin3A (Sema3A) is a repulsive guidance molecule for axons, which acts by inducing growth cone collapse through phosphorylation of CRMP2 (collapsin response mediator protein 2). Here, we show a role for CRMP2 oxidation and thioredoxin (TRX) in the regulation of CRMP2 phosphorylation and growth cone collapse. Sema3A stimulation generated hydrogen peroxide (H2O2) through MICAL (molecule interacting with CasL) and oxidized CRMP2, enabling it to form a disulfide-linked homodimer through cysteine-504. Oxidized CRMP2 then formed a transient disulfide-linked complex with TRX, which stimulated CRMP2 phosphorylation by glycogen synthase kinase-3, leading to growth cone collapse. We also reconstituted oxidation-dependent phosphorylation of CRMP2 in vitro, using a limited set of purified proteins. Our results not only clarify the importance of H2O2 and CRMP2 oxidation in Sema3A-induced growth cone collapse but also indicate an unappreciated role for TRX in linking CRMP2 oxidation to phosphorylation.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "594", "doc_id": "33912020", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Individuals with Alzheimers who participate in six months of physical activity improve cognitive function for up to 18 months.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effect of physical activity on cognitive function in older adults at risk for Alzheimer disease: a randomized trial.\nABSTRACT: CONTEXT Many observational studies have shown that physical activity reduces the risk of cognitive decline; however, evidence from randomized trials is lacking. OBJECTIVE To determine whether physical activity reduces the rate of cognitive decline among older adults at risk. DESIGN AND SETTING Randomized controlled trial of a 24-week physical activity intervention conducted between 2004 and 2007 in metropolitan Perth, Western Australia. Assessors of cognitive function were blinded to group membership. PARTICIPANTS We recruited volunteers who reported memory problems but did not meet criteria for dementia. Three hundred eleven individuals aged 50 years or older were screened for eligibility, 89 were not eligible, and 52 refused to participate. A total of 170 participants were randomized and 138 participants completed the 18-month assessment. INTERVENTION Participants were randomly allocated to an education and usual care group or to a 24-week home-based program of physical activity. MAIN OUTCOME MEASURE Change in Alzheimer Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) scores (possible range, 0-70) over 18 months. RESULTS In an intent-to-treat analysis, participants in the intervention group improved 0.26 points (95% confidence interval, -0.89 to 0.54) and those in the usual care group deteriorated 1.04 points (95% confidence interval, 0.32 to 1.82) on the ADAS-Cog at the end of the intervention. The absolute difference of the outcome measure between the intervention and control groups was -1.3 points (95% confidence interval,-2.38 to -0.22) at the end of the intervention. At 18 months, participants in the intervention group improved 0.73 points (95% confidence interval, -1.27 to 0.03) on the ADAS-Cog, and those in the usual care group improved 0.04 p [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"RESULTS In an intent-to-treat analysis, participants in the intervention group improved 0.26 points (95% confidence interval, -0.89 to 0.54) and those in the usual care group deteriorated 1.04 points (95% confidence interval, 0.32 to 1.82) on the ADAS-Cog at the end of the intervention.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 621, "doc_id": "1642727", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is acute T-cell activation detectable in unstable angina?\n\nABSTRACT:\nRecent studies suggest a role for inflammation in the pathophysiology of unstable angina. This study was designed to investigate whether circulating lymphocytes are involved in the inflammatory reaction associated with the episodes of unstable angina. Twenty-nine patients with proven unstable angina, 36 with stable angina, and 30 healthy subjects were studied. Both early and short-lived (interleukin-2 receptor [IL-2R], alpha-chain CD25, and transferrin receptor CD71) and late antigen (HLA-DR) expression were investigated by flow cytometric analysis. Soluble IL-2R (sIL-2R) was also measured in plasma by ELISA. Lymphocyte activation was studied at day 1 of hospital admission and after 7, 15, 30, 60, and 90 days. In patients with unstable angina, the number of HLA-DR+ CD3 lymphocytes and levels of sIL-2R were higher (P < .001) than in patients with stable angina and control subjects. Both CD4+ and CD8+ lymphocytes expressed HLA-DR antigens. No differences were found among the different groups of subjects in regard to the expression of CD25 and CD71. Lymphocyte activation was more marked in patients with urgent revascularization. No relationships were found between the number of HLA-DR+ lymphocytes and either the severity of coronary angiographic lesions or the number of ischemic episodes. Observations over time showed a gradual decrease in the number of HLA-DR+ lymphocytes and sIL-2R levels from weeks 3 through 8 to 12.", "output": "{\"label\": \"yes\", \"rationale\": \"The present results indicate that (1) CD4+ and CD8+ circulating lymphocytes are activated in patients with unstable angina, and their activation state lasts 6 to 8 weeks; and (2) activation of lymphocytes is not a consequence of myocardial ischemia. These results support the immune system-mediated inflammatory nature of unstable angina.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 9107167, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Activated Cdk5 regulates DNA damage-induced neuronal death.\n\nCANDIDATE_ABSTRACT:\nTITLE: Phosphorylation of ATM by Cdk5 mediates DNA damage signaling and regulates neuronal death\nABSTRACT: The phosphatidylinositol-3-kinase-like kinase ATM (ataxia-telangiectasia mutated) has a central role in coordinating DNA damage responses, including cell-cycle checkpoint control, DNA repair and apoptosis. Mutations of ATM cause a spectrum of defects ranging from neurodegeneration to cancer predisposition. However, the mechanism by which DNA damage activates ATM is poorly understood. Here we show that Cdk5 (cyclin-dependent kinase 5), activated by DNA damage, directly phosphorylates ATM at Ser 794 in post-mitotic neurons. Phosphorylation at Ser 794 precedes, and is required for, ATM autophosphorylation at Ser 1981, and activates ATM kinase activity. The Cdk5-ATM signal regulates phosphorylation and function of the ATM targets p53 and H2AX. Interruption of the Cdk5-ATM pathway attenuates DNA-damage-induced neuronal cell cycle re-entry and expression of the p53 targets PUMA and Bax, protecting neurons from death. Thus, activation of Cdk5 by DNA damage serves as a critical signal to initiate the ATM response and regulate ATM-dependent cellular processes.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Interruption of the Cdk5-ATM pathway attenuates DNA-damage-induced neuronal cell cycle re-entry and expression of the p53 targets PUMA and Bax, protecting neurons from death.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 68, "doc_id": "21295300", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Medications to treat obesity do not have side effects.\n\nCANDIDATE_ABSTRACT:\nTITLE: Long term pharmacotherapy for obesity and overweight: updated meta-analysis.\nABSTRACT: OBJECTIVE To summarise the long term efficacy of anti-obesity drugs in reducing weight and improving health status. DESIGN Updated meta-analysis of randomised trials. DATA SOURCES Medline, Embase, the Cochrane controlled trials register, the Current Science meta-register of controlled trials, and reference lists of identified articles. All data sources were searched from December 2002 (end date of last search) to December 2006. STUDIES REVIEWED Double blind randomised placebo controlled trials of approved anti-obesity drugs used in adults (age over 18) for one year or longer. RESULTS 30 trials of one to four years' duration met the inclusion criteria: 16 orlistat (n=10 631 participants), 10 sibutramine (n=2623), and four rimonabant (n=6365). Of these, 14 trials were new and 16 had previously been identified. Attrition rates averaged 30-40%. Compared with placebo, orlistat reduced weight by 2.9 kg (95% confidence interval 2.5 kg to 3.2 kg), sibutramine by 4.2 kg (3.6 kg to 4.7 kg), and rimonabant by 4.7 kg (4.1 kg to 5.3 kg). Patients receiving active drug treatment were significantly more likely to achieve 5% and 10% weight loss thresholds. Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein. Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorde [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 765, "doc_id": "7552215", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Transcription rates in S. cerevisiae range between 7 and 12 kb/min.\n\nCANDIDATE_ABSTRACT:\nTITLE: Distinction and relationship between elongation rate and processivity of RNA polymerase II in vivo.\nABSTRACT: A number of proteins and drugs have been implicated in the process of transcriptional elongation by RNA polymerase (Pol) II, but the factors that govern the elongation rate (nucleotide additions per min) and processivity (nucleotide additions per initiation event) in vivo are poorly understood. Here, we show that a mutation in the Rpb2 subunit of Pol II reduces both the elongation rate and processivity in vivo. In contrast, none of the putative elongation factors tested affect the elongation rate, although mutations in the THO complex and in Spt4 significantly reduce processivity. The drugs 6-azauracil and mycophenolic acid reduce both the elongation rate and processivity, and this processivity defect is aggravated by mutations in Spt4, TFIIS, and CTDK-1. Our results suggest that, in vivo, a reduced rate of Pol II elongation leads to premature dissociation along the chromatin template and that Pol II processivity can be uncoupled from elongation rate.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1315, "doc_id": "13072112", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Auditory entrainment is strengthened when people see congruent visual and auditory information.\n\nCANDIDATE_PASSAGE:\nThe association between common physical impairments and dementia in low and middle income countries, and, among people with dementia, their association with cognitive function and disability. A 10/66 Dementia Research Group population-based study. OBJECTIVE Chronic physical comorbidity is common in dementia. However, there is an absence of evidence to support good practice guidelines for attention to these problems. We aimed to study the extent of this comorbidity and its impact on cognitive function and disability in population-based studies in low and middle income countries, where chronic diseases and impairments are likely to be both common and undertreated. METHODS A multicentre cross-sectional survey of all over 65 year old residents (n = 15 022) in 11 catchment areas in China, India, Cuba, Dominican Republic, Venezuela, Mexico and Peru. We estimated the prevalence of pain, incontinence, hearing and visual impairments, mobility impairment and undernutrition according to the presence of dementia and its severity, and, among those with dementia, the independent contribution of these impairments to cognitive function and disability, adjusting for age, gender, education and dementia severity. RESULTS Incontinence, hearing impairment, mobility impairment and undernutrition were consistently linearly associated with the presence of dementia and its severity across regions. Among people with dementia, incontinence, hearing impairment and mobility impairment were independently associated with disability in all regions while the contributions of pain, visual impairment and undernutrition were inconsistent. Only hearing impairment made a notable independent contribution to cognitive impairment. CONCLUSIONS There is an urgent need for clinical trials of the feasi [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "141", "doc_id": "21274919", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is perforation of the appendix a risk factor for tubal infertility and ectopic pregnancy?\n\nABSTRACT:\nTo critically assess the evidence that appendiceal perforation is a risk factor for subsequent tubal infertility or ectopic pregnancy. Epidemiologic studies investigating the relationship between appendectomy and infertility or ectopic pregnancy were identified by searching the MEDLINE database from 1966 to 1997. Appropriate citations were also extracted from a manual search of the bibliographies of selected papers. Twenty-three articles were retrieved. Only 4 presented original data including comparisons to a nonexposed control group and they form the basis for this study. Because the raw data or specific techniques of data analysis were not always explicitly described, indices of risk for exposure were extracted from the data as presented and were analysed without attempting to convert them to a common measure. Articles were assessed according to the criteria of the Evidence-Based Medicine Working Group for evaluating articles on harm. Review of the literature yielded estimates of the risk of adverse fertility outcomes ranging from 1.6 (95% confidence interval [CI] 1.1 to 2.5) for ectopic pregnancy after an appendectomy to 4.8 (95% CI 1.5 to 14.9) for tubal infertility from perforation of the appendix. Recall bias, and poor adjustment for confounding variables in some reports, weakened the validity of the studies.", "output": "{\"label\": \"maybe\", \"rationale\": \"The methodologic weaknesses of the studies do not permit acceptance of increased risk of tubal pregnancy or infertility as a consequence of perforation of the appendix, so a causal relationship cannot be supported by the data currently available. Only a well-designed case-control study with unbiased ascertainment of exposure and adjustment for confounding variables will provide a definitive answer.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 10223070, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Decreased conversion of PGE 2 to PPARy ligand 15-ket-PGE 2 causes accumulation of PGE.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pharmacological correction of a defect in PPARγ signaling ameliorates disease severity in Cftr-deficient mice\nABSTRACT: Cystic fibrosis is caused by mutations in the cystic fibrosis transmembrane conductance regulator (encoded by Cftr) that impair its role as an apical chloride channel that supports bicarbonate transport. Individuals with cystic fibrosis show retained, thickened mucus that plugs airways and obstructs luminal organs as well as numerous other abnormalities that include inflammation of affected organs, alterations in lipid metabolism and insulin resistance. Here we show that colonic epithelial cells and whole lung tissue from Cftr-deficient mice show a defect in peroxisome proliferator-activated receptor-gamma (PPAR-gamma, encoded by Pparg) function that contributes to a pathological program of gene expression. Lipidomic analysis of colonic epithelial cells suggests that this defect results in part from reduced amounts of the endogenous PPAR-gamma ligand 15-keto-prostaglandin E(2) (15-keto-PGE(2)). Treatment of Cftr-deficient mice with the synthetic PPAR-gamma ligand rosiglitazone partially normalizes the altered gene expression pattern associated with Cftr deficiency and reduces disease severity. Rosiglitazone has no effect on chloride secretion in the colon, but it increases expression of the genes encoding carbonic anhydrases 4 and 2 (Car4 and Car2), increases bicarbonate secretion and reduces mucus retention. These studies reveal a reversible defect in PPAR-gamma signaling in Cftr-deficient cells that can be pharmacologically corrected to ameliorate the severity of the cystic fibrosis phenotype in mice.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 316, "doc_id": "712078", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Intra-cerebroventricular infusion of amyloid-β oligomers reduces expression of fibronectin type-III domain-containing protein 5 mRNA in mice hippocampi.\n\nCANDIDATE_PASSAGE:\nEpigenetic therapy activates type I interferon signaling in murine ovarian cancer to reduce immunosuppression and tumor burden. Ovarian cancer is the most lethal of all gynecological cancers, and there is an urgent unmet need to develop new therapies. Epithelial ovarian cancer (EOC) is characterized by an immune suppressive microenvironment, and response of ovarian cancers to immune therapies has thus far been disappointing. We now find, in a mouse model of EOC, that clinically relevant doses of DNA methyltransferase and histone deacetylase inhibitors (DNMTi and HDACi, respectively) reduce the immune suppressive microenvironment through type I IFN signaling and improve response to immune checkpoint therapy. These data indicate that the type I IFN response is required for effective in vivo antitumorigenic actions of the DNMTi 5-azacytidine (AZA). Through type I IFN signaling, AZA increases the numbers of CD45+ immune cells and the percentage of active CD8+ T and natural killer (NK) cells in the tumor microenvironment, while reducing tumor burden and extending survival. AZA also increases viral defense gene expression in both tumor and immune cells, and reduces the percentage of macrophages and myeloid-derived suppressor cells in the tumor microenvironment. The addition of an HDACi to AZA enhances the modulation of the immune microenvironment, specifically increasing T and NK cell activation and reducing macrophages over AZA treatment alone, while further increasing the survival of the mice. Finally, a triple combination of DNMTi/HDACi plus the immune checkpoint inhibitor α-PD-1 provides the best antitumor effect and longest overall survival, and may be an attractive candidate for future clinical trials in ovarian cancer.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "655", "doc_id": "9767444", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Articles published in open access format are less likely to be cited than traditional journals.\n\nCANDIDATE_PASSAGE:\nART adherence clubs: A long-term retention strategy for clinically stable patients receiving antiretroviral therapy The ART-adherence club model described here provides patient-friendly access to antiretroviral therapy (ART) for clinically stable patients. It reduces the burden that stable patients place on healthcare facilities, increasing clinical human resources for new patients, and those clinically unstable and at risk of failing treatment. In the model, 30 patients are allocated to an ART club. The group meets either at a facility or community venue for less than an hour every 2 months. Group meetings are facilitated by a lay club facilitator who provides a quick clinical assessment, referral where necessary, and dispenses pre-packed ART. From January 2011 to December 2012, after adoption for phased rollout by the Western Cape Government, more than 600 ART clubs were established in Cape Town, providing ART care to over 16 000 patients. This extensive, rapid rollout demonstrates active buy-in from patients and facility staff. South Africa should consider a similar model for national rollout.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "129", "doc_id": "57121667", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Reduction of purity of cytoplasmic membranes isolated from overexpressors is indicated by stronger spots for OmpF in 2D BN-PAGE gels.\n\nCANDIDATE_PASSAGE:\nCaspase inhibitors promote alternative cell death pathways. The use of caspase inhibitors has revealed the existence of alternative backup cell death programs for apoptosis. The broad-spectrum caspase inhibitor zVAD-fmk modulates the three major types of cell death. Addition of zVAD-fmk blocks apoptotic cell death, sensitizes cells to necrotic cell death, and induces autophagic cell death. Several studies have shown a crucial role for the kinase RIP1 and the adenosine nucleotide translocator (ANT)-cyclophilin D (CypD) complex in necrotic cell death. The underlying mechanism of zVAD-fmk-mediated sensitization to necrotic cell death involves the inhibition of caspase-8-mediated proteolysis of RIP1 and disturbance of the ANT-CypD interaction. RIP1 is also involved in autophagic cell death. Caspase inhibitors and knockdown studies have revealed negative roles for catalase and caspase-8 in autophagic cell death. The positive role of RIP1 and the negative role of caspase-8 in both necrotic and autophagic cell death suggest that the pathways of these two types of cell death are interconnected. Necrotic cell death represents a rapid cellular response involving mitochondrial reactive oxygen species (ROS) production, decreased adenosine triphosphate concentration, and other cellular insults, whereas autophagic cell death first starts as a survival attempt by cleaning up ROS-damaged mitochondria. However, when this process occurs in excess, autophagy itself becomes cytotoxic and eventually leads to autophagic cell death. A better understanding of the molecular mechanisms of these alternative cell death pathways may provide therapeutic tools to combat cell death associated with neurodegenerative diseases, ischemia-reperfusion pathologies, and infectious diseases, and ma [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1033", "doc_id": "25251625", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The minor G allele of FOXO3 is related to less severe symptoms of Crohn's Disease.\n\nCANDIDATE_PASSAGE:\nDeveloping primary palliative care. Although 65% of people with cancer want to die at home, only about 30% are successful in doing so.1,2 A government committed to choice for patients must improve this figure.3 Developing palliative care services in primary care is essential for realising the expectations of dying people. Such services could also offer important opportunities for extending supportive humane care at an earlier stage, and to people not only with cancer but with chronic obstructive pulmonary disease, motor neurone disease, and cardiac failure, for example, who also often have palliative care needs. Primary care professionals have the potential and ability to provide end of life care for most patients, given adequate training, resources, and, when needed, specialist advice.4,5 They share common values with palliative care specialists—holistic, patient centred care, delivered in the context of families and friends.6 However, until recently, apart from Macmillan general practitioners and nurse facilitators, few comprehensive workforce initiatives have been undertaken in primary care that focus on end of life care. Many cancer patients and their carers experience existential distress long before they die.7 Recognising and alleviating such suffering is important, but it often goes unrecognised or is overlooked by services focusing on the terminal phase of illnesses. Primary care teams may know patients over long periods of time. They can readily identify patients from cancer and chronic disease registers who might benefit from an early palliative care approach. Such patients could be identified by clinicians asking one simple question of themselves: “Would I be surprised if my patient were to die in the next 12 months?”8 By identifying such patients [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1231", "doc_id": "10374686", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Pure neural progenitor cell (NPC) populations can only be obtained from cell cultures that undergo passaging, filtration, or other isolation and cell sorting methods.\n\nCANDIDATE_PASSAGE:\nVery small embryonic-like stem cells with maximum regenerative potential get discarded during cord blood banking and bone marrow processing for autologous stem cell therapy. Very small embryonic-like stem cells (VSELs) are possibly lost during cord blood banking and bone marrow (BM) processing for autologus stem cell therapy mainly because of their small size. The present study was conducted on human umbilical cord blood (UCB, n=6) and discarded red blood cells (RBC) fraction obtained after separation of mononuclear cells from human BM (n=6), to test this hypothesis. The results show that VSELs, which are pluripotent stem cells with maximum regenerative potential, settle along with the RBCs during Ficoll-Hypaque density separation. These cells are very small in size (3-5 μm), have high nucleo-cytoplasmic ratio, and express nuclear Oct-4, cell surface protein SSEA-4, and other pluripotent markers such as Nanog, Sox-2, Rex-1, and Tert as indicated by immunolocalization and quantitative polymerase chain reaction (Q-PCR) studies. Interestingly, a distinct population of slightly larger, round hematopoietic stem cells (HSCs) with cytoplasmic Oct-4 were detected in the \"buffy\" coat, which usually gets banked or used during autologus stem cell therapy. Immunohistochemical studies on the umbilical cord tissue (UCT) sections (n=3) showed the presence of nuclear Oct-4-positive VSELs and many fibroblast-like mesenchymal stem cells (MSCs) with cytoplasmic Oct-4. These VSELs with nuclear Oct-4, detected in UCB, UCT, and discarded RBC fraction obtained after BM processing, may persist throughout life, maintain tissue homeostasis, and undergo asymmetric cell division to self-renew as well as produce larger progenitor stem cells, viz. HSCs or MSCs, which follow differentiati [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "989", "doc_id": "25985964", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: 30-Day and 1-year mortality in emergency general surgery laparotomies: an area of concern and need for improvement?\n\nABSTRACT:\nEmergency surgery is associated with poorer outcomes and higher mortality with recent studies suggesting the 30-day mortality to be 14-15%. The aim of this study was to analyse the 30-day mortality, age-related 30-day mortality and 1-year mortality following emergency laparotomy. We hope this will encourage prospective data collection, improvement of care and initiate strategies to establish best practice in this area. This was a retrospective study of patients who underwent emergency laparotomy from June 2010 to May 2012. The primary end point of the study was 30-day mortality, age-related 30-day mortality and 1-year all-cause mortality. 477 laparotomies were performed in 446 patients. 57% were aged<70 and 43% aged>70 years. 30-day mortality was 12, 4% in those aged<70 years and 22% in those>70 years (p<0.001). 1-year mortality was 25, 15% in those aged under 70 years and 38% in those aged>70 years (p<0.001).", "output": "{\"label\": \"maybe\", \"rationale\": \"Emergency laparotomy carries a high rate of mortality, especially in those over the age of 70 years, and more needs to be done to improve outcomes, particularly in this group. This could involve increasing acute surgical care manpower, early recognition of patients requiring emergency surgery, development of clear management protocols for such patients or perhaps even considering centralisation of emergency surgical services to specialist centres with multidisciplinary teams involving emergency surgeons and care of the elderly physicians in hospital and related community outreach services for post-discharge care.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 26037986, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: siRNA knockdown of A20 slows tumor progression in an in vivo murine xenograft model.\n\nCANDIDATE_ABSTRACT:\nTITLE: Quantitative Detection of Hepatitis C Virus RNA by Light Cycler PCR and Comparison with Two Different PCR Assays\nABSTRACT: The new Light Cycler technology was adapted to the detection of hepatitis C virus (HCV) RNA in clinical samples. Sera from 81 patients were tested by Light Cycler PCR, AMPLICOR HCV Monitor assay, and in-house PCR. Our data demonstrate that Light Cycler is a fast and reliable method for the detection and quantitation of HCV RNA.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1404, "doc_id": "285794", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The PRDM1 gene is a key determinant of primordial germ cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effect of physical activity on cognitive function in older adults at risk for Alzheimer disease: a randomized trial.\nABSTRACT: CONTEXT Many observational studies have shown that physical activity reduces the risk of cognitive decline; however, evidence from randomized trials is lacking. OBJECTIVE To determine whether physical activity reduces the rate of cognitive decline among older adults at risk. DESIGN AND SETTING Randomized controlled trial of a 24-week physical activity intervention conducted between 2004 and 2007 in metropolitan Perth, Western Australia. Assessors of cognitive function were blinded to group membership. PARTICIPANTS We recruited volunteers who reported memory problems but did not meet criteria for dementia. Three hundred eleven individuals aged 50 years or older were screened for eligibility, 89 were not eligible, and 52 refused to participate. A total of 170 participants were randomized and 138 participants completed the 18-month assessment. INTERVENTION Participants were randomly allocated to an education and usual care group or to a 24-week home-based program of physical activity. MAIN OUTCOME MEASURE Change in Alzheimer Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) scores (possible range, 0-70) over 18 months. RESULTS In an intent-to-treat analysis, participants in the intervention group improved 0.26 points (95% confidence interval, -0.89 to 0.54) and those in the usual care group deteriorated 1.04 points (95% confidence interval, 0.32 to 1.82) on the ADAS-Cog at the end of the intervention. The absolute difference of the outcome measure between the intervention and control groups was -1.3 points (95% confidence interval,-2.38 to -0.22) at the end of the intervention. At 18 months, participants in the intervention group improved 0.73 points (95% confidence interval, -1.27 to 0.03) on the ADAS-Cog, and those in the usual care group improved 0.04 p [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1176, "doc_id": "1642727", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Non-invasive ventilation use should be decreased if there is inadequate response to conventional treatment.\n\nCANDIDATE_ABSTRACT:\nTITLE: N348I in HIV-1 reverse transcriptase can counteract the nevirapine-mediated bias toward RNase H cleavage during plus-strand initiation.\nABSTRACT: Drug resistance-associated mutations in HIV-1 reverse transcriptase (RT) can affect the balance between polymerase and ribonuclease H (RNase H) activities of the enzyme. We have recently demonstrated that the N348I mutation in the connection domain causes selective dissociation from RNase H-competent complexes, whereas the functional integrity of the polymerase-competent complex remains largely unaffected. N348I has been associated with resistance to the non-nucleoside RT inhibitor (NNRTI), nevirapine; however, a possible mechanism that links changes in RNase H activity to changes in NNRTI susceptibility remains to be established. To address this problem, we consider recent findings suggesting that NNRTIs may affect the orientation of RT on its nucleic acid substrate and increase RNase H activity. Here we demonstrate that RNase H-mediated primer removal is indeed more efficient in the presence of NNRTIs; however, the N348I mutant enzyme is able to counteract this effect. Efavirenz, a tight binding inhibitor, restricts the influence of the mutation. These findings provide strong evidence to suggest that N348I can thwart the inhibitory effects of nevirapine during initiation of (+)-strand DNA synthesis, which provides a novel mechanism for resistance. The data are in agreement with clinical data, which demonstrate a stronger effect of N348I on susceptibility to nevirapine as compared with efavirenz.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 852, "doc_id": "2319305", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Pediatric SCD patients with vaso-occlusive crisis show increased morphine use after breathing 80 ppm iNO for 4 hours.\n\nCANDIDATE_PASSAGE:\nRisk of death with atypical antipsychotic drug treatment for dementia: meta-analysis of randomized placebo-controlled trials. CONTEXT Atypical antipsychotic medications are widely used to treat delusions, aggression, and agitation in people with Alzheimer disease and other dementia; however, concerns have arisen about the increased risk for cerebrovascular adverse events, rapid cognitive decline, and mortality with their use. OBJECTIVE To assess the evidence for increased mortality from atypical antipsychotic drug treatment for people with dementia. DATA SOURCES MEDLINE (1966 to April 2005), the Cochrane Controlled Trials Register (2005, Issue 1), meetings presentations (1997-2004), and information from the sponsors were searched using the terms for atypical antipsychotic drugs (aripiprazole, clozapine, olanzapine, quetiapine, risperidone, and ziprasidone), dementia, Alzheimer disease, and clinical trial. STUDY SELECTION Published and unpublished randomized placebo-controlled, parallel-group clinical trials of atypical antipsychotic drugs marketed in the United States to treat patients with Alzheimer disease or dementia were selected by consensus of the authors. DATA EXTRACTION Trials, baseline characteristics, outcomes, all-cause dropouts, and deaths were extracted by one reviewer; treatment exposure was obtained or estimated. Data were checked by a second reviewer. DATA SYNTHESIS Fifteen trials (9 unpublished), generally 10 to 12 weeks in duration, including 16 contrasts of atypical antipsychotic drugs with placebo met criteria (aripiprazole [n = 3], olanzapine [n = 5], quetiapine [n = 3], risperidone [n = 5]). A total of 3353 patients were randomized to study drug and 1757 were randomized to placebo. Outcomes were assessed using standard methods (with ran [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "933", "doc_id": "5402581", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Diabetic patients with acute coronary syndrome experience increased short-term and long-term risk for bleeding events.\n\nCANDIDATE_PASSAGE:\nSex differences in mortality following acute coronary syndromes. CONTEXT Conflicting information exists about whether sex differences modulate short-term mortality following acute coronary syndromes (ACS). OBJECTIVES To investigate the relationship between sex and 30-day mortality in ACS, and to determine whether this relationship was modified by clinical syndrome or coronary anatomy using a large database across the spectrum of ACS and adjusting for potentially confounding clinical covariates. DESIGN, SETTING, AND PARTICIPANTS A convenience sample of patients pooled from 11 independent, international, randomized ACS clinical trials between 1993 and 2006 whose databases are maintained at the Duke Clinical Research Institute, Durham, North Carolina. Of 136 247 patients, 38 048 (28%) were women; 102 004 (26% women) with ST-segment elevation myocardial infarction (STEMI), 14 466 (29% women) with non-STEMI (NSTEMI), and 19 777 (40% women) with unstable angina. MAIN OUTCOME MEASURE Thirty-day mortality following ACS. RESULTS Thirty-day mortality was 9.6% in women and 5.3% in men (odds ratio [OR], 1.91; 95% confidence interval [CI], 1.83-2.00). After multivariable adjustment, mortality was not significantly different between women and men (adjusted OR, 1.06; 95% CI, 0.99-1.15). A significant sex by type of ACS interaction was demonstrated (P < .001). In STEMI, 30-day mortality was higher among women (adjusted OR, 1.15; 95% CI, 1.06-1.24), whereas in NSTEMI (adjusted OR, 0.77; 95% CI, 0.63-0.95) and unstable angina, mortality was lower among women (adjusted OR, 0.55; 95% CI, 0.43-0.70). In a cohort of 35 128 patients with angiographic data, women more often had nonobstructive (15% vs 8%) and less often had 2-vessel (25% vs 28%) and 3-vessel (23% vs 26%) coronary di [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "343", "doc_id": "7640792", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is acute physiological derangement associated with early radiographic cerebral infarction after subarachnoid haemorrhage?\n\nABSTRACT:\nCerebral infarction after aneurysmal subarachnoid haemorrhage (SAH) is presumed to be due to cerebral vasospasm, defined as arterial lumen narrowing from days 3 to 14. We reviewed the computed tomography scans of 103 patients with aneurysmal SAH for radiographic cerebral infarction and controlled for other predictors of outcome. A blinded neuroradiologist reviewed the angiograms. Cerebral infarction from vasospasm was judged to be unlikely if it was visible on computed tomography within 2 calendar days of SAH or if angiography showed no vasospasm in a referable vessel, or both. Cerebral infarction occurred in 29 (28%) of 103 patients with SAH. 18 patients had cerebral infarction that was unlikely to be due to vasospasm because it was visible on computed tomography by day 2 (6 (33%)) or because angiography showed no vasospasm in a referable artery (7 (39%)), or both (5 (28%)). In a multivariate model, cerebral infarction was significantly related to World Federation of Neurologic Surgeons grade (odds ratio (OR) 1.5/grade, 95% confidence interval (CI) 1.1 to 2.01, p = 0.006) and SAH-Physiologic Derangement Score (PDS) >2 (OR 3.7, 95% CI 1.4 to 9.8, p = 0.01) on admission. Global cerebral oedema (OR 4.3, 95% CI 1.5 to 12.5, p = 0.007) predicted cerebral infarction. Patients with cerebral infarction detectable by day 2 had a higher SAH-PDS than patients with later cerebral infarction (p = 0.025).", "output": "{\"label\": \"yes\", \"rationale\": \"Many cerebral infarctions after SAH are unlikely to be caused by vasospasm because they occur too soon after SAH or because angiography shows no vasospasm in a referable artery, or both. Physiological derangement and cerebral oedema may be worthwhile targets for intervention to decrease the occurrence and clinical impact of cerebral infarction after SAH.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 16820419, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Physical activity level has no association with the difference in maximal oxygen consumption between black and white youth.\n\nCANDIDATE_ABSTRACT:\nTITLE: Maximal aerobic capacity in African-American and Caucasian prepubertal children.\nABSTRACT: The purpose of this study was to examine differences in resting, submaximal, and maximal (VO2max) oxygen consumption (VO2) in African-American (n = 44) and Caucasian (n = 31) prepubertal children aged 5-10 yr. Resting VO2 was measured via indirect calorimetry in the fasted state. Submaximal VO2 and VO2max were determined during an all out, progressive treadmill exercise test appropriate for children. Dual-energy X-ray absorptiometry was used to determine total fat mass (FM), soft lean tissue mass (LTM), and leg soft LTM. Doubly labeled water was used to determine total energy expenditure (TEE) and activity energy expenditure (AEE). A significant effect of ethnicity (P < 0.01) was found for VO2max but not resting or submaximal VO2, with African-American children having absolute VO2max approximately 15% lower than Caucasian children (1.21 +/- 0.032 vs. 1.43 +/- 0.031 l/min, respectively). The lower VO2max persisted in African-American children after adjustment for soft LTM (1.23 +/- 0.025 vs. 1.39 +/- 0.031 l/min; P < 0.01), leg soft LTM (1.20 +/- 0.031 vs. 1.43 +/- 0.042 l/min; P < 0.01), and soft LTM and FM (1.23 +/- 0.025 vs. 1.39 +/- 0.031 l/min; P < 0.01). The lower VO2max persisted also after adjustment for TEE (1.20 +/- 0.02 vs. 1.38 +/- 0.0028 l/min P < 0.001) and AEE (1.20 +/- 0.024 vs. 1.38 +/- 0.028 l/min; P < 0.001). In conclusion, our data indicate that African-American and Caucasian children have similar rates of VO2 at rest and during submaximal exercise, but VO2max is approximately 15% lower in African-American children, independent of soft LTM, FM, leg LTM, TEE, and AEE.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 945, "doc_id": "26112696", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: N-terminal cleavage increases success identifying transcription start sites.\n\nCANDIDATE_PASSAGE:\nUltrasound imaging for lumbar punctures and epidural catheterisations: systematic review and meta-analysis. OBJECTIVE To determine whether ultrasound imaging can reduce the risk of failed lumbar punctures or epidural catheterisations, when compared with standard palpation methods, and whether ultrasound imaging can reduce traumatic procedures, insertion attempts, and needle redirections. DESIGN Systematic review and meta-analysis of randomised controlled trials. DATA SOURCES Ovid Medline, Embase, and Cochrane Central Register of Controlled Trials up to May 2012, without restriction by language or publication status. REVIEW METHODS Randomised trials that compared ultrasound imaging with standard methods (no imaging) in the performance of a lumbar puncture or epidural catheterisation were identified. RESULTS 14 studies with a total of 1334 patients were included (674 patients assigned to the ultrasound group, 660 to the control group). Five studies evaluated lumbar punctures and nine evaluated epidural catheterisations. Six of 624 procedures conducted in the ultrasound group failed; 44 of 610 procedures in the control group failed. Ultrasound imaging reduced the risk of failed procedures (risk ratio 0.21 (95% confidence interval 0.10 to 0.43), P<0.001). Risk reduction was similar when subgroup analysis was performed for lumbar punctures (risk ratio 0.19 (0.07 to 0.56), P=0.002) or epidural catheterisations (0.23 (0.09 to 0.60), P=0.003). Ultrasound imaging also significantly reduced the risk of traumatic procedures (risk ratio 0.27 (0.11 to 0.67), P=0.005), the number of insertion attempts (mean difference -0.44 (-0.64 to -0.24), P<0.001), and the number of needle redirections (mean difference -1.00 (-1.24 to -0.75), P<0.001). CONCLUSIONS Ultrasound imaging ca [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "820", "doc_id": "15482274", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Lupus-prone mice infected with curliproducing bacteria have higher autoantibody titers compared to controls.\n\nCANDIDATE_PASSAGE:\nEvaluating the impact of pharmacists in mental health: a systematic review. Efforts to improve the outcomes of patients with mental illness often have involved incorporating the skills of a variety of health care professionals into collaborative care models. For over 30 years, clinical pharmacists have contributed to these care models in capacities ranging from educator to consultant to provider. This systematic review evaluates the quantity and quality of medical literature examining the impact of pharmacists in mental health from 1972-2003. Although we identified approximately 35 publications describing the roles of clinical pharmacists in this regard, only 16 were of sufficient scientific rigor to permit evaluation and comparison. The 16 studies were divided equally between inpatient and outpatient settings and were conducted in a variety of health care organizations (e.g., Veterans Administration, health maintenance organizations, community mental health clinics, and nursing homes). Nine of the studies examined the role of pharmacists in providing treatment recommendations and patient education, five featured pharmacists as providers (with prescriptive authority), and the remaining two described the impact pharmacists have in delivering education to the psychiatric staff. Six of the 16 studies were prospective, but only three of these incorporated a randomization procedure for patients or facilities. Collectively, the results of the 16 studies were positive, demonstrating improvements in outcomes, prescribing practices, patient satisfaction, and resource use. Unfortunately, most of the investigations were small, and significant limitations in study design limited further comparison. Given the long history and anecdotal success of pharmacists in mental he [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "721", "doc_id": "31612088", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Foxk2 regulates autophagy genes in muscle cells and fibroblast cells.\n\nCANDIDATE_PASSAGE:\nFoxk proteins repress the initiation of starvation-induced atrophy and autophagy programs Autophagy is the primary catabolic process triggered in response to starvation. Although autophagic regulation within the cytosolic compartment is well established, it is becoming clear that nuclear events also regulate the induction or repression of autophagy. Nevertheless, a thorough understanding of the mechanisms by which sequence-specific transcription factors modulate expression of genes required for autophagy is lacking. Here, we identify Foxk proteins (Foxk1 and Foxk2) as transcriptional repressors of autophagy in muscle cells and fibroblasts. Interestingly, Foxk1/2 serve to counter-balance another forkhead transcription factor, Foxo3, which induces an overlapping set of autophagic and atrophic targets in muscle. Foxk1/2 specifically recruits Sin3A-HDAC complexes to restrict acetylation of histone H4 and expression of critical autophagy genes. Remarkably, mTOR promotes the transcriptional activity of Foxk1 by facilitating nuclear entry to specifically limit basal levels of autophagy in nutrient-rich conditions. Our study highlights an ancient, conserved mechanism whereby nutritional status is interpreted by mTOR to restrict autophagy by repressing essential autophagy genes through Foxk-Sin3-mediated transcriptional control.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "432", "doc_id": "8002887", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Converting apoE4 to apoE3 by gene editing worsens the pathology associated with apoE4 in human iPSCderived neurons.\n\nCANDIDATE_PASSAGE:\nAlzheimer’s disease and NGF signaling Age-related degeneration of basal forebrain cholinergic neurons (BFCNs) occurs early and contributes significantly to cognitive decline in Alzheimer’s disease (AD). Proper function and morphology of BFCNs depends on the supply of nerve growth factor (NGF) from the cortex and the hippocampus. A large number of experiments have shown that decreased supply of NGF at the level of BFCN cell bodies leads to loss of neuronal markers and shrinkage, mimicking what is observed in AD. The delivery of sufficient amounts of NGF signal to BFCN cell bodies depends on the effective participation of several factors including sufficient synthesis and release of NGF, adequate synthesis and expression of NGF receptors by BFCNs, normal signaling and retrograde transport of NGF-receptor complex, and finally effective induction of gene expression by NGF. In the past few years it has become clear that decreased amounts of NGF at the level of BFCN cell bodies is largely due to failed retrograde transport rather than decreased synthesis, binding or expression of NGF receptors in the BFCN terminals. We will discuss in vivo evidence supporting decreased retrograde transport of NGF in a mouse model with BFCN degeneration, and will attempt to match these findings with our studies in postmortem human AD brain. We will speculate about the possible mechanisms of failed NGF retrograde transport and its relationship to AD pathology.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "287", "doc_id": "24652030", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Pseudogene PTENP1 encodes a transcript that regulates PTEN expression.\n\nCANDIDATE_PASSAGE:\nGenetic alterations and their relationship in the phosphatidylinositol 3-kinase/Akt pathway in thyroid cancer. PURPOSE To investigate the overall occurrence and relationship of genetic alterations in the phosphatidylinositol 3-kinase (PI3K)/Akt pathway in thyroid tumors and explore the scope of this pathway as a therapeutic target for thyroid cancer. EXPERIMENTAL DESIGN We examined collectively the major genetic alterations and their relationship in this pathway, including PIK3CA copy number gain and mutation, Ras mutation, and PTEN mutation, in a large series of primary thyroid tumors. RESULTS Occurrence of any of these genetic alterations was found in 25 of 81 (31%) benign thyroid adenoma (BTA), 47 of 86 (55%) follicular thyroid cancer (FTC), 21 of 86 (24%) papillary thyroid cancer (PTC), and 29 of 50 (58%) anaplastic thyroid cancer (ATC), with FTC and ATC most frequently harboring these genetic alterations. PIK3CA copy gain was associated with increased PIK3CA protein expression. A mutual exclusivity among these genetic alterations was seen in BTA, FTC, and PTC, suggesting an independent role of each of them through the PI3K/Akt pathway in the tumorigenesis of the differentiated thyroid tumors. However, coexistence of these genetic alterations was increasingly seen with progression from differentiated tumor to undifferentiated ATC. Their coexistence with BRAF mutation was also frequent in PTC and ATC. CONCLUSIONS The data provide strong genetic implication that aberrant activation of PI3K/Akt pathway plays an extensive role in thyroid tumorigenesis, particularly in FTC and ATC, and promotes progression of BTA to FTC and to ATC as the genetic alterations of this pathway accumulate. Progression of PTC to ATC may be facilitated by coexistence of PI3K/Akt pat [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "984", "doc_id": "21551568", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Peroxynitrite is required for nitration of TCR/CD8.\n\nCANDIDATE_PASSAGE:\nDual and opposing roles of primary cilia in medulloblastoma development Recent work has shown that primary cilia are essential for Hedgehog (Hh) signaling during mammalian development. It is also known that aberrant Hh signaling can lead to cancer, but the role of primary cilia in oncogenesis is not known. Cerebellar granule neuron precursors (GNPs) can give rise to medulloblastomas, the most common malignant brain tumor in children. The primary cilium and Hh signaling are required for GNP proliferation. We asked whether primary cilia in GNPs have a role in medulloblastoma growth in mice. Genetic ablation of primary cilia blocked medulloblastoma formation when this tumor was driven by a constitutively active Smoothened protein (Smo), an upstream activator of Hh signaling. In contrast, removal of cilia was required for medulloblastoma growth by a constitutively active glioma-associated oncogene family zinc finger-2 (GLI2), a downstream transcription factor. Thus, primary cilia are either required for or inhibit medulloblastoma formation, depending on the initiating oncogenic event. Remarkably, the presence or absence of cilia was associated with specific variants of human medulloblastomas; primary cilia were found in medulloblastomas with activation in HH or WNT signaling but not in most medulloblastomas in other distinct molecular subgroups. Primary cilia could serve as a diagnostic tool and provide new insights into the mechanism of tumorigenesis.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "936", "doc_id": "8208212", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Stiff substrates encourage mesodermal differentiation by degrading beta-catenin in an integrin-dependent manner.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tissue Mechanics Orchestrate Wnt-Dependent Human Embryonic Stem Cell Differentiation.\nABSTRACT: Regenerative medicine is predicated on understanding the mechanisms regulating development and applying these conditions to direct stem cell fate. Embryogenesis is guided by cell-cell and cell-matrix interactions, but it is unclear how these physical cues influence stem cells in culture. We used human embryonic stem cells (hESCs) to examine whether mechanical features of the extracellular microenvironment could differentially modulate mesoderm specification. We found that, on a hydrogel-based compliant matrix, hESCs accumulate β-catenin at cell-cell adhesions and show enhanced Wnt-dependent mesoderm differentiation. Mechanistically, Src-driven ubiquitination of E-cadherin by Cbl-like ubiquitin ligase releases P120-catenin to facilitate transcriptional activity of β-catenin, which initiates and reinforces mesoderm differentiation. By contrast, on a stiff hydrogel matrix, hESCs show elevated integrin-dependent GSK3 and Src activity that promotes β-catenin degradation and inhibits differentiation. Thus, we found that mechanical features of the microenvironmental matrix influence tissue-specific differentiation of hESCs by altering the cellular response to morphogens.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"By contrast, on a stiff hydrogel matrix, hESCs show elevated integrin-dependent GSK3 and Src activity that promotes β-catenin degradation and inhibits differentiation.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1101, "doc_id": "3874000", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Mutant mice lacking SVCT2 have greatly increased ascorbic acid levels in both brain and adrenals.\n\nCANDIDATE_ABSTRACT:\nTITLE: Ascorbic-acid transporter Slc23a1 is essential for vitamin C transport into the brain and for perinatal survival\nABSTRACT: The only proven requirement for ascorbic acid (vitamin C) is in preventing scurvy, presumably because it is a cofactor for hydroxylases required for post-translational modifications that stabilize collagen. We have created mice deficient in the mouse ortholog (solute carrier family 23 member 1 or Slc23a1) of a rat ascorbic-acid transporter, Svct2 (ref. 4). Cultured embryonic fibroblasts from homozygous Slc23a1−/− mice had less than 5% of normal ascorbic-acid uptake. Ascorbic-acid levels were undetectable or markedly reduced in the blood and tissues of Slc23a1−/− mice. Prenatal supplementation of pregnant females did not elevate blood ascorbic acid in Slc23a1−/− fetuses, suggesting Slc23a1 is important in placental ascorbic-acid transport. Slc23a1−/− mice died within a few minutes of birth with respiratory failure and intraparenchymal brain hemorrhage. Lungs showed no postnatal expansion but had normal surfactant protein B levels. Brain hemorrhage was unlikely to be simply a form of scurvy since Slc23a1−/− mice showed no hemorrhage in any other tissues and their skin had normal skin 4-hydroxyproline levels despite low ascorbic-acid content. We conclude that Slc23a1 is required for transport of ascorbic acid into many tissues and across the placenta. Deficiency of the transporter is lethal in newborn mice, thereby revealing a previously unrecognized requirement for ascorbic acid in the perinatal period.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Ascorbic-acid levels were undetectable or markedly reduced in the blood and tissues of Slc23a1−/− mice.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 811, "doc_id": "19799455", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Incidence of sepsis has fallen substantially from 2009 to 2014.\n\nCANDIDATE_ABSTRACT:\nTITLE: Incidence and Trends of Sepsis in US Hospitals Using Clinical vs Claims Data, 2009-2014\nABSTRACT: Importance Estimates from claims-based analyses suggest that the incidence of sepsis is increasing and mortality rates from sepsis are decreasing. However, estimates from claims data may lack clinical fidelity and can be affected by changing diagnosis and coding practices over time. Objective To estimate the US national incidence of sepsis and trends using detailed clinical data from the electronic health record (EHR) systems of diverse hospitals. Design, Setting, and Population Retrospective cohort study of adult patients admitted to 409 academic, community, and federal hospitals from 2009-2014. Exposures Sepsis was identified using clinical indicators of presumed infection and concurrent acute organ dysfunction, adapting Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) criteria for objective and consistent EHR-based surveillance. Main Outcomes and Measures Sepsis incidence, outcomes, and trends from 2009-2014 were calculated using regression models and compared with claims-based estimates using International Classification of Diseases, Ninth Revision, Clinical Modification codes for severe sepsis or septic shock. Case-finding criteria were validated against Sepsis-3 criteria using medical record reviews. Results A total of 173 690 sepsis cases (mean age, 66.5 [SD, 15.5] y; 77 660 [42.4%] women) were identified using clinical criteria among 2 901 019 adults admitted to study hospitals in 2014 (6.0% incidence). Of these, 26 061 (15.0%) died in the hospital and 10 731 (6.2%) were discharged to hospice. From 2009-2014, sepsis incidence using clinical criteria was stable (+0.6% relative change/y [95% CI, −2.3% to 3.5%], P = .67) whereas incidence per claims increased (+10.3%/y [95% CI, 7.2% to 13.3%], P < .001). In-hospital morta [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Conclusions and Relevance In clinical data from 409 hospitals, sepsis was present in 6% of adult hospitalizations, and in contrast to claims-based analyses, neither the incidence of sepsis nor the combined outcome of death or discharge to hospice changed significantly between 2009-2014.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 595, "doc_id": "4824840", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: RTEL1 interacts with TRF2 through a C4C4 motif\n\nCANDIDATE_ABSTRACT:\nTITLE: TRF2 Recruits RTEL1 to Telomeres in S Phase to Promote T-Loop Unwinding\nABSTRACT: The helicase RTEL1 promotes t-loop unwinding and suppresses telomere fragility to maintain the integrity of vertebrate telomeres. An interaction between RTEL1 and PCNA is important to prevent telomere fragility, but how RTEL1 engages with the telomere to promote t-loop unwinding is unclear. Here, we establish that the shelterin protein TRF2 recruits RTEL1 to telomeres in S phase, which is required to prevent catastrophic t-loop processing by structure-specific nucleases. We show that the TRF2-RTEL1 interaction is mediated by a metal-coordinating C4C4 motif in RTEL1, which is compromised by the Hoyeraal-Hreidarsson syndrome (HHS) mutation, RTEL1(R1264H). Conversely, we define a TRF2(I124D) substitution mutation within the TRFH domain of TRF2, which eliminates RTEL1 binding and phenocopies the RTEL1(R1264H) mutation, giving rise to aberrant t-loop excision, telomere length heterogeneity, and loss of the telomere as a circle. These results implicate TRF2 in the recruitment of RTEL1 to facilitate t-loop disassembly at telomeres in S phase.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We show that the TRF2-RTEL1 interaction is mediated by a metal-coordinating C4C4 motif in RTEL1, which is compromised by the Hoyeraal-Hreidarsson syndrome (HHS) mutation, RTEL1(R1264H).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1006, "doc_id": "4926049", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Weighed food records (WFR) result in high completion since they're cheap to run and impose low participant burden.\n\nCANDIDATE_ABSTRACT:\nTITLE: Accuracy of weighed dietary records in studies of diet and health.\nABSTRACT: OBJECTIVE To provide an independent evaluation of seven day weighed dietary records, which are currently accepted as the most accurate technique for assessing habitual dietary intake in studies investigating the links between diet and health. DESIGN Subjects who had previously participated in the Northern Ireland diet and health study were reselected by stratified random sampling to represent the range of energy intakes in the study as assessed by the seven day weighed dietary record. SETTING Northern Ireland. SUBJECTS 31 Free living adults (16 men and 15 women). MAIN OUTCOME MEASURES Energy intake as measured by the seven day weighed dietary record and total energy expenditure estimated concurrently by the doubly labelled water technique. RESULTS Average recorded energy intakes were significantly lower than measured expenditure in the group overall (9.66 MJ/day v 12.15 MJ/day, 95% confidence interval 1.45 to 3.53 MJ/day). Among those in the upper third of energy intakes the mean (SE) ratio of intake to expenditure was close to 1.0, indicating accurate records (men 1.01 (0.11), women 0.96 (0.08]. In the middle and lower thirds the ratios for men were only 0.74 (0.05) and 0.70 (0.07) respectively and for women 0.89 (0.07) and 0.61 (0.07). CONCLUSIONS These results show a serious bias in reporting habitual energy intake. If substantiated they may have wide implications for the interpretation of many nutritional studies.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1374, "doc_id": "21993510", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: 70% of burn patients are admitted for hospitalization and further treatment after appearing at hospital emergency wards or outpatient clinics.\n\nCANDIDATE_PASSAGE:\nAcute respiratory failure in patients with severe community-acquired pneumonia: a prospective randomized evaluation of noninvasive ventilation. In uncontrolled studies, noninvasive positive pressure ventilation (NPPV) was found useful in avoiding endotracheal intubation in patients with acute respiratory failure (ARF) caused by severe community-acquired pneumonia (CAP). We conducted a prospective, randomized study comparing standard treatment plus NPPV delivered through a face mask to standard treatment alone in patients with severe CAP and ARF. Patients fitting the American Thoracic Society criteria for severe CAP were included in presence of ARF (refractory hypoxemia and/or hypercapnia with acidosis). Exclusion criteria were: severe hemodynamic instability, requirement for emergent cardiopulmonary resuscitation, home mechanical ventilation or oxygen long-term supplementation, concomitant severe disease with a low expectation of life, inability to expectorate or contraindications to the use of the mask. Fifty-six consecutive patients (28 in each arm) were enrolled, and the two groups were similar at study entry. The use of NPPV was well tolerated, safe, and associated with a significant reduction in respiratory rate, need for endotracheal intubation (21% versus 50%; p = 0.03), and duration of intensive care unit (ICU) stay (1.8 ± 0.7 d versus 6 ± 1.8 d; p = 0.04). The two groups had a similar intensity of nursing care workload, time interval from study entry to endotracheal intubation, duration of hospitalization, and hospital mortality. Among patients with chronic obstructive pulmonary disease (COPD), those randomized to NPPV had a lower intensity of nursing care workload (p = 0.04) and improved 2-mo survival (88.9% versus 37.5%; p = 0.05). We conclude tha [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "21", "doc_id": "40867854", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: There is no association between HNF4A mutations and diabetes risks.\n\nCANDIDATE_PASSAGE:\nMigraine and cardiovascular disease: systematic review and meta-analysis. OBJECTIVE To evaluate the association between migraine and cardiovascular disease, including stroke, myocardial infarction, and death due to cardiovascular disease. DESIGN Systematic review and meta-analysis. DATA SOURCES Electronic databases (PubMed, Embase, Cochrane Library) and reference lists of included studies and reviews published until January 2009. Selection criteria Case-control and cohort studies investigating the association between any migraine or specific migraine subtypes and cardiovascular disease. Review methods Two investigators independently assessed eligibility of identified studies in a two step approach. Disagreements were resolved by consensus. Studies were grouped according to a priori categories on migraine and cardiovascular disease. DATA EXTRACTION Two investigators extracted data. Pooled relative risks and 95% confidence intervals were calculated. RESULTS Studies were heterogeneous for participant characteristics and definition of cardiovascular disease. Nine studies investigated the association between any migraine and ischaemic stroke (pooled relative risk 1.73, 95% confidence interval 1.31 to 2.29). Additional analyses indicated a significantly higher risk among people who had migraine with aura (2.16, 1.53 to 3.03) compared with people who had migraine without aura (1.23, 0.90 to 1.69; meta-regression for aura status P=0.02). Furthermore, results suggested a greater risk among women (2.08, 1.13 to 3.84) compared with men (1.37, 0.89 to 2.11). Age less than 45 years, smoking, and oral contraceptive use further increased the risk. Eight studies investigated the association between migraine and myocardial infarction (1.12, 0.95 to 1.32) and five between mig [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1292", "doc_id": "15984735", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Increased vessel density along with a reduction in fibrosis decreases the efficacy of chemotherapy treatments.\n\nCANDIDATE_PASSAGE:\nIDH1 mutations alter citric acid cycle metabolism and increase dependence on oxidative mitochondrial metabolism. Oncogenic mutations in isocitrate dehydrogenase 1 and 2 (IDH1/2) occur in several types of cancer, but the metabolic consequences of these genetic changes are not fully understood. In this study, we performed (13)C metabolic flux analysis on a panel of isogenic cell lines containing heterozygous IDH1/2 mutations. We observed that under hypoxic conditions, IDH1-mutant cells exhibited increased oxidative tricarboxylic acid metabolism along with decreased reductive glutamine metabolism, but not IDH2-mutant cells. However, selective inhibition of mutant IDH1 enzyme function could not reverse the defect in reductive carboxylation activity. Furthermore, this metabolic reprogramming increased the sensitivity of IDH1-mutant cells to hypoxia or electron transport chain inhibition in vitro. Lastly, IDH1-mutant cells also grew poorly as subcutaneous xenografts within a hypoxic in vivo microenvironment. Together, our results suggest therapeutic opportunities to exploit the metabolic vulnerabilities specific to IDH1 mutation.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "619", "doc_id": "14663842", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Antiretroviral therapy increases rates of tuberculosis across a broad range of CD4 strata.\n\nCANDIDATE_PASSAGE:\nComparison of allogeneic vs autologous bone marrow–derived mesenchymal stem cells delivered by transendocardial injection in patients with ischemic cardiomyopathy: the POSEIDON randomized trial. CONTEXT Mesenchymal stem cells (MSCs) are under evaluation as a therapy for ischemic cardiomyopathy (ICM). Both autologous and allogeneic MSC therapies are possible; however, their safety and efficacy have not been compared. OBJECTIVE To test whether allogeneic MSCs are as safe and effective as autologous MSCs in patients with left ventricular (LV) dysfunction due to ICM. DESIGN, SETTING, AND PATIENTS A phase 1/2 randomized comparison (POSEIDON study) in a US tertiary-care referral hospital of allogeneic and autologous MSCs in 30 patients with LV dysfunction due to ICM between April 2, 2010, and September 14, 2011, with 13-month follow-up. INTERVENTION Twenty million, 100 million, or 200 million cells (5 patients in each cell type per dose level) were delivered by transendocardial stem cell injection into 10 LV sites. MAIN OUTCOME MEASURES Thirty-day postcatheterization incidence of predefined treatment-emergent serious adverse events (SAEs). Efficacy assessments included 6-minute walk test, exercise peak VO2, Minnesota Living with Heart Failure Questionnaire (MLHFQ), New York Heart Association class, LV volumes, ejection fraction (EF), early enhancement defect (EED; infarct size), and sphericity index. RESULTS Within 30 days, 1 patient in each group (treatment-emergent SAE rate, 6.7%) was hospitalized for heart failure, less than the prespecified stopping event rate of 25%. The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3% (n = 8) in the autologous group (P = .46). At 1 year, there were no ventricular arrhythmia SAEs observed among all [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "123", "doc_id": "40164383", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Do platelets induce a proinflammatory phenotype in monocytes via the CD147 pathway in rheumatoid arthritis?\n\nABSTRACT:\nActivated platelets exert a proinflammatory action that can be largely ascribed to their ability to interact with monocytes. However, the mechanisms that promote dynamic changes in monocyte subsets in rheumatoid arthritis (RA) have not been clearly identified. The aim of this study was to determine whether platelet activation and the consequent formation of monocyte-platelet aggregates (MPA) might induce a proinflammatory phenotype in circulating monocytes in RA. The surface phenotype of platelets and the frequencies of monocyte subpopulations in the peripheral blood of RA patients were determined using flow cytometry. Platelets were sorted and co-cultured with monocytes. In addition, monocyte activation was assessed by measuring the nuclear factor κB (NF-κB) pathway. The disease activity was evaluated using the 28-joint disease activity score. Platelet activation, circulating intermediate monocytes (Mon2) and MPA formation were significantly elevated in RA, especially in those with active disease status. Furthermore, Mon2 monocytes showed higher CD147 expression and responded to direct cell contact with activated platelets with higher cytokine production and matrix metallopeptidase 9 (MMP-9) secretion, which increased the expression of CD147. After the addition of specific antibodies for CD147, those effects were abolished. Furthermore, the NF-κB-driven inflammatory pathway may be involved in this process.", "output": "{\"label\": \"yes\", \"rationale\": \"These findings indicate an important role of platelet activation and the consequent formation of MPA in the generation of the proinflammatory cytokine milieu and for the promotion and maintenance of the pathogenically relevant Mon2 monocyte compartment in RA, which is likely to play an important role in the pathogenesis of autoimmunity.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25404518, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Hyperfibrinogenemia increases rates of femoropopliteal bypass thrombosis.\n\nCANDIDATE_PASSAGE:\nGlobal, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015 BACKGROUND The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. METHODS We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors-the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "533", "doc_id": "13770184", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Medications to treat obesity do not have side effects.\n\nCANDIDATE_ABSTRACT:\nTITLE: Long term pharmacotherapy for obesity and overweight: updated meta-analysis.\nABSTRACT: OBJECTIVE To summarise the long term efficacy of anti-obesity drugs in reducing weight and improving health status. DESIGN Updated meta-analysis of randomised trials. DATA SOURCES Medline, Embase, the Cochrane controlled trials register, the Current Science meta-register of controlled trials, and reference lists of identified articles. All data sources were searched from December 2002 (end date of last search) to December 2006. STUDIES REVIEWED Double blind randomised placebo controlled trials of approved anti-obesity drugs used in adults (age over 18) for one year or longer. RESULTS 30 trials of one to four years' duration met the inclusion criteria: 16 orlistat (n=10 631 participants), 10 sibutramine (n=2623), and four rimonabant (n=6365). Of these, 14 trials were new and 16 had previously been identified. Attrition rates averaged 30-40%. Compared with placebo, orlistat reduced weight by 2.9 kg (95% confidence interval 2.5 kg to 3.2 kg), sibutramine by 4.2 kg (3.6 kg to 4.7 kg), and rimonabant by 4.7 kg (4.1 kg to 5.3 kg). Patients receiving active drug treatment were significantly more likely to achieve 5% and 10% weight loss thresholds. Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein. Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorde [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Orlistat, sibutramine, and rimonabant modestly reduce weight, have differing effects on cardiovascular risk profiles, and have specific adverse effects.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 765, "doc_id": "7552215", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Major vault protein regulates sorting of tumor suppressive miR-193a into EVs.\n\nCANDIDATE_PASSAGE:\nA SUMO-Dependent Protein Network Regulates Chromosome Congression during Oocyte Meiosis During Caenorhabditis elegans oocyte meiosis, a multi-protein ring complex (RC) localized between homologous chromosomes, promotes chromosome congression through the action of the chromokinesin KLP-19. While some RC components are known, the mechanism of RC assembly has remained obscure. We show that SUMO E3 ligase GEI-17/PIAS is required for KLP-19 recruitment to the RC, and proteomic analysis identified KLP-19 as a SUMO substrate in vivo. In vitro analysis revealed that KLP-19 is efficiently sumoylated in a GEI-17-dependent manner, while GEI-17 undergoes extensive auto-sumoylation. GEI-17 and another RC component, the kinase BUB-1, contain functional SUMO interaction motifs (SIMs), allowing them to recruit SUMO modified proteins, including KLP-19, into the RC. Thus, dynamic SUMO modification and the presence of SIMs in RC components generate a SUMO-SIM network that facilitates assembly of the RC. Our results highlight the importance of SUMO-SIM networks in regulating the assembly of dynamic protein complexes.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "752", "doc_id": "23577014", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: CD44v6 is not associated with constitutive and reprogrammed cancer stem cells driving cancer metastasis.\n\nCANDIDATE_ABSTRACT:\nTITLE: CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis.\nABSTRACT: Cancer stem cells drive tumor formation and metastasis, but how they acquire metastatic traits is not well understood. Here, we show that all colorectal cancer stem cells (CR-CSCs) express CD44v6, which is required for their migration and generation of metastatic tumors. CD44v6 expression is low in primary tumors but demarcated clonogenic CR-CSC populations. Cytokines hepatocyte growth factor (HGF), osteopontin (OPN), and stromal-derived factor 1α (SDF-1), secreted from tumor associated cells, increase CD44v6 expression in CR-CSCs by activating the Wnt/β-catenin pathway, which promotes migration and metastasis. CD44v6(-) progenitor cells do not give rise to metastatic lesions but, when treated with cytokines, acquire CD44v6 expression and metastatic capacity. Importantly, phosphatidylinositol 3-kinase (PI3K) inhibition selectively killed CD44v6 CR-CSCs and reduced metastatic growth. In patient cohorts, low levels of CD44v6 predict increased probability of survival. Thus, the metastatic process in colorectal cancer is initiated by CSCs through the expression of CD44v6, which is both a functional biomarker and therapeutic target.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CD44v6(-) progenitor cells do not give rise to metastatic lesions but, when treated with cytokines, acquire CD44v6 expression and metastatic capacity.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 203, "doc_id": "9558539", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Inhibiting focal adhesion formation enables cells to convert mechanical strain into eventual scarring.\n\nCANDIDATE_ABSTRACT:\nTITLE: Focal adhesion kinase links mechanical force to skin fibrosis via inflammatory signaling\nABSTRACT: Exuberant fibroproliferation is a common complication after injury for reasons that are not well understood. One key component of wound repair that is often overlooked is mechanical force, which regulates cell-matrix interactions through intracellular focal adhesion components, including focal adhesion kinase (FAK). Here we report that FAK is activated after cutaneous injury and that this process is potentiated by mechanical loading. Fibroblast-specific FAK knockout mice have substantially less inflammation and fibrosis than control mice in a model of hypertrophic scar formation. We show that FAK acts through extracellular-related kinase (ERK) to mechanically trigger the secretion of monocyte chemoattractant protein-1 (MCP-1, also known as CCL2), a potent chemokine that is linked to human fibrotic disorders. Similarly, MCP-1 knockout mice form minimal scars, indicating that inflammatory chemokine pathways are a major mechanism by which FAK mechanotransduction induces fibrosis. Small-molecule inhibition of FAK blocks these effects in human cells and reduces scar formation in vivo through attenuated MCP-1 signaling and inflammatory cell recruitment. These findings collectively indicate that physical force regulates fibrosis through inflammatory FAK–ERK–MCP-1 pathways and that molecular strategies targeting FAK can effectively uncouple mechanical force from pathologic scar formation.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"These findings collectively indicate that physical force regulates fibrosis through inflammatory FAK–ERK–MCP-1 pathways and that molecular strategies targeting FAK can effectively uncouple mechanical force from pathologic scar formation.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 632, "doc_id": "5172048", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Discrimination between the initiator and elongation tRNAs depends on the translation initiation factor IF3.\n\nCANDIDATE_ABSTRACT:\nTITLE: Large-Scale Movements of IF3 and tRNA during Bacterial Translation Initiation\nABSTRACT: In bacterial translational initiation, three initiation factors (IFs 1-3) enable the selection of initiator tRNA and the start codon in the P site of the 30S ribosomal subunit. Here, we report 11 single-particle cryo-electron microscopy (cryoEM) reconstructions of the complex of bacterial 30S subunit with initiator tRNA, mRNA, and IFs 1-3, representing different steps along the initiation pathway. IF1 provides key anchoring points for IF2 and IF3, thereby enhancing their activities. IF2 positions a domain in an extended conformation appropriate for capturing the formylmethionyl moiety charged on tRNA. IF3 and tRNA undergo large conformational changes to facilitate the accommodation of the formylmethionyl-tRNA (fMet-tRNA(fMet)) into the P site for start codon recognition.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 350, "doc_id": "16927286", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The density of cytokine receptor bearing cells has no effect on the distance over which cytokines act.\n\nCANDIDATE_ABSTRACT:\nTITLE: CLASPs link focal adhesion-associated microtubule capture to localized exocytosis and adhesion site turnover\nABSTRACT: Turnover of integrin-based focal adhesions (FAs) with the extracellular matrix (ECM) is essential for coordinated cell movement. In collectively migrating human keratinocytes, FAs assemble near the leading edge, grow and mature as a result of contractile forces and disassemble underneath the advancing cell body. We report that clustering of microtubule-associated CLASP1 and CLASP2 proteins around FAs temporally correlates with FA turnover. CLASPs and LL5β (also known as PHLDB2), which recruits CLASPs to FAs, facilitate FA disassembly. CLASPs are further required for FA-associated ECM degradation, and matrix metalloprotease inhibition slows FA disassembly similarly to CLASP or PHLDB2 (LL5β) depletion. Finally, CLASP-mediated microtubule tethering at FAs establishes an FA-directed transport pathway for delivery, docking and localized fusion of exocytic vesicles near FAs. We propose that CLASPs couple microtubule organization, vesicle transport and cell interactions with the ECM, establishing a local secretion pathway that facilitates FA turnover by severing cell-matrix connections.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1211, "doc_id": "1676568", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Diabetes remission occurs less in people treated with conventional therapy than in people treated with laparoscopic adjustable gastric banding surgery.\n\nCANDIDATE_ABSTRACT:\nTITLE: Adjustable gastric banding and conventional therapy for type 2 diabetes: a randomized controlled trial.\nABSTRACT: CONTEXT Observational studies suggest that surgically induced loss of weight may be effective therapy for type 2 diabetes. OBJECTIVE To determine if surgically induced weight loss results in better glycemic control and less need for diabetes medications than conventional approaches to weight loss and diabetes control. DESIGN, SETTING, AND PARTICIPANTS Unblinded randomized controlled trial conducted from December 2002 through December 2006 at the University Obesity Research Center in Australia, with general community recruitment to established treatment programs. Participants were 60 obese patients (BMI >30 and <40) with recently diagnosed (<2 years) type 2 diabetes. INTERVENTIONS Conventional diabetes therapy with a focus on weight loss by lifestyle change vs laparoscopic adjustable gastric banding with conventional diabetes care. MAIN OUTCOME MEASURES Remission of type 2 diabetes (fasting glucose level <126 mg/dL [7.0 mmol/L] and glycated hemoglobin [HbA1c] value <6.2% while taking no glycemic therapy). Secondary measures included weight and components of the metabolic syndrome. Analysis was by intention-to-treat. RESULTS Of the 60 patients enrolled, 55 (92%) completed the 2-year follow-up. Remission of type 2 diabetes was achieved by 22 (73%) in the surgical group and 4 (13%) in the conventional-therapy group. Relative risk of remission for the surgical group was 5.5 (95% confidence interval, 2.2-14.0). Surgical and conventional-therapy groups lost a mean (SD) of 20.7% (8.6%) and 1.7% (5.2%) of weight, respectively, at 2 years (P < .001). Remission of type 2 diabetes was related to weight loss (R2 = 0.46, P < .001) and lower baseline HbA1c levels (combined R2 = 0.52, P < .001). There were no serious complications in either group. CONCLUSIONS Participants r [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Remission of type 2 diabetes was achieved by 22 (73%) in the surgical group and 4 (13%) in the conventional-therapy group.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 340, "doc_id": "7098463", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Human embryonic stem cells have the capacity to give rise to differentiated progeny representative of all three embryonic germ layers.\n\nCANDIDATE_PASSAGE:\nClonally derived human embryonic stem cell lines maintain pluripotency and proliferative potential for prolonged periods of culture. Embryonic stem (ES) cell lines derived from human blastocysts have the developmental potential to form derivatives of all three embryonic germ layers even after prolonged culture. Here we describe the clonal derivation of two human ES cell lines, H9.1 and H9.2. At the time of the clonal derivation of the H9.1 and H9.2 ES cell lines, the parental ES cell line, H9, had already been continuously cultured for 6 months. After an additional 8 months of culture, H9.1 and H9.2 ES cell lines continued to: (1) actively proliferate, (2) express high levels of telomerase, and (3) retain normal karyotypes. Telomere lengths, while somewhat variable, were maintained between 8 and 12 kb in high-passage H9.1 and H9.2 cells. High-passage H9.1 and H9.2 cells both formed teratomas in SCID-beige mice that included differentiated derivatives of all three embryonic germ layers. These results demonstrate the pluripotency of single human ES cells, the maintenance of pluripotency during an extended period of culture, and the long-term self-renewing properties of cultured human ES cells. The remarkable developmental potential, proliferative capacity, and karyotypic stability of human ES cells distinguish them from adult cells.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "531", "doc_id": "25413327", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Mice that lack Interferon-γ or its receptor exhibit high resistance to experimental autoimmune myocarditis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Lethal autoimmune myocarditis in interferon-gamma receptor-deficient mice: enhanced disease severity by impaired inducible nitric oxide synthase induction.\nABSTRACT: BACKGROUND Interferon-gamma (IFN-gamma) is an essential cytokine in the regulation of inflammatory responses in autoimmune diseases. Little is known about its role in inflammatory heart disease. METHODS AND RESULTS We showed that IFN-gamma receptor-deficient mice (IFN-gammaR(-/-)) on a BALB/c background immunized with a peptide derived from cardiac alpha-myosin heavy chain develop severe myocarditis with high mortality. Although myocarditis subsided in wild-type mice after 3 weeks, IFN-gammaR(-/-) mice showed persistent disease. The persistent inflammation was accompanied by vigorous in vitro CD4 T-cell responses and impaired inducible nitric oxide synthase expression, together with evidence of impaired nitric oxide production in IFN-gammaR(-/-) hearts. Treatment of wild-type mice with the nitric oxide synthetase inhibitor N:-nitro-l-arginine-methyl-ester enhanced in vitro CD4 T-cell proliferation and prevented healing of myocarditis. CONCLUSIONS Our data provide evidence that IFN-gamma protects mice from lethal autoimmune myocarditis by inducing the expression of inducible nitric oxide synthase followed by the downregulation of T-cell responses.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"METHODS AND RESULTS We showed that IFN-gamma receptor-deficient mice (IFN-gammaR(-/-)) on a BALB/c background immunized with a peptide derived from cardiac alpha-myosin heavy chain develop severe myocarditis with high mortality.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 781, "doc_id": "24338780", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Walking in traffic areas in London improves lung function in elderly adults.\n\nCANDIDATE_ABSTRACT:\nTITLE: Respiratory and cardiovascular responses to walking down a traffic-polluted road compared with walking in a traffic-free area in participants aged 60 years and older with chronic lung or heart disease and age-matched healthy controls: a randomised, crossover study\nABSTRACT: BACKGROUND Long-term exposure to pollution can lead to an increase in the rate of decline of lung function, especially in older individuals and in those with chronic obstructive pulmonary disease (COPD), whereas shorter-term exposure at higher pollution levels has been implicated in causing excess deaths from ischaemic heart disease and exacerbations of COPD. We aimed to assess the effects on respiratory and cardiovascular responses of walking down a busy street with high levels of pollution compared with walking in a traffic-free area with lower pollution levels in older adults. METHODS In this randomised, crossover study, we recruited men and women aged 60 years and older with angiographically proven stable ischaemic heart disease or stage 2 Global initiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable for 6 months, and age-matched healthy volunteers. Individuals with ischaemic heart disease or COPD were recruited from existing databases or outpatient respiratory and cardiology clinics at the Royal Brompton & Harefield NHS Foundation Trust and age-matched healthy volunteers using advertising and existing databases. All participants had abstained from smoking for at least 12 months and medications were taken as recommended by participants' doctors during the study. Participants were randomly assigned by drawing numbered disks at random from a bag to do a 2 h walk either along a commercial street in London (Oxford Street) or in an urban park (Hyde Park). Baseline measurements of participants were taken before the walk in the hospital laboratory. During each walk session, black carbon, particulate matter (PM) concentrations, ultrafine particles, and nitrogen dioxide (NO2) concentrations were measured. FINDINGS Between October, 2012 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Participants with COPD reported more cough (odds ratio [OR] 1·95, 95% CI 0·96-3·95; p<0·1), sputum (3·15, 1·39-7·13; p<0·05), shortness of breath (1·86, 0·97-3·57; p<0·1), and wheeze (4·00, 1·52-10·50; p<0·05) after walking down Oxford Street compared with Hyde Park.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1373, "doc_id": "21003930", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Diabetic patients with acute coronary syndrome experience increased short-term and long-term risk for bleeding events.\n\nCANDIDATE_PASSAGE:\nPlatelet glycoprotein IIb/IIIa inhibitors reduce mortality in diabetic patients with non-ST-segment-elevation acute coronary syndromes. BACKGROUND Diabetes mellitus is a major risk factor for adverse outcomes after acute coronary syndromes (ACS). Because this disease may be associated with increased platelet aggregation, we investigated whether diabetic patients with ACS derive particular benefit from platelet glycoprotein (GP) IIb/IIIa receptor inhibition. METHODS AND RESULTS We performed a meta-analysis of the diabetic populations enrolled in the 6 large-scale platelet GP IIb/IIIa inhibitor ACS trials: PRISM, PRISM-PLUS, PARAGON A, PARAGON B, PURSUIT, and GUSTO IV. Among 6458 diabetic patients, platelet GP IIb/IIIa inhibition was associated with a significant mortality reduction at 30 days, from 6.2% to 4.6% (OR 0.74; 95% CI 0.59 to 0.92; P=0.007). Conversely, 23 072 nondiabetic patients had no survival benefit (3.0% versus 3.0%). The interaction between platelet GP IIb/IIIa inhibition and diabetic status was statistically significant (P=0.036). Among 1279 diabetic patients undergoing percutaneous coronary intervention (PCI) during index hospitalization, the use of these agents was associated with a mortality reduction at 30 days from 4.0% to 1.2% (OR 0.30; 95% CI 0.14 to 0.69; P=0.002). CONCLUSIONS This meta-analysis, including the entire large-scale trial experience of intravenous platelet GP IIb/IIIa inhibitors for the medical management of non-ST-segment-elevation ACS, shows that these agents may significantly reduce mortality at 30 days in diabetic patients. Although not based on a randomized assessment, the survival benefit appears to be of greater magnitude in patients undergoing PCI. Therefore, the use of platelet GP IIb/IIIa inhibitors should be s [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "343", "doc_id": "7873737", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Patients with microcytosis and higher erythrocyte count are more vulnerable to severe malarial anaemia when infected with Plasmodium falciparum.\n\nCANDIDATE_ABSTRACT:\nTITLE: Increased Microerythrocyte Count in Homozygous α+-Thalassaemia Contributes to Protection against Severe Malarial Anaemia\nABSTRACT: BACKGROUND The heritable haemoglobinopathy alpha(+)-thalassaemia is caused by the reduced synthesis of alpha-globin chains that form part of normal adult haemoglobin (Hb). Individuals homozygous for alpha(+)-thalassaemia have microcytosis and an increased erythrocyte count. Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count. We tested the hypothesis that the erythrocyte indices associated with alpha(+)-thalassaemia homozygosity provide a haematological benefit during acute malaria. METHODS AND FINDINGS Data from children living on the north coast of Papua New Guinea who had participated in a case-control study of the protection afforded by alpha(+)-thalassaemia against severe malaria were reanalysed to assess the genotype-specific reduction in erythrocyte count and Hb levels associated with acute malarial disease. We observed a reduction in median erythrocyte count of approximately 1.5 x 10(12)/l in all children with acute falciparum malaria relative to values in community children (p < 0.001). We developed a simple mathematical model of the linear relationship between Hb concentration and erythrocyte count. This model predicted that children homozygous for alpha(+)-thalassaemia lose less Hb than children of normal genotype for a reduction in erythrocyte count of >1.1 x 10(12)/l as a result of the reduced mean cell Hb in homozygous alpha(+)-thalassaemia. In addition, children homozygous for alpha(+)-thalassaemia require a 10% greater reduction in erythrocyte count than children of normal genotype (p = 0.02) for Hb concentration to fall to 50 g/l, the cutoff for SMA. We estimated that the haematological profile in [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS The increased erythrocyte count and microcytosis in children homozygous for alpha(+)-thalassaemia may contribute substantially to their protection against SMA.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 928, "doc_id": "18174210", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Energy balance requires hypothalamic glutamate neurotransmission.\n\nCANDIDATE_ABSTRACT:\nTITLE: Fasting Activation of AgRP Neurons Requires NMDA Receptors and Involves Spinogenesis and Increased Excitatory Tone\nABSTRACT: AgRP neuron activity drives feeding and weight gain whereas that of nearby POMC neurons does the opposite. However, the role of excitatory glutamatergic input in controlling these neurons is unknown. To address this question, we generated mice lacking NMDA receptors (NMDARs) on either AgRP or POMC neurons. Deletion of NMDARs from AgRP neurons markedly reduced weight, body fat and food intake whereas deletion from POMC neurons had no effect. Activation of AgRP neurons by fasting, as assessed by c-Fos, Agrp and Npy mRNA expression, AMPA receptor-mediated EPSCs, depolarization and firing rates, required NMDARs. Furthermore, AgRP but not POMC neurons have dendritic spines and increased glutamatergic input onto AgRP neurons caused by fasting was paralleled by an increase in spines, suggesting fasting induced synaptogenesis and spinogenesis. Thus glutamatergic synaptic transmission and its modulation by NMDARs play key roles in controlling AgRP neurons and determining the cellular and behavioral response to fasting.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Thus glutamatergic synaptic transmission and its modulation by NMDARs play key roles in controlling AgRP neurons and determining the cellular and behavioral response to fasting.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 378, "doc_id": "10534299", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Differentiation of progenitor cells to myeloid cells is skewed when insulin signaling is suppressed.\n\nCANDIDATE_PASSAGE:\nDirect sensing of systemic and nutritional signals by hematopoietic progenitors in Drosophila The Drosophila lymph gland is a haematopoietic organ in which progenitor cells, which are most akin to the common myeloid progenitor in mammals, proliferate and differentiate into three types of mature cell--plasmatocytes, crystal cells and lamellocytes--the functions of which are reminiscent of mammalian myeloid cells. During the first and early second instars of larval development, the lymph gland contains only progenitors, whereas in the third instar, a medial region of the primary lobe of the lymph gland called the medullary zone contains these progenitors, and maturing blood cells are found juxtaposed in a peripheral region designated the cortical zone. A third group of cells referred to as the posterior signalling centre functions as a haematopoietic niche. Similarly to mammalian myeloid cells, Drosophila blood cells respond to multiple stresses including hypoxia, infection and oxidative stress. However, how systemic signals are sensed by myeloid progenitors to regulate cell-fate determination has not been well described. Here, we show that the haematopoietic progenitors of Drosophila are direct targets of systemic (insulin) and nutritional (essential amino acid) signals, and that these systemic signals maintain the progenitors by promoting Wingless (WNT in mammals) signalling. We expect that this study will promote investigation of such possible direct signal sensing mechanisms by mammalian myeloid progenitors.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "347", "doc_id": "11902109", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Inside the body, falciparum parasites reproduce asexually.\n\nCANDIDATE_PASSAGE:\nMalaria biology and disease pathogenesis: insights for new treatments Plasmodium falciparum malaria, an infectious disease caused by a parasitic protozoan, claims the lives of nearly a million children each year in Africa alone and is a top public health concern. Evidence is accumulating that resistance to artemisinin derivatives, the frontline therapy for the asexual blood stage of the infection, is developing in southeast Asia. Renewed initiatives to eliminate malaria will benefit from an expanded repertoire of antimalarials, including new drugs that kill circulating P. falciparum gametocytes, thereby preventing transmission. Our current understanding of the biology of asexual blood-stage parasites and gametocytes and the ability to culture them in vitro lends optimism that high-throughput screenings of large chemical libraries will produce a new generation of antimalarial drugs. There is also a need for new therapies to reduce the high mortality of severe malaria. An understanding of the pathophysiology of severe disease may identify rational targets for drugs that improve survival.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "640", "doc_id": "6503185", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Ectopic expression of Sall4, Nanog, Esrrb, and Lin28 generates induced pluripotent stem cells from mouse embryonic fibroblasts more efficiently than other factor combinations.\n\nCANDIDATE_ABSTRACT:\nTITLE: The developmental potential of iPSCs is greatly influenced by reprogramming factor selection.\nABSTRACT: Induced pluripotent stem cells (iPSCs) are commonly generated by transduction of Oct4, Sox2, Klf4, and Myc (OSKM) into cells. Although iPSCs are pluripotent, they frequently exhibit high variation in terms of quality, as measured in mice by chimera contribution and tetraploid complementation. Reliably high-quality iPSCs will be needed for future therapeutic applications. Here, we show that one major determinant of iPSC quality is the combination of reprogramming factors used. Based on tetraploid complementation, we found that ectopic expression of Sall4, Nanog, Esrrb, and Lin28 (SNEL) in mouse embryonic fibroblasts (MEFs) generated high-quality iPSCs more efficiently than other combinations of factors including OSKM. Although differentially methylated regions, transcript number of master regulators, establishment of specific superenhancers, and global aneuploidy were comparable between high- and low-quality lines, aberrant gene expression, trisomy of chromosome 8, and abnormal H2A.X deposition were distinguishing features that could potentially also be applicable to human.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Based on tetraploid complementation, we found that ectopic expression of Sall4, Nanog, Esrrb, and Lin28 (SNEL) in mouse embryonic fibroblasts (MEFs) generated high-quality iPSCs more efficiently than other combinations of factors including OSKM.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 369, "doc_id": "6826100", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Flexible molecules experience greater steric hindrance in the tumor microenviroment than rigid molecules.\n\nCANDIDATE_ABSTRACT:\nTITLE: Quantum dots spectrally distinguish multiple species within the tumor milieu in vivo\nABSTRACT: A solid tumor is an organ composed of cancer and host cells embedded in an extracellular matrix and nourished by blood vessels. A prerequisite to understanding tumor pathophysiology is the ability to distinguish and monitor each component in dynamic studies. Standard fluorophores hamper simultaneous intravital imaging of these components. Here, we used multiphoton microscopy techniques and transgenic mice that expressed green fluorescent protein, and combined them with the use of quantum dot preparations. We show that these fluorescent semiconductor nanocrystals can be customized to concurrently image and differentiate tumor vessels from both the perivascular cells and the matrix. Moreover, we used them to measure the ability of particles of different sizes to access the tumor. Finally, we successfully monitored the recruitment of quantum dot–labeled bone marrow–derived precursor cells to the tumor vasculature. These examples show the versatility of quantum dots for studying tumor pathophysiology and creating avenues for treatment.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 421, "doc_id": "11172205", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Transplanted human glial cells can differentiate within the host animal.\n\nCANDIDATE_ABSTRACT:\nTITLE: Forebrain engraftment by human glial progenitor cells enhances synaptic plasticity and learning in adult mice.\nABSTRACT: Human astrocytes are larger and more complex than those of infraprimate mammals, suggesting that their role in neural processing has expanded with evolution. To assess the cell-autonomous and species-selective properties of human glia, we engrafted human glial progenitor cells (GPCs) into neonatal immunodeficient mice. Upon maturation, the recipient brains exhibited large numbers and high proportions of both human glial progenitors and astrocytes. The engrafted human glia were gap-junction-coupled to host astroglia, yet retained the size and pleomorphism of hominid astroglia, and propagated Ca2+ signals 3-fold faster than their hosts. Long-term potentiation (LTP) was sharply enhanced in the human glial chimeric mice, as was their learning, as assessed by Barnes maze navigation, object-location memory, and both contextual and tone fear conditioning. Mice allografted with murine GPCs showed no enhancement of either LTP or learning. These findings indicate that human glia differentially enhance both activity-dependent plasticity and learning in mice.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Upon maturation, the recipient brains exhibited large numbers and high proportions of both human glial progenitors and astrocytes.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1319, "doc_id": "16284655", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Tirasemtiv targets cardiac muscle.\n\nCANDIDATE_PASSAGE:\nAntipsychotic prescribing patterns in Germany: a retrospective analysis using a large outpatient prescription database. Data of prescribing practices for antipsychotics are of great interest with respect to quality of care. Consequently, we analysed all prescriptions under the statutory health insurance redeemed at pharmacies in Southern Germany between July 1999 and December 2001. The database covers prescriptions for approximately 25 million people. Up to 6% of the population were prescribed an antipsychotic at least once during the study period. Most prescriptions were for conventional antipsychotics and written by non-specialists. Patients receiving second generation antipsychotics were more likely to receive continuous antipsychotic therapy. For a large proportion of patients, antipsychotic polypharmacy, as well as comedication for somatic illnesses, were observed. In particular, drugs for the treatment of cardiovascular and metabolic disorders were frequently co-prescribed. Physicians should consider patients' cardiovascular and metabolic risk profile when making treatment choices. The data suggest that the majority of antipsychotics are used for the treatment of disorders other than schizophrenia. It is important to raise awareness among non-specialists about the indications, efficacy and side-effects of the antipsychotics because these physicians account for the majority of antipsychotic prescriptions.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1304", "doc_id": "21590125", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Students who perform poorly in the early years of medical school are at increased risk for professional misconduct later in their careers.\n\nCANDIDATE_ABSTRACT:\nTITLE: Risk factors at medical school for subsequent professional misconduct: multicentre retrospective case-control study\nABSTRACT: OBJECTIVE To determine whether there are risk factors in a doctor's time at medical school that are associated with subsequent professional misconduct. DESIGN Matched case-control study. Setting Records from medical schools and the General Medical Council (GMC). PARTICIPANTS 59 doctors who had graduated from any one of eight medical schools in the United Kingdom in 1958-97 and had a proved finding of serious professional misconduct in GMC proceedings in 1999-2004 (cases); 236 controls (four for each case) were selected by systematic sampling from matching graduation cohorts. Case-control status was revealed by the GMC after completion of data entry. MAIN OUTCOME MEASURE Odds ratios for being a \"case,\" with multivariable conditional logistic regression of potential risk factors including pre-admission characteristics and progress during the course. These data were obtained from anonymised copies of the students' progress files held by their original medical schools. RESULTS Univariate conditional logistic regression analysis found that cases were more likely to be men, to be of lower estimated social class, and to have had academic difficulties during their medical course, especially in the early years. Multivariable analysis showed that male sex (odds ratio 9.80, 95% confidence interval 2.43 to 39.44, P=0.001), lower social class (4.28, 1.52 to 12.09, P=0.006), and failure of early or preclinical examinations (5.47, 2.17 to 13.79, P<0.001) were independently associated with being a case. CONCLUSIONS This small study suggests that male sex, a lower socioeconomic background, and early academic difficulties at medical school could be risk factors for subsequent professional misconduct. The findings are preliminary and should be interpreted with caution. Most do [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Multivariable analysis showed that male sex (odds ratio 9.80, 95% confidence interval 2.43 to 39.44, P=0.001), lower social class (4.28, 1.52 to 12.09, P=0.006), and failure of early or preclinical examinations (5.47, 2.17 to 13.79, P<0.001) were independently associated with being a case.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1105, "doc_id": "6710713", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Glial calcium waves influence seizures.\n\nCANDIDATE_PASSAGE:\nThe importance of engaging policy-makers at the outset to guide research on and introduction of vaccines: the use of policy-maker surveys. Face-to-face surveys of policy-makers and other influential leaders are a useful tool to identify, at an early stage, (a) major issues regarding the introduction of a new vaccine, (b) persons and groups in a country who play a major decision-making or influential role in the introduction of vaccines, (c) potential obstacles to the introduction of vaccines, and (d) data-needs of policy-makers to overcome these obstacles. By surveying the opinions and beliefs of those who will make or influence decisions on whether to introduce a new vaccine, these studies can help ensure that research activities respond to the needs of policy-makers in countries endemic for the target diseases. These surveys can also inform vaccine-introduction strategies by identifying financially and politically feasible means of distributing, targeting, and financing the vaccines. This paper describes the methodology used in conducting such surveys and discusses methodological issues. It also presents lessons learnt from two policy-maker surveys carried out in several Asian countries in regard to new-generation vaccines against cholera, typhoid fever, and shigellosis; and future vaccines against dengue fever/dengue haemorrhagic fever.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "469", "doc_id": "27527854", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Exposure to fine particulate air pollution is unrelated to anxiety prevalence.\n\nCANDIDATE_ABSTRACT:\nTITLE: The relation between past exposure to fine particulate air pollution and prevalent anxiety: observational cohort study\nABSTRACT: OBJECTIVE To determine whether higher past exposure to particulate air pollution is associated with prevalent high symptoms of anxiety. DESIGN Observational cohort study. SETTING Nurses' Health Study. PARTICIPANTS 71,271 women enrolled in the Nurses' Health Study residing throughout the contiguous United States who had valid estimates on exposure to particulate matter for at least one exposure period of interest and data on anxiety symptoms. MAIN OUTCOME MEASURES Meaningfully high symptoms of anxiety, defined as a score of 6 points or greater on the phobic anxiety subscale of the Crown-Crisp index, administered in 2004. RESULTS The 71,271 eligible women were aged between 57 and 85 years (mean 70 years) at the time of assessment of anxiety symptoms, with a prevalence of high anxiety symptoms of 15%. Exposure to particulate matter was characterized using estimated average exposure to particulate matter <2.5 μm in diameter (PM2.5) and 2.5 to 10 μm in diameter (PM2.5-10) in the one month, three months, six months, one year, and 15 years prior to assessment of anxiety symptoms, and residential distance to the nearest major road two years prior to assessment. Significantly increased odds of high anxiety symptoms were observed with higher exposure to PM2.5 for multiple averaging periods (for example, odds ratio per 10 µg/m(3) increase in prior one month average PM2.5: 1.12, 95% confidence interval 1.06 to 1.19; in prior 12 month average PM2.5: 1.15, 1.06 to 1.26). Models including multiple exposure windows suggested short term averaging periods were more relevant than long term averaging periods. There was no association between anxiety and exposure to PM2.5-10. Residential proximity to major roads was not related to anxiety symptoms in a dose dependent manner. CON [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Exposure to fine particulate matter (PM2.5) was associated with high symptoms of anxiety, with more recent exposures potentially more relevant than more distant exposures.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 400, "doc_id": "791050", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: A single nucleotide variant the gene DGKK is strongly associated with increased risk of hypospadias.\n\nCANDIDATE_PASSAGE:\nCommon variants in DGKK are strongly associated with risk of hypospadias Hypospadias is a common congenital malformation of the male external genitalia. We performed a genome-wide association study using pooled DNA from 436 individuals with hypospadias (cases) and 494 controls of European descent and selected the highest ranked SNPs for individual genotyping in the discovery sample, an additional Dutch sample of 133 cases and their parents, and a Swedish series of 266 cases and 402 controls. Individual genotyping of two SNPs (rs1934179 and rs7063116) in DGKK, encoding diacylglycerol kinase κ, produced compelling evidence for association with hypospadias in the discovery sample (allele-specific odds ratio (OR) = 2.5, P = 2.5 × 10−11 and OR = 2.3, P = 2.9 × 10−9, respectively) and in the Dutch (OR = 3.9, P = 2.4 × 10−5 and OR = 3.8, P = 3.4 × 10−5) and Swedish (OR = 2.5, P = 2.6 × 10−8 and OR = 2.2, P = 2.7 × 10−6) replication samples. Expression studies showed expression of DGKK in preputial tissue of cases and controls, which was lower in carriers of the risk allele of rs1934179 (P = 0.047). We propose DGKK as a major risk gene for hypospadias.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "46", "doc_id": "380526", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Treatment with a protein named FN restores regenerative abilities of aged muscles.\n\nCANDIDATE_ABSTRACT:\nTITLE: Loss of fibronectin from the aged stem cell niche affects the regenerative capacity of skeletal muscle in mice\nABSTRACT: Age-related changes in the niche have long been postulated to impair the function of somatic stem cells. Here we demonstrate that the aged stem cell niche in skeletal muscle contains substantially reduced levels of fibronectin (FN), leading to detrimental consequences for the function and maintenance of muscle stem cells (MuSCs). Deletion of the gene encoding FN from young regenerating muscles replicates the aging phenotype and leads to a loss of MuSC numbers. By using an extracellular matrix (ECM) library screen and pathway profiling, we characterize FN as a preferred adhesion substrate for MuSCs and demonstrate that integrin-mediated signaling through focal adhesion kinase and the p38 mitogen-activated protein kinase pathway is strongly de-regulated in MuSCs from aged mice because of insufficient attachment to the niche. Reconstitution of FN levels in the aged niche remobilizes stem cells and restores youth-like muscle regeneration. Taken together, we identify the loss of stem cell adhesion to FN in the niche ECM as a previously unknown aging mechanism.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Deletion of the gene encoding FN from young regenerating muscles replicates the aging phenotype and leads to a loss of MuSC numbers.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1324, "doc_id": "19912367", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Sympathetic nerve activity is reduced throughout normal pregnancy.\n\nCANDIDATE_PASSAGE:\nEmerging role of bisphosphonates in the clinic--antitumor activity and prevention of metastasis to bone. Bisphosphonates are currently used for the treatment of bone metastases, and emerging data suggest that they may also have antitumor properties. Preclinical studies have demonstrated that zoledronic acid can inhibit angiogenesis, invasion and adhesion of tumor cells, and overall tumor progression, and emerging evidence suggests that the use of these agents may impede the development of skeletal metastases. In a recent clinical study in patients with metastatic bone disease, basal levels of vascular endothelial growth factor, a factor essential for angiogenesis, were significantly reduced in patients receiving zoledronic acid, suggesting that zoledronic acid may have clinically relevant antiangiogenic properties. Early clinical data on prevention of bone metastases by the early-generation bisphosphonate clodronate have yielded promising results in patients with breast cancer, and trials are currently ongoing to assess the efficacy of clodronate in this setting. Similarly, the new-generation bisphosphonate zoledronic acid has demonstrated activity in the prevention of bone metastases in small, 18-month pilot studies in patients with high-risk solid tumors (N=40; P=0.0002). Similarly, in a separate 5-year trial, the overall survival of patients with multiple myeloma was greater in patients whose standard treatment regimens included zoledronic acid compared with standard treatment alone (P<0.01). These encouraging early clinical results supported the initiation of larger randomized trials that are currently ongoing.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1120", "doc_id": "25298276", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Lice attenuated SIV vaccines induce a stronger antigen-specific T cell response in lymph node cells.\n\nCANDIDATE_PASSAGE:\nLymph node T cell responses predict the efficacy of live attenuated SIV vaccines Live attenuated simian immunodeficiency virus (SIV) vaccines (LAVs) remain the most efficacious of all vaccines in nonhuman primate models of HIV and AIDS, yet the basis of their robust protection remains poorly understood. Here we show that the degree of LAV-mediated protection against intravenous wild-type SIVmac239 challenge strongly correlates with the magnitude and function of SIV-specific, effector-differentiated T cells in the lymph node but not with the responses of such T cells in the blood or with other cellular, humoral and innate immune parameters. We found that maintenance of protective T cell responses is associated with persistent LAV replication in the lymph node, which occurs almost exclusively in follicular helper T cells. Thus, effective LAVs maintain lymphoid tissue-based, effector-differentiated, SIV-specific T cells that intercept and suppress early wild-type SIV amplification and, if present in sufficient frequencies, can completely control and perhaps clear infection, an observation that provides a rationale for the development of safe, persistent vectors that can elicit and maintain such responses.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "694", "doc_id": "1071991", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Alirocumab treatment reduces apo(a) fractional clearance rate.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effects of PCSK9 Inhibition With Alirocumab on Lipoprotein Metabolism in Healthy Humans\nABSTRACT: BACKGROUND Alirocumab, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), lowers plasma low-density lipoprotein (LDL) cholesterol and apolipoprotein B100 (apoB). Although studies in mice and cells have identified increased hepatic LDL receptors as the basis for LDL lowering by PCSK9 inhibitors, there have been no human studies characterizing the effects of PCSK9 inhibitors on lipoprotein metabolism. In particular, it is not known whether inhibition of PCSK9 has any effects on very low-density lipoprotein or intermediate-density lipoprotein (IDL) metabolism. Inhibition of PCSK9 also results in reductions of plasma lipoprotein (a) levels. The regulation of plasma Lp(a) levels, including the role of LDL receptors in the clearance of Lp(a), is poorly defined, and no mechanistic studies of the Lp(a) lowering by alirocumab in humans have been published to date. METHODS Eighteen (10 F, 8 mol/L) participants completed a placebo-controlled, 2-period study. They received 2 doses of placebo, 2 weeks apart, followed by 5 doses of 150 mg of alirocumab, 2 weeks apart. At the end of each period, fractional clearance rates (FCRs) and production rates (PRs) of apoB and apo(a) were determined. In 10 participants, postprandial triglycerides and apoB48 levels were measured. RESULTS Alirocumab reduced ultracentrifugally isolated LDL-C by 55.1%, LDL-apoB by 56.3%, and plasma Lp(a) by 18.7%. The fall in LDL-apoB was caused by an 80.4% increase in LDL-apoB FCR and a 23.9% reduction in LDL-apoB PR. The latter was due to a 46.1% increase in IDL-apoB FCR coupled with a 27.2% decrease in conversion of IDL to LDL. The FCR of apo(a) tended to increase (24.6%) without any change in apo(a) PR. Alirocumab had no effects on FCRs or PRs of very low-density lipopro [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The FCR of apo(a) tended to increase (24.6%) without any change in apo(a) PR.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 98, "doc_id": "6540064", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Do emergency medical services professionals think they should participate in disease prevention?\n\nABSTRACT:\nThe primary objective of the study was to determine emergency medical services (EMS) professionals' opinions regarding participation in disease and injury prevention programs. A secondary objective was to determine the proportion of EMS professionals who had participated in disease prevention programs. As part of the National Registry of Emergency Medical Technicians' biennial reregistration process, EMS professionals reregistering in 2006 were asked to complete an optional survey regarding their opinions on and participation in disease and injury prevention. Demographic characteristics were also collected. Data were analyzed using descriptive statistics and 99% confidence intervals (CIs). The chi-square test was used to compare differences by responder demographics (alpha = 0.01). A 10% difference between groups was determined to be clinically significant. The survey was completed by 27,233 EMS professionals. Of these responders, 82.7% (99% CI: 82.1-83.3) felt that EMS professionals should participate in disease prevention, with those working 20 to 29 hours per week being the least likely to think they should participate (67.4%, p<0.001). About a third, 33.8% (99% CI: 33.1-34.6), of the respondents reported having provided prevention services, with those having a graduate degree (43.5%, p<0.001), those working in EMS for more than 21 years (44%, p<0.001), those working for the military (57%, p<0.001), those working 60 to 69 hours per week (41%, p<0.001), and those responding to zero emergency calls in a typical week (43%, p<0.001) being the most likely to report having provided prevention services. About half, 51.1% (99% CI: 50.4-51.9), of the respondents agreed that prevention services should be provided during emergency calls, and 7.7% (99% CI: 7.3-8.1) o [TRUNCATED]", "output": "{\"label\": \"maybe\", \"rationale\": \"The majority of EMS professionals thought that they should participate in disease and injury prevention programs. The respondents were mixed as to whether prevention services should be provided while on emergency calls, but those with experience providing these services were more likely to agree with providing them during emergency calls.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 19145527, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: siRNA knockdown of A20 accelerates tumor progression in an in vivo murine xenograft model.\n\nCANDIDATE_ABSTRACT:\nTITLE: A20 is overexpressed in glioma cells and may serve as a potential therapeutic target.\nABSTRACT: OBJECTIVE A20 is a TNF-inducible primary response gene, which has been found to have antiapoptotic function in several cancer cells. This study investigates A20 expression in human glioma tissues and four glioma cell lines, and its effect on tumorigenesis of glioma cells and a mouse tumor model. METHODS Human glioma tissue samples and cells were subject to reverse transcription-PCR (RT-PCR), western blotting and immunohistochemistry. Glioma cells was tested by flow cytometry. A xenograft tumor model in mice was utilized to examine the knock-down effect of specific A20 siRNAs on tumorigenesis. RESULTS A20 was overexpressed in clinical glioma tissue samples (63.9%) and correlated with clinical staging. All four human glioma cell lines expressed A20, among which U87 displayed the strongest expression signals. Inhibiting A20 expression by siRNAs in vitro reduced the growth rates of glioma cells and resulted in G1/S arrest and increased apoptosis. In a mouse tumor model, local administration of siRNA significantly suppressed solid tumor growth. CONCLUSIONS A20 was overexpressed both in human glioma tissues and cell lines, and inhibiting A20 expression greatly slowed tumor cell growth in culture and in mice. These findings indicated that A20 is involved in tumorigenesis of human glioma, and may serve as a future therapeutic target.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In a mouse tumor model, local administration of siRNA significantly suppressed solid tumor growth.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1403, "doc_id": "38355793", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Physical activity level is associated with the difference in maximal oxygen consumption between black and white youth.\n\nCANDIDATE_ABSTRACT:\nTITLE: Determinants of adolescent physical activity and inactivity patterns.\nABSTRACT: OBJECTIVES Despite recognition of the important influence of environmental determinants on physical activity patterns, minimal empirical research has been done to assess the impact of environmental/contextual determinants of physical activity. This article aims to investigate environmental and sociodemographic determinants of physical activity and inactivity patterns among subpopulations of US adolescents. We define environmental determinants as modifiable factors in the physical environment that impose a direct influence on the opportunity to engage in physical activity. The present research examines environmental and sociodemographic determinants of physical activity and inactivity with the implication that these findings can point toward societal-level intervention strategies for increasing physical activity and decreasing inactivity among adolescents. STUDY DESIGN AND METHODOLOGY The study population consists of nationally representative data from the 1996 National Longitudinal Study of Adolescent Health on 17 766 US adolescents enrolled in US middle and high schools (including 3933 non-Hispanic blacks, 3148 Hispanics, and 1337 Asians). Hours/week of inactivity (TV/video viewing and video/computer games) and times/week of moderate to vigorous physical activity were collected by questionnaire. Outcome variables were moderate to vigorous physical activity and inactivity, which were broken into categories (physical activity: 0-2 times/week, 3-4 times/week, and >/=5 times/week; inactivity: 0-10 hours/week, 11-24 hours/week, and >/=25 hours/week). Sociodemographic and environmental correlates of physical activity and inactivity were used as exposure and control variables and included sex, age, urban residence, participation in school physical education progra [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 946, "doc_id": "13083189", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Activated Cdk5 phosphorylates the ATM protein in response to DNA damage.\n\nCANDIDATE_ABSTRACT:\nTITLE: Phosphorylation of ATM by Cdk5 mediates DNA damage signaling and regulates neuronal death\nABSTRACT: The phosphatidylinositol-3-kinase-like kinase ATM (ataxia-telangiectasia mutated) has a central role in coordinating DNA damage responses, including cell-cycle checkpoint control, DNA repair and apoptosis. Mutations of ATM cause a spectrum of defects ranging from neurodegeneration to cancer predisposition. However, the mechanism by which DNA damage activates ATM is poorly understood. Here we show that Cdk5 (cyclin-dependent kinase 5), activated by DNA damage, directly phosphorylates ATM at Ser 794 in post-mitotic neurons. Phosphorylation at Ser 794 precedes, and is required for, ATM autophosphorylation at Ser 1981, and activates ATM kinase activity. The Cdk5-ATM signal regulates phosphorylation and function of the ATM targets p53 and H2AX. Interruption of the Cdk5-ATM pathway attenuates DNA-damage-induced neuronal cell cycle re-entry and expression of the p53 targets PUMA and Bax, protecting neurons from death. Thus, activation of Cdk5 by DNA damage serves as a critical signal to initiate the ATM response and regulate ATM-dependent cellular processes.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Thus, activation of Cdk5 by DNA damage serves as a critical signal to initiate the ATM response and regulate ATM-dependent cellular processes.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 67, "doc_id": "21295300", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Differentiated E2f-1, -2, -3 TKO cells in the intestine do not exhibit apoptosis.\n\nCANDIDATE_PASSAGE:\nRedefining the Genetic Hierarchies Controlling Skeletal Myogenesis: Pax-3 and Myf-5 Act Upstream of MyoD We analyzed Pax-3 (splotch), Myf-5 (targeted with nlacZ), and splotch/Myf-5 homozygous mutant mice to investigate the roles that these genes play in programming skeletal myogenesis. In splotch and Myf-5 homozygous embryos, myogenic progenitor cell perturbations and early muscle defects are distinct. Remarkably, splotch/Myf-5 double homozygotes have a dramatic phenotype not seen in the individual mutants: body muscles are absent. MyoD does not rescue this double mutant phenotype since activation of this gene proves to be dependent on either Pax-3 or Myf-5. Therefore, Pax-3 and Myf-5 define two distinct myogenic pathways, and MyoD acts genetically downstream of these genes for myogenesis in the body. This genetic hierarchy does not appear to operate for head muscle formation.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "345", "doc_id": "18747744", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Depletion of T-helper 17 (Th17) cells during simian immunodeficiency virus (SIV) infection decreases dissemination of Salmonella Typhimurium from the gut.\n\nCANDIDATE_PASSAGE:\nVirus-specific cytotoxic T-lymphocyte responses select for amino-acid variation in simian immunodeficiency virus Env and Nef Cytotoxic T-lymphocyte (CTL) responses to human immunodeficiency virus arise early after infection, but ultimately fail to prevent progression to AIDS. Human immunodeficiency virus may evade the CTL response by accumulating amino-acid replacements within CTL epitopes. We studied 10 CTL epitopes during the course of simian immunodeficiency virus disease progression in three related macaques. All 10 of these CTL epitopes accumulated amino-acid replacements and showed evidence of positive selection by the time the macaques died. Many of the amino-acid replacements in these epitopes reduced or eliminated major histocompatibility complex class I binding and/or CTL recognition. These findings strongly support the CTL 'escape' hypothesis.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "332", "doc_id": "20864487", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Exercise increases cancer mortality rates among Chinese citizens.\n\nCANDIDATE_ABSTRACT:\nTITLE: Combined Impact of Lifestyle-Related Factors on Total and Cause-Specific Mortality among Chinese Women: Prospective Cohort Study\nABSTRACT: BACKGROUND Although cigarette smoking, excessive alcohol drinking, obesity, and several other well-studied unhealthy lifestyle-related factors each have been linked to the risk of multiple chronic diseases and premature death, little is known about the combined impact on mortality outcomes, in particular among Chinese and other non-Western populations. The objective of this study was to quantify the overall impact of lifestyle-related factors beyond that of active cigarette smoking and alcohol consumption on all-cause and cause-specific mortality in Chinese women. METHODS AND FINDINGS We used data from the Shanghai Women's Health Study, an ongoing population-based prospective cohort study in China. Participants included 71,243 women aged 40 to 70 years enrolled during 1996-2000 who never smoked or drank alcohol regularly. A healthy lifestyle score was created on the basis of five lifestyle-related factors shown to be independently associated with mortality outcomes (normal weight, lower waist-hip ratio, daily exercise, never exposed to spouse's smoking, higher daily fruit and vegetable intake). The score ranged from zero (least healthy) to five (most healthy) points. During an average follow-up of 9 years, 2,860 deaths occurred, including 775 from cardiovascular disease (CVD) and 1,351 from cancer. Adjusted hazard ratios for mortality decreased progressively with an increasing number of healthy lifestyle factors. Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality. The inverse association between the healthy lifestyle score and mortality was seen consistently regardless of ch [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The population attributable risks for not having 4-5 healthy lifestyle factors were 33% for total deaths, 59% for CVD deaths, and 19% for cancer deaths.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 396, "doc_id": "1456068", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Cytosolic proteins bind to iron-responsive elements on mRNAs coding for DMT1. Cytosolic proteins bind to iron-responsive elements on mRNAs coding for proteins involved in iron uptake.\n\nCANDIDATE_PASSAGE:\nNeurological outcomes of animal models of uterine artery ligation and relevance to human intrauterine growth restriction: a systematic review AIM This review explores the molecular, neurological, and behavioural outcomes in animal models of uterine artery ligation. We analyse the relevance of this type of model to the pathological and functional phenotypes that are consistent with cerebral palsy and its developmental comorbidities in humans. METHOD A literature search of the PubMed database was conducted for research using the uterine artery ligation model published between 1990 and 2013. From the studies included, any relevant neuroanatomical and behavioural deficits were then summarized from each document and used for further analysis. RESULTS There were 25 papers that met the criteria included for review, and several outcomes were summarized from the results of these papers. Fetuses with growth restriction demonstrated a gradient of reduced body weight with a relative sparing of brain mass. There was a significant reduction in the size of the somatosensory cortex, hippocampus, and corpus callosum. The motor cortex appeared to be spared of identifiable deficits. Apoptotic proteins were upregulated, while those important to neuronal survival, growth, and differentiation were downregulated. Neuronal apoptosis and astrogliosis occurred diffusely throughout the brain regions. White matter injury involved oligodendrocyte precursor maturation arrest, hypomyelination, and an aberrant organization of existing myelin. Animals with growth restriction demonstrated deficits in gait, memory, object recognition, and spatial processing. INTERPRETATION This review concludes that neuronal death, white matter injury, motor abnormalities, and cognitive deficits are important [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "300", "doc_id": "18104691", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Radioiodine treatment of non-toxic multinodular goitre increases thyroid volume.\n\nCANDIDATE_PASSAGE:\nRadioiodine treatment of multinodular non-toxic goitre. OBJECTIVE To investigate the long term effect of radioactive iodine on thyroid function and size in patients with non-toxic multinodular goitre. DESIGN Consecutive patients with multinodular non-toxic goitre selected for radioactive iodine treatment and followed for a minimum of 12 months (median 48 months) after an intended dose of 3.7 MBq/g thyroid tissue corrected to a 100% uptake of iodine-131 in 24 hours. PATIENTS 69 patients with a growing multinodular non-toxic goitre causing local compression symptoms or cosmetic inconveniences. The treatment was chosen because of a high operative risk, previous thyroidectomy, or refusal to be operated on. MAIN OUTCOME MEASUREMENTS Standard thyroid function variables and ultrasonically determined thyroid volume before treatment as well as 1, 2, 3, 6, and 12 months after treatment and then once a year. RESULTS 56 patients were treated with a single dose of 131I, 12 with two doses, and one with four doses. In 45 patients treated with one dose and remaining euthyroid the median thyroid volume was reduced from 73 (interquartile range 50-106) ml to 29 (23-48) ml at 24 months in the 39 patients in whom this was measured during follow up. The median reduction was 40 (22-48) ml (60% reduction, p < 0.0001), half of which occurred within three months. Patients treated with two doses as well as those developing hypothyroidism and hyperthyroidism had a significant reduction in thyroid volume. Eleven patients developed hypothyroidism (cumulative five year risk 22%, 95% confidence interval 4.8% to 38.4%). Side effects were few: three cases of hyperthyroidism and two cases of radiation thyroiditis. Only one patient was dissatisfied with the result; she was referred for operati [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1011", "doc_id": "9745001", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Healthcare delivery efficiency in crowded delivery centers is impaired by improving structural, logistical, and interpersonal elements.\n\nCANDIDATE_PASSAGE:\nMolecular elements of low-oxygen signaling in plants. Oxygen and its limitation are emerging as a crucial factor in plant fitness, growth and development. Recent studies revealed the mechanisms by which oxygen is perceived by plant cells. This sensory system partly relies on an oxygen-mediated branch of the N-end rule pathway for protein degradation acting on a specific clade of ethylene responsive transcription factors (ERF-VII). A complementary regulative step is provided by aerobic sequestration of an ERF-VII protein at the plasma membrane and its timely release when hypoxia occurs. Complete absence of oxygen triggers the transient accumulation of reactive hydrogen peroxide and induces an additional set of reactive oxygen species-related genes involved in both signaling and attenuation of oxidative stress. Moreover, temporary hypoxic environments that are built up as consequence of dense cell packing have been demonstrated to trigger cell-fate determination in maize anthers. Similarly, limited oxygen delivery in bulky fruit or tuber tissues growing in aerobic conditions were shown to stimulate anaerobic-like responses. These advances in low-oxygen signaling and its effect on cell development highlight the importance of taking hypoxia into account in agronomical practices as well as in breeding programs.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "502", "doc_id": "24923605", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does treatment of Cultured Sebocytes with an EGFR Inhibitor Lead to Significant Upregulation of Inflammatory Biomarkers?\n\nABSTRACT:\nEpidermal growth factor receptor (EGFR) inhibitors are being used to treat malignancies originating from epithelia. Unfortunately, blocking the EGFR pathway leads to various side effects, most frequently acneiform eruptions. To probe the mechanism underlying this side effect, we investigated the effect of EGFR inhibitors on cultured sebocytes. To examine the effects of an EGFR inhibitor (cetuximab, Erbitux® 10 ng/ml) and the effects of EGFR ligands, such as epidermal growth factor (EGF, 10 ng/ml) and transforming growth factor-α (TGF-α, 5 ng/ml), on the production of inflammatory cytokines in cultured sebocytes, we used reverse transcriptase-polymerase chain reaction, immunocytofluorescence and Western blots. Outcomes included the expression of interleukin (IL)-1, IL-6, tumor necrosis factor-α (TNF-α), peroxisome proliferator-activated receptor-γ (PPAR-γ) and EGFR. There were no significant differences in the expression of IL-1, IL-6, TNF-α, PPAR-γ and EGFR between (a) groups treated with an EGFR inhibitor or an EGFR ligand and (b) the control group, except for a significant increase in the expression of IL-1 in the EGF-treated group.", "output": "{\"label\": \"no\", \"rationale\": \"EGFR inhibitors and EGFR ligands do not provoke the expression of inflammatory biomarkers in cultured sebocytes. The role of the sebaceous glands in EGFR inhibitor-induced acneiform eruption should be investigated more thoroughly.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 21738357, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The TRaF1/C5 rs10818488 allele polymorphism regulates the neighboring C5 gene.\n\nCANDIDATE_ABSTRACT:\nTITLE: A Candidate Gene Approach Identifies the TRAF1/C5 Region as a Risk Factor for Rheumatoid Arthritis\nABSTRACT: Correction for: Kurreeman FAS, Padyukov L, Marques RB, Schrodi SJ, Seddighzadeh M, et al. (2007) A Candidate Gene Approach Identifies the TRAF1/C5 Region as a Risk Factor for Rheumatoid Arthritis. PLoS Med 4(9): e278. doi:10.1371/journal.pmed.0040278 In Table 1, the allele ratio in column eight (Allele Ratiosb: Cases, Controls) refers to allele A: allele B and not allele1:allele2 as described in footnote b, with Allele A being the Susceptibility Allele as denoted in column seven. The footnote should read: bNumber of alleles were compared in cases versus controls: allele A: allele B cases, allele A: allele B controls. Allele A refers to the susceptibility alleles as given in column seven.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1183, "doc_id": "1967017", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Destination container port throughput(CPT) is positively related to dengue virus (DENV-1) diffusion in air traffic shipments.\n\nCANDIDATE_PASSAGE:\nImmunophenotypic analysis of AIDS-related diffuse large B-cell lymphoma and clinical implications in patients from AIDS malignancies consortium clinical trials 010 and 034 PURPOSE Diffuse large B-cell lymphoma (DLBCL) represents a clinically heterogeneous disease. Models based on immunohistochemistry predict clinical outcome. These include subdivision into germinal center (GC) versus non-GC subtypes; proliferation index (measured by expression of Ki-67), and expression of BCL-2, FOXP1, or B-lymphocyte-induced maturation protein (Blimp-1)/PRDM1. We sought to determine whether immunohistochemical analyses of biopsies from patients with DLBCL having HIV infection are similarly relevant for prognosis. PATIENTS AND METHODS We examined 81 DLBCLs from patients with AIDS in AMC010 (cyclophosphamide, doxorubicin, vincristine, and prednisone [CHOP] v CHOP-rituximab) and AMC034 (etoposide, doxorubicin, vincristine, prednisone, and dose-adjusted cyclophosphamide plus rituximab concurrent v sequential) clinical trials and compared the immunophenotype with survival data, Epstein-Barr virus (EBV) positivity, and CD4 counts. RESULTS The GC and non-GC subtypes of DLBCL did not differ significantly with respect to overall survival or CD4 count at cancer presentation. EBV could be found in both subtypes of DLBCL, although less frequently in the GC subtype, and did not affect survival. Expression of FOXP1, Blimp-1/PRDM1, or BCL-2 was not correlated with the outcome in patients with AIDS-related DLBCL. CONCLUSION These data indicate that with current treatment strategies for lymphoma and control of HIV infection, commonly used immunohistochemical markers may not be clinically relevant in HIV-infected patients with DLBCL. The only predictive immunohistochemical marker was found t [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "337", "doc_id": "23304931", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: MafA phosphorylation enhances its ubiquitination.\n\nCANDIDATE_PASSAGE:\nPancreatic tumor cells with mutant K-ras suppress ERK activity by MEK-dependent induction of MAP kinase phosphatase-2. Activating mutations within the K-ras gene occur in a high percentage of human pancreatic carcinomas. We reported previously that the presence of oncogenic, activated K-ras in human pancreatic carcinoma cell lines did not result in constitutive activation of the extracellular signal-regulated kinases (ERK1 and ERK2). In the present study, we further characterized the ERK signaling pathway in pancreatic tumor cell lines in order to determine whether the ERK pathway is subject to a compensatory downregulation. We found that the attenuation of serum-induced ERK activation was not due to a delay in the kinetics of ERK phosphorylation. Treatment with the tyrosine phosphatase inhibitor orthovanadate increased the level of ERK phosphorylation, implicating a vanadate-sensitive tyrosine phosphatase in the negative regulation of ERK. Furthermore, expression of a dual specificity phosphatase capable of inactivating ERK known as mitogen-activated protein (MAP) kinase phosphatase-2 (MKP-2) was elevated in most of the pancreatic tumor cell lines and correlated with the presence of active MAP kinase kinase (MEK). Taken together, these results suggest that pancreatic tumor cells expressing oncogenic K-ras compensate, in part, by upregulating the expression of MKP-2 to repress the ERK signaling pathway.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "746", "doc_id": "28651643", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does the genotype of the transporter associated with antigen processing gene affect susceptibility to colorectal cancer in Japanese?\n\nABSTRACT:\nAlthough colorectal cancer (CRC) is one of the most frequent malignancies in Japan, the associated genetic factors remain to be elucidated. Functional loss of the transporter associated with antigen processing (TAP) 1 gene induces carcinogenesis. We investigated whether single nucleotide polymorphisms (SNPs) in the TAP1 gene (rs735883) are associated with susceptibility to CRC in a Japanese population. The study participants were 143 cases and 243 clinical controls. After extracting DNA from their peripheral blood cells, genotyping was conducted by the polymerase chain reaction-restriction fragment length polymorphism method. Participants with a mutated allele had an increased risk for CRC. The adjusted odds ratios for the C/T, T/T, and the mutation type (C/T + T/T) compared to that of wild type (C/C) were 2.27 [95 % confidence interval (CI), 1.43-3.67], 1.95 (95 % CI, 0.88-4.30), and 2.22 (95 % CI, 1.42-3.55), respectively. Furthermore, a significant trend in the rate of cases was observed with an increasing number of mutated alleles (P for trend = 0.0068).", "output": "{\"label\": \"yes\", \"rationale\": \"The genotype of the TAP1 gene is associated with susceptibility to CRC.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 24803408, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: siRNA knockdown of A20 accelerates tumor progression in an in vivo murine xenograft model.\n\nCANDIDATE_ABSTRACT:\nTITLE: A20 is overexpressed in glioma cells and may serve as a potential therapeutic target.\nABSTRACT: OBJECTIVE A20 is a TNF-inducible primary response gene, which has been found to have antiapoptotic function in several cancer cells. This study investigates A20 expression in human glioma tissues and four glioma cell lines, and its effect on tumorigenesis of glioma cells and a mouse tumor model. METHODS Human glioma tissue samples and cells were subject to reverse transcription-PCR (RT-PCR), western blotting and immunohistochemistry. Glioma cells was tested by flow cytometry. A xenograft tumor model in mice was utilized to examine the knock-down effect of specific A20 siRNAs on tumorigenesis. RESULTS A20 was overexpressed in clinical glioma tissue samples (63.9%) and correlated with clinical staging. All four human glioma cell lines expressed A20, among which U87 displayed the strongest expression signals. Inhibiting A20 expression by siRNAs in vitro reduced the growth rates of glioma cells and resulted in G1/S arrest and increased apoptosis. In a mouse tumor model, local administration of siRNA significantly suppressed solid tumor growth. CONCLUSIONS A20 was overexpressed both in human glioma tissues and cell lines, and inhibiting A20 expression greatly slowed tumor cell growth in culture and in mice. These findings indicated that A20 is involved in tumorigenesis of human glioma, and may serve as a future therapeutic target.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Inhibiting A20 expression by siRNAs in vitro reduced the growth rates of glioma cells and resulted in G1/S arrest and increased apoptosis.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1403, "doc_id": "38355793", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: A country's Vaccine Alliance (GAVI) eligibility is not indictivate of accelerated adoption of the Hub vaccine.\n\nCANDIDATE_PASSAGE:\nPhysiological implications of hydrogen sulfide: a whiff exploration that blossomed. The important life-supporting role of hydrogen sulfide (H(2)S) has evolved from bacteria to plants, invertebrates, vertebrates, and finally to mammals. Over the centuries, however, H(2)S had only been known for its toxicity and environmental hazard. Physiological importance of H(2)S has been appreciated for about a decade. It started by the discovery of endogenous H(2)S production in mammalian cells and gained momentum by typifying this gasotransmitter with a variety of physiological functions. The H(2)S-catalyzing enzymes are differentially expressed in cardiovascular, neuronal, immune, renal, respiratory, gastrointestinal, reproductive, liver, and endocrine systems and affect the functions of these systems through the production of H(2)S. The physiological functions of H(2)S are mediated by different molecular targets, such as different ion channels and signaling proteins. Alternations of H(2)S metabolism lead to an array of pathological disturbances in the form of hypertension, atherosclerosis, heart failure, diabetes, cirrhosis, inflammation, sepsis, neurodegenerative disease, erectile dysfunction, and asthma, to name a few. Many new technologies have been developed to detect endogenous H(2)S production, and novel H(2)S-delivery compounds have been invented to aid therapeutic intervention of diseases related to abnormal H(2)S metabolism. While acknowledging the challenges ahead, research on H(2)S physiology and medicine is entering an exponential exploration era.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "32", "doc_id": "21932297", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Activation of PPM1D enhances p53 function.\n\nCANDIDATE_PASSAGE:\nThe BLM helicase contributes to telomere maintenance through processing of late-replicating intermediate structures Werner's syndrome (WS) and Bloom's syndrome (BS) are cancer predisposition disorders caused by loss of function of the RecQ helicases WRN or BLM, respectively. BS and WS are characterized by replication defects, hyperrecombination events and chromosomal aberrations, which are hallmarks of cancer. Inefficient replication of the G-rich telomeric strand contributes to chromosome aberrations in WS cells, demonstrating a link between WRN, telomeres and genomic stability. Herein, we provide evidence that BLM also contributes to chromosome-end maintenance. Telomere defects (TDs) are observed in BLM-deficient cells at an elevated frequency, which is similar to cells lacking a functional WRN helicase. Loss of both helicases exacerbates TDs and chromosome aberrations, indicating that BLM and WRN function independently in telomere maintenance. BLM localization, particularly its recruitment to telomeres, changes in response to replication dysfunction, such as in WRN-deficient cells or after aphidicolin treatment. Exposure to replication challenge causes an increase in decatenated deoxyribonucleic acid (DNA) structures and late-replicating intermediates (LRIs), which are visible as BLM-covered ultra-fine bridges (UFBs) in anaphase. A subset of UFBs originates from telomeric DNA and their frequency correlates with telomere replication defects. We propose that the BLM complex contributes to telomere maintenance through its activity in resolving LRIs.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "69", "doc_id": "2679511", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: 53% of perinatal mortality is due to low birth weight.\n\nCANDIDATE_PASSAGE:\nAntidepressant fluoxetine enhances glucocorticoid receptor function in vitro by modulating membrane steroid transporters. 1. Incubation of LMCAT fibroblast cells with antidepressants potentiates glucocorticoid receptor (GR)-mediated gene transcription in the presence of dexamethasone and cortisol, but not of corticosterone. We have shown that antidepressants do so by inhibiting the LMCAT cell membrane steroid transporter (which is virtually identical to the multidrug resistance P-glycoprotein) and thus by increasing dexamethasone or cortisol intracellular concentrations. However, previous experiments with the antidepressant fluoxetine in the presence of dexamethasone have produced negative results (Pariante et al. (2001). Br. J. Pharmacol., 134, 1335-1343). 2. We have since re-examined the effects of fluoxetine on GR-mediated gene transcription in the presence of dexamethasone. Moreover, we have examined the effects of fluoxetine on GR-mediated gene transcription in the presence of cortisol and corticosterone, and on the intracellular accumulation of radioactive cortisol and corticosterone. Finally, we have examined the effects of fluoxetine on inhibition of P-glycoprotein activity in Caco-2 cells. 3. We now find that fluoxetine (1-10 micro M) enhances GR-mediated gene transcription in the presence of dexamethasone and cortisol (+140-170%), but not of corticosterone, and increases the intracellular accumulation of (3)H-cortisol (+5-15%), but not of (3)H-corticosterone. Moreover, fluoxetine (10 micro M) induces approximately 30% inhibition of PGP activity in Caco-2 cells. 4. Our results show that fluoxetine, like other antidepressants, inhibits membrane steroid transporters.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "17", "doc_id": "6083952", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: GATA3 regulates self-renewal capacity in bone marrow hematopoietic stem cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: GATA-3 regulates hematopoietic stem cell maintenance and cell-cycle entry.\nABSTRACT: Maintaining hematopoietic stem cell (HSC) quiescence is a critical property for the life-long generation of blood cells. Approximately 75% of cells in a highly enriched long-term repopulating HSC (LT-HSC) pool (Lin(-)Sca1(+)c-Kit(hi)CD150(+)CD48(-)) are quiescent, with only a small percentage of the LT-HSCs in cycle. Transcription factor GATA-3 is known to be vital for the development of T cells at multiple stages in the thymus and for Th2 differentiation in the peripheral organs. Although it is well documented that GATA-3 is expressed in HSCs, a role for GATA-3 in any prethymic progenitor cell has not been established. In the present study, we show that Gata3-null mutant mice generate fewer LT-HSCs and that fewer Gata3-null LT-HSCs are in cycle. Furthermore, Gata3 mutant hematopoietic progenitor cells fail to be recruited into an increased cycling state after 5-fluorouracil-induced myelosuppression. Therefore, GATA-3 is required for the maintenance of a normal number of LT-HSCs and for their entry into the cell cycle.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In the present study, we show that Gata3-null mutant mice generate fewer LT-HSCs and that fewer Gata3-null LT-HSCs are in cycle.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 445, "doc_id": "10165258", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In British Men, haplogroup I decreases risk of cardiovascular disease.\n\nCANDIDATE_ABSTRACT:\nTITLE: ER-associated mitochondrial division links the distribution of mitochondria and mitochondrial DNA in yeast\nABSTRACT: Mitochondrial division is important for mitochondrial distribution and function. Recent data have demonstrated that ER-mitochondria contacts mark mitochondrial division sites, but the molecular basis and functions of these contacts are not understood. Here we show that in yeast, the ER-mitochondria tethering complex, ERMES, and the highly conserved Miro GTPase, Gem1, are spatially and functionally linked to ER-associated mitochondrial division. Gem1 acts as a negative regulator of ER-mitochondria contacts, an activity required for the spatial resolution and distribution of newly generated mitochondrial tips following division. Previous data have demonstrated that ERMES localizes with a subset of actively replicating mitochondrial nucleoids. We show that mitochondrial division is spatially linked to nucleoids and that a majority of these nucleoids segregate prior to division, resulting in their distribution into newly generated tips in the mitochondrial network. Thus, we postulate that ER-associated division serves to link the distribution of mitochondria and mitochondrial nucleoids in cells. DOI:http://dx.doi.org/10.7554/eLife.00422.001.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 563, "doc_id": "1991105", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Destination container port throughput(CPT) is negatively related to dengue virus (DENV-1) diffusion in air traffic shipments.\n\nCANDIDATE_PASSAGE:\nRecommendations on how to ensure the safety and effectiveness of biosimilars in Latin America: a point of view The use of biotechnology-derived medicines has significantly increased in recent decades. Although biosimilars undergo rigorous characterization as well as clinical studies to document their safety and effectiveness, they are highly complex molecules and small changes in the purification and production process of a biosimilar can have major implications in its safety and effectiveness profile. In Latin America, regulatory authorities have begun to establish well-described and standardized pathways that permit a biosimilar to gain commercial licensure. In order to be certain that a biosimilar reaches its potential in ordinary clinical use, an intensive post-licensing monitoring system must be established since it is the only means to ascertain the true similarity between the original biologic and its biosimilar. Pharmacovigilance allows national authorities to determine a drug's performance in the marketplace. An effective tracking and pharmacovigilance system for biological medicines has many steps and processes. To aid policy makers in Latin American in addressing the many issues surrounding the establishment of an effective pharmacovigilance system, the Americas Health Foundation convened a group of experts to discuss the topic and develop recommendations for implementation. The group discussed current challenges and gaps in pharmacovigilance in Latin America, paying close attention to the major issues associated with traceability and pharmacovigilance of biosimilars following their approval. The recommendations developed should enable countries to accurately document the safety and performance of a biosimilar as experienced by patients under real [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "336", "doc_id": "13031967", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The NF-κB essential modulator gene induces intestinal inflammation by promoting receptor-interacting protein (RIP) kinase 1 kinase activity-mediated epithelial cell death.\n\nCANDIDATE_ABSTRACT:\nTITLE: NEMO Prevents RIP Kinase 1-Mediated Epithelial Cell Death and Chronic Intestinal Inflammation by NF-κB-Dependent and -Independent Functions\nABSTRACT: Intestinal epithelial cells (IECs) regulate gut immune homeostasis, and impaired epithelial responses are implicated in the pathogenesis of inflammatory bowel diseases (IBD). IEC-specific ablation of nuclear factor κB (NF-κB) essential modulator (NEMO) caused Paneth cell apoptosis and impaired antimicrobial factor expression in the ileum, as well as colonocyte apoptosis and microbiota-driven chronic inflammation in the colon. Combined RelA, c-Rel, and RelB deficiency in IECs caused Paneth cell apoptosis but not colitis, suggesting that NEMO prevents colon inflammation by NF-κB-independent functions. Inhibition of receptor-interacting protein kinase 1 (RIPK1) kinase activity or combined deficiency of Fas-associated via death domain protein (FADD) and RIPK3 prevented epithelial cell death, Paneth cell loss, and colitis development in mice with epithelial NEMO deficiency. Therefore, NEMO prevents intestinal inflammation by inhibiting RIPK1 kinase activity-mediated IEC death, suggesting that RIPK1 inhibitors could be effective in the treatment of colitis in patients with NEMO mutations and possibly in IBD.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Inhibition of receptor-interacting protein kinase 1 (RIPK1) kinase activity or combined deficiency of Fas-associated via death domain protein (FADD) and RIPK3 prevented epithelial cell death, Paneth cell loss, and colitis development in mice with epithelial NEMO deficiency.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1170, "doc_id": "18956141", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Klf4 is important for proper myeloid cell differentiation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Kruppel-like factor 4 is essential for inflammatory monocyte differentiation in vivo.\nABSTRACT: Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types. We demonstrate in this study that hematopoietic cells from KLF4(-/-) fetal livers (FL) contained normal numbers of functional hematopoietic progenitor cells, were radioprotective, and performed as well as KLF4(+/+) cells in competitive repopulation assays. However, hematopoietic \"KLF4(-/-) chimeras\" generated by transplantation of KLF4(-/-) fetal livers cells into lethally irradiated wild-type mice completely lacked circulating inflammatory (CD115(+)Gr1(+)) monocytes, and had reduced numbers of resident (CD115(+)Gr1(-)) monocytes. Although the numbers and function of peritoneal macrophages were normal in KLF4(-/-) chimeras, bone marrow monocytic cells from KLF4(-/-) chimeras expressed lower levels of key trafficking molecules and were more apoptotic. Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes. In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells. The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 668, "doc_id": "25148216", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Cell autonomous sex determination in somatic cells occurs in Galliformes.\n\nCANDIDATE_PASSAGE:\nSomatic sex identity is cell-autonomous in the chicken In the mammalian model of sex determination, embryos are considered to be sexually indifferent until the transient action of a sex-determining gene initiates gonadal differentiation. Although this model is thought to apply to all vertebrates, this has yet to be established. Here we have examined three lateral gynandromorph chickens (a rare, naturally occurring phenomenon in which one side of the animal appears male and the other female) to investigate the sex-determining mechanism in birds. These studies demonstrated that gynandromorph birds are genuine male:female chimaeras, and indicated that male and female avian somatic cells may have an inherent sex identity. To test this hypothesis, we transplanted presumptive mesoderm between embryos of reciprocal sexes to generate embryos containing male:female chimaeric gonads. In contrast to the outcome for mammalian mixed-sex chimaeras, in chicken mixed-sex chimaeras the donor cells were excluded from the functional structures of the host gonad. In an example where female tissue was transplanted into a male host, donor cells contributing to the developing testis retained a female identity and expressed a marker of female function. Our study demonstrates that avian somatic cells possess an inherent sex identity and that, in birds, sexual differentiation is substantively cell autonomous.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "235", "doc_id": "4388470", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Are ki-ras gene mutations , LOH of the APC and DCC genes , and microsatellite instability in primary colorectal carcinoma associated with micrometastases in pericolonic lymph nodes or with patients ' survival?\n\nABSTRACT:\nThe primary aim of this study was to look for possible correlations between molecular genetic changes in primary colorectal cancer and the presence or absence of micrometastases in the accompanying pericolonic lymph nodes. The secondary aim was to correlate the data on these molecular genetic changes and micrometastases with survival. One hundred and twenty five Dukes's stage B colorectal cancers from 1989 to 1992 were analysed. The primary tumours were evaluated for Ki-ras mutation, adenomatous polyposis coli (APC) loss of heterozygosity (LOH), deleted in colon cancer (DCC) LOH, and microsatellite instability using standard molecular techniques. All available lymph nodes were immunohistochemically stained for micrometastases. Micrometastases were present in 41% of patients. There were significantly more lymph nodes removed in the patients with micrometastases. Micrometastases were not associated with Ki-ras mutation, APC LOH, DCC LOH, or microsatellite instability, even when controlling for the number of lymph nodes removed. None of the molecular variables considered had a significant impact on either overall survival or on death with disease.", "output": "{\"label\": \"no\", \"rationale\": \"There are insufficient data to justify using molecular genetic changes in primary colorectal carcinomas as prognostic markers. Micrometastases do not provide prognostic information on survival. There is value in increasing the numbers of lymph nodes removed and analysed along with the primary tumour.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 15333653, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Diabetes remission occurs more in people treated with conventional therapy than in people treated with laparoscopic adjustable gastric banding surgery.\n\nCANDIDATE_ABSTRACT:\nTITLE: Adjustable gastric banding and conventional therapy for type 2 diabetes: a randomized controlled trial.\nABSTRACT: CONTEXT Observational studies suggest that surgically induced loss of weight may be effective therapy for type 2 diabetes. OBJECTIVE To determine if surgically induced weight loss results in better glycemic control and less need for diabetes medications than conventional approaches to weight loss and diabetes control. DESIGN, SETTING, AND PARTICIPANTS Unblinded randomized controlled trial conducted from December 2002 through December 2006 at the University Obesity Research Center in Australia, with general community recruitment to established treatment programs. Participants were 60 obese patients (BMI >30 and <40) with recently diagnosed (<2 years) type 2 diabetes. INTERVENTIONS Conventional diabetes therapy with a focus on weight loss by lifestyle change vs laparoscopic adjustable gastric banding with conventional diabetes care. MAIN OUTCOME MEASURES Remission of type 2 diabetes (fasting glucose level <126 mg/dL [7.0 mmol/L] and glycated hemoglobin [HbA1c] value <6.2% while taking no glycemic therapy). Secondary measures included weight and components of the metabolic syndrome. Analysis was by intention-to-treat. RESULTS Of the 60 patients enrolled, 55 (92%) completed the 2-year follow-up. Remission of type 2 diabetes was achieved by 22 (73%) in the surgical group and 4 (13%) in the conventional-therapy group. Relative risk of remission for the surgical group was 5.5 (95% confidence interval, 2.2-14.0). Surgical and conventional-therapy groups lost a mean (SD) of 20.7% (8.6%) and 1.7% (5.2%) of weight, respectively, at 2 years (P < .001). Remission of type 2 diabetes was related to weight loss (R2 = 0.46, P < .001) and lower baseline HbA1c levels (combined R2 = 0.52, P < .001). There were no serious complications in either group. CONCLUSIONS Participants r [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Participants randomized to surgical therapy were more likely to achieve remission of type 2 diabetes through greater weight loss.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 341, "doc_id": "7098463", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: p16INK4A degradation is linked to an abnormal wound response caused by the microinvasive step of advanced Oral Potentially Malignant Lesions (OPMLs).\n\nCANDIDATE_PASSAGE:\nHypoxia in relation to vasculature and proliferation in liver metastases in patients with colorectal cancer. PURPOSE To investigate hypoxia measured by pimonidazole binding, glucose transporter 1 (GLUT1) and carbonic anhydrase IX (CA-IX) expression, proliferation, and vascularity in liver metastases of colorectal cancer and to compare GLUT1 and CA-IX expression in corresponding primary tumors. METHODS AND MATERIALS Twenty-five patients with liver metastases of colorectal cancer, planned for metastasectomy, were included. The hypoxia marker pimonidazole and proliferation marker iododeoxyuridine were administered before surgery. After immunofluorescent staining of the frozen metastases, pimonidazole binding, vascularity, and proliferation were analyzed quantitatively. Thirteen paraffin-embedded primary tumors were stained immunohistochemically for GLUT1 and CA-IX expression, which was analyzed semiquantitatively in primary tumors and corresponding liver metastases. RESULTS In liver metastases, pimonidazole binding showed a pattern consistent with diffusion-limited hypoxia. The mean pimonidazole-positive fraction was 0.146; the mean distance from vessels to pimonidazole-positive areas was 80 microm. When expressed, often co-localization was observed between pimonidazole binding and GLUT1 or CA-IX expression, but microregional areas of mismatch were also observed. No correlation between the level of pimonidazole binding and GLUT1 or CA-IX expression was observed. In some patients, a large fraction (up to 30%) of proliferating cells was present in pimonidazole-stained areas. Expression of CA-IX in primary tumors and metastases showed a significant correlation, which was absent for GLUT1 expression. CONCLUSIONS Compared with other tumor types, liver metastases of [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1397", "doc_id": "24980622", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is p53 protein accumulation in European hepatocellular carcinoma always dependent on p53 gene mutation?\n\nABSTRACT:\nImmunohistochemical reactivity for p53 protein is common in various human malignancies and often related to p53 gene mutation. However, in some tumor types, accumulation of wild-type p53 has been shown. Previously, we analyzed 96 European hepatocellular carcinomas using immunohistochemistry and found that 31% of these tumors overexpressed p53 in the cell nucleus. The aim of the present study was to establish whether p53 positivity correlates with the presence of structural p53 gene abnormalities in European hepatocellular carcinoma. DNA from 20 tumors, 10 with strong immunostaining and 10 with undetectable staining for p53, was extracted from frozen sections, and the entire coding portion of the p53 gene was sequenced. Five of the 10 tumors containing high levels of p53 protein showed missense point mutations. The remaining 5 tumors with high p53 levels showed the wild-type coding sequence. One of the 10 tumors containing undetectable levels of p53 protein had a 1-base pair deletion in the splice acceptor site of intron 4.", "output": "{\"label\": \"no\", \"rationale\": \"The results strongly suggest that, in European hepatocellular carcinomas, stabilization of the p53 protein depends on factors other than p53 gene mutation, such as binding to other molecules of cellular or viral origin.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 7698586, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cost effectiveness evaluations based on cRCT data lack external validity.\n\nCANDIDATE_ABSTRACT:\nTITLE: A Comparison of Cost Effectiveness Using Data from Randomized Trials or Actual Clinical Practice: Selective Cox-2 Inhibitors as an Example\nABSTRACT: BACKGROUND Data on absolute risks of outcomes and patterns of drug use in cost-effectiveness analyses are often based on randomised clinical trials (RCTs). The objective of this study was to evaluate the external validity of published cost-effectiveness studies by comparing the data used in these studies (typically based on RCTs) to observational data from actual clinical practice. Selective Cox-2 inhibitors (coxibs) were used as an example. METHODS AND FINDINGS The UK General Practice Research Database (GPRD) was used to estimate the exposure characteristics and individual probabilities of upper gastrointestinal (GI) events during current exposure to nonsteroidal anti-inflammatory drugs (NSAIDs) or coxibs. A basic cost-effectiveness model was developed evaluating two alternative strategies: prescription of a conventional NSAID or coxib. Outcomes included upper GI events as recorded in GPRD and hospitalisation for upper GI events recorded in the national registry of hospitalisations (Hospital Episode Statistics) linked to GPRD. Prescription costs were based on the prescribed number of tables as recorded in GPRD and the 2006 cost data from the British National Formulary. The study population included over 1 million patients prescribed conventional NSAIDs or coxibs. Only a minority of patients used the drugs long-term and daily (34.5% of conventional NSAIDs and 44.2% of coxibs), whereas coxib RCTs required daily use for at least 6-9 months. The mean cost of preventing one upper GI event as recorded in GPRD was US$104k (ranging from US$64k with long-term daily use to US$182k with intermittent use) and US$298k for hospitalizations. The mean costs (for GPRD events) over calendar time were US$58k during 1990-1993 and US$174k during 2002-2005. Using RCT data rather [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Only a minority of patients used the drugs long-term and daily (34.5% of conventional NSAIDs and 44.2% of coxibs), whereas coxib RCTs required daily use for at least 6-9 months.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 292, "doc_id": "15048300", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Hyperfibrinogenemia decreases rates of femoropopliteal bypass thrombosis.\n\nCANDIDATE_PASSAGE:\nSputum inflammation predicts exacerbations after cessation of inhaled corticosteroids in COPD. INTRODUCTION The GOLD guidelines advocate not to institute inhaled corticosteroids (ICS) in patients with mild-to-moderate COPD. However, many patients do use ICS and in some patients, withdrawal is associated with deteriorating lung function and increased exacerbation rates. Unfortunately, physicians do not know in which patients they can stop ICS treatment safely. AIM To identify predictors of COPD exacerbations after ICS withdrawal. METHODS During ICS treatment, post-bronchodilator spirometry, body plethysmography, and health status assessment were performed in 68 COPD patients using ICS. Additionally, sputum cell differentials, supernatant leukotriene B(4), eosinophilic cationic protein, and myeloperoxidase, serum C-reactive protein and soluble intracellular adhesion molecule, and urinary desmosine were assessed. Sputum was also analysed for mRNA levels of haemoxygenase-1, tumour necrosis factor-α, RANTES, interleukin 5(IL-5), IL-10, IL-12, IL-13, transforming growth factor-β, and interferon-γ. STATISTICS Cox regression analyses were performed using time to exacerbation as outcome variable to identify significant hazards for a COPD exacerbation after ICS withdrawal. RESULTS Higher sputum % eosinophils, higher sputum MPO/neutrophil level, longer duration of COPD symptoms, <40 packyears smoking, and ICS withdrawal in November, December or January were significant hazards (all p<0.05) for experiencing a COPD exacerbation after ICS withdrawal in a monovariate model. In a multivariate model, all factors proved independent predictors except for sputum MPO/neutrophil level. CONCLUSIONS Decisions on whether or not inhaled corticosteroids can be safely withdrawn in mild [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "532", "doc_id": "25319221", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Microglia are an innate immune cell type of the central nervous system.\n\nCANDIDATE_PASSAGE:\nRegulation and function of the E-cadherin/catenin complex in cells of the monocyte-macrophage lineage and DCs. E-cadherin is best characterized as adherens junction protein, which through homotypic interactions contributes to the maintenance of the epithelial barrier function. In epithelial cells, the cytoplasmic tail of E-cadherin forms a dynamic complex with catenins and regulates several intracellular signal transduction pathways, including Wnt/β-catenin, PI3K/Akt, Rho GTPase, and NF-κB signaling. Recent progress uncovered a novel and critical role for this adhesion molecule in mononuclear phagocyte functions. E-cadherin regulates the maturation and migration of Langerhans cells, and its ligation prevents the induction of a tolerogenic state in bone marrow-derived dendritic cells (DCs). In this respect, the functionality of β-catenin could be instrumental in determining the balance between immunogenicity and tolerogenicity of DCs in vitro and in vivo. Fusion of alternatively activated macrophages and osteoclasts is also E-cadherin-dependent. In addition, the E-cadherin ligands CD103 and KLRG1 are expressed on DC-, T-, and NK-cell subsets and contribute to their interaction with E-cadherin-expressing DCs and macrophages. Here we discuss the regulation, function, and implications of E-cadherin expression in these central orchestrators of the immune system.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "789", "doc_id": "3118719", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: APOE4 expression in iPSC-derived neurons results in decreased tau phosphorylation.\n\nCANDIDATE_PASSAGE:\nNeurons derived from reprogrammed fibroblasts functionally integrate into the fetal brain and improve symptoms of rats with Parkinson's disease. The long-term goal of nuclear transfer or alternative reprogramming approaches is to create patient-specific donor cells for transplantation therapy, avoiding immunorejection, a major complication in current transplantation medicine. It was recently shown that the four transcription factors Oct4, Sox2, Klf4, and c-Myc induce pluripotency in mouse fibroblasts. However, the therapeutic potential of induced pluripotent stem (iPS) cells for neural cell replacement strategies remained unexplored. Here, we show that iPS cells can be efficiently differentiated into neural precursor cells, giving rise to neuronal and glial cell types in culture. Upon transplantation into the fetal mouse brain, the cells migrate into various brain regions and differentiate into glia and neurons, including glutamatergic, GABAergic, and catecholaminergic subtypes. Electrophysiological recordings and morphological analysis demonstrated that the grafted neurons had mature neuronal activity and were functionally integrated in the host brain. Furthermore, iPS cells were induced to differentiate into dopamine neurons of midbrain character and were able to improve behavior in a rat model of Parkinson's disease upon transplantation into the adult brain. We minimized the risk of tumor formation from the grafted cells by separating contaminating pluripotent cells and committed neural cells using fluorescence-activated cell sorting. Our results demonstrate the therapeutic potential of directly reprogrammed fibroblasts for neuronal cell replacement in the animal model.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "58", "doc_id": "14192687", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Propriospinal interneurons that play a role in the plastic reorganization of spinal circuits are integral for recovery from spinal cord injury.\n\nCANDIDATE_ABSTRACT:\nTITLE: Recovery of supraspinal control of stepping via indirect propriospinal relay connections after spinal cord injury\nABSTRACT: Spinal cord injuries (SCIs) in humans and experimental animals are often associated with varying degrees of spontaneous functional recovery during the first months after injury. Such recovery is widely attributed to axons spared from injury that descend from the brain and bypass incomplete lesions, but its mechanisms are uncertain. To investigate the neural basis of spontaneous recovery, we used kinematic, physiological and anatomical analyses to evaluate mice with various combinations of spatially and temporally separated lateral hemisections with or without the excitotoxic ablation of intrinsic spinal cord neurons. We show that propriospinal relay connections that bypass one or more injury sites are able to mediate spontaneous functional recovery and supraspinal control of stepping, even when there has been essentially total and irreversible interruption of long descending supraspinal pathways in mice. Our findings show that pronounced functional recovery can occur after severe SCI without the maintenance or regeneration of direct projections from the brain past the lesion and can be mediated by the reorganization of descending and propriospinal connections. Targeting interventions toward augmenting the remodeling of relay connections may provide new therapeutic strategies to bypass lesions and restore function after SCI and in other conditions such as stroke and multiple sclerosis.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Our findings show that pronounced functional recovery can occur after severe SCI without the maintenance or regeneration of direct projections from the brain past the lesion and can be mediated by the reorganization of descending and propriospinal connections.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 980, "doc_id": "20128547", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Therapeutics receiving accelerated approval encounter a lower frequency of post-marketing safety events\n\nCANDIDATE_PASSAGE:\nLysosomal localization of TRPML3 depends on TRPML2 and the mucolipidosis-associated protein TRPML1. Mucolipidosis type IV is an autosomal recessive lysosomal storage disorder characterized by severe neurodegeneration, achlorhydria, and visual impairments such as corneal opacity and strabismus. The disease arises due to mutations in a group 2 transient receptor potential (TRP)-related cation channel, TRPML1. Mammals encode two additional TRPML proteins named TRPML2 and TRPML3. Information regarding the propensity of these proteins to multimerize, their subcellular distribution and mechanisms that regulate their trafficking are limited. Here we demonstrate that TRPMLs interact to form homo- and heteromultimers. Moreover, the presence of either TRPML1 or TRPML2 specifically influences the spatial distribution of TRPML3. TRPML1 and TRPML2 homomultimers are lysosomal proteins, whereas TRPML3 homomultimers are in the endoplasmic reticulum. However, TRPML3 localizes to lysosomes when coexpressed with either TRPML1 or TRPML2 and is comparably mislocalized when lysosomal targeting of TRPML1 and TRPML2 is disrupted. Conversely, TRPML3 does not cause retention of TRPML1 or TRPML2 in the endoplasmic reticulum. These data demonstrate that there is a hierarchy controlling the subcellular distributions of the TRPMLs such that TRPML1 and TRPML2 dictate the localization of TRPML3 and not vice versa.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1284", "doc_id": "19708993", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The latent infection of myeloid cells with human cytomegalovirus induces a number of changes in gene expression.\n\nCANDIDATE_ABSTRACT:\nTITLE: Transcriptome analysis reveals human cytomegalovirus reprograms monocyte differentiation toward an M1 macrophage.\nABSTRACT: Monocytes are primary targets for human CMV (HCMV) infection and are proposed to be responsible for hematogenous dissemination of the virus. Monocytes acquire different functional traits during polarization to the classical proinflammatory M1 macrophage or the alternative antiinflammatory M2 macrophage. We hypothesized that HCMV induced a proinflammatory M1 macrophage following infection to promote viral dissemination because, biologically, a proinflammatory state provides the tools to drive infected monocytes from the blood into the tissue. To test this hypothesis of monocyte conversion from a normal quiescent phenotype to an inflammatory phenotype, we used Affymetrix Microarray to acquire a transcriptional profile of infected monocytes at a time point our data emphasized is a key temporal regulatory point following infection. We found that HCMV significantly up-regulated 583 (5.2%) of the total genes and down-regulated 621 (5.5%) of the total genes>or=1.5-fold at 4 h postinfection. Further ontology analysis revealed that genes implicated in classical M1 macrophage activation were stimulated by HCMV infection. We found that 65% of genes strictly associated with M1 polarization were up-regulated, while only 4% of genes solely associated with M2 polarization were up-regulated. Analysis of the monocyte chemokinome at the transcriptional level showed that 44% of M1 and 33% of M2 macrophage chemokines were up-regulated. Proteomic analysis using chemokine Ab arrays confirmed the secretion of these chemotactic proteins from HCMV-infected monocytes. Overall, the results identify that the HCMV-infected monocyte transcriptome displayed a unique M1/M2 polarization signature that was skewed toward the classical M1 activation phenotype.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Further ontology analysis revealed that genes implicated in classical M1 macrophage activation were stimulated by HCMV infection.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1224, "doc_id": "34016987", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Citrullinated proteins externalized in neutrophil extracellular traps act indirectly to disrupt the inflammatory cycle.\n\nCANDIDATE_ABSTRACT:\nTITLE: NETs are a source of citrullinated autoantigens and stimulate inflammatory responses in rheumatoid arthritis.\nABSTRACT: The early events leading to the development of rheumatoid arthritis (RA) remain unclear, but formation of autoantibodies to citrullinated protein antigens (ACPAs) is considered a key pathogenic event. Neutrophils isolated from patients with various autoimmune diseases display enhanced neutrophil extracellular trap (NET) formation, a phenomenon that exposes autoantigens in the context of immunostimulatory molecules. We investigated whether aberrant NETosis occurs in RA, determined its triggers, and examined its deleterious inflammatory consequences. Enhanced NETosis was observed in circulating and RA synovial fluid neutrophils compared to neutrophils from healthy controls and from patients with osteoarthritis (OA). Further, netting neutrophils infiltrated RA synovial tissue, rheumatoid nodules, and skin. NETosis correlated with ACPA presence and levels and with systemic inflammatory markers. RA sera and immunoglobulin fractions from RA patients with high levels of ACPA and/or rheumatoid factor significantly enhanced NETosis, and the NETs induced by these autoantibodies displayed distinct protein content. Indeed, during NETosis, neutrophils externalized the citrullinated autoantigens implicated in RA pathogenesis, and anti-citrullinated vimentin antibodies potently induced NET formation. Moreover, the inflammatory cytokines interleukin-17A (IL-17A) and tumor necrosis factor-α (TNF-α) induced NETosis in RA neutrophils. In turn, NETs significantly augmented inflammatory responses in RA and OA synovial fibroblasts, including induction of IL-6, IL-8, chemokines, and adhesion molecules. These observations implicate accelerated NETosis in RA pathogenesis, through externalization of citrullinated autoantigens and immunostimulatory molecules that may promote aberrant [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Indeed, during NETosis, neutrophils externalized the citrullinated autoantigens implicated in RA pathogenesis, and anti-citrullinated vimentin antibodies potently induced NET formation. In turn, NETs significantly augmented inflammatory responses in RA and OA synovial fibroblasts, including induction of IL-6, IL-8, chemokines, and adhesion molecules.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 263, "doc_id": "11328820", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Klf2 is important for proper myeloid cell function.\n\nCANDIDATE_ABSTRACT:\nTITLE: The myeloid transcription factor KLF2 regulates the host response to polymicrobial infection and endotoxic shock.\nABSTRACT: Precise control of myeloid cell activation is required for optimal host defense. However, this activation process must be under exquisite control to prevent uncontrolled inflammation. Herein, we identify the Kruppel-like transcription factor 2 (KLF2) as a potent regulator of myeloid cell activation in vivo. Exposure of myeloid cells to hypoxia and/or bacterial products reduced KLF2 expression while inducing hypoxia inducible factor-1α (HIF-1α), findings that were recapitulated in human septic patients. Myeloid KLF2 was found to be a potent inhibitor of nuclear factor-kappaB (NF-κB)-dependent HIF-1α transcription and, consequently, a critical determinant of outcome in models of polymicrobial infection and endotoxemia. Collectively, these observations identify KLF2 as a tonic repressor of myeloid cell activation in vivo and an essential regulator of the innate immune system.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Collectively, these observations identify KLF2 as a tonic repressor of myeloid cell activation in vivo and an essential regulator of the innate immune system.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 667, "doc_id": "6493422", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Beta-band coherence is diminished for visible stimuli over invisible stimuli.\n\nCANDIDATE_PASSAGE:\nA model of multiple myeloma: culture of 5T33 murine myeloma cells and evaluation of tumorigenicity in the C57BL/KaLwRij mouse. The 5T33 multiple myeloma is one of a series of transplantable murine myelomas arising spontaneously in C57BL/KaLwRij mice. This study describes the establishment and characterisation of the 5T33 murine myeloma in vitro as a cultured cell line in terms of its morphology, growth rate, expression of paraprotein (IgG2b) and tumorigenicity in syngeneic animals. The 5T33 cell line has been in continuous culture for over 10 months and has achieved more than passage 34. In culture, 5T33 myeloma grows as single cells or in small clusters of loosely adherent cells on an adherent stromal cell layer. Maximum doubling time is approximately 25 h, and over 90% of the cells express cytoplasmic IgG2b paraprotein. The cultured 5T33 myeloma cells are highly tumorigenic in C57BL/KaLwRij mice with as few as 500 cells inducing paralysis and death as early as day 36 post-tumour inoculation. Kinetics of tumour development and detection of IgG2b paraprotein are dose dependent. Two weeks following intravenous inoculation of 5 x 10(5) cultured 5T33 myeloma cells, tumour cells were readily identified in the bone marrow. By 3 weeks post-tumour inoculation, 5T33 myeloma cells were found in various tissues throughout the animal. Studies are now underway to determine the sensitivity of this cell line to various therapeutic modalities.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "174", "doc_id": "13889962", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: cSMAC formation enhances weak ligand signalling.\n\nCANDIDATE_ABSTRACT:\nTITLE: In vitro differentiation of transplantable neural precursors from human embryonic stem cells\nABSTRACT: The remarkable developmental potential and replicative capacity of human embryonic stem (ES) cells promise an almost unlimited supply of specific cell types for transplantation therapies. Here we describe the in vitro differentiation, enrichment, and transplantation of neural precursor cells from human ES cells. Upon aggregation to embryoid bodies, differentiating ES cells formed large numbers of neural tube–like structures in the presence of fibroblast growth factor 2 (FGF-2). Neural precursors within these formations were isolated by selective enzymatic digestion and further purified on the basis of differential adhesion. Following withdrawal of FGF-2, they differentiated into neurons, astrocytes, and oligodendrocytes. After transplantation into the neonatal mouse brain, human ES cell–derived neural precursors were incorporated into a variety of brain regions, where they differentiated into both neurons and astrocytes. No teratoma formation was observed in the transplant recipients. These results depict human ES cells as a source of transplantable neural precursors for possible nervous system repair.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1385, "doc_id": "2437807", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Mutant mice lacking SVCT2 have greatly increased ascorbic acid levels in both brain and adrenals.\n\nCANDIDATE_ABSTRACT:\nTITLE: Ascorbic-acid transporter Slc23a1 is essential for vitamin C transport into the brain and for perinatal survival\nABSTRACT: The only proven requirement for ascorbic acid (vitamin C) is in preventing scurvy, presumably because it is a cofactor for hydroxylases required for post-translational modifications that stabilize collagen. We have created mice deficient in the mouse ortholog (solute carrier family 23 member 1 or Slc23a1) of a rat ascorbic-acid transporter, Svct2 (ref. 4). Cultured embryonic fibroblasts from homozygous Slc23a1−/− mice had less than 5% of normal ascorbic-acid uptake. Ascorbic-acid levels were undetectable or markedly reduced in the blood and tissues of Slc23a1−/− mice. Prenatal supplementation of pregnant females did not elevate blood ascorbic acid in Slc23a1−/− fetuses, suggesting Slc23a1 is important in placental ascorbic-acid transport. Slc23a1−/− mice died within a few minutes of birth with respiratory failure and intraparenchymal brain hemorrhage. Lungs showed no postnatal expansion but had normal surfactant protein B levels. Brain hemorrhage was unlikely to be simply a form of scurvy since Slc23a1−/− mice showed no hemorrhage in any other tissues and their skin had normal skin 4-hydroxyproline levels despite low ascorbic-acid content. We conclude that Slc23a1 is required for transport of ascorbic acid into many tissues and across the placenta. Deficiency of the transporter is lethal in newborn mice, thereby revealing a previously unrecognized requirement for ascorbic acid in the perinatal period.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Ascorbic-acid levels were undetectable or markedly reduced in the blood and tissues of Slc23a1−/− mice.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 811, "doc_id": "19799455", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Cost effectiveness evaluations based on cRCT data lack external validity.\n\nCANDIDATE_ABSTRACT:\nTITLE: A Comparison of Cost Effectiveness Using Data from Randomized Trials or Actual Clinical Practice: Selective Cox-2 Inhibitors as an Example\nABSTRACT: BACKGROUND Data on absolute risks of outcomes and patterns of drug use in cost-effectiveness analyses are often based on randomised clinical trials (RCTs). The objective of this study was to evaluate the external validity of published cost-effectiveness studies by comparing the data used in these studies (typically based on RCTs) to observational data from actual clinical practice. Selective Cox-2 inhibitors (coxibs) were used as an example. METHODS AND FINDINGS The UK General Practice Research Database (GPRD) was used to estimate the exposure characteristics and individual probabilities of upper gastrointestinal (GI) events during current exposure to nonsteroidal anti-inflammatory drugs (NSAIDs) or coxibs. A basic cost-effectiveness model was developed evaluating two alternative strategies: prescription of a conventional NSAID or coxib. Outcomes included upper GI events as recorded in GPRD and hospitalisation for upper GI events recorded in the national registry of hospitalisations (Hospital Episode Statistics) linked to GPRD. Prescription costs were based on the prescribed number of tables as recorded in GPRD and the 2006 cost data from the British National Formulary. The study population included over 1 million patients prescribed conventional NSAIDs or coxibs. Only a minority of patients used the drugs long-term and daily (34.5% of conventional NSAIDs and 44.2% of coxibs), whereas coxib RCTs required daily use for at least 6-9 months. The mean cost of preventing one upper GI event as recorded in GPRD was US$104k (ranging from US$64k with long-term daily use to US$182k with intermittent use) and US$298k for hospitalizations. The mean costs (for GPRD events) over calendar time were US$58k during 1990-1993 and US$174k during 2002-2005. Using RCT data rather [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS The published cost-effectiveness analyses of coxibs lacked external validity, did not represent patients in actual clinical practice, and should not have been used to inform prescribing policies.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 292, "doc_id": "15048300", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is an elevated ratio of measured to predicted creatinine production in CAPD patients a sensitive predictor of noncompliance with the dialysis prescription?\n\nABSTRACT:\nTo determine the effect a period of \"intentional noncompliance\" in stable continuous ambulatory peritoneal dialysis (CAPD) patients has on the ratio of measured to predicted creatinine generation. Prospective study that compares baseline to noncompliant periods in individual CAPD patients. Nine chronic, stable CAPD patients. At baseline, measured creatinine production and adequacy parameters (KT/V, creatinine clearance, lean body mass, and protein equivalent of nitrogen appearance) were calculated from 24-hour collections of dialysate and urine while patients were performing their routine dialysis prescriptions. After three days of intentional noncompliance (one less exchange/day) the patients repeated their 24-hour collections, again performing their routine number of exchanges. Measured creatinine production and adequacy parameters were again calculated. Predicted creatinine production for each patient was calculated from standard equations. All parameters at baseline were compared to corresponding parameters after intentional noncompliance. In all patients, except one where there was no change, there was a statistically significant increase in not only the ratio of measured to predicted creatinine production but also all other parameters.", "output": "{\"label\": \"no\", \"rationale\": \"As suspected by previous investigators, this study suggests that one cause of an elevated ratio of measured to predicted creatinine production may be a recent period of noncompliance with the patient's dialysis prescription. However, these data suggest that an isolated ratio of measured to predicted creatinine generation is not a sensitive predictor of noncompliance with the peritoneal dialysis prescription.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 9147547, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Intake of folic acid (FA) and vitamin B6 (VB6) increases levels of homocysteine.\n\nCANDIDATE_ABSTRACT:\nTITLE: Differential distribution of IL28B.rs12979860 single-nucleotide polymorphism among Egyptian healthcare workers with and without a hepatitis C virus-specific cellular immune response\nABSTRACT: The CC genotype of the interleukin (IL)-28B.rs12979860 gene has been associated with spontaneous hepatitis C virus (HCV) clearance and treatment response. The distribution and correlation of an IL28B.rs12979860 single-nucleotide polymorphism (SNP) with HCV-specific cell-mediated immune (CMI) responses among Egyptian healthcare workers (HCWs) is not known. We determined this relationship in 402 HCWs who serve a patient cohort with ~85 % HCV prevalence. We enrolled 402 HCWs in four groups: group 1 (n = 258), seronegative aviremic subjects; group 2 (n = 25), seronegative viremic subjects; group 3 (n = 41), subjects with spontaneously resolved HCV infection; and group 4 (n = 78), chronic HCV patients. All subjects were tested for an HCV-specific CMI response using an ex-vivo interferon-gamma (IFNγ) ELISpot assay with nine HCV genotype-4a overlapping 15-mer peptide pools corresponding to all of the HCV proteins. All subjects were tested for IL28B.rs12979860 SNP by real-time PCR. An HCV-specific CMI was demonstrated in ~27 % of the seronegative aviremic HCWs (group 1), suggesting clearance of infection after low-level exposure to HCV. The frequency of IL28B.rs12979860 C allele homozygosity in the four groups was 49 %, 48 %, 49 %, and 23 %, while that of the T allele was 14 %, 16 %, 12 and 19 %, respectively, suggesting differential distributions among subjects with different HCV status. As reported, IL28B.rs12979860 predicted the outcome of HCV infection (p < 0.05), but we did not find any relationship between the IL28B genotypes and the outcome of HCV-specific CMI responses in the four groups (p > 0.05). The data show differential IL28B.rs12979860 genotype distribution among Egyptian HCWs with different HCV status and could not predict the outcome of HCV-specific [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 645, "doc_id": "991139", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: APOE4 expression in iPSC-derived neurons increases AlphaBeta production and tau phosphorylation, delaying GABA neuron degeneration.\n\nCANDIDATE_ABSTRACT:\nTITLE: Gain of toxic Apolipoprotein E4 effects in Human iPSC-Derived Neurons Is Ameliorated by a Small-Molecule Structure Corrector\nABSTRACT: Efforts to develop drugs for Alzheimer's disease (AD) have shown promise in animal studies, only to fail in human trials, suggesting a pressing need to study AD in human model systems. Using human neurons derived from induced pluripotent stem cells that expressed apolipoprotein E4 (ApoE4), a variant of the APOE gene product and the major genetic risk factor for AD, we demonstrated that ApoE4-expressing neurons had higher levels of tau phosphorylation, unrelated to their increased production of amyloid-β (Aβ) peptides, and that they displayed GABAergic neuron degeneration. ApoE4 increased Aβ production in human, but not in mouse, neurons. Converting ApoE4 to ApoE3 by gene editing rescued these phenotypes, indicating the specific effects of ApoE4. Neurons that lacked APOE behaved similarly to those expressing ApoE3, and the introduction of ApoE4 expression recapitulated the pathological phenotypes, suggesting a gain of toxic effects from ApoE4. Treatment of ApoE4-expressing neurons with a small-molecule structure corrector ameliorated the detrimental effects, thus showing that correcting the pathogenic conformation of ApoE4 is a viable therapeutic approach for ApoE4-related AD.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Using human neurons derived from induced pluripotent stem cells that expressed apolipoprotein E4 (ApoE4), a variant of the APOE gene product and the major genetic risk factor for AD, we demonstrated that ApoE4-expressing neurons had higher levels of tau phosphorylation, unrelated to their increased production of amyloid-β (Aβ) peptides, and that they displayed GABAergic neuron degeneration.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 57, "doc_id": "4709641", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Gpr124 suppresses BBB breakdown in mouse models of ischemic stroke.\n\nCANDIDATE_ABSTRACT:\nTITLE: Gpr124 is essential for blood–brain barrier integrity in central nervous system disease\nABSTRACT: Although blood–brain barrier (BBB) compromise is central to the etiology of diverse central nervous system (CNS) disorders, endothelial receptor proteins that control BBB function are poorly defined. The endothelial G-protein-coupled receptor (GPCR) Gpr124 has been reported to be required for normal forebrain angiogenesis and BBB function in mouse embryos, but the role of this receptor in adult animals is unknown. Here Gpr124 conditional knockout (CKO) in the endothelia of adult mice did not affect homeostatic BBB integrity, but resulted in BBB disruption and microvascular hemorrhage in mouse models of both ischemic stroke and glioblastoma, accompanied by reduced cerebrovascular canonical Wnt–β-catenin signaling. Constitutive activation of Wnt–β-catenin signaling fully corrected the BBB disruption and hemorrhage defects of Gpr124-CKO mice, with rescue of the endothelial gene tight junction, pericyte coverage and extracellular-matrix deficits. We thus identify Gpr124 as an endothelial GPCR specifically required for endothelial Wnt signaling and BBB integrity under pathological conditions in adult mice. This finding implicates Gpr124 as a potential therapeutic target for human CNS disorders characterized by BBB disruption.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here Gpr124 conditional knockout (CKO) in the endothelia of adult mice did not affect homeostatic BBB integrity, but resulted in BBB disruption and microvascular hemorrhage in mouse models of both ischemic stroke and glioblastoma, accompanied by reduced cerebrovascular canonical Wnt–β-catenin signaling.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 480, "doc_id": "6325527", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does improved SENSE imaging using accurate coil sensitivity map generated by a global magnitude-phase fitting method?\n\nABSTRACT:\nTo develop a novel coil sensitivity processing technique that is able to reduce or eliminate aliasing artifacts and noise amplification in image-domain parallel imaging (i.e., SENSE). Initial coil sensitivity maps were derived from the center k-space lines by a common self-calibration method. Then continuous trigonometric functions were used to fit both magnitude and phase maps of the self-calibrated coil sensitivity profile globally. Further, the global fitted coil sensitivity maps were adopted for SENSE reconstruction. Numerical simulations, as well as experiments on phantoms and human subjects were performed to evaluate and compare the effectiveness of this global magnitude-phase fitting approach with traditional local fitting methods. Both simulation and experimental results demonstrated that the proposed novel global fitting method was able to obtain accurate coil sensitivity profiles without Gibbs oscillations. The resultant SENSE images were improved substantially in terms of aliasing imaging artifacts.", "output": "{\"label\": \"yes\", \"rationale\": \"A global magnitude-phase fitting method for better estimation of accurate coil sensitivity maps was developed, and it was successfully used in producing high-quality parallel images. Magn Reson Med, 2014. © 2014 Wiley Periodicals, Inc.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25043575, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does rugby headgear prevent concussion?\n\nABSTRACT:\nTo examine the attitudes of players and coaches to the use of protective headgear, particularly with respect to the prevention of concussion. A questionnaire designed to assess attitudes to headgear was administered to 63 players from four different Canadian teams, each representing a different level of play (high school, university, community club, national). In addition, coaches from all four levels were questioned about team policies and their personal opinions about the use of headgear to prevent concussion. Although the players tended to believe that the headgear could prevent concussion (62%), the coaches were less convinced (33%). Despite the players' belief that headgear offers protection against concussion, only a minority reported wearing headgear (27%) and few (24%) felt that its use should be made mandatory. Common reasons for not wearing headgear were \"its use is not mandatory\", \"it is uncomfortable\", and \"it costs too much\".", "output": "{\"label\": \"maybe\", \"rationale\": \"Although most players in the study believe that rugby headgear may prevent concussion, only a minority reported wearing it. Coaches tended to be less convinced than the players that rugby headgear can prevent concussion.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 11867487, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Do approved doctors and medical referees in the UK agree when assessing a seafarer's fitness?\n\nABSTRACT:\nThe seafaring industry remains a hazardous occupation that requires sophisticated systems of risk and fitness assessment. This study aims to investigate the extent of agreement between Approved Doctors (ADs) and Medical Referees (MRs) when they assess a seafarer's fitness. Between 2003 and 2009 a total of 232,878 seafarer medical examinations were carried out by ADs, of which 465 were considered by the MRs because the seafarer appealed against the AD's decision. The extent of agreement between ADs and MRs was studied. Two hundred and sixty-eight (58%) cases seen by the ADs were classed as category 4 \"permanently unfit\"; the referees only placed 85 (18%) of them in this category. On the other hand, 252 (54%) cases seen by the MRs were classed as category 2 \"fit with restrictions\", while the ADs had only placed 111 (24%) in this category. The overall agreement between the assessors (AD vs. MR) was poor (Kappa K = 0.18). For cardiovascular diseases and for mental ill-health, access to additional information by the MR was the commonest reason for changing the fitness category, but for all other conditions factors such as the experience and knowledge of the MRs or their different interpretation of the standards were the most frequent reasons for a change to fitness category or to restrictions.", "output": "{\"label\": \"no\", \"rationale\": \"This study found that there was poor agreement between the AD's decision and the subsequent MR's decision regarding the fitness of those seafarers who decided to appeal against the AD's initial assessment. The reasons for this are considered.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 22972546, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Stroke patients with prior use of direct oral anticoagulants have a higher risk of in-hospital mortality than stroke patients with prior use of warfarin.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association of Intracerebral Hemorrhage Among Patients Taking Non–Vitamin K Antagonist vs Vitamin K Antagonist Oral Anticoagulants With In-Hospital Mortality\nABSTRACT: Importance Although non–vitamin K antagonist oral anticoagulants (NOACs) are increasingly used to prevent thromboembolic disease, there are limited data on NOAC-related intracerebral hemorrhage (ICH). Objective To assess the association between preceding oral anticoagulant use (warfarin, NOACs, and no oral anticoagulants [OACs]) and in-hospital mortality among patients with ICH. Design, Setting, and Participants Retrospective cohort study of 141 311 patients with ICH admitted from October 2013 to December 2016 to 1662 Get With The Guidelines–Stroke hospitals. Exposures Anticoagulation therapy before ICH, defined as any use of OACs within 7 days prior to hospital arrival. Main Outcomes and Measures In-hospital mortality. Results Among 141 311 patients with ICH (mean [SD] age, 68.3 [15.3] years; 48.1% women), 15 036 (10.6%) were taking warfarin and 4918 (3.5%) were taking NOACs preceding ICH, and 39 585 (28.0%) and 5783 (4.1%) were taking concomitant single and dual antiplatelet agents, respectively. Patients with prior use of warfarin or NOACs were older and had higher prevalence of atrial fibrillation and prior stroke. Acute ICH stroke severity (measured by the National Institutes of Health Stroke Scale) was not significantly different across the 3 groups (median, 9 [interquartile range, 2-21] for warfarin, 8 [2-20] for NOACs, and 8 [2-19] for no OACs). The unadjusted in-hospital mortality rates were 32.6% for warfarin, 26.5% for NOACs, and 22.5% for no OACs. Compared with patients without prior use of OACs, the risk of in-hospital mortality was higher among patients with prior use of warfarin (adjusted risk difference [ARD], 9.0% [97.5% CI, 7.9% to 10.1%]; adjusted odds ratio [AOR], 1.62 [97.5% CI, 1.53 to 1.71]) and higher among patients with prior use of [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The unadjusted in-hospital mortality rates were 32.6% for warfarin, 26.5% for NOACs, and 22.5% for no OACs.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1103, "doc_id": "3898784", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Participating in six months of physical activity improves cognitive functioning.\n\nCANDIDATE_PASSAGE:\nDrosophila MICAL regulates myofilament organization and synaptic structure The overall size and structure of a synaptic terminal is an important determinant of its function. In a large-scale mutagenesis screen, designed to identify Drosophila mutants with abnormally structured neuromuscular junctions (NMJs), we discovered mutations in Drosophila mical, a conserved gene encoding a multi-domain protein with a N-terminal monooxygenase domain. In mical mutants, synaptic boutons do not sprout normally over the muscle surface and tend to form clusters along synaptic branches and at nerve entry sites. Consistent with high expression of MICAL in somatic muscles, immunohistochemical stainings reveal that the subcellular localization and architecture of contractile muscle filaments are dramatically disturbed in mical mutants. Instead of being integrated into a regular sarcomeric pattern, actin and myosin filaments are disorganized and accumulate beneath the plasmamembrane. Whereas contractile elements are strongly deranged, the proposed organizer of sarcomeric structure, D-Titin, is much less affected. Transgenic expression of interfering RNA molecules demonstrates that MICAL is required in muscles for the higher order arrangement of myofilaments. Ultrastructural analysis confirms that myosin-rich thick filaments enter submembranous regions and interfere with synaptic development, indicating that the disorganized myofilaments may cause the synaptic growth phenotype. As a model, we suggest that the filamentous network around synaptic boutons restrains the spreading of synaptic branches.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "921", "doc_id": "16562534", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Birth-weight is negatively associated with breast cancer.\n\nCANDIDATE_PASSAGE:\nBody-mass index and risk of 22 specific cancers: a population-based cohort study of 5·24 million UK adults BACKGROUND High body-mass index (BMI) predisposes to several site-specific cancers, but a large-scale systematic and detailed characterisation of patterns of risk across all common cancers adjusted for potential confounders has not previously been undertaken. We aimed to investigate the links between BMI and the most common site-specific cancers. METHODS With primary care data from individuals in the Clinical Practice Research Datalink with BMI data, we fitted Cox models to investigate associations between BMI and 22 of the most common cancers, adjusting for potential confounders. We fitted linear then non-linear (spline) models; investigated effect modification by sex, menopausal status, smoking, and age; and calculated population effects. FINDINGS 5·24 million individuals were included; 166,955 developed cancers of interest. BMI was associated with 17 of 22 cancers, but effects varied substantially by site. Each 5 kg/m(2) increase in BMI was roughly linearly associated with cancers of the uterus (hazard ratio [HR] 1·62, 99% CI 1·56-1·69; p<0·0001), gallbladder (1·31, 1·12-1·52; p<0·0001), kidney (1·25, 1·17-1·33; p<0·0001), cervix (1·10, 1·03-1·17; p=0·00035), thyroid (1·09, 1·00-1·19; p=0·0088), and leukaemia (1·09, 1·05-1·13; p≤0·0001). BMI was positively associated with liver (1·19, 1·12-1·27), colon (1·10, 1·07-1·13), ovarian (1·09, 1.04-1.14), and postmenopausal breast cancers (1·05, 1·03-1·07) overall (all p<0·0001), but these effects varied by underlying BMI or individual-level characteristics. We estimated inverse associations with prostate and premenopausal breast cancer risk, both overall (prostate 0·98, 0·95-1·00; premenopausal breast cance [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "178", "doc_id": "4828631", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: HIF1A as a major vascular endothelial growth factor regulator: do its polymorphisms have an association with age-related macular degeneration?\n\nABSTRACT:\nTo investigate the association between age-related macular degeneration (AMD) and the polymorphisms of HIF1A, a major vascular epithelial growth factor regulator under hypoxic conditions. The associations of AMD and polymorphisms of genes CFH, SKIV2L and MYRIP were also studied. Prospective study. Eighty-seven AMD patients and 80 healthy subjects admitted to the Department of Ophthalmology at Pamukkale University Hospital, Denizli, Turkey, were included: 45 (52%) had wet type AMD, and 42 (48%) had dry type AMD. Polymorphisms rs1061170 (CFH), rs429608 (SKIV2L), rs2679798 (MYRIP) and both rs11549465 and rs11549467 (HIF1A) were investigated in DNA isolated from peripheral blood samples of the cases and controls by dye-termination DNA sequencing. Genotype distribution of rs1061170 (CFH), rs429608 (SKIV2L), rs2679798 (MYRIP) and both rs11549465 and rs11549467 (HIF1A) in AMD cases and healthy controls; association between genotypes and AMD subtypes. Given the significant difference between the mean age of case and control groups (72.13 ± 5.77 vs. 62.80 ± 5.22, respectively) (P = .000), subsequent analyses were adjusted for age. We found that having at least one C allele for polymorphism rs1061170 increases AMD risk independent of age (OR = 2.42, 95% confidence interval [CI], 1.22-4.81). The ancestral T allele for polymorphism rs1061170 has a protective effect for AMD (OR = 0.53, 95% CI, 0.34-0.83). No statistically significant difference for distributions of other single nucleotide polymorphisms (SNPs) emerged between patients and healthy subjects.", "output": "{\"label\": \"maybe\", \"rationale\": \"No associations appeared between HIF1A SNPs and AMD, which were studied here for the first time; however, polymorphism rs1061170 of the CFH gene is associated with AMD in our population.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 24995509, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Long chain polyunsaturated fatty acids supplementation reduces wheezing and asthma.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effect of n-3 long chain polyunsaturated fatty acid supplementation in pregnancy on infants’ allergies in first year of life: randomised controlled trial\nABSTRACT: OBJECTIVE To determine whether dietary n-3 long chain polyunsaturated fatty acid (LCPUFA) supplementation of pregnant women with a fetus at high risk of allergic disease reduces immunoglobulin E associated eczema or food allergy at 1 year of age. DESIGN Follow-up of infants at high hereditary risk of allergic disease in the Docosahexaenoic Acid to Optimise Mother Infant Outcome (DOMInO) randomised controlled trial. SETTING Adelaide, South Australia. PARTICIPANTS 706 infants at high hereditary risk of developing allergic disease whose mothers were participating in the DOMInO trial. INTERVENTIONS The intervention group (n=368) was randomly allocated to receive fish oil capsules (providing 900 mg of n-3 LCPUFA daily) from 21 weeks' gestation until birth; the control group (n=338) received matched vegetable oil capsules without n-3 LCPUFA. MAIN OUTCOME MEASURE Immunoglobulin E associated allergic disease (eczema or food allergy with sensitisation) at 1 year of age. RESULTS No differences were seen in the overall percentage of infants with immunoglobulin E associated allergic disease between the n-3 LCPUFA and control groups (32/368 (9%) v 43/338 (13%); unadjusted relative risk 0.68, 95% confidence interval 0.43 to 1.05, P=0.08; adjusted relative risk 0.70, 0.45 to 1.09, P=0.12), although the percentage of infants diagnosed as having atopic eczema (that is, eczema with associated sensitisation) was lower in the n-3 LCPUFA group (26/368 (7%) v 39/338 (12%); unadjusted relative risk 0.61, 0.38 to 0.98, P=0.04; adjusted relative risk 0.64, 0.40 to 1.02, P=0.06). Fewer infants were sensitised to egg in the n-3 LCPUFA group (34/368 (9%) v 52/338 (15%); unadjusted relative risk 0.61, 0.40 to 0.91, P=0.02; adjusted relative risk 0.62, 0.41 to 0.93, P=0.02), but no diffe [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 710, "doc_id": "22442133", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The DESMOND program demonstrates no significant impact on biochemical outcomes.\n\nCANDIDATE_PASSAGE:\nPharmacologic inhibition of cyclin-dependent kinases 4 and 6 arrests the growth of glioblastoma multiforme intracranial xenografts. Activation of cyclin-dependent kinases 4 and 6 (cdk4/6) occurs in the majority of glioblastoma multiforme (GBM) tumors, and represents a promising molecular target for the development of small molecule inhibitors. In the current study, we investigated the molecular determinants and in vivo response of diverse GBM cell lines and xenografts to PD-0332991, a cdk4/6-specific inhibitor. In vitro testing of PD-0332991 against a panel of GBM cell lines revealed a potent G(1) cell cycle arrest and induction of senescence in each of 16 retinoblastoma protein (Rb)-proficient cell lines regardless of other genetic lesions, whereas 5 cell lines with homozygous inactivation of Rb were completely resistant to treatment. Short hairpin RNA depletion of Rb expression conferred resistance of GBM cells to PD-0332991, further demonstrating a requirement of Rb for sensitivity to cdk4/6 inhibition. PD-0332991 was found to efficiently cross the blood-brain barrier and proved highly effective in suppressing the growth of intracranial GBM xenograft tumors, including those that had recurred after initial therapy with temozolomide. Remarkably, no mice receiving PD-0332991 died as a result of disease progression while on therapy. Additionally, the combination of PD-0332991 and radiation therapy resulted in significantly increased survival benefit compared with either therapy alone. In total, our results support clinical trial evaluation of PD-0332991 against newly diagnosed as well as recurrent GBM, and indicate that Rb status is the primary determinant of potential benefit from this therapy.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1157", "doc_id": "15570691", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: CD28 signals regulate trafficking of murine auto-reactive T cells into target tissues.\n\nCANDIDATE_PASSAGE:\nBlockade of class IB phosphoinositide-3 kinase ameliorates obesity-induced inflammation and insulin resistance. Obesity and insulin resistance, the key features of metabolic syndrome, are closely associated with a state of chronic, low-grade inflammation characterized by abnormal macrophage infiltration into adipose tissues. Although it has been reported that chemokines promote leukocyte migration by activating class IB phosphoinositide-3 kinase (PI3Kγ) in inflammatory states, little is known about the role of PI3Kγ in obesity-induced macrophage infiltration into tissues, systemic inflammation, and the development of insulin resistance. In the present study, we used murine models of both diet-induced and genetically induced obesity to examine the role of PI3Kγ in the accumulation of tissue macrophages and the development of obesity-induced insulin resistance. Mice lacking p110γ (Pik3cg(-/-)), the catalytic subunit of PI3Kγ, exhibited improved systemic insulin sensitivity with enhanced insulin signaling in the tissues of obese animals. In adipose tissues and livers of obese Pik3cg(-/-) mice, the numbers of infiltrated proinflammatory macrophages were markedly reduced, leading to suppression of inflammatory reactions in these tissues. Furthermore, bone marrow-specific deletion and pharmacological blockade of PI3Kγ also ameliorated obesity-induced macrophage infiltration and insulin resistance. These data suggest that PI3Kγ plays a crucial role in the development of both obesity-induced inflammation and systemic insulin resistance and that PI3Kγ can be a therapeutic target for type 2 diabetes.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "201", "doc_id": "10889845", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Transplanted human glial progenitor cells are incapable of forming a neural network with host animals' neurons.\n\nCANDIDATE_ABSTRACT:\nTITLE: Forebrain engraftment by human glial progenitor cells enhances synaptic plasticity and learning in adult mice.\nABSTRACT: Human astrocytes are larger and more complex than those of infraprimate mammals, suggesting that their role in neural processing has expanded with evolution. To assess the cell-autonomous and species-selective properties of human glia, we engrafted human glial progenitor cells (GPCs) into neonatal immunodeficient mice. Upon maturation, the recipient brains exhibited large numbers and high proportions of both human glial progenitors and astrocytes. The engrafted human glia were gap-junction-coupled to host astroglia, yet retained the size and pleomorphism of hominid astroglia, and propagated Ca2+ signals 3-fold faster than their hosts. Long-term potentiation (LTP) was sharply enhanced in the human glial chimeric mice, as was their learning, as assessed by Barnes maze navigation, object-location memory, and both contextual and tone fear conditioning. Mice allografted with murine GPCs showed no enhancement of either LTP or learning. These findings indicate that human glia differentially enhance both activity-dependent plasticity and learning in mice.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Long-term potentiation (LTP) was sharply enhanced in the human glial chimeric mice, as was their learning, as assessed by Barnes maze navigation, object-location memory, and both contextual and tone fear conditioning.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1320, "doc_id": "16284655", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does use of hydrophilic guidewires significantly improve technical success rates of peripheral PTA?\n\nABSTRACT:\nTo determine whether the use of hydrophilic guidewires has increased the technical success rate of peripheral percutaneous transluminal angioplasty (PTA).MATERIAL/ We performed 125 procedures and analyzed the technical success rates of PTA using the conventional guidewire first and then if needed, the hydrophilic guidewire for iliac and SFA stenoses or occlusions. Angioplasty was performed on 25 stenosed, 25 occluded iliac arteries and 25 stenosed, 50 occluded femoral arteries. The result was defined as technical success when the lesion was crossed by a guidewire and balloon, then it was dilated with restoration of vessel lumen and less than 30% residual stenosis and the rise in ABI values was at least 0.15 after 24 hours. The technical success rate after PTA of stenosed iliac arteries was achieved in 96% (24/25) using conventional wires and 100% using hydrophilic guidewire; in iliac occlusions, the rates were 60% (15/25) and 96%, respectively; in femoral stenosis - 84% (21/25) and 100%; in occlusions in the first group: lesions<10 cm -64% (16/25) and 96%, in the second group: lesions>10 cm -48% (12/25) and 88%. In the iliac group, there was no significant difference in the success of iliac stenosis PTA. However, there were significant changes in the success rates of PTA performed for SFA stenosis and iliac and SFA occlusions.", "output": "{\"label\": \"maybe\", \"rationale\": \"In summary, we report an overall improvement and high technical success rate for peripherial PTA. The use of hydrophilic guidewires made significant difference to the technical success rate of PTA, especially in occlusion and more complicated lesions.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 16538201, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: mcm 5 s 2 U is required for proper decoding of NNR codons in eukaryotes.\n\nCANDIDATE_ABSTRACT:\nTITLE: A neural basis for melanocortin-4 receptor regulated appetite\nABSTRACT: Pro-opiomelanocortin (POMC)- and agouti-related peptide (AgRP)-expressing neurons of the arcuate nucleus of the hypothalamus (ARC) are oppositely regulated by caloric depletion and coordinately stimulate and inhibit homeostatic satiety, respectively. This bimodality is principally underscored by the antagonistic actions of these ligands at downstream melanocortin-4 receptors (MC4R) in the paraventricular nucleus of the hypothalamus (PVH). Although this population is critical to energy balance, the underlying neural circuitry remains unknown. Using mice expressing Cre recombinase in MC4R neurons, we demonstrate bidirectional control of feeding following real-time activation and inhibition of PVH(MC4R) neurons and further identify these cells as a functional exponent of ARC(AgRP) neuron-driven hunger. Moreover, we reveal this function to be mediated by a PVH(MC4R)→lateral parabrachial nucleus (LPBN) pathway. Activation of this circuit encodes positive valence, but only in calorically depleted mice. Thus, the satiating and appetitive nature of PVH(MC4R)→LPBN neurons supports the principles of drive reduction and highlights this circuit as a promising target for antiobesity drug development.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1390, "doc_id": "1070920", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: CX3CR1 on the Th2 cells suppresses airway inflammation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Atg5-independent autophagy regulates mitochondrial clearance and is essential for iPSC reprogramming\nABSTRACT: Successful generation of induced pluripotent stem cells entails a major metabolic switch from mitochondrial oxidative phosphorylation to glycolysis during the reprogramming process. The mechanism of this metabolic reprogramming, however, remains elusive. Here, our results suggest that an Atg5-independent autophagic process mediates mitochondrial clearance, a characteristic event involved in the metabolic switch. We found that blocking such autophagy, but not canonical autophagy, inhibits mitochondrial clearance, in turn, preventing iPSC induction. Furthermore, AMPK seems to be upstream of this autophagic pathway and can be targeted by small molecules to modulate mitochondrial clearance during metabolic reprogramming. Our work not only reveals that the Atg5-independent autophagy is crucial for establishing pluripotency, but it also suggests that iPSC generation and tumorigenesis share a similar metabolic switch.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 219, "doc_id": "1605196", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: PD-1 triggering on monocytes enhances IL-10 production by monocytes.\n\nCANDIDATE_PASSAGE:\nMolecular mechanisms of (-)-epicatechin and chlorogenic acid on the regulation of the apoptotic and survival/proliferation pathways in a human hepatoma cell line. Dietary polyphenols have been associated with reduced risk of chronic diseases, but the precise molecular mechanisms of protection remain unclear. This work was aimed at studying the effect of (-)-epicatechin (EC) and chlorogenic acid (CGA) on the regulation of apoptotic and survival/proliferation pathways in a human hepatoma cell line (HepG2). EC or CGA treatment for 18 h had a slight effect on cell viability and decreased reactive oxygen species formation, and EC alone promoted cell proliferation, whereas CGA increased glutathione levels. Phenols neither induced the caspase cascade for apoptosis nor affected expression levels of Bcl-xL or Bax. A sustained activation of the major survival signals AKT/PI-3-kinase and ERK was shown in EC-treated cells, rather than in CGA-exposed cells. These data suggest that EC and CGA have no effect on apoptosis and enhance the intrinsic cellular tolerance against oxidative insults either by activating survival/proliferation pathways or by increasing antioxidant potential in HepG2.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "902", "doc_id": "9197092", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Varying expression levels of EBI2 affect the positioning and migration of B cells.\n\nCANDIDATE_PASSAGE:\nGuidance of B cells by the orphan G protein-coupled receptor EBI2 shapes humoral immune responses. Humoral immunity depends on both rapid and long-term antibody production against invading pathogens. This is achieved by the generation of spatially distinct extrafollicular plasmablast and follicular germinal center (GC) B cell populations, but the signals that guide responding B cells to these alternative compartments have not been fully elucidated. Here, we show that expression of the orphan G protein-coupled receptor Epstein-Barr virus-induced gene 2 (EBI2, also known as GPR183) by activated B cells was essential for their movement to extrafollicular sites and induction of early plasmablast responses. Conversely, downregulation of EBI2 enabled B cells to access the center of follicles and promoted efficient GC formation. EBI2 therefore provides a previously uncharacterized dimension to B cell migration that is crucial for coordinating rapid versus long-term antibody responses.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1361", "doc_id": "15488881", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: IgA plasma cells that are specific for transglutaminase 2 are scarce in the duodenal mucosa of celiac disease patients when the disease is active.\n\nCANDIDATE_ABSTRACT:\nTITLE: High abundance of plasma cells secreting transglutaminase 2–specific IgA autoantibodies with limited somatic hypermutation in celiac disease intestinal lesions\nABSTRACT: Celiac disease is an immune-mediated disorder in which mucosal autoantibodies to the enzyme transglutaminase 2 (TG2) are generated in response to the exogenous antigen gluten in individuals who express human leukocyte antigen HLA-DQ2 or HLA-DQ8 (ref. 3). We assessed in a comprehensive and nonbiased manner the IgA anti-TG2 response by expression cloning of the antibody repertoire of ex vivo–isolated intestinal antibody-secreting cells (ASCs). We found that TG2-specific plasma cells are markedly expanded within the duodenal mucosa in individuals with active celiac disease. TG2-specific antibodies were of high affinity yet showed little adaptation by somatic mutations. Unlike infection-induced peripheral blood plasmablasts, the TG2-specific ASCs had not recently proliferated and were not short-lived ex vivo. Altogether, these observations demonstrate that there is a germline repertoire with high affinity for TG2 that may favor massive generation of autoreactive B cells. TG2-specific antibodies did not block enzymatic activity and served as substrates for TG2-mediated crosslinking when expressed as IgD or IgM but not as IgA1 or IgG1. This could result in preferential recruitment of plasma cells from naive IgD- and IgM-expressing B cells, thus possibly explaining why the antibody response to TG2 bears signs of a primary immune response despite the disease chronicity.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We found that TG2-specific plasma cells are markedly expanded within the duodenal mucosa in individuals with active celiac disease.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 553, "doc_id": "1471041", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Energy balance requires hypothalamic glutamate neurotransmission.\n\nCANDIDATE_PASSAGE:\nFamilial risk of lymphoproliferative tumors in families of patients with chronic lymphocytic leukemia: results from the Swedish Family-Cancer Database. The importance of genetic factors in etiology of chronic lymphocytic leukemia (CLL) is suggested by family and population studies. However, the spectrum of malignancies sharing common genetic factors with CLL and the effects of sex and age on familial risk are unknown. We used the Swedish Family-Cancer Database to test for increased familial risks of CLL and other lymphoproliferative tumors. Cancer diagnoses from 1958 to 1998 were assessed in 14 336 first-degree relatives of 5918 CLL cases and in 28 876 first-degree relatives of 11 778 controls. Cancer risks in relatives of cases were compared with those in relatives of controls using marginal survival models. Relatives of cases were at significantly increased risk for CLL (relative risk [RR] = 7.52; 95% confidence interval [CI], 3.63-15.56), for non-Hodgkin lymphoma (RR = 1.45; 95% CI, 0.98-2.16), and for Hodgkin lymphoma (RR = 2.35; 95% CI, 1.08-5.08). CLL risks were similar in parents, siblings, and offspring of cases, in male and female relatives, and were not affected by the case's age at diagnosis. Anticipation was not significant when analyzed using life table methods. We conclude that the familial component of CLL is shared with other lymphoproliferative malignances, suggesting common genetic pathways. However, because clinically diagnosed CLL is uncommon, absolute excess risk to relatives is small.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "378", "doc_id": "1153655", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Are elevated levels of serum lipoprotein ( a ) and apolipoprotein ( a ) phenotype related to pre-eclampsia?\n\nABSTRACT:\nPre-eclampsia might result from a less effective invasion of trophoblast cells in the myometrium, caused by attenuated immunosuppression in the spiral arteries, resulting from inhibition of plasmin-mediated activation of transforming growth factor-beta-like substances. In vitro evidence indicates that lipoprotein(a) is capable of inhibiting plasmin-mediated activation of transforming growth factor-beta. Thus, high plasma levels of lipoprotein(a) might result in increased incidence of preeclampsia. The patient group consisted of 39 patients with a history of pre-eclampsia in a previous pregnancy: Forty-seven women without pre-eclampsia in their history and matched for age were the control group. All participants gave their informed consent. In both the patient and control group blood pressure, CRP, urinalysis, cholesterol, HDL-cholesterol, triglycerides, lipoprotein(a) level and apolipoprotein(a) phenotype were determined. None of the participants had elevated CRP levels, excluding acute phase related elevations of lipoprotein(a). Proteinuria was present in 33% of patients and in 11% of controls (p=0.01). However, no relation was observed between proteinuria and Lp(a) level. Median Lipoprotein(a) levels in both groups were equal (300 mg/l vs. 275 mg/l; p=0.48), as well as the apo(a) phenotype distribution in both groups.", "output": "{\"label\": \"no\", \"rationale\": \"Lipoprotein(a) and apolipoprotein(a) phenotype do not contribute significantly to the pathogenesis of pre-eclampsia.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 9292635, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_PASSAGE:\nAn Extensive MicroRNA-Mediated Network of RNA-RNA Interactions Regulates Established Oncogenic Pathways in Glioblastoma By analyzing gene expression data in glioblastoma in combination with matched microRNA profiles, we have uncovered a posttranscriptional regulation layer of surprising magnitude, comprising more than 248,000 microRNA (miR)-mediated interactions. These include ∼7,000 genes whose transcripts act as miR \"sponges\" and 148 genes that act through alternative, nonsponge interactions. Biochemical analyses in cell lines confirmed that this network regulates established drivers of tumor initiation and subtype implementation, including PTEN, PDGFRA, RB1, VEGFA, STAT3, and RUNX1, suggesting that these interactions mediate crosstalk between canonical oncogenic pathways. siRNA silencing of 13 miR-mediated PTEN regulators, whose locus deletions are predictive of PTEN expression variability, was sufficient to downregulate PTEN in a 3'UTR-dependent manner and to increase tumor cell growth rates. Thus, miR-mediated interactions provide a mechanistic, experimentally validated rationale for the loss of PTEN expression in a large number of glioma samples with an intact PTEN locus.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "972", "doc_id": "16364639", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: LDL cholesterol has no involvement in the development of cardiovascular disease.\n\nCANDIDATE_ABSTRACT:\nTITLE: LDL-cholesterol concentrations: a genome-wide association study\nABSTRACT: BACKGROUND LDL cholesterol has a causal role in the development of cardiovascular disease. Improved understanding of the biological mechanisms that underlie the metabolism and regulation of LDL cholesterol might help to identify novel therapeutic targets. We therefore did a genome-wide association study of LDL-cholesterol concentrations. METHODS We used genome-wide association data from up to 11,685 participants with measures of circulating LDL-cholesterol concentrations across five studies, including data for 293 461 autosomal single nucleotide polymorphisms (SNPs) with a minor allele frequency of 5% or more that passed our quality control criteria. We also used data from a second genome-wide array in up to 4337 participants from three of these five studies, with data for 290,140 SNPs. We did replication studies in two independent populations consisting of up to 4979 participants. Statistical approaches, including meta-analysis and linkage disequilibrium plots, were used to refine association signals; we analysed pooled data from all seven populations to determine the effect of each SNP on variations in circulating LDL-cholesterol concentrations. FINDINGS In our initial scan, we found two SNPs (rs599839 [p=1.7x10(-15)] and rs4970834 [p=3.0x10(-11)]) that showed genome-wide statistical association with LDL cholesterol at chromosomal locus 1p13.3. The second genome screen found a third statistically associated SNP at the same locus (rs646776 [p=4.3x10(-9)]). Meta-analysis of data from all studies showed an association of SNPs rs599839 (combined p=1.2x10(-33)) and rs646776 (p=4.8x10(-20)) with LDL-cholesterol concentrations. SNPs rs599839 and rs646776 both explained around 1% of the variation in circulating LDL-cholesterol concentrations and were associated wi [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"BACKGROUND LDL cholesterol has a causal role in the development of cardiovascular disease.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 674, "doc_id": "2095573", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: RANK-RANKL pathway signalling is linked to development of Aire-expressing medullary thymic epithelial cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Rank Signaling Links the Development of Invariant γδ T Cell Progenitors and Aire+ Medullary Epithelium\nABSTRACT: The thymic medulla provides a specialized microenvironment for the negative selection of T cells, with the presence of autoimmune regulator (Aire)-expressing medullary thymic epithelial cells (mTECs) during the embryonic-neonatal period being both necessary and sufficient to establish long-lasting tolerance. Here we showed that emergence of the first cohorts of Aire(+) mTECs at this key developmental stage, prior to αβ T cell repertoire selection, was jointly directed by Rankl(+) lymphoid tissue inducer cells and invariant Vγ5(+) dendritic epidermal T cell (DETC) progenitors that are the first thymocytes to express the products of gene rearrangement. In turn, generation of Aire(+) mTECs then fostered Skint-1-dependent, but Aire-independent, DETC progenitor maturation and the emergence of an invariant DETC repertoire. Hence, our data attributed a functional importance to the temporal development of Vγ5(+) γδ T cells during thymus medulla formation for αβ T cell tolerance induction and demonstrated a Rank-mediated reciprocal link between DETC and Aire(+) mTEC maturation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here we showed that emergence of the first cohorts of Aire(+) mTECs at this key developmental stage, prior to αβ T cell repertoire selection, was jointly directed by Rankl(+) lymphoid tissue inducer cells and invariant Vγ5(+) dendritic epidermal T cell (DETC) progenitors that are the first thymocytes to express the products of gene rearrangement.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1005, "doc_id": "301838", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Active Ly49Q induces neutrophil polarization.\n\nCANDIDATE_PASSAGE:\nThe Ly49Q receptor plays a crucial role in neutrophil polarization and migration by regulating raft trafficking. Neutrophils rapidly undergo polarization and directional movement to infiltrate the sites of infection and inflammation. Here, we show that an inhibitory MHC I receptor, Ly49Q, was crucial for the swift polarization of and tissue infiltration by neutrophils. During the steady state, Ly49Q inhibited neutrophil adhesion by preventing focal-complex formation, likely by inhibiting Src and PI3 kinases. However, in the presence of inflammatory stimuli, Ly49Q mediated rapid neutrophil polarization and tissue infiltration in an ITIM-domain-dependent manner. These opposite functions appeared to be mediated by distinct use of effector phosphatase SHP-1 and SHP-2. Ly49Q-dependent polarization and migration were affected by Ly49Q regulation of membrane raft functions. We propose that Ly49Q is pivotal in switching neutrophils to their polarized morphology and rapid migration upon inflammation, through its spatiotemporal regulation of membrane rafts and raft-associated signaling molecules.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "76", "doc_id": "5531479", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Angiotensin converting enzyme inhibitors are associated with increased risk for functional renal insufficiency.\n\nCANDIDATE_PASSAGE:\nRenal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Angiotensin converting enzyme (ACE) inhibitors are now one of the most frequently used classes of antihypertensive drugs. Beyond their utility in the management of hypertension, their use has been extended to the long-term management of patients with congestive heart failure (CHF), as well as diabetic and nondiabetic nephropathies. Although ACE inhibitor therapy usually improves renal blood flow (RBF) and sodium excretion rates in CHF and reduces the rate of progressive renal injury in chronic renal disease, its use can also be associated with a syndrome of “functional renal insufficiency” and/or hyperkalemia. This form of acute renal failure (ARF) most commonly develops shortly after initiation of ACE inhibitor therapy but can be observed after months or years of therapy, even in the absence of prior ill effects. ARF is most likely to occur when renal perfusion pressure cannot be sustained because of substantial decreases in mean arterial pressure (MAP) or when glomerular filtration rate (GFR) is highly angiotensin II (Ang II) dependent. Conditions that predict an adverse hemodynamic effect of ACE inhibitors in patients with CHF are preexisting hypotension and low cardiac filling pressures. The GFR is especially dependent on Ang II during extracellular fluid (ECF) volume depletion, high-grade bilateral renal artery stenosis, or stenosis of a dominant or single kidney, as in a renal transplant recipient. Understanding the pathophysiological mechanisms and the common risk factors for ACE inhibitor–induced fun [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "113", "doc_id": "6157837", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: N348I mutations reduce resistance to nevirapine.\n\nCANDIDATE_ABSTRACT:\nTITLE: N348I in the Connection Domain of HIV-1 Reverse Transcriptase Confers Zidovudine and Nevirapine Resistance\nABSTRACT: Background The catalytically active 66-kDa subunit of the human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) consists of DNA polymerase, connection, and ribonuclease H (RNase H) domains. Almost all known RT inhibitor resistance mutations identified to date map to the polymerase domain of the enzyme. However, the connection and RNase H domains are not routinely analysed in clinical samples and none of the genotyping assays available for patient management sequence the entire RT coding region. The British Columbia Centre for Excellence in HIV/AIDS (the Centre) genotypes clinical isolates up to codon 400 in RT, and our retrospective statistical analyses of the Centre’s database have identified an N348I mutation in the RT connection domain in treatment-experienced individuals. The objective of this multidisciplinary study was to establish the in vivo relevance of this mutation and its role in drug resistance. Methods and Findings The prevalence of N348I in clinical isolates, the time taken for it to emerge under selective drug pressure, and its association with changes in viral load, specific drug treatment, and known drug resistance mutations was analysed from genotypes, viral loads, and treatment histories from the Centre’s database. N348I increased in prevalence from below 1% in 368 treatmentnao ¨ve individuals to 12.1% in 1,009 treatment-experienced patients (p ¼ 7.7 3 10 � 12 ). N348I appeared early in therapy and was highly associated with thymidine analogue mutations (TAMs) M41L and T215Y/F (p , 0.001), the lamivudine resistance mutations M184V/I (p , 0.001), and non-nucleoside RTI (NNRTI) resistance mutations K103N and Y181C/I (p , 0.001). The association with TAMs and NNRTI resistance mutations was consistent with the selection of N3 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"N348I also decreased susceptibility to nevirapine (7.4fold) and efavirenz (2.5-fold) and significantly potentiated resistance to these drugs when combined with K103N.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 825, "doc_id": "15319019", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: miRNAs enforce homeostasis by suppressing low-level ''leaky'' transcription.\n\nCANDIDATE_PASSAGE:\nMicroRNAs can generate thresholds in target gene expression MicroRNAs (miRNAs) are short, highly conserved noncoding RNA molecules that repress gene expression in a sequence-dependent manner. We performed single-cell measurements using quantitative fluorescence microscopy and flow cytometry to monitor a target gene's protein expression in the presence and absence of regulation by miRNA. We find that although the average level of repression is modest, in agreement with previous population-based measurements, the repression among individual cells varies dramatically. In particular, we show that regulation by miRNAs establishes a threshold level of target mRNA below which protein production is highly repressed. Near this threshold, protein expression responds sensitively to target mRNA input, consistent with a mathematical model of molecular titration. These results show that miRNAs can act both as a switch and as a fine-tuner of gene expression.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1393", "doc_id": "2000038", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Input from mental and physical health care professionals is not effective at decreasing homelessness.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mental health problems of homeless children and families: longitudinal study.\nABSTRACT: OBJECTIVE To establish the mental health needs of homeless children and families before and after rehousing. DESIGN Cross sectional, longitudinal study. SETTING City of Birmingham. SUBJECTS 58 rehoused families with 103 children aged 2-16 years and 21 comparison families of low socioeconomic status in stable housing, with 54 children. MAIN OUTCOME MEASURES Children's mental health problems and level of communication; mothers' mental health problems and social support one year after rehousing. RESULTS Mental health problems remained significantly higher in rehoused mothers and their children than in the comparison group (mothers 26% v 5%, P = 0.04; children 39% v 11%, P = 0.0003). Homeless mothers continued to have significantly less social support at follow up. Mothers with a history of abuse and poor social integration were more likely to have children with persistent mental health problems. CONCLUSIONS Homeless families have a high level of complex needs that cannot be met by conventional health services and arrangements. Local strategies for rapid rehousing into permanent accommodation, effective social support and health care for parents and children, and protection from violence and intimidation should be developed and implemented.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 638, "doc_id": "25649714", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Hypothalamic glutamate neurotransmission is unrelated to energy balance.\n\nCANDIDATE_ABSTRACT:\nTITLE: Glutamate mediates the function of melanocortin receptor 4 on Sim1 neurons in body weight regulation.\nABSTRACT: The melanocortin receptor 4 (MC4R) is a well-established mediator of body weight homeostasis. However, the neurotransmitter(s) that mediate MC4R function remain largely unknown; as a result, little is known about the second-order neurons of the MC4R neural pathway. Single-minded 1 (Sim1)-expressing brain regions, which include the paraventricular nucleus of hypothalamus (PVH), represent key brain sites that mediate melanocortin action. We conditionally restored MC4R expression in Sim1 neurons in the background of Mc4r-null mice. The restoration dramatically reduced obesity in Mc4r-null mice. The anti-obesity effect was completely reversed by selective disruption of glutamate release from those same Sim1 neurons. The reversal was caused by lower energy expenditure and hyperphagia. Corroboratively, selective disruption of glutamate release from adult PVH neurons led to rapid obesity development via reduced energy expenditure and hyperphagia. Thus, this study establishes glutamate as the primary neurotransmitter that mediates MC4Rs on Sim1 neurons in body weight regulation.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Corroboratively, selective disruption of glutamate release from adult PVH neurons led to rapid obesity development via reduced energy expenditure and hyperphagia.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 541, "doc_id": "45154987", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Combination nicotine replacement therapies with varenicline or bupropion lead to significantly higher long-term abstinence rates at 52 weeks than varenicline monotherapy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Combination varenicline and bupropion SR for tobacco-dependence treatment in cigarette smokers: a randomized trial.\nABSTRACT: IMPORTANCE Combining pharmacotherapies for tobacco-dependence treatment may increase smoking abstinence. OBJECTIVE To determine efficacy and safety of varenicline and bupropion sustained-release (SR; combination therapy) compared with varenicline (monotherapy) in cigarette smokers. DESIGN, SETTING, AND PARTICIPANTS Randomized, blinded, placebo-controlled multicenter clinical trial with a 12-week treatment period and follow-up through week 52 conducted between October 2009 and April 2013 at 3 midwestern clinical research sites. Five hundred six adult (≥18 years) cigarette smokers were randomly assigned and 315 (62%) completed the study. INTERVENTIONS Twelve weeks of varenicline and bupropion SR or varenicline and placebo. MAIN OUTCOMES AND MEASURES Primary outcome was abstinence rates at week 12, defined as prolonged (no smoking from 2 weeks after the target quit date) abstinence and 7-day point-prevalence (no smoking past 7 days) abstinence. Secondary outcomes were prolonged and point-prevalence smoking abstinence rates at weeks 26 and 52. Outcomes were biochemically confirmed. RESULTS At 12 weeks, 53.0% of the combination therapy group achieved prolonged smoking abstinence and 56.2% achieved 7-day point-prevalence smoking abstinence compared with 43.2% and 48.6% in varenicline monotherapy (odds ratio [OR], 1.49; 95% CI, 1.05-2.12; P = .03 and OR, 1.36; 95% CI, 0.95-1.93; P = .09, respectively). At 26 weeks, 36.6% of the combination therapy group achieved prolonged and 38.2% achieved 7-day point-prevalence smoking abstinence compared with 27.6% and 31.9% in varenicline monotherapy (OR, 1.52; 95% CI, 1.04-2.22; P = .03 and OR, 1.32; 95% CI, 0.91-1.91; P = .14, respectively). At 52 weeks, 30.9% of the combination therapy group achieved prolonged and 36.6% achi [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"At 52 weeks, 30.9% of the combination therapy group achieved prolonged and 36.6% achieved 7-day point-prevalence smoking abstinence compared with 24.5% and 29.2% in varenicline monotherapy (OR, 1.39; 95% CI, 0.93-2.07; P = .11 and OR, 1.40; 95% CI, 0.96-2.05; P = .08, respectively).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 274, "doc_id": "11614737", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The ability of activator E2Fs in preventing cell death is limited to terminally differentiated cells.\n\nCANDIDATE_PASSAGE:\nNatural history of adult T-cell leukemia/lymphoma and approaches to therapy After cell-to-cell transmission, HTLV-I increases its viral genome by de novo infection and proliferation of infected cells. Proliferation of infected cells is clonal and persistent in vivo. During the carrier state, infected cells are selected in vivo by the host's immune system, the genetic and epigenetic environment of proviral integration sites, and other factors. In leukemic cells, tax gene expression is frequently impaired by genetic and epigenetic mechanisms. Such loss of Tax expression enables ATL cells to escape the host immune system. On the other hand, ATL cells acquire the ability to proliferate without Tax by intracellular genetic and epigenetic changes. Despite advances in support and the development of novel treatment agents, the prognosis for ATLL remains poor. A number of therapies, however, do appear to improve prognosis compared to CHOP (VEPA). These include interferon-α plus zidovudine (probably after 1–2 cycles of CHOP), intensive chemotherapy as in LSG-15 with G-CSF support and Allo-SCT (which includes the potential for cure). Emerging novel approaches include HDAC inhibitors, monoclonal antibodies, and proteasome inhibitors. Comparison between different therapeutic approaches is complicated by the range of natural history of ATLL, different recruitments of naïve-to-therapy, refractory or relapsed patients, and variations in the reporting of outcome that frequently excludes difficult-to-evaluate patients. Moreover, results from relatively small proof-of-principle studies have not been extended with randomized, controlled trials. As a result, currently, there is no clear evidence to support the value of any particular treatment approach over others. To avoid furt [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1188", "doc_id": "20754359", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Excess gestational weight gain is associated with obesity-related pregnancy outcomes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effects of interventions in pregnancy on maternal weight and obstetric outcomes: meta-analysis of randomised evidence\nABSTRACT: OBJECTIVE To evaluate the effects of dietary and lifestyle interventions in pregnancy on maternal and fetal weight and to quantify the effects of these interventions on obstetric outcomes. DESIGN Systematic review and meta-analysis. DATA SOURCES Major databases from inception to January 2012 without language restrictions. STUDY SELECTION Randomised controlled trials that evaluated any dietary or lifestyle interventions with potential to influence maternal weight during pregnancy and outcomes of pregnancy. DATA SYNTHESIS Results summarised as relative risks for dichotomous data and mean differences for continuous data. RESULTS We identified 44 relevant randomised controlled trials (7278 women) evaluating three categories of interventions: diet, physical activity, and a mixed approach. Overall, there was 1.42 kg reduction (95% confidence interval 0.95 to 1.89 kg) in gestational weight gain with any intervention compared with control. With all interventions combined, there were no significant differences in birth weight (mean difference -50 g, -100 to 0 g) and the incidence of large for gestational age (relative risk 0.85, 0.66 to 1.09) or small for gestational age (1.00, 0.78 to 1.28) babies between the groups, though by itself physical activity was associated with reduced birth weight (mean difference -60 g, -120 to -10 g). Interventions were associated with a reduced the risk of pre-eclampsia (0.74, 0.60 to 0.92) and shoulder dystocia (0.39, 0.22 to 0.70), with no significant effect on other critically important outcomes. Dietary intervention resulted in the largest reduction in maternal gestational weight gain (3.84 kg, 2.45 to 5.22 kg), with improved pregnancy outcomes compared with other interventions. The overall evidence rating was low to very low for i [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Among the interventions, those based on diet are the most effective and are associated with reductions in maternal gestational weight gain and improved obstetric outcomes.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 394, "doc_id": "11360768", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Female carriers of the Apolipoprotein E4 (APOE4) allele have longer lifetime exposure to estrogen due to an increased reproductive period.\n\nCANDIDATE_PASSAGE:\nBax translocation and mitochondrial fragmentation induced by Helicobacter pylori. BACKGROUND AND AIMS Previous in vitro and in vivo studies have revealed an association between Helicobacter pylori infection and apoptosis in gastric epithelial cells. Although involvement of the Bcl-2 family of proteins as well as cytochrome c release has been demonstrated in H pylori induced cell death, the exact role of the mitochondria during this type of programmed cell death has not been fully elucidated. Therefore, we sought to determine whether or not Bax translocation and mitochondrial fragmentation occur on exposure of gastric epithelial cells to H pylori, resulting in cell death. METHODS Experiments were performed with human gastric adenocarcinoma (AGS) cells, AGS cells transfected with the HPV-E6 gene (which inactivates p53 function), AGS-neo cells (transfected with the backbone construct), mouse embryonic fibroblasts (MEFs), and p19(ARF) null (ARF(-/-)) MEFs. Cells were incubated with a cag positive H pylori strain for up to 24 hours, lysed, and cytoplasmic and mitochondrial membrane fractions were analysed by western blot for Bax translocation. RESULTS Bax translocation was detected in AGS, AGS-neo, and normal MEF cells after exposure to H pylori for three hours, but not in ARF(-/-) MEFs cells. Translocation of Bax after H pylori incubation was also detected in AGS-E6 cells (inactive p53 gene) but to a lesser degree than in AGS-neo cells. In parallel studies, the mitochondrial morphology of living cells infected with H pylori was assessed by confocal microscopy. Mitochondrial fragmentation was detectable after 10 hours of H pylori incubation with AGS cells and after seven hours with MEF cells. In wild-type MEFs, mitochondrial fragmentation was significantly increa [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "416", "doc_id": "8654183", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Cellular clocks are associated with mitosis timing in NIH 3T3 cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Phase locking and multiple oscillating attractors for the coupled mammalian clock and cell cycle.\nABSTRACT: Daily synchronous rhythms of cell division at the tissue or organism level are observed in many species and suggest that the circadian clock and cell cycle oscillators are coupled. For mammals, despite known mechanistic interactions, the effect of such coupling on clock and cell cycle progression, and hence its biological relevance, is not understood. In particular, we do not know how the temporal organization of cell division at the single-cell level produces this daily rhythm at the tissue level. Here we use multispectral imaging of single live cells, computational methods, and mathematical modeling to address this question in proliferating mouse fibroblasts. We show that in unsynchronized cells the cell cycle and circadian clock robustly phase lock each other in a 1:1 fashion so that in an expanding cell population the two oscillators oscillate in a synchronized way with a common frequency. Dexamethasone-induced synchronization reveals additional clock states. As well as the low-period phase-locked state there are distinct coexisting states with a significantly higher period clock. Cells transition to these states after dexamethasone synchronization. The temporal coordination of cell division by phase locking to the clock at a single-cell level has significant implications because disordered circadian function is increasingly being linked to the pathogenesis of many diseases, including cancer.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 241, "doc_id": "10608822", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Human embryonic stem cells give rise to cell types from all three embryonic germ layers.\n\nCANDIDATE_PASSAGE:\nEpigenetic memory and preferential lineage-specific differentiation in induced pluripotent stem cells derived from human pancreatic islet beta cells. Human induced pluripotent stem cells (HiPSCs) appear to be highly similar to human embryonic stem cells (HESCs). Using two genetic lineage-tracing systems, we demonstrate the generation of iPSC lines from human pancreatic islet beta cells. These reprogrammed cells acquired markers of pluripotent cells and differentiated into the three embryonic germ layers. However, the beta cell-derived iPSCs (BiPSCs) maintained open chromatin structure at key beta-cell genes, together with a unique DNA methylation signature that distinguishes them from other PSCs. BiPSCs also demonstrated an increased ability to differentiate into insulin-producing cells both in vitro and in vivo, compared with ESCs and isogenic non-beta iPSCs. Our results suggest that the epigenetic memory may predispose BiPSCs to differentiate more readily into insulin producing cells. These findings demonstrate that HiPSC phenotype may be influenced by their cells of origin, and suggest that their skewed differentiation potential may be advantageous for cell replacement therapy.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "529", "doc_id": "27588420", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Ivermectin is used to treat lymphatic filariasis.\n\nCANDIDATE_PASSAGE:\nPersistent human papillomavirus infection and cervical neoplasia: a systematic review and meta-analysis. Detection of persistent cervical carcinogenic human papillomavirus (HPV) DNA is used as a marker for cervical cancer risk in clinical trials. The authors performed a systematic review and meta-analysis of the association between persistent HPV DNA and high-grade cervical intraepithelial neoplasia (CIN2-3), high-grade squamous intraepithelial lesions (HSIL), and invasive cervical cancer (together designated CIN2-3/HSIL+) to evaluate the robustness of HPV persistence for clinical use. MEDLINE and Current Contents were searched through January 30, 2006. Relative risks (RRs) were stratified by HPV comparison group. Of 2,035 abstracts, 41 studies were eligible for inclusion in the meta-analysis. Over 22,500 women were included in calculation of RRs for persistent HPV DNA detection and cervical neoplasia. RRs ranged from 1.3 (95% confidence interval: 1.1, 1.5) to 813.0 (95% confidence interval: 168.2, 3,229.2) for CIN2-3/HSIL+ versus 12 months), wider testing intervals, CIN2-3/HSIL+, and use of an HPV-negative reference group were consistently associated with higher RRs. Thus, HPV persistence was consistently and strongly associated with CIN2-3/HSIL+, despite wide variation in definitions and study methods. The magnitude of association varied by duration of persistence and testing interval. Precise definition and standardization of HPV testing, sampling procedure, and test interval are needed for reliable clinical testing. These findings validate HPV persistence as a clinical marker and endpoint.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "659", "doc_id": "13857083", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Alteration of origin firing causes changes in termination zones of Okazaki fragments.\n\nCANDIDATE_PASSAGE:\nMechanical regulation of cell function with geometrically modulated elastomeric substrates We report the establishment of a library of micromolded elastomeric micropost arrays to modulate substrate rigidity independently of effects on adhesive and other material surface properties. We demonstrated that micropost rigidity impacts cell morphology, focal adhesions, cytoskeletal contractility and stem cell differentiation. Furthermore, early changes in cytoskeletal contractility predicted later stem cell fate decisions in single cells.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "105", "doc_id": "17388232", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Do dexamethasone and basic-fibroblast growth factor regulate markers of mineralization in cementoblasts in vitro?\n\nABSTRACT:\nThe aim of this study was to determine the effects of basic-fibroblast growth factor (b-FGF) and/or dexamethasone (Dex) on cementoblasts in vitro. Murine cementoblasts were treated as follows: 1) 5% FBS (fetal bovine serum) + ascorbic acid (AA, 50 microg/ml, control); 2) 5% FBS + Dex (10(7)M) + AA; 3) 5% FBS + b-FGF (50 ng/ml)+AA; or 4) 5% FBS + Dex (10(7) M) + b-FGF (50 ng/ml)+AA and then evaluated by Northern analysis for changes in specific genes and by von Kossa stain for changes in mineral nodule formation. Mitotic activity: b-FGF stimulated DNA synthesis significantly versus negative control. Gene expression: osteocalcin (OCN): Dex or b-FGF or the combination resulted in a decrease in expression versus control. Bone sialoprotein (BSP): Dex increased expression of BSP mRNA levels, b-FGF decreased transcript for BSP at 6 and 24 hours. Long-term (8 days) Dex, b-FGF, or Dex plus b-FGF caused a decrease in BSP expression versus control; osteopontin (OPN): both Dex and b-FGF increased transcripts for OPN seen by 6 hours, with a greater increase noted with b-FGF versus Dex. No apparent additive effect of Dex with b-FGF was noted; matrix gamma-carboxyglutamic acid protein (MGP): b-FGF induced transcripts for MGP and addition of Dex increased this effect, while Dex alone had no effect on expression. Biomineralization: Dex increased cementoblast- mediated biomineralization, while b-FGF blocked this activity, and addition of Dex to b-FGF did not alter FGF associated inhibition.", "output": "{\"label\": \"yes\", \"rationale\": \"Dex and FGF alone and in combination alter cementoblast behavior, but additional studies are required to determine whether these factors have beneficial effects at the clinical level.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 16171446, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: ADAR1 binds to Dicer to cleave pre-miRNA.\n\nCANDIDATE_ABSTRACT:\nTITLE: ADAR1 Forms a Complex with Dicer to Promote MicroRNA Processing and RNA-Induced Gene Silencing\nABSTRACT: Adenosine deaminases acting on RNA (ADARs) are involved in RNA editing that converts adenosine residues to inosine specifically in double-stranded RNAs. In this study, we investigated the interaction of the RNA editing mechanism with the RNA interference (RNAi) machinery and found that ADAR1 forms a complex with Dicer through direct protein-protein interaction. Most importantly, ADAR1 increases the maximum rate (Vmax) of pre-microRNA (miRNA) cleavage by Dicer and facilitates loading of miRNA onto RNA-induced silencing complexes, identifying a new role of ADAR1 in miRNA processing and RNAi mechanisms. ADAR1 differentiates its functions in RNA editing and RNAi by the formation of either ADAR1/ADAR1 homodimer or Dicer/ADAR1 heterodimer complexes, respectively. As expected, the expression of miRNAs is globally inhibited in ADAR1(-/-) mouse embryos, which, in turn, alters the expression of their target genes and might contribute to their embryonic lethal phenotype.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In this study, we investigated the interaction of the RNA editing mechanism with the RNA interference (RNAi) machinery and found that ADAR1 forms a complex with Dicer through direct protein-protein interaction.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 49, "doc_id": "5953485", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Risk factors for major depression during midlife among a community sample of women with and without prior major depression: are they the same or different?\n\nABSTRACT:\nWomen's vulnerability for a first lifetime-onset of major depressive disorder (MDD) during midlife is substantial. It is unclear whether risk factors differ for first lifetime-onset and recurrent MDD. Identifying these risk factors can provide more focused depression screening and earlier intervention. This study aims to evaluate whether lifetime psychiatric and health histories, personality traits, menopausal status and factors that vary over time, e.g. symptoms, are independent risk factors for first-onset or recurrent MDD across 13 annual follow-ups. Four hundred and forty-three women, aged 42-52 years, enrolled in the Study of Women's Health Across the Nation in Pittsburgh and participated in the Mental Health Study. Psychiatric interviews obtained information on lifetime psychiatric disorders at baseline and on occurrences of MDD episodes annually. Psychosocial and health-related data were collected annually. Cox multivariable analyses were conducted separately for women with and without a MDD history at baseline. Women without lifetime MDD at baseline had a lower risk of developing MDD during midlife than those with a prior MDD history (28% v. 59%) and their risk profiles differed. Health conditions prior to baseline and during follow-ups perception of functioning (ps<0.05) and vasomotor symptoms (VMS) (p = 0.08) were risk factors for first lifetime-onset MDD. Being peri- and post-menopausal, psychological symptoms and a prior anxiety disorder were predominant risk factors for MDD recurrence.", "output": "{\"label\": \"no\", \"rationale\": \"The menopausal transition warrants attention as a period of vulnerability to MDD recurrence, while health factors and VMS should be considered important risk factors for first lifetime-onset of MDD during midlife.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 25417760, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Medications to treat obesity do not have side effects.\n\nCANDIDATE_ABSTRACT:\nTITLE: Long term pharmacotherapy for obesity and overweight: updated meta-analysis.\nABSTRACT: OBJECTIVE To summarise the long term efficacy of anti-obesity drugs in reducing weight and improving health status. DESIGN Updated meta-analysis of randomised trials. DATA SOURCES Medline, Embase, the Cochrane controlled trials register, the Current Science meta-register of controlled trials, and reference lists of identified articles. All data sources were searched from December 2002 (end date of last search) to December 2006. STUDIES REVIEWED Double blind randomised placebo controlled trials of approved anti-obesity drugs used in adults (age over 18) for one year or longer. RESULTS 30 trials of one to four years' duration met the inclusion criteria: 16 orlistat (n=10 631 participants), 10 sibutramine (n=2623), and four rimonabant (n=6365). Of these, 14 trials were new and 16 had previously been identified. Attrition rates averaged 30-40%. Compared with placebo, orlistat reduced weight by 2.9 kg (95% confidence interval 2.5 kg to 3.2 kg), sibutramine by 4.2 kg (3.6 kg to 4.7 kg), and rimonabant by 4.7 kg (4.1 kg to 5.3 kg). Patients receiving active drug treatment were significantly more likely to achieve 5% and 10% weight loss thresholds. Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein. Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorde [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorders.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 765, "doc_id": "7552215", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: MICAL redox enzymes regulate actin dynamics in many cell types.\n\nCANDIDATE_ABSTRACT:\nTITLE: Differential regulation of actin microfilaments by human MICAL proteins.\nABSTRACT: The Drosophila melanogaster MICAL protein is essential for the neuronal growth cone machinery that functions through plexin- and semaphorin-mediated axonal signaling. Drosophila MICAL is also involved in regulating myofilament organization and synaptic structures, and serves as an actin disassembly factor downstream of plexin-mediated axonal repulsion. In mammalian cells there are three known isoforms, MICAL1, MICAL2 and MICAL3, as well as the MICAL-like proteins MICAL-L1 and MICAL-L2, but little is known of their function, and information comes almost exclusively from neural cells. In this study we show that in non-neural cells human MICALs are required for normal actin organization, and all three MICALs regulate actin stress fibers. Moreover, we provide evidence that the generation of reactive oxygen species by MICAL proteins is crucial for their actin-regulatory function. However, although MICAL1 is auto-inhibited by its C-terminal coiled-coil region, MICAL2 remains constitutively active and affects stress fibers. These data suggest differential but complementary roles for MICAL1 and MICAL2 in actin microfilament regulation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In this study we show that in non-neural cells human MICALs are required for normal actin organization, and all three MICALs regulate actin stress fibers.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 737, "doc_id": "6609935", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_ABSTRACT:\nTITLE: Human papillomavirus and Papanicolaou tests to screen for cervical cancer.\nABSTRACT: BACKGROUND Screening for cervical cancer based on testing for human papillomavirus (HPV) increases the sensitivity of detection of high-grade (grade 2 or 3) cervical intraepithelial neoplasia, but whether this gain represents overdiagnosis or protection against future high-grade cervical epithelial neoplasia or cervical cancer is unknown. METHODS In a population-based screening program in Sweden, 12,527 women 32 to 38 years of age were randomly assigned at a 1:1 ratio to have an HPV test plus a Papanicolaou (Pap) test (intervention group) or a Pap test alone (control group). Women with a positive HPV test and a normal Pap test result were offered a second HPV test at least 1 year later, and those who were found to be persistently infected with the same high-risk type of HPV were then offered colposcopy with cervical biopsy. A similar number of double-blinded Pap smears and colposcopies with biopsy were performed in randomly selected women in the control group. Comprehensive registry data were used to follow the women for a mean of 4.1 years. The relative rates of grade 2 or 3 cervical intraepithelial neoplasia or cancer detected at enrollment and at subsequent screening examinations were calculated. RESULTS At enrollment, the proportion of women in the intervention group who were found to have lesions of grade 2 or 3 cervical intraepithelial neoplasia or cancer was 51% greater (95% confidence interval [CI], 13 to 102) than the proportion of women in the control group who were found to have such lesions. At subsequent screening examinations, the proportion of women in the intervention group who were found to have grade 2 or 3 lesions or cancer was 42% less (95% CI, 4 to 64) and the proportion with grade 3 lesions or cancer was 47% less (95% CI, 2 to 71) than [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS The addition of an HPV test to the Pap test to screen women in their mid-30s for cervical cancer reduces the incidence of grade 2 or 3 cervical intraepithelial neoplasia or cancer detected by subsequent screening examinations.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 972, "doc_id": "46695481", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The proliferative capacity of neural progenitors differs across species.\n\nCANDIDATE_ABSTRACT:\nTITLE: LDL-cholesterol concentrations: a genome-wide association study\nABSTRACT: BACKGROUND LDL cholesterol has a causal role in the development of cardiovascular disease. Improved understanding of the biological mechanisms that underlie the metabolism and regulation of LDL cholesterol might help to identify novel therapeutic targets. We therefore did a genome-wide association study of LDL-cholesterol concentrations. METHODS We used genome-wide association data from up to 11,685 participants with measures of circulating LDL-cholesterol concentrations across five studies, including data for 293 461 autosomal single nucleotide polymorphisms (SNPs) with a minor allele frequency of 5% or more that passed our quality control criteria. We also used data from a second genome-wide array in up to 4337 participants from three of these five studies, with data for 290,140 SNPs. We did replication studies in two independent populations consisting of up to 4979 participants. Statistical approaches, including meta-analysis and linkage disequilibrium plots, were used to refine association signals; we analysed pooled data from all seven populations to determine the effect of each SNP on variations in circulating LDL-cholesterol concentrations. FINDINGS In our initial scan, we found two SNPs (rs599839 [p=1.7x10(-15)] and rs4970834 [p=3.0x10(-11)]) that showed genome-wide statistical association with LDL cholesterol at chromosomal locus 1p13.3. The second genome screen found a third statistically associated SNP at the same locus (rs646776 [p=4.3x10(-9)]). Meta-analysis of data from all studies showed an association of SNPs rs599839 (combined p=1.2x10(-33)) and rs646776 (p=4.8x10(-20)) with LDL-cholesterol concentrations. SNPs rs599839 and rs646776 both explained around 1% of the variation in circulating LDL-cholesterol concentrations and were associated wi [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1254, "doc_id": "2095573", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Inositol lipid 3-phosphatase PTEN converts Ptdlns(3,4)P 2 into phosphatidylinositol 4-phosphate.\n\nCANDIDATE_ABSTRACT:\nTITLE: Sudden infant death syndrome.\nABSTRACT: Despite declines in prevalence during the past two decades, sudden infant death syndrome (SIDS) continues to be the leading cause of death for infants aged between 1 month and 1 year in developed countries. Behavioural risk factors identified in epidemiological studies include prone and side positions for infant sleep, smoke exposure, soft bedding and sleep surfaces, and overheating. Evidence also suggests that pacifier use at sleep time and room sharing without bed sharing are associated with decreased risk of SIDS. Although the cause of SIDS is unknown, immature cardiorespiratory autonomic control and failure of arousal responsiveness from sleep are important factors. Gene polymorphisms relating to serotonin transport and autonomic nervous system development might make affected infants more vulnerable to SIDS. Campaigns for risk reduction have helped to reduce SIDS incidence by 50-90%. However, to reduce the incidence even further, greater strides must be made in reducing prenatal smoke exposure and implementing other recommended infant care practices. Continued research is needed to identify the pathophysiological basis of SIDS.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 636, "doc_id": "2613775", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The first MBT repeat of the four malignant brain tumor (4MBT) domain of Drosophila's Sfmbt and of the orthologous mammalian L3MBTL2 is required for the interaction with the spacer region of Drosophila's Pleiohomeotic (Pho) or its human ortholog YY1.\n\nCANDIDATE_PASSAGE:\nESCRT-III recognition by VPS4 ATPases The ESCRT (endosomal sorting complex required for transport) pathway is required for terminal membrane fission events in several important biological processes, including endosomal intraluminal vesicle formation, HIV budding and cytokinesis. VPS4 ATPases perform a key function in this pathway by recognizing membrane-associated ESCRT-III assemblies and catalysing their disassembly, possibly in conjunction with membrane fission. Here we show that the microtubule interacting and transport (MIT) domains of human VPS4A and VPS4B bind conserved sequence motifs located at the carboxy termini of the CHMP1–3 class of ESCRT-III proteins. Structures of VPS4A MIT–CHMP1A and VPS4B MIT–CHMP2B complexes reveal that the C-terminal CHMP motif forms an amphipathic helix that binds in a groove between the last two helices of the tetratricopeptide-like repeat (TPR) of the VPS4 MIT domain, but in the opposite orientation to that of a canonical TPR interaction. Distinct pockets in the MIT domain bind three conserved leucine residues of the CHMP motif, and mutations that inhibit these interactions block VPS4 recruitment, impair endosomal protein sorting and relieve dominant-negative VPS4 inhibition of HIV budding. Thus, our studies reveal how the VPS4 ATPases recognize their CHMP substrates to facilitate the membrane fission events required for the release of viruses, endosomal vesicles and daughter cells.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1218", "doc_id": "4429388", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: In pediatric tissue, most T cells are naive T cell emigrants from the thymus.\n\nCANDIDATE_PASSAGE:\nThe Molecular Basis for Oat Intolerance in Patients with Celiac Disease Background Celiac disease is a small intestinal inflammatory disorder characterized by malabsorption, nutrient deficiency, and a range of clinical manifestations. It is caused by an inappropriate immune response to dietary gluten and is treated with a gluten-free diet. Recent feeding studies have indicated oats to be safe for celiac disease patients, and oats are now often included in the celiac disease diet. This study aimed to investigate whether oat intolerance exists in celiac disease and to characterize the cells and processes underlying this intolerance. Methods and Findings We selected for study nine adults with celiac disease who had a history of oats exposure. Four of the patients had clinical symptoms on an oats-containing diet, and three of these four patients had intestinal inflammation typical of celiac disease at the time of oats exposure. We established oats-avenin-specific and -reactive intestinal T-cell lines from these three patients, as well as from two other patients who appeared to tolerate oats. The avenin-reactive T-cell lines recognized avenin peptides in the context of HLA-DQ2. These peptides have sequences rich in proline and glutamine residues closely resembling wheat gluten epitopes. Deamidation (glutamine→glutamic acid conversion) by tissue transglutaminase was involved in the avenin epitope formation. Conclusions We conclude that some celiac disease patients have avenin-reactive mucosal T-cells that can cause mucosal inflammation. Oat intolerance may be a reason for villous atrophy and inflammation in patients with celiac disease who are eating oats but otherwise are adhering to a strict gluten-free diet. Clinical follow-up of celiac disease patients eating [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "580", "doc_id": "14340571", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Active Ly49Q induces neutrophil polarization.\n\nCANDIDATE_PASSAGE:\nSteroid receptor interactions with heat shock protein and immunophilin chaperones. We have provided a historical perspective on a body of steroid receptor research dealing with the structure and physiological significance of the untransformed 9S receptor that has often confused both novice and expert investigators. The frequent controversies and equivocations of earlier studies were due to the fact that the native, hormone-free state of these receptors is a large multiprotein complex that resisted description for many years because of its unstable and dynamic nature. The untransformed 9S state of the steroid and dioxin receptors has provided a unique system for studying the function of the ubiquitous, abundant, and conserved heat shock protein, hsp90. The hormonal control of receptor association with hsp90 provided a method of manipulating the receptor heterocomplex in a manner that was physiologically meaningful. For several steroid receptors, binding to hsp90 was required for the receptor to be in a native hormone-binding state, and for all of the receptors, hormone binding promoted dissociation of the receptor from hsp90 and conversion of the receptor to the DNA-binding state. Although the complexes between tyrosine kinases and hsp90 were discovered earlier, the hormonal regulation or steroid receptor association with hsp90 permitted much more rapid and facile study of hsp90 function. The observations that hsp90 binds to the receptors through their HBDs and that these domains can be fused to structurally different proteins bringing their function under hormonal control provided a powerful linkage between the hormonal regulation of receptor binding to hsp90 and the initial step in steroid hormone action. Because the 9S receptor hsp90 heterocomplexes could [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "76", "doc_id": "30184745", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Upregulation of PD1 causes the downmodulation of Satb1.\n\nCANDIDATE_PASSAGE:\nNovel proteinaceous infectious particles cause scrapie. After infection and a prolonged incubation period, the scrapie agent causes a degenerative disease of the central nervous system in sheep and goats. Six lines of evidence including sensitivity to proteases demonstrate that this agent contains a protein that is required for infectivity. Although the scrapie agent is irreversibly inactivated by alkali, five procedures with more specificity for modifying nucleic acids failed to cause inactivation. The agent shows heterogeneity with respect to size, apparently a result of its hydrophobicity; the smallest form may have a molecular weight of 50,000 or less. Because the novel properties of the scrapie agent distinguish it from viruses, plasmids, and viroids, a new term \"prion\" is proposed to denote a small proteinaceous infectious particle which is resistant to inactivation by most procedures that modify nucleic acids. Knowledge of the scrapie agent structure may have significance for understanding the causes of several degenerative diseases.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1349", "doc_id": "7447120", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Clathrin stabilizes the spindle fiber apparatus during mitosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Clathrin is required for the function of the mitotic spindle\nABSTRACT: Clathrin has an established function in the generation of vesicles that transfer membrane and proteins around the cell. The formation of clathrin-coated vesicles occurs continuously in non-dividing cells, but is shut down during mitosis, when clathrin concentrates at the spindle apparatus. Here, we show that clathrin stabilizes fibres of the mitotic spindle to aid congression of chromosomes. Clathrin bound to the spindle directly by the amino-terminal domain of clathrin heavy chain. Depletion of clathrin heavy chain using RNA interference prolonged mitosis; kinetochore fibres were destabilized, leading to defective congression of chromosomes to the metaphase plate and persistent activation of the spindle checkpoint. Normal mitosis was rescued by clathrin triskelia but not the N-terminal domain of clathrin heavy chain, indicating that stabilization of kinetochore fibres was dependent on the unique structure of clathrin. The importance of clathrin for normal mitosis may be relevant to understanding human cancers that involve gene fusions of clathrin heavy chain.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here, we show that clathrin stabilizes fibres of the mitotic spindle to aid congression of chromosomes.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 265, "doc_id": "2033917", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Hypoglycemia increases the risk of dementia.\n\nCANDIDATE_PASSAGE:\nHypoglycemic episodes and risk of dementia in older patients with type 2 diabetes mellitus. CONTEXT Although acute hypoglycemia may be associated with cognitive impairment in children with type 1 diabetes, no studies to date have evaluated whether hypoglycemia is a risk factor for dementia in older patients with type 2 diabetes. OBJECTIVE To determine if hypoglycemic episodes severe enough to require hospitalization are associated with an increased risk of dementia in a population of older patients with type 2 diabetes followed up for 27 years. DESIGN, SETTING, AND PATIENTS A longitudinal cohort study from 1980-2007 of 16,667 patients with a mean age of 65 years and type 2 diabetes who are members of an integrated health care delivery system in northern California. MAIN OUTCOME MEASURE Hypoglycemic events from 1980-2002 were collected and reviewed using hospital discharge and emergency department diagnoses. Cohort members with no prior diagnoses of dementia, mild cognitive impairment, or general memory complaints as of January 1, 2003, were followed up for a dementia diagnosis through January 15, 2007. Dementia risk was examined using Cox proportional hazard regression models, adjusted for age, sex, race/ethnicity, education, body mass index, duration of diabetes, 7-year mean glycated hemoglobin, diabetes treatment, duration of insulin use, hyperlipidemia, hypertension, cardiovascular disease, stroke, transient cerebral ischemia, and end-stage renal disease. RESULTS At least 1 episode of hypoglycemia was diagnosed in 1465 patients (8.8%) and dementia was diagnosed in 1822 patients (11%) during follow-up; 250 patients had both dementia and at least 1 episode of hypoglycemia (16.95%). Compared with patients with no hypoglycemia, patients with single or multipl [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "539", "doc_id": "13282296", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Mutations in G-Beta protein GNB2 are present in many cancers, resulting in loss of interaction with G-alpha subunits and concomitant activation of AKT pathway.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mutations in G protein beta subunits promote transformation and kinase inhibitor resistance\nABSTRACT: Activating mutations in genes encoding G protein α (Gα) subunits occur in 4-5% of all human cancers, but oncogenic alterations in Gβ subunits have not been defined. Here we demonstrate that recurrent mutations in the Gβ proteins GNB1 and GNB2 confer cytokine-independent growth and activate canonical G protein signaling. Multiple mutations in GNB1 affect the protein interface that binds Gα subunits as well as downstream effectors and disrupt Gα interactions with the Gβγ dimer. Different mutations in Gβ proteins clustered partly on the basis of lineage; for example, all 11 GNB1 K57 mutations were in myeloid neoplasms, and seven of eight GNB1 I80 mutations were in B cell neoplasms. Expression of patient-derived GNB1 variants in Cdkn2a-deficient mouse bone marrow followed by transplantation resulted in either myeloid or B cell malignancies. In vivo treatment with the dual PI3K-mTOR inhibitor BEZ235 suppressed GNB1-induced signaling and markedly increased survival. In several human tumors, mutations in the gene encoding GNB1 co-occurred with oncogenic kinase alterations, including the BCR-ABL fusion protein, the V617F substitution in JAK2 and the V600K substitution in BRAF. Coexpression of patient-derived GNB1 variants with these mutant kinases resulted in inhibitor resistance in each context. Thus, GNB1 and GNB2 alterations confer transformed and resistance phenotypes across a range of human tumors and may be targetable with inhibitors of G protein signaling.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 814, "doc_id": "33387953", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Input from mental and physical health care professionals is not effective at decreasing homelessness.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mental health problems of homeless children and families: longitudinal study.\nABSTRACT: OBJECTIVE To establish the mental health needs of homeless children and families before and after rehousing. DESIGN Cross sectional, longitudinal study. SETTING City of Birmingham. SUBJECTS 58 rehoused families with 103 children aged 2-16 years and 21 comparison families of low socioeconomic status in stable housing, with 54 children. MAIN OUTCOME MEASURES Children's mental health problems and level of communication; mothers' mental health problems and social support one year after rehousing. RESULTS Mental health problems remained significantly higher in rehoused mothers and their children than in the comparison group (mothers 26% v 5%, P = 0.04; children 39% v 11%, P = 0.0003). Homeless mothers continued to have significantly less social support at follow up. Mothers with a history of abuse and poor social integration were more likely to have children with persistent mental health problems. CONCLUSIONS Homeless families have a high level of complex needs that cannot be met by conventional health services and arrangements. Local strategies for rapid rehousing into permanent accommodation, effective social support and health care for parents and children, and protection from violence and intimidation should be developed and implemented.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 638, "doc_id": "25649714", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Do cytokine gene polymorphisms predict acute graft rejection following renal transplantation?\n\nABSTRACT:\nThe proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) has been implicated in the pathogenesis of acute rejection, while animal models suggest a role for interleukin-10 (IL-10) in promoting graft survival. It has also been shown that polymorphisms in the TNFA gene promoter (position -308) and in the IL-10 gene promoter (position -1082) correlate with differential production of these cytokines in vitro. The aim of this study was to determine whether TNF-alpha and IL-10 gene polymorphisms influence the incidence and severity of acute rejection in the first six months following renal transplantation. The cytokine genotypes of 115 consecutive first cadaveric kidney allograft recipients and their donors were screened. The rejection episodes (REs) were defined clinically and confirmed histologically where possible and further classified according to severity (RS), namely steroid-resistant or responsive REs. The genotypes were then correlated with the REs and RS. The recipient TNF-alpha high producer genotype and IL-10 high producer genotype were significantly associated with multiple REs (>/=2) in human leukocyte antigen (HLA)-DR mismatched transplants (P = 0.0047 and P = 0.045, respectively), whereas only the TNF-alpha high producer genotype was associated with steroid-resistant REs (P = 0.025). When recipient cytokines were analyzed together, the TNF-alpha high/IL-10 high producer genotype had the worst prognosis, whereas TNF-alpha low/IL-10 low producer genotype was protective.", "output": "{\"label\": \"yes\", \"rationale\": \"We conclude that recipient TNF-alpha and IL-10 gene polymorphisms are determinants of REs and RS following kidney transplantation. Routine screening of these gene polymorphisms may have a clinical role in identifying patients at risk of multiple REs and severe rejections.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 10411704, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Input from mental and physical health care professionals is effective at decreasing homelessness.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mental health problems of homeless children and families: longitudinal study.\nABSTRACT: OBJECTIVE To establish the mental health needs of homeless children and families before and after rehousing. DESIGN Cross sectional, longitudinal study. SETTING City of Birmingham. SUBJECTS 58 rehoused families with 103 children aged 2-16 years and 21 comparison families of low socioeconomic status in stable housing, with 54 children. MAIN OUTCOME MEASURES Children's mental health problems and level of communication; mothers' mental health problems and social support one year after rehousing. RESULTS Mental health problems remained significantly higher in rehoused mothers and their children than in the comparison group (mothers 26% v 5%, P = 0.04; children 39% v 11%, P = 0.0003). Homeless mothers continued to have significantly less social support at follow up. Mothers with a history of abuse and poor social integration were more likely to have children with persistent mental health problems. CONCLUSIONS Homeless families have a high level of complex needs that cannot be met by conventional health services and arrangements. Local strategies for rapid rehousing into permanent accommodation, effective social support and health care for parents and children, and protection from violence and intimidation should be developed and implemented.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 637, "doc_id": "25649714", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The World Health Organization's (WHO) data collection process is biased downward by unequal selection of larger outbreaks.\n\nCANDIDATE_ABSTRACT:\nTITLE: Using Routine Surveillance Data to Estimate the Epidemic Potential of Emerging Zoonoses: Application to the Emergence of US Swine Origin Influenza A H3N2v Virus\nABSTRACT: BACKGROUND Prior to emergence in human populations, zoonoses such as SARS cause occasional infections in human populations exposed to reservoir species. The risk of widespread epidemics in humans can be assessed by monitoring the reproduction number R (average number of persons infected by a human case). However, until now, estimating R required detailed outbreak investigations of human clusters, for which resources and expertise are not always available. Additionally, existing methods do not correct for important selection and under-ascertainment biases. Here, we present simple estimation methods that overcome many of these limitations. METHODS AND FINDINGS Our approach is based on a parsimonious mathematical model of disease transmission and only requires data collected through routine surveillance and standard case investigations. We apply it to assess the transmissibility of swine-origin influenza A H3N2v-M virus in the US, Nipah virus in Malaysia and Bangladesh, and also present a non-zoonotic example (cholera in the Dominican Republic). Estimation is based on two simple summary statistics, the proportion infected by the natural reservoir among detected cases (G) and among the subset of the first detected cases in each cluster (F). If detection of a case does not affect detection of other cases from the same cluster, we find that R can be estimated by 1-G; otherwise R can be estimated by 1-F when the case detection rate is low. In more general cases, bounds on R can still be derived. CONCLUSIONS We have developed a simple approach with limited data requirements that enables robust assessment of the risks posed by emerging zoonoses. We illustrate this by deriving transmissibility estimates for the H3N2v-M virus, an important step in evaluating the possib [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1186, "doc_id": "7485455", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The PRDM1 gene, when combined with the PRDM14 gene, plays an important role during primordial germ cell specification.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Germ Cell Determinant Blimp1 Is Not Required for Derivation of Pluripotent Stem Cells\nABSTRACT: Blimp1 (Prdm1), the key determinant of primordial germ cells (PGCs), plays a combinatorial role with Prdm14 during PGC specification from postimplantation epiblast cells. They together initiate epigenetic reprogramming in early germ cells toward an underlying pluripotent state, which is equivalent to embryonic stem cells (ESCs). Whereas Prdm14 alone can promote reprogramming and is important for the propagation of the pluripotent state, it is not known whether Blimp1 is similarly involved. By using a genetic approach, we demonstrate that Blimp1 is dispensable for the derivation and maintenance of ESCs and postimplantation epiblast stem cells (epiSCs). Notably, Blimp1 is also dispensable for reprogramming epiSCs to ESCs. Thus, although Blimp1 is obligatory for PGC specification, it is not required for the reversion of epiSCs to ESCs and for their maintenance thereafter. This study suggests that reprogramming, including that of somatic cells to ESCs, may not entail an obligatory route through a Blimp1-positive PGC-like state.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Blimp1 (Prdm1), the key determinant of primordial germ cells (PGCs), plays a combinatorial role with Prdm14 during PGC specification from postimplantation epiblast cells.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1177, "doc_id": "13910150", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The G34R/V mutation creates a hypomethylated phenotype at the H3K36 histone.\n\nCANDIDATE_ABSTRACT:\nTITLE: ZMYND11 links histone H3.3K36me3 to transcription elongation and tumour suppression\nABSTRACT: Recognition of modified histones by ‘reader’ proteins plays a critical role in the regulation of chromatin. H3K36 trimethylation (H3K36me3) is deposited onto the nucleosomes in the transcribed regions after RNA polymerase II elongation. In yeast, this mark in turn recruits epigenetic regulators to reset the chromatin to a relatively repressive state, thus suppressing cryptic transcription. However, much less is known about the role of H3K36me3 in transcription regulation in mammals. This is further complicated by the transcription-coupled incorporation of the histone variant H3.3 in gene bodies. Here we show that the candidate tumour suppressor ZMYND11 specifically recognizes H3K36me3 on H3.3 (H3.3K36me3) and regulates RNA polymerase II elongation. Structural studies show that in addition to the trimethyl-lysine binding by an aromatic cage within the PWWP domain, the H3.3-dependent recognition is mediated by the encapsulation of the H3.3-specific ‘Ser 31’ residue in a composite pocket formed by the tandem bromo–PWWP domains of ZMYND11. Chromatin immunoprecipitation followed by sequencing shows a genome-wide co-localization of ZMYND11 with H3K36me3 and H3.3 in gene bodies, and its occupancy requires the pre-deposition of H3.3K36me3. Although ZMYND11 is associated with highly expressed genes, it functions as an unconventional transcription co-repressor by modulating RNA polymerase II at the elongation stage. ZMYND11 is critical for the repression of a transcriptional program that is essential for tumour cell growth; low expression levels of ZMYND11 in breast cancer patients correlate with worse prognosis. Consistently, overexpression of ZMYND11 suppresses cancer cell growth in vitro and tumour formation in mice. Together, this study identifies ZMYND11 as an H3 [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1164, "doc_id": "4455466", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Bacterial meningitis can be diagnosed on the basis of positive cerebrospinal fluid (CSF) cultures.\n\nCANDIDATE_PASSAGE:\nThe psychiatric manifestations of mitochondrial disorders: a case and review of the literature. OBJECTIVE Mitochondrial disorders are caused by gene mutations in mitochondrial or nuclear DNA and affect energy-dependent organs such as the brain. Patients with psychiatric illness, particularly those with medical comorbidities, may have primary mitochondrial disorders. To date, this issue has received little attention in the literature, and mitochondrial disorders are likely underdiagnosed in psychiatric patients. DATA SOURCES This article describes a patient who presented with borderline personality disorder and treatment-resistant depression and was ultimately diagnosed with mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) 3271. We also searched the literature for all case reports of patients with mitochondrial disorders who initially present with prominent psychiatric symptoms by using MEDLINE (from 1948-February 2011), Embase (from 1980-February 2011), PsycINFO (from 1806-February 2011), and the search terms mitochondrial disorder, mitochondria, psychiatry, mental disorders, major depression, anxiety, schizophrenia, and psychosis. STUDY SELECTION Fifty cases of mitochondrial disorders with prominent psychiatric symptomatology were identified. DATA EXTRACTION Information about the psychiatric presentation of the cases was extracted. This information was combined with our case, the most common psychiatric manifestations of mitochondrial disorders were identified, and the important diagnostic and treatment implications for patients with psychiatric illness were reviewed. RESULTS The most common psychiatric presentations in the cases of mitochondrial disorders included mood disorder, cognitive deterioration, psychosis, and a [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "160", "doc_id": "21246752", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does tissue Doppler imaging differentiate physiological from pathological pressure-overload left ventricular hypertrophy in rats?\n\nABSTRACT:\nThe myocardial velocity gradient (MVG) is a recent index of regional myocardial function derived from endocardial and epicardial velocities obtained by tissue Doppler imaging (TDI). This index might be useful for discriminating between physiological and pathological left ventricular hypertrophy (LVH) and for documenting the early transition from compensated LVH to heart failure. We sought to compare MVG measured across the left ventricular posterior wall between normal rats and rats with physiological (exercise) and pathological (pressure-overload) LVH. Wistar rats were assigned to one of the following groups: sedentary, exercise (swimming), and 2-month or 9-month abdominal aortic banding. Compared with sedentary rats, exercise and 2-month banding led to similar and significant LVH. After 2-month banding, conventional parameters of systolic function (left ventricular fractional shortening and dP/dt(max)) were not affected. However, systolic and diastolic MVG were similar in exercise and sedentary rats but were significantly lower in rats with aortic banding. Aortic debanding after 2 months led to a full recovery of MVG, whereas MVG remained decreased when debanding was performed after 9 months.", "output": "{\"label\": \"yes\", \"rationale\": \"Myocardial contraction and relaxation assessed by TDI were impaired in pressure-overload LVH but not in exercise LVH. Therefore, TDI is more sensitive than conventional echocardiography for assessing myocardial dysfunction in pressure-overload LVH and for predicting early recovery in myocardial function after loading conditions normalization.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 11927530, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does systemic atropine administration during cardiac arrest cause fixed and dilated pupils?\n\nABSTRACT:\nSystemic administration of atropine during CPR may postpone brain death determination because of its reputed ability to produce fixed and dilated pupils. We studied the effect of atropine administered in the usual doses as an adjunct to endotracheal intubation and for cardiac arrest to determine if it would interfere with neurological assessment. Two groups of children were studied. Group 1 consisted of 28 patients who received atropine (0.03 +/- 0.003 mg/kg) prior to endotracheal intubation. Group 2 consisted of 21 patients previously without evidence of brainstem disease who suffered a witnessed arrest and had prompt return of spontaneous circulation and received an atropine dose of 0.03 +/- 0.01 mg/kg. In group 1, pupillary size averaged 4.02 +/- 0.78 mm before and 4.75 mm +/- .84 mm after atropine (P less than .001). In group 2, the pupillary examination was conducted 30 minutes after return of spontaneous circulation. The pupillary diameter was 4.80 +/- 0.91 mm. All pupils were reactive to light in both groups.", "output": "{\"label\": \"no\", \"rationale\": \"Atropine administration in conventional dose causes slight pupillary dilation but does not abolish pupillary light reactivity.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 1984729, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Walking in traffic areas in London did not improve lung function in elderly adults.\n\nCANDIDATE_ABSTRACT:\nTITLE: Asthma in United States Olympic athletes who participated in the 1996 Summer Games.\nABSTRACT: BACKGROUND Asthma prevalence appears to be increasing in the general population. We sought to determine whether asthma prevalence has also increased in highly competitive athletes. OBJECTIVE Our aim was to determine how many United States Olympic athletes who were chosen to participate in the 1996 Summer Olympic Games had a past history of asthma or symptoms that suggested asthma or took asthma medications. METHODS We analyzed responses to questions that asked about allergic and respiratory diseases on the United States Olympic Committee (USOC) Medical History Questionnaire that was completed by all athletes who were chosen to represent the US at the 1996 Summer Olympic Games in Atlanta. RESULTS Of the 699 athletes who completed the questionnaire, 107 (15.3%) had a previous diagnosis of asthma, and 97 (13.9%) recorded use of an asthma medication at some time in the past. One hundred seventeen (16.7%) reported use of an asthma medication, a diagnosis of asthma, or both (which was our basis for the diagnosis of asthma). Seventy-three (10. 4%) of the athletes were currently taking an asthma medication at the time that they were processed in Atlanta or noted that they took asthma medications on a permanent or semipermanent basis and were considered to have active asthma. Athletes who participated in cycling and mountain biking had the highest prevalence of having been told that they had asthma or had taken an asthma medication in the past (50%). Frequency of active asthma varied from 45% of cyclists and emountain bikers to none of the divers and weight lifters. Only about 11% of the athletes who participated in the 1984 Summer Olympic Games were reported to have had exercise-induced asthma on the basis of other criteria that may have been less restrictive. On th [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1372, "doc_id": "641459", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Sudden death can occur in patients with orthostatic hypertension without cardiac conduction abnormalities.\n\nCANDIDATE_PASSAGE:\nMyocardial muscarinic receptor upregulation and normal response to isoproterenol in denervated hearts by familial amyloid polyneuropathy. BACKGROUND Patients with familial amyloid polyneuropathy, a rare hereditary form of amyloidosis, have progressive autonomic neuropathy. The disease usually does not induce heart failure but is associated with sudden death, conduction disturbances, and an increased risk of complications during anesthesia. Although cardiac sympathetic denervation has been clearly demonstrated, the postsynaptic status of the cardiac autonomic nervous system remains unelucidated. METHODS AND RESULTS Twenty-one patients were studied (age, 39+/-11 years; normal coronary arteries; left ventricular ejection fraction 68+/-9%). To evaluate the density and affinity constants of myocardial muscarinic receptors, PET with (11)C-MQNB (methylquinuclidinyl benzilate), a specific hydrophilic antagonist, was used. Cardiac beta-receptor functional efficiency was studied by the heart rate (HR) response to intravenous infusion of isoproterenol (5 minutes after 2 mg of atropine, 5, 10, and 15 ng/kg per minute during 5 minutes per step). The mean muscarinic receptor density was higher in patients than in control subjects (B'(max), 35.5+/-8.9 versus 26.1+/-6.7 pmol/mL, P=0.003), without change in receptor affinity. The increase in HR after injection of atropine as well as of MQNB was lower in patients compared with control subjects despite a similar basal HR (DeltaHR after atropine, 11+/-21% versus 62+/-17%; P<0.001), consistent with parasympathetic denervation. Incremental infusion of isoproterenol induced a similar increase in HR in patients and control subjects. CONCLUSIONS Cardiac autonomic denervation in familial amyloid polyneuropathy results in an upregulat [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1112", "doc_id": "1686881", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: cSMAC formation enhances weak ligand signalling.\n\nCANDIDATE_ABSTRACT:\nTITLE: The stimulatory potency of T cell antigens is influenced by the formation of the immunological synapse.\nABSTRACT: T cell activation is predicated on the interaction between the T cell receptor and peptide-major histocompatibility (pMHC) ligands. The factors that determine the stimulatory potency of a pMHC molecule remain unclear. We describe results showing that a peptide exhibiting many hallmarks of a weak agonist stimulates T cells to proliferate more than the wild-type agonist ligand. An in silico approach suggested that the inability to form the central supramolecular activation cluster (cSMAC) could underlie the increased proliferation. This conclusion was supported by experiments that showed that enhancing cSMAC formation reduced stimulatory capacity of the weak peptide. Our studies highlight the fact that a complex interplay of factors determines the quality of a T cell antigen.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"This conclusion was supported by experiments that showed that enhancing cSMAC formation reduced stimulatory capacity of the weak peptide.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1385, "doc_id": "306006", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The Snf1 complex regulates carbon and energy metabolism in baker's yeast (Saccharomyces cerevisiae).\n\nCANDIDATE_ABSTRACT:\nTITLE: Environmental factors that influence the cutaneous production of vitamin D\nABSTRACT: All vertebrates, including humans, obtain most of their daily vitamin D requirement from casual exposure to sunlight. During exposure to sunlight, the solar ultraviolet B photons (290-315 nm) penetrate into the skin where they cause the photolysis of 7-dehydrocholesterol to precholecalciferol. Once formed, precholecalciferol undergoes a thermally induced rearrangement of its double bonds to form cholecalciferol. An increase in skin pigmentation, aging, and the topical application of a sunscreen diminishes the cutaneous production of cholecalciferol. Latitude, season, and time of day as well as ozone pollution in the atmosphere influence the number of solar ultraviolet B photons that reach the earth's surface, and thereby, alter the cutaneous production of cholecalciferol. In Boston, exposure to sunlight during the months of November through February will not produce any significant amounts of cholecalciferol in the skin. Because windowpane glass absorbs ultraviolet B radiation, exposure of sunlight through glass windows will not result in any production of cholecalciferol. It is now recognized that vitamin D insufficiency and vitamin D deficiency are common in elderly people, especially in those who are infirm and not exposed to sunlight or who live at latitudes that do not provide them with sunlight-mediated cholecalciferol during the winter months. Vitamin D insufficiency and deficiency exacerbate osteoporosis, cause osteomalacia, and increase the risk of skeletal fractures. Vitamin D insufficiency and deficiency can be prevented by encouraging responsible exposure to sunlight and/or consumption of a multivitamin tablet that contains 10 micrograms (400 IU) vitamin D.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1182, "doc_id": "275294", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Natriuretic peptides increase susceptibility to diabetes.\n\nCANDIDATE_PASSAGE:\nMendelian Randomization Study of B-Type Natriuretic Peptide and Type 2 Diabetes: Evidence of Causal Association from Population Studies BACKGROUND Genetic and epidemiological evidence suggests an inverse association between B-type natriuretic peptide (BNP) levels in blood and risk of type 2 diabetes (T2D), but the prospective association of BNP with T2D is uncertain, and it is unclear whether the association is confounded. METHODS AND FINDINGS We analysed the association between levels of the N-terminal fragment of pro-BNP (NT-pro-BNP) in blood and risk of incident T2D in a prospective case-cohort study and genotyped the variant rs198389 within the BNP locus in three T2D case-control studies. We combined our results with existing data in a meta-analysis of 11 case-control studies. Using a Mendelian randomization approach, we compared the observed association between rs198389 and T2D to that expected from the NT-pro-BNP level to T2D association and the NT-pro-BNP difference per C allele of rs198389. In participants of our case-cohort study who were free of T2D and cardiovascular disease at baseline, we observed a 21% (95% CI 3%-36%) decreased risk of incident T2D per one standard deviation (SD) higher log-transformed NT-pro-BNP levels in analysis adjusted for age, sex, body mass index, systolic blood pressure, smoking, family history of T2D, history of hypertension, and levels of triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. The association between rs198389 and T2D observed in case-control studies (odds ratio = 0.94 per C allele, 95% CI 0.91-0.97) was similar to that expected (0.96, 0.93-0.98) based on the pooled estimate for the log-NT-pro-BNP level to T2D association derived from a meta-analysis of our study a [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "840", "doc_id": "15663829", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Adult tissue-resident macrophages stem from the embryonal yolk sac and fetal liver.\n\nCANDIDATE_PASSAGE:\nAsymmetric Cell Divisions Sustain Long-Term Hematopoiesis from Single-sorted Human Fetal Liver Cells Hematopoietic stem cells (HSCs) in adult marrow are believed to be derived from fetal liver precursors. To study cell kinetics involved in long-term hematopoiesis, we studied single-sorted candidate HSCs from fetal liver that were cultured in the presence of a mixture of stimulatory cytokines. After 8–10 d, the number of cells in primary cultures varied from 10,000 cells. Single cells in slow growing colonies were recloned upon reaching a 100–200 cell stage. Strikingly, the number of cells in subclones varied widely again. These results are indicative of asymmetric divisions in primitive hematopoietic cells in which proliferative potential and cell cycle properties are unevenly distributed among daughter cells. The continuous generation of functional heterogeneity among the clonal progeny of HSCs is in support of intrinsic control of stem cell fate and provides a model for the long-term maintenance of hematopoiesis in vitro and in vivo.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "89", "doc_id": "14550841", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does timing of initial surfactant treatment make a difference in rates of chronic lung disease or mortality in premature infants?\n\nABSTRACT:\nTo compare two treatment strategies in preterm infants with or at risk of respiratory distress syndrome: early surfactant administration (within one hour of birth) versus late surfactant administration, in a geographically defined population. The primary outcome was chronic lung disease (CLD) and mortality before/at 36 weeks. Secondary outcomes included: duration of mechanical ventilation and continuous positive airway pressure (CPAP), post-natal steroids for CLD and major neonatal morbidities. Premature infants born at 22-32 weeks' gestation between January 2006 and December 2009. Ten neonatal intensive care units (NICUs) in New South Wales (NSW) and Australian Capital Territory (ACT), Australia. Retrospective analysis of prospectively collected data from the regional NICU database in NSW and ACT. Of the 2170 infants who received surfactant, 1182 (54.5%) and 988 (45.5%) received early and late surfactant, respectively. The early surfactant group was less mature (27.1 ± 2.1 versus 29.4 ± 2.1 weeks) and had more CLD and mortality (40.2% versus 20.0%). The multivariable analysis showed early surfactant to be associated with less duration of ventilation, longer duration of CPAP and longer hospital stay but had little or no impact on CLD/mortality.", "output": "{\"label\": \"maybe\", \"rationale\": \"Early surfactant administration is associated with shorter duration of ventilation but does not appear to be significantly protective against CLD/mortality among premature infants. This may support the growing evidence for consideration of CPAP as an alternative to routine intubation and early surfactant administration. Further investigation from large randomized clinical trials is warranted to confirm these results.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 25394614, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Environmental factors can influence the development of breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Gene–environment interactions in 7610 women with breast cancer: prospective evidence from the Million Women Study\nABSTRACT: BACKGROUND Information is scarce about the combined effects on breast cancer incidence of low-penetrance genetic susceptibility polymorphisms and environmental factors (reproductive, behavioural, and anthropometric risk factors for breast cancer). To test for evidence of gene-environment interactions, we compared genotypic relative risks for breast cancer across the other risk factors in a large UK prospective study. METHODS We tested gene-environment interactions in 7610 women who developed breast cancer and 10 196 controls without the disease, studying the effects of 12 polymorphisms (FGFR2-rs2981582, TNRC9-rs3803662, 2q35-rs13387042, MAP3K1-rs889312, 8q24-rs13281615, 2p-rs4666451, 5p12-rs981782, CASP8-rs1045485, LSP1-rs3817198, 5q-rs30099, TGFB1-rs1982073, and ATM-rs1800054) in relation to prospectively collected information about ten established environmental risk factors (age at menarche, parity, age at first birth, breastfeeding, menopausal status, age at menopause, use of hormone replacement therapy, body-mass index, height, and alcohol consumption). FINDINGS After allowance for multiple testing none of the 120 comparisons yielded significant evidence of a gene-environment interaction. By contrast with previous suggestions, there was little evidence that the genotypic relative risks were affected by use of hormone replacement therapy, either overall or for oestrogen-receptor-positive disease. Only one of the 12 polymorphisms was correlated with any of the ten other risk factors: carriers of the high-risk C allele of MAP3K1-rs889312 were significantly shorter than non-carriers (mean height 162.4 cm [95% CI 162.1-162.7] vs 163.1 cm [162.9-163.2]; p=0.01 after allowance for multiple testing). INTERPRETATION Risks of breast cancer associated with low-pene [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"INTERPRETATION Risks of breast cancer associated with low-penetrance susceptibility polymorphisms do not vary significantly with these ten established environmental risk factors.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 381, "doc_id": "18340282", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Upregulation of PD1 causes the upregulation of Satb1.\n\nCANDIDATE_PASSAGE:\nIncreased Microerythrocyte Count in Homozygous α+-Thalassaemia Contributes to Protection against Severe Malarial Anaemia BACKGROUND The heritable haemoglobinopathy alpha(+)-thalassaemia is caused by the reduced synthesis of alpha-globin chains that form part of normal adult haemoglobin (Hb). Individuals homozygous for alpha(+)-thalassaemia have microcytosis and an increased erythrocyte count. Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count. We tested the hypothesis that the erythrocyte indices associated with alpha(+)-thalassaemia homozygosity provide a haematological benefit during acute malaria. METHODS AND FINDINGS Data from children living on the north coast of Papua New Guinea who had participated in a case-control study of the protection afforded by alpha(+)-thalassaemia against severe malaria were reanalysed to assess the genotype-specific reduction in erythrocyte count and Hb levels associated with acute malarial disease. We observed a reduction in median erythrocyte count of approximately 1.5 x 10(12)/l in all children with acute falciparum malaria relative to values in community children (p < 0.001). We developed a simple mathematical model of the linear relationship between Hb concentration and erythrocyte count. This model predicted that children homozygous for alpha(+)-thalassaemia lose less Hb than children of normal genotype for a reduction in erythrocyte count of >1.1 x 10(12)/l as a result of the reduced mean cell Hb in homozygous alpha(+)-thalassaemia. In addition, children homozygous for alpha(+)-thalassaemia require a 10% greater reduction in erythrocyte count than children of normal genotyp [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1350", "doc_id": "18174210", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: TMEM27 is a marker for beta cells.\n\nCANDIDATE_PASSAGE:\nTmem27: a cleaved and shed plasma membrane protein that stimulates pancreatic beta cell proliferation. The signals and molecular mechanisms that regulate the replication of terminally differentiated beta cells are unknown. Here, we report the identification and characterization of transmembrane protein 27 (Tmem27, collectrin) in pancreatic beta cells. Expression of Tmem27 is reduced in Tcf1(-/-) mice and is increased in islets of mouse models with hypertrophy of the endocrine pancreas. Tmem27 forms dimers and its extracellular domain is glycosylated, cleaved and shed from the plasma membrane of beta cells. This cleavage process is beta cell specific and does not occur in other cell types. Overexpression of full-length Tmem27, but not the truncated or soluble protein, leads to increased thymidine incorporation, whereas silencing of Tmem27 using RNAi results in a reduction of cell replication. Furthermore, transgenic mice with increased expression of Tmem27 in pancreatic beta cells exhibit increased beta cell mass. Our results identify a pancreatic beta cell transmembrane protein that regulates cell growth of pancreatic islets.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1133", "doc_id": "24142891", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is the presence of biofilm-producing bacteria on tonsils associated with increased exhaled nitric oxide levels : preliminary data in children who experience recurrent exacerbations of chronic tonsillitis?\n\nABSTRACT:\nIt has been suggested that bacterial biofilms may be a causative factor in the aetiopathogenesis of chronic tonsillitis. Involvement of exhaled nitric oxide has been previously considered, with conflicting findings. A pilot study was performed to investigate the relationship between exhaled nitric oxide levels and the presence of tonsillar biofilm-producing bacteria in children with chronic tonsillitis. Tonsillar biofilm-producing bacteria on bioptic specimens taken during tonsillectomy were assessed by means of spectrophotometry. Analysis was based on 24 children aged 5-10 years (median, 7.5 years). Biofilm-producing bacteria were found in 40.9 per cent of specimens. The median exhaled nitric oxide level was 11.6 ppb (range, 3.2-22.3 ppb). There was a significant relationship between the presence of biofilm-producing bacteria and increased exhaled nitric oxide levels (p = 0.03). Children with exhaled nitric oxide levels of more than 8 ppb were at three times greater risk of developing tonsillar biofilm-producing bacteria than those with lower levels.", "output": "{\"label\": \"yes\", \"rationale\": \"Our findings suggest the possibility of discriminating children with chronic biofilm-sustained tonsillar infections on the basis of exhaled nitric oxide levels.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25655099, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pioglitazone use is significantly associated with an increased risk of pancreatic cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pioglitazone Use and Risk of Bladder Cancer and Other Common Cancers in Persons With Diabetes.\nABSTRACT: IMPORTANCE Studies suggest pioglitazone use may increase risk of cancers. OBJECTIVE To examine whether pioglitazone use for diabetes is associated with risk of bladder and 10 additional cancers. DESIGN, SETTING, AND PARTICIPANTS Cohort and nested case-control analyses among persons with diabetes. A bladder cancer cohort followed 193,099 persons aged 40 years or older in 1997-2002 until December 2012; 464 case patients and 464 matched controls were surveyed about additional confounders. A cohort analysis of 10 additional cancers included 236,507 persons aged 40 years or older in 1997-2005 and followed until June 2012. Cohorts were from Kaiser Permanente Northern California. EXPOSURES Ever use, duration, cumulative dose, and time since initiation of pioglitazone as time dependent. MAIN OUTCOMES AND MEASURES Incident cancer, including bladder, prostate, female breast, lung/bronchus, endometrial, colon, non-Hodgkin lymphoma, pancreas, kidney/renal pelvis, rectum, and melanoma. RESULTS Among 193,099 persons in the bladder cancer cohort, 34,181 (18%) received pioglitazone (median duration, 2.8 years; range, 0.2-13.2 years) and 1261 had incident bladder cancer. Crude incidences of bladder cancer in pioglitazone users and nonusers were 89.8 and 75.9 per 100,000 person-years, respectively. Ever use of pioglitazone was not associated with bladder cancer risk (adjusted hazard ratio [HR], 1.06; 95% CI, 0.89-1.26). Results were similar in case-control analyses (pioglitazone use: 19.6% among case patients and 17.5% among controls; adjusted odds ratio, 1.18; 95% CI, 0.78-1.80). In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95% CI, 1.02-1.26) and p [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The increased prostate and pancreatic cancer risks associated with ever use of pioglitazone merit further investigation to assess whether they are causal or are due to chance, residual confounding, or reverse causality.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 953, "doc_id": "3355397", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: G-CSF increases the expansion and infiltration of MDSCs into tumors.\n\nCANDIDATE_ABSTRACT:\nTITLE: Oncogenic mTOR signaling recruits myeloid-derived suppressor cells to promote tumor initiation\nABSTRACT: Myeloid-derived suppressor cells (MDSCs) play critical roles in primary and metastatic cancer progression. MDSC regulation is widely variable even among patients harbouring the same type of malignancy, and the mechanisms governing such heterogeneity are largely unknown. Here, integrating human tumour genomics and syngeneic mammary tumour models, we demonstrate that mTOR signalling in cancer cells dictates a mammary tumour's ability to stimulate MDSC accumulation through regulating G-CSF. Inhibiting this pathway or its activators (for example, FGFR) impairs tumour progression, which is partially rescued by restoring MDSCs or G-CSF. Tumour-initiating cells (TICs) exhibit elevated G-CSF. MDSCs reciprocally increase TIC frequency through activating Notch in tumour cells, forming a feedforward loop. Analyses of primary breast cancers and patient-derived xenografts corroborate these mechanisms in patients. These findings establish a non-canonical oncogenic role of mTOR signalling in recruiting pro-tumorigenic MDSCs and show how defined cancer subsets may evolve to promote and depend on a distinct immune microenvironment.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here, integrating human tumour genomics and syngeneic mammary tumour models, we demonstrate that mTOR signalling in cancer cells dictates a mammary tumour's ability to stimulate MDSC accumulation through regulating G-CSF.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 441, "doc_id": "2014909", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Helicobacter pylori-induced aberrant NF-kB-dependent expression of activation-induced cytidine deaminase contributes to the mutagenesis of host DNA.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pre-Exposure Prophylaxis to Prevent HIV Infection: Current Status, Future Opportunities and Challenges\nABSTRACT: As the global incidence of HIV exceeds 2 million new infections annually, effective interventions to decrease HIV transmission are needed. Randomized, placebo-controlled studies have demonstrated that daily oral antiretroviral pre-exposure prophylaxis (PrEP) with a fixed-dose combination tablet containing tenofovir disoproxil fumarate and emtricitabine can significantly reduce HIV incidence among diverse at-risk populations. In these studies, the efficacy of PrEP was correlated with levels of adherence. Official guidelines recommend provision of PrEP to people at greatest risk of HIV acquisition, and demonstration projects suggest that high levels of uptake and adherence are possible outside of controlled studies. However, several potential barriers to implementing PrEP remain. These challenges include low awareness and utilization of PrEP by at-risk individuals, uncertainty about adherence in ‘real-world’ settings, the majority of healthcare providers being untrained in PrEP provision, limited data about potential adverse effects from long-term use of tenofovir–emtricitabine, high costs of PrEP medications, and stigma associated with PrEP use and the behaviors that would warrant PrEP. Innovative pharmacologic chemoprophylactic approaches could provide solutions to some of these challenges. Less-than-daily oral dosing regimens and long-acting injectable medications could reduce pill burdens and facilitate adherence, and local delivery of PrEP medications to genital compartments via gels, rings and films may limit systemic drug exposure and potential toxicities. As the portfolio of chemoprophylactic agents and delivery systems expands to meet the diverse sexual health needs and product preferences of individuals who may benefit from PrEP, it is hoped that ant [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 505, "doc_id": "437924", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Hypoglycemia increases the risk of dementia.\n\nCANDIDATE_ABSTRACT:\nTITLE: Hypoglycemic episodes and risk of dementia in older patients with type 2 diabetes mellitus.\nABSTRACT: CONTEXT Although acute hypoglycemia may be associated with cognitive impairment in children with type 1 diabetes, no studies to date have evaluated whether hypoglycemia is a risk factor for dementia in older patients with type 2 diabetes. OBJECTIVE To determine if hypoglycemic episodes severe enough to require hospitalization are associated with an increased risk of dementia in a population of older patients with type 2 diabetes followed up for 27 years. DESIGN, SETTING, AND PATIENTS A longitudinal cohort study from 1980-2007 of 16,667 patients with a mean age of 65 years and type 2 diabetes who are members of an integrated health care delivery system in northern California. MAIN OUTCOME MEASURE Hypoglycemic events from 1980-2002 were collected and reviewed using hospital discharge and emergency department diagnoses. Cohort members with no prior diagnoses of dementia, mild cognitive impairment, or general memory complaints as of January 1, 2003, were followed up for a dementia diagnosis through January 15, 2007. Dementia risk was examined using Cox proportional hazard regression models, adjusted for age, sex, race/ethnicity, education, body mass index, duration of diabetes, 7-year mean glycated hemoglobin, diabetes treatment, duration of insulin use, hyperlipidemia, hypertension, cardiovascular disease, stroke, transient cerebral ischemia, and end-stage renal disease. RESULTS At least 1 episode of hypoglycemia was diagnosed in 1465 patients (8.8%) and dementia was diagnosed in 1822 patients (11%) during follow-up; 250 patients had both dementia and at least 1 episode of hypoglycemia (16.95%). Compared with patients with no hypoglycemia, patients with single or multiple episodes had a graded increase in risk with fully adjusted hazard ratios (HRs): for 1 epis [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Among older patients with type 2 diabetes, a history of severe hypoglycemic episodes was associated with a greater risk of dementia.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 539, "doc_id": "13282296", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Citrullinated proteins externalized in neutrophil extracellular traps act indirectly to disrupt the inflammatory cycle.\n\nCANDIDATE_ABSTRACT:\nTITLE: Antibodies from patients with rheumatoid arthritis target citrullinated histone 4 contained in neutrophils extracellular traps.\nABSTRACT: BACKGROUND Histone deimination regulates gene function and contributes to antimicrobial response, allowing the formation of neutrophil extracellular traps (NETs). Deiminated proteins are target of anti-citrullinated peptides antibodies (ACPA) in rheumatoid arthritis (RA). OBJECTIVE The objective of this paper is to test the hypothesis that RA sera react with deiminated histones contained in NETs. METHODS Neutrophils from peripheral blood were stimulated with A23187 and acid treated; NETosis was induced by phorbol myristate acetate, and NET proteins were isolated. Sera were tested by immunoblot on acid extracted proteins from neutrophils and from NETs, and by ELISA on deiminated histone H4 or H4-derived peptides. Bands reactive with RA sera were excised from gels, digested with trypsin and subjected to matrix-assisted laser desorption/ionisation time of flight (MALDI-TOF) analysis, before and after derivatisation to detect citrullinated peptides. RESULTS RA sera reacted with a deiminated antigen of 11 KDa from activated neutrophils, recognised also by anti-H4 and antideiminated H4 antibodies. A similar reactivity was observed with NET proteins. The antigen from neutrophils or NETs was identified as citrullinated H4 by MALDI-TOF analysis. By ELISA, RA sera bound in vitro citrullinated H4. Citrullinated H4 14-34 and 31-50 peptides detected antibodies in 67% and 63% of RA sera and in less than 5% of controls; antibody titre was correlated with anti-CCP2. CONCLUSIONS Citrullinated H4 from activated neutrophils and NETs is a target of antibodies in RA, and synthetic citrullinated H4-derived peptides are a new substrate for ACPA detection. As NETosis can generate antigens for ACPA, these data suggest a novel connection between innate and adaptive immunity in RA.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Citrullinated H4 from activated neutrophils and NETs is a target of antibodies in RA, and synthetic citrullinated H4-derived peptides are a new substrate for ACPA detection.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 263, "doc_id": "30041340", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Inhibiting focal adhesion formation increases the rate at which cells convert mechanical strain into inflammation and fibrosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Drosophila DHR96 nuclear receptor binds cholesterol and regulates cholesterol homeostasis.\nABSTRACT: Cholesterol homeostasis is required to maintain normal cellular function and avoid the deleterious effects of hypercholesterolemia. Here we show that the Drosophila DHR96 nuclear receptor binds cholesterol and is required for the coordinate transcriptional response of genes that are regulated by cholesterol and involved in cholesterol uptake, trafficking, and storage. DHR96 mutants die when grown on low levels of cholesterol and accumulate excess cholesterol when maintained on a high-cholesterol diet. The cholesterol accumulation phenotype can be attributed to misregulation of npc1b, an ortholog of the mammalian Niemann-Pick C1-like 1 gene NPC1L1, which is essential for dietary cholesterol uptake. These studies define DHR96 as a central regulator of cholesterol homeostasis.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 633, "doc_id": "2423940", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: High cardiopulmonary fitness causes increased mortality rate.\n\nCANDIDATE_ABSTRACT:\nTITLE: Prevalence and cardiovascular disease correlates of low cardiorespiratory fitness in adolescents and adults.\nABSTRACT: CONTEXT Population surveys indicate that physical activity levels are low in the United States. One consequence of inactivity, low cardiorespiratory fitness, is an established risk factor for cardiovascular disease (CVD) morbidity and mortality, but the prevalence of cardiorespiratory fitness has not been quantified in representative US population samples. OBJECTIVES To describe the prevalence of low fitness in the US population aged 12 through 49 years and to relate low fitness to CVD risk factors in this population. DESIGN, SETTING, AND PARTICIPANTS Inception cohort study using data from the cross-sectional nationally representative National Health and Nutrition Examination Survey 1999-2002. Participants were adolescents (aged 12-19 years; n = 3110) and adults (aged 20-49 years; n = 2205) free from previously diagnosed CVD who underwent submaximal graded exercise treadmill testing to achieve at least 75% to 90% of their age-predicted maximum heart rate. Maximal oxygen consumption (VO2max) was estimated by measuring the heart rate response to reference levels of submaximal work. MAIN OUTCOME MEASURES Low fitness defined using percentile cut points of estimated VO2max from existing external referent populations; anthropometric and other CVD risk factors measured according to standard methods. RESULTS Low fitness was identified in 33.6% of adolescents (approximately 7.5 million US adolescents) and 13.9% of adults (approximately 8.5 million US adults); the prevalence was similar in adolescent females (34.4%) and males (32.9%) (P = .40) but was higher in adult females (16.2%) than in males (11.8%) (P = .03). Non-Hispanic blacks and Mexican Americans were less fit than non-Hispanic whites. In all age-sex groups, body mass index and waist circumference were inver [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSION Low fitness in adolescents and adults is common in the US population and is associated with an increased prevalence of CVD risk factors.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 513, "doc_id": "13230773", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Exposure to fine particulate air pollution is unrelated to anxiety prevalence.\n\nCANDIDATE_PASSAGE:\nThe relation between past exposure to fine particulate air pollution and prevalent anxiety: observational cohort study OBJECTIVE To determine whether higher past exposure to particulate air pollution is associated with prevalent high symptoms of anxiety. DESIGN Observational cohort study. SETTING Nurses' Health Study. PARTICIPANTS 71,271 women enrolled in the Nurses' Health Study residing throughout the contiguous United States who had valid estimates on exposure to particulate matter for at least one exposure period of interest and data on anxiety symptoms. MAIN OUTCOME MEASURES Meaningfully high symptoms of anxiety, defined as a score of 6 points or greater on the phobic anxiety subscale of the Crown-Crisp index, administered in 2004. RESULTS The 71,271 eligible women were aged between 57 and 85 years (mean 70 years) at the time of assessment of anxiety symptoms, with a prevalence of high anxiety symptoms of 15%. Exposure to particulate matter was characterized using estimated average exposure to particulate matter <2.5 μm in diameter (PM2.5) and 2.5 to 10 μm in diameter (PM2.5-10) in the one month, three months, six months, one year, and 15 years prior to assessment of anxiety symptoms, and residential distance to the nearest major road two years prior to assessment. Significantly increased odds of high anxiety symptoms were observed with higher exposure to PM2.5 for multiple averaging periods (for example, odds ratio per 10 µg/m(3) increase in prior one month average PM2.5: 1.12, 95% confidence interval 1.06 to 1.19; in prior 12 month average PM2.5: 1.15, 1.06 to 1.26). Models including multiple exposure windows suggested short term averaging periods were more relevant than long term averaging periods. There was no association between anxiety and exposur [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "400", "doc_id": "791050", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Vitamin D deficiency is unrelated to birth weight.\n\nCANDIDATE_ABSTRACT:\nTITLE: Coding of Sweet, Bitter, and Umami Tastes Different Receptor Cells Sharing Similar Signaling Pathways\nABSTRACT: Mammals can taste a wide repertoire of chemosensory stimuli. Two unrelated families of receptors (T1Rs and T2Rs) mediate responses to sweet, amino acids, and bitter compounds. Here, we demonstrate that knockouts of TRPM5, a taste TRP ion channel, or PLCbeta2, a phospholipase C selectively expressed in taste tissue, abolish sweet, amino acid, and bitter taste reception, but do not impact sour or salty tastes. Therefore, despite relying on different receptors, sweet, amino acid, and bitter transduction converge on common signaling molecules. Using PLCbeta2 taste-blind animals, we then examined a fundamental question in taste perception: how taste modalities are encoded at the cellular level. Mice engineered to rescue PLCbeta2 function exclusively in bitter-receptor expressing cells respond normally to bitter tastants but do not taste sweet or amino acid stimuli. Thus, bitter is encoded independently of sweet and amino acids, and taste receptor cells are not broadly tuned across these modalities.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1370, "doc_id": "718601", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Lack of FGF21 in mice leads to reduced lifespan.\n\nCANDIDATE_PASSAGE:\nFibroblast Growth Factor 21 Prevents Atherosclerosis by Suppression of Hepatic Sterol Regulatory Element-Binding Protein-2 and Induction of Adiponectin in Mice BACKGROUND Fibroblast growth factor 21 (FGF21) is a metabolic hormone with pleiotropic effects on glucose and lipid metabolism and insulin sensitivity. It acts as a key downstream target of both peroxisome proliferator-activated receptor α and γ, the agonists of which have been used for lipid lowering and insulin sensitization, respectively. However, the role of FGF21 in the cardiovascular system remains elusive. METHODS AND RESULTS The roles of FGF21 in atherosclerosis were investigated by evaluating the impact of FGF21 deficiency and replenishment with recombinant FGF21 in apolipoprotein E(-/-) mice. FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia. Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia. Chronic treatment with adiponectin partially reverses atherosclerosis without obvious effects on hypercholesterolemia in FGF21-deficient apolipoprotein E(-/-) mice. By contrast, the cholesterol-lowering effects of FGF21 are abrogated by hepatic expression of sterol regulatory element-binding protein-2. CONCLUSIONS FGF21 protects against at [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "682", "doc_id": "9315213", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Ribosomopathies have a low degree of cell and tissue specific pathology.\n\nCANDIDATE_ABSTRACT:\nTITLE: Candida albicans, a distinctive fungal model for cellular aging study\nABSTRACT: The unicellular eukaryotic organisms represent the popular model systems to understand aging in eukaryotes. Candida albicans, a polymorphic fungus, appears to be another distinctive unicellular aging model in addition to the budding yeast Saccharomyces cerevisiae and fission yeast Schizosaccharomyces pombe. The two types of Candida cells, yeast (blastospore) form and hyphal (filamentous) form, have similar replicative lifespan. Taking the advantage of morphologic changes, we are able to obtain cells of different ages. Old Candida cells tend to accumulate glycogen and oxidatively damaged proteins. Deletion of the SIR2 gene causes a decrease of lifespan, while insertion of an extra copy of SIR2 extends lifespan, indicating that like in S. cerevisiae, Sir2 regulates cellular aging in C. albicans. Interestingly, Sir2 deletion does not result in the accumulation of extra-chromosomal rDNA molecules, but influences the retention of oxidized proteins in mother cells, suggesting that the extra-chromosomal rDNA molecules may not be associated with cellular aging in C. albicans. This novel aging model, which allows efficient large-scale isolation of old cells, may facilitate biochemical characterizations and genomics/proteomics studies of cellular aging, and help to verify the aging pathways observed in other organisms including S. cerevisiae.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1049, "doc_id": "516867", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Transplanted human glial progenitor cells can mature in their host animal.\n\nCANDIDATE_ABSTRACT:\nTITLE: Forebrain engraftment by human glial progenitor cells enhances synaptic plasticity and learning in adult mice.\nABSTRACT: Human astrocytes are larger and more complex than those of infraprimate mammals, suggesting that their role in neural processing has expanded with evolution. To assess the cell-autonomous and species-selective properties of human glia, we engrafted human glial progenitor cells (GPCs) into neonatal immunodeficient mice. Upon maturation, the recipient brains exhibited large numbers and high proportions of both human glial progenitors and astrocytes. The engrafted human glia were gap-junction-coupled to host astroglia, yet retained the size and pleomorphism of hominid astroglia, and propagated Ca2+ signals 3-fold faster than their hosts. Long-term potentiation (LTP) was sharply enhanced in the human glial chimeric mice, as was their learning, as assessed by Barnes maze navigation, object-location memory, and both contextual and tone fear conditioning. Mice allografted with murine GPCs showed no enhancement of either LTP or learning. These findings indicate that human glia differentially enhance both activity-dependent plasticity and learning in mice.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Upon maturation, the recipient brains exhibited large numbers and high proportions of both human glial progenitors and astrocytes.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1322, "doc_id": "16284655", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Mice that lack Interferon-γ or its receptor are highly susceptible to experimental autoimmune myocarditis.\n\nCANDIDATE_ABSTRACT:\nTITLE: the Development of Autoimmune Myocarditis in Mice by an\nABSTRACT: BACKGROUND Interleukin (IL)-12 exerts a potent proinflammatory effect by stimulating T-helper (Th) 1 responses. This effect is believed to be mediated primarily through the activation of STAT4 and subsequent production of interferon (IFN)-gamma. Methods and Results- We examined the role of IL-12 receptor (IL-12R) signaling in the development of murine experimental autoimmune myocarditis (EAM) induced by cardiac myosin immunization. Both IL-12Rbeta1-deficient mice and STAT4-deficient mice were resistant to the induction of myocarditis. Treatment with exogenous IL-12 exacerbated disease. We questioned whether IFN-gamma is required for the disease-promoting activity of IL-12. On the contrary, we found that IFN-gamma suppresses EAM. Lack of IFN-gamma due to either depletion with an antibody or a genetic deficiency exacerbated myocarditis. Spleens from IFN-gamma-deficient mice immunized with cardiac myosin showed increased cellularity; greater numbers of CD3+, CD4+, CD8+, and IL-2-producing cells; and heightened ability to produce cytokines on stimulation in vitro. Treatment of mice with recombinant IFN-gamma suppressed the development of myocarditis. CONCLUSIONS IL-12/IL-12R/STAT4 signaling promotes the development of EAM. In contrast, IFN-gamma plays a protective role. The disease-limiting effects of IFN-gamma might be explained by its ability to control the expansion of activated T lymphocytes.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In contrast, IFN-gamma plays a protective role.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 780, "doc_id": "8246922", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Metastatic colorectal cancer treated with a single agent fluoropyrimidines resulted in similar efficacy and better quality of life when compared with oxaliplatin-based chemotherapy in elderly patients.\n\nCANDIDATE_ABSTRACT:\nTITLE: Long-term immune deficiency after allogeneic stem cell transplantation: B-cell deficiency is associated with late infections.\nABSTRACT: Immune reconstitution was analyzed in 140 consecutive patients who were 2-year disease-free and who underwent myeloablative allogeneic transplantation. A CD4 and CD8 defect was observed involving naive, terminally differentiated, memory and competent cells and above limits values for activated subsets. Natural killer cells normalize at six months while we observed expansion of CD19(+)/CD5(+) B cells after three months and a persisting defect of memory B cells. Chronic graft-versus-host disease did not influence significantly those parameters for CD8 subsets while the naïve and competent CD4 subsets were strongly affected. But the most profound impact of chronic graft-versus-host disease was on B-cell subsets, especially on the memory B population. The cumulative incidence of late severe infections was low (14% at four years). Using Cox's models, only low B-cell counts at 12 (P=0.02) and 24 (P=0.001) months were associated with the hazard of developing late infection, in particular if patients did not develop chronic graft-versus-host disease.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 771, "doc_id": "301866", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: IL-6 signaling plays a major role in atherosclerotic cardiovascular disease.\n\nCANDIDATE_PASSAGE:\nRole of RhoA-specific guanine exchange factors in regulation of endomitosis in megakaryocytes. Polyploidization can precede the development of aneuploidy in cancer. Polyploidization in megakaryocytes (Mks), in contrast, is a highly controlled developmental process critical for efficient platelet production via unknown mechanisms. Using primary cells, we demonstrate that the guanine exchange factors GEF-H1 and ECT2, which are often overexpressed in cancer and are essential for RhoA activation during cytokinesis, must be downregulated for Mk polyploidization. The first (2N-4N) endomitotic cycle requires GEF-H1 downregulation, whereas subsequent cycles (>4N) require ECT2 downregulation. Exogenous expression of both GEF-H1 and ECT2 prevents endomitosis, resulting in proliferation of 2N Mks. Furthermore, we have shown that the mechanism by which polyploidization is prevented in Mks lacking Mkl1, which is mutated in megakaryocytic leukemia, is via elevated GEF-H1 expression; shRNA-mediated GEF-H1 knockdown alone rescues this ploidy defect. These mechanistic insights enhance our understanding of normal versus malignant megakaryocytopoiesis, as well as aberrant mitosis in aneuploid cancers.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "548", "doc_id": "33076846", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Cells undergoing methionine restriction may activate miRNAs.\n\nCANDIDATE_PASSAGE:\nInterferons: Success in anti-viral immunotherapy. The interferons (IFNs) are glycoproteins with strong antiviral activities that represent one of the first lines of host defense against invading pathogens. These proteins are classified into three groups, Type I, II and III IFNs, based on the structure of their receptors on the cell surface. Due to their ability to modulate immune responses, they have become attractive therapeutic options to control chronic virus infections. In combination with other drugs, Type I IFNs are considered as \"standard of care\" in suppressing Hepatitis C (HCV) and Hepatitis B (HBV) infections, while Type III IFN has generated encouraging results as a treatment for HCV infection in phase III clinical trials. However, though effective, using IFNs as a treatment is not without the need for caution. IFNs are such powerful cytokines that affect a wide array of cell types; as a result, patients usually experience unpleasant symptoms, with a percentage of patients suffering system wide effects. Thus, constant monitoring is required for patients treated with IFN in order to reach the treatment goals of suppressing virus infection and maintaining quality of life.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "238", "doc_id": "3308636", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nCANDIDATE_PASSAGE:\nRank Signaling Links the Development of Invariant γδ T Cell Progenitors and Aire+ Medullary Epithelium The thymic medulla provides a specialized microenvironment for the negative selection of T cells, with the presence of autoimmune regulator (Aire)-expressing medullary thymic epithelial cells (mTECs) during the embryonic-neonatal period being both necessary and sufficient to establish long-lasting tolerance. Here we showed that emergence of the first cohorts of Aire(+) mTECs at this key developmental stage, prior to αβ T cell repertoire selection, was jointly directed by Rankl(+) lymphoid tissue inducer cells and invariant Vγ5(+) dendritic epidermal T cell (DETC) progenitors that are the first thymocytes to express the products of gene rearrangement. In turn, generation of Aire(+) mTECs then fostered Skint-1-dependent, but Aire-independent, DETC progenitor maturation and the emergence of an invariant DETC repertoire. Hence, our data attributed a functional importance to the temporal development of Vγ5(+) γδ T cells during thymus medulla formation for αβ T cell tolerance induction and demonstrated a Rank-mediated reciprocal link between DETC and Aire(+) mTEC maturation.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1004", "doc_id": "301838", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: CD28 initiates tonic signaling in conventional T cells, which causes an exhaustion phenotype and limited efficiency.\n\nCANDIDATE_PASSAGE:\nRegulation of β-Adrenergic Receptor Signaling by S-Nitrosylation of G-Protein-Coupled Receptor Kinase 2 beta-adrenergic receptors (beta-ARs), prototypic G-protein-coupled receptors (GPCRs), play a critical role in regulating numerous physiological processes. The GPCR kinases (GRKs) curtail G-protein signaling and target receptors for internalization. Nitric oxide (NO) and/or S-nitrosothiols (SNOs) can prevent the loss of beta-AR signaling in vivo, but the molecular details are unknown. Here we show in mice that SNOs increase beta-AR expression and prevent agonist-stimulated receptor downregulation; and in cells, SNOs decrease GRK2-mediated beta-AR phosphorylation and subsequent recruitment of beta-arrestin to the receptor, resulting in the attenuation of receptor desensitization and internalization. In both cells and tissues, GRK2 is S-nitrosylated by SNOs as well as by NO synthases, and GRK2 S-nitrosylation increases following stimulation of multiple GPCRs with agonists. Cys340 of GRK2 is identified as a principal locus of inhibition by S-nitrosylation. Our studies thus reveal a central molecular mechanism through which GPCR signaling is regulated.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "200", "doc_id": "14171859", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Gastric infection with Helicobacter pylori decreases risk of gastric cancer in humans.\n\nCANDIDATE_PASSAGE:\nCombined Impact of Lifestyle-Related Factors on Total and Cause-Specific Mortality among Chinese Women: Prospective Cohort Study BACKGROUND Although cigarette smoking, excessive alcohol drinking, obesity, and several other well-studied unhealthy lifestyle-related factors each have been linked to the risk of multiple chronic diseases and premature death, little is known about the combined impact on mortality outcomes, in particular among Chinese and other non-Western populations. The objective of this study was to quantify the overall impact of lifestyle-related factors beyond that of active cigarette smoking and alcohol consumption on all-cause and cause-specific mortality in Chinese women. METHODS AND FINDINGS We used data from the Shanghai Women's Health Study, an ongoing population-based prospective cohort study in China. Participants included 71,243 women aged 40 to 70 years enrolled during 1996-2000 who never smoked or drank alcohol regularly. A healthy lifestyle score was created on the basis of five lifestyle-related factors shown to be independently associated with mortality outcomes (normal weight, lower waist-hip ratio, daily exercise, never exposed to spouse's smoking, higher daily fruit and vegetable intake). The score ranged from zero (least healthy) to five (most healthy) points. During an average follow-up of 9 years, 2,860 deaths occurred, including 775 from cardiovascular disease (CVD) and 1,351 from cancer. Adjusted hazard ratios for mortality decreased progressively with an increasing number of healthy lifestyle factors. Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for c [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "447", "doc_id": "1456068", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Cellular aging closely links to an older appearance.\n\nCANDIDATE_ABSTRACT:\nTITLE: Perceived age as clinically useful biomarker of ageing: cohort study.\nABSTRACT: OBJECTIVE To determine whether perceived age correlates with survival and important age related phenotypes. DESIGN Follow-up study, with survival of twins determined up to January 2008, by which time 675 (37%) had died. SETTING Population based twin cohort in Denmark. PARTICIPANTS 20 nurses, 10 young men, and 11 older women (assessors); 1826 twins aged >or=70. MAIN OUTCOME MEASURES Assessors: perceived age of twins from photographs. Twins: physical and cognitive tests and molecular biomarker of ageing (leucocyte telomere length). RESULTS For all three groups of assessors, perceived age was significantly associated with survival, even after adjustment for chronological age, sex, and rearing environment. Perceived age was still significantly associated with survival after further adjustment for physical and cognitive functioning. The likelihood that the older looking twin of the pair died first increased with increasing discordance in perceived age within the twin pair-that is, the bigger the difference in perceived age within the pair, the more likely that the older looking twin died first. Twin analyses suggested that common genetic factors influence both perceived age and survival. Perceived age, controlled for chronological age and sex, also correlated significantly with physical and cognitive functioning as well as with leucocyte telomere length. CONCLUSION Perceived age-which is widely used by clinicians as a general indication of a patient's health-is a robust biomarker of ageing that predicts survival among those aged >or=70 and correlates with important functional and molecular ageing phenotypes.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Perceived age, controlled for chronological age and sex, also correlated significantly with physical and cognitive functioning as well as with leucocyte telomere length.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 239, "doc_id": "14079881", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: A diminished ovarian reserve is a very strong indicator of infertility, even in an a priori non-infertile population.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\nABSTRACT: Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential. Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age. Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area. Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH. Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle). Conception was defined as a positive pregnancy test result. Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis. After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively). Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cy [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 40, "doc_id": "13497630", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Recognition of start codons depends on the translation initiation factor IF3.\n\nCANDIDATE_ABSTRACT:\nTITLE: Large-Scale Movements of IF3 and tRNA during Bacterial Translation Initiation\nABSTRACT: In bacterial translational initiation, three initiation factors (IFs 1-3) enable the selection of initiator tRNA and the start codon in the P site of the 30S ribosomal subunit. Here, we report 11 single-particle cryo-electron microscopy (cryoEM) reconstructions of the complex of bacterial 30S subunit with initiator tRNA, mRNA, and IFs 1-3, representing different steps along the initiation pathway. IF1 provides key anchoring points for IF2 and IF3, thereby enhancing their activities. IF2 positions a domain in an extended conformation appropriate for capturing the formylmethionyl moiety charged on tRNA. IF3 and tRNA undergo large conformational changes to facilitate the accommodation of the formylmethionyl-tRNA (fMet-tRNA(fMet)) into the P site for start codon recognition.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"IF3 and tRNA undergo large conformational changes to facilitate the accommodation of the formylmethionyl-tRNA (fMet-tRNA(fMet)) into the P site for start codon recognition.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1023, "doc_id": "16927286", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: There is no relation between Erythromycin use and hypertrophic pyloric stenosis.\n\nCANDIDATE_PASSAGE:\nUse of macrolides in mother and child and risk of infantile hypertrophic pyloric stenosis: nationwide cohort study OBJECTIVE To assess the association between use of macrolide antibiotics in mothers and infants from pregnancy onset until 120 days after birth and infantile hypertrophic pyloric stenosis (IHPS). DESIGN Nationwide register based cohort study. SETTING Denmark, 1996-2011. PARTICIPANTS 999,378 liveborn singletons and linked individual level information on macrolide prescriptions (maternal use during pregnancy, n=30,091; maternal use after birth, n=21,557; use in infants, n=6591), surgery for IHPS, and potential confounders. MAIN OUTCOME MEASURES Surgery for IHPS by three categories of macrolide use: in mothers during pregnancy, in mothers after birth, and in infants after birth. RESULTS 880 infants developed IHPS (0.9 cases per 1000 births). Compared with infants with no use of macrolides, the adjusted rate ratio for IHPS in infants with use of macrolides during days 0 to 13 after birth was 29.8 (95% confidence interval 16.4 to 54.1) and during days 14 to 120 was 3.24 (1.20 to 8.74); the corresponding absolute risk differences were 24.4 (95% confidence interval 13.0 to 44.1) and 0.65 (0.06 to 2.21) cases per 1000 infants exposed to macrolides, respectively. The rate ratio for maternal use of macrolides for days 0 to 13 after birth was 3.49 (1.92 to 6.34) and for days 14 to 120 was 0.70 (0.26 to 1.90); the corresponding absolute risk differences were 2.15 (0.82 to 4.64) and -0.11 (-0.26 to 0.31). The rate ratios for maternal use of macrolides during pregnancy were 1.02 (0.65 to 1.59) for weeks 0 to 27 and 1.77 (0.95 to 3.31) for weeks 28 to birth; the corresponding absolute risk differences were 0.01 (-0.31 to 0.50) and 0.67 (-0.06 to 2.02). CONCLUS [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1295", "doc_id": "21239672", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Physical activity level has no association with the difference in maximal oxygen consumption between black and white youth.\n\nCANDIDATE_PASSAGE:\nPrevalence of the Metabolic Syndrome Among Us Adults: Findings From the Third National Health and Nutrition Examination Survey Metabolic syndrome is diagnosed when three or more of the following criteria are met: abdominal obesity (waist circumference more than 102 cm in men and 88 cm in women); hypertriglyceridemia of 150 mg/dl or above; a high-density lipoprotein (HDL) cholesterol level less than 40 mg/dl in men or 50 mg/dl in women; blood pressure of 130/85 mm Hg or higher; or fasting glucose of at least 110 mg/dl. Individuals with metabolic syndrome are likelier than others to develop diabetes and cardiovascular disease and have increased mortality from all causes (and from cardiovascular disease in particular). The investigators attempted to determine the prevalence of the syndrome in the United States by analyzing data on 8814 men and women 20 years of age or older who took part in the Third National Health and Nutrition Examination Survey in the years 1988 to 1994. This is a cross-sectional health survey of a sample of the noninstitutionalized civilian American population. The overall age-adjusted prevalence of metabolic syndrome was 23.7%. The prevalence rose from 6.7% in persons 20 to 29 years of age to 42% in those aged 70 years and more. There was virtually no gender-related difference in prevalence rates for the combined racial groups. Metabolic syndrome was most prevalent in Mexican Americans and least prevalent in whites, African Americans, and \"others. \" Among both African Americans and Mexican Americans, women had higher prevalence rates than men. Extrapolating from age-specific prevalence rates and US census counts from the year 2000, 47 million US residents have metabolic syndrome. Considering its prevalence, it seems important to estimate [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "945", "doc_id": "75636923", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: A deficiency of vitamin B12 increases blood levels of homocysteine.\n\nCANDIDATE_ABSTRACT:\nTITLE: Randomized trial of folic acid supplementation and serum homocysteine levels.\nABSTRACT: BACKGROUND Lowering serum homocysteine levels with folic acid is expected to reduce mortality from ischemic heart disease. Homocysteine reduction is known to be maximal at a folic acid dosage of 1 mg/d, but the effect of lower doses (relevant to food fortification) is unclear. METHODS We randomized 151 patients with ischemic heart disease to 1 of 5 dosages of folic acid (0.2, 0.4, 0.6, 0.8, and 1.0 mg/d) or placebo. Fasting blood samples for serum homocysteine and serum folate analysis were taken initially, after 3 months of supplementation, and 3 months after folic acid use was discontinued. RESULTS Median serum homocysteine level decreased with increasing folic acid dosage, to a maximum at 0.8 mg of folic acid per day, when the homocysteine reduction (placebo adjusted) was 2.7 micromol/L (23%), similar to the known effect of folic acid dosages of 1 mg/d and above. The higher a person's initial serum homocysteine level, the greater was the response to folic acid, but there were statistically significant reductions regardless of the initial level. Serum folate level increased approximately linearly (5.5 nmol/L for every 0.1 mg of folic acid). Within-person fluctuations over time in serum homocysteine levels, measured in the placebo group, were large compared with the effect of folic acid, indicating that monitoring of the reduction in an individual is impractical. CONCLUSIONS A dosage of folic acid of 0.8 mg/d appears necessary to achieve the maximum reduction in serum homocysteine level across the range of homocysteine levels in the population. Current US food fortification levels will achieve only a small proportion of the achievable homocysteine reduction.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 36, "doc_id": "11705328", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Mutant mice lacking SVCT2 have severely reduced ascorbic acid levels in both brain and adrenals.\n\nCANDIDATE_PASSAGE:\nDisruption of the 5S RNP–Mdm2 interaction significantly improves the erythroid defect in a mouse model for Diamond-Blackfan anemia Diamond-Blackfan anemia (DBA) is a congenital erythroid hypoplasia caused by haploinsufficiency of genes encoding ribosomal proteins (RPs). Perturbed ribosome biogenesis in DBA has been shown to induce a p53-mediated ribosomal stress response. However, the mechanisms of p53 activation and its relevance for the erythroid defect remain elusive. Previous studies have indicated that activation of p53 is caused by the inhibition of mouse double minute 2 (Mdm2), the main negative regulator of p53, by the 5S ribonucleoprotein particle (RNP). Meanwhile, it is not clear whether this mechanism solely mediates the p53-dependent component found in DBA. To approach this question, we crossed our mouse model for RPS19-deficient DBA with Mdm2C305F knock-in mice that have a disrupted 5S RNP–Mdm2 interaction. Upon induction of the Rps19 deficiency, Mdm2C305F reversed the p53 response and improved expansion of hematopoietic progenitors in vitro, and ameliorated the anemia in vivo. Unexpectedly, disruption of the 5S RNP–Mdm2 interaction also led to selective defect in erythropoiesis. Our findings highlight the sensitivity of erythroid progenitor cells to aberrations in p53 homeostasis mediated by the 5S RNP–Mdm2 interaction. Finally, we provide evidence indicating that physiological activation of the 5S RNP-Mdm2-p53 pathway may contribute to functional decline of the hematopoietic system in a cell-autonomous manner over time.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "812", "doc_id": "12240507", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: ART substantially reduces infectiveness of HIV-positive people.\n\nCANDIDATE_PASSAGE:\nCrizotinib in ROS1-rearranged non-small-cell lung cancer. BACKGROUND Chromosomal rearrangements of the gene encoding ROS1 proto-oncogene receptor tyrosine kinase (ROS1) define a distinct molecular subgroup of non-small-cell lung cancers (NSCLCs) that may be susceptible to therapeutic ROS1 kinase inhibition. Crizotinib is a small-molecule tyrosine kinase inhibitor of anaplastic lymphoma kinase (ALK), ROS1, and another proto-oncogene receptor tyrosine kinase, MET. METHODS We enrolled 50 patients with advanced NSCLC who tested positive for ROS1 rearrangement in an expansion cohort of the phase 1 study of crizotinib. Patients were treated with crizotinib at the standard oral dose of 250 mg twice daily and assessed for safety, pharmacokinetics, and response to therapy. ROS1 fusion partners were identified with the use of next-generation sequencing or reverse-transcriptase-polymerase-chain-reaction assays. RESULTS The objective response rate was 72% (95% confidence interval [CI], 58 to 84), with 3 complete responses and 33 partial responses. The median duration of response was 17.6 months (95% CI, 14.5 to not reached). Median progression-free survival was 19.2 months (95% CI, 14.4 to not reached), with 25 patients (50%) still in follow-up for progression. Among 30 tumors that were tested, we identified 7 ROS1 fusion partners: 5 known and 2 novel partner genes. No correlation was observed between the type of ROS1 rearrangement and the clinical response to crizotinib. The safety profile of crizotinib was similar to that seen in patients with ALK-rearranged NSCLC. CONCLUSIONS In this study, crizotinib showed marked antitumor activity in patients with advanced ROS1-rearranged NSCLC. ROS1 rearrangement defines a second molecular subgroup of NSCLC for which crizotinib i [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "61", "doc_id": "26079071", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Macrolides protect against myocardial infarction.\n\nCANDIDATE_ABSTRACT:\nTITLE: Antibiotics and risk of subsequent first-time acute myocardial infarction.\nABSTRACT: CONTEXT Increasing evidence supports the hypothesis of a causal association between certain bacterial infections and increased risk of developing acute myocardial infarction. If such a causal association exists, subjects who used antibiotics active against the bacteria, regardless of indication, might be at lower risk of developing acute myocardial infarction than nonusers. OBJECTIVE To determine whether previous use of antibiotics decreases the risk of developing a first-time acute myocardial infarction. DESIGN Population-based case-control analysis. SETTING The United Kingdom-based General Practice Research Database comprising 350 general practices. PATIENTS A total of 3315 case patients aged 75 years or younger with a diagnosis of first-time acute myocardial infarction between 1992 and 1997 and 13139 controls without myocardial infarction matched to cases for age, sex, general practice attended, and calendar time. MAIN OUTCOME MEASURES Use of antibiotics among those who did or did not have a first-time acute myocardial infarction. RESULTS Cases were significantly less likely to have used tetracycline antibiotics (adjusted odds ratio [OR], 0.70; 95% confidence interval [CI], 0.55-0.90) or quinolones (adjusted OR, 0.45; 95% CI, 0.21-0.95). No effect was found for previous use of macrolides (primarily erythromycin), sulfonamides, penicillins, or cephalosporins. CONCLUSIONS The findings from this large case-control analysis provide further, albeit indirect, evidence for an association between bacterial infections with organisms susceptible to tetracycline or quinolone antibiotics and the risk of acute myocardial infarction. These results of preliminary nature should stimulate more research to further explore the role of infections in the etiology of acute myo [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"No effect was found for previous use of macrolides (primarily erythromycin), sulfonamides, penicillins, or cephalosporins.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 743, "doc_id": "32159283", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Propriospinal interneurons that play a role in the plastic reorganization of spinal circuits are integral for recovery from spinal cord injury.\n\nCANDIDATE_PASSAGE:\nImmune reconstitution after cord blood transplantation: peculiarities, clinical implications and management strategies. Umbilical cord blood (UCB) is now widely used as an alternative hematopoietic stem cell source for patients lacking closely matched related or unrelated adult donors. UCB transplantation has traditionally been associated with delayed engraftment, poor immune reconstitution and consequent increased risk of infection. More recent clinical studies, however, suggest that conditioning regimens and in particular the omission of in vivo T-cell depletion may play a crucial role in post-transplant T-cell expansion, facilitating a uniquely rapid immune recovery after UCB transplantation. The peculiar characteristics of UCB cells, the importance of thymic function and the role of conditioning regimens and graft-versus-host disease influencing immune reconstitution are described. The last part of the review reports available data on UCB, as well as third-party peripheral blood derived anti-viral cell therapy, which provides a novel approach to rescue UCB recipients with viral complications in the post-transplant period.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "980", "doc_id": "27243019", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Artefacts in 24-h pharyngeal and oesophageal pH monitoring: is simplification of pH data analysis feasible?\n\nABSTRACT:\nAmbulatory 24-h dual-channel pharyngeal and oesophageal pH monitoring is the standard test for measuring gastro-oesophageal and gastropharyngeal reflux. Artefacts caused by the intake of food may result in falsely positive gastropharyngeal reflux, which necessitates a manual review of 24-h pH data. The purpose of the study was to investigate the influence of meals and whether leaving out meals affected the reliability of the test. Patients referred for otolaryngological complaints, suspected to have been caused by gastro-oesophageal reflux, underwent 24-h dual-channel pH monitoring. The raw unprocessed pH data were corrected by visual inspection of the 24-h tracings (corrected data), by leaving out meals or meals plus a 2-h postprandrial period. The raw pH data were substantially influenced by artefacts of food intake and pseudoreflux. Data obtained by leaving out meals agreed best with manually corrected data. Many of the falsely positive reflux episodes could be removed, thereby inducing a 9%-18% chance of undetected reflux. When examining the fraction of time supine, manually corrected data and data leaving out meals were fully concordant and detected 79% of patients with gastropharyngeal reflux. However, leaving out meals plus a 2-h postprandrial period resulted in 21%-50% falsely negative tests.", "output": "{\"label\": \"maybe\", \"rationale\": \"Leaving out the period of intake of meals and beverages from the raw pH data might be the second best test after the time-consuming visual correction with a small chance of undetected gastropharyngeal reflux. For scientific purposes and when in doubt, it remains necessary to review the computer-generated data manually to discover every gastropharyngeal reflux event.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 14992556, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Birth-weight is positively associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Intrauterine environments and breast cancer risk: meta-analysis and systematic review\nABSTRACT: INTRODUCTION Various perinatal factors, including birth weight, birth order, maternal age, gestational age, twin status, and parental smoking, have been postulated to affect breast cancer risk in daughters by altering the hormonal environment of the developing fetal mammary glands. Despite ample biologic plausibility, epidemiologic studies to date have yielded conflicting results. We investigated the associations between perinatal factors and subsequent breast cancer risk through meta-analyses. METHODS We reviewed breast cancer studies published from January 1966 to February 2007 that included data on birth weight, birth order, maternal age, gestational age, twin status, and maternal or paternal smoking. Meta-analyses using random effect models were employed to summarize the results. RESULTS We found that heavier birth weights were associated with increased breast cancer risk, with studies involving five categories of birth weight identifying odds ratios (ORs) of 1.24 (95% confidence interval [CI] 1.04 to 1.48) for 4,000 g or more and 1.15 (95% CI 1.04 to 1.26) for 3,500 g to 3,999 g, relative to a birth weight of 2,500 to 2,599 g. These studies provided no support for a J-shaped relationship of birthweight to risk. Support for an association with birthweight was also derived from studies based on three birth weight categories (OR 1.15 [95% CI 1.01 to 1.31] for > or =4,000 g relative to <3,000 g) and two birth weight categories (OR 1.09 [95% CI 1.02 to 1.18] for > or =3,000 g relative to <3,000 g). Women born to older mothers and twins were also at some increased risk, but the results were heterogeneous across studies and publication years. Birth order, prematurity, and maternal smoking were unrelated to breast cancer risk. CONCLUSION Our findings provide so [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"RESULTS We found that heavier birth weights were associated with increased breast cancer risk, with studies involving five categories of birth weight identifying odds ratios (ORs) of 1.24 (95% confidence interval [CI] 1.04 to 1.48) for 4,000 g or more and 1.15 (95% CI 1.04 to 1.26) for 3,500 g to 3,999 g, relative to a birth weight of 2,500 to 2,599 g. These studies provided no support for a J-shaped relationship of birthweight to risk.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 179, "doc_id": "17450673", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: There is an inverse relationship between hip fractures and statin use.\n\nCANDIDATE_ABSTRACT:\nTITLE: HMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients.\nABSTRACT: CONTEXT Recent animal studies have found that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) lipid-lowering drugs (statins) substantially increase bone formation, but whether statin use in humans results in clinically meaningful bone formation or a reduction in the risk of osteoporotic fractures is not known. OBJECTIVE To determine whether the use of statins is associated with reduced hip fracture risk. DESIGN Case-control study. SETTING AND PATIENTS A total of 6110 New Jersey residents aged 65 years or older and enrolled in Medicare and either Medicaid or the Pharmacy Assistance for the Aged and Disabled program. Case patients (n=1222) underwent surgical repair of a hip fracture in 1994. Control patients (n=4888) were identified at a ratio of 4:1 and frequency-matched to case patients for age and sex. MAIN OUTCOME MEASURE Adjusted odds ratio (OR) of hip fracture by statin use in the 180 days and 3 years prior to the index date (the earliest date of admission for surgery), adjusted for demographic and clinical characteristics and health care utilization. RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus. No significant relationship was observed between use of nonstatin lipid-lowering agents and hip fracture risk. Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowe [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowering agents.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1290, "doc_id": "4687948", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Microarray results from culture-amplified mixtures of serotypes correlate poorly with microarray results from uncultured mixtures.\n\nCANDIDATE_PASSAGE:\nIdentifying common impairments in frail and dependent older people: validation of the COPE assessment for non-specialised health workers in low resource primary health care settings BACKGROUND Frail and dependent older people in resource-poor settings are poorly served by health systems that lack outreach capacity. The COPE (Caring for Older PEople) multidimensional assessment tool is designed to help community health workers (CHWs) identify clinically significant impairments and deliver evidence-based interventions METHODS Older people (n = 150) identified by CHWs as frail or dependent, were assessed at home by the CHW using the structured COPE assessment tool, generating information on impairments in nutrition, mobility, vision, hearing, continence, cognition, mood and behaviour. The older people were reassessed by local physicians who reached a clinical judgment regarding the presence or absence of the same impairments based upon clinical examination guided by the EASY-Care assessment tool. RESULTS The COPE tool was considered easy to administer, and gave CHWs a sense of empowerment to understand and act upon the needs of older people. Agreement between COPE assessment by CHW and clinician assessors was modest (ranged from 45.8 to 91.3 %) for most impairments. However, the prevalence of impairments was generally higher according to clinicians, particularly for visual impairment (98.7 vs 45.8 %), cognitive impairment (78.4 vs. 38.2 %) and depression (82.0 vs. 59.9 %). Most cases identified by WHO-COPE were clinician confirmed (positive predictive values - 72.2 to 98.5 %), and levels of disability and needs for care among those identified by COPE were higher than those additionally identified by the clinician alone. CONCLUSIONS The COPE is a feasible tool f [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "785", "doc_id": "10893238", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does epinephrine concentration ( 1:100,000 or 1:200,000 ) affect the clinical efficacy of 4 % articaine for lower third molar removal : a double-blind , randomized , crossover study?\n\nABSTRACT:\nThis study compared the use of 4% articaine in association with 1:100,000 (10 mug/mL; A100) or 1:200,000 (5 mug/mL; A200) epinephrine in lower third molar removal. Fifty healthy volunteers underwent removal of symmetrically positioned lower third molars, in 2 separate appointments, under local anesthesia with either A100 or A200, in a double-blind, randomized, and crossed manner. Latency, duration of postoperative analgesia, duration of anesthetic action on soft tissues, intraoperative bleeding, and hemodynamic parameters were evaluated. A100 and A200 presented very similar latency (1.64 +/- 0.08 and 1.58 +/- 0.08 minutes, respectively; P > .05). Identical volumes of both anesthetic solutions were used: 2.7 mL = 108 mg of articaine plus 27 mug (A100) or 13.5 mug (A200) of epinephrine. The 2 solutions provided similar duration of postoperative analgesia regardless of bone removal (around 200 minutes; P > .05). The 2 solutions also had a similar duration of anesthetic action on soft tissues (around 250 minutes; P > .05). The surgeon's rating of intraoperative bleeding was considered very close to minimal. Transient changes in hemodynamic parameters were observed, but these were neither clinically significant nor attributable to the type of anesthetic used (P > .05).", "output": "{\"label\": \"no\", \"rationale\": \"An epinephrine concentration of 1:100,000 or 1:200,000 in 4% articaine solution does not affect the clinical efficacy of this local anesthetic. It is possible to successfully use the 4% articaine formulation with a lower concentration of epinephrine (1:200,000 or 5 mug/mL) for lower third molar extraction with or without bone removal.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 18022467, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Lymphadenopathy is observed in knockin mouse lacking the SHP-2 MAPK pathway.\n\nCANDIDATE_ABSTRACT:\nTITLE: Dissection of signaling cascades through gp130 in vivo: reciprocal roles for STAT3- and SHP2-mediated signals in immune responses.\nABSTRACT: We generated a series of knockin mouse lines, in which the cytokine receptor gp130-dependent STAT3 and/or SHP2 signals were disrupted, by replacing the mouse gp130 gene with human gp130 mutant cDNAs. The SHP2 signal-deficient mice (gp130F759/F759 were born normal but displayed splenomegaly and lymphadenopathy and an enhanced acute phase reaction. In contrast, the STAT3 signal-deficient mice (gp130FXQ/FXXQ) died perinatally, like the gp130-deficient mice (gp130D/D). The gp130F759/F759 mice showed prolonged gp130-induced STAT3 activation, indicating a negative regulatory role for SHP2. Th1-type cytokine production and IgG2a and IgG2b production were increased in the gp130F759/F759 mice, while they were decreased in the gp130FXXQ/FXXQ immune system. These results indicate that the balance of positive and negative signals generated through gp130 regulates the immune responses.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The SHP2 signal-deficient mice (gp130F759/F759 were born normal but displayed splenomegaly and lymphadenopathy and an enhanced acute phase reaction.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 729, "doc_id": "26851674", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_ABSTRACT:\nTITLE: Efficacy of human papillomavirus testing for the detection of invasive cervical cancers and cervical intraepithelial neoplasia: a randomised controlled trial.\nABSTRACT: BACKGROUND Human papillomavirus (HPV) testing is known to be more sensitive, but less specific than cytology for detecting cervical intraepithelial neoplasia (CIN). We assessed the efficacy of cervical-cancer screening policies that are based on HPV testing. METHODS Between March, 2004, and December, 2004, in two separate recruitment phases, women aged 25-60 years were randomly assigned to conventional cytology or to HPV testing in combination with liquid-based cytology (first phase) or alone (second phase). Randomisation was done by computer in two screening centres and by sequential opening of numbered sealed envelopes in the remaining seven centres. During phase one, women who were HPV-positive and aged 35-60 years were referred to colposcopy, whereas women aged 25-34 years were referred to colposcopy only if cytology was also abnormal or HPV testing was persistently positive. During phase two, women in the HPV group were referred for colposcopy if the HPV test was positive. Two rounds of screening occurred in each phase, and all women had cytology testing only at the second round. The primary endpoint was the detection of grade 2 and 3 CIN, and of invasive cervical cancers during the first and second screening rounds. Analysis was done by intention to screen. This trial is registered, number ISRCTN81678807. FINDINGS In total for both phases, 47,001 women were randomly assigned to the cytology group and 47,369 to HPV testing. 33,851 women from the cytology group and 32,998 from the HPV-testing group had a second round of screening. We also retrieved the histological diagnoses from screening done elsewhere. The detection of invasive cervical cancers was similar for the two groups in the first round of screening (nine in the cytology group vs seven in the H [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Among women aged 35-60 years, at round one the relative detection (HPV vs cytology) was 2.00 (95% CI 1.44-2.77) for CIN2, 2.08 (1.47-2.95) for CIN3, and 2.03 (1.60-2.57) for CIN2 and 3 together.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 972, "doc_id": "27873158", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: GATA3 regulates self-renewal capacity in bone marrow hematopoietic stem cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: GATA-3 regulates hematopoietic stem cell maintenance and cell-cycle entry.\nABSTRACT: Maintaining hematopoietic stem cell (HSC) quiescence is a critical property for the life-long generation of blood cells. Approximately 75% of cells in a highly enriched long-term repopulating HSC (LT-HSC) pool (Lin(-)Sca1(+)c-Kit(hi)CD150(+)CD48(-)) are quiescent, with only a small percentage of the LT-HSCs in cycle. Transcription factor GATA-3 is known to be vital for the development of T cells at multiple stages in the thymus and for Th2 differentiation in the peripheral organs. Although it is well documented that GATA-3 is expressed in HSCs, a role for GATA-3 in any prethymic progenitor cell has not been established. In the present study, we show that Gata3-null mutant mice generate fewer LT-HSCs and that fewer Gata3-null LT-HSCs are in cycle. Furthermore, Gata3 mutant hematopoietic progenitor cells fail to be recruited into an increased cycling state after 5-fluorouracil-induced myelosuppression. Therefore, GATA-3 is required for the maintenance of a normal number of LT-HSCs and for their entry into the cell cycle.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Therefore, GATA-3 is required for the maintenance of a normal number of LT-HSCs and for their entry into the cell cycle.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 445, "doc_id": "10165258", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Basophils promote disease development in patients with systemic lupus erythematosus (SLE).\n\nCANDIDATE_ABSTRACT:\nTITLE: Cancer survivorship research: the challenge of recruiting adult long term cancer survivors from a cooperative clinical trials group\nABSTRACT: INTRODUCTION With the growing number of adult cancer survivors, there is increasing need for information that links potential late and long term effects with specific treatment regimens. Few adult cancer patients are treated on clinical trials; however, patients previously enrolled in these trials are an important source of information about treatment-related late effects. METHODS Focusing on colorectal cancer survivors, we used the database from five phase III randomized clinical trials from the National Surgical Adjuvant Breast & Bowel Project (NSABP) to recruit and enroll long term survivors in a study of late health outcomes and quality of life. We describe the challenges to recruitment of patients more than 5 -20 years after treatment. RESULTS Sixty-five NSABP treatment sites were invited to enroll patients in the study. Sixty participated with the potential to recruit 2,408 patients. We received registration forms on only 976 patients (41%) of whom 744 (76%) expressed interest in participating and 708 completed interviews (95% of those expressing interest; 29% of total potential sample). There were multiple barriers to recruitment (difficulty locating patients, lack of institutional commitment, lack of patient interest). CONCLUSIONS Patients treated on clinical trials are an important potential source for examining the late effects of cancer treatments. Retrospective recruitment has substantial limitations. In the future, mechanisms should be established for prospective long-term follow-up to identify and understand the frequency and type of late effects associated with cancer treatments. IMPLICATIONS FOR CANCER SURVIVORS As cancer patients are living longer, it will be important to learn from participants in clinical trials whether or not specific tre [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 172, "doc_id": "2328272", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: MEK inhibitors are effective treatments in RAS-driven mouse models of cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effective Use of PI3K and MEK Inhibitors to Treat Mutant K-Ras G12D and PIK3CA H1047R Murine Lung Cancers\nABSTRACT: Somatic mutations that activate phosphoinositide 3-kinase (PI3K) have been identified in the p110-alpha catalytic subunit (encoded by PIK3CA). They are most frequently observed in two hotspots: the helical domain (E545K and E542K) and the kinase domain (H1047R). Although the p110-alpha mutants are transforming in vitro, their oncogenic potential has not been assessed in genetically engineered mouse models. Furthermore, clinical trials with PI3K inhibitors have recently been initiated, and it is unknown if their efficacy will be restricted to specific, genetically defined malignancies. In this study, we engineered a mouse model of lung adenocarcinomas initiated and maintained by expression of p110-alpha H1047R. Treatment of these tumors with NVP-BEZ235, a dual pan-PI3K and mammalian target of rapamycin (mTOR) inhibitor in clinical development, led to marked tumor regression as shown by positron emission tomography-computed tomography, magnetic resonance imaging and microscopic examination. In contrast, mouse lung cancers driven by mutant Kras did not substantially respond to single-agent NVP-BEZ235. However, when NVP-BEZ235 was combined with a mitogen-activated protein kinase kinase (MEK) inhibitor, ARRY-142886, there was marked synergy in shrinking these Kras-mutant cancers. These in vivo studies suggest that inhibitors of the PI3K-mTOR pathway may be active in cancers with PIK3CA mutations and, when combined with MEK inhibitors, may effectively treat KRAS mutated lung cancers.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"However, when NVP-BEZ235 was combined with a mitogen-activated protein kinase kinase (MEK) inhibitor, ARRY-142886, there was marked synergy in shrinking these Kras-mutant cancers.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 734, "doc_id": "4961038", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Destination container port throughput(CPT) is negatively related to dengue virus (DENV-1) diffusion in air traffic shipments.\n\nCANDIDATE_ABSTRACT:\nTITLE: Population Density, Water Supply, and the Risk of Dengue Fever in Vietnam: Cohort Study and Spatial Analysis\nABSTRACT: BACKGROUND Aedes aegypti, the major vector of dengue viruses, often breeds in water storage containers used by households without tap water supply, and occurs in high numbers even in dense urban areas. We analysed the interaction between human population density and lack of tap water as a cause of dengue fever outbreaks with the aim of identifying geographic areas at highest risk. METHODS AND FINDINGS We conducted an individual-level cohort study in a population of 75,000 geo-referenced households in Vietnam over the course of two epidemics, on the basis of dengue hospital admissions (n = 3,013). We applied space-time scan statistics and mathematical models to confirm the findings. We identified a surprisingly narrow range of critical human population densities between around 3,000 to 7,000 people/km² prone to dengue outbreaks. In the study area, this population density was typical of villages and some peri-urban areas. Scan statistics showed that areas with a high population density or adequate water supply did not experience severe outbreaks. The risk of dengue was higher in rural than in urban areas, largely explained by lack of piped water supply, and in human population densities more often falling within the critical range. Mathematical modeling suggests that simple assumptions regarding area-level vector/host ratios may explain the occurrence of outbreaks. CONCLUSIONS Rural areas may contribute at least as much to the dissemination of dengue fever as cities. Improving water supply and vector control in areas with a human population density critical for dengue transmission could increase the efficiency of control efforts. Please see later in the article for the Editors' Summary.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 336, "doc_id": "2097256", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Combining phosphatidylinositide 3-kinase and MEK 1/2 inhibitors is effective at treating KRAS mutant tumors.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effective Use of PI3K and MEK Inhibitors to Treat Mutant K-Ras G12D and PIK3CA H1047R Murine Lung Cancers\nABSTRACT: Somatic mutations that activate phosphoinositide 3-kinase (PI3K) have been identified in the p110-alpha catalytic subunit (encoded by PIK3CA). They are most frequently observed in two hotspots: the helical domain (E545K and E542K) and the kinase domain (H1047R). Although the p110-alpha mutants are transforming in vitro, their oncogenic potential has not been assessed in genetically engineered mouse models. Furthermore, clinical trials with PI3K inhibitors have recently been initiated, and it is unknown if their efficacy will be restricted to specific, genetically defined malignancies. In this study, we engineered a mouse model of lung adenocarcinomas initiated and maintained by expression of p110-alpha H1047R. Treatment of these tumors with NVP-BEZ235, a dual pan-PI3K and mammalian target of rapamycin (mTOR) inhibitor in clinical development, led to marked tumor regression as shown by positron emission tomography-computed tomography, magnetic resonance imaging and microscopic examination. In contrast, mouse lung cancers driven by mutant Kras did not substantially respond to single-agent NVP-BEZ235. However, when NVP-BEZ235 was combined with a mitogen-activated protein kinase kinase (MEK) inhibitor, ARRY-142886, there was marked synergy in shrinking these Kras-mutant cancers. These in vivo studies suggest that inhibitors of the PI3K-mTOR pathway may be active in cancers with PIK3CA mutations and, when combined with MEK inhibitors, may effectively treat KRAS mutated lung cancers.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"These in vivo studies suggest that inhibitors of the PI3K-mTOR pathway may be active in cancers with PIK3CA mutations and, when combined with MEK inhibitors, may effectively treat KRAS mutated lung cancers.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 275, "doc_id": "4961038", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Taking 400mg of α-tocopheryl acetate in combination with vitamin C reduces the risk of prostate cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Vitamins E and C in the prevention of prostate and total cancer in men: the Physicians' Health Study II randomized controlled trial.\nABSTRACT: CONTEXT Many individuals take vitamins in the hopes of preventing chronic diseases such as cancer, and vitamins E and C are among the most common individual supplements. A large-scale randomized trial suggested that vitamin E may reduce risk of prostate cancer; however, few trials have been powered to address this relationship. No previous trial in men at usual risk has examined vitamin C alone in the prevention of cancer. OBJECTIVE To evaluate whether long-term vitamin E or C supplementation decreases risk of prostate and total cancer events among men. DESIGN, SETTING, AND PARTICIPANTS The Physicians' Health Study II is a randomized, double-blind, placebo-controlled factorial trial of vitamins E and C that began in 1997 and continued until its scheduled completion on August 31, 2007. A total of 14,641 male physicians in the United States initially aged 50 years or older, including 1307 men with a history of prior cancer at randomization, were enrolled. INTERVENTION Individual supplements of 400 IU of vitamin E every other day and 500 mg of vitamin C daily. MAIN OUTCOME MEASURES Prostate and total cancer. RESULTS During a mean follow-up of 8.0 years, there were 1008 confirmed incident cases of prostate cancer and 1943 total cancers. Compared with placebo, vitamin E had no effect on the incidence of prostate cancer (active and placebo vitamin E groups, 9.1 and 9.5 events per 1000 person-years; hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.85-1.09; P = .58) or total cancer (active and placebo vitamin E groups, 17.8 and 17.3 cases per 1000 person-years; HR, 1.04; 95% CI, 0.95-1.13; P = .41). There was also no significant effect of vitamin C on total cancer (active and placebo vitamin C groups, 17.6 and 17.5 events per 1000 person-years; HR, 1.01; 95% [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Compared with placebo, vitamin E had no effect on the incidence of prostate cancer (active and placebo vitamin E groups, 9.1 and 9.5 events per 1000 person-years; hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.85-1.09; P = .58) or total cancer (active and placebo vitamin E groups, 17.8 and 17.3 cases per 1000 person-years; HR, 1.04; 95% CI, 0.95-1.13; P = .41). There was also no significant effect of vitamin C on total cancer (active and placebo vitamin C groups, 17.6 and 17.5 events per 1000 person-years; HR, 1.01; 95% CI, 0.92-1.10; P = .86) or prostate cancer (active and placebo vitamin C groups, 9.4 and 9.2 cases per 1000 person-years; HR, 1.02; 95% CI, 0.90-1.15; P = .80).\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1141, "doc_id": "12009265", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: DUSP4 downregulation deactivates the Ras-ERK pathway\n\nCANDIDATE_ABSTRACT:\nTITLE: Profiling of residual breast cancers after neoadjuvant chemotherapy identifies DUSP4 deficiency as a mechanism of drug resistance\nABSTRACT: Neoadjuvant chemotherapy (NAC) induces a pathological complete response (pCR) in ∼30% of patients with breast cancer. However, many patients have residual cancer after chemotherapy, which correlates with a higher risk of metastatic recurrence and poorer outcome than those who achieve a pCR. We hypothesized that molecular profiling of tumors after NAC would identify genes associated with drug resistance. Digital transcript counting was used to profile surgically resected breast cancers after NAC. Low concentrations of dual specificity protein phosphatase 4 (DUSP4), an ERK phosphatase, correlated with high post-NAC tumor cell proliferation and with basal-like breast cancer (BLBC) status. BLBC had higher DUSP4 promoter methylation and gene expression patterns of Ras-ERK pathway activation relative to other breast cancer subtypes. DUSP4 overexpression increased chemotherapy-induced apoptosis, whereas DUSP4 depletion dampened the response to chemotherapy. Reduced DUSP4 expression in primary tumors after NAC was associated with treatment-refractory high Ki-67 scores and shorter recurrence-free survival. Finally, inhibition of mitogen-activated protein kinase kinase (MEK) synergized with docetaxel treatment in BLBC xenografts. Thus, DUSP4 downregulation activates the Ras-ERK pathway in BLBC, resulting in an attenuated response to anti-cancer chemotherapy.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Thus, DUSP4 downregulation activates the Ras-ERK pathway in BLBC, resulting in an attenuated response to anti-cancer chemotherapy.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 308, "doc_id": "7821634", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Individuals with low serum vitamin D concentrations have decreased risk of multiple sclerosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Past exposure to sun, skin phenotype, and risk of multiple sclerosis: case-control study.\nABSTRACT: OBJECTIVE To examine whether past high sun exposure is associated with a reduced risk of multiple sclerosis. DESIGN Population based case-control study. SETTING Tasmania, latitudes 41-3 degrees S. PARTICIPANTS 136 cases with multiple sclerosis and 272 controls randomly drawn from the community and matched on sex and year of birth. MAIN OUTCOME MEASURE Multiple sclerosis defined by both clinical and magnetic resonance imaging criteria. RESULTS Higher sun exposure when aged 6-15 years (average 2-3 hours or more a day in summer during weekends and holidays) was associated with a decreased risk of multiple sclerosis (adjusted odds ratio 0.31, 95% confidence interval 0.16 to 0.59). Higher exposure in winter seemed more important than higher exposure in summer. Greater actinic damage was also independently associated with a decreased risk of multiple sclerosis (0.32, 0.11 to 0.88 for grades 4-6 disease). A dose-response relation was observed between multiple sclerosis and decreasing sun exposure when aged 6-15 years and with actinic damage. CONCLUSION Higher sun exposure during childhood and early adolescence is associated with a reduced risk of multiple sclerosis. Insufficient ultraviolet radiation may therefore influence the development of multiple sclerosis.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 622, "doc_id": "17000834", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Integrated care is successful at tackling multiple comorbidities.\n\nCANDIDATE_ABSTRACT:\nTITLE: Functional outcomes of multi-condition collaborative care and successful ageing: results of randomised trial\nABSTRACT: OBJECTIVE To evaluate the effectiveness of integrated care for chronic physical diseases and depression in reducing disability and improving quality of life. DESIGN A randomised controlled trial of multi-condition collaborative care for depression and poorly controlled diabetes and/or risk factors for coronary heart disease compared with usual care among middle aged and elderly people SETTING Fourteen primary care clinics in Seattle, Washington. PARTICIPANTS Patients with diabetes or coronary heart disease, or both, and blood pressure above 140/90 mm Hg, low density lipoprotein concentration >3.37 mmol/L, or glycated haemoglobin 8.5% or higher, and PHQ-9 depression scores of ≥ 10. INTERVENTION A 12 month intervention to improve depression, glycaemic control, blood pressure, and lipid control by integrating a \"treat to target\" programme for diabetes and risk factors for coronary heart disease with collaborative care for depression. The intervention combined self management support, monitoring of disease control, and pharmacotherapy to control depression, hyperglycaemia, hypertension, and hyperlipidaemia. MAIN OUTCOME MEASURES Social role disability (Sheehan disability scale), global quality of life rating, and World Health Organization disability assessment schedule (WHODAS-2) scales to measure disabilities in activities of daily living (mobility, self care, household maintenance). RESULTS Of 214 patients enrolled (106 intervention and 108 usual care), disability and quality of life measures were obtained for 97 intervention patients at six months (92%) and 92 at 12 months (87%), and for 96 usual care patients at six months (89%) and 92 at 12 months (85%). Improvements from baseline on the Sheehan disability scale (-0.9, 95% confidence interval -1.5 to -0.2; [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Improvements from baseline on the Sheehan disability scale (-0.9, 95% confidence interval -1.5 to -0.2; P = 0.006) and global quality of life rating (0.7, 0.2 to 1.2; P = 0.005) were significantly greater at six and 12 months in patients in the intervention group.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 648, "doc_id": "15041758", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does superoxide mediate the acute vasoconstrictor effects of angiotensin II : a study in human and porcine arteries?\n\nABSTRACT:\nTo investigate whether superoxide mediates angiotensin (Ang) II-induced vasoconstriction. Human coronary arteries (HCAs), porcine femoral arteries (PFA) and porcine coronary arteries (PCAs) were mounted in organ baths and concentration-response curves to Ang II, the nitric oxide (NO) donor S-nitroso-N-acetylpenicillamine (SNAP) and the NAD(P)H oxidase substrate NADH were constructed in the absence and presence of superoxide inhibiting and activating drugs. Extracellular superoxide was measured using cytochrome c reduction. Ang II constricted both HCAs and PFAs. In HCAs, the NAD(P)H inhibitors diphenyleneiodonium (DPI) and apocynin, and the xanthine oxidase (XO) inhibitor allopurinol, but not the superoxide dismutase (SOD) mimetic tempol or the SOD inhibitor diethyldithiocarbamate (DETCA), reduced this constriction. Catalase potentiated Ang II in HCAs, indicating a vasodilator role for H2O2. DPI, tempol and SOD did not affect Ang II in PFAs. DPI, apocynin and allopurinol relaxed preconstricted HCAs. Although the relaxant effects of the NO donor SNAP in PCAs was reduced by DETCA, indicating that superoxide-induced constrictions depend on NO inactivation, the apocynin-induced relaxations were NO independent. Moreover, NADH relaxed all vessels, and this effect was blocked by KCl but not DPI or NO removal. Xanthine plus XO also relaxed HCAs and PCAs. Incubation of human or porcine arteries with Ang II or NADH did not result in detectable increases of extracellular superoxide within 1 h.", "output": "{\"label\": \"no\", \"rationale\": \"Acute vasoconstriction by Ang II is not mediated via superoxide generated through NAD(P)H oxidase and/or XO activation. Such activation, if occurring, rather results in the generation of the vasodilator H2O2.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 14654755, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Reduced responsiveness to interleukin-2 in regulatory T cells is associated with autoimmune diseases such as Type 1 Diabetes.\n\nCANDIDATE_PASSAGE:\nShared and distinct genetic variants in type 1 diabetes and celiac disease. BACKGROUND Two inflammatory disorders, type 1 diabetes and celiac disease, cosegregate in populations, suggesting a common genetic origin. Since both diseases are associated with the HLA class II genes on chromosome 6p21, we tested whether non-HLA loci are shared. METHODS We evaluated the association between type 1 diabetes and eight loci related to the risk of celiac disease by genotyping and statistical analyses of DNA samples from 8064 patients with type 1 diabetes, 9339 control subjects, and 2828 families providing 3064 parent-child trios (consisting of an affected child and both biologic parents). We also investigated 18 loci associated with type 1 diabetes in 2560 patients with celiac disease and 9339 control subjects. RESULTS Three celiac disease loci--RGS1 on chromosome 1q31, IL18RAP on chromosome 2q12, and TAGAP on chromosome 6q25--were associated with type 1 diabetes (P<1.00x10(-4)). The 32-bp insertion-deletion variant on chromosome 3p21 was newly identified as a type 1 diabetes locus (P=1.81x10(-8)) and was also associated with celiac disease, along with PTPN2 on chromosome 18p11 and CTLA4 on chromosome 2q33, bringing the total number of loci with evidence of a shared association to seven, including SH2B3 on chromosome 12q24. The effects of the IL18RAP and TAGAP alleles confer protection in type 1 diabetes and susceptibility in celiac disease. Loci with distinct effects in the two diseases included INS on chromosome 11p15, IL2RA on chromosome 10p15, and PTPN22 on chromosome 1p13 in type 1 diabetes and IL12A on 3q25 and LPP on 3q28 in celiac disease. CONCLUSIONS A genetic susceptibility to both type 1 diabetes and celiac disease shares common alleles. These data suggest th [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1028", "doc_id": "25571386", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Rapamycin delays aging in fruit flies.\n\nCANDIDATE_PASSAGE:\nHuman iPSC-based modeling of late-onset disease via progerin-induced aging. Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) resets their identity back to an embryonic age and, thus, presents a significant hurdle for modeling late-onset disorders. In this study, we describe a strategy for inducing aging-related features in human iPSC-derived lineages and apply it to the modeling of Parkinson's disease (PD). Our approach involves expression of progerin, a truncated form of lamin A associated with premature aging. We found that expression of progerin in iPSC-derived fibroblasts and neurons induces multiple aging-related markers and characteristics, including dopamine-specific phenotypes such as neuromelanin accumulation. Induced aging in PD iPSC-derived dopamine neurons revealed disease phenotypes that require both aging and genetic susceptibility, such as pronounced dendrite degeneration, progressive loss of tyrosine hydroxylase (TH) expression, and enlarged mitochondria or Lewy-body-precursor inclusions. Thus, our study suggests that progerin-induced aging can be used to reveal late-onset age-related disease features in hiPSC-based disease models.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1015", "doc_id": "11659421", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Fibroblast growth factor 21 protects against atherosclerosis by modulating adiponectin and SREBP2 levels.\n\nCANDIDATE_PASSAGE:\nCD4+ T cell help guides formation of CD103+ lung-resident memory CD8+ T cells during influenza viral infection. Tissue-resident memory T (Trm) cells provide enhanced protection against infection at mucosal sites. Here we found that CD4(+) T cells are important for the formation of functional lung-resident CD8(+) T cells after influenza virus infection. In the absence of CD4(+) T cells, CD8(+) T cells displayed reduced expression of CD103 (Itgae), were mislocalized away from airway epithelia, and demonstrated an impaired ability to recruit CD8(+) T cells to the lung airways upon heterosubtypic challenge. CD4(+) T cell-derived interferon-γ was necessary for generating lung-resident CD103(+) CD8(+) Trm cells. Furthermore, expression of the transcription factor T-bet was increased in \"unhelped\" lung Trm cells, and a reduction in T-bet rescued CD103 expression in the absence of CD4(+) T cell help. Thus, CD4(+) T cell-dependent signals are important to limit expression of T-bet and allow for the development of CD103(+) CD8(+) Trm cells in the lung airways following respiratory infection.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "420", "doc_id": "3835423", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: HAND2 methylation is a key step in early endometrial carcinogenesis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Role of DNA Methylation and Epigenetic Silencing of HAND2 in Endometrial Cancer Development\nABSTRACT: BACKGROUND Endometrial cancer incidence is continuing to rise in the wake of the current ageing and obesity epidemics. Much of the risk for endometrial cancer development is influenced by the environment and lifestyle. Accumulating evidence suggests that the epigenome serves as the interface between the genome and the environment and that hypermethylation of stem cell polycomb group target genes is an epigenetic hallmark of cancer. The objective of this study was to determine the functional role of epigenetic factors in endometrial cancer development. METHODS AND FINDINGS Epigenome-wide methylation analysis of >27,000 CpG sites in endometrial cancer tissue samples (n = 64) and control samples (n = 23) revealed that HAND2 (a gene encoding a transcription factor expressed in the endometrial stroma) is one of the most commonly hypermethylated and silenced genes in endometrial cancer. A novel integrative epigenome-transcriptome-interactome analysis further revealed that HAND2 is the hub of the most highly ranked differential methylation hotspot in endometrial cancer. These findings were validated using candidate gene methylation analysis in multiple clinical sample sets of tissue samples from a total of 272 additional women. Increased HAND2 methylation was a feature of premalignant endometrial lesions and was seen to parallel a decrease in RNA and protein levels. Furthermore, women with high endometrial HAND2 methylation in their premalignant lesions were less likely to respond to progesterone treatment. HAND2 methylation analysis of endometrial secretions collected using high vaginal swabs taken from women with postmenopausal bleeding specifically identified those patients with early stage endometrial cancer with both high sensitivity and high specificity (rece [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"METHODS AND FINDINGS Epigenome-wide methylation analysis of >27,000 CpG sites in endometrial cancer tissue samples (n = 64) and control samples (n = 23) revealed that HAND2 (a gene encoding a transcription factor expressed in the endometrial stroma) is one of the most commonly hypermethylated and silenced genes in endometrial cancer.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 488, "doc_id": "1780819", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Diabetes remission occurs less in people treated with conventional therapy than in people treated with laparoscopic adjustable gastric banding surgery.\n\nCANDIDATE_PASSAGE:\nUniversal voluntary HIV testing with immediate antiretroviral therapy as a strategy for elimination of HIV transmission: a mathematical model. BACKGROUND Roughly 3 million people worldwide were receiving antiretroviral therapy (ART) at the end of 2007, but an estimated 6.7 million were still in need of treatment and a further 2.7 million became infected with HIV in 2007. Prevention efforts might reduce HIV incidence but are unlikely to eliminate this disease. We investigated a theoretical strategy of universal voluntary HIV testing and immediate treatment with ART, and examined the conditions under which the HIV epidemic could be driven towards elimination. METHODS We used mathematical models to explore the effect on the case reproduction number (stochastic model) and long-term dynamics of the HIV epidemic (deterministic transmission model) of testing all people in our test-case community (aged 15 years and older) for HIV every year and starting people on ART immediately after they are diagnosed HIV positive. We used data from South Africa as the test case for a generalised epidemic, and assumed that all HIV transmission was heterosexual. FINDINGS The studied strategy could greatly accelerate the transition from the present endemic phase, in which most adults living with HIV are not receiving ART, to an elimination phase, in which most are on ART, within 5 years. It could reduce HIV incidence and mortality to less than one case per 1000 people per year by 2016, or within 10 years of full implementation of the strategy, and reduce the prevalence of HIV to less than 1% within 50 years. We estimate that in 2032, the yearly cost of the present strategy and the theoretical strategy would both be US$1.7 billion; however, after this time, the cost of the present st [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "340", "doc_id": "374902", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is subendometrial contractility predictive for in vitro fertilization ( IVF ) outcome?\n\nABSTRACT:\nThe aim of the study was to investigate whether endometrial thickness, endometrial pattern, endometrial movement and serum estradiol and progesterone affect the outcome of in vitro fertilization. Prospectively collected data of endometrial thickness, endometrial pattern and subendometrial activity were analyzed in 122 consecutive in vitro fertilization cycles. All measurements were made on the day of hCG administration (day -2), day of embryo transfer (day +2), day +6 and day +12. It would appear that pregnant women tend to have a thicker endometrium on day +12 than non-pregnant women. There appears to be no appreciable difference between pregnant and non-pregnant women in endometrial movement and thickness, nor in serum estradiol and progesterone on day +2 and day +6. In combining three echographic variables (thickness, pattern and movement) and hormone level (estradiol and progesterone), only progesterone on day +12 could be used to predict the outcome.", "output": "{\"label\": \"no\", \"rationale\": \"Subendometrial contractility plays no important role in implantation on the day of embryo transfer or 4 days later.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 11309175, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does shaving the incision site increase the infection rate after spinal surgery?\n\nABSTRACT:\nA prospective randomized clinical study. To determine whether shaving the incision site before spinal surgery causes postsurgical infection. Spine surgeons usually shave the skin of the incision site immediately before surgery is performed. However, evidence from some surgical series suggests that presurgical shaving may increase the postsurgical infection rate. To our knowledge, no previously published studies have addressed this issue. A total of 789 patients scheduled to undergo spinal surgery were randomly allocated into 2 groups: those in whom the site of operation was shaved immediately before surgery (shaved group; 371 patients) and the patients in whom presurgical shaving was not performed (unshaved group; 418 patients). The mean duration of anesthesia and the infection rates in both groups were recorded and compared. The duration of anesthesia did not differ in the 2 groups (P>0.05). A postoperative infection developed in 4 patients in the shaved group and in 1 patient in the nonshaved group (P<0.01).", "output": "{\"label\": \"maybe\", \"rationale\": \"The shaving of the incision site immediately before spinal surgery may increase the rate of postoperative infection.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 17621202, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Increased diastolic blood pressure (DBP) is associated with abdominal aortic aneurysm.\n\nCANDIDATE_ABSTRACT:\nTITLE: Blood pressure and incidence of twelve cardiovascular diseases: lifetime risks, healthy life-years lost, and age-specific associations in 1·25 million people\nABSTRACT: BACKGROUND The associations of blood pressure with the different manifestations of incident cardiovascular disease in a contemporary population have not been compared. In this study, we aimed to analyse the associations of blood pressure with 12 different presentations of cardiovascular disease. METHODS We used linked electronic health records from 1997 to 2010 in the CALIBER (CArdiovascular research using LInked Bespoke studies and Electronic health Records) programme to assemble a cohort of 1·25 million patients, 30 years of age or older and initially free from cardiovascular disease, a fifth of whom received blood pressure-lowering treatments. We studied the heterogeneity in the age-specific associations of clinically measured blood pressure with 12 acute and chronic cardiovascular diseases, and estimated the lifetime risks (up to 95 years of age) and cardiovascular disease-free life-years lost adjusted for other risk factors at index ages 30, 60, and 80 years. This study is registered at ClinicalTrials.gov, number NCT01164371. FINDINGS During 5·2 years median follow-up, we recorded 83,098 initial cardiovascular disease presentations. In each age group, the lowest risk for cardiovascular disease was in people with systolic blood pressure of 90-114 mm Hg and diastolic blood pressure of 60-74 mm Hg, with no evidence of a J-shaped increased risk at lower blood pressures. The effect of high blood pressure varied by cardiovascular disease endpoint, from strongly positive to no effect. Associations with high systolic blood pressure were strongest for intracerebral haemorrhage (hazard ratio 1·44 [95% CI 1·32-1·58]), subarachnoid haemorrhage (1·43 [1·25-1·63]), and stable angina (1·41 [1·36-1·46]), and weakest for abdominal aortic aneurysm (1·08 [1·00-1·17]). Com [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Compared with diastolic blood pressure, raised systolic blood pressure had a greater effect on angina, myocardial infarction, and peripheral arterial disease, whereas raised diastolic blood pressure had a greater effect on abdominal aortic aneurysm than did raised systolic pressure.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 607, "doc_id": "4506414", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Low expression of miR7a does not repress target genes or exert a biological function in ovaries.\n\nCANDIDATE_PASSAGE:\nDownstream of Mutant KRAS, the Transcription Regulator YAP Is Essential for Neoplastic Progression to Pancreatic Ductal Adenocarcinoma Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with poor survival rates and frequently carries oncogenic KRAS mutation. However, KRAS has thus far not been a viable therapeutic target. We found that the abundance of YAP mRNA, which encodes Yes-associated protein (YAP), a protein regulated by the Hippo pathway during tissue development and homeostasis, was increased in human PDAC tissue compared with that in normal pancreatic epithelia. In genetically engineered KrasG12D and KrasG12D:Trp53R172H mouse models, pancreas-specific deletion of Yap halted the progression of early neoplastic lesions to PDAC without affecting normal pancreatic development and endocrine function. Although Yap was dispensable for acinar to ductal metaplasia (ADM), an initial step in the progression to PDAC, Yap was critically required for the proliferation of mutant Kras or Kras:Trp53 neoplastic pancreatic ductal cells in culture and for their growth and progression to invasive PDAC in mice. Yap functioned as a critical transcriptional switch downstream of the oncogenic KRAS–mitogen-activated protein kinase (MAPK) pathway, promoting the expression of genes encoding secretory factors that cumulatively sustained neoplastic proliferation, a tumorigenic stromal response in the tumor microenvironment, and PDAC progression in Kras and Kras:Trp53 mutant pancreas tissue. Together, our findings identified Yap as a critical oncogenic KRAS effector and a promising therapeutic target for PDAC and possibly other types of KRAS-mutant cancers.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "713", "doc_id": "36310858", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: MICAL redox enzymes regulate actin dynamics.\n\nCANDIDATE_PASSAGE:\nPhosphorylation of histone H3(T118) alters nucleosome dynamics and remodeling Nucleosomes, the fundamental units of chromatin structure, are regulators and barriers to transcription, replication and repair. Post-translational modifications (PTMs) of the histone proteins within nucleosomes regulate these DNA processes. Histone H3(T118) is a site of phosphorylation [H3(T118ph)] and is implicated in regulation of transcription and DNA repair. We prepared H3(T118ph) by expressed protein ligation and determined its influence on nucleosome dynamics. We find H3(T118ph) reduces DNA-histone binding by 2 kcal/mol, increases nucleosome mobility by 28-fold and increases DNA accessibility near the dyad region by 6-fold. Moreover, H3(T118ph) increases the rate of hMSH2-hMSH6 nucleosome disassembly and enables nucleosome disassembly by the SWI/SNF chromatin remodeler. These studies suggest that H3(T118ph) directly enhances and may reprogram chromatin remodeling reactions.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "738", "doc_id": "11532659", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does use of hydrophilic guidewires significantly improve technical success rates of peripheral PTA?\n\nABSTRACT:\nTo determine whether the use of hydrophilic guidewires has increased the technical success rate of peripheral percutaneous transluminal angioplasty (PTA).MATERIAL/ We performed 125 procedures and analyzed the technical success rates of PTA using the conventional guidewire first and then if needed, the hydrophilic guidewire for iliac and SFA stenoses or occlusions. Angioplasty was performed on 25 stenosed, 25 occluded iliac arteries and 25 stenosed, 50 occluded femoral arteries. The result was defined as technical success when the lesion was crossed by a guidewire and balloon, then it was dilated with restoration of vessel lumen and less than 30% residual stenosis and the rise in ABI values was at least 0.15 after 24 hours. The technical success rate after PTA of stenosed iliac arteries was achieved in 96% (24/25) using conventional wires and 100% using hydrophilic guidewire; in iliac occlusions, the rates were 60% (15/25) and 96%, respectively; in femoral stenosis - 84% (21/25) and 100%; in occlusions in the first group: lesions<10 cm -64% (16/25) and 96%, in the second group: lesions>10 cm -48% (12/25) and 88%. In the iliac group, there was no significant difference in the success of iliac stenosis PTA. However, there were significant changes in the success rates of PTA performed for SFA stenosis and iliac and SFA occlusions.", "output": "{\"label\": \"maybe\", \"rationale\": \"In summary, we report an overall improvement and high technical success rate for peripherial PTA. The use of hydrophilic guidewires made significant difference to the technical success rate of PTA, especially in occlusion and more complicated lesions.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 16538201, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Pioneer factor OCT3/4 interacts with major chromatin remodeling factors.\n\nCANDIDATE_PASSAGE:\nImpact of aortic stiffness on survival in end-stage renal disease. BACKGROUND Damage to large arteries is a major factor in the high cardiovascular morbidity and mortality of patients with end-stage renal disease (ESRD). Increased arterial stiffness and intima-media thickness, together with increased pulse pressure, are the principal arterial alterations. Whether increased aortic pulse-wave velocity (PWV), a classic marker of increased arterial stiffness, may predict all-cause and/or cardiovascular mortality has never been investigated. METHODS AND RESULTS A cohort of 241 patients with ESRD undergoing hemodialysis was studied between April 1987 and April 1998. The mean duration of follow-up was 72+/-41 months (mean+/-SD). Mean age at entry was 51.5+/-16.3 years. Seventy-three deaths occurred, including 48 cardiovascular and 25 noncardiovascular fatal events. At entry, together with standard clinical and biochemical analyses, patients underwent echocardiography and aortic PWV measured by Doppler ultrasonography. On the basis of Cox analyses, 2 factors emerged as predictors of all-cause and cardiovascular mortality: age and aortic PWV. Hemoglobin and low diastolic pressure interfered to a smaller extent. After adjustment for all the confounding factors, an OR for PWV >12. 0 versus <9.4 m/s was 5.4 (95% CI, 2.4 to 11.9) for all-cause mortality and 5.9 (95% CI, 2.3 to 15.5) for cardiovascular mortality. For each PWV increase of 1 m/s in our study population, all-cause mortality-adjusted OR was 1.39 (95% CI, 1.19 to 1.62). CONCLUSIONS These results provide the first direct evidence that in patients with ESRD, increased aortic stiffness determined by measurement of aortic PWV is a strong independent predictor of all-cause and mainly cardiovascular mortality.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "955", "doc_id": "6525844", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Epidemiological disease burden from noncommunicable diseases is more prevalent in low economic settings.\n\nCANDIDATE_PASSAGE:\nDetermination of Malaria Epidemiological Status in Iran’s Malarious Areas as Baseline Information for Implementation of Malaria Elimination Program in Iran BACKGROUND According to willingness of the Ministry of Health, Iran and presence of appropriate conditions for disease elimination, national malaria control program decided to conduct a research to clarify malaria status in 2007 and to provide required information to perform the elimination program. This review is comprised of the basis of national malaria elimination program in vision of 2025, which was started in 2010. METHODS In this descriptive study, data were analyzed by applications of different variables at district level. All districts in the three south eastern provinces, in which malaria has local transmission, were considered. Malaria cases has been determined and studied based on the national malaria surveillance system. RESULTS Since vivax malaria is predominant in Sistan & Baluchestan Province, number of vivax cases is equal to malaria positive cases approximately. The important point is that Nikshahr contains the maximum number of local vivax cases in this province and the maximum number of falciparum cases is reported from Sarbaz district. Among all districts of Hormozgan Province, no case of autochthonous falciparum was detected except in Bandar Jask and one case in Minab. There was no case of autochthonous falciparum in Kerman Province, except in Kahnoj and Ghale Ganj that each of them had one case in 2007. CONCLUSION It appears that the report of locally transmitted cases in Iran is increasing over the past few years, before starting malaria elimination plan. Since the Afghan refugees started to return to their own country so the main source of reporting of imported malaria cases reduc [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "384", "doc_id": "17433284", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: IRG1 has antiviral effects against neurotropic viruses.\n\nCANDIDATE_PASSAGE:\nA new look at the heart in diabetes mellitus: from ailing to failing This review discusses some of the mechanisms inherent in diabetes that predispose patients to increased cardiac morbidity and mortality. Single photon emission computerized tomography or photon emission tomography with radioactive labeled analogues of norepinephrine have shown that cardiac sympathetic dysfunction and incompetence are early and also late abnormalities in patients with Type I (insulin-dependent) and Type II (non-insulin-dependent) diabetes mellitus. Furthermore, myocardial blood flow assessment with photon emission tomography has shown that in patients without myocardial perfusion deficits, endothelial-dependent vasodilatation is severely reduced in relation to cardiac sympathetic dysfunction. In addition, signs of endothelial activation have also been found early in patients with Type I and Type II diabetes in whom vascular disease has not been clinically detected. This activation in conjunction with glycaemic control is important in determining macrovascular mortality. Cardiac sympathetic dysfunction is partially restored to normal with near normalisation of glycaemia. Interpretations. Recently unrecognized “subtle” changes predispose the heart to failure, after ischaemia-induced remodelling, and arteriosclerotic plaques to instability and rupture. These changes act in conjunction with effects, driven by hyperglycaemia and diabetes, on the endothelium of large blood vessels, e. g. on nitric oxide release or on protein kinase-C β activation. Meticulous glucose control early on and rapid recompensation of hyperglycaemia in patients with acute coronary syndrome are part of a successful intensive multifactorial approach to prevent the heart in diabetes converting from ailing to [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "549", "doc_id": "13448422", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is iL-10 protective in intestinal ischemia reperfusion injury?\n\nABSTRACT:\nIschemia/reperfusion of the small intestine disrupts gut barrier function, increases bacterial translocation, and activates systemic pro-inflammatory responses. Pharmacological treatment with the anti-inflammatory cytokine interleukin-10 (IL-10) following ischemia to muscle reduces the severity of local and systemic inflammation. While endogenous IL-10 is protective in murine models of acute endotoxemia, its physiological role during direct gut injury is unknown. Mice genetically deficient in IL-10 (IL-10(-/-)) and their normal littermates (IL-10(+/+)) underwent 20 to 50 min of gut ischemia by occlusion of the superior mesenteric artery. Both short- and long-term (>16 h) survival after reperfusion of IL-10(-/-) mice was identical to that of the wild-type littermates, with 50% mortality observed at 35 min of occlusion. The small bowel demonstrated discrete gross areas of hemorrhage and ischemia localized to the jejunum. No significant difference in the extent or time for occurrence of macroscopic or microscopic intestinal damage to the small bowel was observed in IL-10(-/-) or IL-10(+/+) mice, despite the marked elevation in serum IL-6.", "output": "{\"label\": \"no\", \"rationale\": \"The absolute serum concentration of IL-6 in the presence or the absence of IL-10 does not affect local or systemic response to ischemic intestinal injury. These results also demonstrate that the anti-inflammatory cytokine IL-10 does not play a significant local or systemic protective role in this model of ischemia/reperfusion.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 12121701, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Side effects associated with antidepressants lower risk of myocardial infarction.\n\nCANDIDATE_PASSAGE:\nPeroxisome proliferator-activated receptor gamma agonists for the Prevention of Adverse events following percutaneous coronary Revascularization--results of the PPAR study. BACKGROUND Patients with metabolic syndrome are at increased risk for cardiovascular complications. We sought to determine whether peroxisome proliferator-activated receptor gamma agonists had any beneficial effect on patients with metabolic syndrome undergoing percutaneous coronary intervention (PCI). METHODS A total of 200 patients with metabolic syndrome undergoing PCI were randomized to rosiglitazone or placebo and followed for 1 year. Carotid intima-medial thickness (CIMT), inflammatory markers, lipid levels, brain natriuretic peptide, and clinical events were measured at baseline, 6 months, and 12 months. RESULTS There was no significant difference in CIMT between the 2 groups. There was no difference in the 12-month composite end point of death, myocardial infarction (MI), stroke, or any recurrent ischemia (31.4% vs 30.2%, P = .99). The rate of death, MI, or stroke at 12 months was numerically lower in the rosiglitazone group (11.9% vs 6.4%, P = .19). There was a trend toward a greater decrease over time in high-sensitivity C-reactive protein values compared with baseline in the group randomized to rosiglitazone versus placebo both at 6 months (-35.4% vs -15.8%, P = .059) and 12 months (-40.0% vs -20.9%, P = .089) and higher change in high-density lipoprotein (+15.5% vs +4.1%, P = .05) and lower triglycerides (-13.9% vs +14.9%, P = .004) in the rosiglitazone arm. There was a trend toward less new onset diabetes in the rosiglitazone group (0% vs 3.3%, P = .081) and no episodes of symptomatic hypoglycemia. There was no excess of new onset of clinical heart failure in the rosiglitazon [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1085", "doc_id": "24150328", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Leuko-reduced blood reduces infectious complications in red blood cell transfusion.\n\nCANDIDATE_PASSAGE:\nClinical outcomes following institution of the Canadian universal leukoreduction program for red blood cell transfusions. CONTEXT A number of countries have implemented a policy of universal leukoreduction of their blood supply, but the potential role of leukoreduction in decreasing postoperative mortality and infection is unclear. OBJECTIVE To evaluate clinical outcomes following adoption of a national universal prestorage leukoreduction program for blood transfusions. DESIGN, SETTING, AND POPULATION Retrospective before-and-after cohort study conducted from August 1998 to August 2000 in 23 academic and community hospitals throughout Canada, enrolling 14 786 patients who received red blood cell transfusions following cardiac surgery or repair of hip fracture, or who required intensive care following a surgical intervention or multiple trauma. INTERVENTION Universal prestorage leukoreduction program introduced by 2 Canadian blood agencies. A total of 6982 patients were enrolled during the control period and 7804 patients were enrolled following prestorage leukoreduction. MAIN OUTCOME MEASURES All-cause in-hospital mortality and serious nosocomial infections (pneumonia, bacteremia, septic shock, all surgical site infections) occurring after first transfusion and at least 2 days after index procedure or intensive care unit admission. Secondary outcomes included rates of posttransfusion fever and antibiotic use. RESULTS Unadjusted in-hospital mortality rates were significantly lower following the introduction of leukoreduction compared with the control period (6.19% vs 7.03%, respectively; P =.04). Compared with the control period, the adjusted odds of death following leukoreduction were reduced (odds ratio [OR], 0.87; 95% confidence interval [CI], 0.75-0.99), [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "693", "doc_id": "24088502", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Satellite cell dysfunction is a key factor in sarcopenia development.\n\nCANDIDATE_PASSAGE:\ntBid induces alterations of mitochondrial fatty acid oxidation flux by malonyl-CoA-independent inhibition of carnitine palmitoyltransferase-1 Recent studies suggest a close relationship between cell metabolism and apoptosis. We have evaluated changes in lipid metabolism on permeabilized hepatocytes treated with truncated Bid (tBid) in the presence of caspase inhibitors and exogenous cytochrome c. The measurement of β-oxidation flux by labeled palmitate demonstrates that tBid inhibits β-oxidation, thereby resulting in the accumulation of palmitoyl-coenzyme A (CoA) and depletion of acetyl-carnitine and acylcarnitines, which is pathognomonic for inhibition of carnitine palmitoyltransferase-1 (CPT-1). We also show that tBid decreases CPT-1 activity by a mechanism independent of both malonyl-CoA, the key inhibitory molecule of CPT-1, and Bak and/or Bax, but dependent on cardiolipin decrease. Overexpression of Bcl-2, which is able to interact with CPT-1, counteracts the effects exerted by tBid on β-oxidation. The unexpected role of tBid in the regulation of lipid β-oxidation suggests a model in which tBid-induced metabolic decline leads to the accumulation of toxic lipid metabolites such as palmitoyl-CoA, which might become participants in the apoptotic pathway.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1065", "doc_id": "35962023", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Epigenetic modulating agents (EMAs) modulate antitumor immune response in a cancer model system.\n\nCANDIDATE_PASSAGE:\nTh2-mediated host protective immunity to intestinal nematode infections. Despite many years of study, relatively little is known about the effector mechanisms that operate against intestine-dwelling nematodes. Most of the current understanding comes from studies of laboratory model systems in rodents. It is clear that when an intestinal helminth infection takes place the immune system generates a strong Th2-mediated response, which regulates a variety of responses characteristic of helminth infections such as eosinophilia, intestinal mastocytosis and elevated IgE production. The ability to modulate the host's immune response in vivo with cytokine-specific monoclonal antibodies and recombinant cytokines, together with the use of animals with disruption of key genes involved in the immune response, have provided powerful tools with which to dissect the potential effector mechanisms operating. In the absence of a T-cell compartment the host is unable to expel the parasite. If a Th1-dominated response is generated, protective immunity is almost universally compromised. Thus, it it would appear that some aspect of a Th2-mediated response controls effector mechanisms. Although it is clear that for some infections the mast cell appears to be involved in protection, probably through the generation of a non-specific inflammatory response, how these cells become activated remains unclear. Data from infections in transgenic animals suggest that activation is not through the high-affinity receptor for IgE. Such studies also call into doubt the importance of conventional interactions between effector leucocytes and antibody. There is little evidence to support a protective role for eosinophilia in any system. New data also imply that, although interleukin 4 (IL-4) is gen [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "385", "doc_id": "23801039", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: 70% of burn patients are admitted for hospitalization and further treatment after appearing at hospital emergency wards or outpatient clinics.\n\nCANDIDATE_PASSAGE:\nABC of burns. Introduction. Burns are one of the most devastating conditions encountered in medicine. The injury represents an assault on all aspects of the patient, from the physical to the psychological. It affects all ages, from babies to elderly people, and is a problem in both the developed and developing world. All of us have experienced the severe pain that even a small burn can bring. However the pain and distress caused by a large burn are not limited to the immediate event. The visible physical and the invisible psychological scars are long lasting and often lead to chronic disability. Burn injuries represent a diverse and varied challenge to medical and paramedical staff. Correct management requires a skilled multidisciplinary approach that addresses all the problems facing a burn patient. This series provides an overview of the most important aspects of burn injuries for hospital and non-hospital healthcare workers.​workers. Figure 1 Top: Child with 70% full thickness burns, which required resuscitation, intensive care support, and extensive debridement and skin grafting. Left: The same child one year later at a burns camp, having made a good recovery. A reasonable outcome is possible ...", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "21", "doc_id": "41493639", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: HIF1A as a major vascular endothelial growth factor regulator: do its polymorphisms have an association with age-related macular degeneration?\n\nABSTRACT:\nTo investigate the association between age-related macular degeneration (AMD) and the polymorphisms of HIF1A, a major vascular epithelial growth factor regulator under hypoxic conditions. The associations of AMD and polymorphisms of genes CFH, SKIV2L and MYRIP were also studied. Prospective study. Eighty-seven AMD patients and 80 healthy subjects admitted to the Department of Ophthalmology at Pamukkale University Hospital, Denizli, Turkey, were included: 45 (52%) had wet type AMD, and 42 (48%) had dry type AMD. Polymorphisms rs1061170 (CFH), rs429608 (SKIV2L), rs2679798 (MYRIP) and both rs11549465 and rs11549467 (HIF1A) were investigated in DNA isolated from peripheral blood samples of the cases and controls by dye-termination DNA sequencing. Genotype distribution of rs1061170 (CFH), rs429608 (SKIV2L), rs2679798 (MYRIP) and both rs11549465 and rs11549467 (HIF1A) in AMD cases and healthy controls; association between genotypes and AMD subtypes. Given the significant difference between the mean age of case and control groups (72.13 ± 5.77 vs. 62.80 ± 5.22, respectively) (P = .000), subsequent analyses were adjusted for age. We found that having at least one C allele for polymorphism rs1061170 increases AMD risk independent of age (OR = 2.42, 95% confidence interval [CI], 1.22-4.81). The ancestral T allele for polymorphism rs1061170 has a protective effect for AMD (OR = 0.53, 95% CI, 0.34-0.83). No statistically significant difference for distributions of other single nucleotide polymorphisms (SNPs) emerged between patients and healthy subjects.", "output": "{\"label\": \"maybe\", \"rationale\": \"No associations appeared between HIF1A SNPs and AMD, which were studied here for the first time; however, polymorphism rs1061170 of the CFH gene is associated with AMD in our population.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 24995509, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Assessing treatment adherence is more beneficial to clinical practice than measuring routine outcomes.\n\nCANDIDATE_PASSAGE:\nhnRNP A1 associates with telomere ends and stimulates telomerase activity. Telomerase is a ribonucleoprotein enzyme complex that reverse-transcribes an integral RNA template to add short DNA repeats to the 3'-ends of telomeres. G-quadruplex structure in a DNA substrate can block its extension by telomerase. We have found that hnRNP A1--which was previously implicated in telomere length regulation--binds to both single-stranded and structured human telomeric repeats, and in the latter case, it disrupts their higher-order structure. Using an in vitro telomerase assay, we observed that depletion of hnRNP A/B proteins from 293 human embryonic kidney cell extracts dramatically reduced telomerase activity, which was fully recovered upon addition of purified recombinant hnRNP A1. This finding suggests that hnRNP A1 functions as an auxiliary, if not essential, factor of telomerase holoenzyme. We further show, using chromatin immunoprecipitation, that hnRNP A1 associates with human telomeres in vivo. We propose that hnRNP A1 stimulates telomere elongation through unwinding of a G-quadruplex or G-G hairpin structure formed at each translocation step.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "134", "doc_id": "1226452", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Exercise increases cancer mortality rates among Chinese citizens.\n\nCANDIDATE_ABSTRACT:\nTITLE: Combined Impact of Lifestyle-Related Factors on Total and Cause-Specific Mortality among Chinese Women: Prospective Cohort Study\nABSTRACT: BACKGROUND Although cigarette smoking, excessive alcohol drinking, obesity, and several other well-studied unhealthy lifestyle-related factors each have been linked to the risk of multiple chronic diseases and premature death, little is known about the combined impact on mortality outcomes, in particular among Chinese and other non-Western populations. The objective of this study was to quantify the overall impact of lifestyle-related factors beyond that of active cigarette smoking and alcohol consumption on all-cause and cause-specific mortality in Chinese women. METHODS AND FINDINGS We used data from the Shanghai Women's Health Study, an ongoing population-based prospective cohort study in China. Participants included 71,243 women aged 40 to 70 years enrolled during 1996-2000 who never smoked or drank alcohol regularly. A healthy lifestyle score was created on the basis of five lifestyle-related factors shown to be independently associated with mortality outcomes (normal weight, lower waist-hip ratio, daily exercise, never exposed to spouse's smoking, higher daily fruit and vegetable intake). The score ranged from zero (least healthy) to five (most healthy) points. During an average follow-up of 9 years, 2,860 deaths occurred, including 775 from cardiovascular disease (CVD) and 1,351 from cancer. Adjusted hazard ratios for mortality decreased progressively with an increasing number of healthy lifestyle factors. Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality. The inverse association between the healthy lifestyle score and mortality was seen consistently regardless of ch [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS In this first study, to our knowledge, to quantify the combined impact of lifestyle-related factors on mortality outcomes in Chinese women, a healthier lifestyle pattern-including being of normal weight, lower central adiposity, participation in physical activity, nonexposure to spousal smoking, and higher fruit and vegetable intake-was associated with reductions in total and cause-specific mortality among lifetime nonsmoking and nondrinking women, supporting the importance of overall lifestyle modification in disease prevention.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 396, "doc_id": "1456068", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nCANDIDATE_PASSAGE:\nThe tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance. Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens. However, signals underlying mTEC development remain largely unclear. Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals. Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment. Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner. These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1004", "doc_id": "2734421", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: In young and middle-aged adults, current or remote uses of ADHD medications increase the risk of serious cardiovascular events.\n\nCANDIDATE_PASSAGE:\nCharacterization of the adipocyte cellular lineage in vivo Mature adipocytes are generated through the proliferation and differentiation of precursor cells. Our previous studies identified adipocyte progenitors in white adipose tissue (WAT) as Lin(-):CD29(+):CD34(+):Sca-1(+):CD24(+) (CD24(+)) cells that are capable of generating functional WAT (ref. ). Here, we employ several Cre recombinase mouse models to identify the adipocyte cellular lineage in vivo. Although it has been proposed that white adipocytes are derived from endothelial and haematopoietic lineages, we find that neither of these lineages label white adipocytes. However, platelet-derived growth factor receptor α (PdgfRα)-Cre trace labels all white adipocytes. Analysis of WAT from PdgfRα-Cre reporter mice identifies CD24(+) and Lin(-):CD29(+):CD34(+):Sca-1(+): CD24(-) (CD24(-)) cells as adipocyte precursors. We show that CD24(+) cells generate the CD24(-) population in vivo and the CD24(-) cells express late markers of adipogenesis. From these data we propose a model where the CD24(+) adipocyte progenitors become further committed to the adipocyte lineage as CD24 expression is lost, generating CD24(-) preadipocytes. This characterization of the adipocyte cellular lineage will facilitate the study of the mechanisms that regulate WAT formation in vivo and WAT mass expansion in obesity.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "590", "doc_id": "18064113", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: There is no known interaction between Pioneer factor OCT3/4 and major chromatin remodeling factors.\n\nCANDIDATE_PASSAGE:\nDietary factors in chronic inflammation: food tolerances and intolerances of a New Zealand Caucasian Crohn's disease population. Diet is known to play a major role in the symptoms of the inflammatory bowel disease, Crohn's disease (CD). Although no single diet is appropriate to all individuals, most CD patients are aware of foods that provide adverse or beneficial effects. This study seeks to categorise foods in relation to their effects on symptoms of CD, in a New Zealand Caucasian population. Four hundred and forty-six subjects from two different centres in New Zealand were recruited into the study. An extensive dietary questionnaire (257 food items in 15 groups) recorded self-reported dietary tolerances and intolerances. Across each of the food groups, there were statistically significant differences among responses to foods. A two-dimensional graphical summary enabled stratification of foods according to the probability that they will be either beneficial or detrimental. A small number of foods are frequently considered to be beneficial, including white fish, salmon and tuna, gluten-free products, oatmeal, bananas, boiled potatoes, sweet potatoes (kumara), pumpkin, soya milk, goat's milk and yoghurt. Foods that are typically considered detrimental include grapefruit, chilli or chilli sauce, corn and corn products, peanuts, cream, salami, curried foods, cola drinks, high energy drinks, beer, and red wine. For a number of the food items, the same item that was beneficial for one group of subjects was detrimental to others; in particular soya milk, goat's milk, yoghurt, oatmeal, kiwifruit, prunes, apple, broccoli, cauliflower, linseed, pumpkin seed, sunflower seed, ginger and ginger products, beef, lamb, liver, and oily fish. It was not possible to identify [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1294", "doc_id": "9244474", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Early patent ductus ateriosus (PDA) screening increases in-hospital mortality.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association Between Early Screening for Patent Ductus Arteriosus and In-Hospital Mortality Among Extremely Preterm Infants.\nABSTRACT: IMPORTANCE There is currently no consensus for the screening and treatment of patent ductus arteriosus (PDA) in extremely preterm infants. Less pharmacological closure and more supportive management have been observed without evidence to support these changes. OBJECTIVE To evaluate the association between early screening echocardiography for PDA and in-hospital mortality. DESIGN, SETTING, AND PARTICIPANTS Comparison of screened and not screened preterm infants enrolled in the EPIPAGE 2 national prospective population-based cohort study that included all preterm infants born at less than 29 weeks of gestation and hospitalized in 68 neonatal intensive care units in France from April through December 2011. Two main analyses were performed to adjust for potential selection bias, one using propensity score matching and one using neonatal unit preference for early screening echocardiography as an instrumental variable. EXPOSURES Early screening echocardiography before day 3 of life. MAIN OUTCOMES AND MEASURES The primary outcome was death between day 3 and discharge. The secondary outcomes were major neonatal morbidities (pulmonary hemorrhage, severe bronchopulmonary dysplasia, severe cerebral lesions, and necrotizing enterocolitis). RESULTS Among the 1513 preterm infants with data available to determine exposure, 847 were screened for PDA and 666 were not; 605 infants from each group could be paired. Exposed infants were treated for PDA more frequently during their hospitalization than nonexposed infants (55.1% vs 43.1%; odds ratio [OR], 1.62 [95% CI, 1.31 to 2.00]; absolute risk reduction [ARR] in events per 100 infants, -12.0 [95% CI, -17.3 to -6.7). Exposed infants had a lower hospital death rate (14.2% vs 18.5% ; OR, 0.73 [95% CI, 0.54 to 0.98]; ARR, 4.3 [95% [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS AND RELEVANCE In this national population-based cohort of extremely preterm infants, screening echocardiography before day 3 of life was associated with lower in-hospital mortality and likelihood of pulmonary hemorrhage but not with differences in necrotizing enterocolitis, severe bronchopulmonary dysplasia, or severe cerebral lesions.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 368, "doc_id": "27099731", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Excess gestational weight gain is associated with obesity-related pregnancy outcomes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Prevalence of cardiovascular disease risk factor in the Chinese population: the 2007-2008 China National Diabetes and Metabolic Disorders Study.\nABSTRACT: AIMS Cardiovascular disease (CVD) is now the most prevalent and debilitating disease affecting the Chinese population. The goal of the present manuscript was to analyse cardiovascular risk factors and the prevalence of non-fatal CVDs from data gathered from the 2007-2008 China National Diabetes and Metabolic Disorders Study. METHODS AND RESULTS A nationally representative sample of 46 239 adults, 20 years of age or older, was randomly recruited using a multistage stratified design method. Lifestyle factors, diagnosis of CVD, stroke, diabetes, and family history of each subject were collected, and an oral glucose tolerance test or a standard meal test was performed. Various non-fatal CVDs were reported by the subjects. SUDAAN software was used to perform all weighted statistical analyses, with P < 0.05 considered statistically significant. The prevalence of coronary heart disease, stroke, and CVDs was 0.74, 1.07, and 1.78% in males; and 0.51, 0.60, and 1.10% in females, respectively. The presence of CVDs increased with age in both males and females. The prevalence of being overweight or obese, hypertension, dyslipidaemia, or hyperglycaemia was 36.67, 30.09, 67.43, and 26.69% in males; and 29.77, 24.79, 63.98, and 23.62% in females, respectively. In the total sample of 46 239 patients, the prevalence of one subject having 1, 2, 3, or ≥4 of the 5 defined risk factors (i.e. smoking, overweight or obese, hypertension, dyslipidaemia, or hyperglycaemia) was 31.17, 27.38, 17.76, and 10.19%, respectively. Following adjustment for gender and age, the odds ratio of CVDs for those who had 1, 2, 3, or ≥4 risk factors was 2.36, 4.24, 4.88, and 7.22, respectively, when compared with patients with no risk factors. CONCLUSION Morbidity attributed to the five defined cardiova [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 394, "doc_id": "2138767", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: MFGE8 regulates fat absorption by binding to av-Beta3 and av-Beta5 integrins.\n\nCANDIDATE_ABSTRACT:\nTITLE: Dynamics of adherens junctions in epithelial establishment, maintenance, and remodeling\nABSTRACT: The epithelial cadherin (E-cadherin)-catenin complex binds to cytoskeletal components and regulatory and signaling molecules to form a mature adherens junction (AJ). This dynamic structure physically connects neighboring epithelial cells, couples intercellular adhesive contacts to the cytoskeleton, and helps define each cell's apical-basal axis. Together these activities coordinate the form, polarity, and function of all cells in an epithelium. Several molecules regulate AJ formation and integrity, including Rho family GTPases and Par polarity proteins. However, only recently, with the development of live-cell imaging, has the extent to which E-cadherin is actively turned over at junctions begun to be appreciated. This turnover contributes to junction formation and to the maintenance of epithelial integrity during tissue homeostasis and remodeling.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 736, "doc_id": "323030", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does tirilazad mesylate improve early cerebral metabolic recovery following compression ischemia in dogs?\n\nABSTRACT:\nTirilazad mesylate (U74006F) has been reported to improve recovery following cerebral ischemia. We conducted a randomized blinded study to determine if the drug would improve immediate metabolic recovery after complete cerebral compression ischemia. Mongrel dogs were anesthetized with pentobarbital and fentanyl and treated with either vehicle (citrate buffer, n = 8) or tirilazad (1.5 mg/kg i.v. plus 0.18 mg/kg/hr, n = 8). Normothermic complete cerebral compression ischemia was produced for 12 minutes by lateral ventricular fluid infusion to raise intracranial pressure above systolic arterial pressure. Cerebral high-energy phosphate concentrations and intracellular pH were measured by phosphorus magnetic resonance spectroscopy. Cerebral blood flow was measured with radiolabeled microspheres, and oxygen consumption was calculated from sagittal sinus blood samples. Somatosensory evoked potentials were measured throughout the experiment. During ischemia, both groups demonstrated complete loss of high-energy phosphates and a fall in intracellular pH (vehicle, 5.76 +/- 0.23; tirilazad, 5.79 +/- 0.26; mean +/- SEM). At 180 minutes of reperfusion, there were no differences between groups in recovery of intracellular pH (vehicle, 6.89 +/- 0.07; tirilazad, 6.88 +/- 0.18), phosphocreatine concentration (vehicle, 89 +/- 16%; tirilazad, 94 +/- 24% of baseline value), oxygen consumption (vehicle, 2.6 +/- 0.2 ml/min/100 g; tirilazad, 1.8 +/- 0.5 ml/min/100 g), or somatosensory evoked potential amplitude (vehicle, 11 +/- 6%; tirilazad, 7 +/- 4% of baseline value). Forebrain blood flow fell below baseline levels at 180 minutes of reperfusion in the tirilazad-treated animals but not in the vehicle-treated dogs (vehicle, 28 +/- 4 ml/min/100 g; tirilazad, 18 +/- 5 ml/min/100 g).", "output": "{\"label\": \"no\", \"rationale\": \"We conclude that tirilazad pretreatment does not improve immediate metabolic recovery 3 hours following 12 minutes of normothermic complete ischemia produced by cerebral compression.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 1412585, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: CCL19 is absent within dLNs.\n\nCANDIDATE_PASSAGE:\nImmobilized chemokine fields and soluble chemokine gradients cooperatively shape migration patterns of dendritic cells. Chemokines orchestrate immune cell trafficking by eliciting either directed or random migration and by activating integrins in order to induce cell adhesion. Analyzing dendritic cell (DC) migration, we showed that these distinct cellular responses depended on the mode of chemokine presentation within tissues. The surface-immobilized form of the chemokine CCL21, the heparan sulfate-anchoring ligand of the CC-chemokine receptor 7 (CCR7), caused random movement of DCs that was confined to the chemokine-presenting surface because it triggered integrin-mediated adhesion. Upon direct contact with CCL21, DCs truncated the anchoring residues of CCL21, thereby releasing it from the solid phase. Soluble CCL21 functionally resembles the second CCR7 ligand, CCL19, which lacks anchoring residues and forms soluble gradients. Both soluble CCR7 ligands triggered chemotactic movement, but not surface adhesion. Adhesive random migration and directional steering cooperate to produce dynamic but spatially restricted locomotion patterns closely resembling the cellular dynamics observed in secondary lymphoid organs.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "198", "doc_id": "2177022", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Infection of human T-cell lymphotropic virus type 1 is most frequent in individuals of African origin.\n\nCANDIDATE_PASSAGE:\nImmune activation and HIV persistence: implications for curative approaches to HIV infection. Despite complete or near-complete suppression of human immunodeficiency virus (HIV) replication with combination antiretroviral therapy, both HIV and chronic inflammation/immune dysfunction persist indefinitely. Untangling the association between the virus and the host immune environment during therapy might lead to novel interventions aimed at either curing the infection or preventing the development of inflammation-associated end-organ disease. Chronic inflammation and immune dysfunction might lead to HIV persistence by causing virus production, generating new target cells, enabling infecting of activated and resting target cells, altering the migration patterns of susceptible target cells, increasing the proliferation of infected cells, and preventing normal HIV-specific clearance mechanisms from function. Chronic HIV production or replication might contribute to persistent inflammation and immune dysfunction. The rapidly evolving data on these issues strongly suggest that a vicious cycle might exist in which HIV persistence causes inflammation that in turn contributes to HIV persistence.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "628", "doc_id": "44562058", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Surgical treatment is not superior to non-surgical in treating adults with displaced fractures of the proximal humerus.\n\nCANDIDATE_ABSTRACT:\nTITLE: Surgical vs nonsurgical treatment of adults with displaced fractures of the proximal humerus: the PROFHER randomized clinical trial.\nABSTRACT: IMPORTANCE The need for surgery for the majority of patients with displaced proximal humeral fractures is unclear, but its use is increasing. OBJECTIVE To evaluate the clinical effectiveness of surgical vs nonsurgical treatment for adults with displaced fractures of the proximal humerus involving the surgical neck. DESIGN, SETTING, AND PARTICIPANTS A pragmatic, multicenter, parallel-group, randomized clinical trial, the Proximal Fracture of the Humerus Evaluation by Randomization (PROFHER) trial, recruited 250 patients aged 16 years or older (mean age, 66 years [range, 24-92 years]; 192 [77%] were female; and 249 [99.6%] were white) who presented at the orthopedic departments of 32 acute UK National Health Service hospitals between September 2008 and April 2011 within 3 weeks after sustaining a displaced fracture of the proximal humerus involving the surgical neck. Patients were followed up for 2 years (up to April 2013) and 215 had complete follow-up data. The data for 231 patients (114 in surgical group and 117 in nonsurgical group) were included in the primary analysis. INTERVENTIONS Fracture fixation or humeral head replacement were performed by surgeons experienced in these techniques. Nonsurgical treatment was sling immobilization. Standardized outpatient and community-based rehabilitation was provided to both groups. MAIN OUTCOMES AND MEASURES Primary outcome was the Oxford Shoulder Score (range, 0-48; higher scores indicate better outcomes) assessed during a 2-year period, with assessment and data collection at 6, 12, and 24 months. Sample size was based on a minimal clinically important difference of 5 points for the Oxford Shoulder Score. Secondary outcomes were the Short-Form 12 (SF-12), complications, subsequent therapy, and mortality. RESULTS Th [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"There were also no significant between-group differences over 2 years in the mean SF-12 physical component score (surgical group: 1.77 points higher [95% CI, -0.84 to 4.39 points];\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1115, "doc_id": "44048701", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Integrated care is ineffective at tackling multiple comorbidities.\n\nCANDIDATE_ABSTRACT:\nTITLE: Functional outcomes of multi-condition collaborative care and successful ageing: results of randomised trial\nABSTRACT: OBJECTIVE To evaluate the effectiveness of integrated care for chronic physical diseases and depression in reducing disability and improving quality of life. DESIGN A randomised controlled trial of multi-condition collaborative care for depression and poorly controlled diabetes and/or risk factors for coronary heart disease compared with usual care among middle aged and elderly people SETTING Fourteen primary care clinics in Seattle, Washington. PARTICIPANTS Patients with diabetes or coronary heart disease, or both, and blood pressure above 140/90 mm Hg, low density lipoprotein concentration >3.37 mmol/L, or glycated haemoglobin 8.5% or higher, and PHQ-9 depression scores of ≥ 10. INTERVENTION A 12 month intervention to improve depression, glycaemic control, blood pressure, and lipid control by integrating a \"treat to target\" programme for diabetes and risk factors for coronary heart disease with collaborative care for depression. The intervention combined self management support, monitoring of disease control, and pharmacotherapy to control depression, hyperglycaemia, hypertension, and hyperlipidaemia. MAIN OUTCOME MEASURES Social role disability (Sheehan disability scale), global quality of life rating, and World Health Organization disability assessment schedule (WHODAS-2) scales to measure disabilities in activities of daily living (mobility, self care, household maintenance). RESULTS Of 214 patients enrolled (106 intervention and 108 usual care), disability and quality of life measures were obtained for 97 intervention patients at six months (92%) and 92 at 12 months (87%), and for 96 usual care patients at six months (89%) and 92 at 12 months (85%). Improvements from baseline on the Sheehan disability scale (-0.9, 95% confidence interval -1.5 to -0.2; [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Integrated care that covers chronic physical disease and comorbid depression can reduce social role disability and enhance global quality of life.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 647, "doc_id": "15041758", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Increased microtubule acetylation exacerbates LRRK2 Roc-COR domain mutation induced locomotor deficits.\n\nCANDIDATE_ABSTRACT:\nTITLE: Increasing microtubule acetylation rescues axonal transport and locomotor deficits caused by LRRK2 Roc-COR domain mutations\nABSTRACT: Leucine-rich repeat kinase 2 (LRRK2) mutations are the most common genetic cause of Parkinson's disease. LRRK2 is a multifunctional protein affecting many cellular processes and has been described to bind microtubules. Defective microtubule-based axonal transport is hypothesized to contribute to Parkinson's disease, but whether LRRK2 mutations affect this process to mediate pathogenesis is not known. Here we find that LRRK2 containing pathogenic Roc-COR domain mutations (R1441C, Y1699C) preferentially associates with deacetylated microtubules, and inhibits axonal transport in primary neurons and in Drosophila, causing locomotor deficits in vivo. In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport. In vivo knockdown of the deacetylases HDAC6 and Sirt2, or administration of TSA rescues both axonal transport and locomotor behavior. Thus, this study reveals a pathogenic mechanism and a potential intervention for Parkinson's disease.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 612, "doc_id": "9638032", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is the stimulation of mononuclear cells from patients with rheumatoid arthritis to degrade articular cartilage modulated by cartilage itself?\n\nABSTRACT:\nTo study the modulation of mononuclear cell (MNC) activity in patients with rheumatoid arthritis (RA) by constituents released from human articular cartilage, which may be present in vivo during early events of the disease, when articular cartilage is not only mildly damaged. In an attempt to stimulate RA MNC, cells were co-cultured with healthy or mildly damaged articular cartilage tissue. In addition, because of the reported cross-reactivity between cartilage constituents and mycobacterial heat-shock protein (hsp60), RA MNC sensitized with hsp60 were also co-cultured with cartilage tissue. Activation of the RA MNC was assessed by analysing the production of catabolic factors involved in joint damage. For this purpose culture supernatants of the treated RA MNC, comprising the catabolic factors, were added to freshly isolated articular cartilage explants. As a read out for catabolic activity, proteoglycan (PG) turnover by the explants was determined. Spontaneous activity of untreated RA MNC caused inhibition of PG synthesis and increased PG release upon addition of their culture supernatants to the cartilage explants. This MNC activity was not enhanced by the constituents released from healthy or mildly damaged cartilage tissue, whereas sensitization of RA MNC with hsp60 resulted in a 40% enhanced inhibition of PG synthesis. However, even under these pre-activated conditions no reactivity towards the cartilage constituents could be observed.", "output": "{\"label\": \"no\", \"rationale\": \"Cartilage constituents released from mildly damaged cartilage tissue, as may be present during the early events of RA. do not modulate the catabolic activity of RA MNC.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 8737724, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: There is no known interaction between Pioneer factor OCT3/4 and major chromatin remodeling factors.\n\nCANDIDATE_PASSAGE:\nAnti-alphav integrin monoclonal antibody intetumumab enhances the efficacy of radiation therapy and reduces metastasis of human cancer xenografts in nude rats. We previously reported that intetumumab (CNTO 95), a fully human anti-αv integrin monoclonal antibody, is a radiosensitizer in mice with xenograft tumors. Because intetumumab does not cross-react with mouse integrins, but has cross-reactivity with rat integrins, we next studied the potential combined use of radiation therapy and intetumumab in human cancer xenograft models in nude rats to assess effects on both tumor cells and the tumor microenvironment. Nude rats bearing human head and neck cancer and non-small cell lung cancer (NSCLC) xenografts were treated with intetumumab and fractionated local tumor radiotherapy. Effects on tumor growth and metastasis, blood perfusion, oxygenation, and gastrointestinal toxicity were studied. Intetumumab alone had a moderate effect on tumor growth. When combined with fractionated radiation therapy, intetumumab significantly inhibited tumor growth and produced a tumor response rate that was significantly better than with radiation therapy alone. Treatment with intetumumab also significantly reduced lung metastasis in the A549 NSCLC xenograft model. The oxygenation and blood perfusion in xenograft tumors measured by microbubble-enhanced ultrasound imaging were substantially increased after treatment with intetumumab. The combined use of intetumumab and radiation therapy reduced the microvessel density and increased apoptosis in tumor cells and the tumor microenvironment. Toxicity studies showed that treatment with intetumumab did not cause the histopathologic changes in the lungs and did not sensitize the sensitive gastrointestinal epithelium to the effect of radia [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1294", "doc_id": "7986878", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Mutant mice lacking SVCT2 have severely reduced ascorbic acid levels in both brain and adrenals.\n\nCANDIDATE_ABSTRACT:\nTITLE: Array-based Comparative Genomic Hybridization for Genome-Wide Screening of DNA Copy Number in Bladder Tumors\nABSTRACT: Genome-wide copy number profiles were characterized in 41 primary bladder tumors using array-based comparative genomic hybridization (array CGH). In addition to previously identified alterations in large chromosomal regions, alterations were identified in many small genomic regions, some with high-level amplifications or homozygous deletions. High-level amplifications were detected for 192 genomic clones, most frequently at 6p22.3 (E2F3), 8p12 (FGFR1), 8q22.2 (CMYC), 11q13 (CCND1, EMS1, INT2), and 19q13.1 (CCNE). Homozygous deletions were detected in 51 genomic clones, with four showing deletions in more than one case: two clones mapping to 9p21.3 (CDKN2A/p16, in nine cases), one at 8p23.1 (three cases), and one at 11p13 (two cases). Significant correlations were observed between copy number gain of clones containing CCNE1 and gain of ERBB2, and between gain of CCND1 and deletion of TP53. In addition, there was a significant complementary association between gain of CCND1 and gain of E2F3. Although there was no significant relationship between copy number changes and tumor stage or grade, the linked behavior among genomic loci suggests that array CGH will be increasingly important in understanding pathways critical to bladder tumor biology.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 812, "doc_id": "2402323", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Mice that lack Interferon-γ or its receptor exhibit high resistance to experimental autoimmune myocarditis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Lethal autoimmune myocarditis in interferon-gamma receptor-deficient mice: enhanced disease severity by impaired inducible nitric oxide synthase induction.\nABSTRACT: BACKGROUND Interferon-gamma (IFN-gamma) is an essential cytokine in the regulation of inflammatory responses in autoimmune diseases. Little is known about its role in inflammatory heart disease. METHODS AND RESULTS We showed that IFN-gamma receptor-deficient mice (IFN-gammaR(-/-)) on a BALB/c background immunized with a peptide derived from cardiac alpha-myosin heavy chain develop severe myocarditis with high mortality. Although myocarditis subsided in wild-type mice after 3 weeks, IFN-gammaR(-/-) mice showed persistent disease. The persistent inflammation was accompanied by vigorous in vitro CD4 T-cell responses and impaired inducible nitric oxide synthase expression, together with evidence of impaired nitric oxide production in IFN-gammaR(-/-) hearts. Treatment of wild-type mice with the nitric oxide synthetase inhibitor N:-nitro-l-arginine-methyl-ester enhanced in vitro CD4 T-cell proliferation and prevented healing of myocarditis. CONCLUSIONS Our data provide evidence that IFN-gamma protects mice from lethal autoimmune myocarditis by inducing the expression of inducible nitric oxide synthase followed by the downregulation of T-cell responses.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Our data provide evidence that IFN-gamma protects mice from lethal autoimmune myocarditis by inducing the expression of inducible nitric oxide synthase followed by the downregulation of T-cell responses.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 781, "doc_id": "24338780", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: One in five surgical randomized controlled trials are discontinued early.\n\nCANDIDATE_ABSTRACT:\nTITLE: Discontinuation and non-publication of surgical randomised controlled trials: observational study\nABSTRACT: OBJECTIVE To determine the rate of early discontinuation and non-publication of randomised controlled trials involving patients undergoing surgery. DESIGN Cross sectional observational study of registered and published trials. SETTING Randomised controlled trials of interventions in patients undergoing a surgical procedure. DATA SOURCES The ClinicalTrials.gov database was searched for interventional trials registered between January 2008 and December 2009 using the keyword \"surgery\". Recruitment status was extracted from the ClinicalTrials.gov database. A systematic search for studies published in peer reviewed journals was performed; if they were not found, results posted on the ClinicalTrials.gov results database were sought. Email queries were sent to trial investigators of discontinued and unpublished completed trials if no reason for the respective status was disclosed. MAIN OUTCOME MEASURES Trial discontinuation before completion and non-publication after completion. Logistic regression was used to determine the effect of funding source on publication status, with adjustment for intervention type and trial size. RESULTS Of 818 registered trials found using the keyword \"surgery\", 395 met the inclusion criteria. Of these, 21% (81/395) were discontinued early, most commonly owing to poor recruitment (44%, 36/81). The remaining 314 (79%) trials proceeded to completion, with a publication rate of 66% (208/314) at a median time of 4.9 (interquartile range 4.0-6.0) years from study completion to publication search. A further 6% (20/314) of studies presented results on ClinicalTrials.gov without a corresponding peer reviewed publication. Industry funding did not affect the rate of discontinuation (adjusted odds ratio 0.91, 95% confidence interval 0.54 to 1.55) [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS One in five surgical randomised controlled trials are discontinued early, one in three completed trials remain unpublished, and investigators of unpublished studies are frequently not contactable.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 885, "doc_id": "6477536", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Monoclonal antibody targeting of N-cadherin inhibits metastasis.\n\nCANDIDATE_PASSAGE:\nMonoclonal antibody targeting of N-cadherin inhibits prostate cancer growth, metastasis and castration resistance The transition from androgen-dependent to castration-resistant prostate cancer (CRPC) is a lethal event of uncertain molecular etiology. Comparing gene expression in isogenic androgen-dependent and CRPC xenografts, we found a reproducible increase in N-cadherin expression, which was also elevated in primary and metastatic tumors of individuals with CRPC. Ectopic expression of N-cadherin in nonmetastatic, androgen-dependent prostate cancer models caused castration resistance, invasion and metastasis. Monoclonal antibodies against the ectodomain of N-cadherin reduced proliferation, adhesion and invasion of prostate cancer cells in vitro. In vivo, these antibodies slowed the growth of multiple established CRPC xenografts, blocked local invasion and metastasis and, at higher doses, led to complete regression. N-cadherin–specific antibodies markedly delayed the time to emergence of castration resistance, markedly affected tumor histology and angiogenesis, and reduced both AKT serine-threonine kinase activity and serum interleukin-8 (IL-8) secretion. These data indicate that N-cadherin is a major cause of both prostate cancer metastasis and castration resistance. Therapeutic targeting of this factor with monoclonal antibodies may have considerable clinical benefit.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "805", "doc_id": "22180793", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Higher plasma levels of I-carnitine, when associated with trimethylamine N-oxide, are negatively correlated with cardiovascular events in humans.\n\nCANDIDATE_PASSAGE:\nInflammatory biomarkers and exacerbations in chronic obstructive pulmonary disease. IMPORTANCE Exacerbations of respiratory symptoms in chronic obstructive pulmonary disease (COPD) have profound and long-lasting adverse effects on patients. OBJECTIVE To test the hypothesis that elevated levels of inflammatory biomarkers in individuals with stable COPD are associated with an increased risk of having exacerbations. DESIGN, SETTING, AND PARTICIPANTS Prospective cohort study examining 61,650 participants with spirometry measurements from the Copenhagen City Heart Study (2001-2003) and the Copenhagen General Population Study (2003-2008). Of these, 6574 had COPD, defined as a ratio between forced expiratory volume in 1 second (FEV1) and forced vital capacity below 0.7. MAIN OUTCOMES AND MEASURES Baseline levels of C-reactive protein (CRP) and fibrinogen and leukocyte count were measured in participants at a time when they were not experiencing symptoms of exacerbations. Exacerbations were recorded and defined as short-course treatment with oral corticosteroids alone or in combination with an antibiotic or as a hospital admission due to COPD. Levels of CRP and fibrinogen and leukocyte count were defined as high or low according to cut points of 3 mg/L, 14 μmol/L, and 9 ×10(9)/L, respectively. RESULTS During follow-up, 3083 exacerbations were recorded (mean, 0.5/participant). In the first year of follow-up, multivariable-adjusted odds ratios for having frequent exacerbations were 1.2 (95% CI, 0.7-2.2; 17 events/1000 person-years) for individuals with 1 high biomarker, 1.7 (95% CI, 0.9-3.2; 32 events/1000 person-years) for individuals with 2 high biomarkers, and 3.7 (95% CI, 1.9-7.4; 81 events/1000 person-years) for individuals with 3 high biomarkers compared with in [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "523", "doc_id": "29564505", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The DESMOND program caused substantial weight loss in most participants.\n\nCANDIDATE_ABSTRACT:\nTITLE: Junctional actin assembly is mediated by Formin-like 2 downstream of Rac1\nABSTRACT: Epithelial integrity is vitally important, and its deregulation causes early stage cancer. De novo formation of an adherens junction (AJ) between single epithelial cells requires coordinated, spatial actin dynamics, but the mechanisms steering nascent actin polymerization for cell-cell adhesion initiation are not well understood. Here we investigated real-time actin assembly during daughter cell-cell adhesion formation in human breast epithelial cells in 3D environments. We identify formin-like 2 (FMNL2) as being specifically required for actin assembly and turnover at newly formed cell-cell contacts as well as for human epithelial lumen formation. FMNL2 associates with components of the AJ complex involving Rac1 activity and the FMNL2 C terminus. Optogenetic control of Rac1 in living cells rapidly drove FMNL2 to epithelial cell-cell contact zones. Furthermore, Rac1-induced actin assembly and subsequent AJ formation critically depends on FMNL2. These data uncover FMNL2 as a driver for human epithelial AJ formation downstream of Rac1.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1156, "doc_id": "2576811", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Inositol lipid 3-phosphatase PTEN converts Ptdlns(3,4)P 2 into phosphatidylinositol 4-phosphate.\n\nCANDIDATE_PASSAGE:\nPTEN Regulates PI(3,4)P2 Signaling Downstream of Class I PI3K The PI3K signaling pathway regulates cell growth and movement and is heavily mutated in cancer. Class I PI3Ks synthesize the lipid messenger PI(3,4,5)P3. PI(3,4,5)P3 can be dephosphorylated by 3- or 5-phosphatases, the latter producing PI(3,4)P2. The PTEN tumor suppressor is thought to function primarily as a PI(3,4,5)P3 3-phosphatase, limiting activation of this pathway. Here we show that PTEN also functions as a PI(3,4)P2 3-phosphatase, both in vitro and in vivo. PTEN is a major PI(3,4)P2 phosphatase in Mcf10a cytosol, and loss of PTEN and INPP4B, a known PI(3,4)P2 4-phosphatase, leads to synergistic accumulation of PI(3,4)P2, which correlated with increased invadopodia in epidermal growth factor (EGF)-stimulated cells. PTEN deletion increased PI(3,4)P2 levels in a mouse model of prostate cancer, and it inversely correlated with PI(3,4)P2 levels across several EGF-stimulated prostate and breast cancer lines. These results point to a role for PI(3,4)P2 in the phenotype caused by loss-of-function mutations or deletions in PTEN.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "636", "doc_id": "24294572", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Febrile seizures increase the threshold for development of epilepsy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Febrile seizures in the developing brain result in persistent modification of neuronal excitability in limbic circuits\nABSTRACT: Febrile (fever-induced) seizures affect 3–5% of infants and young children. Despite the high incidence of febrile seizures, their contribution to the development of epilepsy later in life has remained controversial. Combining a new rat model of complex febrile seizures and patch clamp techniques, we determined that hyperthermia-induced seizures in the immature rat cause a selective presynaptic increase in inhibitory synaptic transmission in the hippocampus that lasts into adulthood. The long-lasting nature of these potent alterations in synaptic communication after febrile seizures does not support the prevalent view of the 'benign' nature of early-life febrile convulsions.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 410, "doc_id": "14924526", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Weighed food records (WFR) result in poor completion since they're costly to run and impose high participant burden.\n\nCANDIDATE_PASSAGE:\nIn vitro splicing pathways of pre-mRNAs containing multiple intervening sequences? We analyzed the in vitro splicing pathways of three multi-intervening-sequence (IVS) pre-mRNAs: human beta-globin, which contains two IVSs (K. M. Lang, V. L. van Santen, and R. A. Spritz, EMBO J. 4:1991-1996, 1985); rat alpha-lactalbumin, which contains three IVSs; and murine interleukin-3, which contains four IVSs. We found that there are highly preferred pathways of IVS removal from these multi-IVS pre-mRNAs in vitro. The three IVSs of rat alpha-lactalbumin pre-mRNA were excised sequentially from 5' to 3'; in most molecules, IVS1 was removed first, followed by IVS2 and finally by IVS3. The splicing pathway of interleukin-3 pre-mRNA in vitro was more complex. The four IVSs were excised in a highly preferred temporal order, but the order was not strictly sequential or directional. In most molecules, IVS1 and IVS4 were removed first, either simultaneously or in rapid succession. Subsequently, IVS2 was excised, followed by IVS3. The observed splicing pathways apparently resulted from differences in lag times and maximum excision rates of the different IVSs. We detected no exon skipping during splicing of these transcripts in vitro. These observations have implication for proposed models of splice site selection.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1375", "doc_id": "20374609", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Rapid phosphotransfer rates govern fidelity in two component systems\n\nCANDIDATE_PASSAGE:\nMechanisms of endocytosis. Endocytic mechanisms control the lipid and protein composition of the plasma membrane, thereby regulating how cells interact with their environments. Here, we review what is known about mammalian endocytic mechanisms, with focus on the cellular proteins that control these events. We discuss the well-studied clathrin-mediated endocytic mechanisms and dissect endocytic pathways that proceed independently of clathrin. These clathrin-independent pathways include the CLIC/GEEC endocytic pathway, arf6-dependent endocytosis, flotillin-dependent endocytosis, macropinocytosis, circular doral ruffles, phagocytosis, and trans-endocytosis. We also critically review the role of caveolae and caveolin1 in endocytosis. We highlight the roles of lipids, membrane curvature-modulating proteins, small G proteins, actin, and dynamin in endocytic pathways. We discuss the functional relevance of distinct endocytic pathways and emphasize the importance of studying these pathways to understand human disease processes.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1019", "doc_id": "16319097", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Aged patients are more susceptible to ischaemia/reperfusion injury.\n\nCANDIDATE_PASSAGE:\nERS/ESTS clinical guidelines on fitness for radical therapy in lung cancer patients (surgery and chemo-radiotherapy). A collaboration of multidisciplinary experts on the functional evaluation of lung cancer patients has been facilitated by the European Respiratory Society (ERS) and the European Society of Thoracic Surgery (ESTS), in order to draw up recommendations and provide clinicians with clear, up-to-date guidelines on fitness for surgery and chemo-radiotherapy. The subject was divided into different topics, which were then assigned to at least two experts. The authors searched the literature according to their own strategies, with no central literature review being performed. The draft reports written by the experts on each topic were reviewed, discussed and voted on by the entire expert panel. The evidence supporting each recommendation was summarised, and graded as described by the Scottish Intercollegiate Guidelines Network Grading Review Group. Clinical practice guidelines were generated and finalized in a functional algorithm for risk stratification of the lung resection candidates, emphasising cardiological evaluation, forced expiratory volume in 1 s, systematic carbon monoxide lung diffusion capacity and exercise testing. Contrary to lung resection, for which the scientific evidences are more robust, we were unable to recommend any specific test, cut-off value, or algorithm before chemo-radiotherapy due to the lack of data. We recommend that lung cancer patients should be managed in specialised settings by multidisciplinary teams.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "92", "doc_id": "14118484", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Pseudogene PTENP1 regulates the expression of PTEN by functioning as an miRNA decoy.\n\nCANDIDATE_PASSAGE:\nThe p38/MK2-Driven Exchange between Tristetraprolin and HuR Regulates AU–Rich Element–Dependent Translation TNF expression of macrophages is under stringent translational control that depends on the p38 MAPK/MK2 pathway and the AU-rich element (ARE) in the TNF mRNA. Here, we elucidate the molecular mechanism of phosphorylation-regulated translation of TNF. We demonstrate that translation of the TNF-precursor at the ER requires expression of the ARE-binding and -stabilizing factor human antigen R (HuR) together with either activity of the p38 MAPK/MK2 pathway or the absence of the ARE-binding and -destabilizing factor tristetraprolin (TTP). We show that phosphorylation of TTP by MK2 decreases its affinity to the ARE, inhibits its ability to replace HuR, and permits HuR-mediated initiation of translation of TNF mRNA. Since translation of TTP's own mRNA is also regulated by this mechanism, an intrinsic feedback control of the inflammatory response is ensured. The phosphorylation-regulated TTP/HuR exchange at target mRNAs provides a reversible switch between unstable/non-translatable and stable/efficiently translated mRNAs.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "985", "doc_id": "8698857", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: siRNA knockdown of A20 slows tumor progression in an in vivo murine xenograft model.\n\nCANDIDATE_PASSAGE:\n(99m)Tc-HisoDGR as a Potential SPECT Probe for Orthotopic Glioma Detection via Targeting of Integrin α5β1. Integrins, a large family of cell adhesion receptors, have been shown to play an important role for glioma proliferation and invasion. Several integrin receptors, including αvβ3, αvβ5, and α5β1, have generated clinical interest for glioma diagnosis and antitumor therapy. Integrin α5β1 has been highlighted as a prognostic and diagnostic marker in glioma, and its expression is correlated with a worse prognosis in high-grade glioma. However, unlike extensively studied integrins αvβ3 and αvβ5, very few integrin α5β1-specific radiotracers have been reported. Developing α5β1-specific radiotracers may provide alternative diagnosis and evaluation options in addition to well-studied αvβ3/αvβ5-specific tracers, and they may add new documents for profiling tumor progression. Here, a novel integrin α5β1-specific probe (99m)Tc-HisoDGR was fabricated for SPECT (single-photon emission computed tomography) imaging of glioma. To confirm its selective targeting of integrin α5β1 in vivo, the mouse models of α5β1-positive U87MG human glioma were subjected to SPECT/CT scans, and biodistribution experiments and blocking studies were performed. Small-animal SPECT/CT imaging experiments demonstrated that the tumors were clearly visualized in both subcutaneous and orthotopic glioma tumor models with clear background at 0.5, 1, and 2 h p.i. The tumor accumulation of (99m)Tc-HisoDGR showed significant reduction when excess cold isoDGR peptide was coinjected, suggesting that the tumor uptake was specifically mediated. Our work revealed that (99m)Tc-HisoDGR represented a powerful molecular probe for integrin α5β1-positive cancer imaging; moreover, it might be a promising tool for e [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1404", "doc_id": "38808600", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Incidence of sepsis has fallen substantially from 2009 to 2014.\n\nCANDIDATE_PASSAGE:\nTherapeutic equivalence of alendronate 70 mg once-weekly and alendronate 10 mg daily in the treatment of osteoporosis. Alendronate Once-Weekly Study Group. Dosing convenience is a key element in the effective management of any chronic disease, and is particularly important in the long-term management of osteoporosis. Less frequent dosing with any medication may enhance compliance, thereby maximizing the effectiveness of therapy. Animal data support the rationale that once-weekly dosing with alendronate 70 mg (7 times the daily oral treatment dose) could provide similar efficacy to daily dosing with alendronate 10 mg due to its long duration of effect in bone. In addition, dog studies suggest that the potential for esophageal irritation, observed with daily oral bisphosphonates, may be substantially reduced with once-weekly dosing. This dosing regimen would provide patients with increased convenience and would be likely to enhance patient compliance. We compared the efficacy and safety of treatment with oral once-weekly alendronate 70 mg (N=519), twice-weekly alendronate 35 mg (N=369), and daily alendronate 10 mg (N=370) in a one-year, double-blind, multicenter study of postmenopausal women (ages 42 to 95) with osteoporosis (bone mineral density [BMD] of either lumbar spine or femoral neck at least 2.5 SDs below peak premenopausal mean, or prior vertebral or hip fracture). The primary efficacy endpoint was the comparability of increases in lumbar spine BMD, using strict pre-defined equivalence criteria. Secondary endpoints included changes in BMD at the hip and total body and rate of bone turnover, as assessed by biochemical markers. Both of the new regimens fully satisfied the equivalence criteria relative to daily therapy. Mean increases in lumbar spine BMD [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "595", "doc_id": "3613041", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Sympathetic nerve activity is elevated throughout normal pregnancy.\n\nCANDIDATE_PASSAGE:\nInduction of ectopic eyes by targeted expression of the eyeless gene in Drosophila. The Drosophila gene eyeless (ey) encodes a transcription factor with both a paired domain and a homeodomain. It is homologous to the mouse Small eye (Pax-6) gene and to the Aniridia gene in humans. These genes share extensive sequence identity, the position of three intron splice sites is conserved, and these genes are expressed similarly in the developing nervous system and in the eye during morphogenesis. Loss-of-function mutations in both the insect and in the mammalian genes have been shown to lead to a reduction or absence of eye structures, which suggests that ey functions in eye morphogenesis. By targeted expression of the ey complementary DNA in various imaginal disc primordia of Drosophila, ectopic eye structures were induced on the wings, the legs, and on the antennae. The ectopic eyes appeared morphologically normal and consisted of groups of fully differentiated ommatidia with a complete set of photoreceptor cells. These results support the proposition that ey is the master control gene for eye morphogenesis. Because homologous genes are present in vertebrates, ascidians, insects, cephalopods, and nemerteans, ey may function as a master control gene throughout the metazoa.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1119", "doc_id": "9646449", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: IRG1 has antiviral effects against neurotropic viruses.\n\nCANDIDATE_PASSAGE:\nRNA is favourable for analysing EGFR mutations in malignant pleural effusion of lung cancer. Malignant pleural effusion (MPE) is a useful specimen allowing for the evaluation of EGFR status in nonsmall cell lung cancer (NSCLC). However, direct sequencing of genomic DNA from MPE samples was found not to be sensitive for EGFR mutation detection. To test whether EGFR analysis from RNA is less prone to interference from nontumour cells that have no or lower EGFR expression, we compared three methods (sequencing from cell-derived RNA versus sequencing and mass-spectrometric analysis from genomic DNA), in parallel, for EGFR mutation detection from MPE samples in 150 lung adenocarcinoma patients receiving first-line tyrosine kinase inhibitors (TKIs). Among these MPE samples, EGFR mutations were much more frequently identified by sequencing using RNA than by sequencing and mass-spectrometric analysis from genomic DNA (for all mutations, 67.3 versus 44.7 and 46.7%; for L858R or exon 19 deletions, 61.3 versus 41.3 and 46.7%, respectively). The better mutation detection yield of sequencing from RNA was coupled with the superior prediction of clinical efficacy of first-line TKIs. In patients with acquired resistance, EGFR sequencing from RNA provided satisfactory detection of T790M (54.2%). These results demonstrated that EGFR sequencing using RNA as template greatly improves sensitivity for EGFR mutation detection from samples of MPE, highlighting RNA as the favourable source for analysing EGFR mutations from heterogeneous MPE specimens in NSCLC.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "549", "doc_id": "711256", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Beta-band coherence is diminished for visible stimuli over invisible stimuli.\n\nCANDIDATE_PASSAGE:\nA model of multiple myeloma: culture of 5T33 murine myeloma cells and evaluation of tumorigenicity in the C57BL/KaLwRij mouse. The 5T33 multiple myeloma is one of a series of transplantable murine myelomas arising spontaneously in C57BL/KaLwRij mice. This study describes the establishment and characterisation of the 5T33 murine myeloma in vitro as a cultured cell line in terms of its morphology, growth rate, expression of paraprotein (IgG2b) and tumorigenicity in syngeneic animals. The 5T33 cell line has been in continuous culture for over 10 months and has achieved more than passage 34. In culture, 5T33 myeloma grows as single cells or in small clusters of loosely adherent cells on an adherent stromal cell layer. Maximum doubling time is approximately 25 h, and over 90% of the cells express cytoplasmic IgG2b paraprotein. The cultured 5T33 myeloma cells are highly tumorigenic in C57BL/KaLwRij mice with as few as 500 cells inducing paralysis and death as early as day 36 post-tumour inoculation. Kinetics of tumour development and detection of IgG2b paraprotein are dose dependent. Two weeks following intravenous inoculation of 5 x 10(5) cultured 5T33 myeloma cells, tumour cells were readily identified in the bone marrow. By 3 weeks post-tumour inoculation, 5T33 myeloma cells were found in various tissues throughout the animal. Studies are now underway to determine the sensitivity of this cell line to various therapeutic modalities.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "174", "doc_id": "13889962", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Rapid phosphotransfer rates are correlated with histidine kinase regulator specificity.\n\nCANDIDATE_PASSAGE:\nThyroid hormone inhibits lung fibrosis in mice by improving epithelial mitochondrial function Thyroid hormone (TH) is critical for the maintenance of cellular homeostasis during stress responses, but its role in lung fibrosis is unknown. Here we found that the activity and expression of iodothyronine deiodinase 2 (DIO2), an enzyme that activates TH, were higher in lungs from patients with idiopathic pulmonary fibrosis than in control individuals and were correlated with disease severity. We also found that Dio2-knockout mice exhibited enhanced bleomycin-induced lung fibrosis. Aerosolized TH delivery increased survival and resolved fibrosis in two models of pulmonary fibrosis in mice (intratracheal bleomycin and inducible TGF-β1). Sobetirome, a TH mimetic, also blunted bleomycin-induced lung fibrosis. After bleomycin-induced injury, TH promoted mitochondrial biogenesis, improved mitochondrial bioenergetics and attenuated mitochondria-regulated apoptosis in alveolar epithelial cells both in vivo and in vitro. TH did not blunt fibrosis in Ppargc1a- or Pink1-knockout mice, suggesting dependence on these pathways. We conclude that the antifibrotic properties of TH are associated with protection of alveolar epithelial cells and restoration of mitochondrial function and that TH may thus represent a potential therapy for pulmonary fibrosis.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1018", "doc_id": "3619931", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: DUSP4 downregulation deactivates the Ras-ERK pathway\n\nCANDIDATE_PASSAGE:\nA family of phosphoinositide 3-kinases in Drosophila identifies a new mediator of signal transduction BACKGROUND Mammalian phosphoinositide 3-kinases (PI 3-kinases) are involved in receptor-mediated signal transduction and have been implicated in processes such as transformation and mitogenesis through their role in elevating cellular phosphatidylinositol (3,4,5)-trisphosphate. Additionally, a PI 3-kinase activity which generates phosphatidylinositol 3-phosphate has been shown to be required for protein trafficking in yeast. RESULTS We have identified a family of three distinct PI 3-kinases in Drosophila, using an approach based on the polymerase chain reaction to amplify a region corresponding to the conserved catalytic domain of PI 3-kinases. One of these family members, PI3K_92D, is closely related to the prototypical PI 3-kinase, p110 alpha; PI3K_59F is homologous to Vps34p, whereas the third, PI3K_68D, is a novel PI 3-kinase which is widely expressed throughout the Drosophila life cycle. The PI3K_68D cDNA encodes a protein of 210 kDa, which lacks sequences implicated in linking p110 PI 3-kinases to p85 adaptor proteins, but contains an amino-terminal proline-rich sequence, which could bind to SH3 domains, and a carboxy-terminal C2 domain. Biochemical analyses demonstrate that PI3K_68D has a novel substrate specificity in vitro, restricted to phosphatidylinositol and phosphatidylinositol 4-phosphate, and is unable to phosphorylate phosphatidylinositol (4,5)-bisphosphate, the implied in vivo substrate for p110. CONCLUSIONS A family of PI 3-kinases in Drosophila, including a novel class represented by PI3K_68D, is described. PI3K_68D has the potential to bind to signalling molecules containing SH3 domains, lacks p85-adaptor-binding sequences, has a Ca(2+)- [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "308", "doc_id": "14328288", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: ER-localized phosphatase Sac1 processes PI4P through coordination with OSBP and the endosome-localized protein sorting nexin 2.\n\nCANDIDATE_ABSTRACT:\nTITLE: Endosome-ER Contacts Control Actin Nucleation and Retromer Function through VAP-Dependent Regulation of PI4P\nABSTRACT: VAP (VAPA and VAPB) is an evolutionarily conserved endoplasmic reticulum (ER)-anchored protein that helps generate tethers between the ER and other membranes through which lipids are exchanged across adjacent bilayers. Here, we report that by regulating PI4P levels on endosomes, VAP affects WASH-dependent actin nucleation on these organelles and the function of the retromer, a protein coat responsible for endosome-to-Golgi traffic. VAP is recruited to retromer budding sites on endosomes via an interaction with the retromer SNX2 subunit. Cells lacking VAP accumulate high levels of PI4P, actin comets, and trans-Golgi proteins on endosomes. Such defects are mimicked by downregulation of OSBP, a VAP interactor and PI4P transporter that participates in VAP-dependent ER-endosomes tethers. These results reveal a role of PI4P in retromer-/WASH-dependent budding from endosomes. Collectively, our data show how the ER can control budding dynamics and association with the cytoskeleton of another membrane by direct contacts leading to bilayer lipid modifications.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 365, "doc_id": "600437", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Mitochondria are uninvolved in apoptosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mitochondria: Dynamic Organelles in Disease, Aging, and Development\nABSTRACT: Mitochondria are the primary energy-generating system in most eukaryotic cells. Additionally, they participate in intermediary metabolism, calcium signaling, and apoptosis. Given these well-established functions, it might be expected that mitochondrial dysfunction would give rise to a simple and predictable set of defects in all tissues. However, mitochondrial dysfunction has pleiotropic effects in multicellular organisms. Clearly, much about the basic biology of mitochondria remains to be understood. Here we discuss recent work that suggests that the dynamics (fusion and fission) of these organelles is important in development and disease.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Additionally, they participate in intermediary metabolism, calcium signaling, and apoptosis.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 793, "doc_id": "8551160", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Cancer cells can stimulate the accumulation of intra-tumoural myeloid-derived suppressor cells by promoting granulocyte colony stimulating factor production.\n\nCANDIDATE_PASSAGE:\nCENP-B Controls Centromere Formation Depending on the Chromatin Context The centromere is a chromatin region that serves as the spindle attachment point and directs accurate inheritance of eukaryotic chromosomes during cell divisions. However, the mechanism by which the centromere assembles and stabilizes at a specific genomic region is not clear. The de novo formation of a human/mammalian artificial chromosome (HAC/MAC) with a functional centromere assembly requires the presence of alpha-satellite DNA containing binding motifs for the centromeric CENP-B protein. We demonstrate here that de novo centromere assembly on HAC/MAC is dependent on CENP-B. In contrast, centromere formation is suppressed in cells expressing CENP-B when alpha-satellite DNA was integrated into a chromosomal site. Remarkably, on those integration sites CENP-B enhances histone H3-K9 trimethylation and DNA methylation, thereby stimulating heterochromatin formation. Thus, we propose that CENP-B plays a dual role in centromere formation, ensuring de novo formation on DNA lacking a functional centromere but preventing the formation of excess centromeres on chromosomes.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "223", "doc_id": "15960670", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Differentiated E2f-1, -2, -3 TKO cells in the intestine do not exhibit apoptosis.\n\nCANDIDATE_PASSAGE:\nE2F1-3 Switch from Activators in Progenitor Cells to Repressors in Differentiating Cells In the established model of mammalian cell cycle control, the retinoblastoma protein (Rb) functions to restrict cells from entering S phase by binding and sequestering E2f activators (E2f1, E2f2 and E2f3), which are invariably portrayed as the ultimate effectors of a transcriptional program that commit cells to enter and progress through S phase. Using a panel of tissue-specific cre-transgenic mice and conditional E2f alleles we examined the effects of E2f1, E2f2 and E2f3 triple deficiency in murine embryonic stem cells, embryos and small intestines. We show that in normal dividing progenitor cells E2f1-3 function as transcriptional activators, but contrary to the current view, are dispensable for cell division and instead are necessary for cell survival. In differentiating cells E2f1-3 function in a complex with Rb as repressors to silence E2f targets and facilitate exit from the cell cycle. The inactivation of Rb in differentiating cells resulted in a switch of E2f1-3 from repressors to activators, leading to the superactivation of E2f responsive targets and ectopic cell divisions. Loss of E2f1-3 completely suppressed these phenotypes caused by Rb deficiency. This work contextualizes the activator versus repressor functions of E2f1-3 in vivo, revealing distinct roles in dividing versus differentiating cells and in normal versus cancer-like cell cycles.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "345", "doc_id": "4394817", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cognitive behavioral therapy is an ineffective treatment for insomnia\n\nCANDIDATE_ABSTRACT:\nTITLE: Cognitive behavioral therapy vs zopiclone for treatment of chronic primary insomnia in older adults: a randomized controlled trial.\nABSTRACT: CONTEXT Insomnia is a common condition in older adults and is associated with a number of adverse medical, social, and psychological consequences. Previous research has suggested beneficial outcomes of both psychological and pharmacological treatments, but blinded placebo-controlled trials comparing the effects of these treatments are lacking. OBJECTIVE To examine short- and long-term clinical efficacy of cognitive behavioral therapy (CBT) and pharmacological treatment in older adults experiencing chronic primary insomnia. DESIGN, SETTING, AND PARTICIPANTS A randomized, double-blinded, placebo-controlled trial of 46 adults (mean age, 60.8 y; 22 women) with chronic primary insomnia conducted between January 2004 and December 2005 in a single Norwegian university-based outpatient clinic for adults and elderly patients. INTERVENTION CBT (sleep hygiene, sleep restriction, stimulus control, cognitive therapy, and relaxation; n = 18), sleep medication (7.5-mg zopiclone each night; n = 16), or placebo medication (n = 12). All treatment duration was 6 weeks, and the 2 active treatments were followed up at 6 months. MAIN OUTCOME MEASURES Ambulant clinical polysomnographic data and sleep diaries were used to determine total wake time, total sleep time, sleep efficiency, and slow-wave sleep (only assessed using polysomnography) on all 3 assessment points. RESULTS CBT resulted in improved short- and long-term outcomes compared with zopiclone on 3 out of 4 outcome measures. For most outcomes, zopiclone did not differ from placebo. Participants receiving CBT improved their sleep efficiency from 81.4% at pretreatment to 90.1% at 6-month follow-up compared with a decrease from 82.3% to 81.9% in the zopiclone group. Participants in the CBT group spent much more time in slow- [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Participants in the CBT group spent much more time in slow-wave sleep (stages 3 and 4) compared with those in other groups, and spent less time awake during the night.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 267, "doc_id": "5912283", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Measuring routine outcomes is more beneficial to clinical practice than assessing treatment adherence.\n\nCANDIDATE_PASSAGE:\nAnxiety OBJECTIVES To examine the effect of routinely administered psychiatric questionnaires on the recognition, management, and outcome of psychiatric disorders in non-psychiatric settings. DATA SOURCES Embase, Medline, PsycLIT, Cinahl, Cochrane Controlled Trials Register, and hand searches of key journals. METHODS A systematic review of randomised controlled trials of the administration and routine feedback of psychiatric screening and outcome questionnaires to clinicians in non-psychiatric settings. Narrative overview of key design features and end points, together with a random effects quantitative synthesis of comparable studies. MAIN OUTCOME MEASURES Recognition of psychiatric disorders after feedback of questionnaire results; interventions for psychiatric disorders; and outcome of psychiatric disorders. RESULTS Nine randomised studies were identified that examined the use of common psychiatric instruments in primary care and general hospital settings. Studies compared the effect of the administration of these instruments followed by the feedback of the results to clinicians, with administration with no feedback. Meta-analytic pooling was possible for four of these studies (2457 participants), which measured the effect of feedback on the recognition of depressive disorders. Routine administration and feedback of scores for all patients (irrespective of score) did not increase the overall rate of recognition of mental disorders such as anxiety and depression (relative risk of detection of depression by clinician after feedback 0.95, 95% confidence interval 0.83 to 1.09). Two studies showed that routine administration followed by selective feedback for only high scorers increased the rate of recognition of depression (relative risk of detection of depre [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "762", "doc_id": "4695046", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The binding orientation of the ML-SA1 activator at hTRPML2 is different from the binding orientation of the ML-SA1 activator at hTRPML1.\n\nCANDIDATE_PASSAGE:\nRegulation and effects of hypothalamic galanin: relation to dietary fat, alcohol ingestion, circulating lipids and energy homeostasis. Galanin (GAL) is known to stimulate feeding behavior. This peptide has different properties and functions from other feeding stimulants, e.g., neuropeptide Y and agouti-related protein. Hypothalamic GAL is relatively unresponsive to food deprivation and to changes in corticosterone, glucose utilization, dietary carbohydrate and leptin. This indicates that this peptide is not essential under conditions when food is scarce or low-energy, high-carbohydrate diets are being consumed. In contrast, recent evidence suggests that GAL in the paraventricular nucleus (PVN) functions in close relation to dietary fat and alcohol. In particular, it mediates functions that allow animals to adapt to conditions of positive energy balance involving excess consumption of these nutrients. This peptide in the PVN is stimulated by a high-fat diet and also by alcohol. It is stimulated by an increase in circulating lipids caused by a fat-rich meal or alcohol consumption, and it rises during the middle of the active feeding cycle, when fat consumption and triglycerides naturally rise. When centrally injected, GAL in the PVN increases the consumption of food and alcohol. Moreover, it produces a significantly stronger feeding response in rats maintained on a fat-rich diet, which also promotes alcohol intake. This evidence supports the existence of non-homeostatic, positive feedback circuits between GAL and both dietary fat and alcohol. These circuits are believed to contribute to the large meal size, over-consumption of alcohol, and obesity which are generally associated with fat-rich foods.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1200", "doc_id": "11742219", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: There is no known interaction between Pioneer factor OCT3/4 and major chromatin remodeling factors.\n\nCANDIDATE_ABSTRACT:\nTITLE: Oct4 links multiple epigenetic pathways to the pluripotency network\nABSTRACT: Oct4 is a well-known transcription factor that plays fundamental roles in stem cell self-renewal, pluripotency, and somatic cell reprogramming. However, limited information is available on Oct4-associated protein complexes and their intrinsic protein-protein interactions that dictate Oct4's critical regulatory activities. Here we employed an improved affinity purification approach combined with mass spectrometry to purify Oct4 protein complexes in mouse embryonic stem cells (mESCs), and discovered many novel Oct4 partners important for self-renewal and pluripotency of mESCs. Notably, we found that Oct4 is associated with multiple chromatin-modifying complexes with documented as well as newly proved functional significance in stem cell maintenance and somatic cell reprogramming. Our study establishes a solid biochemical basis for genetic and epigenetic regulation of stem cell pluripotency and provides a framework for exploring alternative factor-based reprogramming strategies.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Notably, we found that Oct4 is associated with multiple chromatin-modifying complexes with documented as well as newly proved functional significance in stem cell maintenance and somatic cell reprogramming.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1294, "doc_id": "2078658", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Transcription rates in S. cerevisiae range between 7 and 12 kb/min.\n\nCANDIDATE_PASSAGE:\nSingle-RNA counting reveals alternative modes of gene expression in yeast Proper execution of transcriptional programs is a key requirement of gene expression regulation, demanding accurate control of timing and amplitude. How precisely the transcription machinery fulfills this task is not known. Using an in situ hybridization approach that detects single mRNA molecules, we measured mRNA abundance and transcriptional activity within single Saccharomyces cerevisiae cells. We found that expression levels for particular genes are higher than initially reported and can vary substantially among cells. However, variability for most constitutively expressed genes is unexpectedly small. Combining single-transcript measurements with computational modeling indicates that low expression variation is achieved by transcribing genes using single transcription-initiation events that are clearly separated in time, rather than by transcriptional bursts. In contrast, PDR5, a gene regulated by the transcription coactivator complex SAGA, is expressed using transcription bursts, resulting in larger variation. These data directly demonstrate the existence of multiple expression modes used to modulate the transcriptome.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1315", "doc_id": "16237005", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Ultrasound guidance significantly reduces the number of traumatic procedures when attempting needle insertion.\n\nCANDIDATE_ABSTRACT:\nTITLE: Ultrasound imaging for lumbar punctures and epidural catheterisations: systematic review and meta-analysis.\nABSTRACT: OBJECTIVE To determine whether ultrasound imaging can reduce the risk of failed lumbar punctures or epidural catheterisations, when compared with standard palpation methods, and whether ultrasound imaging can reduce traumatic procedures, insertion attempts, and needle redirections. DESIGN Systematic review and meta-analysis of randomised controlled trials. DATA SOURCES Ovid Medline, Embase, and Cochrane Central Register of Controlled Trials up to May 2012, without restriction by language or publication status. REVIEW METHODS Randomised trials that compared ultrasound imaging with standard methods (no imaging) in the performance of a lumbar puncture or epidural catheterisation were identified. RESULTS 14 studies with a total of 1334 patients were included (674 patients assigned to the ultrasound group, 660 to the control group). Five studies evaluated lumbar punctures and nine evaluated epidural catheterisations. Six of 624 procedures conducted in the ultrasound group failed; 44 of 610 procedures in the control group failed. Ultrasound imaging reduced the risk of failed procedures (risk ratio 0.21 (95% confidence interval 0.10 to 0.43), P<0.001). Risk reduction was similar when subgroup analysis was performed for lumbar punctures (risk ratio 0.19 (0.07 to 0.56), P=0.002) or epidural catheterisations (0.23 (0.09 to 0.60), P=0.003). Ultrasound imaging also significantly reduced the risk of traumatic procedures (risk ratio 0.27 (0.11 to 0.67), P=0.005), the number of insertion attempts (mean difference -0.44 (-0.64 to -0.24), P<0.001), and the number of needle redirections (mean difference -1.00 (-1.24 to -0.75), P<0.001). CONCLUSIONS Ultrasound imaging can reduce the risk of failed or traumatic lumbar punctures and epidural catheterisations, as well as the numb [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Ultrasound imaging can reduce the risk of failed or traumatic lumbar punctures and epidural catheterisations, as well as the number of needle insertions and redirections.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1341, "doc_id": "15482274", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Scapular stabilizer exercises are more effective than general exercise therapy in reducing pain and improving function of the shoulder.\n\nCANDIDATE_PASSAGE:\nBreathing more with weaker respiratory muscles in pulmonary arterial hypertension. Exertional fatigue and dyspnoea limit the daily activities of patients with pulmonary arterial hypertension 1. These symptoms are usually explained by the inability of the overloaded right ventricle to perfuse the lungs and to adapt systemic oxygen delivery to oxygen demand. Accordingly, pulmonary hypertension patients present with reductions in peak oxygen uptake, anaerobic threshold, oxygen pulse, ventilatory efficiency and 6-min walk distance 2–8. This ergospirometric profile is strikingly similar to that of congestive heart failure 8–12, further supporting the notion of impaired cardiac output adaptation to peripheral oxygen requirements as the main cause of decreased exercise capacity. However, in both pulmonary hypertension and heart failure, ergospirometric variables and walk distances are better correlated to functional class and prognosis than to haemodynamic function 3, 6, 7, 10–12. In addition, impaired skeletal muscle function has been repeatedly reported in heart failure, fuelling a “muscle hypothesis” relating dyspnoea and fatigue symptoms to skeletal muscle metaboreceptor and/or ergoreceptor reflexes 13. The muscle hypothesis implies a persistent sympathetic nervous system activation, which has indeed been shown to occur in heart failure 14 and also, more recently, in pulmonary hypertension 15. Until now, there have been no studies on skeletal muscle function in pulmonary arterial hypertension. In the present issue of the European Respiratory Journal , Meyer et al. 16 report data suggesting that respiratory muscle strength is decreased in pulmonary arterial hypertension. In a prospective study on 37 patients with idiopathic pulmonary hypertension, significant de [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1069", "doc_id": "6993046", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Downregulation and mislocalization of Scribble prevents cell transformation and mammary tumorigenesis.\n\nCANDIDATE_PASSAGE:\nPhosphorylation of ATM by Cdk5 mediates DNA damage signaling and regulates neuronal death The phosphatidylinositol-3-kinase-like kinase ATM (ataxia-telangiectasia mutated) has a central role in coordinating DNA damage responses, including cell-cycle checkpoint control, DNA repair and apoptosis. Mutations of ATM cause a spectrum of defects ranging from neurodegeneration to cancer predisposition. However, the mechanism by which DNA damage activates ATM is poorly understood. Here we show that Cdk5 (cyclin-dependent kinase 5), activated by DNA damage, directly phosphorylates ATM at Ser 794 in post-mitotic neurons. Phosphorylation at Ser 794 precedes, and is required for, ATM autophosphorylation at Ser 1981, and activates ATM kinase activity. The Cdk5-ATM signal regulates phosphorylation and function of the ATM targets p53 and H2AX. Interruption of the Cdk5-ATM pathway attenuates DNA-damage-induced neuronal cell cycle re-entry and expression of the p53 targets PUMA and Bax, protecting neurons from death. Thus, activation of Cdk5 by DNA damage serves as a critical signal to initiate the ATM response and regulate ATM-dependent cellular processes.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "354", "doc_id": "21295300", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Are hormonal contraceptives and the length of their use independent risk factors for high-risk HPV infections or high-grade CIN?\n\nABSTRACT:\nTo evaluate the role of hormonal contraceptives as a risk factor of high-risk human papillomavirus (HR-HPV), cervical intraepithelial lesions (CIN) and cervical cancer in our multi-center population-based LAMS (Latin American Screening) study. A cohort study with >12,000 women from Brazil and Argentina using logistic regression to analyze the covariates of hormonal contraception (HOC - oral, injections, patches, implants, vaginal ring and progesterone intrauterine system) use followed by multivariate modeling for predictors of HR-HPV and CIN2+. HR-HPV infection was a consistent risk factor of high-grade CIN in all three groups of women. The length of HOC use was not significantly related to high-grade squamous intraepithelial lesions (HSIL)+ Pap (p = 0.069), LSIL+ Pap (p = 0.781) or ASCUS+ (p = 0.231). The same was true with the length of HOC use and histology CIN3+ (p = 0.115) and CIN2+ (p = 0.515). Frequently, HOC users have previously shown more HPV-related lesions, as well as lower HPV prevalence if they were current smokers. But HOC use and time of usage were not independent risk factors of either HR-HPV infection or high-grade CIN using multiple logistic regressions.", "output": "{\"label\": \"no\", \"rationale\": \"No evidence was found for an association between the use of HOC with an increased risk for HR-HPV infection or high-grade CIN in this cohort.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 21150159, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: After CLASS--Is a voluntary public insurance program a realistic way to meet the long-term support and service needs of adults with disabilities?\n\nABSTRACT:\nThe CLASS Act, which was part of the Affordable Care Act of 2010, established a voluntary personal assistance services (PAS) insurance program. However, concerns about enrollment and adverse selection led to repeal of the CLASS Act in 2013. To estimate the number of middle-aged adults interested in purchasing PAS insurance, the sociodemographic, socioeconomic and disability attributes of this population, and the maximum monthly premium they would be willing to pay for such coverage. A total of 13,384 adults aged 40-65 answered questions about their interest in PAS insurance in the 2011 Sample Adult National Health Interview Survey. We applied survey weights for the U.S. population and conducted logistic regression analyses to identify personal factors associated with interest in paying for the CLASS program. An estimated 25.8 million adults aged 40-65 (26.7%) said they would be interested in paying for a public insurance program to cover PAS benefits. However, interest in PAS insurance varied by age, race, ethnicity, region, income, disability status, and family experience with ADL assistance. Only 1.6 million adults aged 40-65 (1.8%) said they would be willing to pay $100 per month or more for coverage.", "output": "{\"label\": \"no\", \"rationale\": \"While more than a quarter of the middle-aged adult population said they were interested in PAS insurance, actual participation would be highly dependent on premium rates. The current lack of publicly subsidized insurance for long-term care and personal assistance services remains a serious gap in the disability service system.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 26717802, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The PRR MDA5 has a C-terminal domain.\n\nCANDIDATE_PASSAGE:\nImmune signaling by RIG-I-like receptors. The RIG-I-like receptors (RLRs) RIG-I, MDA5, and LGP2 play a major role in pathogen sensing of RNA virus infection to initiate and modulate antiviral immunity. The RLRs detect viral RNA ligands or processed self RNA in the cytoplasm to trigger innate immunity and inflammation and to impart gene expression that serves to control infection. Importantly, RLRs cooperate in signaling crosstalk networks with Toll-like receptors and other factors to impart innate immunity and to modulate the adaptive immune response. RLR regulation occurs at a variety of levels ranging from autoregulation to ligand and cofactor interactions and posttranslational modifications. Abberant RLR signaling or dysregulation of RLR expression is now implicated in the development of autoimmune diseases. Understanding the processes of RLR signaling and response will provide insights to guide RLR-targeted therapeutics for antiviral and immune-modifying applications.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1178", "doc_id": "31272411", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Taking 400mg of α-tocopheryl acetate in combination with vitamin C reduces the risk of prostate cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Vitamins E and C in the prevention of prostate and total cancer in men: the Physicians' Health Study II randomized controlled trial.\nABSTRACT: CONTEXT Many individuals take vitamins in the hopes of preventing chronic diseases such as cancer, and vitamins E and C are among the most common individual supplements. A large-scale randomized trial suggested that vitamin E may reduce risk of prostate cancer; however, few trials have been powered to address this relationship. No previous trial in men at usual risk has examined vitamin C alone in the prevention of cancer. OBJECTIVE To evaluate whether long-term vitamin E or C supplementation decreases risk of prostate and total cancer events among men. DESIGN, SETTING, AND PARTICIPANTS The Physicians' Health Study II is a randomized, double-blind, placebo-controlled factorial trial of vitamins E and C that began in 1997 and continued until its scheduled completion on August 31, 2007. A total of 14,641 male physicians in the United States initially aged 50 years or older, including 1307 men with a history of prior cancer at randomization, were enrolled. INTERVENTION Individual supplements of 400 IU of vitamin E every other day and 500 mg of vitamin C daily. MAIN OUTCOME MEASURES Prostate and total cancer. RESULTS During a mean follow-up of 8.0 years, there were 1008 confirmed incident cases of prostate cancer and 1943 total cancers. Compared with placebo, vitamin E had no effect on the incidence of prostate cancer (active and placebo vitamin E groups, 9.1 and 9.5 events per 1000 person-years; hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.85-1.09; P = .58) or total cancer (active and placebo vitamin E groups, 17.8 and 17.3 cases per 1000 person-years; HR, 1.04; 95% CI, 0.95-1.13; P = .41). There was also no significant effect of vitamin C on total cancer (active and placebo vitamin C groups, 17.6 and 17.5 events per 1000 person-years; HR, 1.01; 95% [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Compared with placebo, vitamin E had no effect on the incidence of prostate cancer (active and placebo vitamin E groups, 9.1 and 9.5 events per 1000 person-years; hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.85-1.09; P = .58) or total cancer (active and placebo vitamin E groups, 17.8 and 17.3 cases per 1000 person-years; HR, 1.04; 95% CI, 0.95-1.13; P = .41). There was also no significant effect of vitamin C on total cancer (active and placebo vitamin C groups, 17.6 and 17.5 events per 1000 person-years; HR, 1.01; 95% CI, 0.92-1.10; P = .86) or prostate cancer (active and placebo vitamin C groups, 9.4 and 9.2 cases per 1000 person-years; HR, 1.02; 95% CI, 0.90-1.15; P = .80).\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1141, "doc_id": "12009265", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: During non-homologous end joining, the ligation step is not as tolerant of disrepairs and other distortions when joining 5' of strand breaks as compared to 3' strand breaks.\n\nCANDIDATE_ABSTRACT:\nTITLE: The fidelity of the ligation step determines how ends are resolved during Nonhomologous end joining\nABSTRACT: Nonhomologous end joining (NHEJ) can effectively resolve chromosome breaks despite diverse end structures; however, it is unclear how the steps employed for resolution are determined. We sought to address this question by analysing cellular NHEJ of ends with systematically mispaired and damaged termini. We show NHEJ is uniquely proficient at bypassing subtle terminal mispairs and radiomimetic damage by direct ligation. Nevertheless, bypass ability varies widely, with increases in mispair severity gradually reducing bypass products from 85 to 6%. End-processing by nucleases and polymerases is increased to compensate, although paths with the fewest number of steps to generate a substrate suitable for ligation are favoured. Thus, both the frequency and nature of end processing are tailored to meet the needs of the ligation step. We propose a model where the ligase organizes all steps during NHEJ within the stable paired-end complex to limit end processing and associated errors.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 358, "doc_id": "18111172", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: A high microerythrocyte count raises vulnerability to severe anemia in homozygous alpha (+)- thalassemia trait subjects.\n\nCANDIDATE_PASSAGE:\nIncreased Microerythrocyte Count in Homozygous α+-Thalassaemia Contributes to Protection against Severe Malarial Anaemia BACKGROUND The heritable haemoglobinopathy alpha(+)-thalassaemia is caused by the reduced synthesis of alpha-globin chains that form part of normal adult haemoglobin (Hb). Individuals homozygous for alpha(+)-thalassaemia have microcytosis and an increased erythrocyte count. Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count. We tested the hypothesis that the erythrocyte indices associated with alpha(+)-thalassaemia homozygosity provide a haematological benefit during acute malaria. METHODS AND FINDINGS Data from children living on the north coast of Papua New Guinea who had participated in a case-control study of the protection afforded by alpha(+)-thalassaemia against severe malaria were reanalysed to assess the genotype-specific reduction in erythrocyte count and Hb levels associated with acute malarial disease. We observed a reduction in median erythrocyte count of approximately 1.5 x 10(12)/l in all children with acute falciparum malaria relative to values in community children (p < 0.001). We developed a simple mathematical model of the linear relationship between Hb concentration and erythrocyte count. This model predicted that children homozygous for alpha(+)-thalassaemia lose less Hb than children of normal genotype for a reduction in erythrocyte count of >1.1 x 10(12)/l as a result of the reduced mean cell Hb in homozygous alpha(+)-thalassaemia. In addition, children homozygous for alpha(+)-thalassaemia require a 10% greater reduction in erythrocyte count than children of normal genotyp [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "42", "doc_id": "18174210", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Pioneer factor OCT3/4 interacts with major chromatin remodeling factors.\n\nCANDIDATE_PASSAGE:\nImpact of aortic stiffness on survival in end-stage renal disease. BACKGROUND Damage to large arteries is a major factor in the high cardiovascular morbidity and mortality of patients with end-stage renal disease (ESRD). Increased arterial stiffness and intima-media thickness, together with increased pulse pressure, are the principal arterial alterations. Whether increased aortic pulse-wave velocity (PWV), a classic marker of increased arterial stiffness, may predict all-cause and/or cardiovascular mortality has never been investigated. METHODS AND RESULTS A cohort of 241 patients with ESRD undergoing hemodialysis was studied between April 1987 and April 1998. The mean duration of follow-up was 72+/-41 months (mean+/-SD). Mean age at entry was 51.5+/-16.3 years. Seventy-three deaths occurred, including 48 cardiovascular and 25 noncardiovascular fatal events. At entry, together with standard clinical and biochemical analyses, patients underwent echocardiography and aortic PWV measured by Doppler ultrasonography. On the basis of Cox analyses, 2 factors emerged as predictors of all-cause and cardiovascular mortality: age and aortic PWV. Hemoglobin and low diastolic pressure interfered to a smaller extent. After adjustment for all the confounding factors, an OR for PWV >12. 0 versus <9.4 m/s was 5.4 (95% CI, 2.4 to 11.9) for all-cause mortality and 5.9 (95% CI, 2.3 to 15.5) for cardiovascular mortality. For each PWV increase of 1 m/s in our study population, all-cause mortality-adjusted OR was 1.39 (95% CI, 1.19 to 1.62). CONCLUSIONS These results provide the first direct evidence that in patients with ESRD, increased aortic stiffness determined by measurement of aortic PWV is a strong independent predictor of all-cause and mainly cardiovascular mortality.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "955", "doc_id": "6525844", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Increased microtubule acetylation repairs interference of axonal transport caused by LRRK2 Roc-COR domain mutations.\n\nCANDIDATE_PASSAGE:\nRibosomal DNA copy loss and repeat instability in ATRX-mutated cancers ATRX (alpha thalassemia/mental retardation X-linked) complexes with DAXX to deposit histone variant H3.3 into repetitive heterochromatin. Recent genome sequencing studies in cancers have revealed mutations in ATRX and their association with ALT (alternative lengthening of telomeres) activation. Here we report depletion of ATRX in mouse ES cells leads to selective loss in ribosomal RNA gene (rDNA) copy number. Supporting this, ATRX-mutated human ALT-positive tumors also show a substantially lower rDNA copy than ALT-negative tumors. Further investigation shows that the rDNA copy loss and repeat instability are caused by a disruption in H3.3 deposition and thus a failure in heterochromatin formation at rDNA repeats in the absence of ATRX. We also find that ATRX-depleted cells are reduced in ribosomal RNA transcription output and show increased sensitivity to RNA polymerase I (Pol I) transcription inhibitor CX5461. In addition, human ALT-positive cancer cell lines are also more sensitive to CX5461 treatment. Our study provides insights into the contribution of ATRX loss of function to tumorigenesis through the loss of rDNA stability and suggests the therapeutic potential of targeting Pol I transcription in ALT cancers.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "614", "doc_id": "4993011", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does perspective-taking increase patient satisfaction in medical encounters?\n\nABSTRACT:\nTo assess whether perspective-taking, which researchers in other fields have shown to induce empathy, improves patient satisfaction in encounters between student-clinicians and standardized patients (SPs). In three studies, randomly assigned students (N = 608) received either a perspective-taking instruction or a neutral instruction prior to a clinical skills examination in 2006-2007. SP satisfaction was the main outcome in all three studies. Study 1 involved 245 third-year medical students from two universities. Studies 2 and 3 extended Study 1 to examine generalizability across student and SP subpopulations. Study 2 (105 physician assistant students, one university) explored the effect of perspective-taking on African American SPs' satisfaction. Study 3 (258 third-year medical students, two universities) examined the intervention's effect on students with high and low baseline perspective-taking tendencies. Intervention students outscored controls in patient satisfaction in all studies: Study 1: P = .01, standardized effect size = 0.16; Study 2: P = .001, standardized effect size = 0.31; Study 3: P = .009, standardized effect size = 0.13. In Study 2, perspective-taking improved African American SPs' satisfaction. In Study 3, intervention students with high baseline perspective-taking tendencies outscored controls (P = .0004, standardized effect size = 0.25), whereas those with low perspective-taking tendencies did not (P = .72, standardized effect size = 0.00).", "output": "{\"label\": \"maybe\", \"rationale\": \"Perspective-taking increased patient satisfaction in all three studies, across medical schools, clinical disciplines, and racially diverse students and SPs. Perspective-taking as a means for improving patient satisfaction deserves further exploration in clinical training and practice.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 20736672, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Occupancy of ribosomes by IncRNAs do not make functional peptides.\n\nCANDIDATE_PASSAGE:\nThe Mismatch Argument: The Construction of a Housing Orthodoxy in Australia Australia's housing policy discourse contains many orthodoxies. While orthodoxies are never totally accepted within a discourse, they are the dominant notions within them and as such carry significant symbolic authority. One orthodoxy that has particular authority in Australia is the notion that there is a 'mismatch' in the housing system between the available stock and the size of households to the extent that there is significant underutilisation and underoccupancy of housing. The mismatch argument's power as orthodoxy is such that the idea is assumed in much housing policy discussion. Criticism of the mismatch orthodoxy can take many approaches, such as empirical, conceptual and discursive. The discursive critique focuses not on the empirical relationship between households and dwellings, but on the statements about that relationship. The resulting analysis shows how the mismatch orthodoxy arose in Australia and its effects on housing discourse. This paper examines the construction of the mismatch orthodoxy, from its first uses in the early 1970s to its entrenchment in national and state housing policy research in the early 1990s. It shows how the structures of the discourse construct the orthodoxy, despite empirical and conceptual criticisms of it. Of particular importance is the effect the orthodoxy has on people deemed to be underutilising their dwellings, and on how the orthodoxy affects policy interpretations, such as occupancy standards.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "879", "doc_id": "154763124", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: There is no relation between Erythromycin use and hypertrophic pyloric stenosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Use of macrolides in mother and child and risk of infantile hypertrophic pyloric stenosis: nationwide cohort study\nABSTRACT: OBJECTIVE To assess the association between use of macrolide antibiotics in mothers and infants from pregnancy onset until 120 days after birth and infantile hypertrophic pyloric stenosis (IHPS). DESIGN Nationwide register based cohort study. SETTING Denmark, 1996-2011. PARTICIPANTS 999,378 liveborn singletons and linked individual level information on macrolide prescriptions (maternal use during pregnancy, n=30,091; maternal use after birth, n=21,557; use in infants, n=6591), surgery for IHPS, and potential confounders. MAIN OUTCOME MEASURES Surgery for IHPS by three categories of macrolide use: in mothers during pregnancy, in mothers after birth, and in infants after birth. RESULTS 880 infants developed IHPS (0.9 cases per 1000 births). Compared with infants with no use of macrolides, the adjusted rate ratio for IHPS in infants with use of macrolides during days 0 to 13 after birth was 29.8 (95% confidence interval 16.4 to 54.1) and during days 14 to 120 was 3.24 (1.20 to 8.74); the corresponding absolute risk differences were 24.4 (95% confidence interval 13.0 to 44.1) and 0.65 (0.06 to 2.21) cases per 1000 infants exposed to macrolides, respectively. The rate ratio for maternal use of macrolides for days 0 to 13 after birth was 3.49 (1.92 to 6.34) and for days 14 to 120 was 0.70 (0.26 to 1.90); the corresponding absolute risk differences were 2.15 (0.82 to 4.64) and -0.11 (-0.26 to 0.31). The rate ratios for maternal use of macrolides during pregnancy were 1.02 (0.65 to 1.59) for weeks 0 to 27 and 1.77 (0.95 to 3.31) for weeks 28 to birth; the corresponding absolute risk differences were 0.01 (-0.31 to 0.50) and 0.67 (-0.06 to 2.02). CONCLUSIONS Treatment of young infants with macrolide antibiotics was strongly associated with IHPS and should therefore o [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Maternal use of macrolides during the first two weeks after birth was also associated with an increased risk of IHPS.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1295, "doc_id": "21239672", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Artefacts in 24-h pharyngeal and oesophageal pH monitoring: is simplification of pH data analysis feasible?\n\nABSTRACT:\nAmbulatory 24-h dual-channel pharyngeal and oesophageal pH monitoring is the standard test for measuring gastro-oesophageal and gastropharyngeal reflux. Artefacts caused by the intake of food may result in falsely positive gastropharyngeal reflux, which necessitates a manual review of 24-h pH data. The purpose of the study was to investigate the influence of meals and whether leaving out meals affected the reliability of the test. Patients referred for otolaryngological complaints, suspected to have been caused by gastro-oesophageal reflux, underwent 24-h dual-channel pH monitoring. The raw unprocessed pH data were corrected by visual inspection of the 24-h tracings (corrected data), by leaving out meals or meals plus a 2-h postprandrial period. The raw pH data were substantially influenced by artefacts of food intake and pseudoreflux. Data obtained by leaving out meals agreed best with manually corrected data. Many of the falsely positive reflux episodes could be removed, thereby inducing a 9%-18% chance of undetected reflux. When examining the fraction of time supine, manually corrected data and data leaving out meals were fully concordant and detected 79% of patients with gastropharyngeal reflux. However, leaving out meals plus a 2-h postprandrial period resulted in 21%-50% falsely negative tests.", "output": "{\"label\": \"maybe\", \"rationale\": \"Leaving out the period of intake of meals and beverages from the raw pH data might be the second best test after the time-consuming visual correction with a small chance of undetected gastropharyngeal reflux. For scientific purposes and when in doubt, it remains necessary to review the computer-generated data manually to discover every gastropharyngeal reflux event.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 14992556, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Women with a lower birth weight are more likely to develop breast cancer later in life.\n\nCANDIDATE_ABSTRACT:\nTITLE: Intrauterine environments and breast cancer risk: meta-analysis and systematic review\nABSTRACT: INTRODUCTION Various perinatal factors, including birth weight, birth order, maternal age, gestational age, twin status, and parental smoking, have been postulated to affect breast cancer risk in daughters by altering the hormonal environment of the developing fetal mammary glands. Despite ample biologic plausibility, epidemiologic studies to date have yielded conflicting results. We investigated the associations between perinatal factors and subsequent breast cancer risk through meta-analyses. METHODS We reviewed breast cancer studies published from January 1966 to February 2007 that included data on birth weight, birth order, maternal age, gestational age, twin status, and maternal or paternal smoking. Meta-analyses using random effect models were employed to summarize the results. RESULTS We found that heavier birth weights were associated with increased breast cancer risk, with studies involving five categories of birth weight identifying odds ratios (ORs) of 1.24 (95% confidence interval [CI] 1.04 to 1.48) for 4,000 g or more and 1.15 (95% CI 1.04 to 1.26) for 3,500 g to 3,999 g, relative to a birth weight of 2,500 to 2,599 g. These studies provided no support for a J-shaped relationship of birthweight to risk. Support for an association with birthweight was also derived from studies based on three birth weight categories (OR 1.15 [95% CI 1.01 to 1.31] for > or =4,000 g relative to <3,000 g) and two birth weight categories (OR 1.09 [95% CI 1.02 to 1.18] for > or =3,000 g relative to <3,000 g). Women born to older mothers and twins were also at some increased risk, but the results were heterogeneous across studies and publication years. Birth order, prematurity, and maternal smoking were unrelated to breast cancer risk. CONCLUSION Our findings provide so [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"RESULTS We found that heavier birth weights were associated with increased breast cancer risk, with studies involving five categories of birth weight identifying odds ratios (ORs) of 1.24 (95% confidence interval [CI] 1.04 to 1.48) for 4,000 g or more and 1.15 (95% CI 1.04 to 1.26) for 3,500 g to 3,999 g, relative to a birth weight of 2,500 to 2,599 g. These studies provided no support for a J-shaped relationship of birthweight to risk.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1380, "doc_id": "17450673", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Reduced responsiveness to interleukin-2 in regulatory T cells is associated with autoimmune diseases such as Type 1 Diabetes.\n\nCANDIDATE_PASSAGE:\nInterleukin-2 gene variation impairs regulatory T cell function and causes autoimmunity Autoimmune diseases are thought to result from imbalances in normal immune physiology and regulation. Here, we show that autoimmune disease susceptibility and resistance alleles on mouse chromosome 3 (Idd3) correlate with differential expression of the key immunoregulatory cytokine interleukin-2 (IL-2). In order to test directly that an approximately twofold reduction in IL-2 underpins the Idd3-linked destabilization of immune homeostasis, we show that engineered haplodeficiency of Il2 gene expression not only reduces T cell IL-2 production by twofold but also mimics the autoimmune dysregulatory effects of the naturally occurring susceptibility alleles of Il2. Reduced IL-2 production achieved by either genetic mechanism correlates with reduced function of CD4+ CD25+ regulatory T cells, which are critical for maintaining immune homeostasis.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1028", "doc_id": "13923140", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: \"Would a man smell a rose then throw it away?\n\nABSTRACT:\nBreast cancer is the most common malignancy afflicting women, and the most common cancer overall in Jordan. A woman's decision to go for screening is influenced by her social support network. This study aims to explore Jordanian men's individual and contextual perspectives on women's breast cancer and their own role in the breast health of the females within their families. An explorative qualitative design was used to purposively recruit 24 married men aged 27 to 65 years (median 43 years) from four governorates in Jordan. Data in the form of interviews transcriptions was subjected to qualitative content analysis. Three themes were identified: a) Supporting one's wife; b) Marital needs and obligations; c) Constrained by a culture of destiny and shame. The first theme was built on men's feelings of responsibility for the family's health and well-being, their experiences of encouraging their wives to seek health care and their providing counselling and instrumental support. The second theme emerged from men's views about other men's rejection of a wife inflicted by breast cancer, their own perceptions of diminished femininity due to mastectomy and their own concerns about protecting the family from the hereditary risk of breast cancer. The third theme was seen in men's perception of breast cancer as an inevitable act of God that is far away from one's own family, in associating breast cancer with improper behaviour and in their readiness to face the culture of Eib (shame).", "output": "{\"label\": \"maybe\", \"rationale\": \"Jordanian men perceive themselves as having a vital role in supporting, guiding and encouraging their wives to follow breast cancer early detection recommendations. Breast health awareness campaigns could involve husbands to capitalize on family support.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 24160268, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Upregulation of mosGCTL-1 is induced upon infection with West Nile virus.\n\nCANDIDATE_ABSTRACT:\nTITLE: A C-Type Lectin Collaborates with a CD45 Phosphatase Homolog to Facilitate West Nile Virus Infection of Mosquitoes\nABSTRACT: West Nile virus (WNV) is the most common arthropod-borne flavivirus in the United States; however, the vector ligand(s) that participate in infection are not known. We now show that an Aedes aegypti C-type lectin, mosGCTL-1, is induced by WNV, interacts with WNV in a calcium-dependent manner, and facilitates infection in vivo and in vitro. A mosquito homolog of human CD45 in A. aegypti, designated mosPTP-1, recruits mosGCTL-1 to enable viral attachment to cells and to enhance viral entry. In vivo experiments show that mosGCTL-1 and mosPTP-1 function as part of the same pathway and are critical for WNV infection of mosquitoes. A similar phenomenon was also observed in Culex quinquefasciatus, a natural vector of WNV, further demonstrating that these genes participate in WNV infection. During the mosquito blood-feeding process, WNV infection was blocked in vivo with mosGCTL-1 antibodies. A molecular understanding of flaviviral-arthropod interactions may lead to strategies to control viral dissemination in nature.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In vivo experiments show that mosGCTL-1 and mosPTP-1 function as part of the same pathway and are critical for WNV infection of mosquitoes.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1352, "doc_id": "12885341", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Pyridostatin induces double-strand breaks accumulation.\n\nCANDIDATE_PASSAGE:\nGenetic and physical analysis of double-strand break repair and recombination in Saccharomyces cerevisiae. We have investigated HO endonuclease-induced double-strand break (DSB) recombination and repair in a LACZ duplication plasmid in yeast. A 117-bp MATa fragment, embedded in one copy of LACZ, served as a site for initiation of a DSB when HO endonuclease was expressed. The DSB could be repaired using wild-type sequences located on a second, promoterless, copy of LACZ on the same plasmid. In contrast to normal mating-type switching, crossing-over associated with gene conversion occurred at least 50% of the time. The proportion of conversion events accompanied by exchange was greater when the two copies of LACZ were in direct orientation (80%), than when inverted (50%). In addition, the fraction of plasmids lost was significantly greater in the inverted orientation. The kinetics of appearance of intermediates and final products were also monitored. The repair of the DSB is slow, requiring at least an hour from the detection of the HO-cut fragments to completion of repair. Surprisingly, the appearance of the two reciprocal products of crossing over did not occur with the same kinetics. For example, when the two LACZ sequences were in the direct orientation, the HO-induced formation of a large circular deletion product was not accompanied by the appearance of a small circular reciprocal product. We suggest that these differences may reflect two kinetically separable processes, one involving only one cut end and the other resulting from the concerted participation of both ends of the DSB.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "997", "doc_id": "25462689", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Intra-cerebroventricular infusion of amyloid-β oligomers reduces expression of fibronectin type-III domain-containing protein 5 mRNA in mice hippocampi.\n\nCANDIDATE_PASSAGE:\nEpigenetic therapy activates type I interferon signaling in murine ovarian cancer to reduce immunosuppression and tumor burden. Ovarian cancer is the most lethal of all gynecological cancers, and there is an urgent unmet need to develop new therapies. Epithelial ovarian cancer (EOC) is characterized by an immune suppressive microenvironment, and response of ovarian cancers to immune therapies has thus far been disappointing. We now find, in a mouse model of EOC, that clinically relevant doses of DNA methyltransferase and histone deacetylase inhibitors (DNMTi and HDACi, respectively) reduce the immune suppressive microenvironment through type I IFN signaling and improve response to immune checkpoint therapy. These data indicate that the type I IFN response is required for effective in vivo antitumorigenic actions of the DNMTi 5-azacytidine (AZA). Through type I IFN signaling, AZA increases the numbers of CD45+ immune cells and the percentage of active CD8+ T and natural killer (NK) cells in the tumor microenvironment, while reducing tumor burden and extending survival. AZA also increases viral defense gene expression in both tumor and immune cells, and reduces the percentage of macrophages and myeloid-derived suppressor cells in the tumor microenvironment. The addition of an HDACi to AZA enhances the modulation of the immune microenvironment, specifically increasing T and NK cell activation and reducing macrophages over AZA treatment alone, while further increasing the survival of the mice. Finally, a triple combination of DNMTi/HDACi plus the immune checkpoint inhibitor α-PD-1 provides the best antitumor effect and longest overall survival, and may be an attractive candidate for future clinical trials in ovarian cancer.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "655", "doc_id": "9767444", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Commelina yellow mottle virus' (ComYMV) genome consists of 7489 baise pairs.\n\nCANDIDATE_ABSTRACT:\nTITLE: PML induces compaction, TRF2 depletion and DNA damage signaling at telomeres and promotes their alternative lengthening.\nABSTRACT: The alternative lengthening of telomeres (ALT) mechanism allows cancer cells to escape senescence and apoptosis in the absence of active telomerase. A characteristic feature of this pathway is the assembly of ALT-associated promyelocytic leukemia (PML) nuclear bodies (APBs) at telomeres. Here, we dissected the role of APBs in a human ALT cell line by performing an RNA interference screen using an automated 3D fluorescence microscopy platform and advanced 3D image analysis. We identified 29 proteins that affected APB formation, which included proteins involved in telomere and chromatin organization, protein sumoylation and DNA repair. By integrating and extending these findings, we found that APB formation induced clustering of telomere repeats, telomere compaction and concomitant depletion of the shelterin protein TRF2 (also known as TERF2). These APB-dependent changes correlated with the induction of a DNA damage response at telomeres in APBs as evident by a strong enrichment of the phosphorylated form of the ataxia telangiectasia mutated (ATM) kinase. Accordingly, we propose that APBs promote telomere maintenance by inducing a DNA damage response in ALT-positive tumor cells through changing the telomeric chromatin state to trigger ATM phosphorylation.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 279, "doc_id": "213017", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: RAD52 is involved in break-induced DNA replication (BIR).\n\nCANDIDATE_PASSAGE:\nHuman cancer cells utilize mitotic DNA synthesis to resist replication stress at telomeres regardless of their telomere maintenance mechanism Telomeres resemble common fragile sites (CFSs) in that they are difficult-to-replicate and exhibit fragility in mitosis in response to DNA replication stress. At CFSs, this fragility is associated with a delay in the completion of DNA replication until early mitosis, whereupon cells are proposed to switch to a RAD52-dependent form of break-induced replication. Here, we show that this mitotic DNA synthesis (MiDAS) is also a feature of human telomeres. Telomeric MiDAS is not restricted to those telomeres displaying overt fragility, and is a feature of a wide range of cell lines irrespective of whether their telomeres are maintained by telomerase or by the alternative lengthening of telomeres (ALT) mechanism. MiDAS at telomeres requires RAD52, and is mechanistically similar to CFS-associated MiDAS, with the notable exception that telomeric MiDAS does not require the MUS81-EME1 endonuclease. We propose a model whereby replication stress initiates a RAD52-dependent form of break-induced replication that bypasses a requirement for MUS81-EME1 to complete DNA synthesis in mitosis.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1003", "doc_id": "4899981", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cancer cells can stimulate the accumulation of intra-tumoural myeloid-derived suppressor cells by promoting granulocyte colony stimulating factor production.\n\nCANDIDATE_ABSTRACT:\nTITLE: Oncogenic mTOR signaling recruits myeloid-derived suppressor cells to promote tumor initiation\nABSTRACT: Myeloid-derived suppressor cells (MDSCs) play critical roles in primary and metastatic cancer progression. MDSC regulation is widely variable even among patients harbouring the same type of malignancy, and the mechanisms governing such heterogeneity are largely unknown. Here, integrating human tumour genomics and syngeneic mammary tumour models, we demonstrate that mTOR signalling in cancer cells dictates a mammary tumour's ability to stimulate MDSC accumulation through regulating G-CSF. Inhibiting this pathway or its activators (for example, FGFR) impairs tumour progression, which is partially rescued by restoring MDSCs or G-CSF. Tumour-initiating cells (TICs) exhibit elevated G-CSF. MDSCs reciprocally increase TIC frequency through activating Notch in tumour cells, forming a feedforward loop. Analyses of primary breast cancers and patient-derived xenografts corroborate these mechanisms in patients. These findings establish a non-canonical oncogenic role of mTOR signalling in recruiting pro-tumorigenic MDSCs and show how defined cancer subsets may evolve to promote and depend on a distinct immune microenvironment.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here, integrating human tumour genomics and syngeneic mammary tumour models, we demonstrate that mTOR signalling in cancer cells dictates a mammary tumour's ability to stimulate MDSC accumulation through regulating G-CSF.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 223, "doc_id": "2014909", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Systemic immunosuppressive (IS) therapy does not enhance the chance of cancer mortality in patients with inflammatory eye disease (IED)\n\nCANDIDATE_ABSTRACT:\nTITLE: Beyond melanoma: inhibiting the PD-1/PD-L1 pathway in solid tumors.\nABSTRACT: Immune checkpoint inhibitors have been identified as breakthrough treatment in melanoma given its dramatic response to PD-1/PD-L1 blockade. This is likely to extend to many other cancers as hundreds of clinical trials are being conducted or proposed using this exciting modality of therapy in a variety of malignancies. While immune checkpoint inhibitors have been extensively studied in melanoma and more recently in lung cancer, little is known regarding immune checkpoint blockade in other cancers. This review will focus on the tumor immune microenvironment, the expression of PD-1/PD-L1 and the effect of immune modulation using PD-1 or PD-L1 inhibitors in patients with head and neck, prostate, urothelial, renal, breast, gastrointestinal and lung cancers.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1125, "doc_id": "1900152", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does rugby headgear prevent concussion?\n\nABSTRACT:\nTo examine the attitudes of players and coaches to the use of protective headgear, particularly with respect to the prevention of concussion. A questionnaire designed to assess attitudes to headgear was administered to 63 players from four different Canadian teams, each representing a different level of play (high school, university, community club, national). In addition, coaches from all four levels were questioned about team policies and their personal opinions about the use of headgear to prevent concussion. Although the players tended to believe that the headgear could prevent concussion (62%), the coaches were less convinced (33%). Despite the players' belief that headgear offers protection against concussion, only a minority reported wearing headgear (27%) and few (24%) felt that its use should be made mandatory. Common reasons for not wearing headgear were \"its use is not mandatory\", \"it is uncomfortable\", and \"it costs too much\".", "output": "{\"label\": \"maybe\", \"rationale\": \"Although most players in the study believe that rugby headgear may prevent concussion, only a minority reported wearing it. Coaches tended to be less convinced than the players that rugby headgear can prevent concussion.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 11867487, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Genetic deficiency of mast cells leads to decreased weight gain in a mouse model of diet-induced obesity.\n\nCANDIDATE_ABSTRACT:\nTITLE: Deficiency and pharmacological stabilization of mast cells reduce diet-induced obesity and diabetes in mice\nABSTRACT: Although mast cell functions have classically been related to allergic responses, recent studies indicate that these cells contribute to other common diseases such as multiple sclerosis, rheumatoid arthritis, atherosclerosis, aortic aneurysm and cancer. This study presents evidence that mast cells also contribute to diet-induced obesity and diabetes. For example, white adipose tissue (WAT) from obese humans and mice contain more mast cells than WAT from their lean counterparts. Furthermore, in the context of mice on a Western diet, genetically induced deficiency of mast cells, or their pharmacological stabilization, reduces body weight gain and levels of inflammatory cytokines, chemokines and proteases in serum and WAT, in concert with improved glucose homeostasis and energy expenditure. Mechanistic studies reveal that mast cells contribute to WAT and muscle angiogenesis and associated cell apoptosis and cathepsin activity. Adoptive transfer experiments of cytokine-deficient mast cells show that these cells, by producing interleukin-6 (IL-6) and interferon-gamma (IFN-gamma), contribute to mouse adipose tissue cysteine protease cathepsin expression, apoptosis and angiogenesis, thereby promoting diet-induced obesity and glucose intolerance. Our results showing reduced obesity and diabetes in mice treated with clinically available mast cell-stabilizing agents suggest the potential of developing new therapies for these common human metabolic disorders.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Furthermore, in the context of mice on a Western diet, genetically induced deficiency of mast cells, or their pharmacological stabilization, reduces body weight gain and levels of inflammatory cytokines, chemokines and proteases in serum and WAT, in concert with improved glucose homeostasis and energy expenditure.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 458, "doc_id": "597790", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Cellular clocks are not predictive of mitosis timing in NIH 3T3 cells.\n\nCANDIDATE_PASSAGE:\nCoding of Sweet, Bitter, and Umami Tastes Different Receptor Cells Sharing Similar Signaling Pathways Mammals can taste a wide repertoire of chemosensory stimuli. Two unrelated families of receptors (T1Rs and T2Rs) mediate responses to sweet, amino acids, and bitter compounds. Here, we demonstrate that knockouts of TRPM5, a taste TRP ion channel, or PLCbeta2, a phospholipase C selectively expressed in taste tissue, abolish sweet, amino acid, and bitter taste reception, but do not impact sour or salty tastes. Therefore, despite relying on different receptors, sweet, amino acid, and bitter transduction converge on common signaling molecules. Using PLCbeta2 taste-blind animals, we then examined a fundamental question in taste perception: how taste modalities are encoded at the cellular level. Mice engineered to rescue PLCbeta2 function exclusively in bitter-receptor expressing cells respond normally to bitter tastants but do not taste sweet or amino acid stimuli. Thus, bitter is encoded independently of sweet and amino acids, and taste receptor cells are not broadly tuned across these modalities.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "242", "doc_id": "718601", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: CRP is positively correlated with postoperative mortality following Coronary Artery Bypass Graft (CABG) surgery.\n\nCANDIDATE_PASSAGE:\nCirculating trimethylamine N‐oxide and the risk of cardiovascular diseases: a systematic review and meta‐analysis of 11 prospective cohort studies Circulating trimethylamine N-oxide (TMAO), a canonical metabolite from gut flora, has been related to the risk of cardiovascular disorders. However, the association between circulating TMAO and the risk of cardiovascular events has not been quantitatively evaluated. We performed a systematic review and meta-analysis of all available cohort studies regarding the association between baseline circulating TMAO and subsequent cardiovascular events. Embase and PubMed databases were searched for relevant cohort studies. The overall hazard ratios for the developing of cardiovascular events (CVEs) and mortality were extracted. Heterogeneity among the included studies was evaluated with Cochran's Q Test and I2 statistics. A random-effect model or a fixed-effect model was applied depending on the heterogeneity. Subgroup analysis and meta-regression were used to evaluate the source of heterogeneity. Among the 11 eligible studies, three reported both CVE and mortality outcome, one reported only CVEs and the other seven provided mortality data only. Higher circulating TMAO was associated with a 23% higher risk of CVEs (HR = 1.23, 95% CI: 1.07-1.42, I2 = 31.4%) and a 55% higher risk of all-cause mortality (HR = 1.55, 95% CI: 1.19-2.02, I2 = 80.8%). Notably, the latter association may be blunted by potential publication bias, although sensitivity analysis by omitting one study at a time did not significantly change the results. Further subgroup analysis and meta-regression did not support that the location of the study, follow-up duration, publication year, population characteristics or the samples of TMAO affect the results sign [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "214", "doc_id": "6793674", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The density of cytokine receptor bearing cells has no effect on the distance over which cytokines act.\n\nCANDIDATE_ABSTRACT:\nTITLE: Transgenic Interleukin 10 Prevents Induction of Experimental Autoimmune Encephalomyelitis \nABSTRACT: The effectiveness of interleukin 10 (IL-10) in the treatment of autoimmune-mediated central nervous system inflammation is controversial. Studies of the model system, experimental autoimmune encephalomyelitis (EAE), using various routes, regimens, and delivery methods of IL-10 suggest that these variables may affect its immunoregulatory function. To study the influence of these factors on IL-10 regulation of EAE pathogenesis, we have analyzed transgenic mice expressing human IL-10 (hIL-10) transgene under the control of a class II major histocompatibility complex (MHC) promoter. The hIL-10 transgenic mice are highly resistant to EAE induced by active immunization, and this resistance appears to be mediated by suppression of autoreactive T cell function. Myelin-reactive T helper 1 cells are induced but nonpathogenic in the IL-10 transgenic mice. Antibody depletion confirmed that EAE resistance is dependent on the presence of the transgenic IL-10. Mice expressing the hIL-10 transgene but not the endogenous murine IL-10 gene demonstrated that transgenic IL-10 from MHC class II–expressing cells is sufficient to block induction of EAE. This study demonstrates that IL-10 can prevent EAE completely if present at appropriate levels and times during disease induction.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1211, "doc_id": "854417", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is the voice of the patients : allergic rhinitis a trivial disease?\n\nABSTRACT:\nPatient and physician perspectives on the impact of allergic rhinitis have previously been studied in the general population. We evaluated the burden of allergic rhinitis among patients from the members of European allergy patient organizations. The Patient Voice Allergy Survey was a quantitative, self-completion survey of 3562 patients with allergic rhinitis (16 years and older). Background information on allergic rhinitis, severity of allergic rhinitis symptoms and their impact on lives, nonmedical measures for relieving of symptoms, types of medications, and concomitant conditions were evaluated. Almost 50% of the responders reported symptoms lasting for more than a season. Preventive household adjustments are expensive with little perceived benefit. Sleep and emotional life are affected by allergic rhinitis. Most patients are satisfied with the current allergic rhinitis medications; at least one-fifth report dissatisfaction. Patients perceive that allergic rhinitis worsens other concomitant allergic diseases.", "output": "{\"label\": \"no\", \"rationale\": \"Future management guidelines for allergic rhinitis must take into account the results of this survey. Such guidelines must promote relief from the emotional burden of allergic rhinitis and from the negative impact on daily activities, encourage patient education, and maintain and build on the strong partnership between patients and healthcare professionals.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 18188010, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: FoxO3a activation in neuronal death is mediated by reactive oxygen species (ROS).\n\nCANDIDATE_PASSAGE:\nFunctional hemichannels in astrocytes: a novel mechanism of glutamate release. Little is known about the expression and possible functions of unopposed gap junction hemichannels in the brain. Emerging evidence suggests that gap junction hemichannels can act as stand-alone functional channels in astrocytes. With immunocytochemistry, dye uptake, and HPLC measurements, we show that astrocytes in vitro express functional hemichannels that can mediate robust efflux of glutamate and aspartate. Functional hemichannels were confirmed by passage of extracellular lucifer yellow (LY) into astrocytes in nominal divalent cation-free solution (DCFS) and the ability to block this passage with gap junction blocking agents. Glutamate/aspartate release (or LY loading) in DCFS was blocked by multivalent cations (Ca2+, Ba2+, Sr2+, Mg2+, and La3+) and by gap junction blocking agents (carbenoxolone, octanol, heptanol, flufenamic acid, and 18alpha-glycyrrhetinic acid) with affinities close to those reported for blockade of gap junction intercellular communication. Glutamate efflux via hemichannels was also accompanied by greatly reduced glutamate uptake. Glutamate release in DCFS, however, was not significantly mediated by reversal of the glutamate transporter: release did not saturate and was not blocked by glutamate transporter blockers. Control experiments in DCFS precluded glutamate release by volume-sensitive anion channels, P2X7 purinergic receptor pores, or general purinergic receptor activation. Blocking intracellular Ca2+ mobilization by BAPTA-AM or thapsigargin did not inhibit glutamate release in DCFS. Divalent cation removal also induced glutamate release from intact CNS white matter (acutely isolated optic nerve) that was blocked by carbenoxolone, suggesting the exist [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "431", "doc_id": "15657779", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Assessing treatment adherence is more beneficial to clinical practice than measuring routine outcomes.\n\nCANDIDATE_PASSAGE:\nAnxiety OBJECTIVES To examine the effect of routinely administered psychiatric questionnaires on the recognition, management, and outcome of psychiatric disorders in non-psychiatric settings. DATA SOURCES Embase, Medline, PsycLIT, Cinahl, Cochrane Controlled Trials Register, and hand searches of key journals. METHODS A systematic review of randomised controlled trials of the administration and routine feedback of psychiatric screening and outcome questionnaires to clinicians in non-psychiatric settings. Narrative overview of key design features and end points, together with a random effects quantitative synthesis of comparable studies. MAIN OUTCOME MEASURES Recognition of psychiatric disorders after feedback of questionnaire results; interventions for psychiatric disorders; and outcome of psychiatric disorders. RESULTS Nine randomised studies were identified that examined the use of common psychiatric instruments in primary care and general hospital settings. Studies compared the effect of the administration of these instruments followed by the feedback of the results to clinicians, with administration with no feedback. Meta-analytic pooling was possible for four of these studies (2457 participants), which measured the effect of feedback on the recognition of depressive disorders. Routine administration and feedback of scores for all patients (irrespective of score) did not increase the overall rate of recognition of mental disorders such as anxiety and depression (relative risk of detection of depression by clinician after feedback 0.95, 95% confidence interval 0.83 to 1.09). Two studies showed that routine administration followed by selective feedback for only high scorers increased the rate of recognition of depression (relative risk of detection of depre [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "134", "doc_id": "4695046", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Distant CREs are important for transcriptional regulation.\n\nCANDIDATE_PASSAGE:\nCell Stem Cell Review FoxO Transcription Factors and Stem Cell Homeostasis: Insights from the Hematopoietic System The forkhead O (FoxO) family of transcription factors participates in diverse physiologic processes, including induction of cell-cycle arrest, stress resistance, differentiation, apoptosis, and metabolism. Several recent studies indicate that FoxO-dependent signaling is required for long-term regenerative potential of the hematopoietic stem cell (HSC) compartment through regulation of HSC response to physiologic oxidative stress, quiescence, and survival. These observations link FoxO function in mammalian systems with the evolutionarily conserved role of FoxO in promotion of stress resistance and longevity in lower phylogenetic systems. Furthermore, these findings have implications for aging in higher organisms and in malignant stem cell biology, and suggest that FoxOs may play an important role in the maintenance and integrity of stem cell compartments in a broad spectrum of tissues.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "351", "doc_id": "16728949", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Birth-weight is positively associated with breast cancer.\n\nCANDIDATE_PASSAGE:\nIbuprofen for the treatment of patent ductus arteriosus in preterm or low birth weight (or both) infants. BACKGROUND Indomethacin is used as standard therapy to close a patent ductus arteriosus (PDA) but is associated with reduced blood flow to several organs. Ibuprofen, another cyclo-oxygenase inhibitor, may be as effective as indomethacin with fewer adverse effects. OBJECTIVES To determine the effectiveness and safety of ibuprofen compared with indomethacin, other cyclo-oxygenase inhibitor, placebo or no intervention for closing a patent ductus arteriosus in preterm, low birth weight, or preterm and low birth weight infants. SEARCH METHODS We searched The Cochrane Library, MEDLINE, EMBASE, Clincialtrials.gov, Controlled-trials.com, and www.abstracts2view.com/pas in May 2014. SELECTION CRITERIA Randomised or quasi-randomised controlled trials of ibuprofen for the treatment of a PDA in newborn infants. DATA COLLECTION AND ANALYSIS Data collection and analysis conformed to the methods of the Cochrane Neonatal Review Group. MAIN RESULTS We included 33 studies enrolling 2190 infants. Two studies compared intravenous (iv) ibuprofen versus placebo (270 infants). In one study (134 infants) ibuprofen reduced the incidence of failure to close a PDA (risk ratio (RR) 0.71, 95% confidence interval (CI) 0.51 to 0.99; risk difference (RD) -0.18, 95% CI -0.35 to -0.01; number needed to treat for an additional beneficial outcome (NNTB) 6, 95% CI 3 to 100). In one study (136 infants), ibuprofen reduced the composite outcome of infant mortality, infants who dropped out, or infants who required rescue treatment (RR 0.58, 95% CI 0.38 to 0.89; RD -0.22, 95% CI -0.38 to -0.06; NNTB 5, 95% CI 3 to 17). One study (64 infants) compared oral ibuprofen with placebo and noted a signif [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "179", "doc_id": "34544514", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Physical activity does not improve cognitive function in individuals with Alzheimers.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effect of physical activity on cognitive function in older adults at risk for Alzheimer disease: a randomized trial.\nABSTRACT: CONTEXT Many observational studies have shown that physical activity reduces the risk of cognitive decline; however, evidence from randomized trials is lacking. OBJECTIVE To determine whether physical activity reduces the rate of cognitive decline among older adults at risk. DESIGN AND SETTING Randomized controlled trial of a 24-week physical activity intervention conducted between 2004 and 2007 in metropolitan Perth, Western Australia. Assessors of cognitive function were blinded to group membership. PARTICIPANTS We recruited volunteers who reported memory problems but did not meet criteria for dementia. Three hundred eleven individuals aged 50 years or older were screened for eligibility, 89 were not eligible, and 52 refused to participate. A total of 170 participants were randomized and 138 participants completed the 18-month assessment. INTERVENTION Participants were randomly allocated to an education and usual care group or to a 24-week home-based program of physical activity. MAIN OUTCOME MEASURE Change in Alzheimer Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) scores (possible range, 0-70) over 18 months. RESULTS In an intent-to-treat analysis, participants in the intervention group improved 0.26 points (95% confidence interval, -0.89 to 0.54) and those in the usual care group deteriorated 1.04 points (95% confidence interval, 0.32 to 1.82) on the ADAS-Cog at the end of the intervention. The absolute difference of the outcome measure between the intervention and control groups was -1.3 points (95% confidence interval,-2.38 to -0.22) at the end of the intervention. At 18 months, participants in the intervention group improved 0.73 points (95% confidence interval, -1.27 to 0.03) on the ADAS-Cog, and those in the usual care group improved 0.04 p [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"RESULTS In an intent-to-treat analysis, participants in the intervention group improved 0.26 points (95% confidence interval, -0.89 to 0.54) and those in the usual care group deteriorated 1.04 points (95% confidence interval, 0.32 to 1.82) on the ADAS-Cog at the end of the intervention.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 944, "doc_id": "1642727", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Podocytes are motile and migrate in the presence of injury.\n\nCANDIDATE_ABSTRACT:\nTITLE: Fructosamine Is a Useful Indicator of Hyperglycaemia and Glucose Control in Clinical and Epidemiological Studies – Cross-Sectional and Longitudinal Experience from the AMORIS Cohort\nABSTRACT: CONTEXT Fructosamine is a glycemic biomarker which may be useful for indication and control of diabetes respectively. OBJECTIVE The objective of the study was to evaluate fructosamine as an indicator of hyperglycaemia and glucose control in subjects with diabetes. DESIGN, SETTING & PATIENTS From the AMORIS cohort, subjects with serum glucose, fructosamine and HbA1c from the same examination were studied cross-sectionally and longitudinally (n = 10,987; 5,590 overnight-fasting). The guidelines of the American Diabetes Association were followed for classification of prediabetes and diabetes. Separate analyses were performed in patients with a newly detected or a known diagnosis of type 1 or type 2 diabetes respectively. RESULTS All three biomarkers were strongly correlated. With regard to the association between fructosamine and HbA1c Pearson linear correlation coefficients in the range of 0.67-0.75 were observed in fasting and non-fasting subjects with type 1 or type 2 diabetes. Analyses of glucose control in fasting patients with type 2 diabetes having all three biomarkers measured at three separate occasions within on average 290 days of the index examination showed similar trends over time for glucose, fructosamine and HbA1c. Discrimination of subjects with and without diabetes across the range of fructosamine levels was good (area under curve (AUC) 0.91-0.95) and a fructosamine level of 2.5 mmol/L classified subjects to diabetes with a sensitivity of 61% and a specificity of 97%. CONCLUSIONS Fructosamine is closely associated with HbA1c and glucose respectively and may be a useful biomarker of hyperglycaemia and glucose control in clinical and epidemiological studies.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 957, "doc_id": "1538080", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Bone marrow cells contribute to adult macrophage compartments.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tissue-resident macrophages self-maintain locally throughout adult life with minimal contribution from circulating monocytes.\nABSTRACT: Despite accumulating evidence suggesting local self-maintenance of tissue macrophages in the steady state, the dogma remains that tissue macrophages derive from monocytes. Using parabiosis and fate-mapping approaches, we confirmed that monocytes do not show significant contribution to tissue macrophages in the steady state. Similarly, we found that after depletion of lung macrophages, the majority of repopulation occurred by stochastic cellular proliferation in situ in a macrophage colony-stimulating factor (M-Csf)- and granulocyte macrophage (GM)-CSF-dependent manner but independently of interleukin-4. We also found that after bone marrow transplantation, host macrophages retained the capacity to expand when the development of donor macrophages was compromised. Expansion of host macrophages was functional and prevented the development of alveolar proteinosis in mice transplanted with GM-Csf-receptor-deficient progenitors. Collectively, these results indicate that tissue-resident macrophages and circulating monocytes should be classified as mononuclear phagocyte lineages that are independently maintained in the steady state.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We also found that after bone marrow transplantation, host macrophages retained the capacity to expand when the development of donor macrophages was compromised.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 183, "doc_id": "12827098", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Pseudogene PTENP1 encodes a transcript that regulates PTEN expression.\n\nCANDIDATE_ABSTRACT:\nTITLE: A coding-independent function of gene and pseudogene mRNAs regulates tumour biology\nABSTRACT: The canonical role of messenger RNA (mRNA) is to deliver protein-coding information to sites of protein synthesis. However, given that microRNAs bind to RNAs, we hypothesized that RNAs could possess a regulatory role that relies on their ability to compete for microRNA binding, independently of their protein-coding function. As a model for the protein-coding-independent role of RNAs, we describe the functional relationship between the mRNAs produced by the PTEN tumour suppressor gene and its pseudogene PTENP1 and the critical consequences of this interaction. We find that PTENP1 is biologically active as it can regulate cellular levels of PTEN and exert a growth-suppressive role. We also show that the PTENP1 locus is selectively lost in human cancer. We extended our analysis to other cancer-related genes that possess pseudogenes, such as oncogenic KRAS. We also demonstrate that the transcripts of protein-coding genes such as PTEN are biologically active. These findings attribute a novel biological role to expressed pseudogenes, as they can regulate coding gene expression, and reveal a non-coding function for mRNAs.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We find that PTENP1 is biologically active as it can regulate cellular levels of PTEN and exert a growth-suppressive role.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 984, "doc_id": "6828370", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: 40mg/day dosage of folic acid and 2mg/day dosage of vitamin B12 does not affect chronic kidney disease (CKD) progression.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effect of homocysteine lowering on mortality and vascular disease in advanced chronic kidney disease and end-stage renal disease: a randomized controlled trial.\nABSTRACT: CONTEXT High plasma homocysteine levels are a risk factor for mortality and vascular disease in observational studies of patients with chronic kidney disease. Folic acid and B vitamins decrease homocysteine levels in this population but whether they lower mortality is unknown. OBJECTIVE To determine whether high doses of folic acid and B vitamins administered daily reduce mortality in patients with chronic kidney disease. DESIGN, SETTING, AND PARTICIPANTS Double-blind randomized controlled trial (2001-2006) in 36 US Department of Veterans Affairs medical centers. Median follow-up was 3.2 years for 2056 participants aged 21 years or older with advanced chronic kidney disease (estimated creatinine clearance < or =30 mL/min) (n = 1305) or end-stage renal disease (n = 751) and high homocysteine levels (> or = 15 micromol/L). INTERVENTION Participants received a daily capsule containing 40 mg of folic acid, 100 mg of pyridoxine hydrochloride (vitamin B6), and 2 mg of cyanocobalamin (vitamin B12) or a placebo. MAIN OUTCOME MEASURES The primary outcome was all-cause mortality. Secondary outcomes included myocardial infarction (MI), stroke, amputation of all or part of a lower extremity, a composite of these 3 plus all-cause mortality, time to initiation of dialysis, and time to thrombosis of arteriovenous access in hemodialysis patients. RESULTS Mean baseline homocysteine level was 24.0 micromol/L in the vitamin group and 24.2 micromol/L in the placebo group. It was lowered 6.3 micromol/L (25.8%; P < .001) in the vitamin group and 0.4 micromol/L (1.7%; P = .14) in the placebo group at 3 months, but there was no significant effect on mortality (448 vitamin group deaths vs 436 placebo group deaths) (hazard ratio [HR], 1.04; 95% CI, 0.91-1.18). No significant effects [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"RESULTS Mean baseline homocysteine level was 24.0 micromol/L in the vitamin group and 24.2 micromol/L in the placebo group.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 12, "doc_id": "33409100", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Participants who quit smoking reduce lung cancer risk by approximately 50%.\n\nCANDIDATE_PASSAGE:\nPredictive value of bone resorption and formation markers in cancer patients with bone metastases receiving the bisphosphonate zoledronic acid. PURPOSE Three large, randomized trials of patients with bone metastases recently demonstrated that zoledronic acid reduces the risk of skeletal-related events. These trials provide an opportunity for investigating the correlation between bone metabolism and clinical outcome during bisphosphonate therapy. PATIENTS AND METHODS Urinary measurements of N-telopeptide (Ntx) and serum bone alkaline phosphatase (BAP) were obtained in 1,824 bisphosphonate-treated patients-1,462 with zoledronic acid (breast, 490; prostate, 411; myeloma, 210; non-small-cell lung, 183; other, 168) and 362 with pamidronate (breast, 254; myeloma, 108). This exploratory cohort analysis grouped patients by baseline and most recent levels of Ntx as low (< 50 nmol/mmol creatinine), moderate (50 to 99 nmol/mmol creatinine), or high (> or = 100 nmol/mmol creatinine), and BAP as low (< 146 U/L) or high (> or = 146 U/L). The relative risks for negative clinical outcomes were estimated for each group using multiple-event and Cox regression models with time-varying covariates. RESULTS Patients with high and moderate Ntx levels had 2-fold increases in their risk of skeletal complications and disease progression compared with patients with low Ntx levels (P < .001 for all). High Ntx levels in each solid tumor category were associated with a 4- to 6-fold increased risk of death on study, and moderate Ntx levels a 2- to 4-fold increased risk compared with low Ntx levels (P < .001 for all). Bone alkaline phosphatase also showed some correlation with risk of negative clinical outcomes. CONCLUSION The bone resorption marker Ntx provides valuable prognostic informa [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "919", "doc_id": "8037453", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: During the primary early antibody response activated B cells migrate toward the inner-and outer paracortical areas where oxysterol accumulation is generated by stromal cells.\n\nCANDIDATE_PASSAGE:\nMonitoring Tumorigenesis and Senescence In Vivo with a p16INK4a-Luciferase Model Monitoring cancer and aging in vivo remains experimentally challenging. Here, we describe a luciferase knockin mouse (p16(LUC)), which faithfully reports expression of p16(INK4a), a tumor suppressor and aging biomarker. Lifelong assessment of luminescence in p16(+/LUC) mice revealed an exponential increase with aging, which was highly variable in a cohort of contemporaneously housed, syngeneic mice. Expression of p16(INK4a) with aging did not predict cancer development, suggesting that the accumulation of senescent cells is not a principal determinant of cancer-related death. In 14 of 14 tested tumor models, expression of p16(LUC) was focally activated by early neoplastic events, enabling visualization of tumors with sensitivity exceeding other imaging modalities. Activation of p16(INK4a) was noted in the emerging neoplasm and surrounding stromal cells. This work suggests that p16(INK4a) activation is a characteristic of all emerging cancers, making the p16(LUC) allele a sensitive, unbiased reporter of neoplastic transformation.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "362", "doc_id": "17717391", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: IgA plasma cells that are specific for transglutaminase 2 are scarce in the duodenal mucosa of celiac disease patients when the disease is active.\n\nCANDIDATE_ABSTRACT:\nTITLE: High abundance of plasma cells secreting transglutaminase 2–specific IgA autoantibodies with limited somatic hypermutation in celiac disease intestinal lesions\nABSTRACT: Celiac disease is an immune-mediated disorder in which mucosal autoantibodies to the enzyme transglutaminase 2 (TG2) are generated in response to the exogenous antigen gluten in individuals who express human leukocyte antigen HLA-DQ2 or HLA-DQ8 (ref. 3). We assessed in a comprehensive and nonbiased manner the IgA anti-TG2 response by expression cloning of the antibody repertoire of ex vivo–isolated intestinal antibody-secreting cells (ASCs). We found that TG2-specific plasma cells are markedly expanded within the duodenal mucosa in individuals with active celiac disease. TG2-specific antibodies were of high affinity yet showed little adaptation by somatic mutations. Unlike infection-induced peripheral blood plasmablasts, the TG2-specific ASCs had not recently proliferated and were not short-lived ex vivo. Altogether, these observations demonstrate that there is a germline repertoire with high affinity for TG2 that may favor massive generation of autoreactive B cells. TG2-specific antibodies did not block enzymatic activity and served as substrates for TG2-mediated crosslinking when expressed as IgD or IgM but not as IgA1 or IgG1. This could result in preferential recruitment of plasma cells from naive IgD- and IgM-expressing B cells, thus possibly explaining why the antibody response to TG2 bears signs of a primary immune response despite the disease chronicity.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We found that TG2-specific plasma cells are markedly expanded within the duodenal mucosa in individuals with active celiac disease.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 553, "doc_id": "1471041", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is parathyroid hormone associated with the LV mass after aortic valve replacement?\n\nABSTRACT:\nLV hypertrophy (LVH) is frequent after aortic valve replacement (AVR) and is often associated with comorbidities, including hypertension, obesity, renal failure and prosthesis-patient mismatch (PPM). However, whether other biological mechanism(s) may participate to LVH after AVR is still unknown. Parathyroid hormone (PTH) may play a role in LVH. However, it is presently unknown whether PTH is associated with LVH in patients that have undergone an AVR. In this cross-sectional study, 195 patients have been investigated at a mean of 8 ± 3.5 years following AVR. LV function and mass were evaluated by Doppler echocardiography. The plasma levels of PTH, 25-hydroxyvitamin D (25-OHD), calcium and phosphate were measured. There were 102 (52%) patients with LVH after AVR. In univariate analyses, PTH blood level was associated with LV mass (LVMi) and LVH. After adjustment for other risk factors, elevated PTH remained associated with LVMi (p=0.003) and LVH (p=0.02). In turn, the blood levels of 25-OHD and the renal function (GFR) were independently and inversely related to the blood level of PTH.", "output": "{\"label\": \"yes\", \"rationale\": \"After AVR, the level of PTH is independently associated with LVH. In turn, the level of PTH is related with the renal function and the level of 25-OHD.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25095827, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Infection of human T-cell lymphotropic virus type 1 is most frequent in individuals of African origin.\n\nCANDIDATE_PASSAGE:\nImmune activation and HIV persistence: implications for curative approaches to HIV infection. Despite complete or near-complete suppression of human immunodeficiency virus (HIV) replication with combination antiretroviral therapy, both HIV and chronic inflammation/immune dysfunction persist indefinitely. Untangling the association between the virus and the host immune environment during therapy might lead to novel interventions aimed at either curing the infection or preventing the development of inflammation-associated end-organ disease. Chronic inflammation and immune dysfunction might lead to HIV persistence by causing virus production, generating new target cells, enabling infecting of activated and resting target cells, altering the migration patterns of susceptible target cells, increasing the proliferation of infected cells, and preventing normal HIV-specific clearance mechanisms from function. Chronic HIV production or replication might contribute to persistent inflammation and immune dysfunction. The rapidly evolving data on these issues strongly suggest that a vicious cycle might exist in which HIV persistence causes inflammation that in turn contributes to HIV persistence.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "628", "doc_id": "44562058", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Transcription rates in S. cerevisiae range between 7 and 12 kb/min.\n\nCANDIDATE_PASSAGE:\nThe Self-Incompatibility Genes of Brassica: Expression and Use in Genetic Ablation of Floral Tissues INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 394 POLLINATION AND POLLEN TUBE GROWTH . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 395 Interaction s between the M ale G ameto phyte and Pistil . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 395 SelfIncom patibili ty Systems: Gameto phytic and S poro phyti c Determin ation of Pollen Phenoty pe . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 397 DEVELOPMENTAL S TUDIES OF REPRODUCTIVE STRUCTURES . . . . . . . . .. . . ... . . . . 398 Tissues of the Pistil with Special Reference to Pollination Functions 398 The Male Gametophyte . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 399 MOLECULAR ANALYSIS OF SELF-INCOMPATIBILITY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40 1 The S-M ultigene F amily o j Brassica. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . 402 Allelism at the S-Lo cus and the SLG Gene\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\" 402 The S-Locus Related (SLR) Genes 405 Molecular Complexity oj the S-Locus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 407 EXPRESSION OF THE SLG GENE IN PIS TILS AND ANTHERS . . . . . . . . . . . . . . . . . . . . . . . 409 Expression in Cruc ifers . . . . . . . . . . . . . . . . . . . . . . . . . [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1315", "doc_id": "86217760", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Increased microtubule acetylation worsens interference of axonal transport caused by LRRK2 Roc-COR domain mutations.\n\nCANDIDATE_PASSAGE:\nIncreasing microtubule acetylation rescues axonal transport and locomotor deficits caused by LRRK2 Roc-COR domain mutations Leucine-rich repeat kinase 2 (LRRK2) mutations are the most common genetic cause of Parkinson's disease. LRRK2 is a multifunctional protein affecting many cellular processes and has been described to bind microtubules. Defective microtubule-based axonal transport is hypothesized to contribute to Parkinson's disease, but whether LRRK2 mutations affect this process to mediate pathogenesis is not known. Here we find that LRRK2 containing pathogenic Roc-COR domain mutations (R1441C, Y1699C) preferentially associates with deacetylated microtubules, and inhibits axonal transport in primary neurons and in Drosophila, causing locomotor deficits in vivo. In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport. In vivo knockdown of the deacetylases HDAC6 and Sirt2, or administration of TSA rescues both axonal transport and locomotor behavior. Thus, this study reveals a pathogenic mechanism and a potential intervention for Parkinson's disease.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "615", "doc_id": "9638032", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does a new guidance device facilitate percutaneous puncture of the foramen ovale in human cadavers?\n\nABSTRACT:\nTrigeminal neuralgia is the most common neurological cause for facial pain. Contemporary interventional treatment relies on surgical microvascular decompression or, alternatively, percutaneous interventions targeting the semilunar ganglion via the foramen ovale. For the latter approach, only free-hand punctures using fluoroscopy devices have been reported. Therefore, the present study aimed to evaluate a new fluoroscopy-based guidance device for transforaminal puncture. Two experienced examiners punctured the foramen ovale bilaterally free-hand, and using a guidance device in human cadavers (n = 9). The number of attempts for puncture was recorded. A new attempt was counted each time the needle had to be retracted for redirection. As compared to the free-hand puncture of the foramen ovale (4.44 +/- 2.79), the new guidance device significantly reduced the number of trials needed (1.37 +/- 0.69).", "output": "{\"label\": \"yes\", \"rationale\": \"The employment of a guidance device facilitated percutaneous transforaminal puncture and resulted in a significantly decreased number of puncture attempts as compared to free-hand techniques in human cadavers.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 15574548, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: RUNX is not expressed in skin tissue.\n\nCANDIDATE_PASSAGE:\nThe Bone and Joint Decade 2000-2010. The World Health Organisation has declared the period 2000 to 2010 the Bone and Joint Decade. This is indeed timely and appropriate. Hundreds of millions of people in the world today are beset with a host of disabilities caused by trauma, ageing and degeneration and other affections of the musculo-skeletal system. With the state of art of orthopaedic surgery and rheumatology, sufferers of bone and joint disabilities have benefited a great deal from advances in pharmacology, newer techniques of imaging, surgery and man-made materials to replace diseased or damaged bone and cartilage. However, man-made materials, being non-living, are subject to wear and tear and loosening in the host bone. As we advance into the Bone and Joint Decade, further improvement in the treatment of bone and joint diseases lies in more basic cartilage and bone research. The Human Genome Project has provided us with a better understanding of disease genes and the possibility of gene manipulation to prevent and treat specific diseases. Cartilage cells culture and transplant are already a reality. Tissue engineering, i.e. growing cells in three-dimensional substrates of collagen or synthetic biodegradable polymers, started in the 1980s, will in future be used to replace damaged bone and cartilage parts with living and bone and cartilaginous tissues, respectively. The first steps have been taken; more research needs to be done. And it is not unreasonable to expect a significant breakthrough in the treatment of bone and joint diseases at the end of this decade. Ann Acad Med Singapore 2002; 31:621-2", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1008", "doc_id": "58050905", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Do living kidney donor informed consent practices vary between US and non-US centers?\n\nABSTRACT:\nLiving kidney donation rates are increasing in the United States and internationally. Major consensus statements on the care of living kidney donors recommend communicating all potential health and psychosocial risks to donors. We evaluated the degree of international variation in the process of informed consent of potential donors during their evaluation. Transplant professionals attending the 2006 World Transplant Congress responded to a survey assessing their process of informed consent, evaluation and communication of living donor risk. US-based respondents were compared to non-US respondents. There were 221 respondents from 177 transplant centers and 40 countries (48% US respondents). Across US and non-US transplant centers, potential donors were most likely to receive written material about living donor risk by mail prior to evaluation, receive risk information in person during evaluation, have a psychosocial evaluation, which usually lasted longer than 30 min and sign an official donation consent form presented to them by a surgeon or nephrologist. Although over 75% of respondents stated that donors received information about medical risks such as hypertension, chronic kidney disease and potential need for dialysis, there was less consistency regarding whether or not respondents conveyed an increased risk of these medical complications to donors. Additionally, the financial and psychosocial costs associated with being a living donor were inconsistently communicated to donors during the informed consent process. Compared to non-US respondents, US respondents were more likely to use written material and visual aids to convey risks to donors, have mandatory psychosocial evaluations and provide access to donor support groups. US transplant centers were al [TRUNCATED]", "output": "{\"label\": \"yes\", \"rationale\": \"As dependence on living organ donation increases best practices for informed consent, donor evaluation and uniform risk conveyance need to be established. This may be accomplished by using a model informed consent template to ensure that informed consent from donors is consistently obtained.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 18599559, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Nigerian physicians constitue the largest component of sub-Saharan Africa-trained physicians in the United States.\n\nCANDIDATE_PASSAGE:\nA feasibility study for a randomised controlled trial of the Positive Reappraisal Coping Intervention, a novel supportive technique for recurrent miscarriage INTRODUCTION Recurrent miscarriage (RM) is diagnosed when a woman has had three or more miscarriages. Increased levels of distress and anxiety are common during the waiting period of any subsequent pregnancies, posing a significant threat to psychological well-being. However, only limited support and therapy are available for these women, and many are left to cope alone. The Positive Reappraisal Coping Intervention (PRCI) is a novel self-administered supportive technique which has been shown to be effective in patients awaiting the outcome of in vitro fertilisation treatment. The primary objective of this study is to assess the feasibility and effectiveness of the PRCI in improving quality of life in the difficult waiting period which women with previous RM endure before an ongoing pregnancy can be confirmed. METHODS AND ANALYSIS A randomised controlled trial (RCT) feasibility study will establish the viability of conducting a multicentre RCT to definitively test the effects of the PRCI on the psychological well-being of women who have experienced RM during the initial waiting period of a subsequent pregnancy. A second component consists of a qualitative process evaluation exploring the initial experience of pregnancy following repeated miscarriages. Participants (n=50) will be randomised into one of two groups. The PRCI intervention group will receive the PRCI card and weekly questionnaires to assess their psychological well-being during the waiting period of their new pregnancy. The non-intervention group will be asked to complete the same weekly questionnaires. The qualitative process analysis will e [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "848", "doc_id": "7751726", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: In mice, P. chabaudi parasites are able to proliferate faster early in infection when inoculated at lower numbers than when inoculated at high numbers.\n\nCANDIDATE_PASSAGE:\nPartitioning regulatory mechanisms of within-host malaria dynamics using the effective propagation number. Immune clearance and resource limitation (via red blood cell depletion) shape the peaks and troughs of malaria parasitemia, which in turn affect disease severity and transmission. Quantitatively partitioning the relative roles of these effects through time is challenging. Using data from rodent malaria, we estimated the effective propagation number, which reflects the relative importance of contrasting within-host control mechanisms through time and is sensitive to the inoculating parasite dose. Our analysis showed that the capacity of innate responses to restrict initial parasite growth saturates with parasite dose and that experimentally enhanced innate immunity can affect parasite density indirectly via resource depletion. Such a statistical approach offers a tool to improve targeting of drugs or vaccines for human therapy by revealing the dynamics and interactions of within-host regulatory mechanisms.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "577", "doc_id": "5289038", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nCANDIDATE_PASSAGE:\nNotch activation promotes cell proliferation and the formation of neural stem cell-like colonies in human glioma cells Since Notch signaling plays a critical role in stem cells and oncogenesis, we hypothesized that Notch signaling might play roles in cancer stem cells and cancer cells with a stem cell phenotype. In this study, we accessed potential functions of the Notch pathway in the formation of cancer stem cells using human glioma. Using RT-PCR, we found that most human astrogliomas of different grades expressed moderate to high level of Notch receptors and ligands. mRNA of Hes5 but not Hes1, both of which are major downstream molecules of the Notch pathway, was also detected. In human glioma cell lines BT325, U251, SHG-44, and U87, mRNA encoding different types of Notch receptors were detected, but active form of Notch1 (NIC) was only detected in SHG-44 and U87 by Western blot. Interestingly, proliferation of these two glioma cell lines appeared faster than that of the other two lines in which NIC was not detected. We have over-expressed NIC of Notch1 in SHG-44 cells by constitutive transfection to evaluate the effects of Notch signaling on glioma cells. Our results showed that over-expression of NIC in SHG-44 cells promoted the growth and the colony-forming activity of SHG-44 cells. Interestingly, over-expression of NIC increased the formation neurosphere-like colonies in the presence of growth factors. These colonies expressed nestin, and could be induced to cells expressing neuron-, astrocyte-, or oligodendrocyte-specific markers, consistent with phenotypes of neural stem cells. These data suggest that Notch signaling promote the formation of cancer stem cell-like cells in human glioma.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1004", "doc_id": "25050969", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pharmacist attendance at ward rounds reduces adverse events in wards.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pharmacist participation on physician rounds and adverse drug events in the intensive care unit.\nABSTRACT: CONTEXT Pharmacist review of medication orders in the intensive care unit (ICU) has been shown to prevent errors, and pharmacist consultation has reduced drug costs. However, whether pharmacist participation in the ICU at the time of drug prescribing reduces adverse events has not been studied. OBJECTIVE To measure the effect of pharmacist participation on medical rounds in the ICU on the rate of preventable adverse drug events (ADEs) caused by ordering errors. DESIGN Before-after comparison between phase 1 (baseline) and phase 2 (after intervention implemented) and phase 2 comparison with a control unit that did not receive the intervention. SETTING A medical ICU (study unit) and a coronary care unit (control unit) in a large urban teaching hospital. PATIENTS Seventy-five patients randomly selected from each of 3 groups: all admissions to the study unit from February 1, 1993, through July 31, 1993 (baseline) and all admissions to the study unit (postintervention) and control unit from October 1, 1994, through July 7, 1995. In addition, 50 patients were selected at random from the control unit during the baseline period. INTERVENTION A senior pharmacist made rounds with the ICU team and remained in the ICU for consultation in the morning, and was available on call throughout the day. MAIN OUTCOME MEASURES Preventable ADEs due to ordering (prescribing) errors and the number, type, and acceptance of interventions made by the pharmacist. Preventable ADEs were identified by review of medical records of the randomly selected patients during both preintervention and postintervention phases. Pharmacists recorded all recommendations, which were then analyzed by type and acceptance. RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 pat [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS The presence of a pharmacist on rounds as a full member of the patient care team in a medical ICU was associated with a substantially lower rate of ADEs caused by prescribing errors.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 941, "doc_id": "12258338", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does potentiation of glucocorticoid release modify the long-term effects of a single exposure to immobilization stress?\n\nABSTRACT:\nPrevious work has shown that a single exposure of rats to a severe stressor (immobilization, IMO) results, days to weeks later, in a reduced response (desensitization) of the hypothalamic-pituitary-adrenal (HPA) axis to a second exposure to the same stressor. In the present work, we studied the influence of both length of exposure to IMO and circulating levels of corticosterone on the first day on the degree of desensitization of two sets of physiological variables: HPA hormones and food intake. Rats were given SC saline or ACTH administration and then exposed to IMO for 0, 1 or 20 min. Seven days later, all rats were exposed to 20 min IMO. HPA response was followed on both experimental days by repeated blood sampling and food intake was measured on a 24-h basis. Both ACTH administration and IMO activates the HPA axis and IMO reduced food intake for several days. A single previous experience with IMO enhanced the post-IMO return of HPA hormones to basal levels on day 8 and reduced the degree of anorexia. The protective effect of previous IMO on food intake was independent of, whereas that on HPA activation was positively related to, the length of exposure on day 1. Concomitant ACTH administration on day 1 did not modify the observed effects.", "output": "{\"label\": \"no\", \"rationale\": \"Long-term protective effects of a single exposure to IMO are observed even with a brief exposure, but they are not potentiated by increasing corticosterone levels during the first exposure.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 15205873, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: JMJD6 slows the hydroxylation of C-terminal lysine\n\nCANDIDATE_PASSAGE:\nResistance to gefitinib in PTEN-null HER-overexpressing tumor cells can be overcome through restoration of PTEN function or pharmacologic modulation of constitutive phosphatidylinositol 3'-kinase/Akt pathway signaling. PURPOSE Tyrosine kinase (TK) inhibitors are emerging as a promising new approach to the treatment of HER overexpressing tumors, however optimal use of these agents awaits further definition of the downstream signaling pathways that mediate their effects. We reported previously that both EGFR- and Her2-overexpressing tumors are sensitive to the new EGFR-selective TK inhibitor gefitinib (ZD1839, \"Iressa\"), and sensitivity to this agent correlated with its ability to down-regulate Akt. However, EGFR-overexpressing MDA-468 cells, which lack PTEN function, are resistant to ZD1839, and ZD1839 is unable to down-regulate Akt activity in these cells. EXPERIMENTAL DESIGN To study the role of PTEN function, we generated MDA468 cells with tet-inducible PTEN expression. RESULTS We show here that the resistance of MDA-468 cells to ZD1839 is attributable to EGFR-independent constitutive Akt activation caused by loss of PTEN function in these cells. Reconstitution of PTEN function through tet-inducible expression restores ZD1839 sensitivity to these cells and reestablishes EGFR-stimulated Akt signaling. Although restoration of PTEN function to tumors is difficult to implement clinically, much of the effects of PTEN loss are attributable to overactive PI3K/Akt pathway signaling, and this overactivity can be modulated by pharmacologic approaches. We show here that pharmacologic down-regulation of constitutive PI3K/Akt pathway signaling using the PI3K inhibitor LY294002 similarly restores EGFR-stimulated Akt signaling and sensitizes MDA-468 cells to ZD1839. CONC [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "662", "doc_id": "34016944", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Bactericidal activity of 3 cutaneous/mucosal antiseptic solutions in the presence of interfering substances: Improvement of the NF EN 13727 European Standard?\n\nABSTRACT:\nThere is no standard protocol for the evaluation of antiseptics used for skin and mucous membranes in the presence of interfering substances. Our objective was to suggest trial conditions adapted from the NF EN 13727 standard, for the evaluation of antiseptics used in gynecology and dermatology. Three antiseptic solutions were tested in vitro: a chlorhexidine-benzalkonium (CB) combination, a hexamidine-chlorhexidine-chlorocresol (HCC) combination, and povidone iodine (P). The adaptation of trial conditions to the standard involved choosing dilutions, solvent, and interfering substances. The activity of solutions was assessed on the recommended strains at concentrations of 97% (pure solution), 50%, and 10% (diluted solution), and 1%. A logarithmic reduction ≥ 5 was expected after 60seconds of contact, to meet requirements of bactericidal activity. HCC did not present any bactericidal activity except on P. aeruginosa at a concentration of 97%. P was not bactericidal on E. hirae at any concentration and on S. aureus at 97%. CB had the most homogeneous bactericidal activity with a reduction>5 log on the 4 bacterial strains at concentrations of 97%, 50% and 10%.", "output": "{\"label\": \"maybe\", \"rationale\": \"Adapting the NF EN 13727 standard allowed assessing the 3 tested solutions: only CB was bactericidal in dirty conditions. This study proved the possibility of validating antiseptic choice in vitro, in current practice conditions, for adjunctive treatment of skin and mucous membranes disorders, primarily of bacterial origin or with a potential of superinfection.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 25779009, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Birth-weight is positively associated with breast cancer.\n\nCANDIDATE_PASSAGE:\nIbuprofen for the treatment of patent ductus arteriosus in preterm or low birth weight (or both) infants. BACKGROUND Indomethacin is used as standard therapy to close a patent ductus arteriosus (PDA) but is associated with reduced blood flow to several organs. Ibuprofen, another cyclo-oxygenase inhibitor, may be as effective as indomethacin with fewer adverse effects. OBJECTIVES To determine the effectiveness and safety of ibuprofen compared with indomethacin, other cyclo-oxygenase inhibitor, placebo or no intervention for closing a patent ductus arteriosus in preterm, low birth weight, or preterm and low birth weight infants. SEARCH METHODS We searched The Cochrane Library, MEDLINE, EMBASE, Clincialtrials.gov, Controlled-trials.com, and www.abstracts2view.com/pas in May 2014. SELECTION CRITERIA Randomised or quasi-randomised controlled trials of ibuprofen for the treatment of a PDA in newborn infants. DATA COLLECTION AND ANALYSIS Data collection and analysis conformed to the methods of the Cochrane Neonatal Review Group. MAIN RESULTS We included 33 studies enrolling 2190 infants. Two studies compared intravenous (iv) ibuprofen versus placebo (270 infants). In one study (134 infants) ibuprofen reduced the incidence of failure to close a PDA (risk ratio (RR) 0.71, 95% confidence interval (CI) 0.51 to 0.99; risk difference (RD) -0.18, 95% CI -0.35 to -0.01; number needed to treat for an additional beneficial outcome (NNTB) 6, 95% CI 3 to 100). In one study (136 infants), ibuprofen reduced the composite outcome of infant mortality, infants who dropped out, or infants who required rescue treatment (RR 0.58, 95% CI 0.38 to 0.89; RD -0.22, 95% CI -0.38 to -0.06; NNTB 5, 95% CI 3 to 17). One study (64 infants) compared oral ibuprofen with placebo and noted a signif [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "179", "doc_id": "34544514", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Androgenetic haploid mouse embryonic stem cells (ESCs) can be derived and genetically manipulated in vitro.\n\nCANDIDATE_ABSTRACT:\nTITLE: Generation of Genetically Modified Mice by Oocyte Injection of Androgenetic Haploid Embryonic Stem Cells\nABSTRACT: Haploid cells are amenable for genetic analysis. Recent success in the derivation of mouse haploid embryonic stem cells (haESCs) via parthenogenesis has enabled genetic screening in mammalian cells. However, successful generation of live animals from these haESCs, which is needed to extend the genetic analysis to the organism level, has not been achieved. Here, we report the derivation of haESCs from androgenetic blastocysts. These cells, designated as AG-haESCs, partially maintain paternal imprints, express classical ESC pluripotency markers, and contribute to various tissues, including the germline, upon injection into diploid blastocysts. Strikingly, live mice can be obtained upon injection of AG-haESCs into MII oocytes, and these mice bear haESC-carried genetic traits and develop into fertile adults. Furthermore, gene targeting via homologous recombination is feasible in the AG-haESCs. Our results demonstrate that AG-haESCs can be used as a genetically tractable fertilization agent for the production of live animals via injection into oocytes.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Strikingly, live mice can be obtained upon injection of AG-haESCs into MII oocytes, and these mice bear haESC-carried genetic traits and develop into fertile adults.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 111, "doc_id": "13513790", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: A deficiency of vitamin B12 increases blood levels of homocysteine.\n\nCANDIDATE_PASSAGE:\nLong-term effect of aspirin on cancer risk in carriers of hereditary colorectal cancer: an analysis from the CAPP2 randomised controlled trial BACKGROUND Observational studies report reduced colorectal cancer in regular aspirin consumers. Randomised controlled trials have shown reduced risk of adenomas but none have employed prevention of colorectal cancer as a primary endpoint. The CAPP2 trial aimed to investigate the antineoplastic effects of aspirin and a resistant starch in carriers of Lynch syndrome, the major form of hereditary colorectal cancer; we now report long-term follow-up of participants randomly assigned to aspirin or placebo. METHODS In the CAPP2 randomised trial, carriers of Lynch syndrome were randomly assigned in a two-by-two factorial design to 600 mg aspirin or aspirin placebo or 30 g resistant starch or starch placebo, for up to 4 years. Randomisation was in blocks of 16 with provision for optional single-agent randomisation and extended postintervention double-blind follow-up; participants and investigators were masked to treatment allocation. The primary endpoint was development of colorectal cancer. Analysis was by intention to treat and per protocol. This trial is registered, ISRCTN59521990. RESULTS 861 participants were randomly assigned to aspirin or aspirin placebo. At a mean follow-up of 55·7 months, 48 participants had developed 53 primary colorectal cancers (18 of 427 randomly assigned to aspirin, 30 of 434 to aspirin placebo). Intention-to-treat analysis of time to first colorectal cancer showed a hazard ratio (HR) of 0·63 (95% CI 0·35-1·13, p=0·12). Poisson regression taking account of multiple primary events gave an incidence rate ratio (IRR) of 0·56 (95% CI 0·32-0·99, p=0·05). For participants completing 2 years of interve [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "36", "doc_id": "15648443", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Self-advocacy training is effective at decreasing homelessness.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mental health problems of homeless children and families: longitudinal study.\nABSTRACT: OBJECTIVE To establish the mental health needs of homeless children and families before and after rehousing. DESIGN Cross sectional, longitudinal study. SETTING City of Birmingham. SUBJECTS 58 rehoused families with 103 children aged 2-16 years and 21 comparison families of low socioeconomic status in stable housing, with 54 children. MAIN OUTCOME MEASURES Children's mental health problems and level of communication; mothers' mental health problems and social support one year after rehousing. RESULTS Mental health problems remained significantly higher in rehoused mothers and their children than in the comparison group (mothers 26% v 5%, P = 0.04; children 39% v 11%, P = 0.0003). Homeless mothers continued to have significantly less social support at follow up. Mothers with a history of abuse and poor social integration were more likely to have children with persistent mental health problems. CONCLUSIONS Homeless families have a high level of complex needs that cannot be met by conventional health services and arrangements. Local strategies for rapid rehousing into permanent accommodation, effective social support and health care for parents and children, and protection from violence and intimidation should be developed and implemented.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1070, "doc_id": "25649714", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Treatment with a protein named FN impairs regenerative abilities of aged muscles.\n\nCANDIDATE_PASSAGE:\nActivation of proteinase-activated receptor 2 in human osteoarthritic cartilage upregulates catabolic and proinflammatory pathways capable of inducing cartilage degradation: a basic science study Proteinase-activated receptors (PARs) belong to a family of G protein-coupled receptors. PARs are activated by a serine-dependent cleavage generating a tethered activating ligand. PAR-2 was shown to be involved in inflammatory pathways. We investigated the in situ levels and modulation of PAR-2 in human normal and osteoarthritis (OA) cartilage/chondrocytes. Furthermore, we evaluated the role of PAR-2 on the synthesis of the major catabolic factors in OA cartilage, including metalloproteinase (MMP)-1 and MMP-13 and the inflammatory mediator cyclooxygenase 2 (COX-2), as well as the PAR-2-activated signalling pathways in OA chondrocytes. PAR-2 expression was determined using real-time reverse transcription-polymerase chain reaction and protein levels by immunohistochemistry in normal and OA cartilage. Protein modulation was investigated in OA cartilage explants treated with a specific PAR-2-activating peptide (PAR-2-AP), SLIGKV-NH2 (1 to 400 μM), interleukin 1 beta (IL-1β) (100 pg/mL), tumor necrosis factor-alpha (TNF-α) (5 ng/mL), transforming growth factor-beta-1 (TGF-β1) (10 ng/mL), or the signalling pathway inhibitors of p38 (SB202190), MEK1/2 (mitogen-activated protein kinase kinase) (PD98059), and nuclear factor-kappa B (NF-κB) (SN50), and PAR-2 levels were determined by immunohistochemistry. Signalling pathways were analyzed on OA chondrocytes by Western blot using specific phospho-antibodies against extracellular signal-regulated kinase 1/2 (Erk1/2), p38, JNK (c-jun N-terminal kinase), and NF-κB in the presence or absence of the PAR-2-AP and/or IL-1β. PAR-2-ind [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1323", "doc_id": "1044552", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Only a minority of cells survive development after differentiation into stress-resistant spores.\n\nCANDIDATE_PASSAGE:\nExploitative and Hierarchical Antagonism in a Cooperative Bacterium Social organisms that cooperate with some members of their own species, such as close relatives, may fail to cooperate with other genotypes of the same species. Such noncooperation may take the form of outright antagonism or social exploitation. Myxococcus xanthus is a highly social prokaryote that cooperatively develops into spore-bearing, multicellular fruiting bodies in response to starvation. Here we have characterized the nature of social interactions among nine developmentally proficient strains of M. xanthus isolated from spatially distant locations. Strains were competed against one another in all possible pairwise combinations during starvation-induced development. In most pairings, at least one competitor exhibited strong antagonism toward its partner and a majority of mixes showed bidirectional antagonism that decreased total spore production, even to the point of driving whole populations to extinction. Differential response to mixing was the primary determinant of competitive superiority rather than the sporulation efficiencies of unmixed populations. In some competitive pairings, the dominant partner sporulated more efficiently in mixed populations than in clonal isolation. This finding represents a novel form of exploitation in bacteria carried out by socially competent genotypes and is the first documentation of social exploitation among natural bacterial isolates. Patterns of antagonistic superiority among these strains form a highly linear dominance hierarchy. At least some competition pairs construct chimeric, rather than segregated, fruiting bodies. The cooperative prokaryote M. xanthus has diverged into a large number of distinct social types that cooperate with clone-ma [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "887", "doc_id": "18855191", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is haematopoietic stem cell migration to the ischemic damaged kidney altered by manipulating the SDF-1/CXCR4-axis?\n\nABSTRACT:\nHaematopoietic stem cells (HSC) have been shown to migrate to the ischemic kidney. The factors that regulate the trafficking of HSC to the ischemic damaged kidney are not fully understood. The stromal cell-derived factor-1 (SDF-1)/CXCR4-axis has been identified as the central signalling axis regulating trafficking of HSC to the bone marrow. Therefore, we hypothesized that SDF-1/CXCR4 interactions are implicated in the migration of HSC to the injured kidney. HSC were isolated from mouse bone marrow and labelled with a cell tracker. Acceptor mice were subjected to unilateral ischemia and received HSC intravenously directly after reperfusion. In addition, in separate groups of acceptor mice, endogenous SDF-1 or HSC-associated CXCR4 was blocked or kidneys were injected with SDF-1. Exogenous HSC could be detected in the tubules and interstitium of the kidney 24 h after ischemic injury. Importantly, the amount of HSC in the ischemic kidney was markedly higher compared to the contralateral kidney. Neutralizing endogenous SDF-1 or HSC-associated CXCR4 did not prevent the migration of HSC. No increase in the number of labelled HSC could be observed after local administration of SDF-1, as was also determined in bilateral kidney ischemia.", "output": "{\"label\": \"no\", \"rationale\": \"In conclusion, systemically administered HSC preferentially migrate to the ischemic injured kidney. This migration could not be prevented by blocking the SDF-1/CXCR4-axis or increased after local administration of SDF-1.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 19223274, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Bariatric surgery increases rates of postmenopausal breast cancer.\n\nCANDIDATE_PASSAGE:\nBreast cancer clusters in the northeast United States: a geographic analysis. High breast cancer mortality rates have been reported in the northeastern part of the United States, with recent attention focused on Long Island, New York. In this study, the authors investigate whether the high breast cancer mortality is evenly spread over the Northeast, in the sense that any observed clusters of deaths can be explained by chance alone, or whether there are clusters of statistical significance. Demographic data and age-specific breast cancer mortality rates for women were obtained for all 244 counties in 11 northeastern states and for the District of Columbia for 1988-1992. A recently developed spatial scan statistic is used, which searches for clusters of cases without specifying their size or location ahead of time, and which tests for their statistical significance while adjusting for the multiple testing inherent in such a procedure. The basic analysis is adjusted for age, with further analyses examining how the results are affected by incorporating race, urbanicity, and parity as confounding variables. There is a statistically significant and geographically broad cluster of breast cancer deaths in the New York City-Philadelphia, Pennsylvania, metropolitan area (p = 0.0001), which has a 7.4% higher mortality rate than the rest of the Northeast. The cluster remains significant when race, urbanicity, and/or parity are included as confounding variables. Four smaller subclusters within this area are also significant on their own strength: Philadelphia with suburbs (p = 0.0001), Long Island (p = 0.0001), central New Jersey (p = 0.0001), and northeastern New Jersey (p = 0.0001). The elevated breast cancer mortality on Long Island might be viewed less as a unique lo [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "165", "doc_id": "3524352", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is Panton-Valentine leucocidin associated with the pathogenesis of Staphylococcus aureus bacteraemia in the UK?\n\nABSTRACT:\nThe morbidity and mortality associated with Panton-Valentine leucocidin (PVL)-positive Staphylococcus aureus suggest that this toxin is a key marker of disease severity. Nevertheless, the importance of PVL in the pathogenesis of primary bacteraemia caused by S. aureus is uncertain. We have determined the prevalence of PVL-encoding genes among isolates of S. aureus from bacteraemic patients. Consecutive bacteraemia isolates of S. aureus (n=244) from patients hospitalized in 25 centres in the UK and Ireland during 2005 were screened for PVL and mecA genes. PVL-positive isolates were characterized by toxin gene profiling, PFGE, spa-typing and MIC determinations for a range of antimicrobials. Four out of 244 isolates (1.6%) were PVL-positive and susceptible to oxacillin [methicillin-susceptible S. aureus (MSSA)]. Eighty-eight out of 244 (36%) were oxacillin-resistant (methicillin-resistant S. aureus), but none was PVL-positive. The four patients (two males: 30 and 33 years; two females: 62 and 80 years) had infection foci of: skin and soft tissue, unknown, indwelling line, and surgical site, and were located at one centre in Wales, one in England and two in Ireland. One of four PVL-positive isolates was resistant to penicillin and fusidic acid, the remainder were susceptible to all antibiotics tested. Genotypic analyses showed that the four isolates represented three distinct strains; the two isolates from Ireland were related.", "output": "{\"label\": \"maybe\", \"rationale\": \"We found that 1.6% of S. aureus (all MSSA) from bacteraemic patients were PVL-positive. This low incidence suggests that PVL-positive S.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 17562682, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Activator-inhibitor pairs are provided ventrally by Xrl-sizzled.\n\nCANDIDATE_PASSAGE:\nRegulation of ADMP and BMP2/4/7 at Opposite Embryonic Poles Generates a Self-Regulating Morphogenetic Field Embryos have the ability to self-regulate and regenerate normal structures after being sectioned in half. How is such a morphogenetic field established? We discovered that quadruple knockdown of ADMP and BMP2/4/7 in Xenopus embryos eliminates self-regulation, causing ubiquitous neural induction throughout the ectoderm. ADMP transcription in the Spemann organizer is activated at low BMP levels. When ventral BMP2/4/7 signals are depleted, Admp expression increases, allowing for self-regulation. ADMP has BMP-like activity and signals via the ALK-2 receptor. It is unable to signal dorsally because of inhibition by Chordin. The ventral BMP antagonists Sizzled and Bambi further refine the pattern. By transplanting dorsal or ventral wild-type grafts into ADMP/BMP2/4/7-depleted hosts, we demonstrate that both poles serve as signaling centers that can induce histotypic differentiation over considerable distances. We conclude that dorsal and ventral BMP signals and their extracellular antagonists expressed under opposing transcriptional regulation provide a molecular mechanism for embryonic self-regulation.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "73", "doc_id": "6076903", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: DUSP4 increases apoptosis.\n\nCANDIDATE_PASSAGE:\nInterleukin-33 prevents apoptosis and improves survival after experimental myocardial infarction through ST2 signaling. BACKGROUND ST2 is an interleukin (IL)-1 receptor family member with membrane-bound (ST2L) and soluble (sST2) isoforms, and sST2 is a biomarker for poor outcome in patients with myocardial infarction (MI). IL-33, the recently discovered ligand for ST2, activates nuclear factor kappaB and thus may regulate apoptotic cell death. We tested the hypothesis that IL-33 is cardioprotective after MI through ST2 signaling. METHODS AND RESULTS IL-33 protected cultured cardiomyocytes from hypoxia-induced apoptosis, and this cardioprotection was partially inhibited by sST2. IL-33 induced expression of the antiapoptotic factors XIAP, cIAP1, and survivin. To define the cardioprotective role of IL-33 in vivo, we performed a blinded and randomized study of ischemia/reperfusion in rats. IL-33 reduced cardiomyocyte apoptosis, suppressed caspase-3 activity, and increased expression of IAP family member proteins. IL-33 decreased both infarct and fibrosis volumes at 15 days; furthermore, both echocardiographic and hemodynamic studies revealed that IL-33 improved ventricular function. To determine whether cardioprotection by IL-33 is mediated through ST2 signaling, a randomized and blinded study of ST2(-/-) versus wild-type littermate mice was performed in 98 mice subjected to MI. At 4 weeks after MI, IL-33 reduced ventricular dilation and improved contractile function in wild-type mice but not in ST2(-/-) mice. Finally, IL-33 improved survival after MI in wild-type but not in ST2(-/-) mice. CONCLUSIONS IL-33 prevents cardiomyocyte apoptosis and improves cardiac function and survival after MI through ST2 signaling.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "309", "doc_id": "10576136", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Suboptimal nutrition is a leading cause of premature death\n\nCANDIDATE_PASSAGE:\nFunctional inhibition of osteoblastic cells in an in vivo mouse model of myeloid leukemia. Pancytopenia is a major cause of morbidity in acute myeloid leukemia (AML), yet its cause is unclear. Normal osteoblastic cells have been shown to support hematopoiesis. To define the effects of leukemia on osteoblastic cells, we used an immunocompetent murine model of AML. Leukemic mice had inhibition of osteoblastic cells, with decreased serum levels of the bone formation marker osteocalcin. Osteoprogenitor cells and endosteal-lining osteopontin(+) cells were reduced, and osteocalcin mRNA in CD45(-) marrow cells was diminished. This resulted in severe loss of mineralized bone. Osteoclasts were only transiently increased without significant increases in bone resorption, and their inhibition only partially rescued leukemia-induced bone loss. In vitro data suggested that a leukemia-derived secreted factor inhibited osteoblastic cells. Because the chemokine CCL-3 was recently reported to inhibit osteoblastic function in myeloma, we tested its expression in our model and in AML patients. Consistent with its potential novel role in leukemic-dependent bone loss, CCL-3 mRNA was significantly increased in malignant marrow cells from leukemic mice and from samples from AML patients. Based on these results, we propose that therapeutic mitigation of leukemia-induced uncoupling of osteoblastic and osteoclastic cells may represent a novel approach to promote normal hematopoiesis in patients with myeloid neoplasms.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1109", "doc_id": "10795340", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Notch signaling occurs between tumor cells and stromal cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Crosstalk between tumor and endothelial cells promotes tumor angiogenesis by MAPK activation of Notch signaling.\nABSTRACT: While significant progress has been made in understanding the induction of tumor vasculature by secreted angiogenic factors, little is known regarding contact-dependent signals that promote tumor angiogenesis. Here, we report that the Notch ligand Jagged1 induced by growth factors via mitogen-activating protein kinase (MAPK) in head and neck squamous cell carcinoma (HNSCC) cells triggered Notch activation in neighboring endothelial cells (ECs) and promoted capillary-like sprout formation. Jagged1-expressing HNSCC cells significantly enhanced neovascularization and tumor growth in vivo. Moreover, the level of Jagged1 was significantly correlated with tumor blood vessel content and associated with HNSCC development. Our results elucidate a novel mechanism by which the direct interplay between tumor cells and ECs promotes angiogenesis through MAPK and Notch signaling pathways.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here, we report that the Notch ligand Jagged1 induced by growth factors via mitogen-activating protein kinase (MAPK) in head and neck squamous cell carcinoma (HNSCC) cells triggered Notch activation in neighboring endothelial cells (ECs) and promoted capillary-like sprout formation.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 863, "doc_id": "20568364", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Sildenafil worsens erectile function in men who experience sexual dysfunction as a result of the use of SSRI antidepressants.\n\nCANDIDATE_ABSTRACT:\nTITLE: Treatment of antidepressant-associated sexual dysfunction with sildenafil: a randomized controlled trial.\nABSTRACT: CONTEXT Sexual dysfunction is a common adverse effect of antidepressants that frequently results in treatment noncompliance. OBJECTIVE To assess the efficacy of sildenafil citrate in men with sexual dysfunction associated with the use of selective and nonselective serotonin reuptake inhibitor (SRI) antidepressants. DESIGN, SETTING, AND PATIENTS Prospective, parallel-group, randomized, double-blind, placebo-controlled trial conducted between November 1, 2000, and January 1, 2001, at 3 US university medical centers among 90 male outpatients (mean [SD] age, 45 [8] years) with major depression in remission and sexual dysfunction associated with SRI antidepressant treatment. INTERVENTION Patients were randomly assigned to take sildenafil (n = 45) or placebo (n = 45) at a flexible dose starting at 50 mg and adjustable to 100 mg before sexual activity for 6 weeks. MAIN OUTCOME MEASURES The primary outcome measure was score on the Clinical Global Impression-Sexual Function (CGI-SF); secondary measures were scores on the International Index of Erectile Function, Arizona Sexual Experience Scale, Massachusetts General Hospital-Sexual Functioning Questionnaire, and Hamilton Rating Scale for Depression (HAM-D). RESULTS Among the 90 randomized patients, 93% (83/89) of patients treated per protocol took at least 1 dose of study drug and 85% (76/89) completed week 6 end-point assessments with last observation carried forward analyses. At a CGI-SF score of 2 or lower, 54.5% (24/44) of sildenafil compared with 4.4% (2/45) of placebo patients were much or very much improved (P<.001). Erectile function, arousal, ejaculation, orgasm, and overall satisfaction domain measures improved significantly in sildenafil compared with placebo patients. Mean depression scores remained consi [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSION In our study, sildenafil effectively improved erectile function and other aspects of sexual function in men with sexual dysfunction associated with the use of SRI antidepressants.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1087, "doc_id": "39281140", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Hematopoietic Stem Cell purification reaches purity rates above 90%.\n\nCANDIDATE_PASSAGE:\nStrong association between respiratory viral infection early after hematopoietic stem cell transplantation and the development of life-threatening acute and chronic alloimmune lung syndromes. Alloimmune lung syndromes (allo-LS), including idiopathic pneumonia syndrome, bronchiolitis obliterans syndrome, and bronchiolitis obliterans organizing pneumonia, are severe complications after hematopoietic stem cell transplantation (HSCT). In our cohort of 110 pediatric patients, 30 had allo-LS (27.3%), 18 with idiopathic pneumonia syndrome and 12 with bronchiolitis obliterans syndrome. Multivariate analysis showed that respiratory viral infection early after HSCT is an important predictor for the development of allo-LS (P <.0001). This was true for all viruses tested. In multivariate analysis, allo-LS was the only predictor for higher mortality (P = .04). Paradoxically, prolonged administration of immunosuppressive agents because of acute graft-versus-host disease had a protective effect on the development of allo-LS (P = .004). We hypothesize that early infection of the respiratory tract with a common cold virus makes the lungs a target for alloimmunity.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "509", "doc_id": "30398773", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The innate immune response struggles to remove small numbers of parasites.\n\nCANDIDATE_ABSTRACT:\nTITLE: Partitioning regulatory mechanisms of within-host malaria dynamics using the effective propagation number.\nABSTRACT: Immune clearance and resource limitation (via red blood cell depletion) shape the peaks and troughs of malaria parasitemia, which in turn affect disease severity and transmission. Quantitatively partitioning the relative roles of these effects through time is challenging. Using data from rodent malaria, we estimated the effective propagation number, which reflects the relative importance of contrasting within-host control mechanisms through time and is sensitive to the inoculating parasite dose. Our analysis showed that the capacity of innate responses to restrict initial parasite growth saturates with parasite dose and that experimentally enhanced innate immunity can affect parasite density indirectly via resource depletion. Such a statistical approach offers a tool to improve targeting of drugs or vaccines for human therapy by revealing the dynamics and interactions of within-host regulatory mechanisms.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Our analysis showed that the capacity of innate responses to restrict initial parasite growth saturates with parasite dose and that experimentally enhanced innate immunity can affect parasite density indirectly via resource depletion.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1223, "doc_id": "5289038", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The US health care system can save up to $750 million if 7% of patients waiting for kidney transplants participate in the optimized national kidney paired donation program.\n\nCANDIDATE_ABSTRACT:\nTITLE: Kidney paired donation and optimizing the use of live donor organs.\nABSTRACT: CONTEXT Blood type and crossmatch incompatibility will exclude at least one third of patients in need from receiving a live donor kidney transplant. Kidney paired donation (KPD) offers incompatible donor/recipient pairs the opportunity to match for compatible transplants. Despite its increasing popularity, very few transplants have resulted from KPD. OBJECTIVE To determine the potential impact of improved matching schemes on the number and quality of transplants achievable with KPD. DESIGN, SETTING, AND POPULATION We developed a model that simulates pools of incompatible donor/recipient pairs. We designed a mathematically verifiable optimized matching algorithm and compared it with the scheme currently used in some centers and regions. Simulated patients from the general community with characteristics drawn from distributions describing end-stage renal disease patients eligible for renal transplantation and their willing and eligible live donors. MAIN OUTCOME MEASURES Number of kidneys matched, HLA mismatch of matched kidneys, and number of grafts surviving 5 years after transplantation. RESULTS A national optimized matching algorithm would result in more transplants (47.7% vs 42.0%, P<.001), better HLA concordance (3.0 vs 4.5 mismatched antigens; P<.001), more grafts surviving at 5 years (34.9% vs 28.7%; P<.001), and a reduction in the number of pairs required to travel (2.9% vs 18.4%; P<.001) when compared with an extension of the currently used first-accept scheme to a national level. Furthermore, highly sensitized patients would benefit 6-fold from a national optimized scheme (2.3% vs 14.1% successfully matched; P<.001). Even if only 7% of patients awaiting kidney transplantation participated in an optimized national KPD program, the health care system c [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Even if only 7% of patients awaiting kidney transplantation participated in an optimized national KPD program, the health care system could save as much as $750 million.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1185, "doc_id": "16737210", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Leukemia associated Rho guanine nucleotide-exchange factor represses RhoA in response to SRC activation.\n\nCANDIDATE_PASSAGE:\nRole of beta adrenergic receptor polymorphisms in heart failure: systematic review and meta-analysis. Heart Failure (HF) is a common disorder associated with substantial morbidity and mortality. beta adrenergic receptors (betaAR) are the primary pathway through which cardiac function is influenced. Chronic beta(1)AR activation is implicated in the pathogenesis of HF and betaAR blockade improves survival in left ventricular systolic dysfunction. Common functional polymorphisms in beta adrenergic receptor genes (ADRB) have been associated with HF phenotypes, and with pharmacogenetic interaction with beta adrenergic receptor blockers (beta blockers). However, these associations have not been consistently replicated. The evidence for ADRB variant involvement in pathogenesis, progression and response to beta blockers in HF is reviewed. In addition, a meta-analysis of three studies analysing the effect of ADRB1 Arg389Gly polymorphism on left ventricular remodelling with the use of beta blockers, demonstrating a 5% improvement in left ventricular ejection fraction in Arg389 homozygotes, is presented. There is now accumulating molecular evidence for a different functional response to beta blockers associated with this polymorphism. In the future, confirmed genotypic associations may enable patients to be identified who are either at greater risk of developing HF, whose HF may rapidly progress, or who are unlikely to benefit from beta blockers, and such patients may benefit from targeted aggressive therapy.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "691", "doc_id": "24586989", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: High-sensitivity cardiac troponin T (HSCT-T) dosage may not be diagnostic if the onset of symptoms occurs less than 3 hours before acute myocardial injury (AMI).\n\nCANDIDATE_ABSTRACT:\nTITLE: Relationship between Sloan-Kettering virus expression and mouse follicular development\nABSTRACT: Sloan-Kettering virus gene product (Ski) is an unique nuclear pro-oncoprotein and belongs to the ski/sno proto-oncogene family. Ski plays multiple roles in a variety of cell types, it can induce both oncogenic transformation and terminal muscle differentiation when expressed at high levels. Ski/SnoN are important transcription regulators of the transforming growth factor-β (TGF-β) superfamily and function mainly through heterodimers. Since TGF-β superfamily are key regulators of follicle development and it has been previously shown that SnoN is also vital to follicle development, this research was conducted to clarify the relationship between Ski expression and mouse follicular development, in ovaries of neonatal and gonadotropin-induced immature mice by immunohistochemical and real-time PCR techniques. In postnatal mice, positive staining for Ski was highly detected in oocyte nuclei at postnatal day 1. With follicular development, the localization moved gradually from oocyte nuclei to perinuclear space and the total levels decreased. During the estrous cycle, Ski expression was apparent at proestrus and estrus, faint at metestrus, highest at diestrus. After injection of gonadotropin, Ski was found in perinuclear space and weak in oocyte nuclei. Following the initiation of luteinization, the expression of Ski was found in corpus luteum. Real-time PCR results also showed that Ski mRNA expression was opposite to ovulation-related genes during the cumulus expansion, with the development of the follicles, its expression level decreased. Ski is expressed in a specific manner during follicle development, ovulation and luteinization. So Ski might play essential roles in these processes especially during early follicular development.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 521, "doc_id": "643765", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Basophils promote disease development in patients with systemic lupus erythematosus (SLE).\n\nCANDIDATE_ABSTRACT:\nTITLE: BASOPHILS AND THE T HELPER 2 ENVIRONMENT CAN PROMOTE THE DEVELOPMENT OF LUPUS NEPHRITIS\nABSTRACT: In systemic lupus erythematosus (SLE), self-reactive antibodies can target the kidney (lupus nephritis), leading to functional failure and possible mortality. We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice). Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis. Basophils were also present in the lymph nodes and spleen of subjects with SLE. Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 172, "doc_id": "12670680", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Upon developing tyrosine-kinase inhibitor resistance, new mutations in epidermal growth factor receptors emerge and cause treatment failure.\n\nCANDIDATE_ABSTRACT:\nTITLE: Acquired EGFR C797S mutation mediates resistance to AZD9291 in non–small cell lung cancer harboring EGFR T790M\nABSTRACT: Here we studied cell-free plasma DNA (cfDNA) collected from subjects with advanced lung cancer whose tumors had developed resistance to the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) AZD9291. We first performed next-generation sequencing of cfDNA from seven subjects and detected an acquired EGFR C797S mutation in one; expression of this mutant EGFR construct in a cell line rendered it resistant to AZD9291. We then performed droplet digital PCR on serial cfDNA specimens collected from 15 AZD9291-treated subjects. All were positive for the T790M mutation before treatment, but upon developing AZD9291 resistance three molecular subtypes emerged: six cases acquired the C797S mutation, five cases maintained the T790M mutation but did not acquire the C797S mutation and four cases lost the T790M mutation despite the presence of the underlying EGFR activating mutation. Our findings provide insight into the diversity of mechanisms through which tumors acquire resistance to AZD9291 and highlight the need for therapies that are able to overcome resistance mediated by the EGFR C797S mutation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"All were positive for the T790M mutation before treatment, but upon developing AZD9291 resistance three molecular subtypes emerged: six cases acquired the C797S mutation, five cases maintained the T790M mutation but did not acquire the C797S mutation and four cases lost the T790M mutation despite the presence of the underlying EGFR activating mutation.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1346, "doc_id": "9505402", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: 30-Day and 1-year mortality in emergency general surgery laparotomies: an area of concern and need for improvement?\n\nABSTRACT:\nEmergency surgery is associated with poorer outcomes and higher mortality with recent studies suggesting the 30-day mortality to be 14-15%. The aim of this study was to analyse the 30-day mortality, age-related 30-day mortality and 1-year mortality following emergency laparotomy. We hope this will encourage prospective data collection, improvement of care and initiate strategies to establish best practice in this area. This was a retrospective study of patients who underwent emergency laparotomy from June 2010 to May 2012. The primary end point of the study was 30-day mortality, age-related 30-day mortality and 1-year all-cause mortality. 477 laparotomies were performed in 446 patients. 57% were aged<70 and 43% aged>70 years. 30-day mortality was 12, 4% in those aged<70 years and 22% in those>70 years (p<0.001). 1-year mortality was 25, 15% in those aged under 70 years and 38% in those aged>70 years (p<0.001).", "output": "{\"label\": \"maybe\", \"rationale\": \"Emergency laparotomy carries a high rate of mortality, especially in those over the age of 70 years, and more needs to be done to improve outcomes, particularly in this group. This could involve increasing acute surgical care manpower, early recognition of patients requiring emergency surgery, development of clear management protocols for such patients or perhaps even considering centralisation of emergency surgical services to specialist centres with multidisciplinary teams involving emergency surgeons and care of the elderly physicians in hospital and related community outreach services for post-discharge care.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 26037986, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Activated Cdk5 regulates DNA damage-induced neuronal death.\n\nCANDIDATE_PASSAGE:\nGreen tea polyphenol causes differential oxidative environments in tumor versus normal epithelial cells. Green tea polyphenols (GTPPs) are considered beneficial to human health, especially as chemopreventive agents. Recently, cytotoxic reactive oxygen species (ROS) were identified in tumor and certain normal cell cultures incubated with high concentrations of the most abundant GTPP, (-)-epigallocatechin-3-gallate (EGCG). If EGCG also provokes the production of ROS in normal epithelial cells, it may preclude the topical use of EGCG at higher doses. The current study examined the oxidative status of normal epithelial, normal salivary gland, and oral carcinoma cells treated with EGCG, using ROS measurement and catalase and superoxide dismutase activity assays. The results demonstrated that high concentrations of EGCG induced oxidative stress only in tumor cells. In contrast, EGCG reduced ROS in normal cells to background levels. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and 5-bromodeoxyuridine incorporation data were also compared between the two oral carcinoma cell lines treated by EGCG, which suggest that a difference in the levels of endogenous catalase activity may play an important role in reducing oxidative stress provoked by EGCG in tumor cells. It is concluded that pathways activated by GTPPs or EGCG in normal epithelial versus tumor cells create different oxidative environments, favoring either normal cell survival or tumor cell destruction. This finding may lead to applications of naturally occurring polyphenols to enhance the effectiveness of chemo/radiation therapy to promote cancer cell death while protecting normal cells.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "68", "doc_id": "6650933", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Knockout proximal tubule-specific deletion of the BMP receptor Alk3 causes epithelial damage.\n\nCANDIDATE_ABSTRACT:\nTITLE: Activin–like kinase–3 activity is important for kidney regeneration and reversal of fibrosis\nABSTRACT: Molecules associated with the transforming growth factor β (TGF-β) superfamily, such as bone morphogenic proteins (BMPs) and TGF-β, are key regulators of inflammation, apoptosis and cellular transitions. Here we show that the BMP receptor activin-like kinase 3 (Alk3) is elevated early in diseased kidneys after injury. We also found that its deletion in the tubular epithelium leads to enhanced TGF-β1-Smad family member 3 (Smad3) signaling, epithelial damage and fibrosis, suggesting a protective role for Alk3-mediated signaling in the kidney. A structure-function analysis of the BMP-Alk3-BMP receptor, type 2 (BMPR2) ligand-receptor complex, along with synthetic organic chemistry, led us to construct a library of small peptide agonists of BMP signaling that function through the Alk3 receptor. One such peptide agonist, THR-123, suppressed inflammation, apoptosis and the epithelial-to-mesenchymal transition program and reversed established fibrosis in five mouse models of acute and chronic renal injury. THR-123 acts specifically through Alk3 signaling, as mice with a targeted deletion for Alk3 in their tubular epithelium did not respond to therapy with THR-123. Combining THR-123 and the angiotensin-converting enzyme inhibitor captopril had an additive therapeutic benefit in controlling renal fibrosis. Our studies show that BMP signaling agonists constitute a new line of therapeutic agents with potential utility in the clinic to induce regeneration, repair and reverse established fibrosis.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We also found that its deletion in the tubular epithelium leads to enhanced TGF-β1-Smad family member 3 (Smad3) signaling, epithelial damage and fibrosis, suggesting a protective role for Alk3-mediated signaling in the kidney.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 670, "doc_id": "5573975", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Rotator cuff exercises are more effective than general exercise therapy in reducing pain and improving function of the shoulder.\n\nCANDIDATE_ABSTRACT:\nTITLE: Exosomal levels of miRNA-21 from cerebrospinal fluids associated with poor prognosis and tumor recurrence of glioma patients\nABSTRACT: Glioma is a most common type of primary brain tumors. Extracellular vesicles, in the form of exosomes, are known to mediate cell-cell communication by transporting cell-derived proteins and nucleic acids, including various microRNAs (miRNAs). Here we examined the cerebrospinal fluid (CSF) from patients with recurrent glioma for the levels of cancer-related miRNAs, and evaluated the values for prognosis by comparing the measures of CSF-, serum-, and exosome-contained miR-21 levels. Samples from seventy glioma patients following surgery were compared with those from brain trauma patients as a non-tumor control group. Exosomal miR-21 levels in the CSF of glioma patients were found significantly higher than in the controls; whereas no difference was detected in serum-derived exosomal miR-21 expression. The CSF-derived exosomal miR-21 levels correlated with tumor spinal/ventricle metastasis and the recurrence with anatomical site preference. From additional 198 glioma tissue samples, we verified that miR-21 levels associated with tumor grade of diagnosis and negatively correlated with the median values of patient overall survival time. We further used a lentiviral inhibitor to suppress miR-21 expression in U251 cells. The results showed that the levels of miR-21 target genes of PTEN, RECK and PDCD4 were up-regulated at protein levels. Therefore, we concluded that the exosomal miR-21 levels could be demonstrated as a promising indicator for glioma diagnosis and prognosis, particularly with values to predict tumor recurrence or metastasis.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1056, "doc_id": "654735", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Immune complex triggered cell death leads to extracellular release of nuclear DNA.\n\nCANDIDATE_PASSAGE:\nLocal changes in lipid environment of TCR microclusters regulate membrane binding by the CD3ε cytoplasmic domain The CD3ε and ζ cytoplasmic domains of the T cell receptor bind to the inner leaflet of the plasma membrane (PM), and a previous nuclear magnetic resonance structure showed that both tyrosines of the CD3ε immunoreceptor tyrosine-based activation motif partition into the bilayer. Electrostatic interactions between acidic phospholipids and clusters of basic CD3ε residues were previously shown to be essential for CD3ε and ζ membrane binding. Phosphatidylserine (PS) is the most abundant negatively charged lipid on the inner leaflet of the PM and makes a major contribution to membrane binding by the CD3ε cytoplasmic domain. Here, we show that TCR triggering by peptide--MHC complexes induces dissociation of the CD3ε cytoplasmic domain from the plasma membrane. Release of the CD3ε cytoplasmic domain from the membrane is accompanied by a substantial focal reduction in negative charge and available PS in TCR microclusters. These changes in the lipid composition of TCR microclusters even occur when TCR signaling is blocked with a Src kinase inhibitor. Local changes in the lipid composition of TCR microclusters thus render the CD3ε cytoplasmic domain accessible during early stages of T cell activation.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "555", "doc_id": "5914739", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nCANDIDATE_ABSTRACT:\nTITLE: Rank Signaling Links the Development of Invariant γδ T Cell Progenitors and Aire+ Medullary Epithelium\nABSTRACT: The thymic medulla provides a specialized microenvironment for the negative selection of T cells, with the presence of autoimmune regulator (Aire)-expressing medullary thymic epithelial cells (mTECs) during the embryonic-neonatal period being both necessary and sufficient to establish long-lasting tolerance. Here we showed that emergence of the first cohorts of Aire(+) mTECs at this key developmental stage, prior to αβ T cell repertoire selection, was jointly directed by Rankl(+) lymphoid tissue inducer cells and invariant Vγ5(+) dendritic epidermal T cell (DETC) progenitors that are the first thymocytes to express the products of gene rearrangement. In turn, generation of Aire(+) mTECs then fostered Skint-1-dependent, but Aire-independent, DETC progenitor maturation and the emergence of an invariant DETC repertoire. Hence, our data attributed a functional importance to the temporal development of Vγ5(+) γδ T cells during thymus medulla formation for αβ T cell tolerance induction and demonstrated a Rank-mediated reciprocal link between DETC and Aire(+) mTEC maturation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Hence, our data attributed a functional importance to the temporal development of Vγ5(+) γδ T cells during thymus medulla formation for αβ T cell tolerance induction and demonstrated a Rank-mediated reciprocal link between DETC and Aire(+) mTEC maturation.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1181, "doc_id": "301838", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Increased mobility of retrotransposons is assosciated with mutation and higher tumorigenesis rates.\n\nCANDIDATE_PASSAGE:\nA novel Ku70 function in colorectal homeostasis separate from nonhomologous end joining Ku70, a known nonhomologous end-joining (NHEJ) factor, also functions in tumor suppression, although this molecular mechanism remains uncharacterized. Previously, we showed that mice deficient for DNA ligase IV (Lig4), another key NHEJ factor, succumbed to aggressive lymphoma in the absence of tumor suppressor p53. However, the tumor phenotype is abrogated by the introduction of a hypomorphic mutant p53R172P, which impaired p53-mediated apoptosis but not cell-cycle arrest. However, Lig4−/−p53R172P mice succumbed to severe diabetes. To further elucidate the role of NHEJ and p53-mediated apoptosis in vivo, we bred Ku70−/− p53R172P mice. Unexpectedly, these mice were free of diabetes, although 80% of the mutant mice had abnormally enlarged colons with pronounced inflammation. Remarkably, most of these mutant mice progressed to dysplasia, adenoma and adenocarcinoma; this is in contrast to the Lig4−/−p53R172P phenotype, strongly suggesting an NHEJ-independent function of Ku70. Significantly, our analyses of Ku70−/−p53R172P colonic epithelial cells show nuclear stabilization of β-catenin accompanied by higher expression of cyclin D1 and c-Myc in affected colon sections than in control samples. This is not due to the p53 mutation, as Ku70−/− mice share this phenotype. Our results not only unravel a novel function of Ku70 essential for colon homeostasis, but also establish an excellent in vivo model in which to study how chronic inflammation and abnormal cellular proliferation underlie tumorigenesis and tumor progression in the colon.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "617", "doc_id": "26059876", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Chlamydia trachomatis is most prevalent in the UK among individuals in their 50s and 60s.\n\nCANDIDATE_PASSAGE:\nMonoallelic expression and methylation of imprinted genes in human and mouse embryonic germ cell lineages. Imprinting is an epigenetic modification leading to monoallelic expression of some genes, and disrupted imprinting is believed to be a barrier to human stem cell transplantation, based on studies that suggest that epigenetic marks are unstable in mouse embryonic germ (EG) and embryonic stem (ES) cells. However, stem cell imprinting has not previously been examined directly in humans. We found that three imprinted genes, TSSC5, H19, and SNRPN, show monoallelic expression in in vitro differentiated human EG-derived cells, and a fourth gene, IGF2, shows partially relaxed imprinting at a ratio from 4:1 to 5:1, comparable to that found in normal somatic cells. In addition, we found normal methylation of an imprinting control region (ICR) that regulates H19 and IGF2 imprinting, suggesting that imprinting may not be a significant epigenetic barrier to human EG cell transplantation. Finally, we were able to construct an in vitro mouse model of genomic imprinting, by generating EG cells from 8.5-day embryos of an interspecific cross, in which undifferentiated cells show biallelic expression and acquire preferential parental allele expression after differentiation. This model should allow experimental manipulation of epigenetic modifications of cultured EG cells that may not be possible in human stem cell studies.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "255", "doc_id": "40087494", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does tissue plasminogen activator alter development of acquired epilepsy?\n\nABSTRACT:\nTissue plasminogen activator (t-PA), a proven therapy for acute ischemic stroke, is an endogenous serine protease associated with neuronal activity and synaptic plasticity in the brain. Its expression is enhanced after seizures, and is involved in seizure propagation throughout the brain. Therefore, the increased use of t-PA to treat stroke may have important implications for the development of poststroke epilepsy. Using experimental and clinical approaches, we investigated the role of t-PA in the development of epilepsy. Mice deficient in t-PA (t-PA(-/-) ) or mice transgenically modified to overexpress neuronal t-PA (T4) underwent amygdala kindling, and seizure threshold and rates of kindling were compared to those in wild-type mice. For the clinical study, we recruited acute ischemic stroke patients who either received intravenous t-PA treatment on admission to hospital (n = 177; cases) or did not (n = 158; controls). We then assessed the incidence of early and late onset seizures and epilepsy in these patients. T4 mice were more seizure-prone than wild-type mice, exhibiting lower seizure thresholds (p = 0.002), but there were no significant differences observed in the rate of kindling development when comparing either T4 mice, or t-PA(-/-) mice, to their wild-type controls. Furthermore, we found no significant differences between the proportion of poststroke patients experiencing early or late seizures, or developing epilepsy, between those who received t-PA and those who did not.", "output": "{\"label\": \"no\", \"rationale\": \"Overexpression of endogenous t-PA lowers seizure threshold but does not influence kindling epileptogenesis. Moreover, the therapeutic administration of t-PA in humans does not influence the development of acquired poststroke epilepsy.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 22957978, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: CHOP is a general endoplasmic reticulum stress marker.\n\nCANDIDATE_PASSAGE:\nReproductive and lifestyle determinants of anti-Müllerian hormone in a large population-based study. CONTEXT Anti-müllerian hormone (AMH) is an ovarian reserve marker that is increasingly applied in clinical practice as a prognostic and diagnostic tool. Despite increased use of AMH in clinical practice, large-scale studies addressing the influence of possible determinants on AMH levels are scarce. OBJECTIVE We aimed to address the role of reproductive and lifestyle determinants of AMH in a large population-based cohort of women. DESIGN In this cross-sectional study, age-specific AMH percentiles were calculated using general linear modeling with CG-LMS (Cole and Green, Lambda, Mu, and Sigma model, an established method to calculate growth curves for children). SETTING Women from the general community participating in the Doetinchem Cohort study were assessed. PARTICIPANTS Two thousand three hundred twenty premenopausal women were included. MAIN OUTCOME MEASURE The effect of female reproductive and lifestyle factors on shifts in age-specific AMH percentiles was studied. RESULTS In comparison to women with a regular menstrual cycle, current oral contraceptive (OC) users, women with menstrual cycle irregularity, and pregnant women had significantly lower age-specific AMH percentiles (for OC use, 11 percentiles lower; for cycle irregularity, 11 percentiles lower; and for pregnancy, 17 percentiles lower [P value for all <.0001]). Age at menarche and age at first childbirth were not associated with the age-specific AMH percentile. Higher parity was associated with 2 percentiles higher age-specific AMH (P = .02). Of the lifestyle factors investigated, current smoking was associated with 4 percentiles lower age-specific AMH percentiles (P = .02), irrespective of the [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "209", "doc_id": "42150015", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Hyperfibrinogenemia increases rates of femoropopliteal bypass thrombosis.\n\nCANDIDATE_PASSAGE:\nGlobal, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015 BACKGROUND The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. METHODS We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors-the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "533", "doc_id": "13770184", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: In a naive state, blocking Wingless-Int-1 secretion from mouse embryonic stem cells inhibits self-renewal of the mouse embryonic stem cells.\n\nCANDIDATE_PASSAGE:\nEmbryonic stem cells require Wnt proteins to prevent differentiation to epiblast stem cells Pluripotent stem cells exist in naive and primed states, epitomized by mouse embryonic stem cells (ESCs) and the developmentally more advanced epiblast stem cells (EpiSCs; ref. ). In the naive state of ESCs, the genome has an unusual open conformation and possesses a minimum of repressive epigenetic marks. In contrast, EpiSCs have activated the epigenetic machinery that supports differentiation towards the embryonic cell types. The transition from naive to primed pluripotency therefore represents a pivotal event in cellular differentiation. But the signals that control this fundamental differentiation step remain unclear. We show here that paracrine and autocrine Wnt signals are essential self-renewal factors for ESCs, and are required to inhibit their differentiation into EpiSCs. Moreover, we find that Wnt proteins in combination with the cytokine LIF are sufficient to support ESC self-renewal in the absence of any undefined factors, and support the derivation of new ESC lines, including ones from non-permissive mouse strains. Our results not only demonstrate that Wnt signals regulate the naive-to-primed pluripotency transition, but also identify Wnt as an essential and limiting ESC self-renewal factor.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "568", "doc_id": "23418635", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: aPKCz causes tumour enhancement by affecting glutamine metabolism.\n\nCANDIDATE_ABSTRACT:\nTITLE: Control of Nutrient Stress-Induced Metabolic Reprogramming by PKCζ in Tumorigenesis\nABSTRACT: Tumor cells have high-energetic and anabolic needs and are known to adapt their metabolism to be able to survive and keep proliferating under conditions of nutrient stress. We show that PKCζ deficiency promotes the plasticity necessary for cancer cells to reprogram their metabolism to utilize glutamine through the serine biosynthetic pathway in the absence of glucose. PKCζ represses the expression of two key enzymes of the pathway, PHGDH and PSAT1, and phosphorylates PHGDH at key residues to inhibit its enzymatic activity. Interestingly, the loss of PKCζ in mice results in enhanced intestinal tumorigenesis and increased levels of these two metabolic enzymes, whereas patients with low levels of PKCζ have a poor prognosis. Furthermore, PKCζ and caspase-3 activities are correlated with PHGDH levels in human intestinal tumors. Taken together, this demonstrates that PKCζ is a critical metabolic tumor suppressor in mouse and human cancer.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Taken together, this demonstrates that PKCζ is a critical metabolic tumor suppressor in mouse and human cancer.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1382, "doc_id": "17755060", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The microtubule-dependent delivery and secretion of matrix metalloproteases (MMPs) is partially responsible for the disassembly of adhesion sites.\n\nCANDIDATE_PASSAGE:\nInflammasome-induced IL-1β secretion in microglia is characterized by delayed kinetics and is only partially dependent on inflammatory caspases. Inflammasomes are multiprotein complexes that link pathogen recognition and cellular stress to the processing of the proinflammatory cytokine interleukin-1β (IL-1β). Whereas inflammasome-mediated activation is heavily studied in hematopoietic macrophages and dendritic cells, much less is known about microglia, resident tissue macrophages of the brain that originate from a distinct progenitor. To directly compare inflammasome-mediated activation in different types of macrophages, we isolated primary microglia and hematopoietic macrophages from adult, healthy rhesus macaques. We analyzed the expression profile of NOD (nucleotide-binding oligomerization domain)-like receptors, adaptor proteins, and caspases and characterized inflammasome activation and regulation in detail. We here demonstrate that primary microglia can respond to the same innate stimuli as hematopoietic macrophages. However, microglial responses are more persistent due to lack of negative regulation on pro-IL-1β expression. In addition, we show that while caspase 1, 4, and 5 activation is pivotal for inflammasome-induced IL-1β secretion by hematopoietic macrophages, microglial secretion of IL-1β is only partially dependent on these inflammatory caspases. These results identify key cell type-specific differences that may aid the development of strategies to modulate innate immune responses in the brain.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1229", "doc_id": "16863359", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Energy balance requires hypothalamic glutamate neurotransmission.\n\nCANDIDATE_PASSAGE:\nActivated AMPK boosts the Nrf2/HO-1 signaling axis—A role for the unfolded protein response In light of the emerging interplay between redox and metabolic signaling pathways we investigated the potential cross talk between nuclear factor E2-related factor 2 (Nrf2) and AMP-activated kinase (AMPK), central regulators of the cellular redox and energy balance, respectively. Making use of xanthohumol (XN) as an activator of both the AMPK and the Nrf2 signaling pathway we show that AMPK exerts a positive influence on Nrf2/heme oxygenase (HO)-1 signaling in mouse embryonic fibroblasts. Genetic ablation and pharmacological inhibition of AMPK blunts Nrf2-dependent HO-1 expression by XN already at the mRNA level. XN leads to AMPK activation via interference with mitochondrial function and activation of liver kinase B1 as upstream AMPK kinase. The subsequent AMPK-mediated enhancement of the Nrf2/HO-1 response does not depend on inhibition of the mammalian target of rapamycin, inhibition of glycogen synthase kinase 3β, or altered abundance of Nrf2 (total and nuclear). However, reduced endoplasmic reticulum stress was identified and elaborated as a step in the AMPK-augmented Nrf2/HO-1 response. Overall, we shed more light on the hitherto incompletely understood cross talk between the LKB1/AMPK and the Nrf2/HO-1 axis revealing for the first time involvement of the unfolded protein response as an additional player and suggesting tight cooperation between signaling pathways controlling cellular redox, energy, or protein homeostasis.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "378", "doc_id": "9752604", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is lIMD1 more frequently altered than RB1 in head and neck squamous cell carcinoma : clinical and prognostic implications?\n\nABSTRACT:\nTo understand the role of two interacting proteins LIMD1 and pRB in development of head and neck squamous cell carcinoma (HNSCC), alterations of these genes were analyzed in 25 dysplastic head and neck lesions, 58 primary HNSCC samples and two HNSCC cell lines. Deletions of LIMD1 and RB1 were analyzed along with mutation and promoter methylation analysis of LIMD1. The genotyping of LIMD1 linked microsatellite marker, hmlimD1, was done to find out any risk allele. The mRNA expression of LIMD1 and RB1 were analyzed by Q-PCR. Immunohistochemical analysis of RB1 was performed. Alterations of these genes were correlated with different clinicopathological parameters. High frequency [94% (78/83)] of LIMD1 alterations was observed in the samples studied. Compare to frequent deletion and methylation, mutation of LIMD1 was increased during tumor progression (P = 0.007). Six novel mutations in exon1 and one novel intron4/exon5 splice-junction mutation were detected in LIMD1 along with a susceptible hmlimD1 (CA)20 allele. Some of these mutations [42% (14/33)] produced non-functional proteins. RB1 deletion was infrequent (27%). Highly reduced mRNA expression of LIMD1 (25.1 +/- 19.04) was seen than RB1 (3.8 +/- 8.09), concordant to their molecular alterations. The pRB expression supported this data. Tumors with LIMD1 alterations in tobacco addicted patients without HPV infection showed poor prognosis. Co-alterations of these genes led the worse patients' outcome.", "output": "{\"label\": \"yes\", \"rationale\": \"Our study suggests LIMD1 inactivation as primary event than inactivation of RB1 in HNSCC development.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 20226061, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Reduced responsiveness to interleukin-2 in regulatory T cells is associated with greater resistance to autoimmune diseases such as Type 1 Diabetes.\n\nCANDIDATE_PASSAGE:\nThe antidiabetic effect of mesenchymal stem cells is unrelated to their transdifferentiation potential but to their capability to restore Th1/Th2 balance and to modify the pancreatic microenvironment. Type 1 diabetes mellitus (T1DM) is a chronic metabolic disease that results from cell-mediated autoimmune destruction of insulin-producing cells. In T1DM animal models, it has been shown that the systemic administration of multipotent mesenchymal stromal cells, also referred as to mesenchymal stem cells (MSCs), results in the regeneration of pancreatic islets. Mechanisms underlying this effect are still poorly understood. Our aims were to assess whether donor MSCs (a) differentiate into pancreatic β-cells and (b) modify systemic and pancreatic pathophysiologic markers of T1DM. After the intravenous administration of 5 × 10(5) syngeneic MSCs, we observed that mice with T1DM reverted their hyperglycemia and presented no donor-derived insulin-producing cells. In contrast, 7 and 65 days post-transplantation, MSCs were engrafted into secondary lymphoid organs. This correlated with a systemic and local reduction in the abundance of autoaggressive T cells together with an increase in regulatory T cells. Additionally, in the pancreas of mice with T1DM treated with MSCs, we observed a cytokine profile shift from proinflammatory to antinflammatory. MSC transplantation did not reduce pancreatic cell apoptosis but recovered local expression and increased the circulating levels of epidermal growth factor, a pancreatic trophic factor. Therefore, the antidiabetic effect of MSCs intravenously administered is unrelated to their transdifferentiation potential but to their capability to restore the balance between Th1 and Th2 immunological responses along with the modification of [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1029", "doc_id": "24101431", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Decreased conversion of PGE 2 to PPARy ligand 15-ket-PGE 2 causes accumulation of PGE.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pharmacological correction of a defect in PPARγ signaling ameliorates disease severity in Cftr-deficient mice\nABSTRACT: Cystic fibrosis is caused by mutations in the cystic fibrosis transmembrane conductance regulator (encoded by Cftr) that impair its role as an apical chloride channel that supports bicarbonate transport. Individuals with cystic fibrosis show retained, thickened mucus that plugs airways and obstructs luminal organs as well as numerous other abnormalities that include inflammation of affected organs, alterations in lipid metabolism and insulin resistance. Here we show that colonic epithelial cells and whole lung tissue from Cftr-deficient mice show a defect in peroxisome proliferator-activated receptor-gamma (PPAR-gamma, encoded by Pparg) function that contributes to a pathological program of gene expression. Lipidomic analysis of colonic epithelial cells suggests that this defect results in part from reduced amounts of the endogenous PPAR-gamma ligand 15-keto-prostaglandin E(2) (15-keto-PGE(2)). Treatment of Cftr-deficient mice with the synthetic PPAR-gamma ligand rosiglitazone partially normalizes the altered gene expression pattern associated with Cftr deficiency and reduces disease severity. Rosiglitazone has no effect on chloride secretion in the colon, but it increases expression of the genes encoding carbonic anhydrases 4 and 2 (Car4 and Car2), increases bicarbonate secretion and reduces mucus retention. These studies reveal a reversible defect in PPAR-gamma signaling in Cftr-deficient cells that can be pharmacologically corrected to ameliorate the severity of the cystic fibrosis phenotype in mice.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 316, "doc_id": "712078", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: B cells go though plasmablast differentiation and antibody production by continuous expression of EBI2.\n\nCANDIDATE_PASSAGE:\nHuman IL-10 is produced by both type 1 helper (Th1) and type 2 helper (Th2) T cell clones and inhibits their antigen-specific proliferation and cytokine production. IL-10 gene transcription and IL-10 protein production was assessed in both type 1 (Th1) and type 2 (Th2) CD4+ human T cell clones by polymerase chain reaction and ELISA, respectively. Although Th2 clones apparently showed higher IL-10 mRNA levels, IL-10 mRNA expression was consistently found in Th1 clones, as well. Likewise, measurable IL-10 levels were found in the supernatants of both Th1 and Th2 clones. The effect of human IL-10 (h-IL-10) and viral IL-10 (v-IL-10) on the proliferative response and cytokine production by Th1 and Th2 human clones was also investigated. Addition in culture of h-IL-10 and v-IL-10 significantly reduced the proliferation of both Th1 and Th2 clones in response to the specific Ag and to PHA, but it had no inhibitory effect on the proliferative response of Th1 and Th2 clones to IL-2. h-IL-10 and v-IL-10 also inhibited the Ag-induced production of gamma-interferon (IFN-gamma) by Th1 clones and the production of IL-4 and IL-5 by Th2 clones, whereas they had no effect on the cytokine synthesis by the same clones stimulated with PMA plus anti-CD3 antibody. Preincubation of APC, but not of clonal T blasts, with h-IL-10 resulted in the inhibition of Ag-induced proliferation of both Th1 and Th2 clones, supporting the view that h-IL-10 primarily affects APC. These data demonstrate that, unlike the murine system where IL-10 is a product of Th2 (but not Th1) cells and seems to mainly down-regulate the Th1 response, in the human system, IL-10 is produced by, and down-regulates the function of, both Th1 and Th2 cells.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "152", "doc_id": "8639034", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: T regulatory cells (tTregs) lacking αvβ8 are more adept at suppressing pathogenic T-cell responses during active inflammation.\n\nCANDIDATE_PASSAGE:\nIntegration of Smad and MAPK pathways: a link and a linker revisited. Cells develop by reading mixed signals. Nowhere is this clearer than in the highly dynamic processes that propel embryogenesis, when critical cell-fate decisions are made swiftly in response to well-orchestrated growthfactor combinations. Learning how diverse signaling pathways are integrated is therefore essential for understanding physiology. This requires the identification, in tangible molecular terms, of key nodes for pathway integration that operate in vivo. A report in this issue, on the integration of Smad and Ras/MAPK pathways during neural induction (Pera et al. 2003), provides timely insights into the relevance of one such node. Pera et al. (2003) report that FGF8 and IGF2—two growth factors that activate the Ras/MAPK pathway— favor neural differentiation and mesoderm dorsalization in Xenopus by inhibiting BMP (Bone Morphogenetic Protein) signaling. Mesoderm is formed from ectoderm in response to Nodal-related signals from the endoderm at the blastula stage and beyond (Fig. 1; for review, see De Robertis et al. 2000). BMP induces differentiation of ectoderm into epidermal cell fates at the expense of neural fates, and it ventralizes the mesoderm at the expense of dorsal fates (for review, see Weinstein and HemmatiBrivanlou 1999; De Robertis et al. 2000). Accordingly, neural differentiation and dorsal mesoderm formation are favored when BMP signaling is attenuated. Noggin, Chordin, Cerberus, and Follistatin, secreted by the Spemann organizer on the dorsal side at the gastrula stage, facilitate the formation of neural tissue by sequestering BMP (Weinstein and Hemmati-Brivanlou 1999; De Robertis et al. 2000). Experimentally blocking BMP signaling with a dominant-negative BMP recept [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1130", "doc_id": "39291138", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Radioiodine treatment of non-toxic multinodular goitre reduces thyroid volume.\n\nCANDIDATE_PASSAGE:\nBody-mass index and risk of 22 specific cancers: a population-based cohort study of 5·24 million UK adults BACKGROUND High body-mass index (BMI) predisposes to several site-specific cancers, but a large-scale systematic and detailed characterisation of patterns of risk across all common cancers adjusted for potential confounders has not previously been undertaken. We aimed to investigate the links between BMI and the most common site-specific cancers. METHODS With primary care data from individuals in the Clinical Practice Research Datalink with BMI data, we fitted Cox models to investigate associations between BMI and 22 of the most common cancers, adjusting for potential confounders. We fitted linear then non-linear (spline) models; investigated effect modification by sex, menopausal status, smoking, and age; and calculated population effects. FINDINGS 5·24 million individuals were included; 166,955 developed cancers of interest. BMI was associated with 17 of 22 cancers, but effects varied substantially by site. Each 5 kg/m(2) increase in BMI was roughly linearly associated with cancers of the uterus (hazard ratio [HR] 1·62, 99% CI 1·56-1·69; p<0·0001), gallbladder (1·31, 1·12-1·52; p<0·0001), kidney (1·25, 1·17-1·33; p<0·0001), cervix (1·10, 1·03-1·17; p=0·00035), thyroid (1·09, 1·00-1·19; p=0·0088), and leukaemia (1·09, 1·05-1·13; p≤0·0001). BMI was positively associated with liver (1·19, 1·12-1·27), colon (1·10, 1·07-1·13), ovarian (1·09, 1.04-1.14), and postmenopausal breast cancers (1·05, 1·03-1·07) overall (all p<0·0001), but these effects varied by underlying BMI or individual-level characteristics. We estimated inverse associations with prostate and premenopausal breast cancer risk, both overall (prostate 0·98, 0·95-1·00; premenopausal breast cance [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1012", "doc_id": "4828631", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Low expression of miR7a does not repress target genes or exert a biological function in ovaries.\n\nCANDIDATE_ABSTRACT:\nTITLE: Assessing the ceRNA hypothesis with quantitative measurements of miRNA and target abundance.\nABSTRACT: Recent studies have reported that competitive endogenous RNAs (ceRNAs) can act as sponges for a microRNA (miRNA) through their binding sites and that changes in ceRNA abundances from individual genes can modulate the activity of miRNAs. Consideration of this hypothesis would benefit from knowing the quantitative relationship between a miRNA and its endogenous target sites. Here, we altered intracellular target site abundance through expression of an miR-122 target in hepatocytes and livers and analyzed the effects on miR-122 target genes. Target repression was released in a threshold-like manner at high target site abundance (≥1.5 × 10(5) added target sites per cell), and this threshold was insensitive to the effective levels of the miRNA. Furthermore, in response to extreme metabolic liver disease models, global target site abundance of hepatocytes did not change sufficiently to affect miRNA-mediated repression. Thus, modulation of miRNA target abundance is unlikely to cause significant effects on gene expression and metabolism through a ceRNA effect.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 713, "doc_id": "18421962", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Cognitive behavioral therapy is an ineffective treatment for insomnia\n\nCANDIDATE_PASSAGE:\nAn overview of the effective combination therapies for the treatment of breast cancer. Breast cancer (BC) is generally classified based on the receptors overexpressed on the cell nucleus, which include hormone receptors such as progesterone (PR) and estrogen (ER), and HER2. Triple-negative breast cancer (TNBC) is a type of cancer that lacks any of these three types of receptor proteins (ER/PR/HER2). Tumor cells exhibit drug resistant phenotypes that decrease the efficacy of chemotherapeutic treatments. Generally, drug resistance has a genetic basis that is caused by an abnormal gene expression, nevertheless, there are several types of drug resistance: efflux pumps reducing the cellular concentration of the drug, alterations in membrane lipids that reduce cellular uptake, increased or altered drug targets, metabolic alteration of the drug, inhibition of apoptosis, repair of the damaged DNA, and alteration of the cell cycle checkpoints. The use of \"combination therapy\" is recognized as an efficient solution to treat human diseases, in particular, breast cancer. In this review, we give examples of different nanocarriers used to co-deliver multiple therapeutics (chemotherapeutic agent and nucleic acid) to drug-resistant tumor cells, and lastly, we give our recommendations for the future directions for the co-delivery treatments.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "267", "doc_id": "22482820", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does danqi Piantan Jiaonang modify hemostasis , hematology , and biochemistry in normal subjects and stroke patients?\n\nABSTRACT:\nPrevious studies on Danqi Piantan Jiaonang (DPJ, NeuroAid), a traditional Chinese medicine, in stroke patients showed promising results. Our aim was to determine the safety of DPJ in normal subjects and stroke patients through a series of studies assessing its immediate and long-term effects, alone and in combination with aspirin, on hematological, hemostatic, and biochemical parameters. We conducted 3 studies from December 2004 to May 2006. Study 1 was a case series which recruited 32 healthy volunteers who were given 2 oral doses of 4 DPJ capsules (0.4 g/capsule) 6 h apart. Study 2 was a randomized controlled trial of 22 healthy volunteers who received either 1 oral dose of aspirin 300 mg alone or a combination of 1 dose of aspirin 300 mg and 2 doses of 4 DPJ capsules taken 6 h apart. For both studies 1 and 2, hemostatic parameters (prothrombin time, activated partial thromboplastin time, fibrinogen, platelet aggregation, D-dimer) were tested at baseline, and after 2 and 8 h. Study 3 was a case series which recruited 10 patients with recent ischemic stroke (within 7 days) who were given 4 DPJ capsules taken orally 3 times a day for 1 month. Blood tests for hemostatic, hematological (complete blood count), and biochemical parameters (glucose, creatinine, alanine aminotransferase, aspartate transaminase, C-reactive protein) were performed at baseline, and after 1 and 4 weeks. Apart from the expected changes in platelet aggregation in subjects taking aspirin, no significant differences were detected in hemostatic parameters at baseline, and 2 and 8 h after oral intake of DPJ alone or in combination with aspirin. Likewise, no significant differences were observed in hematological, hemostatic, and biochemical parameters at baseline, and after 1 and 4 weeks of o [TRUNCATED]", "output": "{\"label\": \"no\", \"rationale\": \"DPJ does not significantly modify hematological, hemostatic, and biochemical parameters in normal subjects and stroke patients.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 18417963, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Inhibiting focal adhesion formation increases the rate at which cells convert mechanical strain into inflammation and fibrosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Focal adhesion kinase links mechanical force to skin fibrosis via inflammatory signaling\nABSTRACT: Exuberant fibroproliferation is a common complication after injury for reasons that are not well understood. One key component of wound repair that is often overlooked is mechanical force, which regulates cell-matrix interactions through intracellular focal adhesion components, including focal adhesion kinase (FAK). Here we report that FAK is activated after cutaneous injury and that this process is potentiated by mechanical loading. Fibroblast-specific FAK knockout mice have substantially less inflammation and fibrosis than control mice in a model of hypertrophic scar formation. We show that FAK acts through extracellular-related kinase (ERK) to mechanically trigger the secretion of monocyte chemoattractant protein-1 (MCP-1, also known as CCL2), a potent chemokine that is linked to human fibrotic disorders. Similarly, MCP-1 knockout mice form minimal scars, indicating that inflammatory chemokine pathways are a major mechanism by which FAK mechanotransduction induces fibrosis. Small-molecule inhibition of FAK blocks these effects in human cells and reduces scar formation in vivo through attenuated MCP-1 signaling and inflammatory cell recruitment. These findings collectively indicate that physical force regulates fibrosis through inflammatory FAK–ERK–MCP-1 pathways and that molecular strategies targeting FAK can effectively uncouple mechanical force from pathologic scar formation.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"These findings collectively indicate that physical force regulates fibrosis through inflammatory FAK–ERK–MCP-1 pathways and that molecular strategies targeting FAK can effectively uncouple mechanical force from pathologic scar formation.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 633, "doc_id": "5172048", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: BCL-2 promotes the apoptotic effects of c-Myc.\n\nCANDIDATE_PASSAGE:\nLarge deformation of red blood cell ghosts in a simple shear flow. Red blood cells are known to change shape in response to local flow conditions. Deformability affects red blood cell physiological function and the hydrodynamic properties of blood. The immersed boundary method is used to simulate three-dimensional membrane-fluid flow interactions for cells with the same internal and external fluid viscosities. The method has been validated for small deformations of an initially spherical capsule in simple shear flow for both neo-Hookean and the Evans-Skalak membrane models. Initially oblate spheroidal capsules are simulated and it is shown that the red blood cell membrane exhibits asymptotic behavior as the ratio of the dilation modulus to the extensional modulus is increased and a good approximation of local area conservation is obtained. Tank treading behavior is observed and its period calculated.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "156", "doc_id": "27049238", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Many transmembrane receptors transmit signals by long-range conformational changes in the association of alpha-helices across the plasma membrane.\n\nCANDIDATE_ABSTRACT:\nTITLE: Dynamic Helix Interactions in Transmembrane Signaling\nABSTRACT: Studying how protein transmembrane domains transmit signals across membranes is beset by unique challenges. Here, we discuss the circumstances that have led to success and reflect on what has been learned from these examples. Such efforts suggest that some of the most interesting properties of transmembrane helix interactions may be the least amenable to study by current techniques.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 757, "doc_id": "17123657", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Whole brain radiotherapy increases the occurrence of new brain metastases.\n\nCANDIDATE_ABSTRACT:\nTITLE: Stereotactic radiosurgery plus whole-brain radiation therapy vs stereotactic radiosurgery alone for treatment of brain metastases: a randomized controlled trial.\nABSTRACT: CONTEXT In patients with brain metastases, it is unclear whether adding up-front whole-brain radiation therapy (WBRT) to stereotactic radiosurgery (SRS) has beneficial effects on mortality or neurologic function compared with SRS alone. OBJECTIVE To determine if WBRT combined with SRS results in improvements in survival, brain tumor control, functional preservation rate, and frequency of neurologic death. DESIGN, SETTING, AND PATIENTS Randomized controlled trial of 132 patients with 1 to 4 brain metastases, each less than 3 cm in diameter, enrolled at 11 hospitals in Japan between October 1999 and December 2003. INTERVENTIONS Patients were randomly assigned to receive WBRT plus SRS (65 patients) or SRS alone (67 patients). MAIN OUTCOME MEASURES The primary end point was overall survival; secondary end points were brain tumor recurrence, salvage brain treatment, functional preservation, toxic effects of radiation, and cause of death. RESULTS The median survival time and the 1-year actuarial survival rate were 7.5 months and 38.5% (95% confidence interval, 26.7%-50.3%) in the WBRT + SRS group and 8.0 months and 28.4% (95% confidence interval, 17.6%-39.2%) for SRS alone (P = .42). The 12-month brain tumor recurrence rate was 46.8% in the WBRT + SRS group and 76.4% for SRS alone group (P<.001). Salvage brain treatment was less frequently required in the WBRT + SRS group (n = 10) than with SRS alone (n = 29) (P<.001). Death was attributed to neurologic causes in 22.8% of patients in the WBRT + SRS group and in 19.3% of those treated with SRS alone (P = .64). There were no significant differences in systemic and neurologic functional preservation and toxic effects of radiation. CONCLUSIONS Compared with SRS alone, the use of WBRT plus SRS did not improve survival [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The 12-month brain tumor recurrence rate was 46.8% in the WBRT + SRS group and 76.4% for SRS alone group (P<.001).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1376, "doc_id": "3944632", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Are poor diet quality and postoperative time independent risk factors for weight regain after Roux-en-Y gastric bypass?\n\nABSTRACT:\nIn this study, multivariate analyses was used to investigate factors associated with weight regain long after Roux-en-Y gastric bypass. This retrospective study comprised 80 patients (88.8% female) with at least 24 mo of postoperative time. Weight regain was defined as an increase of at least 10% of the lowest postoperative weight. The following data were collected: demographic characteristics, eating behavior, food intake, diet quality measured by the Healthy Eating Index, level of physical activity, follow-up visit attendance, anthropometric history, and postoperative time. Multivariate logistic regression generated a controlled analysis, followed by calculation of the odds ratio (OR). The mean postoperative time was 47.0 ± 18.0 mo. The mean pre- and postoperative body mass indexes were 49.8 ± 9.3 kg/m(2) and 33.6 ± 7.2 kg/m(2), respectively. Despite satisfactory postoperative weight loss, 23.7% of the patients regained weight. After controlling for confounders, only postoperative time (OR 1.08; P < 0.01) and Healthy Eating Index (OR 0.95; P = 0.04) remained associated with weight regain.", "output": "{\"label\": \"yes\", \"rationale\": \"Patients with long-term obesity and poor diet quality were at high risk of weight regain. These results suggest the need of nutritional monitoring during the late postoperative period, paying special attention to eating patterns.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 27544005, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Klf4 is not required for proper myeloid cell differentiation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Kruppel-like factor 4 is essential for inflammatory monocyte differentiation in vivo.\nABSTRACT: Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types. We demonstrate in this study that hematopoietic cells from KLF4(-/-) fetal livers (FL) contained normal numbers of functional hematopoietic progenitor cells, were radioprotective, and performed as well as KLF4(+/+) cells in competitive repopulation assays. However, hematopoietic \"KLF4(-/-) chimeras\" generated by transplantation of KLF4(-/-) fetal livers cells into lethally irradiated wild-type mice completely lacked circulating inflammatory (CD115(+)Gr1(+)) monocytes, and had reduced numbers of resident (CD115(+)Gr1(-)) monocytes. Although the numbers and function of peritoneal macrophages were normal in KLF4(-/-) chimeras, bone marrow monocytic cells from KLF4(-/-) chimeras expressed lower levels of key trafficking molecules and were more apoptotic. Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes. In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells. The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 669, "doc_id": "25148216", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Auditory entrainment is strengthened when people see congruent visual and auditory information.\n\nCANDIDATE_ABSTRACT:\nTITLE: Congruent Visual Speech Enhances Cortical Entrainment to Continuous Auditory Speech in Noise-Free Conditions.\nABSTRACT: UNLABELLED Congruent audiovisual speech enhances our ability to comprehend a speaker, even in noise-free conditions. When incongruent auditory and visual information is presented concurrently, it can hinder a listener's perception and even cause him or her to perceive information that was not presented in either modality. Efforts to investigate the neural basis of these effects have often focused on the special case of discrete audiovisual syllables that are spatially and temporally congruent, with less work done on the case of natural, continuous speech. Recent electrophysiological studies have demonstrated that cortical response measures to continuous auditory speech can be easily obtained using multivariate analysis methods. Here, we apply such methods to the case of audiovisual speech and, importantly, present a novel framework for indexing multisensory integration in the context of continuous speech. Specifically, we examine how the temporal and contextual congruency of ongoing audiovisual speech affects the cortical encoding of the speech envelope in humans using electroencephalography. We demonstrate that the cortical representation of the speech envelope is enhanced by the presentation of congruent audiovisual speech in noise-free conditions. Furthermore, we show that this is likely attributable to the contribution of neural generators that are not particularly active during unimodal stimulation and that it is most prominent at the temporal scale corresponding to syllabic rate (2-6 Hz). Finally, our data suggest that neural entrainment to the speech envelope is inhibited when the auditory and visual streams are incongruent both temporally and contextually. SIGNIFICANCE STATEMENT Seeing a speaker's face as he or she talks can greatly help in understan [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"UNLABELLED Congruent audiovisual speech enhances our ability to comprehend a speaker, even in noise-free conditions.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 141, "doc_id": "14437255", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Can surgeon familiarization with current evidence lead to a change in practice?\n\nABSTRACT:\nDespite evidence against its utility, many surgeons continue to employ prophylactic nasogastric decompression in elective colonic resection. This study aimed to establish whether an easy and practical intervention, mailing out a summary of current evidence to surgeons, can change surgeons practice to bring it more in line with current evidence. The use of prophylactic nasogastric (NG) decompression in elective colonic resections was documented for the 2 consecutive months of October and November, 2004 at the Royal Alexandra Hospital (RAH). A one page summary of recent evidence concerning this practice was then mailed to all general surgeons at that institution. A similar second review was carried out for the months of January and February, 2005. The two periods were compared with regards to prophylactic NG use. Twenty two patients underwent elective colonic resections during the months of October and November, 2004. Twenty one patients underwent such procedures in January and February, 2005. Seven out of the 22 cases in the first group (the pre-intervention block) received prophylactic NG decompression. Five out of the 21 cases in the second group (the post-intervention block) received prophylactic NG decompression. The difference in prophylactic NG use between the two groups was not statistically significant.", "output": "{\"label\": \"no\", \"rationale\": \"This study has shown that mailing out a summary of current evidence to surgeons concerning a certain issue is not sufficient to lead to a change in practice.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 18708308, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Mutant mice lacking SVCT2 have severely reduced ascorbic acid levels in both brain and adrenals.\n\nCANDIDATE_PASSAGE:\nPredicting immunogenic tumour mutations by combining mass spectrometry and exome sequencing Human tumours typically harbour a remarkable number of somatic mutations. If presented on major histocompatibility complex class I molecules (MHCI), peptides containing these mutations could potentially be immunogenic as they should be recognized as ‘non-self’ neo-antigens by the adaptive immune system. Recent work has confirmed that mutant peptides can serve as T-cell epitopes. However, few mutant epitopes have been described because their discovery required the laborious screening of patient tumour-infiltrating lymphocytes for their ability to recognize antigen libraries constructed following tumour exome sequencing. We sought to simplify the discovery of immunogenic mutant peptides by characterizing their general properties. We developed an approach that combines whole-exome and transcriptome sequencing analysis with mass spectrometry to identify neo-epitopes in two widely used murine tumour models. Of the >1,300 amino acid changes identified, ∼13% were predicted to bind MHCI, a small fraction of which were confirmed by mass spectrometry. The peptides were then structurally modelled bound to MHCI. Mutations that were solvent-exposed and therefore accessible to T-cell antigen receptors were predicted to be immunogenic. Vaccination of mice confirmed the approach, with each predicted immunogenic peptide yielding therapeutically active T-cell responses. The predictions also enabled the generation of peptide–MHCI dextramers that could be used to monitor the kinetics and distribution of the anti-tumour T-cell response before and after vaccination. These findings indicate that a suitable prediction algorithm may provide an approach for the pharmacodynamic monitoring of T- [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "812", "doc_id": "4462777", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Incidence rates of cervical cancer have decreased.\n\nCANDIDATE_PASSAGE:\nMass screening programmes and trends in cervical cancer in Finland and the Netherlands. With respect to cervical cancer management, Finland and the Netherlands are comparable in relevant characteristics, e.g., fertility rate, age-of-mother at first birth and a national screening programme for several years. The aim of this study is to compare trends in incidence of and mortality from cervical cancer in Finland and the Netherlands in relation to the introduction and intensity of the screening programmes. Therefore, incidence and mortality rates were calculated using the Cancer Registries of Finland and the Netherlands. Data on screening intensity were obtained from the Finnish Cancer Registry and the Dutch evaluation centre at ErasmusMC-Rotterdam. Women aged 30-60 have been screened every 5 years, in Finland since 1992 and in the Netherlands since 1996. Screening protocols for smear taking and referral to the gynaecologist are comparable. Incidence and mortality rates have declined more in Finland. In 2003, age-adjusted incidence and mortality in Finland were 4.0 and 0.9 and in the Netherlands 4.9 and 1.4 per 100,000 woman-years, respectively. Excess smear use in the Netherlands was estimated to be 24 per 1,000 women during a 5-year interval compared to 121 in Finland. The decline in mortality in Finland seems to be almost completely related to the screening programme whereas in the Netherlands it was initially considered to be a natural decline. Differences in risk factors might also play a role: the Netherlands has higher population density and higher percentages of immigrants and (female) smokers. The greater excess smear use in Finland might also have affected incidence.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "597", "doc_id": "25742130", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Polymeal nutrition increases cardiovascular mortality.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Polymeal: a more natural, safer, and probably tastier (than the Polypill) strategy to reduce cardiovascular disease by more than 75%.\nABSTRACT: OBJECTIVE Although the Polypill concept (proposed in 2003) is promising in terms of benefits for cardiovascular risk management, the potential costs and adverse effects are its main pitfalls. The objective of this study was to identify a tastier and safer alternative to the Polypill: the Polymeal. METHODS Data on the ingredients of the Polymeal were taken from the literature. The evidence based recipe included wine, fish, dark chocolate, fruits, vegetables, garlic, and almonds. Data from the Framingham heart study and the Framingham offspring study were used to build life tables to model the benefits of the Polymeal in the general population from age 50, assuming multiplicative correlations. RESULTS Combining the ingredients of the Polymeal would reduce cardiovascular disease events by 76%. For men, taking the Polymeal daily represented an increase in total life expectancy of 6.6 years, an increase in life expectancy free from cardiovascular disease of 9.0 years, and a decrease in life expectancy with cardiovascular disease of 2.4 years. The corresponding differences for women were 4.8, 8.1, and 3.3 years. CONCLUSION The Polymeal promises to be an effective, non-pharmacological, safe, cheap, and tasty alternative to reduce cardiovascular morbidity and increase life expectancy in the general population.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"For men, taking the Polymeal daily represented an increase in total life expectancy of 6.6 years, an increase in life expectancy free from cardiovascular disease of 9.0 years, and a decrease in life expectancy with cardiovascular disease of 2.4 years.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 959, "doc_id": "8780599", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: A T helper 2 cell (Th2) environment impedes disease development in patients with systemic lupus erythematosus (SLE).\n\nCANDIDATE_PASSAGE:\nBASOPHILS AND THE T HELPER 2 ENVIRONMENT CAN PROMOTE THE DEVELOPMENT OF LUPUS NEPHRITIS In systemic lupus erythematosus (SLE), self-reactive antibodies can target the kidney (lupus nephritis), leading to functional failure and possible mortality. We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice). Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis. Basophils were also present in the lymph nodes and spleen of subjects with SLE. Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "28", "doc_id": "12670680", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Eliminating the last sporadic cases of malaria requires considerable funding.\n\nCANDIDATE_ABSTRACT:\nTITLE: Costs and financial feasibility of malaria elimination\nABSTRACT: The marginal costs and benefits of converting malaria programmes from a control to an elimination goal are central to strategic decisions, but empirical evidence is scarce. We present a conceptual framework to assess the economics of elimination and analyse a central component of that framework-potential short-term to medium-term financial savings. After a review that showed a dearth of existing evidence, the net present value of elimination in five sites was calculated and compared with effective control. The probability that elimination would be cost-saving over 50 years ranged from 0% to 42%, with only one site achieving cost-savings in the base case. These findings show that financial savings should not be a primary rationale for elimination, but that elimination might still be a worthy investment if total benefits are sufficient to outweigh marginal costs. Robust research into these elimination benefits is urgently needed.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 376, "doc_id": "22401061", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Downregulation and mislocalization of Scribble prevents cell transformation and mammary tumorigenesis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Deregulation of Scribble Promotes Mammary Tumorigenesis and Reveals a Role for Cell Polarity in Carcinoma\nABSTRACT: Loss of cell polarity proteins such as Scribble induces neoplasia in Drosophila by promoting uncontrolled proliferation. In mammals, the role that polarity proteins play during tumorigenesis is not well understood. Here, we demonstrate that depletion of Scribble in mammary epithelia disrupts cell polarity, blocks three-dimensional morphogenesis, inhibits apoptosis, and induces dysplasia in vivo that progress to tumors after long latency. Loss of Scribble cooperates with oncogenes such as c-myc to transform epithelial cells and induce tumors in vivo by blocking activation of an apoptosis pathway. Like depletion, mislocalization of Scribble from cell-cell junction was sufficient to promote cell transformation. Interestingly, spontaneous mammary tumors in mice and humans possess both downregulated and mislocalized Scribble. Thus, we demonstrate that scribble inhibits breast cancer formation and that deregulation of polarity pathways promotes dysplastic and neoplastic growth in mammals by disrupting morphogenesis and inhibiting cell death.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 354, "doc_id": "8774475", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Rapamycin increases the concentration of triacylglycerols in fruit flies.\n\nCANDIDATE_PASSAGE:\nEffects of Abciximab on the architecture of platelet-rich clots in patients with acute myocardial infarction undergoing primary coronary intervention. BACKGROUND Abciximab plus aspirin improves the TIMI 3 flow rate of the infarct-related artery in patients treated with either percutaneous coronary intervention or thrombolysis. The present study investigated whether the reperfusion efficacy of abciximab relates to modifications of clot architecture in patients admitted for acute myocardial infarction (AMI). METHODS AND RESULTS A total of 23 AMI patients in the Abciximab before Direct angioplasty and stenting in Myocardial Infarction Regarding Acute and Long term follow-up (ADMIRAL) trial received, in a double-blind fashion, either abciximab (n=13) or placebo (n=10) before primary stenting. Viscoelastic (G' in dyne/cm(2)) and morphological (mean platelet aggregate surface area [SAG] in micrometer(2)) indexes of ex vivo platelet-rich clots (PRC) were assessed in a double-blind fashion before and after the bolus administration of abciximab or placebo. G' and SAG reflect the mechanical and morphological impact of activated platelets on the PRC fibrin network, respectively. Abciximab administration reduced G' by 63% (P=0.0001) and SAG by 65% (P=0.0007), and no effect was seen in the placebo group. These abciximab-related changes increased fibrin exposure as a consequence of the platelet-aggregate surface reduction and may have improved endogenous fibrinolysis. These effects were identified in all patients, independent of previous heparin administration. CONCLUSIONS Abciximab dramatically reduces platelet aggregate size and increases the fibrin accessibility of ex vivo PRC in AMI patients. These modifications could participate in the better coronary artery patency [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1016", "doc_id": "17897801", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does timing of initial surfactant treatment make a difference in rates of chronic lung disease or mortality in premature infants?\n\nABSTRACT:\nTo compare two treatment strategies in preterm infants with or at risk of respiratory distress syndrome: early surfactant administration (within one hour of birth) versus late surfactant administration, in a geographically defined population. The primary outcome was chronic lung disease (CLD) and mortality before/at 36 weeks. Secondary outcomes included: duration of mechanical ventilation and continuous positive airway pressure (CPAP), post-natal steroids for CLD and major neonatal morbidities. Premature infants born at 22-32 weeks' gestation between January 2006 and December 2009. Ten neonatal intensive care units (NICUs) in New South Wales (NSW) and Australian Capital Territory (ACT), Australia. Retrospective analysis of prospectively collected data from the regional NICU database in NSW and ACT. Of the 2170 infants who received surfactant, 1182 (54.5%) and 988 (45.5%) received early and late surfactant, respectively. The early surfactant group was less mature (27.1 ± 2.1 versus 29.4 ± 2.1 weeks) and had more CLD and mortality (40.2% versus 20.0%). The multivariable analysis showed early surfactant to be associated with less duration of ventilation, longer duration of CPAP and longer hospital stay but had little or no impact on CLD/mortality.", "output": "{\"label\": \"maybe\", \"rationale\": \"Early surfactant administration is associated with shorter duration of ventilation but does not appear to be significantly protective against CLD/mortality among premature infants. This may support the growing evidence for consideration of CPAP as an alternative to routine intubation and early surfactant administration. Further investigation from large randomized clinical trials is warranted to confirm these results.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 25394614, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is perforation of the appendix a risk factor for tubal infertility and ectopic pregnancy?\n\nABSTRACT:\nTo critically assess the evidence that appendiceal perforation is a risk factor for subsequent tubal infertility or ectopic pregnancy. Epidemiologic studies investigating the relationship between appendectomy and infertility or ectopic pregnancy were identified by searching the MEDLINE database from 1966 to 1997. Appropriate citations were also extracted from a manual search of the bibliographies of selected papers. Twenty-three articles were retrieved. Only 4 presented original data including comparisons to a nonexposed control group and they form the basis for this study. Because the raw data or specific techniques of data analysis were not always explicitly described, indices of risk for exposure were extracted from the data as presented and were analysed without attempting to convert them to a common measure. Articles were assessed according to the criteria of the Evidence-Based Medicine Working Group for evaluating articles on harm. Review of the literature yielded estimates of the risk of adverse fertility outcomes ranging from 1.6 (95% confidence interval [CI] 1.1 to 2.5) for ectopic pregnancy after an appendectomy to 4.8 (95% CI 1.5 to 14.9) for tubal infertility from perforation of the appendix. Recall bias, and poor adjustment for confounding variables in some reports, weakened the validity of the studies.", "output": "{\"label\": \"maybe\", \"rationale\": \"The methodologic weaknesses of the studies do not permit acceptance of increased risk of tubal pregnancy or infertility as a consequence of perforation of the appendix, so a causal relationship cannot be supported by the data currently available. Only a well-designed case-control study with unbiased ascertainment of exposure and adjustment for confounding variables will provide a definitive answer.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 10223070, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Women with a higher birth weight are more likely to develop breast cancer later in life.\n\nCANDIDATE_ABSTRACT:\nTITLE: Intrauterine factors and risk of breast cancer: a systematic review and meta-analysis of current evidence.\nABSTRACT: BACKGROUND Emerging evidence suggests an association between female prenatal experience and her subsequent risk of developing breast cancer. Potential underlying mechanisms include variation in amounts of maternal endogenous sex hormones and growth hormones, germ-cell mutations, formation of cancer stem-cells, and other genetic or epigenetic events. We reviewed and summarised quantitatively the available data on intrauterine exposures and risk of breast cancer. METHODS We systematically searched for studies that assessed association between perinatal factors and risk of breast cancer. We reviewed separately each of the perinatal factors, including birthweight, birth length, parental age at delivery, gestational age, intrauterine exposure to diethylstilbestrol, twin membership, maternal pre-eclampsia or eclampsia, and other factors. FINDINGS We identified 57 studies published between Oct 1, 1980, and June 21, 2007. Increased risk of breast cancer was noted with increased birthweight (relative risk [RR] 1.15 [95% CI 1.09-1.21]), birth length (1.28 [1.11-1.48]), higher maternal age (1.13 [1.02-1.25]), and paternal age (1.12 [1.05-1.19]). Decreased risk of breast cancer was noted for maternal pre-eclampsia and eclampsia (0.48 [0.30-0.78]) and twin membership (0.93 [0.87-1.00]). No association was noted between risk of breast cancer and gestational age at birth (0.95 [0.71-1.26]) or maternal diethylstilbestrol treatment (1.40 [0.86-2.28]). INTERPRETATION The intrauterine environment contributes to the predisposition of women to breast cancer in adulthood. The in-utero mechanisms responsible for such predisposition need to be elucidated.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Increased risk of breast cancer was noted with increased birthweight (relative risk [RR] 1.15 [95% CI 1.09-1.21]), birth length (1.28 [1.11-1.48]), higher maternal age (1.13 [1.02-1.25]), and paternal age (1.12 [1.05-1.19]).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1379, "doc_id": "23557241", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cancer-associated fibroblasts (CAFs) are constituents of tumor microenvironments\n\nCANDIDATE_ABSTRACT:\nTITLE: Microenvironmental regulation of tumor progression and metastasis\nABSTRACT: Cancers develop in complex tissue environments, which they depend on for sustained growth, invasion and metastasis. Unlike tumor cells, stromal cell types within the tumor microenvironment (TME) are genetically stable and thus represent an attractive therapeutic target with reduced risk of resistance and tumor recurrence. However, specifically disrupting the pro-tumorigenic TME is a challenging undertaking, as the TME has diverse capacities to induce both beneficial and adverse consequences for tumorigenesis. Furthermore, many studies have shown that the microenvironment is capable of normalizing tumor cells, suggesting that re-education of stromal cells, rather than targeted ablation per se, may be an effective strategy for treating cancer. Here we discuss the paradoxical roles of the TME during specific stages of cancer progression and metastasis, as well as recent therapeutic attempts to re-educate stromal cells within the TME to have anti-tumorigenic effects.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 224, "doc_id": "6944800", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: High-sensitivity cardiac troponin T (HSCT-T) dosage may not be diagnostic if the onset of symptoms occurs less than 3 hours before acute myocardial injury (AMI).\n\nCANDIDATE_PASSAGE:\nPlacebo-Controlled Trials and Active-Control Trials in the Evaluation of New Treatments. Part 1: Ethical and Scientific Issues Placebo-controlled trials are used extensively in the development of new pharmaceuticals. They are sometimes challenged as unethical in settings in which patients could be treated with an existing therapy (1-7). The issues of when placebo controls are ethically acceptable and when they are scientifically necessary are important and worthy of discussion. The Ethics of Placebo Controls The Declaration of Helsinki The Declaration of Helsinki (8) is an international document that describes ethical principles for clinical investigation. Those who contend that placebo controls are unethical whenever known effective therapy exists for a condition usually cite the following sentence in the Declaration as support for that position: In any medical study, every patientincluding those of a control group, if anyshould be assured of the best proven diagnostic and therapeutic method. We believe that an interpretation of this sentence as barring placebo controls whenever an effective treatment exists is untenable. First, the requirement that all patients receive the best proven diagnostic and therapeutic method would bar not only placebo-controlled trials but also active-control and historically controlled trials. When effective treatment exists, the patient receiving the investigational treatment instead of the established therapy is clearly not getting the best proven treatment. Second, it does not seem reasonable to consider as equivalent all failures to use known effective therapy. Historically, concerns about placebo use have usually arisen in the context of serious illness. There is universal agreement that use of placebo or otherwise untreate [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "521", "doc_id": "10749308", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Occupancy of ribosomes by IncRNAs mirror 5 0-UTRs\n\nCANDIDATE_ABSTRACT:\nTITLE: Ribosome Profiling Provides Evidence that Large Noncoding RNAs Do Not Encode Proteins\nABSTRACT: Large noncoding RNAs are emerging as an important component in cellular regulation. Considerable evidence indicates that these transcripts act directly as functional RNAs rather than through an encoded protein product. However, a recent study of ribosome occupancy reported that many large intergenic ncRNAs (lincRNAs) are bound by ribosomes, raising the possibility that they are translated into proteins. Here, we show that classical noncoding RNAs and 5' UTRs show the same ribosome occupancy as lincRNAs, demonstrating that ribosome occupancy alone is not sufficient to classify transcripts as coding or noncoding. Instead, we define a metric based on the known property of translation whereby translating ribosomes are released upon encountering a bona fide stop codon. We show that this metric accurately discriminates between protein-coding transcripts and all classes of known noncoding transcripts, including lincRNAs. Taken together, these results argue that the large majority of lincRNAs do not function through encoded proteins.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here, we show that classical noncoding RNAs and 5' UTRs show the same ribosome occupancy as lincRNAs, demonstrating that ribosome occupancy alone is not sufficient to classify transcripts as coding or noncoding.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 880, "doc_id": "8426046", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Surgical treatment is not superior to non-surgical in treating adults with displaced fractures of the proximal humerus.\n\nCANDIDATE_ABSTRACT:\nTITLE: Surgical vs nonsurgical treatment of adults with displaced fractures of the proximal humerus: the PROFHER randomized clinical trial.\nABSTRACT: IMPORTANCE The need for surgery for the majority of patients with displaced proximal humeral fractures is unclear, but its use is increasing. OBJECTIVE To evaluate the clinical effectiveness of surgical vs nonsurgical treatment for adults with displaced fractures of the proximal humerus involving the surgical neck. DESIGN, SETTING, AND PARTICIPANTS A pragmatic, multicenter, parallel-group, randomized clinical trial, the Proximal Fracture of the Humerus Evaluation by Randomization (PROFHER) trial, recruited 250 patients aged 16 years or older (mean age, 66 years [range, 24-92 years]; 192 [77%] were female; and 249 [99.6%] were white) who presented at the orthopedic departments of 32 acute UK National Health Service hospitals between September 2008 and April 2011 within 3 weeks after sustaining a displaced fracture of the proximal humerus involving the surgical neck. Patients were followed up for 2 years (up to April 2013) and 215 had complete follow-up data. The data for 231 patients (114 in surgical group and 117 in nonsurgical group) were included in the primary analysis. INTERVENTIONS Fracture fixation or humeral head replacement were performed by surgeons experienced in these techniques. Nonsurgical treatment was sling immobilization. Standardized outpatient and community-based rehabilitation was provided to both groups. MAIN OUTCOMES AND MEASURES Primary outcome was the Oxford Shoulder Score (range, 0-48; higher scores indicate better outcomes) assessed during a 2-year period, with assessment and data collection at 6, 12, and 24 months. Sample size was based on a minimal clinically important difference of 5 points for the Oxford Shoulder Score. Secondary outcomes were the Short-Form 12 (SF-12), complications, subsequent therapy, and mortality. RESULTS Th [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"There were also no significant between-group differences over 2 years in the mean SF-12 physical component score (surgical group: 1.77 points higher [95% CI, -0.84 to 4.39 points];\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1115, "doc_id": "44048701", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Antiretroviral therapy increases rates of tuberculosis across a broad range of CD4 strata.\n\nCANDIDATE_PASSAGE:\nCytokinesis failure generating tetraploids promotes tumorigenesis in p53-null cells A long-standing hypothesis on tumorigenesis is that cell division failure, generating genetically unstable tetraploid cells, facilitates the development of aneuploid malignancies. Here we test this idea by transiently blocking cytokinesis in p53-null (p53-/-) mouse mammary epithelial cells (MMECs), enabling the isolation of diploid and tetraploid cultures. The tetraploid cells had an increase in the frequency of whole-chromosome mis-segregation and chromosomal rearrangements. Only the tetraploid cells were transformed in vitro after exposure to a carcinogen. Furthermore, in the absence of carcinogen, only the tetraploid cells gave rise to malignant mammary epithelial cancers when transplanted subcutaneously into nude mice. These tumours all contained numerous non-reciprocal translocations and an 8–30-fold amplification of a chromosomal region containing a cluster of matrix metalloproteinase (MMP) genes. MMP overexpression is linked to mammary tumours in humans and animal models. Thus, tetraploidy enhances the frequency of chromosomal alterations and promotes tumour development in p53-/- MMECs.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "123", "doc_id": "34103335", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: 53% of perinatal mortality is due to low birth weight.\n\nCANDIDATE_ABSTRACT:\nTITLE: Estimates of global prevalence of childhood underweight in 1990 and 2015.\nABSTRACT: CONTEXT One key target of the United Nations Millennium Development goals is to reduce the prevalence of underweight among children younger than 5 years by half between 1990 and 2015. OBJECTIVE To estimate trends in childhood underweight by geographic regions of the world. DESIGN, SETTING, AND PARTICIPANTS Time series study of prevalence of underweight, defined as weight 2 SDs below the mean weight for age of the National Center for Health Statistics and World Health Organization (WHO) reference population. National prevalence rates derived from the WHO Global Database on Child Growth and Malnutrition, which includes data on approximately 31 million children younger than 5 years who participated in 419 national nutritional surveys in 139 countries from 1965 through 2002. MAIN OUTCOME MEASURES Linear mixed-effects modeling was used to estimate prevalence rates and numbers of underweight children by region in 1990 and 2015 and to calculate the changes (ie, increase or decrease) to these values between 1990 and 2015. RESULTS Worldwide, underweight prevalence was projected to decline from 26.5% in 1990 to 17.6% in 2015, a change of -34% (95% confidence interval [CI], -43% to -23%). In developed countries, the prevalence was estimated to decrease from 1.6% to 0.9%, a change of -41% (95% CI, -92% to 343%). In developing regions, the prevalence was forecasted to decline from 30.2% to 19.3%, a change of -36% (95% CI, -45% to -26%). In Africa, the prevalence of underweight was forecasted to increase from 24.0% to 26.8%, a change of 12% (95% CI, 8%-16%). In Asia, the prevalence was estimated to decrease from 35.1% to 18.5%, a change of -47% (95% CI, -58% to -34%). Worldwide, the number of underweight children was projected to decline from 163.8 million in 1990 to 113. [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 17, "doc_id": "1606628", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Treatment with a protein named FN impairs regenerative abilities of aged muscles.\n\nCANDIDATE_ABSTRACT:\nTITLE: Loss of fibronectin from the aged stem cell niche affects the regenerative capacity of skeletal muscle in mice\nABSTRACT: Age-related changes in the niche have long been postulated to impair the function of somatic stem cells. Here we demonstrate that the aged stem cell niche in skeletal muscle contains substantially reduced levels of fibronectin (FN), leading to detrimental consequences for the function and maintenance of muscle stem cells (MuSCs). Deletion of the gene encoding FN from young regenerating muscles replicates the aging phenotype and leads to a loss of MuSC numbers. By using an extracellular matrix (ECM) library screen and pathway profiling, we characterize FN as a preferred adhesion substrate for MuSCs and demonstrate that integrin-mediated signaling through focal adhesion kinase and the p38 mitogen-activated protein kinase pathway is strongly de-regulated in MuSCs from aged mice because of insufficient attachment to the niche. Reconstitution of FN levels in the aged niche remobilizes stem cells and restores youth-like muscle regeneration. Taken together, we identify the loss of stem cell adhesion to FN in the niche ECM as a previously unknown aging mechanism.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Reconstitution of FN levels in the aged niche remobilizes stem cells and restores youth-like muscle regeneration.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1323, "doc_id": "19912367", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Headaches are correlated with cognitive impairment.\n\nCANDIDATE_PASSAGE:\nAortic stiffness, blood pressure progression, and incident hypertension. CONTEXT Vascular stiffness increases with advancing age and is a major risk factor for age-related morbidity and mortality. Vascular stiffness and blood pressure pulsatility are related; however, temporal relationships between vascular stiffening and blood pressure elevation have not been fully delineated. OBJECTIVE To examine temporal relationships among vascular stiffness, central hemodynamics, microvascular function, and blood pressure progression. DESIGN, SETTING, AND PARTICIPANTS Longitudinal community-based cohort study conducted in Framingham, Massachusetts. The present investigation is based on the 2 latest examination cycles (cycle 7: 1998-2001; cycle 8: 2005-2008 [last visit: January 25, 2008]) of the Framingham Offspring study (recruited: 1971-1975). Temporal relationships among blood pressure and 3 measures of vascular stiffness and pressure pulsatility derived from arterial tonometry (carotid-femoral pulse wave velocity [CFPWV], forward wave amplitude [FWA], and augmentation index) were examined over a 7-year period in 1759 participants (mean [SD] age: 60 [9] years; 974 women). MAIN OUTCOME MEASURES The primary outcomes were blood pressure and incident hypertension during examination cycle 8. The secondary outcomes were CFPWV, FWA, and augmentation index during examination cycle 8. RESULTS In a multivariable-adjusted regression model, higher FWA (β, 1.3 [95% CI, 0.5-2.1] mm Hg per 1 SD; P = .002) and higher CFPWV (β, 1.5 [95% CI, 0.5-2.6] mm Hg per 1 SD; P = .006) during examination cycle 7 were jointly associated with systolic blood pressure during examination cycle 8. Similarly, in a model that included systolic and diastolic blood pressure and additional risk factors dur [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "500", "doc_id": "30639847", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does rugby headgear prevent concussion?\n\nABSTRACT:\nTo examine the attitudes of players and coaches to the use of protective headgear, particularly with respect to the prevention of concussion. A questionnaire designed to assess attitudes to headgear was administered to 63 players from four different Canadian teams, each representing a different level of play (high school, university, community club, national). In addition, coaches from all four levels were questioned about team policies and their personal opinions about the use of headgear to prevent concussion. Although the players tended to believe that the headgear could prevent concussion (62%), the coaches were less convinced (33%). Despite the players' belief that headgear offers protection against concussion, only a minority reported wearing headgear (27%) and few (24%) felt that its use should be made mandatory. Common reasons for not wearing headgear were \"its use is not mandatory\", \"it is uncomfortable\", and \"it costs too much\".", "output": "{\"label\": \"maybe\", \"rationale\": \"Although most players in the study believe that rugby headgear may prevent concussion, only a minority reported wearing it. Coaches tended to be less convinced than the players that rugby headgear can prevent concussion.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 11867487, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Glycolysis is one of the primary glycometabolic pathways in cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Vesicular Glycolysis Provides On-Board Energy for Fast Axonal Transport\nABSTRACT: Fast axonal transport (FAT) requires consistent energy over long distances to fuel the molecular motors that transport vesicles. We demonstrate that glycolysis provides ATP for the FAT of vesicles. Although inhibiting ATP production from mitochondria did not affect vesicles motility, pharmacological or genetic inhibition of the glycolytic enzyme GAPDH reduced transport in cultured neurons and in Drosophila larvae. GAPDH localizes on vesicles via a huntingtin-dependent mechanism and is transported on fast-moving vesicles within axons. Purified motile vesicles showed GAPDH enzymatic activity and produced ATP. Finally, we show that vesicular GAPDH is necessary and sufficient to provide on-board energy for fast vesicular transport. Although detaching GAPDH from vesicles reduced transport, targeting GAPDH to vesicles was sufficient to promote FAT in GAPDH deficient neurons. This specifically localized glycolytic machinery may supply constant energy, independent of mitochondria, for the processive movement of vesicles over long distances in axons.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We demonstrate that glycolysis provides ATP for the FAT of vesicles.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 475, "doc_id": "18678095", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does mechanical limitation of pulmonary blood flow facilitate heart transplantation in older infants with hypoplastic left heart syndrome?\n\nABSTRACT:\nProgression of pulmonary vascular disease limits heart transplantation for hypoplastic left heart syndrome (HLHS) to early infancy. Our objective was to assess the impact of bilateral pulmonary artery banding (PAB) on the operative courses of HLHS infants transplanted at ages older than 4 months. Courses of all HLHS patients in our center who remained listed to age >or=120 days before heart transplantation were assessed. Patients undergoing transplantation after standard management (control group) were compared to patients having a prior pulmonary blood flow limiting procedure (PAB group). Of 16 identified patients, one crossed over to stage I Norwood on day 185 and died post-operatively. Fifteen patients were transplanted at age >or=120 days (control group n=9, PAB group n=6). Four PAB patients had open PA band placement. Two PAB patients underwent experimental percutaneous bilateral internal pulmonary artery flow limiting device insertion. The PAB group mean age at banding was 141+/-54 days, and mean interval from PAB to transplant was 35+/-31 days (range 1.5-68 days). No differences in age at transplant, weight at transplant, warm graft ischemia time or total graft ischemia time were detected between groups. Mean times of mechanical ventilation (control 143+/-69h vs. PAB 44+/-13h), inhaled nitric oxide (control 126+/-70h vs. PAB 37+/-9h), inotropic support (control 171+/-64h vs. PAB 87+/-17h), intensive care unit (ICU) stay (control 8.3+/-2.7 days vs. PAB 4.5+/-1.4 days), and hospital stay (control 10.4+/-3.9 days vs. PAB 7.0+/-1.1 days) were all lower in the PAB group (P<0.05 all comparisons). Two control patients died, three required extracorporeal membrane oxygenation (ECMO), and six did not tolerate primary chest closure. No PAB patient died or requir [TRUNCATED]", "output": "{\"label\": \"yes\", \"rationale\": \"Pre-transplant mechanical limitation of pulmonary blood flow simplified management and reduced morbidity for HLHS patients undergoing heart transplantation at ages >or=4 months. This strategy extends the permissible transplant waiting time in older infants with HLHS.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 12754026, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Commelina yellow mottle virus' (ComYMV) genome consists of 2140 baise pairs.\n\nCANDIDATE_ABSTRACT:\nTITLE: Histone deacetylases (HDACs) in frontotemporal lobar degeneration.\nABSTRACT: AIMS Frontotemporal lobar degeneration (FTLD) is clinically and pathologically heterogeneous. Although associated with variations in MAPT, GRN and C9ORF72, the pathogenesis of these, and of other nongenetic, forms of FTLD, remains unknown. Epigenetic factors such as histone regulation by histone deacetylases (HDAC) may play a role in the dysregulation of transcriptional activity, thought to underpin the neurodegenerative process. METHODS The distribution and intensity of HDACs 4, 5 and 6 was assessed semi-quantitatively in immunostained sections of temporal cortex with hippocampus, and cerebellum, from 33 pathologically confirmed cases of FTLD and 27 controls. RESULTS We found a significantly greater intensity of cytoplasmic immunostaining for HDAC4 and HDAC6 in granule cells of the dentate gyrus in cases of FTLD overall compared with controls, and specifically in cases of FTLD tau-Picks compared with FTLD tau-MAPT and controls. No differences were noted between FTLD-TDP subtypes, or between the different genetic and nongenetic forms of FTLD. No changes were seen in HDAC5 in any FTLD or control cases. CONCLUSIONS Dysregulation of HDAC4 and/or HDAC6 could play a role in the pathogenesis of FTLD-tau associated with Pick bodies, although their lack of immunostaining implies that such changes do not contribute directly to the formation of Pick bodies.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 278, "doc_id": "665817", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Bariatric surgery reduces postmenopausal breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Bariatric Surgery in the United Kingdom: A Cohort Study of Weight Loss and Clinical Outcomes in Routine Clinical Care.\nABSTRACT: BACKGROUND Bariatric surgery is becoming a more widespread treatment for obesity. Comprehensive evidence of the long-term effects of contemporary surgery on a broad range of clinical outcomes in large populations treated in routine clinical practice is lacking. The objective of this study was to measure the association between bariatric surgery, weight, body mass index, and obesity-related co-morbidities. METHODS AND FINDINGS This was an observational retrospective cohort study using data from the United Kingdom Clinical Practice Research Datalink. All 3,882 patients registered in the database and with bariatric surgery on or before 31 December 2014 were included and matched by propensity score to 3,882 obese patients without surgery. The main outcome measures were change in weight and body mass index over 4 y; incident diagnoses of type 2 diabetes mellitus (T2DM), hypertension, angina, myocardial infarction (MI), stroke, fractures, obstructive sleep apnoea, and cancer; mortality; and resolution of hypertension and T2DM. Weight measures were available for 3,847 patients between 1 and 4 mo, 2,884 patients between 5 and 12 mo, and 2,258 patients between 13 and 48 mo post-procedure. Bariatric surgery patients exhibited rapid weight loss for the first four postoperative months, at a rate of 4.98 kg/mo (95% CI 4.88-5.08). Slower weight loss was sustained to the end of 4 y. Gastric bypass (6.56 kg/mo) and sleeve gastrectomy (6.29 kg/mo) were associated with greater initial weight reduction than gastric banding (2.77 kg/mo). Protective hazard ratios (HRs) were detected for bariatric surgery for incident T2DM, 0.68 (95% CI 0.55-0.83); hypertension, 0.35 (95% CI 0.27-0.45); angina, 0.59 (95% CI 0.40-0.87);MI, 0.28 (95% CI 0.10-0.74); and obstructive sleep apnoea, 0.5 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"No association was detected between bariatric surgery and fractures, cancer, or stroke.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 169, "doc_id": "5824985", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: KLF4 is necessary for VSMCs to gain genetic characteristics of other cell types within atherosclerotic lesions.\n\nCANDIDATE_PASSAGE:\nThe transcription factor c-Maf controls the production of interleukin-4 but not other Th2 cytokines. IL-4 promotes the differentiation of naive CD4+ T cells into IL-4-producing T helper 2 (Th2) cells. Previous work provided suggestive but not conclusive evidence that the transcription factor c-Maf directed the tissue-specific expression of IL-4. It was not known whether c-Maf controlled the transcription of other Th2 cytokine genes. To elucidate the role of c-Maf in vivo, we examined cytokine production in mice lacking c-Maf (c-maf(-/-)). CD4+ T cells and NK T cells from c-maf(-/-) mice were markedly deficient in IL-4 production. However, the mice produced normal levels of IL-13 and IgE, and, when differentiated in the presence of exogenous IL-4, c-maf(-/-) T cells produced approximately normal levels of other Th2 cytokines. We conclude that c-Maf has a critical and selective function in IL-4 gene transcription in vivo.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "663", "doc_id": "20388894", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Overexpressing Cnp1 N-tail variants rescues the temperature-sensitive growth defect of scm3-139.\n\nCANDIDATE_PASSAGE:\nFission Yeast Scm3: A CENP-A Receptor Required for Integrity of Subkinetochore Chromatin The mechanisms ensuring specific incorporation of CENP-A at centromeres are poorly understood. Mis16 and Mis18 are required for CENP-A localization at centromeres and form a complex that is conserved from fission yeast to human. Fission yeast sim1 mutants that alleviate kinetochore domain silencing are defective in Scm3(Sp), the ortholog of budding yeast Scm3(Sc). Scm3(Sp) depends on Mis16/18 for its centromere localization and like them is recruited to centromeres in late anaphase. Importantly, Scm3(Sp) coaffinity purifies with CENP-A(Cnp1) and associates with CENP-A(Cnp1) in vitro, yet localizes independently of intact CENP-A(Cnp1) chromatin and is differentially released from chromatin. While Scm3(Sc) has been proposed to form a unique hexameric nucleosome with CENP-A(Cse4) and histone H4 at budding yeast point centromeres, we favor a model in which Scm3(Sp) acts as a CENP-A(Cnp1) receptor/assembly factor, cooperating with Mis16 and Mis18 to receive CENP-A(Cnp1) from the Sim3 escort and mediate assembly of CENP-A(Cnp1) into subkinetochore chromatin.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "897", "doc_id": "14338915", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Intake of folic acid (FA) and vitamin B6 (VB6) increases levels of homocysteine.\n\nCANDIDATE_PASSAGE:\nNIPBL, encoding a homolog of fungal Scc2-type sister chromatid cohesion proteins and fly Nipped-B, is mutated in Cornelia de Lange syndrome Cornelia de Lange syndrome (CdLS) is a multiple malformation disorder characterized by dysmorphic facial features, mental retardation, growth delay and limb reduction defects. We indentified and characterized a new gene, NIPBL, that is mutated in individuals with CdLS and determined its structure and the structures of mouse, rat and zebrafish homologs. We named its protein product delangin. Vertebrate delangins have substantial homology to orthologs in flies, worms, plants and fungi, including Scc2-type sister chromatid cohesion proteins, and D. melanogaster Nipped-B. We propose that perturbed delangin function may inappropriately activate DLX genes, thereby contributing to the proximodistal limb patterning defects in CdLS. Genome analyses typically identify individual delangin or Nipped-B-like orthologs in diploid animal and plant genomes. The evolution of an ancestral sister chromatid cohesion protein to acquire an additional role in developmental gene regulation suggests that there are parallels between CdLS and Roberts syndrome.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "645", "doc_id": "18662787", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is dimensions and wall force development capacity of human pial arteries from normotensives altered in obesity?\n\nABSTRACT:\nThe dimensions and maximum wall tension capacity of segments of human pial arteries from normotensive obese and non-obese patients were compared. Segment size was assessed by quantitative morphometry of fixed sections and wall force by in vitro myography. Twenty normotensive non-obese and 13 normotensive obese humans body mass index (BMI) 22.4+/-0.5 and 33.9+/-1.7 kg/m(2), respectively) were studied. There was no significant difference in the perimeter of the outer medial border, the smoothed out length of the internal elastic lamina, the ratios of media thickness to area and lumen diameter and the maximum wall force development between the two groups.", "output": "{\"label\": \"no\", \"rationale\": \"Obesity per se is not associated with initial dimensional changes nor capacity to develop wall tension that might lead to the emergence of hypertension.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 11360162, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The G34R/V mutation creates a hypomethylated phenotype at the H3K36 histone.\n\nCANDIDATE_PASSAGE:\nHigh CTLA-4 expression on Th17 cells results in increased sensitivity to CTLA-4 coinhibition and resistance to belatacept. The CD28/cytotoxic T-lymphocyte antigen 4 (CTLA-4)blocker belatacept selectively inhibits alloreactive T cell responses but is associated with a high incidence of acute rejection following renal transplantation,which led us to investigate the etiology of belatacept–resistant graft rejection. T cells can differentiate into functionally distinct subsets of memory T cellsthat collectively enable protection against diverse classes of pathogens and can cross-react with allogeneicantigen and mediate graft rejection. T helper 17(Th17) cells are a pro-inflammatory CD4+ lineage that provides immunity to pathogens and are pathogenic in autoimmune disease. We found that T helper 1 (Th1)and Th17 memory compartments contained a similar frequency of divided cells following allogeneic stimulation. Compared to Th1 cells, Th17 memory cells expressed significantly higher levels of the coinhibitory molecule CTLA-4. Stimulation in the presence of belatacept inhibited Th1 responses but augmented Th17 cells due to greater sensitivity to coinhibition by CTLA-4. Th17 cells from renal transplant recipients were resistant to ex vivo CD28/CTLA-4 blockade with belatacept, and an elevated frequency of Th17 memory cells was associated with acute rejection during belatacept therapy. These data highlight important differences in costimulatory and coinhibitory requirements of CD4+ memory subsets, and demonstrate that the heterogeneity of pathogen-derived memory has implications for immunomodulation strategies.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1164", "doc_id": "13398997", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Individuals with Alzheimers who participate in six months of physical activity improve cognitive function for up to 18 months.\n\nCANDIDATE_PASSAGE:\nGene regulation by the act of long non-coding RNA transcription Long non-protein-coding RNAs (lncRNAs) are proposed to be the largest transcript class in the mouse and human transcriptomes. Two important questions are whether all lncRNAs are functional and how they could exert a function. Several lncRNAs have been shown to function through their product, but this is not the only possible mode of action. In this review we focus on a role for the process of lncRNA transcription, independent of the lncRNA product, in regulating protein-coding-gene activity in cis. We discuss examples where lncRNA transcription leads to gene silencing or activation, and describe strategies to determine if the lncRNA product or its transcription causes the regulatory effect.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "621", "doc_id": "14050257", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Patients with microcytosis and higher erythrocyte count are more vulnerable to severe malarial anaemia when infected with Plasmodium falciparum.\n\nCANDIDATE_ABSTRACT:\nTITLE: Murine Dishevelled 3 Functions in Redundant Pathways with Dishevelled 1 and 2 in Normal Cardiac Outflow Tract, Cochlea, and Neural Tube Development\nABSTRACT: Dishevelled (Dvl) proteins are important signaling components of both the canonical beta-catenin/Wnt pathway, which controls cell proliferation and patterning, and the planar cell polarity (PCP) pathway, which coordinates cell polarity within a sheet of cells and also directs convergent extension cell (CE) movements that produce narrowing and elongation of the tissue. Three mammalian Dvl genes have been identified and the developmental roles of Dvl1 and Dvl2 were previously determined. Here, we identify the functions of Dvl3 in development and provide evidence of functional redundancy among the three murine Dvls. Dvl3(-/-) mice died perinatally with cardiac outflow tract abnormalities, including double outlet right ventricle and persistent truncus arteriosis. These mutants also displayed a misorientated stereocilia in the organ of Corti, a phenotype that was enhanced with the additional loss of a single allele of the PCP component Vangl2/Ltap (LtapLp/+). Although neurulation appeared normal in both Dvl3(-/-) and LtapLp/+ mutants, Dvl3(+/-);LtapLp/+ combined mutants displayed incomplete neural tube closure. Importantly, we show that many of the roles of Dvl3 are also shared by Dvl1 and Dvl2. More severe phenotypes were observed in Dvl3 mutants with the deficiency of another Dvl, and increasing Dvl dosage genetically with Dvl transgenes demonstrated the ability of Dvls to compensate for each other to enable normal development. Interestingly, global canonical Wnt signaling appeared largely unaffected in the double Dvl mutants, suggesting that low Dvl levels are sufficient for functional canonical Wnt signals. In summary, we demonstrate that Dvl3 is required for cardiac outflow tract development and describe its importance in the PCP pathway during neurulation a [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 928, "doc_id": "317204", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The relationship between a breast cancer patient's capacity to metabolize tamoxifen and treatment outcome is dependent on the patient's genetic make-up.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association between CYP2D6 polymorphisms and outcomes among women with early stage breast cancer treated with tamoxifen.\nABSTRACT: CONTEXT The growth inhibitory effect of tamoxifen, which is used for the treatment of hormone receptor-positive breast cancer, is mediated by its metabolites, 4-hydroxytamoxifen and endoxifen. The formation of active metabolites is catalyzed by the polymorphic cytochrome P450 2D6 (CYP2D6) enzyme. OBJECTIVE To determine whether CYP2D6 variation is associated with clinical outcomes in women receiving adjuvant tamoxifen. DESIGN, SETTING, AND PATIENTS Retrospective analysis of German and US cohorts of patients treated with adjuvant tamoxifen for early stage breast cancer. The 1325 patients had diagnoses between 1986 and 2005 of stage I through III breast cancer and were mainly postmenopausal (95.4%). Last follow-up was in December 2008; inclusion criteria were hormone receptor positivity, no metastatic disease at diagnosis, adjuvant tamoxifen therapy, and no chemotherapy. DNA from tumor tissue or blood was genotyped for CYP2D6 variants associated with reduced (*10, *41) or absent (*3, *4, *5) enzyme activity. Women were classified as having an extensive (n=609), heterozygous extensive/intermediate (n=637), or poor (n=79) CYP2D6 metabolism. MAIN OUTCOME MEASURES Time to recurrence, event-free survival, disease-free survival, and overall survival. RESULTS Median follow-up was 6.3 years. At 9 years of follow-up, the recurrence rates were 14.9% for extensive metabolizers, 20.9% for heterozygous extensive/intermediate metabolizers, and 29.0% for poor metabolizers, and all-cause mortality rates were 16.7%, 18.0%, and 22.8%, respectively. Compared with extensive metabolizers, there was a significantly increased risk of recurrence for heterozygous extensive/intermediate metabolizers (time to recurrence adjusted hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.04 [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Compared with extensive metabolizers, those with decreased CYP2D6 activity (heterozygous extensive/intermediate and poor metabolism) had worse event-free survival (HR, 1.33; 95% CI, 1.06-1.68) and disease-free survival (HR, 1.29; 95% CI, 1.03-1.61), but there was no significant difference in overall survival (HR, 1.15; 95% CI, 0.88-1.51).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1259, "doc_id": "24341590", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: p16INK4A accumulation is linked to an abnormal wound response caused by the microinvasive step of advanced Oral Potentially Malignant Lesions (OPMLs).\n\nCANDIDATE_PASSAGE:\nMonitoring Tumorigenesis and Senescence In Vivo with a p16INK4a-Luciferase Model Monitoring cancer and aging in vivo remains experimentally challenging. Here, we describe a luciferase knockin mouse (p16(LUC)), which faithfully reports expression of p16(INK4a), a tumor suppressor and aging biomarker. Lifelong assessment of luminescence in p16(+/LUC) mice revealed an exponential increase with aging, which was highly variable in a cohort of contemporaneously housed, syngeneic mice. Expression of p16(INK4a) with aging did not predict cancer development, suggesting that the accumulation of senescent cells is not a principal determinant of cancer-related death. In 14 of 14 tested tumor models, expression of p16(LUC) was focally activated by early neoplastic events, enabling visualization of tumors with sensitivity exceeding other imaging modalities. Activation of p16(INK4a) was noted in the emerging neoplasm and surrounding stromal cells. This work suggests that p16(INK4a) activation is a characteristic of all emerging cancers, making the p16(LUC) allele a sensitive, unbiased reporter of neoplastic transformation.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1395", "doc_id": "17717391", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: HbA1c consistently overestimates glycemic control in black individuals with Sickle cell trait (SCT).\n\nCANDIDATE_ABSTRACT:\nTITLE: Gastric juice miR-129 as a potential biomarker for screening gastric cancer\nABSTRACT: MicroRNAs (miRNAs) play crucial roles during the occurrence and development of gastric cancer. Conventional serological tests for screening gastric cancer have limits on sensitivity and specificity. Several miRNAs in peripheral blood have been used as biomarkers of gastric cancer. However, most of these miRNAs are shared by several types of cancer. Thanks to the tissue specificity of gastric juice, here we examined the feasibility of using gastric juice miR-129-1/2, which are aberrantly expressed in gastric cancer, to screen gastric cancer. Total of 141 gastric juices samples from gastric cancer, gastric ulcer, atrophic gastritis, and minimal gastritis patients or subjects with normal mucosa were collected by gastroscopy. The gastric juice miR-129-1/2 levels were detected by quantitative reverse transcription-polymerase chain reaction. A receiver operating characteristic (ROC) curve was constructed for differentiating patients with gastric cancer from patients with benign gastric diseases. We showed that, compared with patients with benign gastric diseases, patients with gastric cancer had significantly lower levels of gastric juice miR-129-1-3p and miR-129-2-3p. The areas under ROC curve (AUC) were 0.639 and 0.651 for miR-129-1-3p and miR-129-2-3p, respectively. Using the parallel combination test, the AUC was up to 0.656. In summary, our results suggest that gastric juice miR-129-1-3p and miR-129-2-3p are potential biomarkers for the screening gastric cancer, and the detection of gastric juice miRNAs is a convenient non-invasion method for the diagnosis of gastric cancer.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 499, "doc_id": "2205779", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Knockout proximal tubule-specific deletion of the BMP receptor Alk3 causes epithelial damage.\n\nCANDIDATE_ABSTRACT:\nTITLE: Loss of immune escape mutations during persistent HCV infection in pregnancy enhances replication of vertically transmitted viruses\nABSTRACT: Globally, about 1% of pregnant women are persistently infected with the hepatitis C virus (HCV). Mother-to-child transmission of HCV occurs in 3-5% of pregnancies and accounts for most new childhood infections. HCV-specific CD8(+) cytotoxic T lymphocytes (CTLs) are vital in the clearance of acute HCV infections, but in the 60-80% of infections that persist, these cells become functionally exhausted or select for mutant viruses that escape T cell recognition. Increased HCV replication during pregnancy suggests that maternofetal immune tolerance mechanisms may further impair HCV-specific CTLs, limiting their selective pressure on persistent viruses. To assess this possibility, we characterized circulating viral quasispecies during and after consecutive pregnancies in two women. This revealed a loss of some escape mutations in HLA class I epitopes during pregnancy that was associated with emergence of more fit viruses. CTL selective pressure was reimposed after childbirth, at which point escape mutations in these epitopes again predominated in the quasispecies and viral load dropped sharply. Importantly, the viruses transmitted perinatally were those with enhanced fitness due to reversion of escape mutations. Our findings indicate that the immunoregulatory changes of pregnancy reduce CTL selective pressure on HCV class I epitopes, thereby facilitating vertical transmission of viruses with optimized replicative fitness.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 670, "doc_id": "92308", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Microcin J25 encourages nucleoside triphosphate (NTP) binding.\n\nCANDIDATE_ABSTRACT:\nTITLE: The atypical antipsychotic olanzapine causes weight gain by targeting serotonin receptor 2C.\nABSTRACT: Atypical antipsychotics such as olanzapine often induce excessive weight gain and type 2 diabetes. However, the mechanisms underlying these drug-induced metabolic perturbations remain poorly understood. Here, we used an experimental model that reproduces olanzapine-induced hyperphagia and obesity in female C57BL/6 mice. We found that olanzapine treatment acutely increased food intake, impaired glucose tolerance, and altered physical activity and energy expenditure in mice. Furthermore, olanzapine-induced hyperphagia and weight gain were blunted in mice lacking the serotonin 2C receptor (HTR2C). Finally, we showed that treatment with the HTR2C-specific agonist lorcaserin suppressed olanzapine-induced hyperphagia and weight gain. Lorcaserin treatment also improved glucose tolerance in olanzapine-fed mice. Collectively, our studies suggest that olanzapine exerts some of its untoward metabolic effects via antagonism of HTR2C.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 787, "doc_id": "1428830", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Ultrasound guidance significantly reduces the number of traumatic procedures when attempting needle insertion.\n\nCANDIDATE_ABSTRACT:\nTITLE: Ultrasound imaging for lumbar punctures and epidural catheterisations: systematic review and meta-analysis.\nABSTRACT: OBJECTIVE To determine whether ultrasound imaging can reduce the risk of failed lumbar punctures or epidural catheterisations, when compared with standard palpation methods, and whether ultrasound imaging can reduce traumatic procedures, insertion attempts, and needle redirections. DESIGN Systematic review and meta-analysis of randomised controlled trials. DATA SOURCES Ovid Medline, Embase, and Cochrane Central Register of Controlled Trials up to May 2012, without restriction by language or publication status. REVIEW METHODS Randomised trials that compared ultrasound imaging with standard methods (no imaging) in the performance of a lumbar puncture or epidural catheterisation were identified. RESULTS 14 studies with a total of 1334 patients were included (674 patients assigned to the ultrasound group, 660 to the control group). Five studies evaluated lumbar punctures and nine evaluated epidural catheterisations. Six of 624 procedures conducted in the ultrasound group failed; 44 of 610 procedures in the control group failed. Ultrasound imaging reduced the risk of failed procedures (risk ratio 0.21 (95% confidence interval 0.10 to 0.43), P<0.001). Risk reduction was similar when subgroup analysis was performed for lumbar punctures (risk ratio 0.19 (0.07 to 0.56), P=0.002) or epidural catheterisations (0.23 (0.09 to 0.60), P=0.003). Ultrasound imaging also significantly reduced the risk of traumatic procedures (risk ratio 0.27 (0.11 to 0.67), P=0.005), the number of insertion attempts (mean difference -0.44 (-0.64 to -0.24), P<0.001), and the number of needle redirections (mean difference -1.00 (-1.24 to -0.75), P<0.001). CONCLUSIONS Ultrasound imaging can reduce the risk of failed or traumatic lumbar punctures and epidural catheterisations, as well as the numb [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Ultrasound imaging reduced the risk of failed procedures (risk ratio 0.21 (95% confidence interval 0.10 to 0.43), P<0.001). Risk reduction was similar when subgroup analysis was performed for lumbar punctures (risk ratio 0.19 (0.07 to 0.56), P=0.002) or epidural catheterisations (0.23 (0.09 to 0.60), P=0.003).\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1341, "doc_id": "15482274", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_PASSAGE:\nGeovisual analytics to enhance spatial scan statistic interpretation: an analysis of U.S. cervical cancer mortality BACKGROUND Kulldorff's spatial scan statistic and its software implementation - SaTScan - are widely used for detecting and evaluating geographic clusters. However, two issues make using the method and interpreting its results non-trivial: (1) the method lacks cartographic support for understanding the clusters in geographic context and (2) results from the method are sensitive to parameter choices related to cluster scaling (abbreviated as scaling parameters), but the system provides no direct support for making these choices. We employ both established and novel geovisual analytics methods to address these issues and to enhance the interpretation of SaTScan results. We demonstrate our geovisual analytics approach in a case study analysis of cervical cancer mortality in the U.S. RESULTS We address the first issue by providing an interactive visual interface to support the interpretation of SaTScan results. Our research to address the second issue prompted a broader discussion about the sensitivity of SaTScan results to parameter choices. Sensitivity has two components: (1) the method can identify clusters that, while being statistically significant, have heterogeneous contents comprised of both high-risk and low-risk locations and (2) the method can identify clusters that are unstable in location and size as the spatial scan scaling parameter is varied. To investigate cluster result stability, we conducted multiple SaTScan runs with systematically selected parameters. The results, when scanning a large spatial dataset (e.g., U.S. data aggregated by county), demonstrate that no single spatial scan scaling value is known to be optimal to identif [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "972", "doc_id": "10692412", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: There is no relation between Erythromycin use and hypertrophic pyloric stenosis.\n\nCANDIDATE_PASSAGE:\nEffect of homocysteine lowering on mortality and vascular disease in advanced chronic kidney disease and end-stage renal disease: a randomized controlled trial. CONTEXT High plasma homocysteine levels are a risk factor for mortality and vascular disease in observational studies of patients with chronic kidney disease. Folic acid and B vitamins decrease homocysteine levels in this population but whether they lower mortality is unknown. OBJECTIVE To determine whether high doses of folic acid and B vitamins administered daily reduce mortality in patients with chronic kidney disease. DESIGN, SETTING, AND PARTICIPANTS Double-blind randomized controlled trial (2001-2006) in 36 US Department of Veterans Affairs medical centers. Median follow-up was 3.2 years for 2056 participants aged 21 years or older with advanced chronic kidney disease (estimated creatinine clearance < or =30 mL/min) (n = 1305) or end-stage renal disease (n = 751) and high homocysteine levels (> or = 15 micromol/L). INTERVENTION Participants received a daily capsule containing 40 mg of folic acid, 100 mg of pyridoxine hydrochloride (vitamin B6), and 2 mg of cyanocobalamin (vitamin B12) or a placebo. MAIN OUTCOME MEASURES The primary outcome was all-cause mortality. Secondary outcomes included myocardial infarction (MI), stroke, amputation of all or part of a lower extremity, a composite of these 3 plus all-cause mortality, time to initiation of dialysis, and time to thrombosis of arteriovenous access in hemodialysis patients. RESULTS Mean baseline homocysteine level was 24.0 micromol/L in the vitamin group and 24.2 micromol/L in the placebo group. It was lowered 6.3 micromol/L (25.8%; P < .001) in the vitamin group and 0.4 micromol/L (1.7%; P = .14) in the placebo group at 3 months, but there wa [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1295", "doc_id": "33409100", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is periventricular demyelination and axonal pathology associated with subependymal virus spread in a murine model for multiple sclerosis?\n\nABSTRACT:\nTheiler's murine encephalomyelitis virus (TMEV) infection of mice is a widely used animal model for demyelinating disorders, such as multiple sclerosis (MS). The aim of the present study was to identify topographical differences of TMEV spread and demyelination in the brain of experimentally infected susceptible SJL/J mice and resistant C57BL/6 mice. Demyelination was confirmed by Luxol fast blue and cresyl violet staining and axonal damage by neurofilament-specific and β-amyloid precursor protein-specific immunohistochemistry. Viral dissemination within the central nervous system (CNS) was quantified by immunohistochemistry and in situ hybridization. Further, the phenotype of infected cells was determined by confocal laser scanning microscopy. An early transient infection of periventricular cells followed by demyelination and axonopathies around the fourth ventricle in SJL/J mice was noticed. Periventricular and brain stem demyelination was associated with a predominant infection of microglia/macrophages and oligodendrocytes.", "output": "{\"label\": \"yes\", \"rationale\": \"Summarized, the demonstration of ependymal infection and subjacent spread into the brain parenchyma as well as regional virus clearance despite ongoing demyelination and axonal damage in other CNS compartments allows new insights into TME pathogenesis. This novel aspect of TMEV CNS interaction will enhance the understanding of region-specific susceptibilities to injury and regenerative capacities of the brain in this MS model.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 22538300, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nCANDIDATE_ABSTRACT:\nTITLE: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\nABSTRACT: Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens. However, signals underlying mTEC development remain largely unclear. Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals. Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment. Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner. These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1181, "doc_id": "2734421", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: RAD52 is involved in break-induced DNA replication (BIR).\n\nCANDIDATE_ABSTRACT:\nTITLE: Alternative Lengthening of Telomeres Mediated by Mitotic DNA Synthesis Engages Break-Induced Replication Processes.\nABSTRACT: Alternative lengthening of telomeres (ALT) is a telomerase-independent telomere maintenance mechanism that occurs in a subset of cancers. By analyzing telomerase-positive cells and their human TERC knockout-derived ALT human cell lines, we show that ALT cells harbor more fragile telomeres representing telomere replication problems. ALT-associated replication defects trigger mitotic DNA synthesis (MiDAS) at telomeres in a RAD52-dependent, but RAD51-independent, manner. Telomeric MiDAS is a conservative DNA synthesis process, potentially mediated by break-induced replication, similar to type II ALT survivors in Saccharomyces cerevisiae Replication stresses induced by ectopic oncogenic expression of cyclin E, G-quadruplexes, or R-loop formation facilitate the ALT pathway and lead to telomere clustering, a hallmark of ALT cancers. The TIMELESS/TIPIN complex suppresses telomere clustering and telomeric MiDAS, whereas the SMC5/6 complex promotes them. In summary, ALT cells exhibit more telomere replication defects that result in persistent DNA damage responses at telomeres, leading to the engagement of telomeric MiDAS (spontaneous mitotic telomere synthesis) that is triggered by DNA replication stress, a potential driver of genomic duplications in cancer.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"ALT-associated replication defects trigger mitotic DNA synthesis (MiDAS) at telomeres in a RAD52-dependent, but RAD51-independent, manner.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1003, "doc_id": "4319844", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is Panton-Valentine leucocidin associated with the pathogenesis of Staphylococcus aureus bacteraemia in the UK?\n\nABSTRACT:\nThe morbidity and mortality associated with Panton-Valentine leucocidin (PVL)-positive Staphylococcus aureus suggest that this toxin is a key marker of disease severity. Nevertheless, the importance of PVL in the pathogenesis of primary bacteraemia caused by S. aureus is uncertain. We have determined the prevalence of PVL-encoding genes among isolates of S. aureus from bacteraemic patients. Consecutive bacteraemia isolates of S. aureus (n=244) from patients hospitalized in 25 centres in the UK and Ireland during 2005 were screened for PVL and mecA genes. PVL-positive isolates were characterized by toxin gene profiling, PFGE, spa-typing and MIC determinations for a range of antimicrobials. Four out of 244 isolates (1.6%) were PVL-positive and susceptible to oxacillin [methicillin-susceptible S. aureus (MSSA)]. Eighty-eight out of 244 (36%) were oxacillin-resistant (methicillin-resistant S. aureus), but none was PVL-positive. The four patients (two males: 30 and 33 years; two females: 62 and 80 years) had infection foci of: skin and soft tissue, unknown, indwelling line, and surgical site, and were located at one centre in Wales, one in England and two in Ireland. One of four PVL-positive isolates was resistant to penicillin and fusidic acid, the remainder were susceptible to all antibiotics tested. Genotypic analyses showed that the four isolates represented three distinct strains; the two isolates from Ireland were related.", "output": "{\"label\": \"maybe\", \"rationale\": \"We found that 1.6% of S. aureus (all MSSA) from bacteraemic patients were PVL-positive. This low incidence suggests that PVL-positive S.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 17562682, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: YAP/TAZ is required in intestinal regeneration in mouse models of ulcerative colitis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cell death: the significance of apoptosis.\nABSTRACT: Publisher Summary The classification of cell death can be based on morphological or biochemical criteria or on the circumstances of its occurrence. Currently, irreversible structural alteration provides the only unequivocal evidence of death; biochemical indicators of cell death that are universally applicable have to be precisely defined and studies of cell function or of reproductive capacity do not necessarily differentiate between death and dormant states from which recovery may be possible. It has also proved feasible to categorize most if not all dying cells into one or the other of two discrete and distinctive patterns of morphological change, which have, generally, been found to occur under disparate but individually characteristic circumstances. One of these patterns is the swelling proceeding to rupture of plasma and organelle membranes and dissolution of organized structure—termed “coagulative necrosis. ” It results from injury by agents, such as toxins and ischemia, affects cells in groups rather than singly, and evokes exudative inflammation when it develops in vivo. The other morphological pattern is characterized by condensation of the cell with maintenance of organelle integrity and the formation of surface protuberances that separate as membrane-bounded globules; in tissues, these are phagocytosed and digested by resident cells, there being no associated inflammation.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1381, "doc_id": "935034", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Bariatric surgery increases rates of postmenopausal breast cancer.\n\nCANDIDATE_PASSAGE:\nBreast cancer clusters in the northeast United States: a geographic analysis. High breast cancer mortality rates have been reported in the northeastern part of the United States, with recent attention focused on Long Island, New York. In this study, the authors investigate whether the high breast cancer mortality is evenly spread over the Northeast, in the sense that any observed clusters of deaths can be explained by chance alone, or whether there are clusters of statistical significance. Demographic data and age-specific breast cancer mortality rates for women were obtained for all 244 counties in 11 northeastern states and for the District of Columbia for 1988-1992. A recently developed spatial scan statistic is used, which searches for clusters of cases without specifying their size or location ahead of time, and which tests for their statistical significance while adjusting for the multiple testing inherent in such a procedure. The basic analysis is adjusted for age, with further analyses examining how the results are affected by incorporating race, urbanicity, and parity as confounding variables. There is a statistically significant and geographically broad cluster of breast cancer deaths in the New York City-Philadelphia, Pennsylvania, metropolitan area (p = 0.0001), which has a 7.4% higher mortality rate than the rest of the Northeast. The cluster remains significant when race, urbanicity, and/or parity are included as confounding variables. Four smaller subclusters within this area are also significant on their own strength: Philadelphia with suburbs (p = 0.0001), Long Island (p = 0.0001), central New Jersey (p = 0.0001), and northeastern New Jersey (p = 0.0001). The elevated breast cancer mortality on Long Island might be viewed less as a unique lo [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "165", "doc_id": "3524352", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Birth-weight is negatively associated with breast cancer.\n\nCANDIDATE_PASSAGE:\nBody-mass index and risk of 22 specific cancers: a population-based cohort study of 5·24 million UK adults BACKGROUND High body-mass index (BMI) predisposes to several site-specific cancers, but a large-scale systematic and detailed characterisation of patterns of risk across all common cancers adjusted for potential confounders has not previously been undertaken. We aimed to investigate the links between BMI and the most common site-specific cancers. METHODS With primary care data from individuals in the Clinical Practice Research Datalink with BMI data, we fitted Cox models to investigate associations between BMI and 22 of the most common cancers, adjusting for potential confounders. We fitted linear then non-linear (spline) models; investigated effect modification by sex, menopausal status, smoking, and age; and calculated population effects. FINDINGS 5·24 million individuals were included; 166,955 developed cancers of interest. BMI was associated with 17 of 22 cancers, but effects varied substantially by site. Each 5 kg/m(2) increase in BMI was roughly linearly associated with cancers of the uterus (hazard ratio [HR] 1·62, 99% CI 1·56-1·69; p<0·0001), gallbladder (1·31, 1·12-1·52; p<0·0001), kidney (1·25, 1·17-1·33; p<0·0001), cervix (1·10, 1·03-1·17; p=0·00035), thyroid (1·09, 1·00-1·19; p=0·0088), and leukaemia (1·09, 1·05-1·13; p≤0·0001). BMI was positively associated with liver (1·19, 1·12-1·27), colon (1·10, 1·07-1·13), ovarian (1·09, 1.04-1.14), and postmenopausal breast cancers (1·05, 1·03-1·07) overall (all p<0·0001), but these effects varied by underlying BMI or individual-level characteristics. We estimated inverse associations with prostate and premenopausal breast cancer risk, both overall (prostate 0·98, 0·95-1·00; premenopausal breast cance [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "178", "doc_id": "4828631", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The most prevalent adverse events to Semaglutide are cardiovascular.\n\nCANDIDATE_PASSAGE:\nRelation of plasma leptin concentrations to sex, body fat, dietary intake, and peak oxygen uptake in young adult women and men. The purpose of this study was to examine the relation of leptin to metabolic and dietary factors in college-age adults. Young adult women and men (n = 32) were recruited and underwent testing for measurement of body mass index, body composition, peak oxygen consumption (VO2peak), dietary intake, and plasma levels of leptin and insulin. Ln leptin was significantly greater for women than for men (2.1 versus 1.2 ng/mL, respectively). This difference remained significant even after adjusting ln leptin for fat mass and fat-free mass as covariates in separate analyses. VO2peak was higher for men than for women and this remained significant after adjustment for differences in fat-free mass and total body mass. Significant correlations were found between ln leptin and indicators of fat mass in women and men, with higher correlations for similar variables observed in men (r = 0.548, 0.674, and 0.732 for body mass index, percentage of body fat, and fat mass [kg] for women, respectively, and r = 0.740, 0.888, 0.858 for body mass index, percentage of body fat, and fat mass [kg] for men, respectively). Ln leptin showed a significant inverse relationship with VO2peak (r = -0.751) in men only. After adjusting ln leptin for body fat mass using partial correlations, ln leptin was not significantly associated with any of the measured variables. Alternatively, after normalization of ln leptin using fat mass as the divisor, a less adequate statistical analysis method, men showed statistical significant correlations between ln leptin and dietary intake and VO2peak. Although plasma leptin values were higher in women, stronger associations were evident fo [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1237", "doc_id": "25135304", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Vaccinating the gastrointestinal tract induces protection of rectal and vaginal mucosa.\n\nCANDIDATE_PASSAGE:\n[Pharmacokinetics and biotransformation of the antimycotic drug ciclopiroxolamine in animals and man after topical and systemic administration]. 1. Following the dermal application of the carbon-14 labelled broad spectrum antimycotic 6-cyclohexyl-1-hydroxy-4-methyl-2(1H)-pyridone, 2-aminoethanol salt (ciclopiroxolamine, Hoe 296, Batrafen) in the form of a 1% aqueous cream to healthy human dorsal skin (penetration time: 6 h; occlusive dressing for 5 h), percutaneous absorption accounted on average for 1.3% of the dose applied. Excretion occurred via the kidney, with biological half-lives of 1.7 h. As can be seen from penetration studies of cadaverous skin, the horny layer contained the highest concentrations, with values of 2300-4500 microgram/cm3. The levels determined in the corium were still above the minimum inhibitory concentrations. These concentrations were already obtained at the first test stage (1.5 h after application) and did not change virtually at all over the longer penetration period. According to studies using histoautoradiography, ciclopirox can penetrate the skin via the epidermis and the hair follicles. When ciclopirox-14C-olamine aqueous cream was spread on the surface of fingernails, the radioactive-labelled compound penetrated right through the nail. The percutaneous absorption in dogs was higher, at 5-15% of the dose, than it was in humans. 2. After vaginal application (1 mg/kg) of ciclopirox-14C-olamine in the form of a 1% aqueous cream to bitches, between 42 and 97% of the dose (depending on the animal) was recovered in the urine and faeces, the remainder having penetrated into the tampon used to close the vagina. 3. Ciclopirox is excreted by dogs and man in the urine, primarily as a glucuronide. In humans another glucuronide with pr [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1356", "doc_id": "26461066", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The treatment of cancer patients with co-IR blockade does not cause any adverse autoimmune events.\n\nCANDIDATE_PASSAGE:\nIs autoimmunity the Achilles' heel of cancer immunotherapy? The emergence of immuno-oncology as the first broadly successful strategy for metastatic cancer will require clinicians to integrate this new pillar of medicine with chemotherapy, radiation, and targeted small-molecule compounds. Of equal importance is gaining an understanding of the limitations and toxicities of immunotherapy. Immunotherapy was initially perceived to be a relatively less toxic approach to cancer treatment than other available therapies—and surely it is, when compared to those. However, as the use of immunotherapy becomes more common, especially as first- and second-line treatments, immunotoxicity and autoimmunity are emerging as the Achilles' heel of immunotherapy. In this Perspective, we discuss evidence that the occurrence of immunotoxicity bodes well for the patient, and describe mechanisms that might be related to the induction of autoimmunity. We then explore approaches to limit immunotoxicity, and discuss the future directions of research and reporting that are needed to diminish it.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1278", "doc_id": "11335781", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Deltex has no known interactions with eIF3f.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Translation Initiation Factor 3f (eIF3f) Exhibits a Deubiquitinase Activity Regulating Notch Activation\nABSTRACT: Activation of the mammalian Notch receptor after ligand binding relies on a succession of events including metalloprotease-cleavage, endocytosis, monoubiquitination, and eventually processing by the gamma-secretase, giving rise to a soluble, transcriptionally active molecule. The Notch1 receptor was proposed to be monoubiquitinated before its gamma-secretase cleavage; the targeted lysine has been localized to its submembrane domain. Investigating how this step might be regulated by a deubiquitinase (DUB) activity will provide new insight for understanding Notch receptor activation and downstream signaling. An immunofluorescence-based screening of an shRNA library allowed us to identify eIF3f, previously known as one of the subunits of the translation initiation factor eIF3, as a DUB targeting the activated Notch receptor. We show that eIF3f has an intrinsic DUB activity. Knocking down eIF3f leads to an accumulation of monoubiquitinated forms of activated Notch, an effect counteracted by murine WT eIF3f but not by a catalytically inactive mutant. We also show that eIF3f is recruited to activated Notch on endocytic vesicles by the putative E3 ubiquitin ligase Deltex1, which serves as a bridging factor. Finally, catalytically inactive forms of eIF3f as well as shRNAs targeting eIF3f repress Notch activation in a coculture assay, showing that eIF3f is a new positive regulator of the Notch pathway. Our results support two new and provocative conclusions: (1) The activated form of Notch needs to be deubiquitinated before being processed by the gamma-secretase activity and entering the nucleus, where it fulfills its transcriptional function. (2) The enzyme accounting for this deubiquitinase activity is eIF3f, known so far as a translation initiation factor. These d [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We also show that eIF3f is recruited to activated Notch on endocytic vesicles by the putative E3 ubiquitin ligase Deltex1, which serves as a bridging factor.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 330, "doc_id": "9505448", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Arterioles have a larger lumen diameter than venules.\n\nCANDIDATE_PASSAGE:\nReprogramming of human somatic cells to pluripotency with defined factors Pluripotency pertains to the cells of early embryos that can generate all of the tissues in the organism. Embryonic stem cells are embryo-derived cell lines that retain pluripotency and represent invaluable tools for research into the mechanisms of tissue formation. Recently, murine fibroblasts have been reprogrammed directly to pluripotency by ectopic expression of four transcription factors (Oct4, Sox2, Klf4 and Myc) to yield induced pluripotent stem (iPS) cells. Using these same factors, we have derived iPS cells from fetal, neonatal and adult human primary cells, including dermal fibroblasts isolated from a skin biopsy of a healthy research subject. Human iPS cells resemble embryonic stem cells in morphology and gene expression and in the capacity to form teratomas in immune-deficient mice. These data demonstrate that defined factors can reprogramme human cells to pluripotency, and establish a method whereby patient-specific cells might be established in culture.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "128", "doc_id": "4380451", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Mathematical models predict that using Artemisinin-based combination therapy over nongametocytocidal drugs have only a modest impact in reducing malaria transmission.\n\nCANDIDATE_ABSTRACT:\nTITLE: Modelling the Impact of Artemisinin Combination Therapy and Long-Acting Treatments on Malaria Transmission Intensity\nABSTRACT: BACKGROUND Artemisinin derivatives used in recently introduced combination therapies (ACTs) for Plasmodium falciparum malaria significantly lower patient infectiousness and have the potential to reduce population-level transmission of the parasite. With the increased interest in malaria elimination, understanding the impact on transmission of ACT and other antimalarial drugs with different pharmacodynamics becomes a key issue. This study estimates the reduction in transmission that may be achieved by introducing different types of treatment for symptomatic P. falciparum malaria in endemic areas. METHODS AND FINDINGS We developed a mathematical model to predict the potential impact on transmission outcomes of introducing ACT as first-line treatment for uncomplicated malaria in six areas of varying transmission intensity in Tanzania. We also estimated the impact that could be achieved by antimalarials with different efficacy, prophylactic time, and gametocytocidal effects. Rates of treatment, asymptomatic infection, and symptomatic infection in the six study areas were estimated using the model together with data from a cross-sectional survey of 5,667 individuals conducted prior to policy change from sulfadoxine-pyrimethamine to ACT. The effects of ACT and other drug types on gametocytaemia and infectiousness to mosquitoes were independently estimated from clinical trial data. Predicted percentage reductions in prevalence of infection and incidence of clinical episodes achieved by ACT were highest in the areas with low initial transmission. A 53% reduction in prevalence of infection was seen if 100% of current treatment was switched to ACT in the area where baseline slide-prevalence of parasitaemia was lowest (3.7%), compared to an 11% reduction in the highest [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"An efficacious antimalarial regimen with no specific gametocytocidal properties but a long prophylactic time was estimated to be more effective at reducing transmission than a short-acting ACT in the highest-transmission setting.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 760, "doc_id": "1805641", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: RANK-RANKL pathway signalling is linked to development of Aire-expressing medullary thymic epithelial cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: RANK signals from CD4+3− inducer cells regulate development of Aire-expressing epithelial cells in the thymic medulla\nABSTRACT: Aire-expressing medullary thymic epithelial cells (mTECs) play a key role in preventing autoimmunity by expressing tissue-restricted antigens to help purge the emerging T cell receptor repertoire of self-reactive specificities. Here we demonstrate a novel role for a CD4+3− inducer cell population, previously linked to development of organized secondary lymphoid structures and maintenance of T cell memory in the functional regulation of Aire-mediated promiscuous gene expression in the thymus. CD4+3− cells are closely associated with mTECs in adult thymus, and in fetal thymus their appearance is temporally linked with the appearance of Aire+ mTECs. We show that RANKL signals from this cell promote the maturation of RANK-expressing CD80−Aire− mTEC progenitors into CD80+Aire+ mTECs, and that transplantation of RANK-deficient thymic stroma into immunodeficient hosts induces autoimmunity. Collectively, our data reveal cellular and molecular mechanisms leading to the generation of Aire+ mTECs and highlight a previously unrecognized role for CD4+3−RANKL+ inducer cells in intrathymic self-tolerance.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We show that RANKL signals from this cell promote the maturation of RANK-expressing CD80−Aire− mTEC progenitors into CD80+Aire+ mTECs, and that transplantation of RANK-deficient thymic stroma into immunodeficient hosts induces autoimmunity.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1005, "doc_id": "3952288", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Birth-weight is positively associated with breast cancer.\n\nCANDIDATE_PASSAGE:\nVegan proteins may reduce risk of cancer, obesity, and cardiovascular disease by promoting increased glucagon activity. Amino acids modulate the secretion of both insulin and glucagon; the composition of dietary protein therefore has the potential to influence the balance of glucagon and insulin activity. Soy protein, as well as many other vegan proteins, are higher in non-essential amino acids than most animal-derived food proteins, and as a result should preferentially favor glucagon production. Acting on hepatocytes, glucagon promotes (and insulin inhibits) cAMP-dependent mechanisms that down-regulate lipogenic enzymes and cholesterol synthesis, while up-regulating hepatic LDL receptors and production of the IGF-I antagonist IGFBP-1. The insulin-sensitizing properties of many vegan diets--high in fiber, low in saturated fat--should amplify these effects by down-regulating insulin secretion. Additionally, the relatively low essential amino acid content of some vegan diets may decrease hepatic IGF-I synthesis. Thus, diets featuring vegan proteins can be expected to lower elevated serum lipid levels, promote weight loss, and decrease circulating IGF-I activity. The latter effect should impede cancer induction (as is seen in animal studies with soy protein), lessen neutrophil-mediated inflammatory damage, and slow growth and maturation in children. In fact, vegans tend to have low serum lipids, lean physiques, shorter stature, later puberty, and decreased risk for certain prominent 'Western' cancers; a vegan diet has documented clinical efficacy in rheumatoid arthritis. Low-fat vegan diets may be especially protective in regard to cancers linked to insulin resistance--namely, breast and colon cancer--as well as prostate cancer; conversely, the high IGF-I acti [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "179", "doc_id": "6327940", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Distant CREs are less conserved among species.\n\nCANDIDATE_PASSAGE:\nElevated expression of miR-24-3p is a potentially adverse prognostic factor in colorectal adenocarcinoma. OBJECTIVES Several miRNAs are aberrantly expressed in cancer. miR-24-3p is involved in cancer-related cellular processes, including cell cycle control, cell growth, proliferation, and apoptosis. In this study, we examined the potential diagnostic and prognostic significance of miR-24-3p expression in colorectal adenocarcinoma. DESIGN AND METHODS Total RNA was isolated from 182 colorectal adenocarcinoma specimens and 86 paired non-cancerous colorectal mucosae. After polyadenylation of 2μg total RNA and reverse transcription into first-strand cDNA using an oligo-dT-adapter primer, miR-24-3p expression was quantified using an in-house-developed reverse-transcription real-time quantitative PCR method, based on the SYBR Green chemistry. SNORD43 (RNU43) was used as a reference gene. RESULTS miR-24-3p levels do not significantly differ between colorectal adenocarcinoma and non-cancerous colorectal mucosae. Thus, miR-24-3p expression cannot be used for diagnostic purposes. However, high miR-24-3p expression predicts poor disease-free survival (DFS) and overall survival (OS) of colorectal adenocarcinoma patients. Multivariate Cox regression analysis confirmed that miR-24-3p overexpression is a significant predictor of relapse in colorectal adenocarcinoma and that its prognostic significance is independent of other established prognostic factors and treatment of patients. Of note, miR-24-3p overexpression retains its rather unfavorable prognostic value in the subgroup of patients with advanced yet locally restricted colorectal adenocarcinoma (T3) and in those without distant metastasis (M0). Moreover, miR-24-3p overexpression is a potentially unfavorable prognosti [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "352", "doc_id": "39580129", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: RAD52 is involved in break-induced DNA replication (BIR).\n\nCANDIDATE_ABSTRACT:\nTITLE: Mammalian RAD52 Functions in Break-Induced Replication Repair of Collapsed DNA Replication Forks\nABSTRACT: Human cancers are characterized by the presence of oncogene-induced DNA replication stress (DRS), making them dependent on repair pathways such as break-induced replication (BIR) for damaged DNA replication forks. To better understand BIR, we performed a targeted siRNA screen for genes whose depletion inhibited G1 to S phase progression when oncogenic cyclin E was overexpressed. RAD52, a gene dispensable for normal development in mice, was among the top hits. In cells in which fork collapse was induced by oncogenes or chemicals, the Rad52 protein localized to DRS foci. Depletion of Rad52 by siRNA or knockout of the gene by CRISPR/Cas9 compromised restart of collapsed forks and led to DNA damage in cells experiencing DRS. Furthermore, in cancer-prone, heterozygous APC mutant mice, homozygous deletion of the Rad52 gene suppressed tumor growth and prolonged lifespan. We therefore propose that mammalian RAD52 facilitates repair of collapsed DNA replication forks in cancer cells.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We therefore propose that mammalian RAD52 facilitates repair of collapsed DNA replication forks in cancer cells.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1003, "doc_id": "14332945", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Long chain polyunsaturated fatty acids supplementation is associated with lower rates of atopic eczema at 1 year.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effect of n-3 long chain polyunsaturated fatty acid supplementation in pregnancy on infants’ allergies in first year of life: randomised controlled trial\nABSTRACT: OBJECTIVE To determine whether dietary n-3 long chain polyunsaturated fatty acid (LCPUFA) supplementation of pregnant women with a fetus at high risk of allergic disease reduces immunoglobulin E associated eczema or food allergy at 1 year of age. DESIGN Follow-up of infants at high hereditary risk of allergic disease in the Docosahexaenoic Acid to Optimise Mother Infant Outcome (DOMInO) randomised controlled trial. SETTING Adelaide, South Australia. PARTICIPANTS 706 infants at high hereditary risk of developing allergic disease whose mothers were participating in the DOMInO trial. INTERVENTIONS The intervention group (n=368) was randomly allocated to receive fish oil capsules (providing 900 mg of n-3 LCPUFA daily) from 21 weeks' gestation until birth; the control group (n=338) received matched vegetable oil capsules without n-3 LCPUFA. MAIN OUTCOME MEASURE Immunoglobulin E associated allergic disease (eczema or food allergy with sensitisation) at 1 year of age. RESULTS No differences were seen in the overall percentage of infants with immunoglobulin E associated allergic disease between the n-3 LCPUFA and control groups (32/368 (9%) v 43/338 (13%); unadjusted relative risk 0.68, 95% confidence interval 0.43 to 1.05, P=0.08; adjusted relative risk 0.70, 0.45 to 1.09, P=0.12), although the percentage of infants diagnosed as having atopic eczema (that is, eczema with associated sensitisation) was lower in the n-3 LCPUFA group (26/368 (7%) v 39/338 (12%); unadjusted relative risk 0.61, 0.38 to 0.98, P=0.04; adjusted relative risk 0.64, 0.40 to 1.02, P=0.06). Fewer infants were sensitised to egg in the n-3 LCPUFA group (34/368 (9%) v 52/338 (15%); unadjusted relative risk 0.61, 0.40 to 0.91, P=0.02; adjusted relative risk 0.62, 0.41 to 0.93, P=0.02), but no diffe [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSION n-3 LCPUFA supplementation in pregnancy did not reduce the overall incidence of immunoglobulin E associated allergies in the first year of life, although atopic eczema and egg sensitisation were lower.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 709, "doc_id": "22442133", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Diabetic patients with acute coronary syndrome experience decreased short-term and long-term risk for bleeding events.\n\nCANDIDATE_PASSAGE:\nThe Drosophila DHR96 nuclear receptor binds cholesterol and regulates cholesterol homeostasis. Cholesterol homeostasis is required to maintain normal cellular function and avoid the deleterious effects of hypercholesterolemia. Here we show that the Drosophila DHR96 nuclear receptor binds cholesterol and is required for the coordinate transcriptional response of genes that are regulated by cholesterol and involved in cholesterol uptake, trafficking, and storage. DHR96 mutants die when grown on low levels of cholesterol and accumulate excess cholesterol when maintained on a high-cholesterol diet. The cholesterol accumulation phenotype can be attributed to misregulation of npc1b, an ortholog of the mammalian Niemann-Pick C1-like 1 gene NPC1L1, which is essential for dietary cholesterol uptake. These studies define DHR96 as a central regulator of cholesterol homeostasis.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "342", "doc_id": "2423940", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Induced hepatic stem cells possess the potential to differentiate into hepatocytic cells.\n\nCANDIDATE_PASSAGE:\nTet1 and Tet2 regulate 5-hydroxymethylcytosine production and cell lineage specification in mouse embryonic stem cells. TET family enzymes convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) in DNA. Here, we show that Tet1 and Tet2 are Oct4-regulated enzymes that together sustain 5hmC in mouse embryonic stem cells (ESCs) and are induced concomitantly with 5hmC during reprogramming of fibroblasts to induced pluripotent stem cells. ESCs depleted of Tet1 by RNAi show diminished expression of the Nodal antagonist Lefty1 and display hyperactive Nodal signaling and skewed differentiation into the endoderm-mesoderm lineage in embryoid bodies in vitro. In Fgf4- and heparin-supplemented culture conditions, Tet1-depleted ESCs activate the trophoblast stem cell lineage determinant Elf5 and can colonize the placenta in midgestation embryo chimeras. Consistent with these findings, Tet1-depleted ESCs form aggressive hemorrhagic teratomas with increased endoderm, reduced neuroectoderm, and ectopic appearance of trophoblastic giant cells. Thus, 5hmC is an epigenetic modification associated with the pluripotent state, and Tet1 functions to regulate the lineage differentiation potential of ESCs.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "625", "doc_id": "13777138", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Glycan adaptation involves insertion-deletion events.\n\nCANDIDATE_PASSAGE:\nNanoenzymology of the 20S proteasome: proteasomal actions are controlled by the allosteric transition. The proteasome is a major cytosolic proteolytic assembly, essential for the physiology of eukaryotic cells. Both the architecture and enzymatic properties of the 20S proteasome are relatively well understood. However, despite longstanding interest, the integration of structural and functional properties of the proteasome into a coherent model explaining the mechanism of its enzymatic actions has been difficult. Recently, we used tapping mode atomic force microscopy (AFM) in liquid to demonstrate that the alpha-rings of the proteasome imaged in a top-view position repeatedly switched between their open and closed conformations, apparently to control access to the central channel. Here, we show with AFM that the molecules in a side-view position acquired two stable conformations. The overall shapes of the 20S particles were classified as either barrel-like or cylinder-like. The relative abundance of the two conformers depended on the nature of their interactions with ligands. Similarly to the closed molecules in top view, the barrels predominated in control or inhibited molecules. The cylinders and open molecules prevailed when the proteasome was observed in the presence of peptide substrates. Based on these data, we developed the two-state model of allosteric transitions to explain the dynamics of proteasomal structure. This model helps to better understand the observed properties of the 20S molecule, and sets foundations for further studies of the structural dynamics of the proteasome.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "473", "doc_id": "19651306", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: IFIT1 restricts viral replication by sequestrating mis-capped viral RNAs.\n\nCANDIDATE_PASSAGE:\nEB virus-encoded RNAs are recognized by RIG-I and activate signaling to induce type I IFN. Epstein-Barr virus (EBV)-encoded small RNAs (EBERs) are nonpolyadenylated, untranslated RNAs, exist most abundantly in latently EBV-infected cells, and are expected to show secondary structures with many short stem-loops. Retinoic acid-inducible gene I (RIG-I) is a cytosolic protein that detects viral double-stranded RNA (dsRNA) inside the cell and initiates signaling pathways leading to the induction of protective cellular genes, including type I interferons (IFNs). We investigated whether EBERs were recognized by RIG-I as dsRNA. Transfection of RIG-I plasmid induced IFNs and IFN-stimulated genes (ISGs) in EBV-positive Burkitt's lymphoma (BL) cells, but not in their EBV-negative counterparts or EBER-knockout EBV-infected BL cells. Transfection of EBER plasmid or in vitro-synthesized EBERs induced expression of type I IFNs and ISGs in RIG-I-expressing, EBV-negative BL cells, but not in RIG-I-minus counterparts. EBERs activated RIG-I's substrates, NF-kappaB and IFN regulatory factor 3, which were necessary for type I IFN activation. It was also shown that EBERs co-precipitated with RIG-I. These results indicate that EBERs are recognized by RIG-I and activate signaling to induce type I IFN in EBV-infected cells.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "544", "doc_id": "37727521", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is caspase-1 genetic variation associated with Alzheimer 's disease risk?\n\nABSTRACT:\nInterleukin (IL)-1beta is a potent proinflammatory cytokine markedly overexpressed in the brains of patients with Alzheimer's disease (AD), and also involved in development of atherosclerosis and coronary artery disease. Caspase-1 (CASP1), formerly called IL-1beta converting enzyme (ICE), mediates the cleavage of the inactive precursor of IL-1beta into the biologically active form. CASP1 genetic variation (G+7/in6A, rs501192) has been associated with susceptibility to myocardial infarction and cardiovascular death risk. We examined the contribution of this gene to the susceptibility for AD. We examined genetic variations of CASP1 by genotyping haplotype tagging SNPs (htSNPs) (rs501192, rs556205 and rs530537) in a group of 628 Spanish AD cases and 722 controls. There were no differences in the genotypic, allelic or haplotypic distributions between cases and controls in the overall analysis or after stratification by age, gender or APOE epsilon4 allele.", "output": "{\"label\": \"no\", \"rationale\": \"Our negative findings in the Spanish population argue against the hypothesis that CASP1 genetic variations are causally related to AD risk.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 20184726, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Do coping skills and parent support mediate the association between childhood attention-deficit/hyperactivity disorder and adolescent cigarette use?\n\nABSTRACT:\nTo examine mediators of the association between childhood attention-deficit/hyperactivity disorder (ADHD) and adolescent cigarette use. Participants were 142 adolescents diagnosed with ADHD in childhood and 100 adolescents without ADHD. Among probands, cigarette smoking was more frequent, adaptive coping skills (behavioral and cognitive) were fewer, and parental support was lower. Coping and support partially mediated the ADHD association with smoking. Persistence of ADHD and adolescent conduct disorder were also important.", "output": "{\"label\": \"yes\", \"rationale\": \"Vulnerability to smoking among probands may be partly due to fewer problem-solving resources. Coping skill deficits and parent-child communication may be important treatment targets for smoking prevention.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 15863431, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: H4 G94P proteins inhibit chromatin assembly, which decreases free histones.\n\nCANDIDATE_ABSTRACT:\nTITLE: Histone levels are regulated by phosphorylation and ubiquitylation dependent proteolysis\nABSTRACT: Histone levels are tightly regulated to prevent harmful effects such as genomic instability and hypersensitivity to DNA-damaging agents due to the accumulation of these highly basic proteins when DNA replication slows down or stops. Although chromosomal histones are stable, excess (non-chromatin bound) histones are rapidly degraded in a Rad53 (radiation sensitive 53) kinase-dependent manner in Saccharomyces cerevisiae. Here we demonstrate that excess histones associate with Rad53 in vivo and seem to undergo modifications such as tyrosine phosphorylation and polyubiquitylation, before their proteolysis by the proteasome. We have identified the Tyr 99 residue of histone H3 as being critical for the efficient ubiquitylation and degradation of this histone. We have also identified the ubiquitin conjugating enzymes (E2) Ubc4 and Ubc5, as well as the ubiquitin ligase (E3) Tom1 (temperature dependent organization in mitotic nucleus 1), as enzymes involved in the ubiquitylation of excess histones. Regulated histone proteolysis has major implications for the maintenance of epigenetic marks on chromatin, genomic stability and the packaging of sperm DNA.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 486, "doc_id": "14637235", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does high glucose-induced oxidative stress increase IL-8 production in human gingival epithelial cells?\n\nABSTRACT:\nDiabetes is often associated with increased prevalence and severity of periodontal disease. We hypothesized that gingival epithelial cells modify periodontal disease progression and predicted that hyperglycemia would activate an inflammatory response in human gingival epithelial cells (HGECs). We tested our hypothesis in immortalized HGECs (epi 4 cells) isolated from periodontal tissue and transfected with the simian virus 40 T antigen. The epi 4 cells were cultured in high (25 mM, HG) and normal (6 mM, NG) glucose conditions. The epi 4 cells showed increased interleukin-8 (IL-8) protein secretion and mRNA expression when cultured in HG, compared with in NG. These effects were not associated with increased cell proliferation and were not observed in a hyperosmolar control group (normal glucose with 19 mM mannitol). Increased IL-8 secretion in HG was inhibited by pretreatment with an antioxidant, N-acetylcysteine, or a protein kinase C inhibitor, Ro31-8220. Hyperglycemia did not affect IL-8 secretion by gingival fibroblasts or periodontal ligament cells. In epi 4 cells, hyperglycemia also induced expression of toll-like receptor 2 (TLR2) but not TLR4.", "output": "{\"label\": \"yes\", \"rationale\": \"These findings suggest a potential participation of epithelial cells in periodontal disease during diabetes by evoking an excessive host inflammatory response.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 27171647, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Lice attenuated SIV vaccines induce a stronger antigen-specific T cell response in lymph node cells.\n\nCANDIDATE_PASSAGE:\nDual role of interleukin-10 in the regulation of respiratory syncitial virus (RSV)-induced lung inflammation. RSV lower respiratory tract infections (LRTI) are among the most common diseases necessitating hospital admission in children. In addition to causing acute respiratory failure, RSV infections are associated with sequelae such as secondary bacterial infections and reactive airway disease. One characteristic host response observed in severe RSV-induced LRTI and/or subsequent development of asthma is increased expression of interleukin (IL)-10. However, contradictory results have been reported regarding whether IL-10 inhibits asthmatic responses or intensifies the disease. We aimed to reconcile these discordant observations by elucidating the role of IL-10 in regulating the host response to RSV LRTI. In this study, we used a lung-specific, inducible IL-10 over-expression (OE) transgenic mouse model to address this question. Our results showed that the presence of IL-10 at the time of RSV infection not only attenuated acute inflammatory process (i.e. 24 h post-infection), but also late inflammatory changes [characterized by T helper type 2 (Th2) cytokine and chemokine expression]. While this result appears contradictory to some clinical observations where elevated IL-10 levels are observed in asthmatic patients, we also found that delaying IL-10 OE until the late immune response to RSV infection, additive effects rather than inhibitory effects were observed. Importantly, in non-infected, IL-10 OE mice, IL-10 OE alone induced up-regulation of Th2 cytokine (IL-13 and IL-5) and Th2-related chemokine [monocyte chemoattractant protein 1 (MCP-1), chemokine (C-C motif) ligand 3 (CCL3) and regulated upon activation normal T cell expressed and secreted (RANTES)] [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "694", "doc_id": "26068103", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Higher plasma levels of I-carnitine, when associated with trimethylamine N-oxide, are negatively correlated with cardiovascular events in humans.\n\nCANDIDATE_ABSTRACT:\nTITLE: Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis\nABSTRACT: Intestinal microbiota metabolism of choline and phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO). We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice. Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism. The presence of specific bacterial taxa in human feces was associated with both plasma TMAO concentration and dietary status. Plasma L-carnitine levels in subjects undergoing cardiac evaluation (n = 2,595) predicted increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels. Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed. In mice with an intact intestinal microbiota, dietary supplementation with TMAO or either carnitine or choline reduced in vivo reverse cholesterol transport. Intestinal microbiota may thus contribute to the well-established link between high levels of red meat consumption and CVD risk.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 523, "doc_id": "14803797", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Elevated cell-free mitochondrial DNA levels are associated with mortality.\n\nCANDIDATE_PASSAGE:\nLDL inhibits the mediation of cholesterol efflux from macrophage foam cells by apoA-I-containing lipoproteins. A putative mechanism for foam cell formation. Although the accumulation of cholesterol in macrophages appears to be an initial step in atherogenesis, low-density lipoprotein (LDL), a major risk factor for atherosclerosis, does not promote cholesterol accumulation in macrophages in its native form. On the other hand, apolipoprotein (apo) A-I-containing lipoprotein removes cholesterol from cholesterol-loaded macrophages (foam cells) and prevents cholesterol from accumulating in the cells. We examined the effect of LDL on cholesterol removal by two species of apoA-I-containing lipoproteins, one containing only apoA-I (LpA-I) and the other containing apoA-I and apoA-II (LpA-I/A-II). When foam cells were incubated with LpA-I or LpA-I/A-II, cellular cholesterol mass was reduced. In contrast, when LDL was added, the cholesterol-reducing capacities of these lipoproteins were dose-dependently inhibited by LDL. In the presence of LDL, LpA-I and LpA-I/A-II removed free cholesterol preferentially from LDL rather than from the plasma membrane of foam cells. In addition, a fair amount of cellular cholesterol was directly moved to LDL rather than to LpA-I or LpA-I/A-II. The cellular cholesterol that moved to LDL was completely compensated for by the cholesterol influx from LDL to foam cells. Thus, net cholesterol efflux (a combination of influx and efflux) from foam cells was inhibited by LDL. These results, taken together, indicate that LDL may accelerate foam cell formation by inhibiting cholesterol removal from the cells and that elevated levels of plasma LDL may become a risk factor for atherosclerosis by inhibiting the function of LpA-I and LpA-I/A-II at the [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "375", "doc_id": "9814332", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Hypothalamic glutamate neurotransmission is unrelated to energy balance.\n\nCANDIDATE_ABSTRACT:\nTITLE: Glutamate mediates the function of melanocortin receptor 4 on Sim1 neurons in body weight regulation.\nABSTRACT: The melanocortin receptor 4 (MC4R) is a well-established mediator of body weight homeostasis. However, the neurotransmitter(s) that mediate MC4R function remain largely unknown; as a result, little is known about the second-order neurons of the MC4R neural pathway. Single-minded 1 (Sim1)-expressing brain regions, which include the paraventricular nucleus of hypothalamus (PVH), represent key brain sites that mediate melanocortin action. We conditionally restored MC4R expression in Sim1 neurons in the background of Mc4r-null mice. The restoration dramatically reduced obesity in Mc4r-null mice. The anti-obesity effect was completely reversed by selective disruption of glutamate release from those same Sim1 neurons. The reversal was caused by lower energy expenditure and hyperphagia. Corroboratively, selective disruption of glutamate release from adult PVH neurons led to rapid obesity development via reduced energy expenditure and hyperphagia. Thus, this study establishes glutamate as the primary neurotransmitter that mediates MC4Rs on Sim1 neurons in body weight regulation.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Thus, this study establishes glutamate as the primary neurotransmitter that mediates MC4Rs on Sim1 neurons in body weight regulation.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 541, "doc_id": "45154987", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The composition of myosin-II isoform switches from the A isoform to the B isoform during hematopoietic differentiation.\n\nCANDIDATE_PASSAGE:\nNature and anisotropy of cortical forces orienting Drosophila tissue morphogenesis The morphogenesis of developing embryos and organs relies on the ability of cells to remodel their contacts with neighbouring cells. Using quantitative modelling and laser nano-dissection, we probed the mechanics of a morphogenetic process, the elongation of Drosophila melanogaster embryos, which results from polarized cell neighbour exchanges. We show that anisotropy of cortical tension at apical cell junctions is sufficient to drive tissue elongation. We estimated its value through comparisons between in silico and in vivo data using various tissue descriptors. Nano-dissection of the actomyosin network indicates that tension is anisotropically distributed and depends on myosin II accumulation. Junction relaxation after nano-dissection also suggests that cortical elastic forces are dominant in this process. Interestingly, fluctuations in vertex position (points where three or more cells meet) facilitate neighbour exchanges. We delineate the contribution of subcellular tensile activity polarizing junction remodelling, and the permissive role of vertex fluctuations during tissue elongation.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1206", "doc_id": "23141360", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: BiP is a general endoplasmic reticulum stress marker.\n\nCANDIDATE_PASSAGE:\nTunable signal processing through modular control of transcription factor translocation. Signaling pathways can induce different dynamics of transcription factor (TF) activation. We explored how TFs process signaling inputs to generate diverse dynamic responses. The budding yeast general stress-responsive TF Msn2 acted as a tunable signal processor that could track, filter, or integrate signals in an input-dependent manner. This tunable signal processing appears to originate from dual regulation of both nuclear import and export by phosphorylation, as mutants with one form of regulation sustained only one signal-processing function. Versatile signal processing by Msn2 is crucial for generating distinct dynamic responses to different natural stresses. Our findings reveal how complex signal-processing functions are integrated into a single molecule and provide a guide for the design of TFs with \"programmable\" signal-processing functions.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "176", "doc_id": "24742375", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Deleting Raptor increases G-CSF levels.\n\nCANDIDATE_PASSAGE:\nCocoa flavonols and procyanidins promote transforming growth factor-beta1 homeostasis in peripheral blood mononuclear cells. Evidence suggests that certain flavan-3-ols and procyanidins (FP) can have a positive influence on cardiovascular health. It has been previously reported that FP isolated from cocoa can potentially modulate the level and production of several signaling molecules associated with immune function and inflammation, including several cytokines and eicosanoids. In the present study, we examined whether FP fractions monomers through decamers modulate secretion of the cytokine transforming growth factor (TGF)-beta(1) from resting human peripheral blood mononuclear cells (PBMC). A total of 13 healthy subjects were studied and grouped according to their baseline production of TGF-beta(1). When cells from individuals with low baseline levels of TGF-beta(1) (n = 7) were stimulated by individual FP fractions (25 microg/ml), TGF-beta(1) release was enhanced in the range of 15%-66% over baseline (P < 0.05; monomer, dimer, and tetramer). The low-molecular-weight FP fractions (or=hexamer), with the monomer and dimer inducing the greatest increases (66% and 68%, respectively). In contrast to the above, TGF-beta(1) secretion from high TGF-beta(1) baseline subjects (n = 6) was inhibited by individual FP fractions (P < 0.05; trimer through decamer). The inhibition was most pronounced with trimeric through decameric fractions (28%-42%), and monomers and dimers moderately inhibited TGF-beta(1) release (17% and 23%, respectively). Given the vascular actions associated with TGF-beta(1), we suggest that in healthy individuals, homeostatic modulation of its pro [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "323", "doc_id": "38712515", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: BRCA 1 mutation carriers' risk of breast and ovarian cancer depends on where the mutation is located.\n\nCANDIDATE_PASSAGE:\nAssociation of type and location of BRCA1 and BRCA2 mutations with risk of breast and ovarian cancer. IMPORTANCE Limited information about the relationship between specific mutations in BRCA1 or BRCA2 (BRCA1/2) and cancer risk exists. OBJECTIVE To identify mutation-specific cancer risks for carriers of BRCA1/2. DESIGN, SETTING, AND PARTICIPANTS Observational study of women who were ascertained between 1937 and 2011 (median, 1999) and found to carry disease-associated BRCA1 or BRCA2 mutations. The international sample comprised 19,581 carriers of BRCA1 mutations and 11,900 carriers of BRCA2 mutations from 55 centers in 33 countries on 6 continents. We estimated hazard ratios for breast and ovarian cancer based on mutation type, function, and nucleotide position. We also estimated RHR, the ratio of breast vs ovarian cancer hazard ratios. A value of RHR greater than 1 indicated elevated breast cancer risk; a value of RHR less than 1 indicated elevated ovarian cancer risk. EXPOSURES Mutations of BRCA1 or BRCA2. MAIN OUTCOMES AND MEASURES Breast and ovarian cancer risks. RESULTS Among BRCA1 mutation carriers, 9052 women (46%) were diagnosed with breast cancer, 2317 (12%) with ovarian cancer, 1041 (5%) with breast and ovarian cancer, and 7171 (37%) without cancer. Among BRCA2 mutation carriers, 6180 women (52%) were diagnosed with breast cancer, 682 (6%) with ovarian cancer, 272 (2%) with breast and ovarian cancer, and 4766 (40%) without cancer. In BRCA1, we identified 3 breast cancer cluster regions (BCCRs) located at c.179 to c.505 (BCCR1; RHR = 1.46; 95% CI, 1.22-1.74; P = 2 × 10(-6)), c.4328 to c.4945 (BCCR2; RHR = 1.34; 95% CI, 1.01-1.78; P = .04), and c. 5261 to c.5563 (BCCR2', RHR = 1.38; 95% CI, 1.22-1.55; P = 6 × 10(-9)). We also identified an ovarian can [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "159", "doc_id": "9394119", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Major antigen-induced signals from the T cell receptor and secondary signals from costimulatory receptors are required for T cell activation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Relationship between activity levels, aerobic fitness, and body fat in 8- to 10-yr-old children.\nABSTRACT: The relationships between children's activity, aerobic fitness, and fatness are unclear. Indirect estimates of activity, e.g., heart rate (HR) and recall, may mask any associations. The purpose of this study was to assess these relationships by using the Tritrac-R3D, a pedometer, and heart rate. Thirty-four children, ages 8-10 yr, participated in the study. The Tritrac and pedometer were worn for up to 6 days. HR was measured for 1 day. Activity measured by Tritrac or pedometer correlated positively to fitness in the whole group (Tritrac, r = 0.66; pedometer, r = 0.59; P < 0.01) and in boys and girls separately (P < 0.05) and correlated negatively to fatness in the whole group (r = -0.42, P < 0.05). In contrast, HR did not correlate significantly to fitness, and HR of >139 beats/min correlated positively to fatness in girls (r = 0.64, P < 0.05). This suggests that HR is misleading as a measure of activity. This study supports a positive relationship between activity and fitness and suggests a negative relationship between fatness and activity.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 749, "doc_id": "2575938", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: BLM gene encodes RecQ-class DNA helicase.\n\nCANDIDATE_PASSAGE:\nA versatile zero background T-vector system for gene cloning and functional genomics. With the recent availability of complete genomic sequences of many organisms, high-throughput and cost-efficient systems for gene cloning and functional analysis are in great demand. Although site-specific recombination-based cloning systems, such as Gateway cloning technology, are extremely useful for efficient transfer of DNA fragments into multiple destination vectors, the two-step cloning process is time consuming and expensive. Here, we report a zero background TA cloning system that provides simple and high-efficiency direct cloning of PCR-amplified DNA fragments with almost no self-ligation. The improved T-vector system takes advantage of the restriction enzyme XcmI to generate a T-overhang after digestion and the negative selection marker gene ccdB to eliminate the self-ligation background after transformation. We demonstrate the feasibility and flexibility of the technology by developing a set of transient and stable transformation vectors for constitutive gene expression, gene silencing, protein tagging, protein subcellular localization detection, and promoter fragment activity analysis in plants. Because the system can be easily adapted for developing specialized expression vectors for other organisms, zero background TA provides a general, cost-efficient, and high-throughput platform that complements the Gateway cloning system for gene cloning and functional genomics.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "157", "doc_id": "9599194", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Patients in stable partnerships progress from HIV to death at the same rate as patients not in partnerships.\n\nCANDIDATE_PASSAGE:\nTreatment of active tuberculosis in HIV-coinfected patients: a systematic review and meta-analysis. BACKGROUND Patients with human immunodeficiency virus (HIV) infection and tuberculosis have an increased risk of death, treatment failure, and relapse. METHODS A systematic review and meta-analysis of randomized, controlled trials and cohort studies was conducted to evaluate the impact of duration and dosing schedule of rifamycin and use of antiretroviral therapy in the treatment of active tuberculosis in HIV-positive patients. In included studies, the initial tuberculosis diagnosis, failure, and/or relapse were microbiologically confirmed, and patients received standardized rifampin- or rifabutin-containing regimens. Pooled cumulative incidence of treatment failure, death during treatment, and relapse were calculated using random-effects models. Multivariable meta-regression was performed using negative binomial regression. RESULTS After screening 5158 citations, 6 randomized trials and 21 cohort studies were included. Relapse was more common with regimens using 2 months rifamycin (adjusted risk ratio, 3.6; 95% confidence interval, 1.1-11.7) than with regimens using rifamycin for at least 8 months. Compared with daily therapy in the initial phase (n=3352 patients from 35 study arms), thrice-weekly therapy (n=211 patients from 5 study arms) was associated with higher rates of failure (adjusted risk ratio, 4.0; 95% confidence interval, 1.5-10.4) and relapse [adjusted risk ratio, 4.8; 95% confidence interval, 1.8-12.8). There were trends toward higher relapse rates if rifamycins were used for only 6 months, compared with > or =8 months, or if antiretroviral therapy was not used. CONCLUSIONS This review raises serious concerns regarding current recommendations fo [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "925", "doc_id": "31363207", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Hypothalamic glutamate neurotransmission is crucial to energy balance.\n\nCANDIDATE_PASSAGE:\nDefining early lineage specification of human embryonic stem cells by the orchestrated balance of canonical Wnt/beta-catenin, Activin/Nodal and BMP signaling. The canonical Wnt/beta-catenin signaling has remarkably diverse roles in embryonic development, stem cell self-renewal and cancer progression. Here, we show that stabilized expression of beta-catenin perturbed human embryonic stem (hES)-cell self-renewal, such that up to 80% of the hES cells developed into the primitive streak (PS)/mesoderm progenitors, reminiscent of early mammalian embryogenesis. The formation of the PS/mesoderm progenitors essentially depended on the cooperative action of beta-catenin together with Activin/Nodal and BMP signaling pathways. Intriguingly, blockade of BMP signaling completely abolished mesoderm generation, and induced a cell fate change towards the anterior PS progenitors. The PI3-kinase/Akt, but not MAPK, signaling pathway had a crucial role in the anterior PS specification, at least in part, by enhancing beta-catenin stability. In addition, Activin/Nodal and Wnt/beta-catenin signaling synergistically induced the generation and specification of the anterior PS/endoderm. Taken together, our findings clearly demonstrate that the orchestrated balance of Activin/Nodal and BMP signaling defines the cell fate of the nascent PS induced by canonical Wnt/beta-catenin signaling in hES cells.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "540", "doc_id": "43661837", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Clathrin stabilizes the spindle fiber apparatus during mitosis.\n\nCANDIDATE_PASSAGE:\nClathrin is required for the function of the mitotic spindle Clathrin has an established function in the generation of vesicles that transfer membrane and proteins around the cell. The formation of clathrin-coated vesicles occurs continuously in non-dividing cells, but is shut down during mitosis, when clathrin concentrates at the spindle apparatus. Here, we show that clathrin stabilizes fibres of the mitotic spindle to aid congression of chromosomes. Clathrin bound to the spindle directly by the amino-terminal domain of clathrin heavy chain. Depletion of clathrin heavy chain using RNA interference prolonged mitosis; kinetochore fibres were destabilized, leading to defective congression of chromosomes to the metaphase plate and persistent activation of the spindle checkpoint. Normal mitosis was rescued by clathrin triskelia but not the N-terminal domain of clathrin heavy chain, indicating that stabilization of kinetochore fibres was dependent on the unique structure of clathrin. The importance of clathrin for normal mitosis may be relevant to understanding human cancers that involve gene fusions of clathrin heavy chain.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "265", "doc_id": "2033917", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does methotrexate inhibit NF-κB activity via long intergenic ( noncoding ) RNA-p21 induction?\n\nABSTRACT:\nTo determine interrelationships between the expression of long intergenic (noncoding) RNA-p21 (lincRNA-p21), NF-κB activity, and responses to methotrexate (MTX) in rheumatoid arthritis (RA) by analyzing patient blood samples and cell culture models. Expression levels of long noncoding RNA and messenger RNA (mRNA) were determined by quantitative reverse transcription-polymerase chain reaction. Western blotting and flow cytometry were used to quantify levels of intracellular proteins. Intracellular NF-κB activity was determined using an NF-κB luciferase reporter plasmid. Patients with RA expressed reduced basal levels of lincRNA-p21 and increased basal levels of phosphorylated p65 (RelA), a marker of NF-κB activation. Patients with RA who were not treated with MTX expressed lower levels of lincRNA-p21 and higher levels of phosphorylated p65 compared with RA patients treated with low-dose MTX. In cell culture using primary cells and transformed cell lines, MTX induced lincRNA-p21 through a DNA-dependent protein kinase catalytic subunit (DNA PKcs)-dependent mechanism. Deficiencies in the levels of PRKDC mRNA in patients with RA were also corrected by MTX in vivo. Furthermore, MTX reduced NF-κB activity in tumor necrosis factor α-treated cells through a DNA PKcs-dependent mechanism via induction of lincRNA-p21. Finally, we observed that depressed levels of TP53 and lincRNA-p21 increased NF-κB activity in cell lines. Decreased levels of lincRNA-p21 did not alter NFKB1 or RELA transcripts; rather, lincRNA-p21 physically bound to RELA mRNA.", "output": "{\"label\": \"yes\", \"rationale\": \"Our findings support a model whereby depressed levels of lincRNA-p21 in RA contribute to increased NF-κB activity. MTX decreases basal levels of NF-κB activity by increasing lincRNA-p21 levels through a DNA PKcs-dependent mechanism.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25077978, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does limb-salvage surgery offer patients better quality of life and functional capacity than amputation?\n\nABSTRACT:\nPatients with aggressive lower extremity musculoskeletal tumors may be candidates for either above-knee amputation or limb-salvage surgery. However, the subjective and objective benefits of limb-salvage surgery compared with amputation are not fully clear.QUESTIONS/ We therefore compared functional status and quality of life for patients treated with above-knee amputation versus limb-salvage surgery. We reviewed 20 of 51 patients aged 15 years and older treated with above-knee amputation or limb-salvage surgery for aggressive musculoskeletal tumors around the knee between 1994 and 2004 as a retrospective cohort study. At last followup we obtained the Physiological Cost Index, the Reintegration to Normal Living Index, SF-36, and the Toronto Extremity Salvage Score questionnaires. The minimum followup was 12 months (median, 56 months; range, 12-108 months). Compared with patients having above-knee amputation, patients undergoing limb-salvage surgery had superior Physiological Cost Index scores and Reintegration to Normal Living Index. The Toronto Extremity Salvage scores and SF-36 scores were similar in the two groups.", "output": "{\"label\": \"maybe\", \"rationale\": \"These data suggest that limb-salvage surgery offers better gait efficiency and return to normal living compared with above-knee amputation, but does not improve the patient's perception of quality of life.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 22302658, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Do hydrophobic profiles of the tail anchors in SLMAP dictate subcellular targeting?\n\nABSTRACT:\nTail anchored (TA) membrane proteins target subcellular structures via a C-terminal transmembrane domain and serve prominent roles in membrane fusion and vesicle transport. Sarcolemmal Membrane Associated Protein (SLMAP) possesses two alternatively spliced tail anchors (TA1 or TA2) but their specificity of subcellular targeting remains unknown. TA1 or TA2 can direct SLMAP to reticular structures including the endoplasmic reticulum (ER), whilst TA2 directs SLMAP additionally to the mitochondria. Despite the general structural similarity of SLMAP to other vesicle trafficking proteins, we found no evidence for its localization with the vesicle transport machinery or a role in vesicle transport. The predicted transmembrane region of TA2 is flanked on either side by a positively charged amino acid and is itself less hydrophobic than the transmembrane helix present in TA1. Substitution of the positively charged amino acids, in the regions flanking the transmembrane helix of TA2, with leucine did not alter its subcellular targeting. The targeting of SLMAP to the mitochondria was dependent on the hydrophobic nature of TA2 since targeting of SLMAP-TA2 was prevented by the substitution of leucine (L) for moderately hydrophobic amino acid residues within the transmembrane region. The SLMAP-TA2-4L mutant had a hydrophobic profile that was comparable to that of SLMAP-TA1 and had identical targeting properties to SLMAP-TA1.", "output": "{\"label\": \"yes\", \"rationale\": \"Thus the overall hydrophobicity of the two alternatively spliced TAs in SLMAP determines its subcellular targeting and TA2 predominantly directs SLMAP to the mitochondira where it may serve roles in the function of this organelle.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 19538755, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Ly49Q directs the organization of neutrophil migration to inflammation sites by regulating membrane raft functions.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Ly49Q receptor plays a crucial role in neutrophil polarization and migration by regulating raft trafficking.\nABSTRACT: Neutrophils rapidly undergo polarization and directional movement to infiltrate the sites of infection and inflammation. Here, we show that an inhibitory MHC I receptor, Ly49Q, was crucial for the swift polarization of and tissue infiltration by neutrophils. During the steady state, Ly49Q inhibited neutrophil adhesion by preventing focal-complex formation, likely by inhibiting Src and PI3 kinases. However, in the presence of inflammatory stimuli, Ly49Q mediated rapid neutrophil polarization and tissue infiltration in an ITIM-domain-dependent manner. These opposite functions appeared to be mediated by distinct use of effector phosphatase SHP-1 and SHP-2. Ly49Q-dependent polarization and migration were affected by Ly49Q regulation of membrane raft functions. We propose that Ly49Q is pivotal in switching neutrophils to their polarized morphology and rapid migration upon inflammation, through its spatiotemporal regulation of membrane rafts and raft-associated signaling molecules.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Ly49Q-dependent polarization and migration were affected by Ly49Q regulation of membrane raft functions.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 723, "doc_id": "5531479", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: New drugs for tuberculosis often do not penetrate the necrotic portion of a tuberculosis lesion in high concentrations.\n\nCANDIDATE_ABSTRACT:\nTITLE: An Excitatory Loop with Astrocytes Contributes to Drive Neurons to Seizure Threshold\nABSTRACT: Seizures in focal epilepsies are sustained by a highly synchronous neuronal discharge that arises at restricted brain sites and subsequently spreads to large portions of the brain. Despite intense experimental research in this field, the earlier cellular events that initiate and sustain a focal seizure are still not well defined. Their identification is central to understand the pathophysiology of focal epilepsies and to develop new pharmacological therapies for drug-resistant forms of epilepsy. The prominent involvement of astrocytes in ictogenesis was recently proposed. We test here whether a cooperation between astrocytes and neurons is a prerequisite to support ictal (seizure-like) and interictal epileptiform events. Simultaneous patch-clamp recording and Ca2+ imaging techniques were performed in a new in vitro model of focal seizures induced by local applications of N-methyl-D-aspartic acid (NMDA) in rat entorhinal cortex slices. We found that a Ca2+ elevation in astrocytes correlates with both the initial development and the maintenance of a focal, seizure-like discharge. A delayed astrocyte activation during ictal discharges was also observed in other models (including the whole in vitro isolated guinea pig brain) in which the site of generation of seizure activity cannot be precisely monitored. In contrast, interictal discharges were not associated with Ca2+ changes in astrocytes. Selective inhibition or stimulation of astrocyte Ca2+ signalling blocked or enhanced, respectively, ictal discharges, but did not affect interictal discharge generation. Our data reveal that neurons engage astrocytes in a recurrent excitatory loop (possibly involving gliotransmission) that promotes seizure ignition and sustains the ictal discharge. This neuron-astrocyte int [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 847, "doc_id": "1410197", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Hyperfibrinogenemia decreases rates of femoropopliteal bypass thrombosis.\n\nCANDIDATE_PASSAGE:\nInfluence of smoking and plasma factors on patency of femoropopliteal vein grafts. OBJECTIVE To determine the effects of smoking, plasma lipids, lipoproteins, apolipoproteins, and fibrinogen on the patency of saphenous vein femoropopliteal bypass grafts at one year. DESIGN Prospective study of patients with saphenous vein femoropopliteal bypass grafts entered into a multicentre trial. SETTING Surgical wards, outpatient clinics, and home visits coordinated by two tertiary referral centres in London and Birmingham. PATIENTS 157 Patients (mean age 66.6 (SD 8.2) years), 113 with patent grafts and 44 with occluded grafts one year after bypass. MAIN OUTCOME MEASURE Cumulative percentage patency at one year. RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts. Serum cholesterol concentrations were significantly higher in patients with grafts that remained patent one year after bypass (p less than 0.005). Analysis of the smoking markers indicated that a quarter of patients (40) were untruthful in their claims to have stopped smoking. Based on smoking markers, patency of grafts in smokers was significantly lower at one year by life table analysis than in non-smokers (63% v 84%, p less than 0.02). Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002). Surprisingly, increased plasma low density lipoprotein cholesterol concentration was significantly assoc [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "532", "doc_id": "12991445", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: In transgenic mice harboring green florescent protein under the control of the Sox2 promoter, less than ten percent of the cells with green florescent colocalize with cell proliferation markers.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cell Stem Cell Article In Vivo Fate Analysis Reveals the Multipotent and Self-Renewal Capacities of Sox2 + Neural Stem Cells in the Adult Hippocampus\nABSTRACT: To characterize the properties of adult neural stem cells (NSCs), we generated and analyzed Sox2-GFP transgenic mice. Sox2-GFP cells in the subgranular zone (SGZ) express markers specific for progenitors, but they represent two morphologically distinct populations that differ in proliferation levels. Lentivirus- and retrovirus-mediated fate-tracing studies showed that Sox2+ cells in the SGZ have potential to give rise to neurons and astrocytes, revealing their multipotency at the population as well as at a single-cell level. A subpopulation of Sox2+ cells gives rise to cells that retain Sox2, highlighting Sox2+ cells as a primary source for adult NSCs. In response to mitotic signals, increased proliferation of Sox2+ cells is coupled with the generation of Sox2+ NSCs as well as neuronal precursors. An asymmetric contribution of Sox2+ NSCs may play an important role in maintaining the constant size of the NSC pool and producing newly born neurons during adult neurogenesis.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 587, "doc_id": "16999023", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Expression of oncolytic virus antigens as peptides makes relapse more likely.\n\nCANDIDATE_PASSAGE:\nDetecting and targeting tumor relapse by its resistance to innate effectors at early recurrence Tumor recurrence represents a major clinical challenge. Our data show that emergent recurrent tumors acquire a phenotype radically different from that of their originating primary tumors. This phenotype allows them to evade a host-derived innate immune response elicited by the progression from minimal residual disease (MRD) to actively growing recurrence. Screening for this innate response predicted accurately in which mice recurrence would occur. Premature induction of recurrence resensitized MRD to the primary therapy, suggesting a possible paradigm shift for clinical treatment of dormant disease in which the current expectant approach is replaced with active attempts to uncover MRD before evolution of the escape phenotype is complete. By combining screening with second-line treatments targeting innate insensitivity, up to 100% of mice that would have otherwise relapsed were cured. These data may open new avenues for early detection and appropriately timed, highly targeted treatment of tumor recurrence irrespective of tumor type or frontline treatment.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "403", "doc_id": "1921218", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Cognitive behavioral therapy is an ineffective treatment for insomnia\n\nCANDIDATE_ABSTRACT:\nTITLE: Cognitive behavioral therapy vs zopiclone for treatment of chronic primary insomnia in older adults: a randomized controlled trial.\nABSTRACT: CONTEXT Insomnia is a common condition in older adults and is associated with a number of adverse medical, social, and psychological consequences. Previous research has suggested beneficial outcomes of both psychological and pharmacological treatments, but blinded placebo-controlled trials comparing the effects of these treatments are lacking. OBJECTIVE To examine short- and long-term clinical efficacy of cognitive behavioral therapy (CBT) and pharmacological treatment in older adults experiencing chronic primary insomnia. DESIGN, SETTING, AND PARTICIPANTS A randomized, double-blinded, placebo-controlled trial of 46 adults (mean age, 60.8 y; 22 women) with chronic primary insomnia conducted between January 2004 and December 2005 in a single Norwegian university-based outpatient clinic for adults and elderly patients. INTERVENTION CBT (sleep hygiene, sleep restriction, stimulus control, cognitive therapy, and relaxation; n = 18), sleep medication (7.5-mg zopiclone each night; n = 16), or placebo medication (n = 12). All treatment duration was 6 weeks, and the 2 active treatments were followed up at 6 months. MAIN OUTCOME MEASURES Ambulant clinical polysomnographic data and sleep diaries were used to determine total wake time, total sleep time, sleep efficiency, and slow-wave sleep (only assessed using polysomnography) on all 3 assessment points. RESULTS CBT resulted in improved short- and long-term outcomes compared with zopiclone on 3 out of 4 outcome measures. For most outcomes, zopiclone did not differ from placebo. Participants receiving CBT improved their sleep efficiency from 81.4% at pretreatment to 90.1% at 6-month follow-up compared with a decrease from 82.3% to 81.9% in the zopiclone group. Participants in the CBT group spent much more time in slow- [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Participants receiving CBT improved their sleep efficiency from 81.4% at pretreatment to 90.1% at 6-month follow-up compared with a decrease from 82.3% to 81.9% in the zopiclone group.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 267, "doc_id": "5912283", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Birth-weight is positively associated with breast cancer.\n\nCANDIDATE_PASSAGE:\nIntegrated molecular genetic profiling of pediatric high-grade gliomas reveals key differences with the adult disease. PURPOSE To define copy number alterations and gene expression signatures underlying pediatric high-grade glioma (HGG). PATIENTS AND METHODS We conducted a high-resolution analysis of genomic imbalances in 78 de novo pediatric HGGs, including seven diffuse intrinsic pontine gliomas, and 10 HGGs arising in children who received cranial irradiation for a previous cancer using single nucleotide polymorphism microarray analysis. Gene expression was analyzed with gene expression microarrays for 53 tumors. Results were compared with publicly available data from adult tumors. RESULTS Significant differences in copy number alterations distinguish childhood and adult glioblastoma. PDGFRA was the predominant target of focal amplification in childhood HGG, including diffuse intrinsic pontine gliomas, and gene expression analyses supported an important role for deregulated PDGFRalpha signaling in pediatric HGG. No IDH1 hotspot mutations were found in pediatric tumors, highlighting molecular differences with adult secondary glioblastoma. Pediatric and adult glioblastomas were clearly distinguished by frequent gain of chromosome 1q (30% v 9%, respectively) and lower frequency of chromosome 7 gain (13% v 74%, respectively) and 10q loss (35% v 80%, respectively). PDGFRA amplification and 1q gain occurred at significantly higher frequency in irradiation-induced tumors, suggesting that these are initiating events in childhood gliomagenesis. A subset of pediatric HGGs showed minimal copy number changes. CONCLUSION Integrated molecular profiling showed substantial differences in the molecular features underlying pediatric and adult HGG, indicating that findings [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "179", "doc_id": "2360905", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Allogeneic mechanical circulatory support is not as effective as autologous mechanical circulatory support for treating acute myocardial infarction.\n\nCANDIDATE_ABSTRACT:\nTITLE: Comparison of allogeneic vs autologous bone marrow–derived mesenchymal stem cells delivered by transendocardial injection in patients with ischemic cardiomyopathy: the POSEIDON randomized trial.\nABSTRACT: CONTEXT Mesenchymal stem cells (MSCs) are under evaluation as a therapy for ischemic cardiomyopathy (ICM). Both autologous and allogeneic MSC therapies are possible; however, their safety and efficacy have not been compared. OBJECTIVE To test whether allogeneic MSCs are as safe and effective as autologous MSCs in patients with left ventricular (LV) dysfunction due to ICM. DESIGN, SETTING, AND PATIENTS A phase 1/2 randomized comparison (POSEIDON study) in a US tertiary-care referral hospital of allogeneic and autologous MSCs in 30 patients with LV dysfunction due to ICM between April 2, 2010, and September 14, 2011, with 13-month follow-up. INTERVENTION Twenty million, 100 million, or 200 million cells (5 patients in each cell type per dose level) were delivered by transendocardial stem cell injection into 10 LV sites. MAIN OUTCOME MEASURES Thirty-day postcatheterization incidence of predefined treatment-emergent serious adverse events (SAEs). Efficacy assessments included 6-minute walk test, exercise peak VO2, Minnesota Living with Heart Failure Questionnaire (MLHFQ), New York Heart Association class, LV volumes, ejection fraction (EF), early enhancement defect (EED; infarct size), and sphericity index. RESULTS Within 30 days, 1 patient in each group (treatment-emergent SAE rate, 6.7%) was hospitalized for heart failure, less than the prespecified stopping event rate of 25%. The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3% (n = 8) in the autologous group (P = .46). At 1 year, there were no ventricular arrhythmia SAEs observed among allogeneic recipients compared with 4 patients (26.7%) in the autologous group (P = .10). Relative to baseline, autologous but not allogeneic MSC therapy was associated with an improvement in the 6- [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS In this early-stage study of patients with ICM, transendocardial injection of allogeneic and autologous MSCs without a placebo control were both associated with low rates of treatment-emergent SAEs, including immunologic reactions.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 104, "doc_id": "40164383", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The availability of safe places to study is effective at decreasing homelessness.\n\nCANDIDATE_PASSAGE:\nComparison of allogeneic vs autologous bone marrow–derived mesenchymal stem cells delivered by transendocardial injection in patients with ischemic cardiomyopathy: the POSEIDON randomized trial. CONTEXT Mesenchymal stem cells (MSCs) are under evaluation as a therapy for ischemic cardiomyopathy (ICM). Both autologous and allogeneic MSC therapies are possible; however, their safety and efficacy have not been compared. OBJECTIVE To test whether allogeneic MSCs are as safe and effective as autologous MSCs in patients with left ventricular (LV) dysfunction due to ICM. DESIGN, SETTING, AND PATIENTS A phase 1/2 randomized comparison (POSEIDON study) in a US tertiary-care referral hospital of allogeneic and autologous MSCs in 30 patients with LV dysfunction due to ICM between April 2, 2010, and September 14, 2011, with 13-month follow-up. INTERVENTION Twenty million, 100 million, or 200 million cells (5 patients in each cell type per dose level) were delivered by transendocardial stem cell injection into 10 LV sites. MAIN OUTCOME MEASURES Thirty-day postcatheterization incidence of predefined treatment-emergent serious adverse events (SAEs). Efficacy assessments included 6-minute walk test, exercise peak VO2, Minnesota Living with Heart Failure Questionnaire (MLHFQ), New York Heart Association class, LV volumes, ejection fraction (EF), early enhancement defect (EED; infarct size), and sphericity index. RESULTS Within 30 days, 1 patient in each group (treatment-emergent SAE rate, 6.7%) was hospitalized for heart failure, less than the prespecified stopping event rate of 25%. The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3% (n = 8) in the autologous group (P = .46). At 1 year, there were no ventricular arrhythmia SAEs observed among all [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1196", "doc_id": "40164383", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: PKG-la plays an essential role in expression of pain hypersensitivity in PGK-la knockout mice.\n\nCANDIDATE_PASSAGE:\nPresynaptically Localized Cyclic GMP-Dependent Protein Kinase 1 Is a Key Determinant of Spinal Synaptic Potentiation and Pain Hypersensitivity Synaptic long-term potentiation (LTP) at spinal neurons directly communicating pain-specific inputs from the periphery to the brain has been proposed to serve as a trigger for pain hypersensitivity in pathological states. Previous studies have functionally implicated the NMDA receptor-NO pathway and the downstream second messenger, cGMP, in these processes. Because cGMP can broadly influence diverse ion-channels, kinases, and phosphodiesterases, pre- as well as post-synaptically, the precise identity of cGMP targets mediating spinal LTP, their mechanisms of action, and their locus in the spinal circuitry are still unclear. Here, we found that Protein Kinase G1 (PKG-I) localized presynaptically in nociceptor terminals plays an essential role in the expression of spinal LTP. Using the Cre-lox P system, we generated nociceptor-specific knockout mice lacking PKG-I specifically in presynaptic terminals of nociceptors in the spinal cord, but not in post-synaptic neurons or elsewhere (SNS-PKG-I(-/-) mice). Patch clamp recordings showed that activity-induced LTP at identified synapses between nociceptors and spinal neurons projecting to the periaqueductal grey (PAG) was completely abolished in SNS-PKG-I(-/-) mice, although basal synaptic transmission was not affected. Analyses of synaptic failure rates and paired-pulse ratios indicated a role for presynaptic PKG-I in regulating the probability of neurotransmitter release. Inositol 1,4,5-triphosphate receptor 1 and myosin light chain kinase were recruited as key phosphorylation targets of presynaptic PKG-I in nociceptive neurons. Finally, behavioural analyses in vivo showed ma [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "911", "doc_id": "11254556", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Monoclonal antibody targeting of N-cadherin encourages metastasis.\n\nCANDIDATE_ABSTRACT:\nTITLE: A mutation in Orai1 causes immune deficiency by abrogating CRAC channel function\nABSTRACT: Antigen stimulation of immune cells triggers Ca2+ entry through Ca2+ release-activated Ca2+ (CRAC) channels, promoting the immune response to pathogens by activating the transcription factor NFAT. We have previously shown that cells from patients with one form of hereditary severe combined immune deficiency (SCID) syndrome are defective in store-operated Ca2+ entry and CRAC channel function. Here we identify the genetic defect in these patients, using a combination of two unbiased genome-wide approaches: a modified linkage analysis with single-nucleotide polymorphism arrays, and a Drosophila RNA interference screen designed to identify regulators of store-operated Ca2+ entry and NFAT nuclear import. Both approaches converged on a novel protein that we call Orai1, which contains four putative transmembrane segments. The SCID patients are homozygous for a single missense mutation in ORAI1, and expression of wild-type Orai1 in SCID T cells restores store-operated Ca2+ influx and the CRAC current (ICRAC). We propose that Orai1 is an essential component or regulator of the CRAC channel complex.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 802, "doc_id": "1605392", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Do emergency medical services professionals think they should participate in disease prevention?\n\nABSTRACT:\nThe primary objective of the study was to determine emergency medical services (EMS) professionals' opinions regarding participation in disease and injury prevention programs. A secondary objective was to determine the proportion of EMS professionals who had participated in disease prevention programs. As part of the National Registry of Emergency Medical Technicians' biennial reregistration process, EMS professionals reregistering in 2006 were asked to complete an optional survey regarding their opinions on and participation in disease and injury prevention. Demographic characteristics were also collected. Data were analyzed using descriptive statistics and 99% confidence intervals (CIs). The chi-square test was used to compare differences by responder demographics (alpha = 0.01). A 10% difference between groups was determined to be clinically significant. The survey was completed by 27,233 EMS professionals. Of these responders, 82.7% (99% CI: 82.1-83.3) felt that EMS professionals should participate in disease prevention, with those working 20 to 29 hours per week being the least likely to think they should participate (67.4%, p<0.001). About a third, 33.8% (99% CI: 33.1-34.6), of the respondents reported having provided prevention services, with those having a graduate degree (43.5%, p<0.001), those working in EMS for more than 21 years (44%, p<0.001), those working for the military (57%, p<0.001), those working 60 to 69 hours per week (41%, p<0.001), and those responding to zero emergency calls in a typical week (43%, p<0.001) being the most likely to report having provided prevention services. About half, 51.1% (99% CI: 50.4-51.9), of the respondents agreed that prevention services should be provided during emergency calls, and 7.7% (99% CI: 7.3-8.1) o [TRUNCATED]", "output": "{\"label\": \"maybe\", \"rationale\": \"The majority of EMS professionals thought that they should participate in disease and injury prevention programs. The respondents were mixed as to whether prevention services should be provided while on emergency calls, but those with experience providing these services were more likely to agree with providing them during emergency calls.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 19145527, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does nerve growth factor promote corneal epithelial migration by enhancing expression of matrix metalloprotease-9?\n\nABSTRACT:\nNerve growth factor (NGF) is a neuropeptide essential for the development, survival, growth, and differentiation of corneal cells. Its effects are mediated by both TrkA and p75 receptors. Clinically relevant use of NGF was introduced to treat neurotrophic ulcerations in patients. Herein, we examine the mechanisms by which NGF enhances epithelial wound healing both in vivo and in vitro. An animal model using adult hens was implemented for the in vivo experiments. Laser ablation keratectomy was performed and animals were observed for up to 7 days. Epithelial healing was measured with fluorescein. In addition, proliferation was measured using BrdU incorporation and both TrkA and matrix metalloprotease-9 (MMP-9) expression were measured by immunohistochemistry (IHC) and Western blot (WB). In vitro experiments were carried out with telomerase-immortalized human corneal epithelial cells (HCLE). The rate of proliferation was measured using a colorimetric assay and BrdU incorporation. Real-time migration was evaluated with an inverted microscope. MMP-9 expression was evaluated by immunocytochemistry (ICC), WB, zymography, and RT-PCR. Finally, beta-4 integrin (β4) expression was assessed by ICC and WB. Faster epithelial healing was observed in NGF-treated corneas compared with controls (P < 0.01). These corneas showed increased proliferation, TrkA upregulation, and enhanced MMP-9 presence (P < 0.01). In vitro, faster spreading and migration were observed in response to NGF (P < 0.01). Enhanced proliferation, as well as enhanced TrkA and MMP-9 expression, and decreased β4 levels were observed after adding NGF (P < 0.01).", "output": "{\"label\": \"yes\", \"rationale\": \"NGF plays a major role during the epithelial healing process by promoting migration, a process that is accelerated by cell spreading. This effect is mediated by both the upregulation of MMP-9 and cleavage of β4 integrin.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 23640040, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Intramembrane cleavage by signal peptide peptidase aids in the degradation of proteins with a complex membrane orientation.\n\nCANDIDATE_PASSAGE:\nSuccinate is an inflammatory signal that induces IL-1β through HIF-1α Macrophages activated by the Gram-negative bacterial product lipopolysaccharide switch their core metabolism from oxidative phosphorylation to glycolysis. Here we show that inhibition of glycolysis with 2-deoxyglucose suppresses lipopolysaccharide-induced interleukin-1β but not tumour-necrosis factor-α in mouse macrophages. A comprehensive metabolic map of lipopolysaccharide-activated macrophages shows upregulation of glycolytic and downregulation of mitochondrial genes, which correlates directly with the expression profiles of altered metabolites. Lipopolysaccharide strongly increases the levels of the tricarboxylic-acid cycle intermediate succinate. Glutamine-dependent anerplerosis is the principal source of succinate, although the ‘GABA (γ-aminobutyric acid) shunt’ pathway also has a role. Lipopolysaccharide-induced succinate stabilizes hypoxia-inducible factor-1α, an effect that is inhibited by 2-deoxyglucose, with interleukin-1β as an important target. Lipopolysaccharide also increases succinylation of several proteins. We therefore identify succinate as a metabolite in innate immune signalling, which enhances interleukin-1β production during inflammation.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "657", "doc_id": "4423401", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Prescribed exercise training improves quality of life.\n\nCANDIDATE_PASSAGE:\nCost-effectiveness comparison between topical silver sulfadiazine and enclosed silver dressing for partial-thickness burn treatment. The standard treatment of partial-thickness burns includes topical silver products such as silver sulfadiazine (SSD) cream and enclosed dressings including silver-impregnated foam (Mepilex Ag; Molnlycke Health Care, Gothenburg, Sweden) and silver-laden sheets (Aquacel Ag; ConvaTec, Skillman, NJ). The current state of health care is limited by resources, with an emphasis on evidence-based outcomes and cost-effective treatments. This study includes a decision analysis with an incremental cost-utility ratio comparing enclosed silver dressings with SSD in partial-thickness burn patients with TBSA less than 20%. A comprehensive literature review was conducted to identify clinically relevant health states in partial-thickness burn patients. These health states include successful healing, infection, and noninfected delayed healing requiring either surgery or conservative management. The probabilities of these health states were combined with Medicare CPT reimbursement codes (cost) and patient-derived utilities to fit into the decision model. Utilities were obtained using a visual analog scale during patient interviews. Expected cost and quality-adjusted life years (QALYs) were calculated using the roll-back method. The incremental cost-utility ratio for enclosed silver dressing relative to SSD was $40,167.99/QALY. One-way sensitivity analysis of complication rates confirmed robustness of the model. Assuming a maximum willingness to pay $50,000/QALY, the complication rate for SSD must be 22% or higher for enclosed silver dressing to be cost effective. By varying complication rates for SSD and enclosed silver dressings, the two-way sens [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "965", "doc_id": "3690068", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Reduced responsiveness to interleukin-2 in regulatory T cells is associated with greater resistance to autoimmune diseases such as Type 1 Diabetes.\n\nCANDIDATE_PASSAGE:\nAnti-CD3 monoclonal antibody in new-onset type 1 diabetes mellitus. BACKGROUND Type 1 diabetes mellitus is a chronic autoimmune disease caused by the pathogenic action of T lymphocytes on insulin-producing beta cells. Previous clinical studies have shown that continuous immune suppression temporarily slows the loss of insulin production. Preclinical studies suggested that a monoclonal antibody against CD3 could reverse hyperglycemia at presentation and induce tolerance to recurrent disease. METHODS We studied the effects of a nonactivating humanized monoclonal antibody against CD3--hOKT3gamma1(Ala-Ala)--on the loss of insulin production in patients with type 1 diabetes mellitus. Within 6 weeks after diagnosis, 24 patients were randomly assigned to receive either a single 14-day course of treatment with the monoclonal antibody or no antibody and were studied during the first year of disease. RESULTS Treatment with the monoclonal antibody maintained or improved insulin production after one year in 9 of the 12 patients in the treatment group, whereas only 2 of the 12 controls had a sustained response (P=0.01). The treatment effect on insulin responses lasted for at least 12 months after diagnosis. Glycosylated hemoglobin levels and insulin doses were also reduced in the monoclonal-antibody group. No severe side effects occurred, and the most common side effects were fever, rash, and anemia. Clinical responses were associated with a change in the ratio of CD4+ T cells to CD8+ T cells 30 and 90 days after treatment. CONCLUSIONS Treatment with hOKT3gamma1(Ala-Ala) mitigates the deterioration in insulin production and improves metabolic control during the first year of type 1 diabetes mellitus in the majority of patients. The mechanism of action of the anti-CD3 mon [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1029", "doc_id": "36642096", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: NF2 (Merlin) causes phosphorylation and subsequent cytoplasmic sequestration of YAP in Drosophila by activating LATS1/2 kinases.\n\nCANDIDATE_PASSAGE:\nA genetic screen identifies an LKB1–MARK signalling axis controlling the Hippo–YAP pathway The Hippo–YAP pathway is an emerging signalling cascade involved in the regulation of stem cell activity and organ size. To identify components of this pathway, we performed an RNAi-based kinome screen in human cells. Our screen identified several kinases not previously associated with Hippo signalling that control multiple cellular processes. One of the hits, LKB1, is a common tumour suppressor whose mechanism of action is only partially understood. We demonstrate that LKB1 acts through its substrates of the microtubule affinity-regulating kinase family to regulate the localization of the polarity determinant Scribble and the activity of the core Hippo kinases. Our data also indicate that YAP is functionally important for the tumour suppressive effects of LKB1. Our results identify a signalling axis that links YAP activation with LKB1 mutations, and have implications for the treatment of LKB1-mutant human malignancies. In addition, our findings provide insight into upstream signals of the Hippo–YAP signalling cascade.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "830", "doc_id": "1897324", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: CD44v6 is not associated with constitutive and reprogrammed cancer stem cells driving cancer metastasis.\n\nCANDIDATE_PASSAGE:\nBest--worst scaling: What it can do for health care research and how to do it. Statements like \"quality of care is more highly valued than waiting time\" can neither be supported nor refuted by comparisons of utility parameters from a traditional discrete choice experiment (DCE). Best--worst scaling can overcome this problem because it asks respondents to perform a different choice task. However, whilst the nature of the best--worst task is generally understood, there are a number of issues relating to the design and analysis of a best--worst choice experiment that require further exposition. This paper illustrates how to aggregate and analyse such data and using a quality of life pilot study demonstrates how richer insights can be drawn by the use of best--worst tasks.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "203", "doc_id": "3222122", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The minor G allele of FOXO3 is related to more severe symptoms of Crohn's Disease.\n\nCANDIDATE_ABSTRACT:\nTITLE: Innate lymphoid cells mediate influenza-induced airway hyper-reactivity independently of adaptive immunity\nABSTRACT: Patients with asthma, a major public health problem, are at high risk for serious disease from influenza virus infection, but the pathogenic mechanisms by which influenza A causes airway disease and asthma are not fully known. We show here in a mouse model that influenza infection acutely induced airway hyper-reactivity (AHR), a cardinal feature of asthma, independently of T helper type 2 (TH2) cells and adaptive immunity. Instead, influenza infection induced AHR through a previously unknown pathway that required the interleukin 13 (IL-13)–IL-33 axis and cells of the non-T cell, non-B cell innate lymphoid type called 'natural helper cells'. Infection with influenza A virus, which activates the NLRP3 inflammasome, resulted in much more production of IL-33 by alveolar macrophages, which in turn activated natural helper cells producing substantial IL-13.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1232, "doc_id": "696006", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Headaches are correlated with cognitive impairment.\n\nCANDIDATE_PASSAGE:\nAortic stiffness, blood pressure progression, and incident hypertension. CONTEXT Vascular stiffness increases with advancing age and is a major risk factor for age-related morbidity and mortality. Vascular stiffness and blood pressure pulsatility are related; however, temporal relationships between vascular stiffening and blood pressure elevation have not been fully delineated. OBJECTIVE To examine temporal relationships among vascular stiffness, central hemodynamics, microvascular function, and blood pressure progression. DESIGN, SETTING, AND PARTICIPANTS Longitudinal community-based cohort study conducted in Framingham, Massachusetts. The present investigation is based on the 2 latest examination cycles (cycle 7: 1998-2001; cycle 8: 2005-2008 [last visit: January 25, 2008]) of the Framingham Offspring study (recruited: 1971-1975). Temporal relationships among blood pressure and 3 measures of vascular stiffness and pressure pulsatility derived from arterial tonometry (carotid-femoral pulse wave velocity [CFPWV], forward wave amplitude [FWA], and augmentation index) were examined over a 7-year period in 1759 participants (mean [SD] age: 60 [9] years; 974 women). MAIN OUTCOME MEASURES The primary outcomes were blood pressure and incident hypertension during examination cycle 8. The secondary outcomes were CFPWV, FWA, and augmentation index during examination cycle 8. RESULTS In a multivariable-adjusted regression model, higher FWA (β, 1.3 [95% CI, 0.5-2.1] mm Hg per 1 SD; P = .002) and higher CFPWV (β, 1.5 [95% CI, 0.5-2.6] mm Hg per 1 SD; P = .006) during examination cycle 7 were jointly associated with systolic blood pressure during examination cycle 8. Similarly, in a model that included systolic and diastolic blood pressure and additional risk factors dur [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "500", "doc_id": "30639847", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Microarray results from culture-amplified mixtures of serotypes correlate poorly with microarray results from uncultured mixtures.\n\nCANDIDATE_ABSTRACT:\nTITLE: The PneuCarriage Project: A Multi-Centre Comparative Study to Identify the Best Serotyping Methods for Examining Pneumococcal Carriage in Vaccine Evaluation Studies\nABSTRACT: BACKGROUND The pneumococcus is a diverse pathogen whose primary niche is the nasopharynx. Over 90 different serotypes exist, and nasopharyngeal carriage of multiple serotypes is common. Understanding pneumococcal carriage is essential for evaluating the impact of pneumococcal vaccines. Traditional serotyping methods are cumbersome and insufficient for detecting multiple serotype carriage, and there are few data comparing the new methods that have been developed over the past decade. We established the PneuCarriage project, a large, international multi-centre study dedicated to the identification of the best pneumococcal serotyping methods for carriage studies. METHODS AND FINDINGS Reference sample sets were distributed to 15 research groups for blinded testing. Twenty pneumococcal serotyping methods were used to test 81 laboratory-prepared (spiked) samples. The five top-performing methods were used to test 260 nasopharyngeal (field) samples collected from children in six high-burden countries. Sensitivity and positive predictive value (PPV) were determined for the test methods and the reference method (traditional serotyping of >100 colonies from each sample). For the alternate serotyping methods, the overall sensitivity ranged from 1% to 99% (reference method 98%), and PPV from 8% to 100% (reference method 100%), when testing the spiked samples. Fifteen methods had ≥70% sensitivity to detect the dominant (major) serotype, whilst only eight methods had ≥70% sensitivity to detect minor serotypes. For the field samples, the overall sensitivity ranged from 74.2% to 95.8% (reference method 93.8%), and PPV from 82.2% to 96.4% (reference method 99.6%). The microarray had the highest sensitivity (95.8%) and high PPV (93.7%). The major limitation of this study is th [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 785, "doc_id": "12471115", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is cD44v6 relevant in colorectal tumour progression?\n\nABSTRACT:\nThere is a lack of consensus regarding the role of CD44 variants in colorectal cancer, with conflicting reports regarding their expression and correlation with prognosis. We investigated the expression and prognostic significance of CD44v6 protein in our series of colorectal tumour specimens and then analysed the pattern of CD44 variant mRNA transcript expression in a smaller series of colorectal tumour/normal tissue specimens, thus assessing what our data contributes to this debate. Immunohistochemistry was used to detect CD44v6 protein expression, while reverse transcriptase-polymerase chain reaction in combination with Southern blotting was used to analyse CD44 mRNA transcript expression. Similar levels of expression of CD44v6 protein were observed in each of the Dukes' stages, ranging from 50% to 67%, indicating no correlation with progression of disease or survival rates. CD44 variant mRNA expression was found in 85% of the tumours and 75% of the normal specimens. The majority of tumours expressed each of the variants. The pattern of variant expression was maintained in the corresponding normal tissue in nearly one-half (47%) of the tumour specimens. A sequential pattern of variant expression was observed in the majority of specimens. There was no association between CD44 variant mRNA expression and Dukes' stage, tumour differentiation or survival.", "output": "{\"label\": \"no\", \"rationale\": \"The data reported here, along with those already in the literature, suggest that CD44v6 does not play a pivotal role in colorectal cancer progression. Moreover, due to the pattern of expression of contiguous blocks of variant transcripts it is unlikely that expression of any single variant can predict outcome in vivo.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 12018451, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Are head and neck specific quality of life measures necessary?\n\nABSTRACT:\nThe purpose of this study was to determine whether head and neck-specific health status domains are distinct from those assessed by general measures of quality-of-life (QOL). Cross-sectional study of 55 head and neck cancer patients in tertiary academic center was made. Three head and neck-specific measures,-including the Head&Neck Survey (H&NS); a brief, multi-item test which generates domain scores; and a general health measure,-were administered. The H&NS was highly reliable and more strongly correlated to the specific measures than to the general measure. Eating/swallowing (ES) and speech/communication (SC) were not well correlated with general health domains. Head and neck pain was highly correlated to general bodily pain (0.88, p<.0001). Despite correlations to some general health domains, appearance (AP) was not fully reflected by any other domain.", "output": "{\"label\": \"yes\", \"rationale\": \"Head and neck-specific QOL measures are necessary and should include domains that reflect ES, SC, and AP.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 9278754, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: High cardiopulmonary fitness causes increased mortality rate.\n\nCANDIDATE_ABSTRACT:\nTITLE: Prevalence and cardiovascular disease correlates of low cardiorespiratory fitness in adolescents and adults.\nABSTRACT: CONTEXT Population surveys indicate that physical activity levels are low in the United States. One consequence of inactivity, low cardiorespiratory fitness, is an established risk factor for cardiovascular disease (CVD) morbidity and mortality, but the prevalence of cardiorespiratory fitness has not been quantified in representative US population samples. OBJECTIVES To describe the prevalence of low fitness in the US population aged 12 through 49 years and to relate low fitness to CVD risk factors in this population. DESIGN, SETTING, AND PARTICIPANTS Inception cohort study using data from the cross-sectional nationally representative National Health and Nutrition Examination Survey 1999-2002. Participants were adolescents (aged 12-19 years; n = 3110) and adults (aged 20-49 years; n = 2205) free from previously diagnosed CVD who underwent submaximal graded exercise treadmill testing to achieve at least 75% to 90% of their age-predicted maximum heart rate. Maximal oxygen consumption (VO2max) was estimated by measuring the heart rate response to reference levels of submaximal work. MAIN OUTCOME MEASURES Low fitness defined using percentile cut points of estimated VO2max from existing external referent populations; anthropometric and other CVD risk factors measured according to standard methods. RESULTS Low fitness was identified in 33.6% of adolescents (approximately 7.5 million US adolescents) and 13.9% of adults (approximately 8.5 million US adults); the prevalence was similar in adolescent females (34.4%) and males (32.9%) (P = .40) but was higher in adult females (16.2%) than in males (11.8%) (P = .03). Non-Hispanic blacks and Mexican Americans were less fit than non-Hispanic whites. In all age-sex groups, body mass index and waist circumference were inver [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSION Low fitness in adolescents and adults is common in the US population and is associated with an increased prevalence of CVD risk factors.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 513, "doc_id": "13230773", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Breast cancer development is determined exclusively by genetic factors.\n\nCANDIDATE_PASSAGE:\nGene–environment interactions in 7610 women with breast cancer: prospective evidence from the Million Women Study BACKGROUND Information is scarce about the combined effects on breast cancer incidence of low-penetrance genetic susceptibility polymorphisms and environmental factors (reproductive, behavioural, and anthropometric risk factors for breast cancer). To test for evidence of gene-environment interactions, we compared genotypic relative risks for breast cancer across the other risk factors in a large UK prospective study. METHODS We tested gene-environment interactions in 7610 women who developed breast cancer and 10 196 controls without the disease, studying the effects of 12 polymorphisms (FGFR2-rs2981582, TNRC9-rs3803662, 2q35-rs13387042, MAP3K1-rs889312, 8q24-rs13281615, 2p-rs4666451, 5p12-rs981782, CASP8-rs1045485, LSP1-rs3817198, 5q-rs30099, TGFB1-rs1982073, and ATM-rs1800054) in relation to prospectively collected information about ten established environmental risk factors (age at menarche, parity, age at first birth, breastfeeding, menopausal status, age at menopause, use of hormone replacement therapy, body-mass index, height, and alcohol consumption). FINDINGS After allowance for multiple testing none of the 120 comparisons yielded significant evidence of a gene-environment interaction. By contrast with previous suggestions, there was little evidence that the genotypic relative risks were affected by use of hormone replacement therapy, either overall or for oestrogen-receptor-positive disease. Only one of the 12 polymorphisms was correlated with any of the ten other risk factors: carriers of the high-risk C allele of MAP3K1-rs889312 were significantly shorter than non-carriers (mean height 162.4 cm [95% CI 162.1-162.7] vs 163.1 cm [162.9-16 [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "185", "doc_id": "18340282", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Activation of PPM1D suppresses p53 function.\n\nCANDIDATE_ABSTRACT:\nTITLE: Genetic and Functional Diversification of Small RNA Pathways in Plants\nABSTRACT: Multicellular eukaryotes produce small RNA molecules (approximately 21–24 nucleotides) of two general types, microRNA (miRNA) and short interfering RNA (siRNA). They collectively function as sequence-specific guides to silence or regulate genes, transposons, and viruses and to modify chromatin and genome structure. Formation or activity of small RNAs requires factors belonging to gene families that encode DICER (or DICER-LIKE [DCL]) and ARGONAUTE proteins and, in the case of some siRNAs, RNA-dependent RNA polymerase (RDR) proteins. Unlike many animals, plants encode multiple DCL and RDR proteins. Using a series of insertion mutants of Arabidopsis thaliana, unique functions for three DCL proteins in miRNA (DCL1), endogenous siRNA (DCL3), and viral siRNA (DCL2) biogenesis were identified. One RDR protein (RDR2) was required for all endogenous siRNAs analyzed. The loss of endogenous siRNA in dcl3 and rdr2 mutants was associated with loss of heterochromatic marks and increased transcript accumulation at some loci. Defects in siRNA-generation activity in response to turnip crinkle virus in dcl2 mutant plants correlated with increased virus susceptibility. We conclude that proliferation and diversification of DCL and RDR genes during evolution of plants contributed to specialization of small RNA-directed pathways for development, chromatin structure, and defense.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 70, "doc_id": "1333643", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Nanoparticles can be targeted against specific cell types by incorporating aptamers into lipid nanoparticles.\n\nCANDIDATE_ABSTRACT:\nTITLE: Aptamer-functionalized lipid nanoparticles targeting osteoblasts as a novel RNA interference–based bone anabolic strategy\nABSTRACT: Currently, major concerns about the safety and efficacy of RNA interference (RNAi)-based bone anabolic strategies still exist because of the lack of direct osteoblast-specific delivery systems for osteogenic siRNAs. Here we screened the aptamer CH6 by cell-SELEX, specifically targeting both rat and human osteoblasts, and then we developed CH6 aptamer–functionalized lipid nanoparticles (LNPs) encapsulating osteogenic pleckstrin homology domain-containing family O member 1 (Plekho1) siRNA (CH6-LNPs-siRNA). Our results showed that CH6 facilitated in vitro osteoblast-selective uptake of Plekho1 siRNA, mainly via macropinocytosis, and boosted in vivo osteoblast-specific Plekho1 gene silencing, which promoted bone formation, improved bone microarchitecture, increased bone mass and enhanced mechanical properties in both osteopenic and healthy rodents. These results indicate that osteoblast-specific aptamer-functionalized LNPs could act as a new RNAi-based bone anabolic strategy, advancing the targeted delivery selectivity of osteogenic siRNAs from the tissue level to the cellular level.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Our results showed that CH6 facilitated in vitro osteoblast-selective uptake of Plekho1 siRNA, mainly via macropinocytosis, and boosted in vivo osteoblast-specific Plekho1 gene silencing, which promoted bone formation, improved bone microarchitecture, increased bone mass and enhanced mechanical properties in both osteopenic and healthy rodents.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 839, "doc_id": "1469751", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Ubiquitin ligase UBC13 generates a K63-linked polyubiquitin moiety at PCNA K164.\n\nCANDIDATE_PASSAGE:\nReplication Fork Slowing and Reversal upon DNA Damage Require PCNA Polyubiquitination and ZRANB3 DNA Translocase Activity DNA damage tolerance during eukaryotic replication is orchestrated by PCNA ubiquitination. While monoubiquitination activates mutagenic translesion synthesis, polyubiquitination activates an error-free pathway, elusive in mammals, enabling damage bypass by template switching. Fork reversal is driven in vitro by multiple enzymes, including the DNA translocase ZRANB3, shown to bind polyubiquitinated PCNA. However, whether this interaction promotes fork remodeling and template switching in vivo was unknown. Here we show that damage-induced fork reversal in mammalian cells requires PCNA ubiquitination, UBC13, and K63-linked polyubiquitin chains, previously involved in error-free damage tolerance. Fork reversal in vivo also requires ZRANB3 translocase activity and its interaction with polyubiquitinated PCNA, pinpointing ZRANB3 as a key effector of error-free DNA damage tolerance. Mutations affecting fork reversal also induced unrestrained fork progression and chromosomal breakage, suggesting fork remodeling as a global fork slowing and protection mechanism. Targeting these fork protection systems represents a promising strategy to potentiate cancer chemotherapy.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1337", "doc_id": "20231138", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Androgenetic haploid mouse embryonic stem cells (ESCs) can be derived and genetically manipulated in vitro.\n\nCANDIDATE_PASSAGE:\nDerivation of novel human ground state naive pluripotent stem cells Mouse embryonic stem (ES) cells are isolated from the inner cell mass of blastocysts, and can be preserved in vitro in a naive inner-cell-mass-like configuration by providing exogenous stimulation with leukaemia inhibitory factor (LIF) and small molecule inhibition of ERK1/ERK2 and GSK3β signalling (termed 2i/LIF conditions). Hallmarks of naive pluripotency include driving Oct4 (also known as Pou5f1) transcription by its distal enhancer, retaining a pre-inactivation X chromosome state, and global reduction in DNA methylation and in H3K27me3 repressive chromatin mark deposition on developmental regulatory gene promoters. Upon withdrawal of 2i/LIF, naive mouse ES cells can drift towards a primed pluripotent state resembling that of the post-implantation epiblast. Although human ES cells share several molecular features with naive mouse ES cells, they also share a variety of epigenetic properties with primed murine epiblast stem cells (EpiSCs). These include predominant use of the proximal enhancer element to maintain OCT4 expression, pronounced tendency for X chromosome inactivation in most female human ES cells, increase in DNA methylation and prominent deposition of H3K27me3 and bivalent domain acquisition on lineage regulatory genes. The feasibility of establishing human ground state naive pluripotency in vitro with equivalent molecular and functional features to those characterized in mouse ES cells remains to be defined. Here we establish defined conditions that facilitate the derivation of genetically unmodified human naive pluripotent stem cells from already established primed human ES cells, from somatic cells through induced pluripotent stem (iPS) cell reprogramming or directly from b [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "111", "doc_id": "4462419", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Pleiotropic coupling of GLP-1R to intracellular effectors promotes distinct profiles of cellular signaling.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Extracellular Surface of the GLP-1 Receptor Is a Molecular Trigger for Biased Agonism\nABSTRACT: Ligand-directed signal bias offers opportunities for sculpting molecular events, with the promise of better, safer therapeutics. Critical to the exploitation of signal bias is an understanding of the molecular events coupling ligand binding to intracellular signaling. Activation of class B G protein-coupled receptors is driven by interaction of the peptide N terminus with the receptor core. To understand how this drives signaling, we have used advanced analytical methods that enable separation of effects on pathway-specific signaling from those that modify agonist affinity and mapped the functional consequence of receptor modification onto three-dimensional models of a receptor-ligand complex. This yields molecular insights into the initiation of receptor activation and the mechanistic basis for biased agonism. Our data reveal that peptide agonists can engage different elements of the receptor extracellular face to achieve effector coupling and biased signaling providing a foundation for rational design of biased agonists.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 956, "doc_id": "12956194", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: MEK inhibitors are effective treatments in RAS-driven mouse models of cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effective Use of PI3K and MEK Inhibitors to Treat Mutant K-Ras G12D and PIK3CA H1047R Murine Lung Cancers\nABSTRACT: Somatic mutations that activate phosphoinositide 3-kinase (PI3K) have been identified in the p110-alpha catalytic subunit (encoded by PIK3CA). They are most frequently observed in two hotspots: the helical domain (E545K and E542K) and the kinase domain (H1047R). Although the p110-alpha mutants are transforming in vitro, their oncogenic potential has not been assessed in genetically engineered mouse models. Furthermore, clinical trials with PI3K inhibitors have recently been initiated, and it is unknown if their efficacy will be restricted to specific, genetically defined malignancies. In this study, we engineered a mouse model of lung adenocarcinomas initiated and maintained by expression of p110-alpha H1047R. Treatment of these tumors with NVP-BEZ235, a dual pan-PI3K and mammalian target of rapamycin (mTOR) inhibitor in clinical development, led to marked tumor regression as shown by positron emission tomography-computed tomography, magnetic resonance imaging and microscopic examination. In contrast, mouse lung cancers driven by mutant Kras did not substantially respond to single-agent NVP-BEZ235. However, when NVP-BEZ235 was combined with a mitogen-activated protein kinase kinase (MEK) inhibitor, ARRY-142886, there was marked synergy in shrinking these Kras-mutant cancers. These in vivo studies suggest that inhibitors of the PI3K-mTOR pathway may be active in cancers with PIK3CA mutations and, when combined with MEK inhibitors, may effectively treat KRAS mutated lung cancers.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"However, when NVP-BEZ235 was combined with a mitogen-activated protein kinase kinase (MEK) inhibitor, ARRY-142886, there was marked synergy in shrinking these Kras-mutant cancers.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 734, "doc_id": "4961038", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Female carriers of the Apolipoprotein E4 (APOE4) allele have longer lifetime exposure to estrogen due to an increased reproductive period.\n\nCANDIDATE_PASSAGE:\nBax translocation and mitochondrial fragmentation induced by Helicobacter pylori. BACKGROUND AND AIMS Previous in vitro and in vivo studies have revealed an association between Helicobacter pylori infection and apoptosis in gastric epithelial cells. Although involvement of the Bcl-2 family of proteins as well as cytochrome c release has been demonstrated in H pylori induced cell death, the exact role of the mitochondria during this type of programmed cell death has not been fully elucidated. Therefore, we sought to determine whether or not Bax translocation and mitochondrial fragmentation occur on exposure of gastric epithelial cells to H pylori, resulting in cell death. METHODS Experiments were performed with human gastric adenocarcinoma (AGS) cells, AGS cells transfected with the HPV-E6 gene (which inactivates p53 function), AGS-neo cells (transfected with the backbone construct), mouse embryonic fibroblasts (MEFs), and p19(ARF) null (ARF(-/-)) MEFs. Cells were incubated with a cag positive H pylori strain for up to 24 hours, lysed, and cytoplasmic and mitochondrial membrane fractions were analysed by western blot for Bax translocation. RESULTS Bax translocation was detected in AGS, AGS-neo, and normal MEF cells after exposure to H pylori for three hours, but not in ARF(-/-) MEFs cells. Translocation of Bax after H pylori incubation was also detected in AGS-E6 cells (inactive p53 gene) but to a lesser degree than in AGS-neo cells. In parallel studies, the mitochondrial morphology of living cells infected with H pylori was assessed by confocal microscopy. Mitochondrial fragmentation was detectable after 10 hours of H pylori incubation with AGS cells and after seven hours with MEF cells. In wild-type MEFs, mitochondrial fragmentation was significantly increa [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "416", "doc_id": "8654183", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The peak incidence of fractures occurs in toddlers.\n\nCANDIDATE_PASSAGE:\nIncidence of childhood distal forearm fractures over 30 years: a population-based study. CONTEXT The incidence of distal forearm fractures in children peaks around the time of the pubertal growth spurt, possibly because physical activity increases at the time of a transient deficit in cortical bone mass due to the increased calcium demand during maximal skeletal growth. Changes in physical activity or diet may therefore influence risk of forearm fracture. OBJECTIVE To determine whether there has been a change in the incidence of distal forearm fractures in children in recent years. DESIGN, SETTING, AND PATIENTS Population-based study among Rochester, Minn, residents younger than 35 years with distal forearm fractures in 1969-1971, 1979-1981, 1989-1991, and 1999-2001. MAIN OUTCOME MEASURE Estimated incidence of distal forearm fractures in 4 time periods. RESULTS Comparably age- and sex-adjusted annual incidence rates per 100 000 increased from 263.3 (95% confidence interval [CI], 231.1-295.4) in 1969-1971 to 322.3 (95% CI, 285.3-359.4) in 1979-1981 and to 399.8 (95% CI, 361.0-438.6) in 1989-1991 before leveling off at 372.9 (95% CI, 339.1-406.7) in 1999-2001. Age-adjusted incidence rates per 100 000 were 32% greater among male residents in 1999-2001 compared with 1969-1971 (409.4 [95% CI, 359.9-459.0] vs 309.4 [95% CI, 259.3-359.5]; P =.01) and 56% greater among female residents in the same time periods (334.3 [95% CI, 288.6-380.1] vs 214.6 [95% CI, 174.9-254.4]; P<.001). The peak incidence and greatest increase occurred between ages 11 and 14 years in boys and 8 and 11 years in girls. CONCLUSIONS There has been a statistically significant increase in the incidence of distal forearm fractures in children and adolescents, but whether this is due to changing pa [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1249", "doc_id": "7209559", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: A 100g dose of chloroquine chemoprophylactic regimen results in retinal toxicity after 1 year of weekly intake.\n\nCANDIDATE_PASSAGE:\nTreatment of active tuberculosis in HIV-coinfected patients: a systematic review and meta-analysis. BACKGROUND Patients with human immunodeficiency virus (HIV) infection and tuberculosis have an increased risk of death, treatment failure, and relapse. METHODS A systematic review and meta-analysis of randomized, controlled trials and cohort studies was conducted to evaluate the impact of duration and dosing schedule of rifamycin and use of antiretroviral therapy in the treatment of active tuberculosis in HIV-positive patients. In included studies, the initial tuberculosis diagnosis, failure, and/or relapse were microbiologically confirmed, and patients received standardized rifampin- or rifabutin-containing regimens. Pooled cumulative incidence of treatment failure, death during treatment, and relapse were calculated using random-effects models. Multivariable meta-regression was performed using negative binomial regression. RESULTS After screening 5158 citations, 6 randomized trials and 21 cohort studies were included. Relapse was more common with regimens using 2 months rifamycin (adjusted risk ratio, 3.6; 95% confidence interval, 1.1-11.7) than with regimens using rifamycin for at least 8 months. Compared with daily therapy in the initial phase (n=3352 patients from 35 study arms), thrice-weekly therapy (n=211 patients from 5 study arms) was associated with higher rates of failure (adjusted risk ratio, 4.0; 95% confidence interval, 1.5-10.4) and relapse [adjusted risk ratio, 4.8; 95% confidence interval, 1.8-12.8). There were trends toward higher relapse rates if rifamycins were used for only 6 months, compared with > or =8 months, or if antiretroviral therapy was not used. CONCLUSIONS This review raises serious concerns regarding current recommendations fo [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "26", "doc_id": "31363207", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does rugby headgear prevent concussion?\n\nABSTRACT:\nTo examine the attitudes of players and coaches to the use of protective headgear, particularly with respect to the prevention of concussion. A questionnaire designed to assess attitudes to headgear was administered to 63 players from four different Canadian teams, each representing a different level of play (high school, university, community club, national). In addition, coaches from all four levels were questioned about team policies and their personal opinions about the use of headgear to prevent concussion. Although the players tended to believe that the headgear could prevent concussion (62%), the coaches were less convinced (33%). Despite the players' belief that headgear offers protection against concussion, only a minority reported wearing headgear (27%) and few (24%) felt that its use should be made mandatory. Common reasons for not wearing headgear were \"its use is not mandatory\", \"it is uncomfortable\", and \"it costs too much\".", "output": "{\"label\": \"maybe\", \"rationale\": \"Although most players in the study believe that rugby headgear may prevent concussion, only a minority reported wearing it. Coaches tended to be less convinced than the players that rugby headgear can prevent concussion.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 11867487, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Macrolides protect against myocardial infarction.\n\nCANDIDATE_ABSTRACT:\nTITLE: Antibiotics and risk of subsequent first-time acute myocardial infarction.\nABSTRACT: CONTEXT Increasing evidence supports the hypothesis of a causal association between certain bacterial infections and increased risk of developing acute myocardial infarction. If such a causal association exists, subjects who used antibiotics active against the bacteria, regardless of indication, might be at lower risk of developing acute myocardial infarction than nonusers. OBJECTIVE To determine whether previous use of antibiotics decreases the risk of developing a first-time acute myocardial infarction. DESIGN Population-based case-control analysis. SETTING The United Kingdom-based General Practice Research Database comprising 350 general practices. PATIENTS A total of 3315 case patients aged 75 years or younger with a diagnosis of first-time acute myocardial infarction between 1992 and 1997 and 13139 controls without myocardial infarction matched to cases for age, sex, general practice attended, and calendar time. MAIN OUTCOME MEASURES Use of antibiotics among those who did or did not have a first-time acute myocardial infarction. RESULTS Cases were significantly less likely to have used tetracycline antibiotics (adjusted odds ratio [OR], 0.70; 95% confidence interval [CI], 0.55-0.90) or quinolones (adjusted OR, 0.45; 95% CI, 0.21-0.95). No effect was found for previous use of macrolides (primarily erythromycin), sulfonamides, penicillins, or cephalosporins. CONCLUSIONS The findings from this large case-control analysis provide further, albeit indirect, evidence for an association between bacterial infections with organisms susceptible to tetracycline or quinolone antibiotics and the risk of acute myocardial infarction. These results of preliminary nature should stimulate more research to further explore the role of infections in the etiology of acute myo [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"No effect was found for previous use of macrolides (primarily erythromycin), sulfonamides, penicillins, or cephalosporins.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 743, "doc_id": "32159283", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pioglitazone use is not associated with an increased risk of prostate cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pioglitazone Use and Risk of Bladder Cancer and Other Common Cancers in Persons With Diabetes.\nABSTRACT: IMPORTANCE Studies suggest pioglitazone use may increase risk of cancers. OBJECTIVE To examine whether pioglitazone use for diabetes is associated with risk of bladder and 10 additional cancers. DESIGN, SETTING, AND PARTICIPANTS Cohort and nested case-control analyses among persons with diabetes. A bladder cancer cohort followed 193,099 persons aged 40 years or older in 1997-2002 until December 2012; 464 case patients and 464 matched controls were surveyed about additional confounders. A cohort analysis of 10 additional cancers included 236,507 persons aged 40 years or older in 1997-2005 and followed until June 2012. Cohorts were from Kaiser Permanente Northern California. EXPOSURES Ever use, duration, cumulative dose, and time since initiation of pioglitazone as time dependent. MAIN OUTCOMES AND MEASURES Incident cancer, including bladder, prostate, female breast, lung/bronchus, endometrial, colon, non-Hodgkin lymphoma, pancreas, kidney/renal pelvis, rectum, and melanoma. RESULTS Among 193,099 persons in the bladder cancer cohort, 34,181 (18%) received pioglitazone (median duration, 2.8 years; range, 0.2-13.2 years) and 1261 had incident bladder cancer. Crude incidences of bladder cancer in pioglitazone users and nonusers were 89.8 and 75.9 per 100,000 person-years, respectively. Ever use of pioglitazone was not associated with bladder cancer risk (adjusted hazard ratio [HR], 1.06; 95% CI, 0.89-1.26). Results were similar in case-control analyses (pioglitazone use: 19.6% among case patients and 17.5% among controls; adjusted odds ratio, 1.18; 95% CI, 0.78-1.80). In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95% CI, 1.02-1.26) and p [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The increased prostate and pancreatic cancer risks associated with ever use of pioglitazone merit further investigation to assess whether they are causal or are due to chance, residual confounding, or reverse causality.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 952, "doc_id": "3355397", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: H4 G94P proteins suppress degradation of free histones via Rad53-dependent mechanisms.\n\nCANDIDATE_PASSAGE:\nTit-for-Tat: Type VI Secretion System Counterattack during Bacterial Cell-Cell Interactions The bacterial type VI secretion system (T6SS) is a dynamic organelle that bacteria use to target prey cells for inhibition via translocation of effector proteins. Time-lapse fluorescence microscopy has documented striking dynamics of opposed T6SS organelles in adjacent sister cells of Pseudomonas aeruginosa. Such cell-cell interactions have been termed \"T6SS dueling\" and likely reflect a biological process that is driven by T6SS antibacterial attack. Here, we show that T6SS dueling behavior strongly influences the ability of P. aeruginosa to prey upon heterologous bacterial species. We show that, in the case of P. aeruginosa, T6SS-dependent killing of either Vibrio cholerae or Acinetobacter baylyi is greatly stimulated by T6SS activity occurring in those prey species. Our data suggest that, in P. aeruginosa, T6SS organelle assembly and lethal counterattack are regulated by a signal that corresponds to the point of attack of the T6SS apparatus elaborated by a second aggressive T6SS(+) bacterial cell. PAPERFLICK:", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "487", "doc_id": "7145763", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is macular Retinal Ganglion Cell Layer Thickness Reduced in Patients with Obstructive Sleep Apnea?\n\nABSTRACT:\nTo evaluate macular ganglion cell layer (GCL) and ganglion cell-inner plexiform layer (GCIPL) thicknesses in patients with obstructive sleep apnea (OSA) syndrome. 73 OSA patients and 67 age-matched controls were consecutively and prospectively enrolled. All participants underwent at least one reliable standard automated perimetry (SAP) and were imaged with spectral-domain optical coherence tomography (OCT) using two different devices. The OCT parameters were compared between groups, and Pearson correlations between main indices of SAP and OCT parameters were calculated. The pattern standard deviation of SAP was higher in the OSA group (p = 0.001). Mean GCIPL thickness was 82.99 ± 10.30 and 80.78 ± 12.15 µm in the control and OSA groups, respectively (p = 0.25), and GCL thickness was 44.93 ± 11.42 µm in the control group and 48.81 ± 10.85 µm in OSA individuals (p = 0.47). Pearson correlations between the GCIPL-GCL measurements and the main indices of SAP were not significant.", "output": "{\"label\": \"no\", \"rationale\": \"Neither GCIPL nor GCL thickness were reduced in OSA subjects compared with healthy individuals. Retinal sensitivity evaluated with SAP was however decreased in OSA patients.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 27192975, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Lack of FGF21 in mice slows the rate of atherosclerotic plaque formation.\n\nCANDIDATE_PASSAGE:\nIslet1 deletion causes kidney agenesis and hydroureter resembling CAKUT. Islet1 (Isl1) is a transcription factor transiently expressed in a subset of heart and limb progenitors. During studies of limb development, conditional Isl1 deletion produced unexpected kidney abnormalities. Here, we studied the renal expression of Isl1 and whether it has a role in kidney development. In situ hybridization revealed Isl1 expression in the mesenchymal cells surrounding the base of the ureteric bud in mice. Conditional deletion of Isl1 caused kidney agenesis or hypoplasia and hydroureter, a phenotype resembling human congenital anomalies of the kidney and urinary tract (CAKUT). The absence of Isl1 led to ectopic branching of the ureteric bud out from the nephric duct or to the formation of accessory buds, both of which could lead to obstruction of the ureter-bladder junction and consequent hydroureter. The abnormal elongation and poor branching of the ureteric buds were the likely causes of the kidney agenesis or hypoplasia. Furthermore, the lack of Isl1 reduced the expression of Bmp4, a gene implicated in the CAKUT-like phenotype, in the metanephric region before ureteric budding. In conclusion, Isl1 is essential for proper development of the kidney and ureter by repressing the aberrant formation of the ureteric bud. These observations call for further studies to investigate whether Isl1 may be a causative gene for human CAKUT.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "683", "doc_id": "26008063", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Ivermectin is used to treat lymphatic filariasis.\n\nCANDIDATE_PASSAGE:\nPersistent human papillomavirus infection and cervical neoplasia: a systematic review and meta-analysis. Detection of persistent cervical carcinogenic human papillomavirus (HPV) DNA is used as a marker for cervical cancer risk in clinical trials. The authors performed a systematic review and meta-analysis of the association between persistent HPV DNA and high-grade cervical intraepithelial neoplasia (CIN2-3), high-grade squamous intraepithelial lesions (HSIL), and invasive cervical cancer (together designated CIN2-3/HSIL+) to evaluate the robustness of HPV persistence for clinical use. MEDLINE and Current Contents were searched through January 30, 2006. Relative risks (RRs) were stratified by HPV comparison group. Of 2,035 abstracts, 41 studies were eligible for inclusion in the meta-analysis. Over 22,500 women were included in calculation of RRs for persistent HPV DNA detection and cervical neoplasia. RRs ranged from 1.3 (95% confidence interval: 1.1, 1.5) to 813.0 (95% confidence interval: 168.2, 3,229.2) for CIN2-3/HSIL+ versus 12 months), wider testing intervals, CIN2-3/HSIL+, and use of an HPV-negative reference group were consistently associated with higher RRs. Thus, HPV persistence was consistently and strongly associated with CIN2-3/HSIL+, despite wide variation in definitions and study methods. The magnitude of association varied by duration of persistence and testing interval. Precise definition and standardization of HPV testing, sampling procedure, and test interval are needed for reliable clinical testing. These findings validate HPV persistence as a clinical marker and endpoint.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "659", "doc_id": "13857083", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Binding of p53 to enhancer regions (p53BERs) regulates the activity of p53 transcription and cell cycle arrest through the production of p53-dependent eRNAs.\n\nCANDIDATE_ABSTRACT:\nTITLE: eRNAs are required for p53-dependent enhancer activity and gene transcription.\nABSTRACT: Binding within or nearby target genes involved in cell proliferation and survival enables the p53 tumor suppressor gene to regulate their transcription and cell-cycle progression. Using genome-wide chromatin-binding profiles, we describe binding of p53 also to regions located distantly from any known p53 target gene. Interestingly, many of these regions possess conserved p53-binding sites and all known hallmarks of enhancer regions. We demonstrate that these p53-bound enhancer regions (p53BERs) indeed contain enhancer activity and interact intrachromosomally with multiple neighboring genes to convey long-distance p53-dependent transcription regulation. Furthermore, p53BERs produce, in a p53-dependent manner, enhancer RNAs (eRNAs) that are required for efficient transcriptional enhancement of interacting target genes and induction of a p53-dependent cell-cycle arrest. Thus, our results ascribe transcription enhancement activity to p53 with the capacity to regulate multiple genes from a single genomic binding site. Moreover, eRNA production from p53BERs is required for efficient p53 transcription enhancement.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Moreover, eRNA production from p53BERs is required for efficient p53 transcription enhancement.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 177, "doc_id": "9669099", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Human embryonic stem cells give rise to cell types from all three embryonic germ layers.\n\nCANDIDATE_ABSTRACT:\nTITLE: Establishment and in vitro differentiation of a new embryonic stem cell line from human blastocyst.\nABSTRACT: Embryonic stem cells have the ability to remain undifferentiated and proliferate indefinitely in vitro while maintaining the potential to differentiate into derivatives of all three embryonic germ layers. These cells have, therefore, potential for in vitro differentiation studies, gene function, and so on. The aim of this study was to produce a human embryonic stem cell line. An inner cell mass of a human blastocyst was separated and cultured on mouse embryonic fibroblasts in embryonic stem cell medium with related additives. The established line was evaluated by morphology; passaging; freezing and thawing; alkaline phosphatase; Oct-4 expression; anti-surface markers including Tra-1-60 and Tra-1-81; and karyotype and spontaneous differentiation. Differentiated cardiomyocytes and neurons were evaluated by transmission electron microscopy and immunocytochemistry. Here, we report the derivation of a new embryonic stem cell line (Royan H1) from a human blastocyst that remains undifferentiated in morphology during continuous passaging for more than 30 passages, maintains a normal XX karyotype, is viable after freezing and thawing, and expresses alkaline phosphatase, Oct-4, Tra-1-60, and Tra-1-81. These cells remain undifferentiated when grown on mouse embryonic fibroblast feeder layers in the presence or absence of recombinant human leukemia inhibitory factor. Royan H1 cells can differentiate in vitro in the absence of feeder cells and can produce embryoid bodies that can further differentiate into beating cardiomyocytes as well as neurons. These results define Royan H1 cells as a new human embryonic stem cell line.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Embryonic stem cells have the ability to remain undifferentiated and proliferate indefinitely in vitro while maintaining the potential to differentiate into derivatives of all three embryonic germ layers.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 529, "doc_id": "36651210", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The combination of H3K4me3 and H3K79me2 is found in quiescent hair follicle stem cells.\n\nCANDIDATE_PASSAGE:\nWnt5a functions in planar cell polarity regulation in mice. Planar cell polarity (PCP) refers to the polarization of cells within the plane of a cell sheet. A distinctive epithelial PCP in vertebrates is the uniform orientation of stereociliary bundles of the sensory hair cells in the mammalian cochlea. In addition to establishing epithelial PCP, planar polarization is also required for convergent extension (CE); a polarized cellular movement that occurs during neural tube closure and cochlear extension. Studies in Drosophila and vertebrates have revealed a conserved PCP pathway, including Frizzled (Fz) receptors. Here we use the cochlea as a model system to explore the involvement of known ligands of Fz, Wnt morphogens, in PCP regulation. We show that Wnt5a forms a reciprocal expression pattern with a Wnt antagonist, the secreted frizzled-related protein 3 (Sfrp3 or Frzb), along the axis of planar polarization in the cochlear epithelium. We further demonstrate that Wnt5a antagonizes Frzb in regulating cochlear extension and stereociliary bundle orientation in vitro, and that Wnt5a(-/-) animals have a shortened and widened cochlea. Finally, we show that Wnt5a is required for proper subcellular distribution of a PCP protein, Ltap/Vangl2, and that Wnt5a interacts genetically with Ltap/Vangl2 for uniform orientation of stereocilia, cochlear extension, and neural tube closure. Together, these findings demonstrate that Wnt5a functions in PCP regulation in mice.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1204", "doc_id": "18575183", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Articles published in open access format are less likely to be cited than traditional journals.\n\nCANDIDATE_ABSTRACT:\nTITLE: Open Access Increases Citation Rate\nABSTRACT: PLoS Biology publishes today a research article by Gunther Eysenbach that is not about biology. It is about citations. It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles. As such, it adds objective support to the belief we have always held that open-access publication speeds up scientific dialog between researchers and, consequently, should be extended to the whole scientific literature as quickly as possible. It is therefore fitting that we publish such a paper. We have long argued that papers freely available in a journal will be more often read and cited than those behind a subscription barrier. However, solid evidence to support or refute such a claim has been surprisingly hard to find. Since most open-access journals are new, comparisons of the effects of open access with established subscription-based journals are easily confounded by age and reputation. In the current study, Eysenbach compared citations compiled by Thomson Scientific (formerly Thomson ISI) to individual articles published between June 2004 and December 2004 in the same journal—namely, Proceedings of the National Academy of Sciences (PNAS), which announced its open-access option for authors on June 8 of that year, with an associated publication charge of US$1,000. Non-OA articles in PNAS are subject to a six-month “toll-access” delay before the article becomes publicly available. The results of this natural experiment are clear: in the 4 to 16 months following publication, OA articles gained a significant citation advantage over non-OA articles during the same period. They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely between 10 and 16 months. Given that P [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 129, "doc_id": "27768226", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Increased microtubule acetylation exacerbates LRRK2 Roc-COR domain mutation induced locomotor deficits.\n\nCANDIDATE_ABSTRACT:\nTITLE: Increasing microtubule acetylation rescues axonal transport and locomotor deficits caused by LRRK2 Roc-COR domain mutations\nABSTRACT: Leucine-rich repeat kinase 2 (LRRK2) mutations are the most common genetic cause of Parkinson's disease. LRRK2 is a multifunctional protein affecting many cellular processes and has been described to bind microtubules. Defective microtubule-based axonal transport is hypothesized to contribute to Parkinson's disease, but whether LRRK2 mutations affect this process to mediate pathogenesis is not known. Here we find that LRRK2 containing pathogenic Roc-COR domain mutations (R1441C, Y1699C) preferentially associates with deacetylated microtubules, and inhibits axonal transport in primary neurons and in Drosophila, causing locomotor deficits in vivo. In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport. In vivo knockdown of the deacetylases HDAC6 and Sirt2, or administration of TSA rescues both axonal transport and locomotor behavior. Thus, this study reveals a pathogenic mechanism and a potential intervention for Parkinson's disease.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 612, "doc_id": "9638032", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Lack of FGF21 in mice slows the rate of atherosclerotic plaque formation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Fibroblast Growth Factor 21 Prevents Atherosclerosis by Suppression of Hepatic Sterol Regulatory Element-Binding Protein-2 and Induction of Adiponectin in Mice\nABSTRACT: BACKGROUND Fibroblast growth factor 21 (FGF21) is a metabolic hormone with pleiotropic effects on glucose and lipid metabolism and insulin sensitivity. It acts as a key downstream target of both peroxisome proliferator-activated receptor α and γ, the agonists of which have been used for lipid lowering and insulin sensitization, respectively. However, the role of FGF21 in the cardiovascular system remains elusive. METHODS AND RESULTS The roles of FGF21 in atherosclerosis were investigated by evaluating the impact of FGF21 deficiency and replenishment with recombinant FGF21 in apolipoprotein E(-/-) mice. FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia. Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia. Chronic treatment with adiponectin partially reverses atherosclerosis without obvious effects on hypercholesterolemia in FGF21-deficient apolipoprotein E(-/-) mice. By contrast, the cholesterol-lowering effects of FGF21 are abrogated by hepatic expression of sterol regulatory element-binding protein-2. CONCLUSIONS FGF21 protects against atherosclerosis via fine tuning the multiorgan crosstalk among liver, adipose tissue, and blood vessels.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS FGF21 protects against atherosclerosis via fine tuning the multiorgan crosstalk among liver, adipose tissue, and blood vessels.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 683, "doc_id": "9315213", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is ulcerative colitis as common in Crete as in northern Europe : a 5-year prospective study?\n\nABSTRACT:\nTo study the incidence of ulcerative colitis and to analyse the pattern of the disease in the prefecture of Heraklion, Crete. The population at risk comprised 263,670 inhabitants in the prefecture of Heraklion (2641 km2). The two regional hospitals, five health centres, 109 private family doctors and 145 specialists participated in the study. A prospective and population-based epidemiological study of ulcerative colitis over five years from 1990 to the end of 1994. Overall, 117 patients with ulcerative colitis (75 males and 42 females) were newly diagnosed during the study period. The mean annual incidence of the disease for the years 1990-1994 was 8.9 per 10(5) inhabitants (95% CI 7.2-10.4). The male to female ratio was 1.8:1. There were no significant difference between the age-specific incidences of the age groups. The majority (51.3%) of the patients were exsmokers and one-third had never smoked. A family history of first-degree relatives positive for inflammatory bowel disease was obtained in 9.6% of our patients.", "output": "{\"label\": \"yes\", \"rationale\": \"Ulcerative colitis is common in Crete; its incidence is as high as in Northern Europe.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 8889457, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: CX3CR1 on the Th2 cells suppresses airway inflammation.\n\nCANDIDATE_PASSAGE:\nCX3CR1 is required for airway inflammation by promoting T helper cell survival and maintenance in inflamed lung Allergic asthma is a T helper type 2 (T(H)2)-dominated disease of the lung. In people with asthma, a fraction of CD4(+) T cells express the CX3CL1 receptor, CX3CR1, and CX3CL1 expression is increased in airway smooth muscle, lung endothelium and epithelium upon allergen challenge. Here we found that untreated CX3CR1-deficient mice or wild-type (WT) mice treated with CX3CR1-blocking reagents show reduced lung disease upon allergen sensitization and challenge. Transfer of WT CD4(+) T cells into CX3CR1-deficient mice restored the cardinal features of asthma, and CX3CR1-blocking reagents prevented airway inflammation in CX3CR1-deficient recipients injected with WT T(H)2 cells. We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma. CX3CR1-induced survival was also observed for T(H)1 cells upon airway inflammation but not under homeostatic conditions or upon peripheral inflammation. Therefore, CX3CR1 and CX3CL1 may represent attractive therapeutic targets in asthma.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "219", "doc_id": "21366394", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is a mandatory general surgery rotation necessary in the surgical clerkship?\n\nABSTRACT:\nChanges in the spectrum of general surgery and the delivery of surgical care have placed the requirement for a mandatory general surgery rotation in the surgical clerkship in question. We tested the hypothesis that equal mastery of surgical clerkship objectives can be obtained in a clerkship with and without general surgery. Students chose any two surgical rotations and were assessed by written examination, objective structured clinical examination (OSCE), ward evaluations, self-assessment objectives questionnaire, and satisfaction survey. Data for 54 students showed no differences in scores between groups on any parameter. No specific concerns related to the absence of general surgery were identified.", "output": "{\"label\": \"no\", \"rationale\": \"Effective undergraduate surgical education can be offered in many specialty settings. Removal of the requirement for general surgery in clerkship may lead to a more effective use of all educational opportunities. A careful analysis of local programs and facilities is necessary before suggesting this change to other institutions.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 9645785, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does endothelium-derived endothelin-1 reduce cerebral artery sensitivity to nitric oxide by a protein kinase C-independent pathway?\n\nABSTRACT:\nNitric oxide (NO) reduces endothelin-1 (ET-1) production and blunts ET-1 dependent vasoconstriction. The direct effects of smooth muscle ET(A) receptor stimulation on NO-mediated relaxation are unknown. We hypothesized that endothelium-derived ET-1 regulates vascular tone by reducing smooth muscle sensitivity to NO, possibly through activation of protein kinase C (PKC). Rings of rabbit middle cerebral artery were mounted on microvessel myographs to measure isometric tension. Dose-response curves to acetylcholine (ACh) and sodium nitroprusside (SNP; an NO donor) were obtained with or without ET-1 receptor blockade. Experiments were performed in the presence of indomethacin (10 micromol/L). Results are expressed as mean+/-SEM. In depolarized conditions (40 mmol/L KCl physiological solution), ACh-induced relaxation was entirely NO-dependent, as indicated by its suppression by N(omega)-nitro-L-arginine (P<0.05). Arterial sensitivity (pD(2)) to ACh (6.32+/-0.11, n=6) was increased (P<0.05) to 6.77+/-0.10 (n=6) by BQ123 (ET(A) receptor antagonist, 5 micromol/L) but not by BQ788 (ET(B) receptor antagonist, 5 micromol/L; 6.08+/-0.22, n=5). Consistent with this finding, blockade of ET(A) receptors increased (P<0.05) vascular sensitivity to SNP (6.95+/-0.10, n=8), whereas BQ788 had no influence on arterial sensitivity to SNP (6.17+/-0.07, n=7) compared with control (6.43+/-0.13, n=11). In denuded arteries, the sensitivity to SNP (7.10+/-0.08, n=8) was reduced by exogenous ET-1 (6.51+/-0.35, n=7, P<0.05). Chelerythrine, a PKC inhibitor, did not alter smooth muscle sensitivity to NO, whereas phorbol 12-myristate 13-acetate, a PKC activator, strongly increased it.", "output": "{\"label\": \"yes\", \"rationale\": \"Blockade of ET(A) but not ET(B) receptors sensitizes vascular smooth muscle to exogenous and endothelium-derived NO. This suggests that ET-1 regulates smooth muscle sensitivity to NO by a PKC-independent pathway. This represents an alternative pathway by which NO and ET-1 interact to regulate vascular tone.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 11588325, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Carriers of the alcohol aldehyde dehydrogenase deficiency mutation drink less that non-carries.\n\nCANDIDATE_ABSTRACT:\nTITLE: Brain-Specific Phosphorylation of MeCP2 Regulates Activity-Dependent Bdnf Transcription, Dendritic Growth, and Spine Maturation\nABSTRACT: Mutations or duplications in MECP2 cause Rett and Rett-like syndromes, neurodevelopmental disorders characterized by mental retardation, motor dysfunction, and autistic behaviors. MeCP2 is expressed in many mammalian tissues and functions as a global repressor of transcription; however, the molecular mechanisms by which MeCP2 dysfunction leads to the neural-specific phenotypes of RTT remain poorly understood. Here, we show that neuronal activity and subsequent calcium influx trigger the de novo phosphorylation of MeCP2 at serine 421 (S421) by a CaMKII-dependent mechanism. MeCP2 S421 phosphorylation is induced selectively in the brain in response to physiological stimuli. Significantly, we find that S421 phosphorylation controls the ability of MeCP2 to regulate dendritic patterning, spine morphogenesis, and the activity-dependent induction of Bdnf transcription. These findings suggest that, by triggering MeCP2 phosphorylation, neuronal activity regulates a program of gene expression that mediates nervous system maturation and that disruption of this process in individuals with mutations in MeCP2 may underlie the neural-specific pathology of RTT.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 230, "doc_id": "1964163", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Diabetes remission occurs less in people treated with conventional therapy than in people treated with laparoscopic adjustable gastric banding surgery.\n\nCANDIDATE_PASSAGE:\nKnowledge of young African American adults about heart disease: a cross-sectional survey BACKGROUND African Americans have higher rates of cardiovascular disease (CVD) mortality than other ethnic groups. Young adults are prime targets for intervention strategies to prevent and reduce disease risk. The study purpose was to determine the level of knowledge of lifestyle risk factors for CVD among young African American adults in Phoenix. The results will be used to guide the development of CVD outreach programs targeted to this population. The Health Belief Model was used as a conceptual framework. METHODS A convenience sample of 172 African American men and women aged 18-26 years completed a questionnaire adapted from the American Heart Association national surveys. Descriptive statistics were compared by age, gender, education level, and health status variables including BMI, smoking status, and physical activity. RESULTS Some aspects of heart-disease were well known among young adult African Americans. Knowledge of certain other important risk factors (menopause) and preventive behaviors (eating fewer animal products), however, was more variable and inconsistent among the respondents. Differences in knowledge of individual variables was greater by education level than by gender overall. Predictors of a summary CVD knowledge score included higher education, female gender, and high self-efficacy (adjusted R2 = 0.158, p < .001). Predictors of self-efficacy in changing CVD risk were higher education and perceived low risk of CVD (adjusted R2 = 0.064, p < .001), but these characteristics explained only 6% of the variance. CONCLUSIONS Evaluation of baseline knowledge of CVD is essential before designing and implementing health promotion programs. Existing strength [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "340", "doc_id": "17914395", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: 4-PBA treatment raises endoplasmic reticulum stress in response to general endoplasmic reticulum stress markers.\n\nCANDIDATE_PASSAGE:\nWolfram syndrome 1 and adenylyl cyclase 8 interact at the plasma membrane to regulate insulin production and secretion Endoplasmic reticulum (ER) stress causes pancreatic β-cell dysfunction and contributes to β-cell loss and the progression of type 2 diabetes. Wolfram syndrome 1 (WFS1) has been shown to be an important regulator of the ER stress signalling pathway; however, its role in β-cell function remains unclear. Here we provide evidence that WFS1 is essential for glucose- and glucagon-like peptide 1 (GLP-1)-stimulated cyclic AMP production and regulation of insulin biosynthesis and secretion. Stimulation with glucose causes WFS1 translocation from the ER to the plasma membrane, where it forms a complex with adenylyl cyclase 8 (AC8), an essential cAMP-generating enzyme in the β-cell that integrates glucose and GLP-1 signalling. ER stress and mutant WFS1 inhibit complex formation and activation of AC8, reducing cAMP synthesis and insulin secretion. These findings reveal that an ER-stress-related protein has a distinct role outside the ER regulating both insulin biosynthesis and secretion. The reduction of WFS1 protein on the plasma membrane during ER stress is a contributing factor for β-cell dysfunction and progression of type 2 diabetes.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "11", "doc_id": "32587939", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Forkhead 0 (fox0) transcription factors are involved in cellular differentiation.\n\nCANDIDATE_PASSAGE:\nGenerating diploid embryos from Xenopus tropicalis. A spectacular advantage of Xenopus tropicalis is the ease with which diploid embryos can be generated year round. By the simple administration of human chorionic gonadotropin, an investigator can generate many hundreds of synchronized embryos by in vitro fertilization or thousands of embryos from a mating pair. The ability to induce ovulations when desired facilitates many different experiments such as experimental embryology, molecular manipulation of gene products, and genetics.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "428", "doc_id": "1624106", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Assembly of invadopodia is triggered by focal generation of phosphatidylinositol-3,4-biphosphate and the activation of the nonreceptor tyrosine kinase Src.\n\nCANDIDATE_PASSAGE:\nPhosphorylation site mutations in heterochromatin protein 1 (HP1) reduce or eliminate silencing activity. HP1 is an essential heterochromatin-associated protein in Drosophila. HP1 has dosage-dependent effects on the silencing of euchromatic genes that are mislocalized to heterochromatin and is required for the normal expression of at least two heterochromatic genes. HP1 is multiply phosphorylated in vivo, and HP1 hyperphosphorylation is correlated with heterochromatin assembly during development. The purpose of this study was to test whether HP1 phosphorylation modifies biological activity and biochemical properties of HP1. To determine sites of HP1 phosphorylation in vivo and whether phosphorylation affects any biochemical properties of HP1, we expressed Drosophila HP1 in lepidopteran cultured cells using a recombinant baculovirus vector. Phosphopeptides were identified by matrix-assisted laser desorption ionization/time of flight mass spectroscopy; these peptides contain target sites for casein kinase II, protein tyrosine kinase, and PIM-1 kinase. Purified HP1 from bacterial (unphosphorylated) and lepidopteran (phosphorylated) cells has similar secondary structure. Phosphorylation has no effect on HP1 self-association but alters the DNA binding properties of HP1, suggesting that phosphorylation could differentially regulate HP1-dependent interactions. Serine-to-alanine and serine-to-glutamate substitutions at consensus protein kinase motifs resulted in reduction or loss of silencing activity of mutant HP1 in transgenic flies. These results suggest that dynamic phosphorylation/dephosphorylation regulates HP1 activity in heterochromatic silencing.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "133", "doc_id": "8417211", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Headaches are correlated with cognitive impairment.\n\nCANDIDATE_PASSAGE:\nHeadache, migraine, and structural brain lesions and function: population based Epidemiology of Vascular Ageing-MRI study OBJECTIVE To evaluate the association of overall and specific headaches with volume of white matter hyperintensities, brain infarcts, and cognition. DESIGN Population based, cross sectional study. SETTING Epidemiology of Vascular Ageing study, Nantes, France. PARTICIPANTS 780 participants (mean age 69, 58.5% women) with detailed headache assessment. MAIN OUTCOME MEASURES Brain scans were evaluated for volume of white matter hyperintensities (by fully automated imaging processing) and for classification of infarcts (by visual reading with a standardised assessment grid). Cognitive function was assessed by a battery of tests including the mini-mental state examination. RESULTS 163 (20.9%) participants reported a history of severe headache and 116 had migraine, of whom 17 (14.7%) reported aura symptoms. An association was found between any history of severe headache and increasing volume of white matter hyperintensities. The adjusted odds ratio of being in the highest third for total volume of white matter hyperintensities was 2.0 (95% confidence interval 1.3 to 3.1, P for trend 0.002) for participants with any history of severe headache when compared with participants without severe headache being in the lowest third. The association pattern was similar for all headache types. Migraine with aura was the only headache type strongly associated with volume of deep white matter hyperintensities (highest third odds ratio 12.4, 1.6 to 99.4, P for trend 0.005) and with brain infarcts (3.4, 1.2 to 9.3). The location of infarcts was predominantly outside the cerebellum and brain stem. Evidence was lacking for cognitive impairment for any headache ty [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "500", "doc_id": "17930286", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: CDK6 shows improved binding to loss-of-function variants of p18 INK4C.\n\nCANDIDATE_PASSAGE:\nFeedback Circuit among INK4 Tumor Suppressors Constrains Human Glioblastoma Development We have developed a nonheuristic genome topography scan (GTS) algorithm to characterize the patterns of genomic alterations in human glioblastoma (GBM), identifying frequent p18(INK4C) and p16(INK4A) codeletion. Functional reconstitution of p18(INK4C) in GBM cells null for both p16(INK4A) and p18(INK4C) resulted in impaired cell-cycle progression and tumorigenic potential. Conversely, RNAi-mediated depletion of p18(INK4C) in p16(INK4A)-deficient primary astrocytes or established GBM cells enhanced tumorigenicity in vitro and in vivo. Furthermore, acute suppression of p16(INK4A) in primary astrocytes induced a concomitant increase in p18(INK4C). Together, these findings uncover a feedback regulatory circuit in the astrocytic lineage and demonstrate a bona fide tumor suppressor role for p18(INK4C) in human GBM wherein it functions cooperatively with other INK4 family members to constrain inappropriate proliferation.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "205", "doc_id": "7898952", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Cellular clocks are associated with mitosis timing in NIH 3T3 cells.\n\nCANDIDATE_PASSAGE:\nOnce-a-day Concerta methylphenidate versus three-times-daily methylphenidate in laboratory and natural settings. OBJECTIVE Methylphenidate (MPH), the most commonly prescribed drug for attention-deficit/hyperactivity disorder (ADHD), has a short half-life, which necessitates multiple daily doses. The need for multiple doses produces problems with medication administration during school and after-school hours, and therefore with compliance. Previous long-acting stimulants and preparations have shown effects equivalent to twice-daily dosing of MPH. This study tests the efficacy and duration of action, in natural and laboratory settings, of an extended-release MPH preparation designed to last 12 hours and therefore be equivalent to 3-times-daily dosing. METHODS Sixty-eight children with ADHD, 6 to 12 years old, participated in a within-subject, double-blind comparison of placebo, immediate-release (IR) MPH 3 times a day (tid), and Concerta, a once-daily MPH formulation. Three dosing levels of medication were used: 5 mg IR MPH tid/18 mg Concerta once a day (qd); 10 mg IR MPH tid/36 mg Concerta qd; and 15 mg IR MPH tid/54 mg Concerta qd. All children were currently medicated with MPH at enrollment, and each child's dose level was based on that child's MPH dosing before the study. The doses of Concerta were selected to be comparable to the daily doses of MPH that each child received. To achieve the ascending rate of MPH delivery determined by initial investigations to provide the necessary continuous coverage, Concerta doses were 20% higher on a daily basis than a comparable tid regimen of IR MPH. Children received each medication condition for 7 days. The investigation was conducted in the context of a background clinical behavioral intervention in both the natura [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "241", "doc_id": "2475059", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Birth-weight is negatively associated with breast cancer.\n\nCANDIDATE_PASSAGE:\nIL-18 induction of osteopontin mediates cardiac fibrosis and diastolic dysfunction in mice. Osteopontin (OPN), a key component of the extracellular matrix, is associated with the fibrotic process during tissue remodeling. OPN and the cytokine interleukin (IL)-18 have been shown to be overexpressed in an array of human cardiac pathologies. In the present study, we determined the role of IL-18 in the regulation of cardiac OPN expression and the subsequent interstitial fibrosis and diastolic dysfunction. We demonstrated parallel increases in IL-18, OPN expression, and interstitial fibrosis in murine models of left ventricular pressure and volume overload. Exogenous recombinant (r)IL-18 administered for 2 wk increased cardiac OPN expression, interstitial fibrosis, and diastolic dysfunction. Stimulation of the T helper (Th)1 lymphocyte phenotype with a selective toll-like receptor (TLR)9 agonist induced cardiac IL-18 and OPN expression, which was associated with increased cardiac fibrillar collagen concentrations and interstitial fibrosis resulting in diastolic dysfunction. rIL-18 induced OPN expression and protein levels in primary of cardiac fibroblast cultures. Conditioned media from TLR9-stimulated T lymphocyte cultures induced IL-18 and OPN expression in cardiac fibroblasts, while blockade of the IL-18 receptor with a neutralizing antibody abolished the increase in OPN expression. Furthermore, a mutation in the transcriptional factor interferon regulatory factor (IRF)1 or IRF1 small interfering RNA (siRNA) resulted in the decreased expression of IL-18 and OPN in cardiac fibroblasts. With pressure overload, IRF1-mutant mice showed downregulation of IL-18 and OPN expression in cardiac tissue, reduced cardiac fibrotic development, and increased left ventricular [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "178", "doc_id": "13108582", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: AMP-activated protein kinase (AMPK) activation reduces inflammation-related fibrosis in the lungs.\n\nCANDIDATE_ABSTRACT:\nTITLE: Metformin reverses established lung fibrosis in a bleomycin model\nABSTRACT: Fibrosis is a pathological result of a dysfunctional repair response to tissue injury and occurs in a number of organs, including the lungs1. Cellular metabolism regulates tissue repair and remodelling responses to injury2-4. AMPK is a critical sensor of cellular bioenergetics and controls the switch from anabolic to catabolic metabolism5. However, the role of AMPK in fibrosis is not well understood. Here, we demonstrate that in humans with idiopathic pulmonary fibrosis (IPF) and in an experimental mouse model of lung fibrosis, AMPK activity is lower in fibrotic regions associated with metabolically active and apoptosis-resistant myofibroblasts. Pharmacological activation of AMPK in myofibroblasts from lungs of humans with IPF display lower fibrotic activity, along with enhanced mitochondrial biogenesis and normalization of sensitivity to apoptosis. In a bleomycin model of lung fibrosis in mice, metformin therapeutically accelerates the resolution of well-established fibrosis in an AMPK-dependent manner. These studies implicate deficient AMPK activation in non-resolving, pathologic fibrotic processes, and support a role for metformin (or other AMPK activators) to reverse established fibrosis by facilitating deactivation and apoptosis of myofibroblasts.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"These studies implicate deficient AMPK activation in non-resolving, pathologic fibrotic processes, and support a role for metformin (or other AMPK activators) to reverse established fibrosis by facilitating deactivation and apoptosis of myofibroblasts.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 55, "doc_id": "49556906", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Transplanted human glial progenitor cells are incapable of forming a neural network with host animals' neurons.\n\nCANDIDATE_ABSTRACT:\nTITLE: Forebrain engraftment by human glial progenitor cells enhances synaptic plasticity and learning in adult mice.\nABSTRACT: Human astrocytes are larger and more complex than those of infraprimate mammals, suggesting that their role in neural processing has expanded with evolution. To assess the cell-autonomous and species-selective properties of human glia, we engrafted human glial progenitor cells (GPCs) into neonatal immunodeficient mice. Upon maturation, the recipient brains exhibited large numbers and high proportions of both human glial progenitors and astrocytes. The engrafted human glia were gap-junction-coupled to host astroglia, yet retained the size and pleomorphism of hominid astroglia, and propagated Ca2+ signals 3-fold faster than their hosts. Long-term potentiation (LTP) was sharply enhanced in the human glial chimeric mice, as was their learning, as assessed by Barnes maze navigation, object-location memory, and both contextual and tone fear conditioning. Mice allografted with murine GPCs showed no enhancement of either LTP or learning. These findings indicate that human glia differentially enhance both activity-dependent plasticity and learning in mice.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Long-term potentiation (LTP) was sharply enhanced in the human glial chimeric mice, as was their learning, as assessed by Barnes maze navigation, object-location memory, and both contextual and tone fear conditioning.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1320, "doc_id": "16284655", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Patients with panic anxiety show decreased CSF levels of hypocretin.\n\nCANDIDATE_ABSTRACT:\nTITLE: A KEY ROLE FOR OREXIN IN PANIC ANXIETY\nABSTRACT: Panic disorder is a severe anxiety disorder with recurrent, debilitating panic attacks. In individuals with panic disorder there is evidence of decreased central gamma-aminobutyric acid (GABA) activity as well as marked increases in autonomic and respiratory responses after intravenous infusions of hypertonic sodium lactate. In a rat model of panic disorder, chronic inhibition of GABA synthesis in the dorsomedial-perifornical hypothalamus of rats produces anxiety-like states and a similar vulnerability to sodium lactate-induced cardioexcitatory responses. The dorsomedial-perifornical hypothalamus is enriched in neurons containing orexin (ORX, also known as hypocretin), which have a crucial role in arousal, vigilance and central autonomic mobilization, all of which are key components of panic. Here we show that activation of ORX-synthesizing neurons is necessary for developing a panic-prone state in the rat panic model, and either silencing of the hypothalamic gene encoding ORX (Hcrt) with RNAi or systemic ORX-1 receptor antagonists blocks the panic responses. Moreover, we show that human subjects with panic anxiety have elevated levels of ORX in the cerebrospinal fluid compared to subjects without panic anxiety. Taken together, our results suggest that the ORX system may be involved in the pathophysiology of panic anxiety and that ORX antagonists constitute a potential new treatment strategy for panic disorder.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Moreover, we show that human subjects with panic anxiety have elevated levels of ORX in the cerebrospinal fluid compared to subjects without panic anxiety.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 930, "doc_id": "16056514", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Metastatic colorectal cancer treated with a single agent fluoropyrimidines resulted in similar efficacy and better quality of life when compared with oxaliplatin-based chemotherapy in elderly patients.\n\nCANDIDATE_ABSTRACT:\nTITLE: Chemotherapy options in elderly and frail patients with metastatic colorectal cancer (MRC FOCUS2): an open-label, randomised factorial trial\nABSTRACT: BACKGROUND Elderly and frail patients with cancer, although often treated with chemotherapy, are under-represented in clinical trials. We designed FOCUS2 to investigate reduced-dose chemotherapy options and to seek objective predictors of outcome in frail patients with advanced colorectal cancer. METHODS We undertook an open, 2 × 2 factorial trial in 61 UK centres for patients with previously untreated advanced colorectal cancer who were considered unfit for full-dose chemotherapy. After comprehensive health assessment (CHA), patients were randomly assigned by minimisation to: 48-h intravenous fluorouracil with levofolinate (group A); oxaliplatin and fluorouracil (group B); capecitabine (group C); or oxaliplatin and capecitabine (group D). Treatment allocation was not masked. Starting doses were 80% of standard doses, with discretionary escalation to full dose after 6 weeks. The two primary outcome measures were: addition of oxaliplatin ([A vs B] + [C vs D]), assessed with progression-free survival (PFS); and substitution of fluorouracil with capecitabine ([A vs C] + [B vs D]), assessed by change from baseline to 12 weeks in global quality of life (QoL). Analysis was by intention to treat. Baseline clinical and CHA data were modelled against outcomes with a novel composite measure, overall treatment utility (OTU). This study is registered, number ISRCTN21221452. FINDINGS 459 patients were randomly assigned (115 to each of groups A-C, 114 to group D). Factorial comparison of addition of oxaliplatin versus no addition suggested some improvement in PFS, but the finding was not significant (median 5·8 months [IQR 3·3-7·5] vs 4·5 months [2·8-6·4]; hazard ratio 0·84, 95% CI 0·69-1·01, p=0·07). Replacement of fluorouracil with capecitabine did not improve global Qo [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"On balance, a combination including oxaliplatin was preferable to single-agent fluoropyrimidines, although the primary endpoint of PFS was not met.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 771, "doc_id": "15476777", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: MICAL redox enzymes regulate actin dynamics.\n\nCANDIDATE_ABSTRACT:\nTITLE: Differential regulation of actin microfilaments by human MICAL proteins.\nABSTRACT: The Drosophila melanogaster MICAL protein is essential for the neuronal growth cone machinery that functions through plexin- and semaphorin-mediated axonal signaling. Drosophila MICAL is also involved in regulating myofilament organization and synaptic structures, and serves as an actin disassembly factor downstream of plexin-mediated axonal repulsion. In mammalian cells there are three known isoforms, MICAL1, MICAL2 and MICAL3, as well as the MICAL-like proteins MICAL-L1 and MICAL-L2, but little is known of their function, and information comes almost exclusively from neural cells. In this study we show that in non-neural cells human MICALs are required for normal actin organization, and all three MICALs regulate actin stress fibers. Moreover, we provide evidence that the generation of reactive oxygen species by MICAL proteins is crucial for their actin-regulatory function. However, although MICAL1 is auto-inhibited by its C-terminal coiled-coil region, MICAL2 remains constitutively active and affects stress fibers. These data suggest differential but complementary roles for MICAL1 and MICAL2 in actin microfilament regulation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In this study we show that in non-neural cells human MICALs are required for normal actin organization, and all three MICALs regulate actin stress fibers.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 738, "doc_id": "6609935", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Replacement of histone H2A with H2A.Z accelerates gene activation in yeasts by destabilizing +1 nucleosomes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Genome-Wide Dynamics of Htz1, a Histone H2A Variant that Poises Repressed/Basal Promoters for Activation through Histone Loss\nABSTRACT: Histone variants help specialize chromatin regions; however, their impact on transcriptional regulation is largely unknown. Here, we determined the genome-wide localization and dynamics of Htz1, the yeast histone H2A variant. Htz1 localizes to hundreds of repressed/basal Pol II promoters and prefers TATA-less promoters. Specific Htz1 deposition requires the SWR1 complex, which largely colocalizes with Htz1. Htz1 occupancy correlates with particular histone modifications, and Htz1 deposition is partially reliant on Gcn5 (a histone acetyltransferase) and Bdf1, an SWR1 complex member that binds acetylated histones. Changes in growth conditions cause a striking redistribution of Htz1 from activated to repressed/basal promoters. Furthermore, Htz1 promotes full gene activation but does not generally impact repression. Importantly, Htz1 releases from purified chromatin in vitro under conditions where H2A and H3 remain associated. We suggest that Htz1-bearing nucleosomes are deposited at repressed/basal promoters but facilitate activation through their susceptibility to loss, thereby helping to expose promoter DNA.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1040, "doc_id": "16626264", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: PKG-la does not have a large impact on expression of pain hypersensitivity in PGK-la knockout mice.\n\nCANDIDATE_ABSTRACT:\nTITLE: Presynaptically Localized Cyclic GMP-Dependent Protein Kinase 1 Is a Key Determinant of Spinal Synaptic Potentiation and Pain Hypersensitivity\nABSTRACT: Synaptic long-term potentiation (LTP) at spinal neurons directly communicating pain-specific inputs from the periphery to the brain has been proposed to serve as a trigger for pain hypersensitivity in pathological states. Previous studies have functionally implicated the NMDA receptor-NO pathway and the downstream second messenger, cGMP, in these processes. Because cGMP can broadly influence diverse ion-channels, kinases, and phosphodiesterases, pre- as well as post-synaptically, the precise identity of cGMP targets mediating spinal LTP, their mechanisms of action, and their locus in the spinal circuitry are still unclear. Here, we found that Protein Kinase G1 (PKG-I) localized presynaptically in nociceptor terminals plays an essential role in the expression of spinal LTP. Using the Cre-lox P system, we generated nociceptor-specific knockout mice lacking PKG-I specifically in presynaptic terminals of nociceptors in the spinal cord, but not in post-synaptic neurons or elsewhere (SNS-PKG-I(-/-) mice). Patch clamp recordings showed that activity-induced LTP at identified synapses between nociceptors and spinal neurons projecting to the periaqueductal grey (PAG) was completely abolished in SNS-PKG-I(-/-) mice, although basal synaptic transmission was not affected. Analyses of synaptic failure rates and paired-pulse ratios indicated a role for presynaptic PKG-I in regulating the probability of neurotransmitter release. Inositol 1,4,5-triphosphate receptor 1 and myosin light chain kinase were recruited as key phosphorylation targets of presynaptic PKG-I in nociceptive neurons. Finally, behavioural analyses in vivo showed marked defects in SNS-PKG-I(-/-) mice in several models of activity-induced nociceptive hypersensitivity, and pharmacological studies identified [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Our results thus indicate that presynaptic mechanisms involving an increase in release probability from nociceptors are operational in the expression of synaptic LTP on spinal-PAG projection neurons and that PKG-I localized in presynaptic nociceptor terminals plays an essential role in this process to regulate pain sensitivity.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 909, "doc_id": "11254556", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: ALDH1 expression is associated with better breast cancer outcomes.\n\nCANDIDATE_ABSTRACT:\nTITLE: ALDH1 is a marker of normal and malignant human mammary stem cells and a predictor of poor clinical outcome.\nABSTRACT: Application of stem cell biology to breast cancer research has been limited by the lack of simple methods for identification and isolation of normal and malignant stem cells. Utilizing in vitro and in vivo experimental systems, we show that normal and cancer human mammary epithelial cells with increased aldehyde dehydrogenase activity (ALDH) have stem/progenitor properties. These cells contain the subpopulation of normal breast epithelium with the broadest lineage differentiation potential and greatest growth capacity in a xenotransplant model. In breast carcinomas, high ALDH activity identifies the tumorigenic cell fraction, capable of self-renewal and of generating tumors that recapitulate the heterogeneity of the parental tumor. In a series of 577 breast carcinomas, expression of ALDH1 detected by immunostaining correlated with poor prognosis. These findings offer an important new tool for the study of normal and malignant breast stem cells and facilitate the clinical application of stem cell concepts.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In a series of 577 breast carcinomas, expression of ALDH1 detected by immunostaining correlated with poor prognosis.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 51, "doc_id": "45638119", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Basophils counteract disease development in patients with systemic lupus erythematosus (SLE).\n\nCANDIDATE_ABSTRACT:\nTITLE: BASOPHILS AND THE T HELPER 2 ENVIRONMENT CAN PROMOTE THE DEVELOPMENT OF LUPUS NEPHRITIS\nABSTRACT: In systemic lupus erythematosus (SLE), self-reactive antibodies can target the kidney (lupus nephritis), leading to functional failure and possible mortality. We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice). Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis. Basophils were also present in the lymph nodes and spleen of subjects with SLE. Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 171, "doc_id": "12670680", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Upregulation of mosGCTL-1 is induced upon infection with West Nile virus.\n\nCANDIDATE_PASSAGE:\nA C-Type Lectin Collaborates with a CD45 Phosphatase Homolog to Facilitate West Nile Virus Infection of Mosquitoes West Nile virus (WNV) is the most common arthropod-borne flavivirus in the United States; however, the vector ligand(s) that participate in infection are not known. We now show that an Aedes aegypti C-type lectin, mosGCTL-1, is induced by WNV, interacts with WNV in a calcium-dependent manner, and facilitates infection in vivo and in vitro. A mosquito homolog of human CD45 in A. aegypti, designated mosPTP-1, recruits mosGCTL-1 to enable viral attachment to cells and to enhance viral entry. In vivo experiments show that mosGCTL-1 and mosPTP-1 function as part of the same pathway and are critical for WNV infection of mosquitoes. A similar phenomenon was also observed in Culex quinquefasciatus, a natural vector of WNV, further demonstrating that these genes participate in WNV infection. During the mosquito blood-feeding process, WNV infection was blocked in vivo with mosGCTL-1 antibodies. A molecular understanding of flaviviral-arthropod interactions may lead to strategies to control viral dissemination in nature.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1352", "doc_id": "12885341", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Mutations in RIM1 raise levels of IME1 RNA.\n\nCANDIDATE_ABSTRACT:\nTITLE: Molecular characterization of the yeast meiotic regulatory gene RIM1.\nABSTRACT: In the yeast Saccharomyces cerevisiae, genetic studies suggest that the RIM1 gene encodes a positive regulator of meiosis. rim1 mutations cause reduced expression of IME1, which is required for expression of many meiotic genes, and thus lead to a partial defect in meiosis and spore formation. We report the sequence of RIM1 and functional analysis of its coding region. The RIM1 gene product (RIM1) contains three regions similar to C2H2 zinc fingers. Serine substitutions for cysteine in each of the putative zinc fingers abolish RIM1 function. The carboxyl-terminus of RIM1 is enriched in acidic amino acids and is required for full RIM1 activity. RIM1 also contains two putative cAMP-dependent protein kinase (cAPK) phosphorylation sites. At one site, substitution of alanine for serine does not affect RIM1 activity; at the other site, this substitution impairs activity. This analysis of RIM1 suggests that the protein may function as a transcriptional activator. We have used the cloned RIM1 gene to create a complete rim1 deletion. This null allele, like previously isolated rim1 mutations, causes a partial meiotic defect. In addition to RIM1, maximum IME1 expression requires the MCK1 and IME4 gene products. Defects associated with rim1, mck1, and ime4 mutations in expression of a meiotic reporter gene (ime2-lacZ) and in sporulation are additive. These findings suggest that RIM1 acts independently of MCK1 and IME4 to stimulate IME1 expression.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"rim1 mutations cause reduced expression of IME1, which is required for expression of many meiotic genes, and thus lead to a partial defect in meiosis and spore formation.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 816, "doc_id": "8148304", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Nonsteroidal antinflammatory drugs are ineffective as cancer treatments.\n\nCANDIDATE_ABSTRACT:\nTITLE: High-Threshold Mechanosensitive Ion Channels Blocked by a Novel Conopeptide Mediate Pressure-Evoked Pain\nABSTRACT: Little is known about the molecular basis of somatosensory mechanotransduction in mammals. We screened a library of peptide toxins for effects on mechanically activated currents in cultured dorsal root ganglion neurons. One conopeptide analogue, termed NMB-1 for noxious mechanosensation blocker 1, selectively inhibits (IC50 1 µM) sustained mechanically activated currents in a subset of sensory neurons. Biotinylated NMB-1 retains activity and binds selectively to peripherin-positive nociceptive sensory neurons. The selectivity of NMB-1 was confirmed by the fact that it has no inhibitory effects on voltage-gated sodium and calcium channels, or ligand-gated channels such as acid-sensing ion channels or TRPA1 channels. Conversely, the tarantula toxin, GsMTx-4, which inhibits stretch-activated ion channels, had no effects on mechanically activated currents in sensory neurons. In behavioral assays, NMB-1 inhibits responses only to high intensity, painful mechanical stimulation and has no effects on low intensity mechanical stimulation or thermosensation. Unexpectedly, NMB-1 was found to also be an inhibitor of rapid FM1-43 loading (a measure of mechanotransduction) in cochlear hair cells. These data demonstrate that pharmacologically distinct channels respond to distinct types of mechanical stimuli and suggest that mechanically activated sustained currents underlie noxious mechanosensation. NMB-1 thus provides a novel diagnostic tool for the molecular definition of channels involved in hearing and pressure-evoked pain.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 856, "doc_id": "1275505", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Sequence conservation in gene regulatory regions between species is a high-accuracy predictor of conserved functionality.\n\nCANDIDATE_PASSAGE:\nEnhancer Evolution across 20 Mammalian Species The mammalian radiation has corresponded with rapid changes in noncoding regions of the genome, but we lack a comprehensive understanding of regulatory evolution in mammals. Here, we track the evolution of promoters and enhancers active in liver across 20 mammalian species from six diverse orders by profiling genomic enrichment of H3K27 acetylation and H3K4 trimethylation. We report that rapid evolution of enhancers is a universal feature of mammalian genomes. Most of the recently evolved enhancers arise from ancestral DNA exaptation, rather than lineage-specific expansions of repeat elements. In contrast, almost all liver promoters are partially or fully conserved across these species. Our data further reveal that recently evolved enhancers can be associated with genes under positive selection, demonstrating the power of this approach for annotating regulatory adaptations in genomic sequences. These results provide important insight into the functional genetics underpinning mammalian regulatory evolution.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1074", "doc_id": "14658685", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: MICAL redox enzymes regulate actin dynamics.\n\nCANDIDATE_PASSAGE:\nWolfram syndrome 1 and adenylyl cyclase 8 interact at the plasma membrane to regulate insulin production and secretion Endoplasmic reticulum (ER) stress causes pancreatic β-cell dysfunction and contributes to β-cell loss and the progression of type 2 diabetes. Wolfram syndrome 1 (WFS1) has been shown to be an important regulator of the ER stress signalling pathway; however, its role in β-cell function remains unclear. Here we provide evidence that WFS1 is essential for glucose- and glucagon-like peptide 1 (GLP-1)-stimulated cyclic AMP production and regulation of insulin biosynthesis and secretion. Stimulation with glucose causes WFS1 translocation from the ER to the plasma membrane, where it forms a complex with adenylyl cyclase 8 (AC8), an essential cAMP-generating enzyme in the β-cell that integrates glucose and GLP-1 signalling. ER stress and mutant WFS1 inhibit complex formation and activation of AC8, reducing cAMP synthesis and insulin secretion. These findings reveal that an ER-stress-related protein has a distinct role outside the ER regulating both insulin biosynthesis and secretion. The reduction of WFS1 protein on the plasma membrane during ER stress is a contributing factor for β-cell dysfunction and progression of type 2 diabetes.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "738", "doc_id": "32587939", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: A mutation in HNF4A leads to an increased risk of developing diabetes by the age of 14 years.\n\nCANDIDATE_PASSAGE:\nIL-17 promotes tumor development through the induction of tumor promoting microenvironments at tumor sites and myeloid-derived suppressor cells. The role of immune responses in tumor development is a central issue for tumor biology and immunology. IL-17 is an important cytokine for inflammatory and autoimmune diseases. Although IL-17-producing cells are detected in cancer patients and tumor-bearing mice, the role of IL-17 in tumor development is controversial, and mechanisms remain to be fully elucidated. In the current study, we found that the development of tumors was inhibited in IL-17R-deficient mice. A defect in IFN-gammaR increased tumor growth, whereas tumor growth was inhibited in mice that were deficient in both IL-17R and IFN-gammaR compared with wild-type animals. Further experiments showed that neutralization of IL-17 by Abs inhibited tumor growth in wild-type mice, whereas systemic administration of IL-17 promoted tumor growth. The IL-17R deficiency increased CD8 T cell infiltration, whereas it reduced the infiltration of myeloid-derived suppressor cells (MDSCs) in tumors. In contrast, administration of IL-17 inhibited CD8 T cell infiltration and increased MDSCs in tumors. Further analysis indicated that IL-17 was required for the development and tumor-promoting activity of MDSCs in tumor-bearing mice. These data demonstrate that IL-17-mediated responses promote tumor development through the induction of tumor-promoting microenvironments at tumor sites. IL-17-mediated regulation of MDSCs is a primary mechanism for its tumor-promoting effects. The study provides novel insights into the role of IL-17 in tumor development and has major implications for targeting IL-17 in treatment of tumors.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "44", "doc_id": "25726838", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Chinese individuals with TT homozygosity in the MTHFR gene are less vulnerable to strokes caused by low levels of folate intake.\n\nCANDIDATE_PASSAGE:\nIncreased Microerythrocyte Count in Homozygous α+-Thalassaemia Contributes to Protection against Severe Malarial Anaemia BACKGROUND The heritable haemoglobinopathy alpha(+)-thalassaemia is caused by the reduced synthesis of alpha-globin chains that form part of normal adult haemoglobin (Hb). Individuals homozygous for alpha(+)-thalassaemia have microcytosis and an increased erythrocyte count. Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count. We tested the hypothesis that the erythrocyte indices associated with alpha(+)-thalassaemia homozygosity provide a haematological benefit during acute malaria. METHODS AND FINDINGS Data from children living on the north coast of Papua New Guinea who had participated in a case-control study of the protection afforded by alpha(+)-thalassaemia against severe malaria were reanalysed to assess the genotype-specific reduction in erythrocyte count and Hb levels associated with acute malarial disease. We observed a reduction in median erythrocyte count of approximately 1.5 x 10(12)/l in all children with acute falciparum malaria relative to values in community children (p < 0.001). We developed a simple mathematical model of the linear relationship between Hb concentration and erythrocyte count. This model predicted that children homozygous for alpha(+)-thalassaemia lose less Hb than children of normal genotype for a reduction in erythrocyte count of >1.1 x 10(12)/l as a result of the reduced mean cell Hb in homozygous alpha(+)-thalassaemia. In addition, children homozygous for alpha(+)-thalassaemia require a 10% greater reduction in erythrocyte count than children of normal genotyp [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "253", "doc_id": "18174210", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Inositol lipid 3-phosphatase PTEN converts Ptdlns(3,4)P 2 into phosphatidylinositol 4-phosphate.\n\nCANDIDATE_ABSTRACT:\nTITLE: Air pollution and cardiovascular disease: a statement for healthcare professionals from the Expert Panel on Population and Prevention Science of the American Heart Association.\nABSTRACT: Air pollution is a heterogeneous, complex mixture of gases, liquids, and particulate matter. Epidemiological studies have demonstrated a consistent increased risk for cardiovascular events in relation to both short- and long-term exposure to present-day concentrations of ambient particulate matter. Several plausible mechanistic pathways have been described, including enhanced coagulation/thrombosis, a propensity for arrhythmias, acute arterial vasoconstriction, systemic inflammatory responses, and the chronic promotion of atherosclerosis. The purpose of this statement is to provide healthcare professionals and regulatory agencies with a comprehensive review of the literature on air pollution and cardiovascular disease. In addition, the implications of these findings in relation to public health and regulatory policies are addressed. Practical recommendations for healthcare providers and their patients are outlined. In the final section, suggestions for future research are made to address a number of remaining scientific questions.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 636, "doc_id": "471921", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Tetraspanin-3 is a causative factor in the development of acute myelogenous leukemia\n\nCANDIDATE_PASSAGE:\nCoronary plaque disruption. Coronary atherosclerosis is by far the most frequent cause of ischemic heart disease, and plaque disruption with superimposed thrombosis is the main cause of the acute coronary syndromes of unstable angina, myocardial infarction, and sudden death.1 2 3 4 5 Therefore, for event-free survival, the vital question is not why atherosclerosis develops but rather why, after years of indolent growth, it suddenly becomes complicated by life-threatening thrombosis. The composition and vulnerability of plaque rather than its volume or the consequent severity of stenosis produced have emerged as being the most important determinants for the development of the thrombus-mediated acute coronary syndromes; lipid-rich and soft plaques are more dangerous than collagen-rich and hard plaques because they are more unstable and rupture-prone and highly thrombogenic after disruption.6 This review will explore potential mechanisms responsible for the sudden conversion of a stable atherosclerotic plaque to an unstable and life-threatening atherothrombotic lesion—an event known as plaque fissuring, rupture, or disruption.7 8 Atherosclerosis is the result of a complex interaction between blood elements, disturbed flow, and vessel wall abnormality, involving several pathological processes: inflammation, with increased endothelial permeability, endothelial activation, and monocyte recruitment9 10 11 12 13 14 ; growth, with smooth muscle cell (SMC) proliferation, migration, and matrix synthesis15 16 ; degeneration, with lipid accumulation17 18 ; necrosis, possibly related to the cytotoxic effect of oxidized lipid19 ; calcification/ossification, which may represent an active rather than a dystrophic process20 21 ; and thrombosis, with platelet recruitment and f [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1150", "doc_id": "19332616", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: De novo assembly of sequence data has more specific contigs than unassembled sequence data.\n\nCANDIDATE_ABSTRACT:\nTITLE: A culture-independent sequence-based metagenomics approach to the investigation of an outbreak of Shiga-toxigenic Escherichia coli O104:H4.\nABSTRACT: IMPORTANCE Identification of the bacterium responsible for an outbreak can aid in disease management. However, traditional culture-based diagnosis can be difficult, particularly if no specific diagnostic test is available for an outbreak strain. OBJECTIVE To explore the potential of metagenomics, which is the direct sequencing of DNA extracted from microbiologically complex samples, as an open-ended clinical discovery platform capable of identifying and characterizing bacterial strains from an outbreak without laboratory culture. DESIGN, SETTING, AND PATIENTS In a retrospective investigation, 45 samples were selected from fecal specimens obtained from patients with diarrhea during the 2011 outbreak of Shiga-toxigenic Escherichia coli (STEC) O104:H4 in Germany. Samples were subjected to high-throughput sequencing (August-September 2012), followed by a 3-phase analysis (November 2012-February 2013). In phase 1, a de novo assembly approach was developed to obtain a draft genome of the outbreak strain. In phase 2, the depth of coverage of the outbreak strain genome was determined in each sample. In phase 3, sequences from each sample were compared with sequences from known bacteria to identify pathogens other than the outbreak strain. MAIN OUTCOMES AND MEASURES The recovery of genome sequence data for the purposes of identification and characterization of the outbreak strain and other pathogens from fecal samples. RESULTS During phase 1, a draft genome of the STEC outbreak strain was obtained. During phase 2, the outbreak strain genome was recovered from 10 samples at greater than 10-fold coverage and from 26 samples at greater than 1-fold coverage. Sequences from the Shiga-toxin genes were detected in 27 of 40 STEC-positive samples (67%). In phase 3, sequences [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 312, "doc_id": "6173523", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Lupus-prone mice infected with curliproducing bacteria have higher autoantibody titers compared to controls.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mechanisms that Specify Promoter Nucleosome Location and Identity\nABSTRACT: The chromatin architecture of eukaryotic gene promoters is generally characterized by a nucleosome-free region (NFR) flanked by at least one H2A.Z variant nucleosome. Computational predictions of nucleosome positions based on thermodynamic properties of DNA-histone interactions have met with limited success. Here we show that the action of the essential RSC remodeling complex in S. cerevisiae helps explain the discrepancy between theory and experiment. In RSC-depleted cells, NFRs shrink such that the average positions of flanking nucleosomes move toward predicted sites. Nucleosome positioning at distinct subsets of promoters additionally requires the essential Myb family proteins Abf1 and Reb1, whose binding sites are enriched in NFRs. In contrast, H2A.Z deposition is dispensable for nucleosome positioning. By regulating H2A.Z deposition using a steroid-inducible protein splicing strategy, we show that NFR establishment is necessary for H2A.Z deposition. These studies suggest an ordered pathway for the assembly of promoter chromatin architecture.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 721, "doc_id": "1259280", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Are eGFR overexpressing cells and tumors dependent on autophagy for growth and survival?\n\nABSTRACT:\nThe epidermal growth factor receptor (EGFR) is overexpressed, amplified or mutated in various human epithelial tumors, and is associated with tumor aggressiveness and therapy resistance. Autophagy activation provides a survival advantage for cells in the tumor microenvironment. In the current study, we assessed the potential of autophagy inhibition (using chloroquine (CQ)) in treatment of EGFR expressing tumors. Quantitative PCR, immunohistochemistry, clonogenic survival, proliferation assays and in vivo tumor growth were used to assess this potential. We show that EGFR overexpressing xenografts are sensitive to CQ treatment and are sensitized to irradiation by autophagy inhibition. In HNSSC xenografts, a correlation between EGFR and expression of the autophagy marker LC3b is observed, suggesting a role for autophagy in EGFR expressing tumors. This observation was substantiated in cell lines, showing high EGFR expressing cells to be more sensitive to CQ addition as reflected by decreased proliferation and survival. Surprisingly high EGFR expressing cells display a lower autophagic flux.", "output": "{\"label\": \"yes\", \"rationale\": \"The EGFR high expressing cells and tumors investigated in this study are highly dependent on autophagy for growth and survival. Inhibition of autophagy may therefore provide a novel treatment opportunity for EGFR overexpressing tumors.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 23891088, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In young and middle-aged adults, current or remote uses of ADHD medications do not increase the risk of serious cardiovascular events.\n\nCANDIDATE_ABSTRACT:\nTITLE: ADHD medications and risk of serious cardiovascular events in young and middle-aged adults.\nABSTRACT: CONTEXT More than 1.5 million US adults use stimulants and other medications labeled for treatment of attention-deficit/hyperactivity disorder (ADHD). These agents can increase heart rate and blood pressure, raising concerns about their cardiovascular safety. OBJECTIVE To examine whether current use of medications prescribed primarily to treat ADHD is associated with increased risk of serious cardiovascular events in young and middle-aged adults. DESIGN, SETTING, AND PARTICIPANTS Retrospective, population-based cohort study using electronic health care records from 4 study sites (OptumInsight Epidemiology, Tennessee Medicaid, Kaiser Permanente California, and the HMO Research Network), starting in 1986 at 1 site and ending in 2005 at all sites, with additional covariate assessment using 2007 survey data. Participants were adults aged 25 through 64 years with dispensed prescriptions for methylphenidate, amphetamine, or atomoxetine at baseline. Each medication user (n = 150,359) was matched to 2 nonusers on study site, birth year, sex, and calendar year (443,198 total users and nonusers). MAIN OUTCOME MEASURES Serious cardiovascular events, including myocardial infarction (MI), sudden cardiac death (SCD), or stroke, with comparison between current or new users and remote users to account for potential healthy-user bias. RESULTS During 806,182 person-years of follow-up (median, 1.3 years per person), 1357 cases of MI, 296 cases of SCD, and 575 cases of stroke occurred. There were 107,322 person-years of current use (median, 0.33 years), with a crude incidence per 1000 person-years of 1.34 (95% CI, 1.14-1.57) for MI, 0.30 (95% CI, 0.20-0.42) for SCD, and 0.56 (95% CI, 0.43-0.72) for stroke. The multivariable-adjusted rate ratio (RR) of serious cardiovascular eve [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The multivariable-adjusted rate ratio (RR) of serious cardiovascular events for current use vs nonuse of ADHD medications was 0.83 (95% CI, 0.72-0.96). Among new users of ADHD medications, the adjusted RR was 0.77 (95% CI, 0.63-0.94).\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 589, "doc_id": "10984005", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Egr2 regulates the homeostasis of B and T cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Transcription Factors Egr2 and Egr3 Are Essential for the Control of Inflammation and Antigen-Induced Proliferation of B and T Cells\nABSTRACT: Lymphocytes provide optimal responses against pathogens with minimal inflammatory pathology. However, the intrinsic mechanisms regulating these responses are unknown. Here, we report that deletion of both transcription factors Egr2 and Egr3 in lymphocytes resulted in a lethal autoimmune syndrome with excessive serum proinflammatory cytokines but also impaired antigen receptor-induced proliferation of B and T cells. Egr2- and Egr3-defective B and T cells had hyperactive signal transducer and activator of transcription-1 (STAT1) and STAT3 while antigen receptor-induced activation of transcription factor AP-1 was severely impaired. We discovered that Egr2 and/or Egr3 directly induced expression of suppressor of cytokine signaling-1 (SOCS1) and SOCS3, inhibitors of STAT1 and STAT3, and also blocked the function of Batf, an AP-1 inhibitor, in B and T cells. Thus, Egr2 and Egr3 regulate B and T cell function in adaptive immune responses and homeostasis by promoting antigen receptor signaling and controlling inflammation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Thus, Egr2 and Egr3 regulate B and T cell function in adaptive immune responses and homeostasis by promoting antigen receptor signaling and controlling inflammation.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 370, "doc_id": "1550937", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: During the primary early antibody response activated B cells migrate toward the inner-and outer paracortical areas where oxysterol accumulation is generated by stromal cells.\n\nCANDIDATE_PASSAGE:\nMonitoring Tumorigenesis and Senescence In Vivo with a p16INK4a-Luciferase Model Monitoring cancer and aging in vivo remains experimentally challenging. Here, we describe a luciferase knockin mouse (p16(LUC)), which faithfully reports expression of p16(INK4a), a tumor suppressor and aging biomarker. Lifelong assessment of luminescence in p16(+/LUC) mice revealed an exponential increase with aging, which was highly variable in a cohort of contemporaneously housed, syngeneic mice. Expression of p16(INK4a) with aging did not predict cancer development, suggesting that the accumulation of senescent cells is not a principal determinant of cancer-related death. In 14 of 14 tested tumor models, expression of p16(LUC) was focally activated by early neoplastic events, enabling visualization of tumors with sensitivity exceeding other imaging modalities. Activation of p16(INK4a) was noted in the emerging neoplasm and surrounding stromal cells. This work suggests that p16(INK4a) activation is a characteristic of all emerging cancers, making the p16(LUC) allele a sensitive, unbiased reporter of neoplastic transformation.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "362", "doc_id": "17717391", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Monoclonal antibody targeting of N-cadherin inhibits metastasis.\n\nCANDIDATE_PASSAGE:\nMonoclonal antibody targeting of N-cadherin inhibits prostate cancer growth, metastasis and castration resistance The transition from androgen-dependent to castration-resistant prostate cancer (CRPC) is a lethal event of uncertain molecular etiology. Comparing gene expression in isogenic androgen-dependent and CRPC xenografts, we found a reproducible increase in N-cadherin expression, which was also elevated in primary and metastatic tumors of individuals with CRPC. Ectopic expression of N-cadherin in nonmetastatic, androgen-dependent prostate cancer models caused castration resistance, invasion and metastasis. Monoclonal antibodies against the ectodomain of N-cadherin reduced proliferation, adhesion and invasion of prostate cancer cells in vitro. In vivo, these antibodies slowed the growth of multiple established CRPC xenografts, blocked local invasion and metastasis and, at higher doses, led to complete regression. N-cadherin–specific antibodies markedly delayed the time to emergence of castration resistance, markedly affected tumor histology and angiogenesis, and reduced both AKT serine-threonine kinase activity and serum interleukin-8 (IL-8) secretion. These data indicate that N-cadherin is a major cause of both prostate cancer metastasis and castration resistance. Therapeutic targeting of this factor with monoclonal antibodies may have considerable clinical benefit.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "805", "doc_id": "22180793", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Rapid up-regulation and higher basal expression of interferon-induced genes increase survival of granule cell neurons that are infected by West Nile virus.\n\nCANDIDATE_PASSAGE:\nNrf2 protects human alveolar epithelial cells against injury induced by influenza A virus BACKGROUND Influenza A virus (IAV) infection primarily targets respiratory epithelial cells and produces clinical outcomes ranging from mild upper respiratory infection to severe pneumonia. Recent studies have shown the importance of lung antioxidant defense systems against injury by IAV. Nuclear factor-erythroid 2 related factor 2 (Nrf2) activates the majority of antioxidant genes. METHODS Alveolar type II (ATII) cells and alveolar macrophages (AM) were isolated from human lungs not suitable for transplantation and donated for medical research. In some studies ATII cells were transdifferentiated to alveolar type I-like (ATI-like) cells. Alveolar epithelial cells were infected with A/PR/8/34 (PR8) virus. We analyzed PR8 virus production, influenza A nucleoprotein levels, ROS generation and expression of antiviral genes. Immunocytofluorescence was used to determine Nrf2 translocation and western blotting to detect Nrf2, HO-1 and caspase 1 and 3 cleavage. We also analyzed ingestion of PR8 virus infected apoptotic ATII cells by AM, cytokine levels by ELISA, glutathione levels, necrosis and apoptosis by TUNEL assay. Moreover, we determined the critical importance of Nrf2 using adenovirus Nrf2 (AdNrf2) or Nrf2 siRNA to overexpress or knockdown Nrf2, respectively. RESULTS We found that IAV induced oxidative stress, cytotoxicity and apoptosis in ATI-like and ATII cells. We also found that AM can ingest PR8 virus-induced apoptotic ATII cells (efferocytosis) but not viable cells, whereas ATII cells did not ingest these apoptotic cells. PR8 virus increased ROS production, Nrf2, HO-1, Mx1 and OAS1 expression and Nrf2 translocation to the nucleus. Nrf2 knockdown with siRNA sensitiz [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1020", "doc_id": "6182947", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Natriuretic peptides protect against diabetes.\n\nCANDIDATE_PASSAGE:\nPhase-plate cryo-EM structure of a biased agonist-bound human GLP-1 receptor–Gs complex The class B glucagon-like peptide-1 (GLP-1) G protein-coupled receptor is a major target for the treatment of type 2 diabetes and obesity. Endogenous and mimetic GLP-1 peptides exhibit biased agonism—a difference in functional selectivity—that may provide improved therapeutic outcomes. Here we describe the structure of the human GLP-1 receptor in complex with the G protein-biased peptide exendin-P5 and a Gαs heterotrimer, determined at a global resolution of 3.3 Å. At the extracellular surface, the organization of extracellular loop 3 and proximal transmembrane segments differs between our exendin-P5-bound structure and previous GLP-1-bound GLP-1 receptor structure. At the intracellular face, there was a six-degree difference in the angle of the Gαs–α5 helix engagement between structures, which was propagated across the G protein heterotrimer. In addition, the structures differed in the rate and extent of conformational reorganization of the Gαs protein. Our structure provides insights into the molecular basis of biased agonism.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "841", "doc_id": "3610282", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Women with a lower birth weight are more likely to develop breast cancer later in life.\n\nCANDIDATE_ABSTRACT:\nTITLE: Birth Size and Breast Cancer Risk: Re-analysis of Individual Participant Data from 32 Studies\nABSTRACT: BACKGROUND Birth size, perhaps a proxy for prenatal environment, might be a correlate of subsequent breast cancer risk, but findings from epidemiological studies have been inconsistent. We re-analysed individual participant data from published and unpublished studies to obtain more precise estimates of the magnitude and shape of the birth size-breast cancer association. METHODS AND FINDINGS Studies were identified through computer-assisted and manual searches, and personal communication with investigators. Individual participant data from 32 studies, comprising 22,058 breast cancer cases, were obtained. Random effect models were used, if appropriate, to combine study-specific estimates of effect. Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003). Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data. Birth length and head circumference from birth records were also positively associated with breast cancer risk (pooled RR per one SD increment: 1.06 [95% CI 1.03-1.10] and 1.09 [95% CI 1.03-1.15], respectively). Simultaneous adjustment for these three birth size variables showed that length was the strongest independent predictor of risk. The birth size effec [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1380, "doc_id": "16322674", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is amino-terminal pro-brain natriuretic peptide ( NT-proBNP ) a biomarker of cardiac filling pressures in pre-eclampsia?\n\nABSTRACT:\nTo evaluate if amino-terminal pro-brain natriuretic peptide (NT-proBNP) plasma levels reflect intracardiac filling pressures in pre-eclamptic patients. In a cross-sectional study we investigated 22 untreated critically ill pre-eclamptic women between 22 and 34 weeks gestation. All patients underwent intra-arterial blood pressure and central hemodynamic measurements and NT-proBNP was determined in stored plasma. Baseline characteristics, plasma NT-proBNP concentrations and relevant laboratory variables were investigated for correlations with hemodynamic values using Spearman's rank correlation test. No significant correlations were demonstrated between NT-proBNP concentrations and variables associated with the severity of the pre-eclampsia. We found significant positive correlations between NT-proBNP and diastolic pulmonary pressure (r = 0.59; p = 0.005) and pulmonary capillary wedge pressure (PCWP) (r = 0.51; p = 0.015). Multiple linear regression analysis showed that the association between NT-proBNP and PCWP was not affected by creatinine level.", "output": "{\"label\": \"yes\", \"rationale\": \"NT-proBNP is a biomarker of left ventricular cardiac filling pressures in untreated pre-eclamptic patients.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 20674138, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: All hematopoietic stem cells segregate their chromosomes randomly.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effect of lowering blood pressure on cardiovascular events and mortality in patients on dialysis: a systematic review and meta-analysis of randomised controlled trials\nABSTRACT: BACKGROUND Patients undergoing dialysis have a substantially increased risk of cardiovascular mortality and morbidity. Although several trials have shown the cardiovascular benefits of lowering blood pressure in the general population, there is uncertainty about the efficacy and tolerability of reducing blood pressure in patients on dialysis. We did a systematic review and meta-analysis to assess the effect of blood pressure lowering in patients on dialysis. METHODS We systematically searched Medline, Embase, and the Cochrane Library database for trials reported between 1950 and November, 2008, without language restriction. We extracted a standardised dataset from randomised controlled trials of blood pressure lowering in patients on dialysis that reported cardiovascular outcomes. Meta-analysis was done with a random effects model. FINDINGS We identified eight relevant trials, which provided data for 1679 patients and 495 cardiovascular events. Weighted mean systolic blood pressure was 4.5 mm Hg lower and diastolic blood pressure 2.3 mm Hg lower in actively treated patients than in controls. Blood pressure lowering treatment was associated with lower risks of cardiovascular events (RR 0.71, 95% CI 0.55-0.92; p=0.009), all-cause mortality (RR 0.80, 0.66-0.96; p=0.014), and cardiovascular mortality (RR 0.71, 0.50-0.99; p=0.044) than control regimens. The effects seem to be consistent across a range of patient groups included in the studies. INTERPRETATION Treatment with agents that lower blood pressure should routinely be considered for individuals undergoing dialysis to reduce the very high cardiovascular morbidity and mortality rate in this population.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 100, "doc_id": "202259", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Inhibiting glucose-6-phospate dehydrogenase improves lipogenesis by deactivating LKB1-AMPK signaling.\n\nCANDIDATE_ABSTRACT:\nTITLE: 6-phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumor growth by inhibiting LKB1-AMPK signaling\nABSTRACT: The oxidative pentose phosphate pathway (PPP) contributes to tumour growth, but the precise contribution of 6-phosphogluconate dehydrogenase (6PGD), the third enzyme in this pathway, to tumorigenesis remains unclear. We found that suppression of 6PGD decreased lipogenesis and RNA biosynthesis and elevated ROS levels in cancer cells, attenuating cell proliferation and tumour growth. 6PGD-mediated production of ribulose-5-phosphate (Ru-5-P) inhibits AMPK activation by disrupting the active LKB1 complex, thereby activating acetyl-CoA carboxylase 1 and lipogenesis. Ru-5-P and NADPH are thought to be precursors in RNA biosynthesis and lipogenesis, respectively; thus, our findings provide an additional link between the oxidative PPP and lipogenesis through Ru-5-P-dependent inhibition of LKB1-AMPK signalling. Moreover, we identified and developed 6PGD inhibitors, physcion and its derivative S3, that effectively inhibited 6PGD, cancer cell proliferation and tumour growth in nude mice xenografts without obvious toxicity, suggesting that 6PGD could be an anticancer target.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We found that suppression of 6PGD decreased lipogenesis and RNA biosynthesis and elevated ROS levels in cancer cells, attenuating cell proliferation and tumour growth. 6PGD-mediated production of ribulose-5-phosphate (Ru-5-P) inhibits AMPK activation by disrupting the active LKB1 complex, thereby activating acetyl-CoA carboxylase 1 and lipogenesis.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 635, "doc_id": "1686997", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: De novo assembly of sequence data has fewer specific contigs than unassembled sequence data.\n\nCANDIDATE_PASSAGE:\nIdentification of T6SS-dependent effector and immunity proteins by Tn-seq in Vibrio cholerae. Type VI protein secretion system (T6SS) is important for bacterial competition through contact-dependent killing of competitors. T6SS delivers effectors to neighboring cells and corresponding antagonistic proteins confer immunity against effectors that are delivered by sister cells. Although T6SS has been found in more than 100 gram-negative bacteria including many important human pathogens, few T6SS-dependent effector and immunity proteins have been experimentally determined. Here we report a high-throughput approach using transposon mutagenesis and deep sequencing (Tn-seq) to identify T6SS immunity proteins in Vibrio cholerae. Saturating transposon mutagenesis was performed in wild type and a T6SS null mutant. Genes encoding immunity proteins were predicted to be essential in the wild type but dispensable in the T6SS mutant. By comparing the relative abundance of each transposon mutant in the mutant library using deep sequencing, we identified three immunity proteins that render protection against killing by T6SS predatory cells. We also identified their three cognate T6SS-secreted effectors and show these are important for not only antibacterial and antieukaryotic activities but also assembly of T6SS apparatus. The lipase and muramidase T6SS effectors identified in this study underscore the diversity of T6SS-secreted substrates and the distinctly different mechanisms that target these for secretion by the dynamic T6SS organelle.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "310", "doc_id": "22632303", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Lack of FGF21 in mice leads to reduced lifespan.\n\nCANDIDATE_PASSAGE:\nDementia incidence and mortality in middle-income countries, and associations with indicators of cognitive reserve: a 10/66 Dementia Research Group population-based cohort study BACKGROUND Results of the few cohort studies from countries with low incomes or middle incomes suggest a lower incidence of dementia than in high-income countries. We assessed incidence of dementia according to criteria from the 10/66 Dementia Research Group and Diagnostic and Statistical Manual of Mental Disorders (DSM) IV, the effect of dementia at baseline on mortality, and the independent effects of age, sex, socioeconomic position, and indicators of cognitive reserve. METHODS We did a population-based cohort study of all people aged 65 years and older living in urban sites in Cuba, the Dominican Republic, and Venezuela, and rural and urban sites in Peru, Mexico, and China, with ascertainment of incident 10/66 and DSM-IV dementia 3-5 years after cohort inception. We used questionnaires to obtain information about age in years, sex, educational level, literacy, occupational attainment, and number of household assets. We obtained information about mortality from all sites. For participants who had died, we interviewed a friend or relative to ascertain the likelihood that they had dementia before death. FINDINGS 12,887 participants were interviewed at baseline. 11,718 were free of dementia, of whom 8137 (69%) were reinterviewed, contributing 34,718 person-years of follow-up. Incidence for 10/66 dementia varied between 18·2 and 30·4 per 1000 person-years, and were 1·4-2·7 times higher than were those for DSM-IV dementia (9·9-15·7 per 1000 person-years). Mortality hazards were 1·56-5·69 times higher in individuals with dementia at baseline than in those who were dementia-free. Informa [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "682", "doc_id": "14682243", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does shaving the incision site increase the infection rate after spinal surgery?\n\nABSTRACT:\nA prospective randomized clinical study. To determine whether shaving the incision site before spinal surgery causes postsurgical infection. Spine surgeons usually shave the skin of the incision site immediately before surgery is performed. However, evidence from some surgical series suggests that presurgical shaving may increase the postsurgical infection rate. To our knowledge, no previously published studies have addressed this issue. A total of 789 patients scheduled to undergo spinal surgery were randomly allocated into 2 groups: those in whom the site of operation was shaved immediately before surgery (shaved group; 371 patients) and the patients in whom presurgical shaving was not performed (unshaved group; 418 patients). The mean duration of anesthesia and the infection rates in both groups were recorded and compared. The duration of anesthesia did not differ in the 2 groups (P>0.05). A postoperative infection developed in 4 patients in the shaved group and in 1 patient in the nonshaved group (P<0.01).", "output": "{\"label\": \"maybe\", \"rationale\": \"The shaving of the incision site immediately before spinal surgery may increase the rate of postoperative infection.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 17621202, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Patients with microcytosis and higher erythrocyte count were more resistant to severe malarial anaemia when infected with Plasmodium falciparum.\n\nCANDIDATE_ABSTRACT:\nTITLE: Increased Microerythrocyte Count in Homozygous α+-Thalassaemia Contributes to Protection against Severe Malarial Anaemia\nABSTRACT: BACKGROUND The heritable haemoglobinopathy alpha(+)-thalassaemia is caused by the reduced synthesis of alpha-globin chains that form part of normal adult haemoglobin (Hb). Individuals homozygous for alpha(+)-thalassaemia have microcytosis and an increased erythrocyte count. Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count. We tested the hypothesis that the erythrocyte indices associated with alpha(+)-thalassaemia homozygosity provide a haematological benefit during acute malaria. METHODS AND FINDINGS Data from children living on the north coast of Papua New Guinea who had participated in a case-control study of the protection afforded by alpha(+)-thalassaemia against severe malaria were reanalysed to assess the genotype-specific reduction in erythrocyte count and Hb levels associated with acute malarial disease. We observed a reduction in median erythrocyte count of approximately 1.5 x 10(12)/l in all children with acute falciparum malaria relative to values in community children (p < 0.001). We developed a simple mathematical model of the linear relationship between Hb concentration and erythrocyte count. This model predicted that children homozygous for alpha(+)-thalassaemia lose less Hb than children of normal genotype for a reduction in erythrocyte count of >1.1 x 10(12)/l as a result of the reduced mean cell Hb in homozygous alpha(+)-thalassaemia. In addition, children homozygous for alpha(+)-thalassaemia require a 10% greater reduction in erythrocyte count than children of normal genotype (p = 0.02) for Hb concentration to fall to 50 g/l, the cutoff for SMA. We estimated that the haematological profile in [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We estimated that the haematological profile in children homozygous for alpha(+)-thalassaemia reduces the risk of SMA during acute malaria compared to children of normal genotype (relative risk 0.52; 95% confidence interval [CI] 0.24-1.12, p = 0.09).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 929, "doc_id": "18174210", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Surfactin producing cells and exopolymer producing cells cooperate to generate \"Van Gogh\" bundles that have sliding abilities on specialized media.\n\nCANDIDATE_PASSAGE:\nFrom Cell Differentiation to Cell Collectives: Bacillus subtilis Uses Division of Labor to Migrate The organization of cells, emerging from cell-cell interactions, can give rise to collective properties. These properties are adaptive when together cells can face environmental challenges that they separately cannot. One particular challenge that is important for microorganisms is migration. In this study, we show how flagellum-independent migration is driven by the division of labor of two cell types that appear during Bacillus subtilis sliding motility. Cell collectives organize themselves into bundles (called \"van Gogh bundles\") of tightly aligned cell chains that form filamentous loops at the colony edge. We show, by time-course microscopy, that these loops migrate by pushing themselves away from the colony. The formation of van Gogh bundles depends critically on the synergistic interaction of surfactin-producing and matrix-producing cells. We propose that surfactin-producing cells reduce the friction between cells and their substrate, thereby facilitating matrix-producing cells to form bundles. The folding properties of these bundles determine the rate of colony expansion. Our study illustrates how the simple organization of cells within a community can yield a strong ecological advantage. This is a key factor underlying the diverse origins of multicellularity.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1114", "doc_id": "12824568", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: CX3CR1 on the Th2 cells impairs T cell survival\n\nCANDIDATE_ABSTRACT:\nTITLE: CX3CR1 is required for airway inflammation by promoting T helper cell survival and maintenance in inflamed lung\nABSTRACT: Allergic asthma is a T helper type 2 (T(H)2)-dominated disease of the lung. In people with asthma, a fraction of CD4(+) T cells express the CX3CL1 receptor, CX3CR1, and CX3CL1 expression is increased in airway smooth muscle, lung endothelium and epithelium upon allergen challenge. Here we found that untreated CX3CR1-deficient mice or wild-type (WT) mice treated with CX3CR1-blocking reagents show reduced lung disease upon allergen sensitization and challenge. Transfer of WT CD4(+) T cells into CX3CR1-deficient mice restored the cardinal features of asthma, and CX3CR1-blocking reagents prevented airway inflammation in CX3CR1-deficient recipients injected with WT T(H)2 cells. We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma. CX3CR1-induced survival was also observed for T(H)1 cells upon airway inflammation but not under homeostatic conditions or upon peripheral inflammation. Therefore, CX3CR1 and CX3CL1 may represent attractive therapeutic targets in asthma.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 216, "doc_id": "21366394", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Cellular clocks are associated with mitosis timing in NIH 3T3 cells.\n\nCANDIDATE_PASSAGE:\nOnce-a-day Concerta methylphenidate versus three-times-daily methylphenidate in laboratory and natural settings. OBJECTIVE Methylphenidate (MPH), the most commonly prescribed drug for attention-deficit/hyperactivity disorder (ADHD), has a short half-life, which necessitates multiple daily doses. The need for multiple doses produces problems with medication administration during school and after-school hours, and therefore with compliance. Previous long-acting stimulants and preparations have shown effects equivalent to twice-daily dosing of MPH. This study tests the efficacy and duration of action, in natural and laboratory settings, of an extended-release MPH preparation designed to last 12 hours and therefore be equivalent to 3-times-daily dosing. METHODS Sixty-eight children with ADHD, 6 to 12 years old, participated in a within-subject, double-blind comparison of placebo, immediate-release (IR) MPH 3 times a day (tid), and Concerta, a once-daily MPH formulation. Three dosing levels of medication were used: 5 mg IR MPH tid/18 mg Concerta once a day (qd); 10 mg IR MPH tid/36 mg Concerta qd; and 15 mg IR MPH tid/54 mg Concerta qd. All children were currently medicated with MPH at enrollment, and each child's dose level was based on that child's MPH dosing before the study. The doses of Concerta were selected to be comparable to the daily doses of MPH that each child received. To achieve the ascending rate of MPH delivery determined by initial investigations to provide the necessary continuous coverage, Concerta doses were 20% higher on a daily basis than a comparable tid regimen of IR MPH. Children received each medication condition for 7 days. The investigation was conducted in the context of a background clinical behavioral intervention in both the natura [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "241", "doc_id": "2475059", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Rapid phosphotransfer rates govern fidelity in two component systems\n\nCANDIDATE_PASSAGE:\nMechanisms of endocytosis. Endocytic mechanisms control the lipid and protein composition of the plasma membrane, thereby regulating how cells interact with their environments. Here, we review what is known about mammalian endocytic mechanisms, with focus on the cellular proteins that control these events. We discuss the well-studied clathrin-mediated endocytic mechanisms and dissect endocytic pathways that proceed independently of clathrin. These clathrin-independent pathways include the CLIC/GEEC endocytic pathway, arf6-dependent endocytosis, flotillin-dependent endocytosis, macropinocytosis, circular doral ruffles, phagocytosis, and trans-endocytosis. We also critically review the role of caveolae and caveolin1 in endocytosis. We highlight the roles of lipids, membrane curvature-modulating proteins, small G proteins, actin, and dynamin in endocytic pathways. We discuss the functional relevance of distinct endocytic pathways and emphasize the importance of studying these pathways to understand human disease processes.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1019", "doc_id": "16319097", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: ART has no effect on the infectiveness of HIV-positive people.\n\nCANDIDATE_PASSAGE:\nHIV Treatment as Prevention: Systematic Comparison of Mathematical Models of the Potential Impact of Antiretroviral Therapy on HIV Incidence in South Africa BACKGROUND Many mathematical models have investigated the impact of expanding access to antiretroviral therapy (ART) on new HIV infections. Comparing results and conclusions across models is challenging because models have addressed slightly different questions and have reported different outcome metrics. This study compares the predictions of several mathematical models simulating the same ART intervention programmes to determine the extent to which models agree about the epidemiological impact of expanded ART. METHODS AND FINDINGS Twelve independent mathematical models evaluated a set of standardised ART intervention scenarios in South Africa and reported a common set of outputs. Intervention scenarios systematically varied the CD4 count threshold for treatment eligibility, access to treatment, and programme retention. For a scenario in which 80% of HIV-infected individuals start treatment on average 1 y after their CD4 count drops below 350 cells/µl and 85% remain on treatment after 3 y, the models projected that HIV incidence would be 35% to 54% lower 8 y after the introduction of ART, compared to a counterfactual scenario in which there is no ART. More variation existed in the estimated long-term (38 y) reductions in incidence. The impact of optimistic interventions including immediate ART initiation varied widely across models, maintaining substantial uncertainty about the theoretical prospect for elimination of HIV from the population using ART alone over the next four decades. The number of person-years of ART per infection averted over 8 y ranged between 5.8 and 18.7. Considering the actual scal [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "60", "doc_id": "13899137", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Pharmacist attendance at ward rounds reduces adverse events in wards.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pharmacist participation on physician rounds and adverse drug events in the intensive care unit.\nABSTRACT: CONTEXT Pharmacist review of medication orders in the intensive care unit (ICU) has been shown to prevent errors, and pharmacist consultation has reduced drug costs. However, whether pharmacist participation in the ICU at the time of drug prescribing reduces adverse events has not been studied. OBJECTIVE To measure the effect of pharmacist participation on medical rounds in the ICU on the rate of preventable adverse drug events (ADEs) caused by ordering errors. DESIGN Before-after comparison between phase 1 (baseline) and phase 2 (after intervention implemented) and phase 2 comparison with a control unit that did not receive the intervention. SETTING A medical ICU (study unit) and a coronary care unit (control unit) in a large urban teaching hospital. PATIENTS Seventy-five patients randomly selected from each of 3 groups: all admissions to the study unit from February 1, 1993, through July 31, 1993 (baseline) and all admissions to the study unit (postintervention) and control unit from October 1, 1994, through July 7, 1995. In addition, 50 patients were selected at random from the control unit during the baseline period. INTERVENTION A senior pharmacist made rounds with the ICU team and remained in the ICU for consultation in the morning, and was available on call throughout the day. MAIN OUTCOME MEASURES Preventable ADEs due to ordering (prescribing) errors and the number, type, and acceptance of interventions made by the pharmacist. Preventable ADEs were identified by review of medical records of the randomly selected patients during both preintervention and postintervention phases. Pharmacists recorded all recommendations, which were then analyzed by type and acceptance. RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 pat [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 patient-days (95% confidence interval [CI], 7-14) before the intervention to 3.5 (95% CI, 1-5; P<.001) after the intervention.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 941, "doc_id": "12258338", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: aPKCz causes tumour enhancement by affecting glutamine metabolism.\n\nCANDIDATE_ABSTRACT:\nTITLE: Junctional actin assembly is mediated by Formin-like 2 downstream of Rac1\nABSTRACT: Epithelial integrity is vitally important, and its deregulation causes early stage cancer. De novo formation of an adherens junction (AJ) between single epithelial cells requires coordinated, spatial actin dynamics, but the mechanisms steering nascent actin polymerization for cell-cell adhesion initiation are not well understood. Here we investigated real-time actin assembly during daughter cell-cell adhesion formation in human breast epithelial cells in 3D environments. We identify formin-like 2 (FMNL2) as being specifically required for actin assembly and turnover at newly formed cell-cell contacts as well as for human epithelial lumen formation. FMNL2 associates with components of the AJ complex involving Rac1 activity and the FMNL2 C terminus. Optogenetic control of Rac1 in living cells rapidly drove FMNL2 to epithelial cell-cell contact zones. Furthermore, Rac1-induced actin assembly and subsequent AJ formation critically depends on FMNL2. These data uncover FMNL2 as a driver for human epithelial AJ formation downstream of Rac1.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1382, "doc_id": "2576811", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Commelina yellow mottle virus' (ComYMV) genome consists of 2140 baise pairs.\n\nCANDIDATE_ABSTRACT:\nTITLE: Properties of Commelina yellow mottle virus's complete DNA sequence, genomic discontinuities and transcript suggest that it is a pararetrovirus.\nABSTRACT: The non-enveloped bacilliform viruses are the second group of plant viruses known to possess a genome consisting of circular double-stranded DNA. We have characterized the viral transcript and determined the complete sequence of the genome of Commelina mellow mottle virus (CoYMV), a member of this group. Analysis of the viral transcript indicates that the virus encodes a single terminally-redundant genome-length plus 120 nucleotide transcript. A fraction of the transcripts is polyadenylated, although the majority of the transcript is not polyadenylated. Analysis of the genome sequence indicates that the genome is 7489 bp in size and that the transcribed strand contains three open reading frames capable of encoding proteins of 23, 15 and 216 kd. The function of the 25 and 15 kd proteins is unknown. Similarities between the 216 kd polypeptide and the cauliflower mosaic virus coat protein and protease/reverse transcriptase polyprotein suggest that the 216 kd polypeptide is a polyprotein that is proteolytically processed to yield the virion coat protein, a protease, and replicase (reverse transcriptase and ribonuclease H). Each strand of the CoYMV genome is interrupted by site-specific discontinuities. The locations of the 5'-ends of these discontinuities, and the presence and location of a region on the CoYMV transcript capable of annealing with the 3'-end of cytosolic initiator methionine tRNA are consistent with replication by reverse transcription. We have demonstrated that a construct containing 1.3 CoYMV genomes is infective when introduced into Commelina diffusa, the host for CoYMV, using Agrobacterium-mediated infection.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Analysis of the genome sequence indicates that the genome is 7489 bp in size and that the transcribed strand contains three open reading frames capable of encoding proteins of 23, 15 and 216 kd.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 278, "doc_id": "14376683", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does serum adiponectin correlate with viral characteristics but not histologic features in patients with chronic hepatitis C?\n\nABSTRACT:\nAdiponectin induces insulin sensitivity and modulates inflammatory responses. We thus studied the implications of adiponectin in patients with chronic hepatitis C virus (HCV) infection inherently linked to insulin resistance. We analyzed the association of serum adiponectin levels with clinical, virologic, and histologic findings in 95 naive Taiwanese patients with chronic hepatitis C before and after antiviral therapy. At baseline, 14 (15%) of the 95 patients were obese and 26 (27%) had type 2 diabetes mellitus. Fifty-seven patients were infected with HCV genotype 1 and 38 with genotype 2. Steatosis and periportal fibrosis was present in 44 (46%) and 69 (73%), respectively. In multivariate analysis, male gender, insulin resistance, high HCV load and genotype 2 were significantly associated with a lower serum adiponectin level. In contrast, intrahepatic gene expression of adiponectin receptors was higher in genotype 2 compared with genotype 1. Serum adiponectin level did not correlate with other clinical or histologic parameters. After treatment, change of steatosis also did not correlate with the change of adiponectin level (P=0.61).", "output": "{\"label\": \"yes\", \"rationale\": \"Adiponectin correlated with hepatitis C viral factors at both serum and liver tissue levels. The interactions among adiponectin, insulin resistance and chronic HCV infection merit further studies.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 15964656, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: ALDH1 expression is associated with poorer prognosis for breast cancer primary tumors.\n\nCANDIDATE_ABSTRACT:\nTITLE: ALDH1 is a marker of normal and malignant human mammary stem cells and a predictor of poor clinical outcome.\nABSTRACT: Application of stem cell biology to breast cancer research has been limited by the lack of simple methods for identification and isolation of normal and malignant stem cells. Utilizing in vitro and in vivo experimental systems, we show that normal and cancer human mammary epithelial cells with increased aldehyde dehydrogenase activity (ALDH) have stem/progenitor properties. These cells contain the subpopulation of normal breast epithelium with the broadest lineage differentiation potential and greatest growth capacity in a xenotransplant model. In breast carcinomas, high ALDH activity identifies the tumorigenic cell fraction, capable of self-renewal and of generating tumors that recapitulate the heterogeneity of the parental tumor. In a series of 577 breast carcinomas, expression of ALDH1 detected by immunostaining correlated with poor prognosis. These findings offer an important new tool for the study of normal and malignant breast stem cells and facilitate the clinical application of stem cell concepts.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In a series of 577 breast carcinomas, expression of ALDH1 detected by immunostaining correlated with poor prognosis.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 52, "doc_id": "45638119", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Do emergency medical services professionals think they should participate in disease prevention?\n\nABSTRACT:\nThe primary objective of the study was to determine emergency medical services (EMS) professionals' opinions regarding participation in disease and injury prevention programs. A secondary objective was to determine the proportion of EMS professionals who had participated in disease prevention programs. As part of the National Registry of Emergency Medical Technicians' biennial reregistration process, EMS professionals reregistering in 2006 were asked to complete an optional survey regarding their opinions on and participation in disease and injury prevention. Demographic characteristics were also collected. Data were analyzed using descriptive statistics and 99% confidence intervals (CIs). The chi-square test was used to compare differences by responder demographics (alpha = 0.01). A 10% difference between groups was determined to be clinically significant. The survey was completed by 27,233 EMS professionals. Of these responders, 82.7% (99% CI: 82.1-83.3) felt that EMS professionals should participate in disease prevention, with those working 20 to 29 hours per week being the least likely to think they should participate (67.4%, p<0.001). About a third, 33.8% (99% CI: 33.1-34.6), of the respondents reported having provided prevention services, with those having a graduate degree (43.5%, p<0.001), those working in EMS for more than 21 years (44%, p<0.001), those working for the military (57%, p<0.001), those working 60 to 69 hours per week (41%, p<0.001), and those responding to zero emergency calls in a typical week (43%, p<0.001) being the most likely to report having provided prevention services. About half, 51.1% (99% CI: 50.4-51.9), of the respondents agreed that prevention services should be provided during emergency calls, and 7.7% (99% CI: 7.3-8.1) o [TRUNCATED]", "output": "{\"label\": \"maybe\", \"rationale\": \"The majority of EMS professionals thought that they should participate in disease and injury prevention programs. The respondents were mixed as to whether prevention services should be provided while on emergency calls, but those with experience providing these services were more likely to agree with providing them during emergency calls.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 19145527, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Intra-cerebroventricular infusion of amyloid-β oligomers increases expression of fibronectin type-III domain-containing protein 5 mRNA in mice hippocampi.\n\nCANDIDATE_PASSAGE:\nTargeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs). GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets. We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels. To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA). Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis. The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays. The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts. In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival. Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation. Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "654", "doc_id": "33370", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: In mice, P. chabaudi parasites are able to proliferate faster early in infection when inoculated at lower numbers than when inoculated at high numbers.\n\nCANDIDATE_ABSTRACT:\nTITLE: Partitioning regulatory mechanisms of within-host malaria dynamics using the effective propagation number.\nABSTRACT: Immune clearance and resource limitation (via red blood cell depletion) shape the peaks and troughs of malaria parasitemia, which in turn affect disease severity and transmission. Quantitatively partitioning the relative roles of these effects through time is challenging. Using data from rodent malaria, we estimated the effective propagation number, which reflects the relative importance of contrasting within-host control mechanisms through time and is sensitive to the inoculating parasite dose. Our analysis showed that the capacity of innate responses to restrict initial parasite growth saturates with parasite dose and that experimentally enhanced innate immunity can affect parasite density indirectly via resource depletion. Such a statistical approach offers a tool to improve targeting of drugs or vaccines for human therapy by revealing the dynamics and interactions of within-host regulatory mechanisms.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 577, "doc_id": "5289038", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Replacement of histone H2A with H2A.Z accelerates gene activation in yeasts by destabilizing +1 nucleosomes.\n\nCANDIDATE_PASSAGE:\nInferring nucleosome positions with their histone mark annotation from ChIP data MOTIVATION The nucleosome is the basic repeating unit of chromatin. It contains two copies each of the four core histones H2A, H2B, H3 and H4 and about 147 bp of DNA. The residues of the histone proteins are subject to numerous post-translational modifications, such as methylation or acetylation. Chromatin immunoprecipitiation followed by sequencing (ChIP-seq) is a technique that provides genome-wide occupancy data of these modified histone proteins, and it requires appropriate computational methods. RESULTS We present NucHunter, an algorithm that uses the data from ChIP-seq experiments directed against many histone modifications to infer positioned nucleosomes. NucHunter annotates each of these nucleosomes with the intensities of the histone modifications. We demonstrate that these annotations can be used to infer nucleosomal states with distinct correlations to underlying genomic features and chromatin-related processes, such as transcriptional start sites, enhancers, elongation by RNA polymerase II and chromatin-mediated repression. Thus, NucHunter is a versatile tool that can be used to predict positioned nucleosomes from a panel of histone modification ChIP-seq experiments and infer distinct histone modification patterns associated to different chromatin states. AVAILABILITY The software is available at http://epigen.molgen.mpg.de/nuchunter/.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1040", "doc_id": "175735", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does use of hydrophilic guidewires significantly improve technical success rates of peripheral PTA?\n\nABSTRACT:\nTo determine whether the use of hydrophilic guidewires has increased the technical success rate of peripheral percutaneous transluminal angioplasty (PTA).MATERIAL/ We performed 125 procedures and analyzed the technical success rates of PTA using the conventional guidewire first and then if needed, the hydrophilic guidewire for iliac and SFA stenoses or occlusions. Angioplasty was performed on 25 stenosed, 25 occluded iliac arteries and 25 stenosed, 50 occluded femoral arteries. The result was defined as technical success when the lesion was crossed by a guidewire and balloon, then it was dilated with restoration of vessel lumen and less than 30% residual stenosis and the rise in ABI values was at least 0.15 after 24 hours. The technical success rate after PTA of stenosed iliac arteries was achieved in 96% (24/25) using conventional wires and 100% using hydrophilic guidewire; in iliac occlusions, the rates were 60% (15/25) and 96%, respectively; in femoral stenosis - 84% (21/25) and 100%; in occlusions in the first group: lesions<10 cm -64% (16/25) and 96%, in the second group: lesions>10 cm -48% (12/25) and 88%. In the iliac group, there was no significant difference in the success of iliac stenosis PTA. However, there were significant changes in the success rates of PTA performed for SFA stenosis and iliac and SFA occlusions.", "output": "{\"label\": \"maybe\", \"rationale\": \"In summary, we report an overall improvement and high technical success rate for peripherial PTA. The use of hydrophilic guidewires made significant difference to the technical success rate of PTA, especially in occlusion and more complicated lesions.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 16538201, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Auditory entrainment is strengthened when people see congruent visual and auditory information.\n\nCANDIDATE_ABSTRACT:\nTITLE: Congruent Visual Speech Enhances Cortical Entrainment to Continuous Auditory Speech in Noise-Free Conditions.\nABSTRACT: UNLABELLED Congruent audiovisual speech enhances our ability to comprehend a speaker, even in noise-free conditions. When incongruent auditory and visual information is presented concurrently, it can hinder a listener's perception and even cause him or her to perceive information that was not presented in either modality. Efforts to investigate the neural basis of these effects have often focused on the special case of discrete audiovisual syllables that are spatially and temporally congruent, with less work done on the case of natural, continuous speech. Recent electrophysiological studies have demonstrated that cortical response measures to continuous auditory speech can be easily obtained using multivariate analysis methods. Here, we apply such methods to the case of audiovisual speech and, importantly, present a novel framework for indexing multisensory integration in the context of continuous speech. Specifically, we examine how the temporal and contextual congruency of ongoing audiovisual speech affects the cortical encoding of the speech envelope in humans using electroencephalography. We demonstrate that the cortical representation of the speech envelope is enhanced by the presentation of congruent audiovisual speech in noise-free conditions. Furthermore, we show that this is likely attributable to the contribution of neural generators that are not particularly active during unimodal stimulation and that it is most prominent at the temporal scale corresponding to syllabic rate (2-6 Hz). Finally, our data suggest that neural entrainment to the speech envelope is inhibited when the auditory and visual streams are incongruent both temporally and contextually. SIGNIFICANCE STATEMENT Seeing a speaker's face as he or she talks can greatly help in understan [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Specifically, we show that the brain's representation of auditory speech is enhanced when the accompanying visual speech signal shares the same timing.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 141, "doc_id": "14437255", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Dexamethasone decreases risk of postoperative bleeding.\n\nCANDIDATE_ABSTRACT:\nTITLE: Dexamethasone and risk of nausea and vomiting and postoperative bleeding after tonsillectomy in children: a randomized trial.\nABSTRACT: CONTEXT Dexamethasone is widely used to prevent postoperative nausea and vomiting (PONV) in pediatric tonsillectomy. OBJECTIVE To assess whether dexamethasone dose-dependently reduces the risk of PONV at 24 hours after tonsillectomy. DESIGN, SETTING, AND PATIENTS Randomized placebo-controlled trial conducted among 215 children undergoing elective tonsillectomy at a major public teaching hospital in Switzerland from February 2005 to December 2007. INTERVENTIONS Children were randomly assigned to receive dexamethasone (0.05, 0.15, or 0.5 mg/kg) or placebo intravenously after induction of anesthesia. Acetaminophen-codeine and ibuprofen were given as postoperative analgesia. Follow-up continued until the 10th postoperative day. MAIN OUTCOME MEASURES The primary end point was prevention of PONV at 24 hours; secondary end points were decrease in the need for ibuprofen at 24 hours and evaluation of adverse effects. RESULTS At 24 hours, 24 of 54 participants who received placebo (44%; 95% confidence interval [CI], 31%-59%) had experienced PONV compared with 20 of 53 (38%; 95% CI, 25%-52%), 13 of 54 (24%; 95% CI, 13%-38%), and 6 of 52 (12%; 95% CI, 4%-23%) who received dexamethasone at 0.05, 0.15, and 0.5 mg/kg, respectively (P<.001 for linear trend). Children who received dexamethasone received significantly less ibuprofen. There were 26 postoperative bleeding episodes in 22 children. Two of 53 (4%; 95% CI, 0.5%-13%) children who received placebo had bleeding compared with 6 of 53 (11%; 95% CI, 4%-23%), 2 of 51 (4%; 95% CI, 0.5%-13%), and 12 of 50 (24%; 95% CI, 13%-38%) who received dexamethasone at 0.05, 0.15, and 0.5 mg/kg, respectively (P = .003). Dexamethasone, 0.5 mg/kg, was associated with the highest bleeding risk (adjusted relative risk, 6.80; 95% CI, 1.77-1 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Dexamethasone, 0.5 mg/kg, was associated with the highest bleeding risk (adjusted relative risk, 6.80; 95% CI, 1.77-16.5).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 338, "doc_id": "23349986", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does ultrasound imaging before puncture facilitate internal jugular vein cannulation?\n\nABSTRACT:\nTo investigate whether prepuncture ultrasound evaluation of vascular anatomy facilitates internal jugular vein cannulation compared with landmark-guided puncture. Prospective randomized study. Single community hospital. Adult patients undergoing general anesthesia (n = 240). The right internal jugular vein was cannulated using either anatomic landmarks or prepuncture ultrasound (3.75/7.5 MHz) guidance. In the landmark group, respiratory jugular venodilation was used as the primary landmark for locating the vein. Results of cannulation and the incidence of complications were compared. Patients were randomly assigned to the ultrasound or landmark group. Respiratory jugular venodilation was identified in 188 patients (78.3%), in whom results of cannulation did not differ between the 2 techniques with respect to the venous access rate (cannulated at the first attempt: 83.5% in the landmark v 85.7% in the ultrasound group), the success rate (cannulated within 3 attempts: 96.9% v 95.6%), and the incidence of arterial puncture (1.0% v 3.3%). In the remaining 52 respiratory jugular venodilation-unidentified patients, the access rate (30.4% v 86.2%, p<0.001) and the success rate (78.3 v 100%, p<0.05) were significantly better in the ultrasound group, and no arterial puncture was recorded in the ultrasound group, whereas the incidence was 13.0% in the landmark group. The results were similar regardless of the ultrasound frequency used.", "output": "{\"label\": \"maybe\", \"rationale\": \"Prepuncture ultrasound evaluation did not improve the result of right internal jugular vein cannulation compared with the respiratory jugular venodilation-guided approach. When the landmark was not observed, however, the prepuncture ultrasound guidance was helpful in facilitating the cannulation.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 12407608, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Primary cervical cancer screening with HPV detection has higher longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_PASSAGE:\nHuman papillomavirus testing for the detection of high-grade cervical intraepithelial neoplasia and cancer: final results of the POBASCAM randomised controlled trial. BACKGROUND Human papillomavirus (HPV) testing is more sensitive for the detection of high-grade cervical lesions than is cytology, but detection of HPV by DNA screening in two screening rounds 5 years apart has not been assessed. The aim of this study was to assess whether HPV DNA testing in the first screen decreases detection of cervical intraepithelial neoplasia (CIN) grade 3 or worse, CIN grade 2 or worse, and cervical cancer in the second screening. METHODS In this randomised trial, women aged 29-56 years participating in the cervical screening programme in the Netherlands were randomly assigned to receive HPV DNA (GP5+/6+-PCR method) and cytology co-testing or cytology testing alone, from January, 1999, to September, 2002. Randomisation (in a 1:1 ratio) was done with computer-generated random numbers after the cervical specimen had been taken. At the second screening 5 years later, HPV DNA and cytology co-testing was done in both groups; researchers were masked to the patient's assignment. The primary endpoint was the number of CIN grade 3 or worse detected. Analysis was done by intention to screen. The trial is now finished and is registered, number ISRCTN20781131. FINDINGS 22,420 women were randomly assigned to the intervention group and 22 518 to the control group; 19 999 in the intervention group and 20,106 in the control group were eligible for analysis at the first screen. At the second screen, 19 579 women in the intervention group and 19,731 in the control group were eligible, of whom 16,750 and 16,743, respectively, attended the second screen. In the second round, CIN grade 3 or [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "971", "doc_id": "9764256", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Epidemiological disease burden from noncommunicable diseases is more prevalent in high economic settings.\n\nCANDIDATE_PASSAGE:\nPrevalence of late-life depression and gap in mental health service use across European regions. Background We aimed to determine the prevalence and gap in use of mental health services for late-life depression in four European regions (Western Europe, Scandinavia, Southern Europe and Central and Eastern Europe) and explore socio-demographic, social and health-related factors associated with it. Methods We conducted a cross-sectional study based on data from the Survey on Health, Ageing and Retirement in Europe. Participants were a population-based sample of 28 796 persons (53% women, mean age 74 years old) residing in Europe. Mental health service use was estimated using information about the diagnosis or treatment for depression. Results The prevalence of late-life depression was 29% in the whole sample and was highest in Southern Europe (35%), followed by Central and Eastern Europe (32%), Western Europe (26%) and lowest in Scandinavia (17%). Factors that had the strongest association with depression were total number of chronic diseases, pain, limitations in instrumental activities of daily living, grip strength and cognitive impairment. The gap in mental health service use was 79%. Conclusions We suggest that interventions to decrease the burden of late-life depression should be targeted at individuals that are affected by chronic somatic comorbidities and are limited in mental and physical functioning. Promotion of help-seeking of older adults, de-stigmatization of mental illness and education of general practitioners could help decrease the gap in mental health service utilization.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "383", "doc_id": "58564850", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Increased LDL receptors plays a role in the reduction of plasma Lp(a).\n\nCANDIDATE_PASSAGE:\nEnhancement of proteasome function by PA28α overexpression protects against oxidative stress. The principal function of the proteasome is targeted degradation of intracellular proteins. Proteasome dysfunction has been observed in experimental cardiomyopathies and implicated in human congestive heart failure. Measures to enhance proteasome proteolytic function are currently lacking but would be beneficial in testing the pathogenic role of proteasome dysfunction and could have significant therapeutic potential. The association of proteasome activator 28 (PA28) with the 20S proteasome may play a role in antigen processing. It is unclear, however, whether the PA28 plays any important role outside of antigen presentation, although up-regulation of PA28 has been observed in certain types of cardiomyopathy. Here, we show that PA28α overexpression (PA28αOE) stabilized PA28β, increased 11S proteasomes, and enhanced the degradation of a previously validated proteasome surrogate substrate (GFPu) in cultured neonatal rat cardiomyocytes. PA28αOE significantly attenuated H(2)O(2)-induced increases in the protein carbonyls and markedly suppressed apoptosis in cultured cardiomyocytes under basal conditions or when stressed by H(2)O(2). We conclude that PA28αOE is sufficient to up-regulate 11S proteasomes, enhance proteasome-mediated removal of misfolded and oxidized proteins, and protect against oxidative stress in cardiomyocytes, providing a highly sought means to increase proteasomal degradation of abnormal cellular proteins.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "603", "doc_id": "28164534", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Deltex interacts with eIF3. There is no known interaction between Deltex and elF3\n\nCANDIDATE_PASSAGE:\nChromatin remodelling at promoters suppresses antisense transcription Chromatin allows the eukaryotic cell to package its DNA efficiently. To understand how chromatin structure is controlled across the Saccharomyces cerevisiae genome, we have investigated the role of the ATP-dependent chromatin remodelling complex Isw2 in positioning nucleosomes. We find that Isw2 functions adjacent to promoter regions where it repositions nucleosomes at the interface between genic and intergenic sequences. Nucleosome repositioning by Isw2 is directional and results in increased nucleosome occupancy of the intergenic region. Loss of Isw2 activity leads to inappropriate transcription, resulting in the generation of both coding and noncoding transcripts. Here we show that Isw2 repositions nucleosomes to enforce directionality on transcription by preventing transcription initiation from cryptic sites. Our analyses reveal how chromatin is organized on a global scale and advance our understanding of how transcription is regulated.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "331", "doc_id": "4305576", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Homozygous deletion of murine Sbds gene from osterix-expressing mesenchymal stem and progenitor cells (MPCs) prevents oxidative stress.\n\nCANDIDATE_PASSAGE:\nMesenchymal Inflammation Drives Genotoxic Stress in Hematopoietic Stem Cells and Predicts Disease Evolution in Human Pre-leukemia. Mesenchymal niche cells may drive tissue failure and malignant transformation in the hematopoietic system, but the underlying molecular mechanisms and relevance to human disease remain poorly defined. Here, we show that perturbation of mesenchymal cells in a mouse model of the pre-leukemic disorder Shwachman-Diamond syndrome (SDS) induces mitochondrial dysfunction, oxidative stress, and activation of DNA damage responses in hematopoietic stem and progenitor cells. Massive parallel RNA sequencing of highly purified mesenchymal cells in the SDS mouse model and a range of human pre-leukemic syndromes identified p53-S100A8/9-TLR inflammatory signaling as a common driving mechanism of genotoxic stress. Transcriptional activation of this signaling axis in the mesenchymal niche predicted leukemic evolution and progression-free survival in myelodysplastic syndrome (MDS), the principal leukemia predisposition syndrome. Collectively, our findings identify mesenchymal niche-induced genotoxic stress in heterotypic stem and progenitor cells through inflammatory signaling as a targetable determinant of disease outcome in human pre-leukemia.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "527", "doc_id": "3863543", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Omnivores produce less trimethylamine N-oxide from dietary I-carnitine than vegans.\n\nCANDIDATE_ABSTRACT:\nTITLE: Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis\nABSTRACT: Intestinal microbiota metabolism of choline and phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO). We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice. Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism. The presence of specific bacterial taxa in human feces was associated with both plasma TMAO concentration and dietary status. Plasma L-carnitine levels in subjects undergoing cardiac evaluation (n = 2,595) predicted increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels. Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed. In mice with an intact intestinal microbiota, dietary supplementation with TMAO or either carnitine or choline reduced in vivo reverse cholesterol transport. Intestinal microbiota may thus contribute to the well-established link between high levels of red meat consumption and CVD risk.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 881, "doc_id": "14803797", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Beta-band coherence is diminished for visible stimuli over invisible stimuli.\n\nCANDIDATE_PASSAGE:\nA model of multiple myeloma: culture of 5T33 murine myeloma cells and evaluation of tumorigenicity in the C57BL/KaLwRij mouse. The 5T33 multiple myeloma is one of a series of transplantable murine myelomas arising spontaneously in C57BL/KaLwRij mice. This study describes the establishment and characterisation of the 5T33 murine myeloma in vitro as a cultured cell line in terms of its morphology, growth rate, expression of paraprotein (IgG2b) and tumorigenicity in syngeneic animals. The 5T33 cell line has been in continuous culture for over 10 months and has achieved more than passage 34. In culture, 5T33 myeloma grows as single cells or in small clusters of loosely adherent cells on an adherent stromal cell layer. Maximum doubling time is approximately 25 h, and over 90% of the cells express cytoplasmic IgG2b paraprotein. The cultured 5T33 myeloma cells are highly tumorigenic in C57BL/KaLwRij mice with as few as 500 cells inducing paralysis and death as early as day 36 post-tumour inoculation. Kinetics of tumour development and detection of IgG2b paraprotein are dose dependent. Two weeks following intravenous inoculation of 5 x 10(5) cultured 5T33 myeloma cells, tumour cells were readily identified in the bone marrow. By 3 weeks post-tumour inoculation, 5T33 myeloma cells were found in various tissues throughout the animal. Studies are now underway to determine the sensitivity of this cell line to various therapeutic modalities.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "174", "doc_id": "13889962", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: In melanoma, anti-CTLA-4 treatment reinvigorates exhausted PD-1+Eomes+CD8 T cells.\n\nCANDIDATE_PASSAGE:\nThe inflammasome component NLRP3 impairs antitumor vaccine by enhancing the accumulation of tumor-associated myeloid-derived suppressor cells. The inflammasome is a proteolysis complex that generates the active forms of the proinflammatory cytokines interleukin (IL)-1β and IL-18. Inflammasome activation is mediated by NLR proteins that respond to microbial and nonmicrobial stimuli. Among NLRs, NLRP3 senses the widest array of stimuli and enhances adaptive immunity. However, its role in antitumor immunity is unknown. Therefore, we evaluated the function of the NLRP3 inflammasome in the immune response using dendritic cell vaccination against the poorly immunogenic melanoma cell line B16-F10. Vaccination of Nlrp3(-/-) mice led to a relative 4-fold improvement in survival relative to control animals. Immunity depended on CD8(+) T cells and exhibited immune specificity and memory. Increased vaccine efficacy in Nlrp3(-/-) hosts did not reflect differences in dendritic cells but rather differences in myeloid-derived suppressor cells (MDSC). Although Nlrp3 was expressed in MDSCs, the absence of Nlrp3 did not alter either their functional capacity to inhibit T cells or their presence in peripheral lymphoid tissues. Instead, the absence of Nlrp3 caused a 5-fold reduction in the number of tumor-associated MDSCs found in host mice. Adoptive transfer experiments also showed that Nlrp3(-/-) MDSCs were less efficient in reaching the tumor site. Depleting MDSCs with an anti-Gr-1 antibody increased the survival of tumor-bearing wild-type mice but not Nlrp3(-/-) mice. We concluded that Nlrp3 was critical for accumulation of MDSCs in tumors and for inhibition of antitumor T-cell immunity after dendritic cell vaccination. Our findings establish an unexpected role for Nlrp3 in [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "576", "doc_id": "15435343", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does valve system reduce the catheter-related bloodstream infection?\n\nABSTRACT:\nThe Groshong catheter (GC) is considered to have a lower risk of central venous catheter-related bloodstream infection (CVC-RBSI) than conventional catheters because of its valve system (closed-end) for preventing blood reflux. However, few studies have compared the GC with conventional (open-end) catheters in terms of catheter-related complications. To compare the incidence of catheter-related complications including CVC-RBSI between the GC and the Argyle catheter (AC). The GC and the AC were inserted in the same way from the internal jugular vein. Catheter-related complications were evaluated from the database retrospectively. Two hundred seventy GCs were inserted in 123 patients, and 251 ACs were inserted in 135 patients. There were no significant differences in patient background factors between GC and AC use, except for the following two parameters. Use of GC was associated with a longer catheter insertion length and a younger patient age. Univariate analysis revealed that neither type of catheter reduced the incidence of CVC-RBSI. Kaplan-Meier analysis and log rank test revealed no significant difference between the GC and the AC in the period from insertion to development of complications.", "output": "{\"label\": \"no\", \"rationale\": \"The GC has no superiority over the conventional AC for preventing CVC-RBSI.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 20001813, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Gastric infection with Helicobacter pylori decreases risk of gastric cancer in humans.\n\nCANDIDATE_PASSAGE:\nCombined Impact of Lifestyle-Related Factors on Total and Cause-Specific Mortality among Chinese Women: Prospective Cohort Study BACKGROUND Although cigarette smoking, excessive alcohol drinking, obesity, and several other well-studied unhealthy lifestyle-related factors each have been linked to the risk of multiple chronic diseases and premature death, little is known about the combined impact on mortality outcomes, in particular among Chinese and other non-Western populations. The objective of this study was to quantify the overall impact of lifestyle-related factors beyond that of active cigarette smoking and alcohol consumption on all-cause and cause-specific mortality in Chinese women. METHODS AND FINDINGS We used data from the Shanghai Women's Health Study, an ongoing population-based prospective cohort study in China. Participants included 71,243 women aged 40 to 70 years enrolled during 1996-2000 who never smoked or drank alcohol regularly. A healthy lifestyle score was created on the basis of five lifestyle-related factors shown to be independently associated with mortality outcomes (normal weight, lower waist-hip ratio, daily exercise, never exposed to spouse's smoking, higher daily fruit and vegetable intake). The score ranged from zero (least healthy) to five (most healthy) points. During an average follow-up of 9 years, 2,860 deaths occurred, including 775 from cardiovascular disease (CVD) and 1,351 from cancer. Adjusted hazard ratios for mortality decreased progressively with an increasing number of healthy lifestyle factors. Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for c [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "447", "doc_id": "1456068", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: There is a relation between Erythromycin use and hypertrophic pyloric stenosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Specificity Residues Determine Binding Affinity for Two-Component Signal Transduction Systems\nABSTRACT: UNLABELLED Two-component systems (TCS) comprise histidine kinases and their cognate response regulators and allow bacteria to sense and respond to a wide variety of signals. Histidine kinases (HKs) phosphorylate and dephosphorylate their cognate response regulators (RRs) in response to stimuli. In general, these reactions appear to be highly specific and require an appropriate association between the HK and RR proteins. The Myxococcus xanthus genome encodes one of the largest repertoires of signaling proteins in bacteria (685 open reading frames [ORFs]), including at least 127 HKs and at least 143 RRs. Of these, 27 are bona fide NtrC-family response regulators, 21 of which are encoded adjacent to their predicted cognate kinases. Using system-wide profiling methods, we determined that the HK-NtrC RR pairs display a kinetic preference during both phosphotransfer and phosphatase functions, thereby defining cognate signaling systems in M. xanthus. Isothermal titration calorimetry measurements indicated that cognate HK-RR pairs interact with dissociation constants (Kd) of approximately 1 µM, while noncognate pairs had no measurable binding. Lastly, a chimera generated between the histidine kinase, CrdS, and HK1190 revealed that residues conferring phosphotransfer and phosphatase specificity dictate binding affinity, thereby establishing discrete protein-protein interactions which prevent cross talk. The data indicate that binding affinity is a critical parameter governing system-wide signaling fidelity for bacterial signal transduction proteins. IMPORTANCE Using in vitro phosphotransfer and phosphatase profiling assays and isothermal titration calorimetry, we have taken a system-wide approach to demonstrate specificity for a family of two-component signaling prot [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1289, "doc_id": "1225513", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Incidence rates of cervical cancer have decreased.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mass screening programmes and trends in cervical cancer in Finland and the Netherlands.\nABSTRACT: With respect to cervical cancer management, Finland and the Netherlands are comparable in relevant characteristics, e.g., fertility rate, age-of-mother at first birth and a national screening programme for several years. The aim of this study is to compare trends in incidence of and mortality from cervical cancer in Finland and the Netherlands in relation to the introduction and intensity of the screening programmes. Therefore, incidence and mortality rates were calculated using the Cancer Registries of Finland and the Netherlands. Data on screening intensity were obtained from the Finnish Cancer Registry and the Dutch evaluation centre at ErasmusMC-Rotterdam. Women aged 30-60 have been screened every 5 years, in Finland since 1992 and in the Netherlands since 1996. Screening protocols for smear taking and referral to the gynaecologist are comparable. Incidence and mortality rates have declined more in Finland. In 2003, age-adjusted incidence and mortality in Finland were 4.0 and 0.9 and in the Netherlands 4.9 and 1.4 per 100,000 woman-years, respectively. Excess smear use in the Netherlands was estimated to be 24 per 1,000 women during a 5-year interval compared to 121 in Finland. The decline in mortality in Finland seems to be almost completely related to the screening programme whereas in the Netherlands it was initially considered to be a natural decline. Differences in risk factors might also play a role: the Netherlands has higher population density and higher percentages of immigrants and (female) smokers. The greater excess smear use in Finland might also have affected incidence.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Incidence and mortality rates have declined more in Finland.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 597, "doc_id": "25742130", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Lmna knock-in models are appropriate for testing therapeutic approaches against Hutchinson-Gilford progeria syndrome (HGPS).\n\nCANDIDATE_PASSAGE:\nOptimal therapy for reduction of lipoprotein(a). WHAT IS KNOWN AND OBJECTIVE There is a growing body of experimental and clinical evidence for the atherogenic and pro-thrombotic potential of Lipoprotein(a) [Lp(a)], as well as for its causative role in coronary heart disease and stroke. We comment on novel strategies for reducing Lp(a) levels. COMMENT Irrespective of the underlying biological mechanisms explaining the athero-thrombotic potential of this lipoprotein, most work has focused on the identification of suitable therapies for hyperlipoproteinemia(a). These include apheresis techniques, nicotinic acid and statins. None of these strategies have been shown to be definitely effective or convenient for the patient and new strategies are being attempted. Promising results are emerging with therapeutic interventions targeting the 'inflammatory pathways' by inhibition of Interleukin-6 (IL-6) signalling with natural compounds (e.g., Ginko biloba) or the IL-6 receptor antibody Tocilizumab. These may both lower Lp(a) and cardiovascular risk of the patients. Besides inhibiting platelet function, antiplatelet therapy with aspirin may also decrease the plasma concentration of Lp(a) and modulate its influence on platelets. WHAT IS NEW AND CONCLUSION We highlight the inadequacy of current approaches for lowering Lp(a) and draw attention to novel insights that may lead to better treatment.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "698", "doc_id": "33118292", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is contralateral high-grade carotid artery stenosis or occlusion associated with increased risk for poor neurologic outcome after elective carotid stent placement?\n\nABSTRACT:\nTo compare neurologic outcome after elective internal carotid artery (ICA) stents have been placed in patients with and in patients without contralateral ICA obstructions. This study included 471 consecutive patients from a registry database who underwent elective ICA stent placement without cerebral protection for high-grade (greater than 70% stenosis of the ICA, according to the North American Symptomatic Carotid Endarterectomy Trial) symptomatic (n = 147) or asymptomatic (n = 324) ICA stenosis. Contralateral carotid arteries were investigated with angiography. Patients with and patients without contralateral high-grade stenosis (70%-99% stenosis, according to the North American Symptomatic Carotid Endarterectomy Trial) or occlusion were compared with respect to 30-day neurologic outcome by using the chi2 test and multivariate logistic regression analysis. Neurologic events were observed in 33 patients (7%) with 15 transient ischemic attacks, eight minor strokes, and 10 major strokes that led to death in two patients (combined stroke and death rate, 4%). Eighty-eight patients (19%) with contralateral high-grade ICA stenosis and 43 patients (9%) with contralateral ICA occlusion exhibited a similar rate of postintervention combined neurologic events (n = 9, 7%) compared with patients without contralateral high-grade ICA stenosis or occlusion (n = 24, 7%) (P =.94). No differences were observed between symptomatic and asymptomatic patients. Combined stroke and death rates were also comparable between symptomatic (four of 131, 3%) and asymptomatic (14 of 340, 4%) patients (P =.59). Of all variables tested, multivariate analysis did not detect any predictor for peri- or postinterventional neurologic events.", "output": "{\"label\": \"no\", \"rationale\": \"Contralateral high-grade ICA stenosis or occlusion was not associated with an increased risk for neurologic events after elective ICA stent placement.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 14695388, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Concentrations of SNV and CNV in stem-cell regulatory elements and binding sites of transcription factors in iPSC-lines are distinct from their founding cells.\n\nCANDIDATE_PASSAGE:\nLip movements entrain the observers’ low-frequency brain oscillations to facilitate speech intelligibility During continuous speech, lip movements provide visual temporal signals that facilitate speech processing. Here, using MEG we directly investigated how these visual signals interact with rhythmic brain activity in participants listening to and seeing the speaker. First, we investigated coherence between oscillatory brain activity and speaker's lip movements and demonstrated significant entrainment in visual cortex. We then used partial coherence to remove contributions of the coherent auditory speech signal from the lip-brain coherence. Comparing this synchronization between different attention conditions revealed that attending visual speech enhances the coherence between activity in visual cortex and the speaker's lips. Further, we identified a significant partial coherence between left motor cortex and lip movements and this partial coherence directly predicted comprehension accuracy. Our results emphasize the importance of visually entrained and attention-modulated rhythmic brain activity for the enhancement of audiovisual speech processing.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "281", "doc_id": "10624000", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Do alpha1-Adrenoceptor Antagonists Improve Memory by Activating N-methyl-D-Aspartate-Induced Ion Currents in the Rat Hippocampus?\n\nABSTRACT:\nAlpha1 (α1)-adrenoceptor antagonists are widely used to treat lower urinary tract symptoms. These drugs not only act on peripheral tissues, but also cross the blood-brain barrier and affect the central nervous system. Therefore, α1-adrenoceptor antagonists may enhance brain functions. In the present study, we investigated the effects of tamsulosin, an α1-adrenoceptor antagonist, on short-term memory, as well as spatial learning and memory, in rats. The step-down avoidance test was used to evaluate short-term memory, and an eight-arm radial maze test was used to evaluate spatial learning and memory. TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling) staining was performed in order to evaluate the effect of tamsulosin on apoptosis in the hippocampal dentate gyrus. Patch clamp recordings were used to evaluate the effect of tamsulosin on ionotropic glutamate receptors, such as N-methyl-D-aspartate (NMDA), amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), and kainate receptors, in hippocampal CA1 neurons. Tamsulosin treatment improved short-term memory, as well as spatial learning and memory, without altering apoptosis. The amplitudes of NMDA-induced ion currents were dose-dependently increased by tamsulosin. However, the amplitudes of AMPA- and kainate-induced ion currents were not affected by tamsulosin.", "output": "{\"label\": \"yes\", \"rationale\": \"Tamsulosin enhanced memory function by activating NMDA receptor-mediated ion currents in the hippocampus without initiating apoptosis. The present study suggests the possibility of using tamsulosin to enhance memory under normal conditions, in addition to its use in treating overactive bladder.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 26739177, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is revascularization of smokers with claudication predicted to limit quality of life despite a higher risk of late failure?\n\nABSTRACT:\nTobacco smoking after lower extremity revascularization for claudication has repeatedly been shown to increase the risk of adverse events, such that many vascular specialists consider that refusal to abstain from smoking constitutes a major contraindication to open surgical bypass or endovascular intervention. A Markov decision analysis (DA) model was used to compare the options of direct revascularization vs medical therapy only in smokers with claudication. The primary outcome was calculated quality of life (cQoL), determined for each patient at follow-up based on the outcomes of the treatment received. Markov DA software was used to predict the QoL for each treatment option preoperatively based on smoking status. Among patients referred during a recent 64-month period with vasculogenic claudication, 94 were actively smoking compared with 217 who were not. The DA model predicted that if the patients who smoked were to discontinue smoking, the best therapy would be bypass surgery for 77% and endovascular intervention for 17%. However, despite at least doubling the risks with intervention in the patients who continue to smoke, the DA model still predicted that 78% and 9% would fare better with open surgical or endovascular intervention, respectively. Among actively smoking patients, open surgical (3%) or endovascular (4%) therapies were initially performed in few patients, whereas 93% were offered only medical therapy. Among initial nonsmokers, revascularization was performed by open (27%) or endovascular (42%) means. At 3 years, the median (interquartile range [IQR]) cQoL was lower in initial smokers than in nonsmokers (0.73 [IQR, 0.73-0.77] vs 0.82 [IQR, 0.75-0.86]; P < .0001), primarily because of a lack of revascularization for smokers. Among initial smo [TRUNCATED]", "output": "{\"label\": \"no\", \"rationale\": \"Patients with claudication who smoke may be denied the symptom improvement associated with revascularization, yet recidivism for smoking also occurs among patients who have stopped smoking in order to receive revascularization. The strategy not to directly revascularize patients with claudication who continue to smoke does not appear to maximize patient midterm QoL.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 27687324, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Gpr124 increases BBB breakdown in mouse models of ischemic stroke.\n\nCANDIDATE_ABSTRACT:\nTITLE: Gpr124 is essential for blood–brain barrier integrity in central nervous system disease\nABSTRACT: Although blood–brain barrier (BBB) compromise is central to the etiology of diverse central nervous system (CNS) disorders, endothelial receptor proteins that control BBB function are poorly defined. The endothelial G-protein-coupled receptor (GPCR) Gpr124 has been reported to be required for normal forebrain angiogenesis and BBB function in mouse embryos, but the role of this receptor in adult animals is unknown. Here Gpr124 conditional knockout (CKO) in the endothelia of adult mice did not affect homeostatic BBB integrity, but resulted in BBB disruption and microvascular hemorrhage in mouse models of both ischemic stroke and glioblastoma, accompanied by reduced cerebrovascular canonical Wnt–β-catenin signaling. Constitutive activation of Wnt–β-catenin signaling fully corrected the BBB disruption and hemorrhage defects of Gpr124-CKO mice, with rescue of the endothelial gene tight junction, pericyte coverage and extracellular-matrix deficits. We thus identify Gpr124 as an endothelial GPCR specifically required for endothelial Wnt signaling and BBB integrity under pathological conditions in adult mice. This finding implicates Gpr124 as a potential therapeutic target for human CNS disorders characterized by BBB disruption.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Here Gpr124 conditional knockout (CKO) in the endothelia of adult mice did not affect homeostatic BBB integrity, but resulted in BBB disruption and microvascular hemorrhage in mouse models of both ischemic stroke and glioblastoma, accompanied by reduced cerebrovascular canonical Wnt–β-catenin signaling.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 479, "doc_id": "6325527", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: 90% of patients with melanoma and an objective response to PD-1 blockade will experience a progression in their melanoma.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association of Pembrolizumab With Tumor Response and Survival Among Patients With Advanced Melanoma.\nABSTRACT: IMPORTANCE The programmed death 1 (PD-1) pathway limits immune responses to melanoma and can be blocked with the humanized anti-PD-1 monoclonal antibody pembrolizumab. OBJECTIVE To characterize the association of pembrolizumab with tumor response and overall survival among patients with advanced melanoma. DESIGN, SETTINGS, AND PARTICIPANTS Open-label, multicohort, phase 1b clinical trials (enrollment, December 2011-September 2013). Median duration of follow-up was 21 months. The study was performed in academic medical centers in Australia, Canada, France, and the United States. Eligible patients were aged 18 years and older and had advanced or metastatic melanoma. Data were pooled from 655 enrolled patients (135 from a nonrandomized cohort [n = 87 ipilimumab naive; n = 48 ipilimumab treated] and 520 from randomized cohorts [n = 226 ipilimumab naive; n = 294 ipilimumab treated]). Cutoff dates were April 18, 2014, for safety analyses and October 18, 2014, for efficacy analyses. EXPOSURES Pembrolizumab 10 mg/kg every 2 weeks, 10 mg/kg every 3 weeks, or 2 mg/kg every 3 weeks continued until disease progression, intolerable toxicity, or investigator decision. MAIN OUTCOMES AND MEASURES The primary end point was confirmed objective response rate (best overall response of complete response or partial response) in patients with measurable disease at baseline per independent central review. Secondary end points included toxicity, duration of response, progression-free survival, and overall survival. RESULTS Among the 655 patients (median [range] age, 61 [18-94] years; 405 [62%] men), 581 had measurable disease at baseline. An objective response was reported in 194 of 581 patients (33% [95% CI, 30%-37%]) and in 60 of 133 treatment-naive patients (45% [95% CI, 36% to 5 [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 24, "doc_id": "3471191", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The risk of breast cancer among parous women decreases with placental weight of pregnancies.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pregnancy characteristics and maternal risk of breast cancer.\nABSTRACT: CONTEXT During pregnancy, serum levels of estrogen, progesterone, and other hormones are markedly higher than during other periods of life. Pregnancy hormones primarily are produced in the placenta, and signs of placental impairment may serve as indirect markers of hormone exposures during pregnancy. During pregnancy, these markers have been inconsistently associated with subsequent risk of breast cancer in the mother. OBJECTIVE To examine associations between indirect markers of hormonal exposures, such as placental weight and other pregnancy characteristics, and maternal risk of developing breast cancer. DESIGN AND SETTING Population-based cohort study using data from the Swedish Birth Register, the Swedish Cancer Register, the Swedish Cause of Death Register, and the Swedish Register of Population and Population Changes. PARTICIPANTS Women included in the Sweden Birth Register who delivered singletons between 1982 and 1989, with complete information on date of birth and gestational age. Women were followed up until the occurrence of breast cancer, death, or end of follow-up (December 31, 2001). Cox proportional hazards models were used to estimate associations between hormone exposures and risks of breast cancer. MAIN OUTCOME MEASURE Incidence of invasive breast cancer. RESULTS Of 314,019 women in the cohort, 2216 (0.7%) developed breast cancer during the follow-up through 2001, of whom 2100 (95%) were diagnosed before age 50 years. Compared with women who had placentas weighing less than 500 g in 2 consecutive pregnancies, the risk of breast cancer was increased among women whose placentas weighed between 500 and 699 g in their first pregnancy and at least 700 g in their second pregnancy (or vice versa) (adjusted hazard ratio, 1.82; 95% confidence interv [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Compared with women who had placentas weighing less than 500 g in 2 consecutive pregnancies, the risk of breast cancer was increased among women whose placentas weighed between 500 and 699 g in their first pregnancy and at least 700 g in their second pregnancy (or vice versa) (adjusted hazard ratio, 1.82; 95% confidence interval [CI], 1.07-3.08), and the corresponding risk was doubled among women whose placentas weighed at least 700 g in both pregnancies (adjusted hazard ratio, 2.05; 95% CI, 1.15-3.64).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1265, "doc_id": "37480103", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Removal of H3K9me3 improves reprogramming efficiency in human somatic cell nuclear transfer experiments.\n\nCANDIDATE_PASSAGE:\nHuman somatic cell nuclear transfer using adult cells. Derivation of patient-specific human pluripotent stem cells via somatic cell nuclear transfer (SCNT) has the potential for applications in a range of therapeutic contexts. However, successful SCNT with human cells has proved challenging to achieve, and thus far has only been reported with fetal or infant somatic cells. In this study, we describe the application of a recently developed methodology for the generation of human ESCs via SCNT using dermal fibroblasts from 35- and 75-year-old males. Our study therefore demonstrates the applicability of SCNT for adult human cells and supports further investigation of SCNT as a strategy for regenerative medicine.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1036", "doc_id": "37822406", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Integrating classroom-based collaborative learning with Web-based collaborative learning leads to subpar class performance\n\nCANDIDATE_PASSAGE:\nEMT, the cytoskeleton, and cancer cell invasion The metastatic process, i.e. the dissemination of cancer cells throughout the body to seed secondary tumors at distant sites, requires cancer cells to leave the primary tumor and to acquire migratory and invasive capabilities. In a process of epithelial-mesenchymal transition (EMT), besides changing their adhesive repertoire, cancer cells employ developmental processes to gain migratory and invasive properties that involve a dramatic reorganization of the actin cytoskeleton and the concomitant formation of membrane protrusions required for invasive growth. The molecular processes underlying such cellular changes are still only poorly understood, and the various migratory organelles, including lamellipodia, filopodia, invadopodia and podosomes, still require a better functional and molecular characterization. Notably, direct experimental evidence linking the formation of migratory membrane protrusions and the process of EMT and tumor metastasis is still lacking. In this review, we have summarized recent novel insights into the molecular processes and players underlying EMT on one side and the formation of invasive membrane protrusions on the other side.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "649", "doc_id": "40667577", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: YAP/TAZ is required in intestinal regeneration in mouse models of ulcerative colitis.\n\nCANDIDATE_ABSTRACT:\nTITLE: YAP/TAZ-Dependent Reprogramming of Colonic Epithelium Links ECM Remodeling to Tissue Regeneration\nABSTRACT: Tissue regeneration requires dynamic cellular adaptation to the wound environment. It is currently unclear how this is orchestrated at the cellular level and how cell fate is affected by severe tissue damage. Here we dissect cell fate transitions during colonic regeneration in a mouse dextran sulfate sodium (DSS) colitis model, and we demonstrate that the epithelium is transiently reprogrammed into a primitive state. This is characterized by de novo expression of fetal markers as well as suppression of markers for adult stem and differentiated cells. The fate change is orchestrated by remodeling the extracellular matrix (ECM), increased FAK/Src signaling, and ultimately YAP/TAZ activation. In a defined cell culture system recapitulating the extracellular matrix remodeling observed in vivo, we show that a collagen 3D matrix supplemented with Wnt ligands is sufficient to sustain endogenous YAP/TAZ and induce conversion of cell fate. This provides a simple model for tissue regeneration, implicating cellular reprogramming as an essential element.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In a defined cell culture system recapitulating the extracellular matrix remodeling observed in vivo, we show that a collagen 3D matrix supplemented with Wnt ligands is sufficient to sustain endogenous YAP/TAZ and induce conversion of cell fate.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1381, "doc_id": "13481880", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does combining antiretroviral agents in a single dosage form enhance quality of life of HIV/AIDS patients?\n\nABSTRACT:\nCombining various antiretroviral agents into one single dosage form has been a strategy to reduce pill burden and enhance medication adherence among human immunodeficiency virus /AIDS (HIV/AIDS) patients. This is a cost-utility study from a health care system's perspective comparing coformulated fixed dose (FXD) strategy versus multiple free dose combination (FRC) in antiretroviral therapy. The Medical Expenditure Panel Survey (MEPS) was used to identify HIV/AIDS patients with ≥2 active antiretroviral medications. Patients on FXD were matched in 1:1 ratio with the FRC group using propensity scores. All medical costs excluding those paid by patients and families were included. Utility was measured using SF-6D scores from the SF-12 questionnaire. Incremental cost-utility ratios (ICURs) were calculated using the mean annual estimates. A cost-effectiveness acceptability curve was determined using a Monte Carlo probabilistic simulation technique. Nine FXD antiretroviral formulations approved by the U.S. Food and Drug Administration by 2005 was included in this study. One hundred seventy HIV/AIDS patients with ≥2 antiretroviral agents were identified from the MEPS database, of which 53% (n=92) were on FXD formulation. On matching, 70 patients from FXD had a match from the FRC group. No differences in sociodemographic and health status variables were observed between the matched groups. The mean annual cost was $15,766.15 for FXD patients and $11,875.21 for FRC patients. The mean utility gained by using FXD over FRC was 0.085; however, this difference was not statistically significant. The ICUR for the FXD treatment over FRC treatment was $45,540.49/quality-adjusted life years (QALYs). Probabilistic sensitivity analysis showed FXD to dominate FRC (>50% probability [TRUNCATED]", "output": "{\"label\": \"no\", \"rationale\": \"Although the cost-effectiveness of a single-pill strategy was within the acceptable willingness-to-pay threshold, the QALY difference were minimal. Further research is recommended to explore the long-term impact of the strategy.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 21712147, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does inferior tilt of the glenoid component decrease scapular notching in reverse shoulder arthroplasty : results of a prospective randomized study?\n\nABSTRACT:\nThe purpose of this study was to determine if inferior tilt of the glenoid component decreased the amount of radiographic scapular notching after reverse shoulder arthroplasty. A secondary goal was to determine if inferior tilt had any effect on clinical outcome. A prospective randomized trial of 52 consecutive reverse shoulder arthroplasties performed by 1 surgeon for cuff tear arthropathy was performed. The subjects were randomly assigned to receive a glenoid component with no inferior tilt (control group) or a glenoid component that was inferiorly tilted 10° to protect the inferior glenoid (inferior tilt group). All glenoid components were placed in 3 mm of inferior translation. Radiographic notching was graded at a minimum of 1 year after surgery. Clinical outcomes of the groups were recorded. Follow-up radiographs and data were available for 42 subjects, 20 in the inferior tilt group and 22 in the control group. The experimental groups did not differ significantly in the notch ratings or clinical outcomes. Notching occurred in 15 patients (75%) in the inferior tilt group and in 19 (86%) in the control group. Notching scores were 2 or greater in 10 patients (50%) in the inferior tilt group and in 11 (50%) in the control group.", "output": "{\"label\": \"no\", \"rationale\": \"Placing the glenoid component with inferior tilt does not reduce the incidence or severity of radiographic scapular notching after reverse shoulder arthroplasty. No clinical differences were observed between the groups.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 22079769, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Malaria has a high vectorial capacity.\n\nCANDIDATE_PASSAGE:\nALDH1 is a marker of normal and malignant human mammary stem cells and a predictor of poor clinical outcome. Application of stem cell biology to breast cancer research has been limited by the lack of simple methods for identification and isolation of normal and malignant stem cells. Utilizing in vitro and in vivo experimental systems, we show that normal and cancer human mammary epithelial cells with increased aldehyde dehydrogenase activity (ALDH) have stem/progenitor properties. These cells contain the subpopulation of normal breast epithelium with the broadest lineage differentiation potential and greatest growth capacity in a xenotransplant model. In breast carcinomas, high ALDH activity identifies the tumorigenic cell fraction, capable of self-renewal and of generating tumors that recapitulate the heterogeneity of the parental tumor. In a series of 577 breast carcinomas, expression of ALDH1 detected by immunostaining correlated with poor prognosis. These findings offer an important new tool for the study of normal and malignant breast stem cells and facilitate the clinical application of stem cell concepts.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "753", "doc_id": "45638119", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The center of the granuloma in an immune cell induces a pro-inflammatory immune response.\n\nCANDIDATE_ABSTRACT:\nTITLE: Inflammatory signaling in human Tuberculosis granulomas is spatially organized\nABSTRACT: Granulomas are the pathological hallmark of tuberculosis (TB). However, their function and mechanisms of formation remain poorly understood. To understand the role of granulomas in TB, we analyzed the proteomes of granulomas from subjects with tuberculosis in an unbiased manner. Using laser-capture microdissection, mass spectrometry and confocal microscopy, we generated detailed molecular maps of human granulomas. We found that the centers of granulomas have a pro-inflammatory environment that is characterized by the presence of antimicrobial peptides, reactive oxygen species and pro-inflammatory eicosanoids. Conversely, the tissue surrounding the caseum has a comparatively anti-inflammatory signature. These findings are consistent across a set of six human subjects and in rabbits. Although the balance between systemic pro- and anti-inflammatory signals is crucial to TB disease outcome, here we find that these signals are physically segregated within each granuloma. From the protein and lipid snapshots of human and rabbit lesions analyzed here, we hypothesize that the pathologic response to TB is shaped by the precise anatomical localization of these inflammatory pathways during the development of the granuloma.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We found that the centers of granulomas have a pro-inflammatory environment that is characterized by the presence of antimicrobial peptides, reactive oxygen species and pro-inflammatory eicosanoids.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1202, "doc_id": "3475317", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Scapular stabilizer exercises are more effective than general exercise therapy in reducing pain and improving function of the shoulder.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effect of specific exercise strategy on need for surgery in patients with subacromial impingement syndrome: randomised controlled study\nABSTRACT: OBJECTIVE To evaluate if a specific exercise strategy, targeting the rotator cuff and scapula stabilisers, improves shoulder function and pain more than unspecific exercises in patients with subacromial impingement syndrome, thereby decreasing the need for arthroscopic subacromial decompression. DESIGN Randomised, participant and single assessor blinded, controlled study. SETTING Department of orthopaedics in a Swedish university hospital. PARTICIPANTS 102 patients with long standing (over six months) persistent subacromial impingement syndrome in whom earlier conservative treatment had failed, recruited through orthopaedic specialists. INTERVENTIONS The specific exercise strategy consisted of strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers in combination with manual mobilisation. The control exercise programme consisted of unspecific movement exercises for the neck and shoulder. Patients in both groups received five to six individual guided treatment sessions during 12 weeks. In between these supervised sessions the participants performed home exercises once or twice a day for 12 weeks. MAIN OUTCOME MEASURES The primary outcome was the Constant-Murley shoulder assessment score evaluating shoulder function and pain. Secondary outcomes were patients' global impression of change because of treatment and decision regarding surgery. RESULTS Most (97, 95%) participants completed the 12 week study. There was a significantly greater improvement in the Constant-Murley score in the specific exercise group than in the control exercise group (24 points (95% confidence interval 19 to 28.0) v 9 points (5 to 13); mean difference between group: 15 points (8.5 to 20.6)). Significantly more patients in the [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSION A specific exercise strategy, focusing on strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers, is effective in reducing pain and improving shoulder function in patients with persistent subacromial impingement syndrome.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1069, "doc_id": "4200695", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Transcription factor EB induces transcription of pro-inflammatory cytokines in macrophages infected with Staphylococcus aureus.\n\nCANDIDATE_ABSTRACT:\nTITLE: A global role for KLF1 in erythropoiesis revealed by ChIP-seq in primary erythroid cells.\nABSTRACT: KLF1 regulates a diverse suite of genes to direct erythroid cell differentiation from bipotent progenitors. To determine the local cis-regulatory contexts and transcription factor networks in which KLF1 operates, we performed KLF1 ChIP-seq in the mouse. We found at least 945 sites in the genome of E14.5 fetal liver erythroid cells which are occupied by endogenous KLF1. Many of these recovered sites reside in erythroid gene promoters such as Hbb-b1, but the majority are distant to any known gene. Our data suggests KLF1 directly regulates most aspects of terminal erythroid differentiation including production of alpha- and beta-globin protein chains, heme biosynthesis, coordination of proliferation and anti-apoptotic pathways, and construction of the red cell membrane and cytoskeleton by functioning primarily as a transcriptional activator. Additionally, we suggest new mechanisms for KLF1 cooperation with other transcription factors, in particular the erythroid transcription factor GATA1, to maintain homeostasis in the erythroid compartment.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1312, "doc_id": "2452989", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Side effects associated with antidepressants lower risk of myocardial infarction.\n\nCANDIDATE_PASSAGE:\nPeroxisome proliferator-activated receptor gamma agonists for the Prevention of Adverse events following percutaneous coronary Revascularization--results of the PPAR study. BACKGROUND Patients with metabolic syndrome are at increased risk for cardiovascular complications. We sought to determine whether peroxisome proliferator-activated receptor gamma agonists had any beneficial effect on patients with metabolic syndrome undergoing percutaneous coronary intervention (PCI). METHODS A total of 200 patients with metabolic syndrome undergoing PCI were randomized to rosiglitazone or placebo and followed for 1 year. Carotid intima-medial thickness (CIMT), inflammatory markers, lipid levels, brain natriuretic peptide, and clinical events were measured at baseline, 6 months, and 12 months. RESULTS There was no significant difference in CIMT between the 2 groups. There was no difference in the 12-month composite end point of death, myocardial infarction (MI), stroke, or any recurrent ischemia (31.4% vs 30.2%, P = .99). The rate of death, MI, or stroke at 12 months was numerically lower in the rosiglitazone group (11.9% vs 6.4%, P = .19). There was a trend toward a greater decrease over time in high-sensitivity C-reactive protein values compared with baseline in the group randomized to rosiglitazone versus placebo both at 6 months (-35.4% vs -15.8%, P = .059) and 12 months (-40.0% vs -20.9%, P = .089) and higher change in high-density lipoprotein (+15.5% vs +4.1%, P = .05) and lower triglycerides (-13.9% vs +14.9%, P = .004) in the rosiglitazone arm. There was a trend toward less new onset diabetes in the rosiglitazone group (0% vs 3.3%, P = .081) and no episodes of symptomatic hypoglycemia. There was no excess of new onset of clinical heart failure in the rosiglitazon [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1085", "doc_id": "24150328", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Macrolides have no protective effect against myocardial infarction.\n\nCANDIDATE_ABSTRACT:\nTITLE: Antibiotics and risk of subsequent first-time acute myocardial infarction.\nABSTRACT: CONTEXT Increasing evidence supports the hypothesis of a causal association between certain bacterial infections and increased risk of developing acute myocardial infarction. If such a causal association exists, subjects who used antibiotics active against the bacteria, regardless of indication, might be at lower risk of developing acute myocardial infarction than nonusers. OBJECTIVE To determine whether previous use of antibiotics decreases the risk of developing a first-time acute myocardial infarction. DESIGN Population-based case-control analysis. SETTING The United Kingdom-based General Practice Research Database comprising 350 general practices. PATIENTS A total of 3315 case patients aged 75 years or younger with a diagnosis of first-time acute myocardial infarction between 1992 and 1997 and 13139 controls without myocardial infarction matched to cases for age, sex, general practice attended, and calendar time. MAIN OUTCOME MEASURES Use of antibiotics among those who did or did not have a first-time acute myocardial infarction. RESULTS Cases were significantly less likely to have used tetracycline antibiotics (adjusted odds ratio [OR], 0.70; 95% confidence interval [CI], 0.55-0.90) or quinolones (adjusted OR, 0.45; 95% CI, 0.21-0.95). No effect was found for previous use of macrolides (primarily erythromycin), sulfonamides, penicillins, or cephalosporins. CONCLUSIONS The findings from this large case-control analysis provide further, albeit indirect, evidence for an association between bacterial infections with organisms susceptible to tetracycline or quinolone antibiotics and the risk of acute myocardial infarction. These results of preliminary nature should stimulate more research to further explore the role of infections in the etiology of acute myo [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"No effect was found for previous use of macrolides (primarily erythromycin), sulfonamides, penicillins, or cephalosporins.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 742, "doc_id": "32159283", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Chenodeoxycholic acid treatment decreases brown adipose tissue activity.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Bile Acid Chenodeoxycholic Acid Increases Human Brown Adipose Tissue Activity.\nABSTRACT: The interest in brown adipose tissue (BAT) as a target to combat metabolic disease has recently been renewed with the discovery of functional BAT in humans. In rodents, BAT can be activated by bile acids, which activate type 2 iodothyronine deiodinase (D2) in BAT via the G-coupled protein receptor TGR5, resulting in increased oxygen consumption and energy expenditure. Here we examined the effects of oral supplementation of the bile acid chenodeoxycholic acid (CDCA) on human BAT activity. Treatment of 12 healthy female subjects with CDCA for 2 days resulted in increased BAT activity. Whole-body energy expenditure was also increased upon CDCA treatment. In vitro treatment of primary human brown adipocytes derived with CDCA or specific TGR5 agonists increased mitochondrial uncoupling and D2 expression, an effect that was absent in human primary white adipocytes. These findings identify bile acids as a target to activate BAT in humans.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Treatment of 12 healthy female subjects with CDCA for 2 days resulted in increased BAT activity.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 250, "doc_id": "1568684", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Healthy volunteers exhibit rapid and transient increase of cellular ATP after being bolus-injected with fructose.\n\nCANDIDATE_PASSAGE:\nIonic mechanism of ouabain-induced concurrent apoptosis and necrosis in individual cultured cortical neurons Energy deficiency and dysfunction of the Na+, K+-ATPase are common consequences of many pathological insults. The nature and mechanism of cell injury induced by impaired Na+, K+-ATPase, however, are not well defined. We used cultured cortical neurons to examine the hypothesis that blocking the Na+, K+-ATPase induces apoptosis by depleting cellular K+ and, concurrently, induces necrotic injury in the same cells by increasing intracellular Ca2+ and Na+. The Na+, K+-ATPase inhibitor ouabain induced concentration-dependent neuronal death. Ouabain triggered transient neuronal cell swelling followed by cell shrinkage, accompanied by intracellular Ca2+ and Na+ increase, K+ decrease, cytochrome c release, caspase-3 activation, and DNA laddering. Electron microscopy revealed the coexistence of ultrastructural features of both apoptosis and necrosis in individual cells. The caspase inhibitor Z-Val-Ala-Asp(OMe)-fluoromethyl ketone (Z-VAD-FMK) blocked >50% of ouabain-induced neuronal death. Potassium channel blockers or high K+ medium, but not Ca2+ channel blockade, prevented cytochrome c release, caspase activation, and DNA damage. Blocking of K+, Ca2+, or Na+ channels or high K+ medium each attenuated the ouabain-induced cell death; combined inhibition of K+ channels and Ca2+ or Na+ channels resulted in additional protection. Moreover, coapplication of Z-VAD-FMK and nifedipine produced virtually complete neuroprotection. These results suggest that the neuronal death associated with Na+, K+-pump failure consists of concurrent apoptotic and necrotic components, mediated by intracellular depletion of K+ and accumulation of Ca2+ and Na+, respectively. The ouabain-i [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "504", "doc_id": "17231273", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Tetraspanin-3 is a causative factor in the development of acute myelogenous leukemia\n\nCANDIDATE_PASSAGE:\nTetraspanin 3 Is Required for the Development and Propagation of Acute Myelogenous Leukemia. Acute Myelogenous Leukemia (AML) is an aggressive cancer that strikes both adults and children and is frequently resistant to therapy. Thus, identifying signals needed for AML propagation is a critical step toward developing new approaches for treating this disease. Here, we show that Tetraspanin 3 is a target of the RNA binding protein Musashi 2, which plays a key role in AML. We generated Tspan3 knockout mice that were born without overt defects. However, Tspan3 deletion impaired leukemia stem cell self-renewal and disease propagation and markedly improved survival in mouse models of AML. Additionally, Tspan3 inhibition blocked growth of AML patient samples, suggesting that Tspan3 is also important in human disease. As part of the mechanism, we show that Tspan3 deficiency disabled responses to CXCL12/SDF-1 and led to defects in AML localization within the niche. These identify Tspan3 as an important regulator of aggressive leukemias and highlight a role for Tspan3 in oncogenesis.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1150", "doc_id": "11369420", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: High levels of copeptin decrease risk of diabetes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mendelian Randomization Study of B-Type Natriuretic Peptide and Type 2 Diabetes: Evidence of Causal Association from Population Studies\nABSTRACT: BACKGROUND Genetic and epidemiological evidence suggests an inverse association between B-type natriuretic peptide (BNP) levels in blood and risk of type 2 diabetes (T2D), but the prospective association of BNP with T2D is uncertain, and it is unclear whether the association is confounded. METHODS AND FINDINGS We analysed the association between levels of the N-terminal fragment of pro-BNP (NT-pro-BNP) in blood and risk of incident T2D in a prospective case-cohort study and genotyped the variant rs198389 within the BNP locus in three T2D case-control studies. We combined our results with existing data in a meta-analysis of 11 case-control studies. Using a Mendelian randomization approach, we compared the observed association between rs198389 and T2D to that expected from the NT-pro-BNP level to T2D association and the NT-pro-BNP difference per C allele of rs198389. In participants of our case-cohort study who were free of T2D and cardiovascular disease at baseline, we observed a 21% (95% CI 3%-36%) decreased risk of incident T2D per one standard deviation (SD) higher log-transformed NT-pro-BNP levels in analysis adjusted for age, sex, body mass index, systolic blood pressure, smoking, family history of T2D, history of hypertension, and levels of triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. The association between rs198389 and T2D observed in case-control studies (odds ratio = 0.94 per C allele, 95% CI 0.91-0.97) was similar to that expected (0.96, 0.93-0.98) based on the pooled estimate for the log-NT-pro-BNP level to T2D association derived from a meta-analysis of our study and published data (hazard ratio = 0.82 per SD, 0.74-0.90) and the difference in NT-pro-BNP levels (0.22 SD, 0.15-0.29) per C allele of r [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 517, "doc_id": "15663829", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cell autonomous sex determination in somatic cells occurs in Galliformes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Somatic sex identity is cell-autonomous in the chicken\nABSTRACT: In the mammalian model of sex determination, embryos are considered to be sexually indifferent until the transient action of a sex-determining gene initiates gonadal differentiation. Although this model is thought to apply to all vertebrates, this has yet to be established. Here we have examined three lateral gynandromorph chickens (a rare, naturally occurring phenomenon in which one side of the animal appears male and the other female) to investigate the sex-determining mechanism in birds. These studies demonstrated that gynandromorph birds are genuine male:female chimaeras, and indicated that male and female avian somatic cells may have an inherent sex identity. To test this hypothesis, we transplanted presumptive mesoderm between embryos of reciprocal sexes to generate embryos containing male:female chimaeric gonads. In contrast to the outcome for mammalian mixed-sex chimaeras, in chicken mixed-sex chimaeras the donor cells were excluded from the functional structures of the host gonad. In an example where female tissue was transplanted into a male host, donor cells contributing to the developing testis retained a female identity and expressed a marker of female function. Our study demonstrates that avian somatic cells possess an inherent sex identity and that, in birds, sexual differentiation is substantively cell autonomous.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"These studies demonstrated that gynandromorph birds are genuine male:female chimaeras, and indicated that male and female avian somatic cells may have an inherent sex identity.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 235, "doc_id": "4388470", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Forkhead 0 (fox0) transcription factors are involved in apoptosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cell Stem Cell Review FoxO Transcription Factors and Stem Cell Homeostasis: Insights from the Hematopoietic System\nABSTRACT: The forkhead O (FoxO) family of transcription factors participates in diverse physiologic processes, including induction of cell-cycle arrest, stress resistance, differentiation, apoptosis, and metabolism. Several recent studies indicate that FoxO-dependent signaling is required for long-term regenerative potential of the hematopoietic stem cell (HSC) compartment through regulation of HSC response to physiologic oxidative stress, quiescence, and survival. These observations link FoxO function in mammalian systems with the evolutionarily conserved role of FoxO in promotion of stress resistance and longevity in lower phylogenetic systems. Furthermore, these findings have implications for aging in higher organisms and in malignant stem cell biology, and suggest that FoxOs may play an important role in the maintenance and integrity of stem cell compartments in a broad spectrum of tissues.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The forkhead O (FoxO) family of transcription factors participates in diverse physiologic processes, including induction of cell-cycle arrest, stress resistance, differentiation, apoptosis, and metabolism.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 426, "doc_id": "16728949", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Interleukin-18 plays an important role in the pathogenesis of atherosclerosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Familial amyloidotic polyneuropathy: current and emerging treatment options for transthyretin-mediated amyloidosis\nABSTRACT: Transthyretin familial amyloid polyneuropathy (TTR-FAP) is a fatal clinical disorder characterized by extracellular deposition of abnormal fibrils derived from misfolded, normally soluble transthyretin (TTR) molecules. The disease is most commonly caused by a point mutation within the TTR gene inherited in an autosomal dominant fashion. Over 100 of such mutations have been identified, leading to destabilization of the physiological TTR tetramer. As a result, many monomers originate with a tendency for spontaneous conformational changes and self-aggregation. The main clinical feature of TTR-FAP is progressive sensorimotor and autonomic neuropathy. In the beginning, this polyneuropathy predominantly involves small unmyelinated nerve fibers with the result of dissociated sensory loss disproportionately affecting sensation of pain and temperature. Autonomic neuropathy typically accompanies sensory deficits early in the disease course. The symptoms include orthostatic hypotension, constipation alternating with diarrhea, erectile dysfunction, anhydrosis, and urinary retention or incontinence. Later, involvement of motor fibers causes rapidly progressive weakness and gait disturbances. In addition to the peripheral nervous system, the heart and the gut are frequently affected. Onset of symptoms is bimodal, with one peak at age 33 years (early onset) and another distinct peak in the sixth decade of life (late onset). The course of TTR-FAP is uniformly progressive and fatal. Death occurs an average of 10.8 years after the onset of symptoms in Portuguese patients, and 7.3 years in late-onset Japanese patients. Common causes include cachexia, cardiac failure, arrhythmia, and secondary infections. Liver transplantation is the standard therapy for patients who are in a c [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 653, "doc_id": "2496002", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Omnivores produce more trimethylamine N-oxide from dietary I-carnitine than vegetarians.\n\nCANDIDATE_PASSAGE:\nReduction of transmission from malaria patients by artemisinin combination therapies: a pooled analysis of six randomized trials BACKGROUND Artemisinin combination therapies (ACT), which are increasingly being introduced for treatment of Plasmodium falciparum malaria, are more effective against sexual stage parasites (gametocytes) than previous first-line antimalarials and therefore have the potential to reduce parasite transmission. The size of this effect is estimated in symptomatic P. falciparum infections. METHODS Data on 3,174 patients were pooled from six antimalarial trials conducted in The Gambia and Kenya. Multivariable regression was used to investigate the role of ACT versus non-artemisinin antimalarial treatment, treatment failure, presence of pre-treatment gametocytes and submicroscopic gametocytaemia on transmission to mosquitoes and the area under the curve (AUC) of gametocyte density during the 28 days of follow up. RESULTS ACT treatment was associated with a significant reduction in the probability of being gametocytaemic on the day of transmission experiments (OR 0.20 95% CI 0.16-0.26), transmission to mosquitoes by slide-positive gametocyte carriers (OR mosquito infection 0.49 95% CI 0.33-0.73) and AUC of gametocyte density (ratio of means 0.35 95% CI 0.31-0.41). Parasitological treatment failure did not account for the difference between ACT and non-artemisinin impact. The presence of slide-positive gametocytaemia prior to treatment significantly reduced ACT impact on gametocytaemia (p < 0.001). Taking account of submicroscopic gametocytaemia reduced estimates of ACT impact in a high transmission setting in Kenya, but not in a lower transmission setting in the Gambia. CONCLUSION Treatment with ACT significantly reduces infectiousness of i [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "884", "doc_id": "12409683", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pleiotropic coupling of GLP-1R to intracellular effectors promotes distinct profiles of cellular signaling.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Extracellular Surface of the GLP-1 Receptor Is a Molecular Trigger for Biased Agonism\nABSTRACT: Ligand-directed signal bias offers opportunities for sculpting molecular events, with the promise of better, safer therapeutics. Critical to the exploitation of signal bias is an understanding of the molecular events coupling ligand binding to intracellular signaling. Activation of class B G protein-coupled receptors is driven by interaction of the peptide N terminus with the receptor core. To understand how this drives signaling, we have used advanced analytical methods that enable separation of effects on pathway-specific signaling from those that modify agonist affinity and mapped the functional consequence of receptor modification onto three-dimensional models of a receptor-ligand complex. This yields molecular insights into the initiation of receptor activation and the mechanistic basis for biased agonism. Our data reveal that peptide agonists can engage different elements of the receptor extracellular face to achieve effector coupling and biased signaling providing a foundation for rational design of biased agonists.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 956, "doc_id": "12956194", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Increased vessel density along with a reduction in fibrosis improves the efficacy of chemotherapy treatments.\n\nCANDIDATE_PASSAGE:\nPhase II study of panobinostat in combination with bevacizumab for recurrent glioblastoma and anaplastic glioma. BACKGROUND Panobinostat is a histone deacetylase inhibitor with antineoplastic and antiangiogenic effects in glioma that may work synergistically with bevacizumab. We conducted a multicenter phase II trial of panobinostat combined with bevacizumab in patients with recurrent high-grade glioma (HGG). METHODS Patients with recurrent HGG were treated with oral panobinostat 30 mg 3 times per week, every other week, in combination with bevacizumab 10 mg/kg every other week. The primary endpoint was a 6-month progression-fee survival (PFS6) rate for participants with recurrent glioblastoma (GBM). Patients with recurrent anaplastic glioma (AG) were evaluated as an exploratory arm of the study. RESULTS At interim analysis, the GBM arm did not meet criteria for continued accrual, and the GBM arm was closed. A total of 24 patients with GBM were accrued prior to closure. The PFS6 rate was 30.4% (95%, CI 12.4%-50.7%), median PFS was 5 months (range, 3-9 months), and median overall survival (OS) was 9 months (range, 6-19 months). Accrual in the AG arm continued to completion, and a total of 15 patients were enrolled. The PFS6 rate was 46.7% (range, 21%-73%), median PFS was 7 months (range, 2-10 months), and median OS was 17 months (range, 5 months-27 months). CONCLUSIONS This phase II study of panobinostat and bevacizumab in participants with recurrent GBM did not meet criteria for continued accrual, and the GBM cohort of the study was closed. Although it was reasonably well tolerated, the addition of panobinostat to bevacizumab did not significantly improve PFS6 compared with historical controls of bevacizumab monotherapy in either cohort.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "620", "doc_id": "14482051", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The removal of reactive oxygen species by activated oncogenes contributes to the increased genomic instability of leukaemia cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: BCR/ABL oncogenic kinase promotes unfaithful repair of the reactive oxygen species-dependent DNA double-strand breaks.\nABSTRACT: The oncogenic BCR/ABL tyrosine kinase induces constitutive DNA damage in Philadelphia chromosome (Ph)-positive leukemia cells. We find that BCR/ABL-induced reactive oxygen species (ROSs) cause chronic oxidative DNA damage resulting in double-strand breaks (DSBs) in S and G(2)/M cell cycle phases. These lesions are repaired by BCR/ABL-stimulated homologous recombination repair (HRR) and nonhomologous end-joining (NHEJ) mechanisms. A high mutation rate is detected in HRR products in BCR/ABL-positive cells, but not in the normal counterparts. In addition, large deletions are found in NHEJ products exclusively in BCR/ABL cells. We propose that the following series of events may contribute to genomic instability of Ph-positive leukemias: BCR/ABL --> ROSs --> oxidative DNA damage --> DSBs in proliferating cells --> unfaithful HRR and NHEJ repair.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We propose that the following series of events may contribute to genomic instability of Ph-positive leukemias: BCR/ABL --> ROSs --> oxidative DNA damage --> DSBs in proliferating cells --> unfaithful HRR and NHEJ repair.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1261, "doc_id": "13023410", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Are diffusion tensor imaging findings strongly associated with postconcussional disorder 2 months following mild traumatic brain injury?\n\nABSTRACT:\nTo examine the relation between diffusion tensor imaging (DTI) of the corpus callosum and postconcussion symptom reporting following mild traumatic brain injury (MTBI). Sixty patients with MTBI and 34 patients with orthopedic/soft-tissue injuries (Trauma Controls) prospectively enrolled from consecutive admissions to a level 1 trauma center. Diffusion tensor imaging of the corpus callosum was undertaken using a Phillips 3T scanner at 6 to 8 weeks postinjury. Participants also completed a postconcussion symptom checklist. The MTBI group was divided into 2 subgroups based on the International Classification of Diseases, Tenth Revision symptom criteria for postconcussion disorder (PCD): PCD Present (n = 21), PCD Absent (n = 39). Measures of fractional anisotropy and mean diffusivity for the genu, body, and splenium of the corpus callosum. Participants also completed the British Columbia Post-Concussion Symptom Inventory. The MTBI group reported more postconcussion symptoms than the trauma controls. There were no significant differences between MTBI and trauma control groups on all DTI measures. In the MTBI sample, there were no significant differences on all DTI measures between those who did and did not meet the International Classification of Diseases, Tenth Revision research criteria for postconcussion disorder.", "output": "{\"label\": \"no\", \"rationale\": \"These data do not support an association between white matter integrity in the corpus callosum and self-reported postconcussion syndrome 6 to 8 weeks post-MTBI.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 21642855, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Fibroblast Growth Factor is a ligand which signals through receptor tyrosine kinases.\n\nCANDIDATE_PASSAGE:\nBasic residues in the T-cell receptor ζ cytoplasmic domain mediate membrane association and modulate signaling. The T-cell receptor (TCR) consists of a TCRαβ heterodimer, a TCRζ homodimer, and CD3γε and CD3δε heterodimers. The precise mechanism of T-cell triggering following TCR ligand engagement remains elusive. Previous studies reported that the cytoplasmic tail of CD3ε binds to the plasma membrane through a basic residue-rich stretch (BRS) and proposed that dissociation from the membrane is required for phosphorylation thereof. In this report we show that BRS motifs within the cytoplasmic tail of TCRζ mediate association with the plasma membrane and that TCR engagement results in TCRζ dissociation from the membrane. This dissociation requires phosphorylation of the TCRζ immunoreceptor tyrosine-based activation motifs by lymphocyte cell-specificprotein tyrosine kinase (Lck) but not ζ-chain-associated protein kinase 70 binding. Mutations of the TCRζ BRS motifs that disrupt this membrane association attenuate proximal and distal responses induced by TCR engagement. These mutations appear to alter the localization of TCRζ with respect to Lck as well as the mobility of the TCR complex. This study reveals that tyrosine phosphorylation of the TCRζ cytoplasmic domain regulates its association with the plasma membrane and highlights the functional importance of TCRζ BRS motifs.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "418", "doc_id": "8903143", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Cell autonomous sex determination in somatic cells does not occur in Galliformes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Somatic sex identity is cell-autonomous in the chicken\nABSTRACT: In the mammalian model of sex determination, embryos are considered to be sexually indifferent until the transient action of a sex-determining gene initiates gonadal differentiation. Although this model is thought to apply to all vertebrates, this has yet to be established. Here we have examined three lateral gynandromorph chickens (a rare, naturally occurring phenomenon in which one side of the animal appears male and the other female) to investigate the sex-determining mechanism in birds. These studies demonstrated that gynandromorph birds are genuine male:female chimaeras, and indicated that male and female avian somatic cells may have an inherent sex identity. To test this hypothesis, we transplanted presumptive mesoderm between embryos of reciprocal sexes to generate embryos containing male:female chimaeric gonads. In contrast to the outcome for mammalian mixed-sex chimaeras, in chicken mixed-sex chimaeras the donor cells were excluded from the functional structures of the host gonad. In an example where female tissue was transplanted into a male host, donor cells contributing to the developing testis retained a female identity and expressed a marker of female function. Our study demonstrates that avian somatic cells possess an inherent sex identity and that, in birds, sexual differentiation is substantively cell autonomous.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In an example where female tissue was transplanted into a male host, donor cells contributing to the developing testis retained a female identity and expressed a marker of female function.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 233, "doc_id": "4388470", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Early patent ductus ateriosus (PDA) screening increases in-hospital mortality.\n\nCANDIDATE_PASSAGE:\nUp-regulation of PPAR-gamma mRNA expression in the liver of obese patients: an additional reinforcing lipogenic mechanism to SREBP-1c induction. INTRODUCTION Triglyceride accumulation in the liver is an early feature in the development of nonalcoholic fatty liver disease (NAFLD) associated with human obesity, which is a multifactorial syndrome and whose underlying mechanisms are beginning to be understood. OBJECTIVES Liver peroxisome proliferator-activated receptor-γ (PPAR-γ) mRNA expression was measured as a signaling mechanism related to steatosis in obese patients with NAFLD. METHODS Liver PPAR-γ and sterol receptor element-binding protein 1c (SREBP-1c) mRNA (real-time RT-PCR), serum total adiponectin (RIA), and high molecular weight (HMW)-adiponectin (ELISA) levels, and insulin resistance (IR) evolution (homeostasis model assessment-IR) were determined in 22 obese NAFLD patients (16 with steatosis and six with steatohepatitis) who underwent subtotal gastrectomy with gastrojejunal anastomosis in Roux-en-Y and 16 nonobese subjects who underwent laparoscopic cholecystectomy (controls). RESULTS Liver PPAR-γ mRNA levels were 112 and 188% higher (P < 0.05) than control values in obese patients with steatosis and steatohepatitis, respectively, who also exhibited 70 and 62% increases in those of SREBP-1c, concomitantly with IR and lower levels of serum total adiponectin and HMW-adiponectin (P < 0.05). Liver PPAR-γ expression showed positive associations with SREBP-1c mRNA levels (r = 0.86; P < 0.0001), serum insulin levels (r = 0.39; P < 0.01), and homeostasis model assessment-IR (r = 0.60; P < 0.0001), and negative correlations with total adiponectin (r = -0.37; P < 0.01) and HMW-adiponectin (r = -0.51; P < 0.001) levels in serum. CONCLUSIONS PPAR-γ is up-regul [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "368", "doc_id": "22478394", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: General exercise therapy is more effective than scapular stabilizer exercises in reducing pain and improving function of the shoulder.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effect of specific exercise strategy on need for surgery in patients with subacromial impingement syndrome: randomised controlled study\nABSTRACT: OBJECTIVE To evaluate if a specific exercise strategy, targeting the rotator cuff and scapula stabilisers, improves shoulder function and pain more than unspecific exercises in patients with subacromial impingement syndrome, thereby decreasing the need for arthroscopic subacromial decompression. DESIGN Randomised, participant and single assessor blinded, controlled study. SETTING Department of orthopaedics in a Swedish university hospital. PARTICIPANTS 102 patients with long standing (over six months) persistent subacromial impingement syndrome in whom earlier conservative treatment had failed, recruited through orthopaedic specialists. INTERVENTIONS The specific exercise strategy consisted of strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers in combination with manual mobilisation. The control exercise programme consisted of unspecific movement exercises for the neck and shoulder. Patients in both groups received five to six individual guided treatment sessions during 12 weeks. In between these supervised sessions the participants performed home exercises once or twice a day for 12 weeks. MAIN OUTCOME MEASURES The primary outcome was the Constant-Murley shoulder assessment score evaluating shoulder function and pain. Secondary outcomes were patients' global impression of change because of treatment and decision regarding surgery. RESULTS Most (97, 95%) participants completed the 12 week study. There was a significantly greater improvement in the Constant-Murley score in the specific exercise group than in the control exercise group (24 points (95% confidence interval 19 to 28.0) v 9 points (5 to 13); mean difference between group: 15 points (8.5 to 20.6)). Significantly more patients in the [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"There was a significantly greater improvement in the Constant-Murley score in the specific exercise group than in the control exercise group (24 points (95% confidence interval 19 to 28.0) v 9 points (5 to 13); mean difference between group: 15 points (8.5 to 20.6)).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 454, "doc_id": "4200695", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Hyperfibrinogenemia increases rates of femoropopliteal bypass thrombosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Influence of smoking and plasma factors on patency of femoropopliteal vein grafts.\nABSTRACT: OBJECTIVE To determine the effects of smoking, plasma lipids, lipoproteins, apolipoproteins, and fibrinogen on the patency of saphenous vein femoropopliteal bypass grafts at one year. DESIGN Prospective study of patients with saphenous vein femoropopliteal bypass grafts entered into a multicentre trial. SETTING Surgical wards, outpatient clinics, and home visits coordinated by two tertiary referral centres in London and Birmingham. PATIENTS 157 Patients (mean age 66.6 (SD 8.2) years), 113 with patent grafts and 44 with occluded grafts one year after bypass. MAIN OUTCOME MEASURE Cumulative percentage patency at one year. RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts. Serum cholesterol concentrations were significantly higher in patients with grafts that remained patent one year after bypass (p less than 0.005). Analysis of the smoking markers indicated that a quarter of patients (40) were untruthful in their claims to have stopped smoking. Based on smoking markers, patency of grafts in smokers was significantly lower at one year by life table analysis than in non-smokers (63% v 84%, p less than 0.02). Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002). Surprisingly, increased plasma low density lipoprotein cholesterol concentration was significantly associated with improved patency at one year (85%) at values above the median compared w [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"A more forceful approach is needed to stop patients smoking; therapeutic measures to improve patency of vein grafts should focus on decreasing plasma fibrinogen concentration rather than serum cholesterol concentration.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 533, "doc_id": "12991445", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Oxidative phosphorylation is one of the primary glycometabolic pathways in cells.\n\nCANDIDATE_PASSAGE:\nDiverse tumorigenic pathways in ovarian serous carcinoma. This study was undertaken to analyze genetic alterations in 108 sporadic serous ovarian neoplasms to elucidate ovarian serous carcinogenesis. Our results demonstrate that K-ras mutations occur in approximately 50% of serous borderline tumors (SBTs), non-invasive micropapillary serous carcinomas (MPSCs), and invasive micropapillary serous carcinomas, which represent a morphological continuum of tumor progression. Moreover, progressive increase in the degree of allelic imbalance of chromosomes 1p, 5q, 8p, 18q, 22q, and Xp was observed comparing serous borderline tumors to noninvasive and invasive micropapillary serous carcinomas. In contrast, high-grade (conventional serous carcinoma) tumors contained wild-type K-ras in all 23 cases studied and a high frequency of allelic imbalance even in small (early) primary tumors similar to that found in advanced stage tumors. Based on these findings, we propose a dualistic model for ovarian serous carcinogenesis. One pathway involves a stepwise progression from SBT to noninvasive and then invasive MPSC. The other pathway is characterized by rapid progression from the ovarian surface epithelium or inclusion cysts to a conventional (high-grade) serous carcinoma.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "900", "doc_id": "42836872", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: LDL cholesterol has a causal role in the development of cardiovascular disease.\n\nCANDIDATE_PASSAGE:\nRandomized trial of folic acid supplementation and serum homocysteine levels. BACKGROUND Lowering serum homocysteine levels with folic acid is expected to reduce mortality from ischemic heart disease. Homocysteine reduction is known to be maximal at a folic acid dosage of 1 mg/d, but the effect of lower doses (relevant to food fortification) is unclear. METHODS We randomized 151 patients with ischemic heart disease to 1 of 5 dosages of folic acid (0.2, 0.4, 0.6, 0.8, and 1.0 mg/d) or placebo. Fasting blood samples for serum homocysteine and serum folate analysis were taken initially, after 3 months of supplementation, and 3 months after folic acid use was discontinued. RESULTS Median serum homocysteine level decreased with increasing folic acid dosage, to a maximum at 0.8 mg of folic acid per day, when the homocysteine reduction (placebo adjusted) was 2.7 micromol/L (23%), similar to the known effect of folic acid dosages of 1 mg/d and above. The higher a person's initial serum homocysteine level, the greater was the response to folic acid, but there were statistically significant reductions regardless of the initial level. Serum folate level increased approximately linearly (5.5 nmol/L for every 0.1 mg of folic acid). Within-person fluctuations over time in serum homocysteine levels, measured in the placebo group, were large compared with the effect of folic acid, indicating that monitoring of the reduction in an individual is impractical. CONCLUSIONS A dosage of folic acid of 0.8 mg/d appears necessary to achieve the maximum reduction in serum homocysteine level across the range of homocysteine levels in the population. Current US food fortification levels will achieve only a small proportion of the achievable homocysteine reduction.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "673", "doc_id": "11705328", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: AMP-activated protein kinase (AMPK) activation reduces inflammation-related fibrosis in the lungs.\n\nCANDIDATE_ABSTRACT:\nTITLE: Metformin reverses established lung fibrosis in a bleomycin model\nABSTRACT: Fibrosis is a pathological result of a dysfunctional repair response to tissue injury and occurs in a number of organs, including the lungs1. Cellular metabolism regulates tissue repair and remodelling responses to injury2-4. AMPK is a critical sensor of cellular bioenergetics and controls the switch from anabolic to catabolic metabolism5. However, the role of AMPK in fibrosis is not well understood. Here, we demonstrate that in humans with idiopathic pulmonary fibrosis (IPF) and in an experimental mouse model of lung fibrosis, AMPK activity is lower in fibrotic regions associated with metabolically active and apoptosis-resistant myofibroblasts. Pharmacological activation of AMPK in myofibroblasts from lungs of humans with IPF display lower fibrotic activity, along with enhanced mitochondrial biogenesis and normalization of sensitivity to apoptosis. In a bleomycin model of lung fibrosis in mice, metformin therapeutically accelerates the resolution of well-established fibrosis in an AMPK-dependent manner. These studies implicate deficient AMPK activation in non-resolving, pathologic fibrotic processes, and support a role for metformin (or other AMPK activators) to reverse established fibrosis by facilitating deactivation and apoptosis of myofibroblasts.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"These studies implicate deficient AMPK activation in non-resolving, pathologic fibrotic processes, and support a role for metformin (or other AMPK activators) to reverse established fibrosis by facilitating deactivation and apoptosis of myofibroblasts.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 55, "doc_id": "49556906", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: One in two surgical randomized controlled trials are discontinued early.\n\nCANDIDATE_ABSTRACT:\nTITLE: Discontinuation and non-publication of surgical randomised controlled trials: observational study\nABSTRACT: OBJECTIVE To determine the rate of early discontinuation and non-publication of randomised controlled trials involving patients undergoing surgery. DESIGN Cross sectional observational study of registered and published trials. SETTING Randomised controlled trials of interventions in patients undergoing a surgical procedure. DATA SOURCES The ClinicalTrials.gov database was searched for interventional trials registered between January 2008 and December 2009 using the keyword \"surgery\". Recruitment status was extracted from the ClinicalTrials.gov database. A systematic search for studies published in peer reviewed journals was performed; if they were not found, results posted on the ClinicalTrials.gov results database were sought. Email queries were sent to trial investigators of discontinued and unpublished completed trials if no reason for the respective status was disclosed. MAIN OUTCOME MEASURES Trial discontinuation before completion and non-publication after completion. Logistic regression was used to determine the effect of funding source on publication status, with adjustment for intervention type and trial size. RESULTS Of 818 registered trials found using the keyword \"surgery\", 395 met the inclusion criteria. Of these, 21% (81/395) were discontinued early, most commonly owing to poor recruitment (44%, 36/81). The remaining 314 (79%) trials proceeded to completion, with a publication rate of 66% (208/314) at a median time of 4.9 (interquartile range 4.0-6.0) years from study completion to publication search. A further 6% (20/314) of studies presented results on ClinicalTrials.gov without a corresponding peer reviewed publication. Industry funding did not affect the rate of discontinuation (adjusted odds ratio 0.91, 95% confidence interval 0.54 to 1.55) [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS One in five surgical randomised controlled trials are discontinued early, one in three completed trials remain unpublished, and investigators of unpublished studies are frequently not contactable.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 886, "doc_id": "6477536", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Physical injury represses transgultaminase activity.\n\nCANDIDATE_ABSTRACT:\nTITLE: Transglutaminase 2 Undergoes a Large Conformational Change upon Activation \nABSTRACT: Human transglutaminase 2 (TG2), a member of a large family of enzymes that catalyze protein crosslinking, plays an important role in the extracellular matrix biology of many tissues and is implicated in the gluten-induced pathogenesis of celiac sprue. Although vertebrate transglutaminases have been studied extensively, thus far all structurally characterized members of this family have been crystallized in conformations with inaccessible active sites. We have trapped human TG2 in complex with an inhibitor that mimics inflammatory gluten peptide substrates and have solved, at 2-A resolution, its x-ray crystal structure. The inhibitor stabilizes TG2 in an extended conformation that is dramatically different from earlier transglutaminase structures. The active site is exposed, revealing that catalysis takes place in a tunnel, bridged by two tryptophan residues that separate acyl-donor from acyl-acceptor and stabilize the tetrahedral reaction intermediates. Site-directed mutagenesis was used to investigate the acyl-acceptor side of the tunnel, yielding mutants with a marked increase in preference for hydrolysis over transamidation. By providing the ability to visualize this activated conformer, our results create a foundation for understanding the catalytic as well as the non-catalytic roles of TG2 in biology, and for dissecting the process by which the autoantibody response to TG2 is induced in celiac sprue patients.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 949, "doc_id": "13578199", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Ambulatory blood pressure monitoring is inaccurate at diagnosing hypertension.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cost-effectiveness of options for the diagnosis of high blood pressure in primary care: a modelling study.\nABSTRACT: BACKGROUND The diagnosis of hypertension has traditionally been based on blood-pressure measurements in the clinic, but home and ambulatory measurements better correlate with cardiovascular outcome, and ambulatory monitoring is more accurate than both clinic and home monitoring in diagnosing hypertension. We aimed to compare the cost-effectiveness of different diagnostic strategies for hypertension. METHODS We did a Markov model-based probabilistic cost-effectiveness analysis. We used a hypothetical primary-care population aged 40 years or older with a screening blood-pressure measurement greater than 140/90 mm Hg and risk-factor prevalence equivalent to the general population. We compared three diagnostic strategies-further blood pressure measurement in the clinic, at home, and with an ambulatory monitor-in terms of lifetime costs, quality-adjusted life years, and cost-effectiveness. FINDINGS Ambulatory monitoring was the most cost-effective strategy for the diagnosis of hypertension for men and women of all ages. It was cost-saving for all groups (from -£56 [95% CI -105 to -10] in men aged 75 years to -£323 [-389 to -222] in women aged 40 years) and resulted in more quality-adjusted life years for men and women older than 50 years (from 0·006 [0·000 to 0·015] for women aged 60 years to 0·022 [0·012 to 0·035] for men aged 70 years). This finding was robust when assessed with a wide range of deterministic sensitivity analyses around the base case, but was sensitive if home monitoring was judged to have equal test performance to ambulatory monitoring or if treatment was judged effective irrespective of whether an individual was hypertensive. INTERPRETATION Ambulatory monitoring as a diagnostic strategy for hypertension after an initial raised reading in the c [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"BACKGROUND The diagnosis of hypertension has traditionally been based on blood-pressure measurements in the clinic, but home and ambulatory measurements better correlate with cardiovascular outcome, and ambulatory monitoring is more accurate than both clinic and home monitoring in diagnosing hypertension.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 106, "doc_id": "5151024", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Cellular clocks are associated with mitosis timing in NIH 3T3 cells.\n\nCANDIDATE_PASSAGE:\nRobust synchronization of coupled circadian and cell cycle oscillators in single mammalian cells Circadian cycles and cell cycles are two fundamental periodic processes with a period in the range of 1 day. Consequently, coupling between such cycles can lead to synchronization. Here, we estimated the mutual interactions between the two oscillators by time-lapse imaging of single mammalian NIH3T3 fibroblasts during several days. The analysis of thousands of circadian cycles in dividing cells clearly indicated that both oscillators tick in a 1:1 mode-locked state, with cell divisions occurring tightly 5 h before the peak in circadian Rev-Erbα-YFP reporter expression. In principle, such synchrony may be caused by either unidirectional or bidirectional coupling. While gating of cell division by the circadian cycle has been most studied, our data combined with stochastic modeling unambiguously show that the reverse coupling is predominant in NIH3T3 cells. Moreover, temperature, genetic, and pharmacological perturbations showed that the two interacting cellular oscillators adopt a synchronized state that is highly robust over a wide range of parameters. These findings have implications for circadian function in proliferative tissues, including epidermis, immune cells, and cancer.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "241", "doc_id": "2212067", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Ultrasound guidance significantly raises the number of traumatic procedures when attempting needle insertion.\n\nCANDIDATE_ABSTRACT:\nTITLE: Ultrasound imaging for lumbar punctures and epidural catheterisations: systematic review and meta-analysis.\nABSTRACT: OBJECTIVE To determine whether ultrasound imaging can reduce the risk of failed lumbar punctures or epidural catheterisations, when compared with standard palpation methods, and whether ultrasound imaging can reduce traumatic procedures, insertion attempts, and needle redirections. DESIGN Systematic review and meta-analysis of randomised controlled trials. DATA SOURCES Ovid Medline, Embase, and Cochrane Central Register of Controlled Trials up to May 2012, without restriction by language or publication status. REVIEW METHODS Randomised trials that compared ultrasound imaging with standard methods (no imaging) in the performance of a lumbar puncture or epidural catheterisation were identified. RESULTS 14 studies with a total of 1334 patients were included (674 patients assigned to the ultrasound group, 660 to the control group). Five studies evaluated lumbar punctures and nine evaluated epidural catheterisations. Six of 624 procedures conducted in the ultrasound group failed; 44 of 610 procedures in the control group failed. Ultrasound imaging reduced the risk of failed procedures (risk ratio 0.21 (95% confidence interval 0.10 to 0.43), P<0.001). Risk reduction was similar when subgroup analysis was performed for lumbar punctures (risk ratio 0.19 (0.07 to 0.56), P=0.002) or epidural catheterisations (0.23 (0.09 to 0.60), P=0.003). Ultrasound imaging also significantly reduced the risk of traumatic procedures (risk ratio 0.27 (0.11 to 0.67), P=0.005), the number of insertion attempts (mean difference -0.44 (-0.64 to -0.24), P<0.001), and the number of needle redirections (mean difference -1.00 (-1.24 to -0.75), P<0.001). CONCLUSIONS Ultrasound imaging can reduce the risk of failed or traumatic lumbar punctures and epidural catheterisations, as well as the numb [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Ultrasound imaging reduced the risk of failed procedures (risk ratio 0.21 (95% confidence interval 0.10 to 0.43), P<0.001). Risk reduction was similar when subgroup analysis was performed for lumbar punctures (risk ratio 0.19 (0.07 to 0.56), P=0.002) or epidural catheterisations (0.23 (0.09 to 0.60), P=0.003).\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1339, "doc_id": "15482274", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Varenicline monotherapy is more effective after 26 weeks of treatment compared to combination nicotine replacement therapies with varenicline or bupropion.\n\nCANDIDATE_ABSTRACT:\nTITLE: Combination varenicline and bupropion SR for tobacco-dependence treatment in cigarette smokers: a randomized trial.\nABSTRACT: IMPORTANCE Combining pharmacotherapies for tobacco-dependence treatment may increase smoking abstinence. OBJECTIVE To determine efficacy and safety of varenicline and bupropion sustained-release (SR; combination therapy) compared with varenicline (monotherapy) in cigarette smokers. DESIGN, SETTING, AND PARTICIPANTS Randomized, blinded, placebo-controlled multicenter clinical trial with a 12-week treatment period and follow-up through week 52 conducted between October 2009 and April 2013 at 3 midwestern clinical research sites. Five hundred six adult (≥18 years) cigarette smokers were randomly assigned and 315 (62%) completed the study. INTERVENTIONS Twelve weeks of varenicline and bupropion SR or varenicline and placebo. MAIN OUTCOMES AND MEASURES Primary outcome was abstinence rates at week 12, defined as prolonged (no smoking from 2 weeks after the target quit date) abstinence and 7-day point-prevalence (no smoking past 7 days) abstinence. Secondary outcomes were prolonged and point-prevalence smoking abstinence rates at weeks 26 and 52. Outcomes were biochemically confirmed. RESULTS At 12 weeks, 53.0% of the combination therapy group achieved prolonged smoking abstinence and 56.2% achieved 7-day point-prevalence smoking abstinence compared with 43.2% and 48.6% in varenicline monotherapy (odds ratio [OR], 1.49; 95% CI, 1.05-2.12; P = .03 and OR, 1.36; 95% CI, 0.95-1.93; P = .09, respectively). At 26 weeks, 36.6% of the combination therapy group achieved prolonged and 38.2% achieved 7-day point-prevalence smoking abstinence compared with 27.6% and 31.9% in varenicline monotherapy (OR, 1.52; 95% CI, 1.04-2.22; P = .03 and OR, 1.32; 95% CI, 0.91-1.91; P = .14, respectively). At 52 weeks, 30.9% of the combination therapy group achieved prolonged and 36.6% achi [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"At 26 weeks, 36.6% of the combination therapy group achieved prolonged and 38.2% achieved 7-day point-prevalence smoking abstinence compared with 27.6% and 31.9% in varenicline monotherapy (OR, 1.52; 95% CI, 1.04-2.22; P = .03 and OR, 1.32; 95% CI, 0.91-1.91; P = .14, respectively).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1360, "doc_id": "11614737", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: siRNA knockdown of A20 slows tumor progression in an in vivo murine xenograft model.\n\nCANDIDATE_ABSTRACT:\nTITLE: Targeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth\nABSTRACT: Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs). GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets. We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels. To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA). Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis. The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays. The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts. In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival. Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation. Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may funct [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1404, "doc_id": "33370", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Stroke patients with prior use of direct oral anticoagulants have a higher risk of in-hospital mortality than stroke patients with prior use of warfarin.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association of Intracerebral Hemorrhage Among Patients Taking Non–Vitamin K Antagonist vs Vitamin K Antagonist Oral Anticoagulants With In-Hospital Mortality\nABSTRACT: Importance Although non–vitamin K antagonist oral anticoagulants (NOACs) are increasingly used to prevent thromboembolic disease, there are limited data on NOAC-related intracerebral hemorrhage (ICH). Objective To assess the association between preceding oral anticoagulant use (warfarin, NOACs, and no oral anticoagulants [OACs]) and in-hospital mortality among patients with ICH. Design, Setting, and Participants Retrospective cohort study of 141 311 patients with ICH admitted from October 2013 to December 2016 to 1662 Get With The Guidelines–Stroke hospitals. Exposures Anticoagulation therapy before ICH, defined as any use of OACs within 7 days prior to hospital arrival. Main Outcomes and Measures In-hospital mortality. Results Among 141 311 patients with ICH (mean [SD] age, 68.3 [15.3] years; 48.1% women), 15 036 (10.6%) were taking warfarin and 4918 (3.5%) were taking NOACs preceding ICH, and 39 585 (28.0%) and 5783 (4.1%) were taking concomitant single and dual antiplatelet agents, respectively. Patients with prior use of warfarin or NOACs were older and had higher prevalence of atrial fibrillation and prior stroke. Acute ICH stroke severity (measured by the National Institutes of Health Stroke Scale) was not significantly different across the 3 groups (median, 9 [interquartile range, 2-21] for warfarin, 8 [2-20] for NOACs, and 8 [2-19] for no OACs). The unadjusted in-hospital mortality rates were 32.6% for warfarin, 26.5% for NOACs, and 22.5% for no OACs. Compared with patients without prior use of OACs, the risk of in-hospital mortality was higher among patients with prior use of warfarin (adjusted risk difference [ARD], 9.0% [97.5% CI, 7.9% to 10.1%]; adjusted odds ratio [AOR], 1.62 [97.5% CI, 1.53 to 1.71]) and higher among patients with prior use of [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The unadjusted in-hospital mortality rates were 32.6% for warfarin, 26.5% for NOACs, and 22.5% for no OACs.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1103, "doc_id": "3898784", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Varying expression levels of EBI2 affect the positioning and migration of B cells.\n\nCANDIDATE_PASSAGE:\nType 1 diabetes-associated IL2RA variation lowers IL-2 signaling and contributes to diminished CD4+CD25+ regulatory T cell function. Numerous reports have demonstrated that CD4(+)CD25(+) regulatory T cells (Tregs) from individuals with a range of human autoimmune diseases, including type 1 diabetes, are deficient in their ability to control autologous proinflammatory responses when compared with nondiseased, control individuals. Treg dysfunction could be a primary, causal event or may result from perturbations in the immune system during disease development. Polymorphisms in genes associated with Treg function, such as IL2RA, confer a higher risk of autoimmune disease. Although this suggests a primary role for defective Tregs in autoimmunity, a link between IL2RA gene polymorphisms and Treg function has not been examined. We addressed this by examining the impact of an IL2RA haplotype associated with type 1 diabetes on Treg fitness and suppressive function. Studies were conducted using healthy human subjects to avoid any confounding effects of disease. We demonstrated that the presence of an autoimmune disease-associated IL2RA haplotype correlates with diminished IL-2 responsiveness in Ag-experienced CD4(+) T cells, as measured by phosphorylation of STAT5a, and is associated with lower levels of FOXP3 expression by Tregs and a reduction in their ability to suppress proliferation of autologous effector T cells. These data offer a rationale that contributes to the molecular and cellular mechanisms through which polymorphisms in the IL-2RA gene affect immune regulation, and consequently upon susceptibility to autoimmune and inflammatory diseases.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1361", "doc_id": "11899391", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: General exercise therapy is more effective than rotator cuff exercises in reducing pain and improving function of the shoulder.\n\nCANDIDATE_PASSAGE:\n15-Hydroxyprostaglandin dehydrogenase is down-regulated in colorectal cancer. Prostaglandin E2 (PGE2) can stimulate tumor progression by modulating several proneoplastic pathways, including proliferation, angiogenesis, cell migration, invasion, and apoptosis. Although steady-state tissue levels of PGE2 stem from relative rates of biosynthesis and breakdown, most reports examining PGE2 have focused solely on the cyclooxygenase-dependent formation of this bioactive lipid. Enzymatic degradation of PGE2 involves the NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH). The present study examined a range of normal tissues in the human and mouse and found high levels of 15-PGDH in the large intestine. By contrast, the expression of 15-PGDH is decreased in several colorectal carcinoma cell lines and in other human malignancies such as breast and lung carcinomas. Consistent with these findings, we observe diminished 15-Pgdh expression in ApcMin+/- mouse adenomas. Enzymatic activity of 15-PGDH correlates with expression levels and the genetic disruption of 15-Pgdh completely blocks production of the urinary PGE2 metabolite. Finally, 15-PGDH expression and activity are significantly down-regulated in human colorectal carcinomas relative to matched normal tissue. In summary, these results suggest a novel tumor suppressive role for 15-PGDH due to loss of expression during colorectal tumor progression.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "453", "doc_id": "21181273", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Foxp3 enables the expression of transcriptional regulators implicated in memory T cell development.\n\nCANDIDATE_PASSAGE:\nResponse to self antigen imprints regulatory memory in tissues Immune homeostasis in tissues is achieved through a delicate balance between pathogenic T-cell responses directed at tissue-specific antigens and the ability of the tissue to inhibit these responses. The mechanisms by which tissues and the immune system communicate to establish and maintain immune homeostasis are currently unknown. Clinical evidence suggests that chronic or repeated exposure to self antigen within tissues leads to an attenuation of pathological autoimmune responses, possibly as a means to mitigate inflammatory damage and preserve function. Many human organ-specific autoimmune diseases are characterized by the initial presentation of the disease being the most severe, with subsequent flares being of lesser severity and duration. In fact, these diseases often spontaneously resolve, despite persistent tissue autoantigen expression. In the practice of antigen-specific immunotherapy, allergens or self antigens are repeatedly injected in the skin, with a diminution of the inflammatory response occurring after each successive exposure. Although these findings indicate that tissues acquire the ability to attenuate autoimmune reactions upon repeated responses to antigens, the mechanism by which this occurs is unknown. Here we show that upon expression of self antigen in a peripheral tissue, thymus-derived regulatory T cells (Treg cells) become activated, proliferate and differentiate into more potent suppressors, which mediate resolution of organ-specific autoimmunity in mice. After resolution of the inflammatory response, activated Treg cells are maintained in the target tissue and are primed to attenuate subsequent autoimmune reactions when antigen is re-expressed. Thus, Treg cells func [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "434", "doc_id": "4380287", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: General exercise therapy is more effective than rotator cuff exercises in reducing pain and improving function of the shoulder.\n\nCANDIDATE_ABSTRACT:\nTITLE: Oct4-Induced Pluripotency in Adult Neural Stem Cells\nABSTRACT: The four transcription factors Oct4, Sox2, Klf4, and c-Myc can induce pluripotency in mouse and human fibroblasts. We previously described direct reprogramming of adult mouse neural stem cells (NSCs) by Oct4 and either Klf4 or c-Myc. NSCs endogenously express Sox2, c-Myc, and Klf4 as well as several intermediate reprogramming markers. Here we report that exogenous expression of the germline-specific transcription factor Oct4 is sufficient to generate pluripotent stem cells from adult mouse NSCs. These one-factor induced pluripotent stem cells (1F iPS) are similar to embryonic stem cells in vitro and in vivo. Not only can these cells can be efficiently differentiated into NSCs, cardiomyocytes, and germ cells in vitro, but they are also capable of teratoma formation and germline transmission in vivo. Our results demonstrate that Oct4 is required and sufficient to directly reprogram NSCs to pluripotency.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 453, "doc_id": "1630949", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is the clinical diagnosis of meniscal tear easy . Reliability of two clinical meniscal tests and magnetic resonance imaging?\n\nABSTRACT:\nto clarify the reliability of two clinical meniscal tests, McMurray's and Apley's and the MRI imaging, in order to establish how to reduce unjustified arthroscopies. 102 patients were selected out of 160. All patients were submitted to a triple clinical examination (by a young surgeon and two skilled surgeons), MRI and an arthroscopic procedure. The investigated clinical tests were McMurray's and Apley's test. The positivity or negativity of the tests and MRI were compared to arthroscopic findings. Arthroscopy is considered the gold standard for the diagnosis of meniscal lesions. We measured the length of the meniscal lesions in order to correlate it to the clinical findings. From the clinical examination, we got the following data: McMurray's test: sensitivity 79.7%, specificity 78.5%, accuracy 79.4%, positive likelihood ratio 3.7, negative likelihood ratio 0.2. Apley's test: sensitivity 83.7%, specificity 71.4%, accuracy 80.3%, positive likelihood ratio 2.9, negative likelihood ratio 0.2. The composite assessment is strictly dependent on how the discordance of the two tests is evaluated. The assessment of the clinical tests was done even in relation to medial or lateral meniscal lesion. No statistical difference was found about the length of the meniscal tear. MRI gave the following results: sensitivity 78.3%, specificity 85.7%, accuracy 80.3%.", "output": "{\"label\": \"no\", \"rationale\": \"If we use, as diagnostic means, McMurray's and Apley's clinical tests and MRI as imaging procedure, we have an accuracy of about 80%. It is important to keep in mind that it is not possible to have the absolute certainty of make a correct diagnosis in case of meniscal lesions. Patients, too, have to be informed about the risk of a negative arthroscopy.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 21669136, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Sympathetic nerve activity is elevated throughout normal pregnancy.\n\nCANDIDATE_PASSAGE:\nInduction of ectopic eyes by targeted expression of the eyeless gene in Drosophila. The Drosophila gene eyeless (ey) encodes a transcription factor with both a paired domain and a homeodomain. It is homologous to the mouse Small eye (Pax-6) gene and to the Aniridia gene in humans. These genes share extensive sequence identity, the position of three intron splice sites is conserved, and these genes are expressed similarly in the developing nervous system and in the eye during morphogenesis. Loss-of-function mutations in both the insect and in the mammalian genes have been shown to lead to a reduction or absence of eye structures, which suggests that ey functions in eye morphogenesis. By targeted expression of the ey complementary DNA in various imaginal disc primordia of Drosophila, ectopic eye structures were induced on the wings, the legs, and on the antennae. The ectopic eyes appeared morphologically normal and consisted of groups of fully differentiated ommatidia with a complete set of photoreceptor cells. These results support the proposition that ey is the master control gene for eye morphogenesis. Because homologous genes are present in vertebrates, ascidians, insects, cephalopods, and nemerteans, ey may function as a master control gene throughout the metazoa.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1119", "doc_id": "9646449", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Bcp1 is a chaperone for Rpl23.\n\nCANDIDATE_PASSAGE:\nRational Extension of the Ribosome Biogenesis Pathway Using Network-Guided Genetics Biogenesis of ribosomes is an essential cellular process conserved across all eukaryotes and is known to require >170 genes for the assembly, modification, and trafficking of ribosome components through multiple cellular compartments. Despite intensive study, this pathway likely involves many additional genes. Here, we employ network-guided genetics-an approach for associating candidate genes with biological processes that capitalizes on recent advances in functional genomic and proteomic studies-to computationally identify additional ribosomal biogenesis genes. We experimentally evaluated >100 candidate yeast genes in a battery of assays, confirming involvement of at least 15 new genes, including previously uncharacterized genes (YDL063C, YIL091C, YOR287C, YOR006C/TSR3, YOL022C/TSR4). We associate the new genes with specific aspects of ribosomal subunit maturation, ribosomal particle association, and ribosomal subunit nuclear export, and we identify genes specifically required for the processing of 5S, 7S, 20S, 27S, and 35S rRNAs. These results reveal new connections between ribosome biogenesis and mRNA splicing and add >10% new genes-most with human orthologs-to the biogenesis pathway, significantly extending our understanding of a universally conserved eukaryotic process.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "173", "doc_id": "8126244", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Pyridostatin prevents double-strand breaks accumulation.\n\nCANDIDATE_PASSAGE:\nTargeting BRCA1 and BRCA2 Deficiencies with G-Quadruplex-Interacting Compounds G-quadruplex (G4)-forming genomic sequences, including telomeres, represent natural replication fork barriers. Stalled replication forks can be stabilized and restarted by homologous recombination (HR), which also repairs DNA double-strand breaks (DSBs) arising at collapsed forks. We have previously shown that HR facilitates telomere replication. Here, we demonstrate that the replication efficiency of guanine-rich (G-rich) telomeric repeats is decreased significantly in cells lacking HR. Treatment with the G4-stabilizing compound pyridostatin (PDS) increases telomere fragility in BRCA2-deficient cells, suggesting that G4 formation drives telomere instability. Remarkably, PDS reduces proliferation of HR-defective cells by inducing DSB accumulation, checkpoint activation, and deregulated G2/M progression and by enhancing the replication defect intrinsic to HR deficiency. PDS toxicity extends to HR-defective cells that have acquired olaparib resistance through loss of 53BP1 or REV7. Altogether, these results highlight the therapeutic potential of G4-stabilizing drugs to selectively eliminate HR-compromised cells and tumors, including those resistant to PARP inhibition.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "998", "doc_id": "16472469", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Depletion of T-helper 17 (Th17) cells during simian immunodeficiency virus (SIV) infection decreases dissemination of Salmonella Typhimurium from the gut.\n\nCANDIDATE_PASSAGE:\nSimian immunodeficiency virus–induced mucosal interleukin-17 deficiency promotes Salmonella dissemination from the gut Salmonella typhimurium causes a localized enteric infection in immunocompetent individuals, whereas HIV-infected individuals develop a life-threatening bacteremia. Here we show that simian immunodeficiency virus (SIV) infection results in depletion of T helper type 17 (TH17) cells in the ileal mucosa of rhesus macaques, thereby impairing mucosal barrier functions to S. typhimurium dissemination. In SIV-negative macaques, the gene expression profile induced by S. typhimurium in ligated ileal loops was dominated by TH17 responses, including the expression of interleukin-17 (IL-17) and IL-22. TH17 cells were markedly depleted in SIV-infected rhesus macaques, resulting in blunted TH17 responses to S. typhimurium infection and increased bacterial dissemination. IL-17 receptor–deficient mice showed increased systemic dissemination of S. typhimurium from the gut, suggesting that IL-17 deficiency causes defects in mucosal barrier function. We conclude that SIV infection impairs the IL-17 axis, an arm of the mucosal immune response preventing systemic microbial dissemination from the gastrointestinal tract.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "332", "doc_id": "29023309", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Patients in stable partnerships have a faster progression from HIV to AIDS.\n\nCANDIDATE_ABSTRACT:\nTITLE: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\nABSTRACT: OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART). DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study). SETTING Seven outpatient clinics throughout Switzerland. PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years). MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound. RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion. When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership. In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without. Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression. CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 922, "doc_id": "17077004", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Notch signaling occurs between tumor cells and stromal cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Jagged1-induced Notch signaling drives proliferation of multiple myeloma cells.\nABSTRACT: Notch receptors expressed on hematopoietic stem cells interact with their ligands on bone marrow stromal cells and thereby control cell fate decisions and survival. We recently demonstrated that Notch signaling is involved in proliferation and survival of B cell-derived tumor cells of classic Hodgkin disease and described a novel mechanism for the oncogenic capacity of Notch. In this study we investigated whether Notch signaling is involved in the tight interactions between neoplastic plasma cells and their bone marrow microenvironment, which are essential for tumor cell growth in multiple myeloma (MM). Here we demonstrate that Notch receptors and their ligand Jagged1 are highly expressed in cultured and primary MM cells, whereas nonneoplastic counterparts show low to undetectable levels of Notch. Functional data indicate that ligand-induced Notch signaling is a growth factor for MM cells and suggest that these interactions contribute to myelomagenesis in vivo.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We recently demonstrated that Notch signaling is involved in proliferation and survival of B cell-derived tumor cells of classic Hodgkin disease and described a novel mechanism for the oncogenic capacity of Notch.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 863, "doc_id": "16361581", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pioglitazone use is not associated with an increased risk of prostate cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pioglitazone Use and Risk of Bladder Cancer and Other Common Cancers in Persons With Diabetes.\nABSTRACT: IMPORTANCE Studies suggest pioglitazone use may increase risk of cancers. OBJECTIVE To examine whether pioglitazone use for diabetes is associated with risk of bladder and 10 additional cancers. DESIGN, SETTING, AND PARTICIPANTS Cohort and nested case-control analyses among persons with diabetes. A bladder cancer cohort followed 193,099 persons aged 40 years or older in 1997-2002 until December 2012; 464 case patients and 464 matched controls were surveyed about additional confounders. A cohort analysis of 10 additional cancers included 236,507 persons aged 40 years or older in 1997-2005 and followed until June 2012. Cohorts were from Kaiser Permanente Northern California. EXPOSURES Ever use, duration, cumulative dose, and time since initiation of pioglitazone as time dependent. MAIN OUTCOMES AND MEASURES Incident cancer, including bladder, prostate, female breast, lung/bronchus, endometrial, colon, non-Hodgkin lymphoma, pancreas, kidney/renal pelvis, rectum, and melanoma. RESULTS Among 193,099 persons in the bladder cancer cohort, 34,181 (18%) received pioglitazone (median duration, 2.8 years; range, 0.2-13.2 years) and 1261 had incident bladder cancer. Crude incidences of bladder cancer in pioglitazone users and nonusers were 89.8 and 75.9 per 100,000 person-years, respectively. Ever use of pioglitazone was not associated with bladder cancer risk (adjusted hazard ratio [HR], 1.06; 95% CI, 0.89-1.26). Results were similar in case-control analyses (pioglitazone use: 19.6% among case patients and 17.5% among controls; adjusted odds ratio, 1.18; 95% CI, 0.78-1.80). In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95% CI, 1.02-1.26) and p [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95% CI, 1.02-1.26) and pancreatic cancer (HR, 1.41; 95% CI, 1.16-1.71).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 952, "doc_id": "3355397", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Physical activity level has no association with the difference in maximal oxygen consumption between black and white youth.\n\nCANDIDATE_PASSAGE:\nEffects of exercise intensity on cardiovascular fitness, total body composition, and visceral adiposity of obese adolescents. BACKGROUND Little is known about how the intensity of exercise influences cardiovascular fitness and body composition, especially in obese adolescents. OBJECTIVE Our goal was to determine the effects of physical training intensity on the cardiovascular fitness, percentage of body fat (%BF), and visceral adipose tissue (VAT) of obese adolescents. DESIGN Obese 13-16-y-olds (n = 80) were assigned to 1) biweekly lifestyle education (LSE), 2) LSE + moderate-intensity physical training, or 3) LSE + high-intensity physical training. The intervention lasted 8 mo. Physical training was offered 5 d/wk, and the target energy expenditure for all subjects in physical training groups was 1047 kJ (250 kcal)/session. Cardiovascular fitness was measured with a multistage treadmill test, %BF with dual-energy X-ray absorptiometry, and VAT with magnetic resonance imaging. RESULTS The increase in cardiovascular fitness in the high-intensity physical training group, but not in the moderate-intensity group, was significantly greater than that in the LSE alone group (P = 0.009); no other comparisons of the 3 groups were significant. Compared with the LSE alone group, a group composed of subjects in both physical training groups combined who attended training sessions >or=2 d/wk showed favorable changes in cardiovascular fitness (P < 0.001), %BF (P = 0.001), and VAT (P = 0.029). We found no evidence that the high-intensity physical training was more effective than the moderate-intensity physical training in enhancing body composition. CONCLUSIONS The cardiovascular fitness of obese adolescents was significantly improved by physical training, especially high-i [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "945", "doc_id": "4463588", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does inhibition of the renin-angiotensin system reduce platelet activity at rest or during stress in hypertension?\n\nABSTRACT:\nWe investigated the influence of angiotensin receptor blockade and angiotensin-converting enzyme inhibition on stress-induced platelet activation in hypertensive patients. Secondary aims were effects on inflammation, coagulation, and endothelial function. Following a 4-week placebo period, 25 hypertensive patients entered a double-blind, crossover study comparing enalapril (20 mg once daily) and losartan (100 mg once daily) treatment (each for 8 weeks). Patients were studied at rest and after a standardized exercise test. Mean arterial pressure was reduced from 119 ± 2 to 104 ± 2 (enalapril) and 106 ± 2 (losartan) mmHg (both P <0.001). Plasma angiotensin II decreased from 2.4 ± 0.4 to 0.5 ± 0.1 pmol/l with enalapril, and increased to 7.2 ± 1.3 pmol/l with losartan (both P <0.001). Exercise-evoked platelet activation, as evidenced by increased numbers of P-selectin-positive platelets (P <0.01), elevated circulating platelet-platelet aggregates (P <0.01) and soluble P-selectin levels (P <0.001), and increased platelet responsiveness to adenosine diphosphate and thrombin (both P <0.05). Neither drug influenced these markers of platelet activation at rest or following exercise. Markers of inflammation (high-sensitivity C reactive protein, interleukin-6, tissue necrosis factor-α), coagulation (tissue plasminogen activator antigen, prothrombin fragment F1+2), and endothelial function (von Willebrand factor, soluble vascular cellular adhesion molecule-1, and intercellular adhesion molecule-1) were also uninfluenced by treatment.", "output": "{\"label\": \"no\", \"rationale\": \"Enalapril and losartan failed to reduce platelet activity both at rest and during exercise in hypertensive patients. Markers of inflammation, coagulation, and endothelial function were similarly unaffected. Inhibition of the renin-angiotensin system promotes its beneficial effects in hypertension through mechanisms other than platelet inhibition.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 23625113, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Microglia are an innate immune cell type of the peripheral nervous system.\n\nCANDIDATE_PASSAGE:\nA tumor necrosis factor-α–mediated pathway promoting autosomal dominant polycystic kidney disease Autosomal dominant polycystic kidney disease (ADPKD) is caused by heterozygous mutations in either PKD1 or PKD2, genes that encode polycystin-1 and polycystin-2, respectively. We show here that tumor necrosis factor-α (TNF-α), an inflammatory cytokine present in the cystic fluid of humans with ADPKD, disrupts the localization of polycystin-2 to the plasma membrane and primary cilia through a scaffold protein, FIP2, which is induced by TNF-α. Treatment of mouse embryonic kidney organ cultures with TNF-α resulted in formation of cysts, and this effect was exacerbated in the Pkd2+/− kidneys. TNF-α also stimulated cyst formation in vivo in Pkd2+/− mice. In contrast, treatment of Pkd2+/− mice with the TNF-α inhibitor etanercept prevented cyst formation. These data reveal a pathway connecting TNF-α signaling, polycystins and cystogenesis, the activation of which may reduce functional polycystin-2 below a critical threshold, precipitating the ADPKD cellular phenotype.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "790", "doc_id": "25089501", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Teaching hospitals do not provide better care than non-teaching hospitals.\n\nCANDIDATE_ABSTRACT:\nTITLE: Patient Outcomes with Teaching Versus Nonteaching Healthcare: A Systematic Review\nABSTRACT: Background Extensive debate exists in the healthcare community over whether outcomes of medical care at teaching hospitals and other healthcare units are better or worse than those at the respective nonteaching ones. Thus, our goal was to systematically evaluate the evidence pertaining to this question. Methods and Findings We reviewed all studies that compared teaching versus nonteaching healthcare structures for mortality or any other patient outcome, regardless of health condition. Studies were retrieved from PubMed, contact with experts, and literature cross-referencing. Data were extracted on setting, patients, data sources, author affiliations, definition of compared groups, types of diagnoses considered, adjusting covariates, and estimates of effect for mortality and for each other outcome. Overall, 132 eligible studies were identified, including 93 on mortality and 61 on other eligible outcomes (22 addressed both). Synthesis of the available adjusted estimates on mortality yielded a summary relative risk of 0.96 (95% confidence interval [CI], 0.93–1.00) for teaching versus nonteaching healthcare structures and 1.04 (95% CI, 0.99–1.10) for minor teaching versus nonteaching ones. There was considerable heterogeneity between studies (I2 = 72% for the main analysis). Results were similar in studies using clinical and those using administrative databases. No differences were seen in the 14 studies fully adjusting for volume/experience, severity, and comorbidity (relative risk 1.01). Smaller studies did not differ in their results from larger studies. Differences were seen for some diagnoses (e.g., significantly better survival for breast cancer and cerebrovascular accidents in teaching hospitals and significantly better survival from cholecystectomy in no [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Other outcomes were diverse, but typically teaching healthcare structures did not do better than nonteaching ones.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1146, "doc_id": "13906581", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Combination nicotine replacement therapies with varenicline or bupropion lead to significantly higher long-term abstinence rates at 52 weeks than varenicline monotherapy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Combination varenicline and bupropion SR for tobacco-dependence treatment in cigarette smokers: a randomized trial.\nABSTRACT: IMPORTANCE Combining pharmacotherapies for tobacco-dependence treatment may increase smoking abstinence. OBJECTIVE To determine efficacy and safety of varenicline and bupropion sustained-release (SR; combination therapy) compared with varenicline (monotherapy) in cigarette smokers. DESIGN, SETTING, AND PARTICIPANTS Randomized, blinded, placebo-controlled multicenter clinical trial with a 12-week treatment period and follow-up through week 52 conducted between October 2009 and April 2013 at 3 midwestern clinical research sites. Five hundred six adult (≥18 years) cigarette smokers were randomly assigned and 315 (62%) completed the study. INTERVENTIONS Twelve weeks of varenicline and bupropion SR or varenicline and placebo. MAIN OUTCOMES AND MEASURES Primary outcome was abstinence rates at week 12, defined as prolonged (no smoking from 2 weeks after the target quit date) abstinence and 7-day point-prevalence (no smoking past 7 days) abstinence. Secondary outcomes were prolonged and point-prevalence smoking abstinence rates at weeks 26 and 52. Outcomes were biochemically confirmed. RESULTS At 12 weeks, 53.0% of the combination therapy group achieved prolonged smoking abstinence and 56.2% achieved 7-day point-prevalence smoking abstinence compared with 43.2% and 48.6% in varenicline monotherapy (odds ratio [OR], 1.49; 95% CI, 1.05-2.12; P = .03 and OR, 1.36; 95% CI, 0.95-1.93; P = .09, respectively). At 26 weeks, 36.6% of the combination therapy group achieved prolonged and 38.2% achieved 7-day point-prevalence smoking abstinence compared with 27.6% and 31.9% in varenicline monotherapy (OR, 1.52; 95% CI, 1.04-2.22; P = .03 and OR, 1.32; 95% CI, 0.91-1.91; P = .14, respectively). At 52 weeks, 30.9% of the combination therapy group achieved prolonged and 36.6% achi [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Neither outcome was significantly different at 52 weeks.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 274, "doc_id": "11614737", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Ly6C hi monocytes have a lower inflammatory capacity than Ly6C lo monocytes.\n\nCANDIDATE_PASSAGE:\nA randomized, placebo-controlled trial of diindolylmethane for breast cancer biomarker modulation in patients taking tamoxifen Diindolylmethane (DIM), a bioactive metabolite of indole-3-carbinol found in cruciferous vegetables, has proposed cancer chemoprevention activity in the breast. There is limited evidence of clinically relevant activity of DIM or long-term safety data of its regular use. A randomized, double-blind, placebo-controlled trial was conducted to determine the activity and safety of combined use of BioResponse DIM® (BR-DIM) with tamoxifen. Women prescribed tamoxifen (n = 130) were randomly assigned oral BR-DIM at 150 mg twice daily or placebo, for 12 months. The primary study endpoint was change in urinary 2/16α-hydroxyestrone (2/16α-OHE1) ratio. Changes in 4-hydroxyestrone (4-OHE1), serum estrogens, sex hormone-binding globulin (SHBG), breast density, and tamoxifen metabolites were assessed. Ninety-eight women (51 placebo, 47 DIM) completed intervention; compliance with treatment was >91%. BR-DIM increased the 2/16α-OHE1 ratio (+3.2 [0.8, 8.4]) compared to placebo (−0.7 [−1.7, 0.8], P < 0.001). Serum SHBG increased with BR-DIM compared to placebo (+25 ± 22 and +1.1 ± 19 nmol/L, respectively). No change in breast density measured by mammography or by MRI was observed. Plasma tamoxifen metabolites (endoxifen, 4-OH tamoxifen, and N-desmethyl-tamoxifen) were reduced in women receiving BR-DIM versus placebo (P < 0.001). Minimal adverse events were reported and did not differ by treatment arm. In patients taking tamoxifen for breast cancer, daily BR-DIM promoted favorable changes in estrogen metabolism and circulating levels of SHBG. Further research is warranted to determine whether BR-DIM associated decreases in tamoxifen metabolites, including [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "728", "doc_id": "20454006", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Monoclonal antibody targeting of N-cadherin encourages metastasis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Monoclonal antibody targeting of N-cadherin inhibits prostate cancer growth, metastasis and castration resistance\nABSTRACT: The transition from androgen-dependent to castration-resistant prostate cancer (CRPC) is a lethal event of uncertain molecular etiology. Comparing gene expression in isogenic androgen-dependent and CRPC xenografts, we found a reproducible increase in N-cadherin expression, which was also elevated in primary and metastatic tumors of individuals with CRPC. Ectopic expression of N-cadherin in nonmetastatic, androgen-dependent prostate cancer models caused castration resistance, invasion and metastasis. Monoclonal antibodies against the ectodomain of N-cadherin reduced proliferation, adhesion and invasion of prostate cancer cells in vitro. In vivo, these antibodies slowed the growth of multiple established CRPC xenografts, blocked local invasion and metastasis and, at higher doses, led to complete regression. N-cadherin–specific antibodies markedly delayed the time to emergence of castration resistance, markedly affected tumor histology and angiogenesis, and reduced both AKT serine-threonine kinase activity and serum interleukin-8 (IL-8) secretion. These data indicate that N-cadherin is a major cause of both prostate cancer metastasis and castration resistance. Therapeutic targeting of this factor with monoclonal antibodies may have considerable clinical benefit.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In vivo, these antibodies slowed the growth of multiple established CRPC xenografts, blocked local invasion and metastasis and, at higher doses, led to complete regression.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 802, "doc_id": "22180793", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Bariatric surgery reduces postmenopausal breast cancer.\n\nCANDIDATE_PASSAGE:\nBariatric Surgery in the United Kingdom: A Cohort Study of Weight Loss and Clinical Outcomes in Routine Clinical Care. BACKGROUND Bariatric surgery is becoming a more widespread treatment for obesity. Comprehensive evidence of the long-term effects of contemporary surgery on a broad range of clinical outcomes in large populations treated in routine clinical practice is lacking. The objective of this study was to measure the association between bariatric surgery, weight, body mass index, and obesity-related co-morbidities. METHODS AND FINDINGS This was an observational retrospective cohort study using data from the United Kingdom Clinical Practice Research Datalink. All 3,882 patients registered in the database and with bariatric surgery on or before 31 December 2014 were included and matched by propensity score to 3,882 obese patients without surgery. The main outcome measures were change in weight and body mass index over 4 y; incident diagnoses of type 2 diabetes mellitus (T2DM), hypertension, angina, myocardial infarction (MI), stroke, fractures, obstructive sleep apnoea, and cancer; mortality; and resolution of hypertension and T2DM. Weight measures were available for 3,847 patients between 1 and 4 mo, 2,884 patients between 5 and 12 mo, and 2,258 patients between 13 and 48 mo post-procedure. Bariatric surgery patients exhibited rapid weight loss for the first four postoperative months, at a rate of 4.98 kg/mo (95% CI 4.88-5.08). Slower weight loss was sustained to the end of 4 y. Gastric bypass (6.56 kg/mo) and sleeve gastrectomy (6.29 kg/mo) were associated with greater initial weight reduction than gastric banding (2.77 kg/mo). Protective hazard ratios (HRs) were detected for bariatric surgery for incident T2DM, 0.68 (95% CI 0.55-0.83); hypertension, [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "169", "doc_id": "5824985", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The proportion of people with visual difficulty is two times higher in low-income countries than in high-income countries.\n\nCANDIDATE_PASSAGE:\nRenal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Angiotensin converting enzyme (ACE) inhibitors are now one of the most frequently used classes of antihypertensive drugs. Beyond their utility in the management of hypertension, their use has been extended to the long-term management of patients with congestive heart failure (CHF), as well as diabetic and nondiabetic nephropathies. Although ACE inhibitor therapy usually improves renal blood flow (RBF) and sodium excretion rates in CHF and reduces the rate of progressive renal injury in chronic renal disease, its use can also be associated with a syndrome of “functional renal insufficiency” and/or hyperkalemia. This form of acute renal failure (ARF) most commonly develops shortly after initiation of ACE inhibitor therapy but can be observed after months or years of therapy, even in the absence of prior ill effects. ARF is most likely to occur when renal perfusion pressure cannot be sustained because of substantial decreases in mean arterial pressure (MAP) or when glomerular filtration rate (GFR) is highly angiotensin II (Ang II) dependent. Conditions that predict an adverse hemodynamic effect of ACE inhibitors in patients with CHF are preexisting hypotension and low cardiac filling pressures. The GFR is especially dependent on Ang II during extracellular fluid (ECF) volume depletion, high-grade bilateral renal artery stenosis, or stenosis of a dominant or single kidney, as in a renal transplant recipient. Understanding the pathophysiological mechanisms and the common risk factors for ACE inhibitor–induced fun [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1257", "doc_id": "6157837", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does use of hydrophilic guidewires significantly improve technical success rates of peripheral PTA?\n\nABSTRACT:\nTo determine whether the use of hydrophilic guidewires has increased the technical success rate of peripheral percutaneous transluminal angioplasty (PTA).MATERIAL/ We performed 125 procedures and analyzed the technical success rates of PTA using the conventional guidewire first and then if needed, the hydrophilic guidewire for iliac and SFA stenoses or occlusions. Angioplasty was performed on 25 stenosed, 25 occluded iliac arteries and 25 stenosed, 50 occluded femoral arteries. The result was defined as technical success when the lesion was crossed by a guidewire and balloon, then it was dilated with restoration of vessel lumen and less than 30% residual stenosis and the rise in ABI values was at least 0.15 after 24 hours. The technical success rate after PTA of stenosed iliac arteries was achieved in 96% (24/25) using conventional wires and 100% using hydrophilic guidewire; in iliac occlusions, the rates were 60% (15/25) and 96%, respectively; in femoral stenosis - 84% (21/25) and 100%; in occlusions in the first group: lesions<10 cm -64% (16/25) and 96%, in the second group: lesions>10 cm -48% (12/25) and 88%. In the iliac group, there was no significant difference in the success of iliac stenosis PTA. However, there were significant changes in the success rates of PTA performed for SFA stenosis and iliac and SFA occlusions.", "output": "{\"label\": \"maybe\", \"rationale\": \"In summary, we report an overall improvement and high technical success rate for peripherial PTA. The use of hydrophilic guidewires made significant difference to the technical success rate of PTA, especially in occlusion and more complicated lesions.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 16538201, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Myelin sheaths play a role in action potential propagation.\n\nCANDIDATE_ABSTRACT:\nTITLE: High-mobility group box-1 protein induces osteogenic phenotype changes in aortic valve interstitial cells.\nABSTRACT: OBJECTIVES Calcific aortic valve (AV) disease is known to be an inflammation-related process. High-mobility group box-1 (HMGB1) protein and Toll-like receptor 4 (TLR4) have been reported to participate in several inflammatory diseases. The purpose of the present study was to determine whether the HMGB1-TLR4 axis is involved in calcific AV disease, and to evaluate the effect of HMGB1, and its potential mechanisms, on the pro-osteogenic phenotype change of valvular interstitial cells (VICs). METHODS Expression of HMGB1 and TLR4 in human calcific AVs was evaluated using immunohistochemical staining and immunoblotting. Cultured VICs were used as an in vitro model. The VICs were stimulated with HMGB1 for analysis, with versus without TLR4 small interfering ribonucleic acid (siRNA), c-Jun N-terminal kinase mitogen-activated protein kinase (JNK MAPK), and nuclear factor kappa-B (NF-κB) inhibitors. RESULTS Enhanced accumulation of HMGB1 and TLR4 was observed in calcific valves. Moreover, we found that HMGB1 induced high levels of pro-inflammatory cytokine production and promoted the osteoblastic differentiation and calcification of VICs. In addition, HMGB1 induced phosphorylation of JNK MAPK and NF-κB. However, these effects were markedly suppressed by siRNA silencing of TLR4. In addition, blockade of JNK MAPK and NF-κB phosphorylation prohibited HMGB1-induced production of pro-osteogenic factors, and mineralization of VICs. CONCLUSIONS The HMGB1 protein may promote osteoblastic differentiation and calcification of VICs, through the TLR4-JNK-NF-κB signaling pathway.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 818, "doc_id": "364522", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Birth-weight is negatively associated with breast cancer.\n\nCANDIDATE_PASSAGE:\nBody-mass index and risk of 22 specific cancers: a population-based cohort study of 5·24 million UK adults BACKGROUND High body-mass index (BMI) predisposes to several site-specific cancers, but a large-scale systematic and detailed characterisation of patterns of risk across all common cancers adjusted for potential confounders has not previously been undertaken. We aimed to investigate the links between BMI and the most common site-specific cancers. METHODS With primary care data from individuals in the Clinical Practice Research Datalink with BMI data, we fitted Cox models to investigate associations between BMI and 22 of the most common cancers, adjusting for potential confounders. We fitted linear then non-linear (spline) models; investigated effect modification by sex, menopausal status, smoking, and age; and calculated population effects. FINDINGS 5·24 million individuals were included; 166,955 developed cancers of interest. BMI was associated with 17 of 22 cancers, but effects varied substantially by site. Each 5 kg/m(2) increase in BMI was roughly linearly associated with cancers of the uterus (hazard ratio [HR] 1·62, 99% CI 1·56-1·69; p<0·0001), gallbladder (1·31, 1·12-1·52; p<0·0001), kidney (1·25, 1·17-1·33; p<0·0001), cervix (1·10, 1·03-1·17; p=0·00035), thyroid (1·09, 1·00-1·19; p=0·0088), and leukaemia (1·09, 1·05-1·13; p≤0·0001). BMI was positively associated with liver (1·19, 1·12-1·27), colon (1·10, 1·07-1·13), ovarian (1·09, 1.04-1.14), and postmenopausal breast cancers (1·05, 1·03-1·07) overall (all p<0·0001), but these effects varied by underlying BMI or individual-level characteristics. We estimated inverse associations with prostate and premenopausal breast cancer risk, both overall (prostate 0·98, 0·95-1·00; premenopausal breast cance [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "178", "doc_id": "4828631", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Are mitochondrial mutations a late event in the progression of head and neck squamous cell cancer?\n\nABSTRACT:\nTo determine the timing of mitochondrial mutations in the progression of head and neck squamous cell carcinoma. Twenty-three mitochondrial mutations were identified in 12 tumors using a high-throughput mitochondrial sequencing array. Areas of adjacent dysplastic and normal epithelium adjacent to tumors were sequenced using conventional methods for the presence of mutations that occurred in the corresponding tumor. Two of 23 (8.7%) tumor mitochondrial mutations (2 of 12 tumors) were present in both the areas of adjacent dysplasia and normal epithelium. Five of 23 (21.7%) tumor mitochondrial mutations (4 of 12 tumors) were present in areas of adjacent dysplasia. Eleven of 12 tumors contained nonsynonymous mutations that resulted in protein coding alterations. A significant difference (P < 0.01, chi(2)) was found in the incidence of mitochondrial mutation that occurred after development of cancer compared with adjacent areas dysplasia and normal epithelium.", "output": "{\"label\": \"yes\", \"rationale\": \"The majority of mitochondrial mutations occur during or after the transition of preneoplastic epithelium to cancer in head and neck squamous cell carcinoma, indicating that these are a late event in head and neck carcinogenesis.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 17671113, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: RUNX is not expressed in skin tissue.\n\nCANDIDATE_ABSTRACT:\nTITLE: Human epidermal stem cell function is regulated by circadian oscillations.\nABSTRACT: Human skin copes with harmful environmental factors that are circadian in nature, yet how circadian rhythms modulate the function of human epidermal stem cells is mostly unknown. Here we show that in human epidermal stem cells and their differentiated counterparts, core clock genes peak in a successive and phased manner, establishing distinct temporal intervals during the 24 hr day period. Each of these successive clock waves is associated with a peak in the expression of subsets of transcripts that temporally segregate the predisposition of epidermal stem cells to respond to cues that regulate their proliferation or differentiation, such as TGFβ and calcium. Accordingly, circadian arrhythmia profoundly affects stem cell function in culture and in vivo. We hypothesize that this intricate mechanism ensures homeostasis by providing epidermal stem cells with environmentally relevant temporal functional cues during the course of the day and that its perturbation may contribute to aging and carcinogenesis.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1008, "doc_id": "2547636", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Thigh-length graduated compression stockings (GCS) did not reduce deep vein thrombosis in patients admitted to hospital who are immobile because of acute stroke.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effectiveness of thigh-length graduated compression stockings to reduce the risk of deep vein thrombosis after stroke (CLOTS trial 1): a multicentre, randomised controlled trial\nABSTRACT: BACKGROUND Deep vein thrombosis (DVT) and pulmonary embolism are common after stroke. In small trials of patients undergoing surgery, graduated compression stockings (GCS) reduce the risk of DVT. National stroke guidelines extrapolating from these trials recommend their use in patients with stroke despite insufficient evidence. We assessed the effectiveness of thigh-length GCS to reduce DVT after stroke. METHODS In this outcome-blinded, randomised controlled trial, 2518 patients who were admitted to hospital within 1 week of an acute stroke and who were immobile were enrolled from 64 centres in the UK, Italy, and Australia. Patients were allocated via a central randomisation system to routine care plus thigh-length GCS (n=1256) or to routine care plus avoidance of GCS (n=1262). A technician who was blinded to treatment allocation undertook compression Doppler ultrasound of both legs at about 7-10 days and, when practical, again at 25-30 days after enrolment. The primary outcome was the occurrence of symptomatic or asymptomatic DVT in the popliteal or femoral veins. Analyses were by intention to treat. This study is registered, number ISRCTN28163533. FINDINGS All patients were included in the analyses. The primary outcome occurred in 126 (10.0%) patients allocated to thigh-length GCS and in 133 (10.5%) allocated to avoid GCS, resulting in a non-significant absolute reduction in risk of 0.5% (95% CI -1.9% to 2.9%). Skin breaks, ulcers, blisters, and skin necrosis were significantly more common in patients allocated to GCS than in those allocated to avoid their use (64 [5%] vs 16 [1%]; odds ratio 4.18, 95% CI 2.40-7.27). INTERPRETATION These data do not lend support to the use of thigh-length GCS in patients admitted to hospital with acute stroke. National guid [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"INTERPRETATION These data do not lend support to the use of thigh-length GCS in patients admitted to hospital with acute stroke.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1298, "doc_id": "11718220", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: A total of 1,000 people in the UK are asymptomatic carriers of vCJD infection.\n\nCANDIDATE_PASSAGE:\nHigh-throughput sequencing reveals extensive variation in human-specific L1 content in individual human genomes. Using high-throughput sequencing, we devised a technique to determine the insertion sites of virtually all members of the human-specific L1 retrotransposon family in any human genome. Using diagnostic nucleotides, we were able to locate the approximately 800 L1Hs copies corresponding specifically to the pre-Ta, Ta-0, and Ta-1 L1Hs subfamilies, with over 90% of sequenced reads corresponding to human-specific elements. We find that any two individual genomes differ at an average of 285 sites with respect to L1 insertion presence or absence. In total, we assayed 25 individuals, 15 of which are unrelated, at 1139 sites, including 772 shared with the reference genome and 367 nonreference L1 insertions. We show that L1Hs profiles recapitulate genetic ancestry, and determine the chromosomal distribution of these elements. Using these data, we estimate that the rate of L1 retrotransposition in humans is between 1/95 and 1/270 births, and the number of dimorphic L1 elements in the human population with gene frequencies greater than 0.05 is between 3000 and 10,000.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "48", "doc_id": "10944947", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Cytochrome c is transferred from cytosol to the mitochondrial intermembrane space during apoptosis.\n\nCANDIDATE_PASSAGE:\nPrimPol, an Archaic Primase/Polymerase Operating in Human Cells We describe a second primase in human cells, PrimPol, which has the ability to start DNA chains with deoxynucleotides unlike regular primases, which use exclusively ribonucleotides. Moreover, PrimPol is also a DNA polymerase tailored to bypass the most common oxidative lesions in DNA, such as abasic sites and 8-oxoguanine. Subcellular fractionation and immunodetection studies indicated that PrimPol is present in both nuclear and mitochondrial DNA compartments. PrimPol activity is detectable in mitochondrial lysates from human and mouse cells but is absent from mitochondria derived from PRIMPOL knockout mice. PRIMPOL gene silencing or ablation in human and mouse cells impaired mitochondrial DNA replication. On the basis of the synergy observed with replicative DNA polymerases Polγ and Polε, PrimPol is proposed to facilitate replication fork progression by acting as a translesion DNA polymerase or as a specific DNA primase reinitiating downstream of lesions that block synthesis during both mitochondrial and nuclear DNA replication.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "299", "doc_id": "17368516", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does rugby headgear prevent concussion?\n\nABSTRACT:\nTo examine the attitudes of players and coaches to the use of protective headgear, particularly with respect to the prevention of concussion. A questionnaire designed to assess attitudes to headgear was administered to 63 players from four different Canadian teams, each representing a different level of play (high school, university, community club, national). In addition, coaches from all four levels were questioned about team policies and their personal opinions about the use of headgear to prevent concussion. Although the players tended to believe that the headgear could prevent concussion (62%), the coaches were less convinced (33%). Despite the players' belief that headgear offers protection against concussion, only a minority reported wearing headgear (27%) and few (24%) felt that its use should be made mandatory. Common reasons for not wearing headgear were \"its use is not mandatory\", \"it is uncomfortable\", and \"it costs too much\".", "output": "{\"label\": \"maybe\", \"rationale\": \"Although most players in the study believe that rugby headgear may prevent concussion, only a minority reported wearing it. Coaches tended to be less convinced than the players that rugby headgear can prevent concussion.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 11867487, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_ABSTRACT:\nTITLE: Efficacy of human papillomavirus testing for the detection of invasive cervical cancers and cervical intraepithelial neoplasia: a randomised controlled trial.\nABSTRACT: BACKGROUND Human papillomavirus (HPV) testing is known to be more sensitive, but less specific than cytology for detecting cervical intraepithelial neoplasia (CIN). We assessed the efficacy of cervical-cancer screening policies that are based on HPV testing. METHODS Between March, 2004, and December, 2004, in two separate recruitment phases, women aged 25-60 years were randomly assigned to conventional cytology or to HPV testing in combination with liquid-based cytology (first phase) or alone (second phase). Randomisation was done by computer in two screening centres and by sequential opening of numbered sealed envelopes in the remaining seven centres. During phase one, women who were HPV-positive and aged 35-60 years were referred to colposcopy, whereas women aged 25-34 years were referred to colposcopy only if cytology was also abnormal or HPV testing was persistently positive. During phase two, women in the HPV group were referred for colposcopy if the HPV test was positive. Two rounds of screening occurred in each phase, and all women had cytology testing only at the second round. The primary endpoint was the detection of grade 2 and 3 CIN, and of invasive cervical cancers during the first and second screening rounds. Analysis was done by intention to screen. This trial is registered, number ISRCTN81678807. FINDINGS In total for both phases, 47,001 women were randomly assigned to the cytology group and 47,369 to HPV testing. 33,851 women from the cytology group and 32,998 from the HPV-testing group had a second round of screening. We also retrieved the histological diagnoses from screening done elsewhere. The detection of invasive cervical cancers was similar for the two groups in the first round of screening (nine in the cytology group vs seven in the H [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Among women aged 35-60 years, at round one the relative detection (HPV vs cytology) was 2.00 (95% CI 1.44-2.77) for CIN2, 2.08 (1.47-2.95) for CIN3, and 2.03 (1.60-2.57) for CIN2 and 3 together.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 972, "doc_id": "27873158", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Vitamin D deficiency is unrelated to birth weight.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association between maternal serum 25-hydroxyvitamin D level and pregnancy and neonatal outcomes: systematic review and meta-analysis of observational studies.\nABSTRACT: OBJECTIVE To assess the effect of 25-hydroxyvitamin D (25-OHD) levels on pregnancy outcomes and birth variables. DESIGN Systematic review and meta-analysis. DATA SOURCES Medline (1966 to August 2012), PubMed (2008 to August 2012), Embase (1980 to August 2012), CINAHL (1981 to August 2012), the Cochrane database of systematic reviews, and the Cochrane database of registered clinical trials. STUDY SELECTION Studies reporting on the association between serum 25-OHD levels during pregnancy and the outcomes of interest (pre-eclampsia, gestational diabetes, bacterial vaginosis, caesarean section, small for gestational age infants, birth weight, birth length, and head circumference). DATA EXTRACTION Two authors independently extracted data from original research articles, including key indicators of study quality. We pooled the most adjusted odds ratios and weighted mean differences. Associations were tested in subgroups representing different patient characteristics and study quality. RESULTS 3357 studies were identified and reviewed for eligibility. 31 eligible studies were included in the final analysis. Insufficient serum levels of 25-OHD were associated with gestational diabetes (pooled odds ratio 1.49, 95% confidence interval 1.18 to 1.89), pre-eclampsia (1.79, 1.25 to 2.58), and small for gestational age infants (1.85, 1.52 to 2.26). Pregnant women with low serum 25-OHD levels had an increased risk of bacterial vaginosis and low birthweight infants but not delivery by caesarean section. CONCLUSION Vitamin D insufficiency is associated with an increased risk of gestational diabetes, pre-eclampsia, and small for gestational age infants. Pregnant women with low 25-OHD levels had an increased risk of bacterial vaginosis and lower birth weight infants, but not de [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Pregnant women with low 25-OHD levels had an increased risk of bacterial vaginosis and lower birth weight infants, but not delivery by caesarean section.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1370, "doc_id": "2425364", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Anthrax spores are very difficult to dispose once they are dispersed.\n\nCANDIDATE_PASSAGE:\nNanog safeguards pluripotency and mediates germline development Nanog is a divergent homeodomain protein found in mammalian pluripotent cells and developing germ cells. Deletion of Nanog causes early embryonic lethality, whereas constitutive expression enables autonomous self-renewal of embryonic stem cells. Nanog is accordingly considered a core element of the pluripotent transcriptional network. However, here we report that Nanog fluctuates in mouse embryonic stem cells. Transient downregulation of Nanog appears to predispose cells towards differentiation but does not mark commitment. By genetic deletion we show that, although they are prone to differentiate, embryonic stem cells can self-renew indefinitely in the permanent absence of Nanog. Expanded Nanog null cells colonize embryonic germ layers and exhibit multilineage differentiation both in fetal and adult chimaeras. Although they are also recruited to the germ line, primordial germ cells lacking Nanog fail to mature on reaching the genital ridge. This defect is rescued by repair of the mutant allele. Thus Nanog is dispensible for expression of somatic pluripotency but is specifically required for formation of germ cells. Nanog therefore acts primarily in construction of inner cell mass and germ cell states rather than in the housekeeping machinery of pluripotency. We surmise that Nanog stabilizes embryonic stem cells in culture by resisting or reversing alternative gene expression states.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "114", "doc_id": "4423327", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: NAC inhibits the generation of angiotensin-converting enzyme.\n\nCANDIDATE_PASSAGE:\nAcetylcysteine for prevention of acute deterioration of renal function following elective coronary angiography and intervention: a randomized controlled trial. CONTEXT The antioxidant acetylcysteine prevents acute contrast nephrotoxicity in patients with impaired renal function who undergo computed tomography scanning. However, its role in coronary angiography is unclear. OBJECTIVE To determine whether oral acetylcysteine prevents acute deterioration in renal function in patients with moderate renal insufficiency who undergo elective coronary angiography. DESIGN AND SETTING Prospective, randomized, double-blind, placebo-controlled trial conducted from May 2000 to December 2001 at the Grantham Hospital at the University of Hong Kong. PARTICIPANTS Two hundred Chinese patients aged mean (SD) 68 (6.5) years with stable moderate renal insufficiency (creatinine clearance <60 mL/min [1.00 mL/s]) who were undergoing elective coronary angiography with or without intervention. INTERVENTION Participants were randomly assigned to receive oral acetylcysteine(600 mg twice per day; n = 102) or matching placebo tablets (n = 98) on the day before and the day of angiography. All patients received low-osmolality contrast agent. MAIN OUTCOME MEASURES Occurrence of more than a 25% increase in serum creatinine level within 48 hours after contrast administration; change in creatinine clearance and serum creatinine level. RESULTS Twelve control patients (12%) and 4 acetylcysteine patients (4%) developed a more than 25% increase in serum creatinine level within 48 hours after contrast administration (relative risk, 0.32; 95% confidence interval [CI], 0.10-0.96; P =.03). Serum creatinine was lower in the acetylcysteine group (1.22 mg/dL [107.8 micromol/L]; 95% CI, 1.11-1.33 mg/dL vs [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "828", "doc_id": "4678846", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is aortic vasoconstriction related to smooth muscle cells ET-A and ET-B receptors involved in hypoxia-induced sustained systemic arterial hypertension in rats?\n\nABSTRACT:\nWe report in the present study the role of endothelin (ET-1) and ET-1 receptors in the sustained hypoxia-induced systemic hypertension. Wistar rats were randomly assigned to live continuously in hypobaric hypoxia (CH rats) or normoxia (N rats). At the end of hypoxic stress exposure (5 weeks at 450 mm Hg), measurements of mean systemic arterial pressure were done. The effects of ET-1 in the presence or not of the endothelium and/or of specific ET-A inhibitors (BQ-123) or ET-B inhibitors (BQ-788), have been investigated in an isolated model of rat thoracic aorta. Finally, plasmatic ET-1 concentrations have been determined by assay procedure. Following five weeks of chronic hypoxic stress, CH rats presented a significant increase of mean systemic arterial pressure (N: 129.1+/-6.8 mm Hg vs CH: 152.5+/-3.4 mm Hg; P<0.05). Despite of this hypoxia-induced hypertension, ET-1 plasmatic concentration was not different between N and CH rats. Finally, CH rats presented a reduce response to ET-1 when compared to N rats. This phenomenon seems to be associated to the ET-A vascular smooth muscle cell receptors, since difference between N and CH rats was still present in endothelium denuded aortic rings in the presence or not of the specific ET-B inhibitors (BQ-788). In addition, in the presence of the specific ET-A inhibitor (BQ-123) response to ET-1 was abolished in N and CH rats to the same extent (N:-98%; CH:-99%).", "output": "{\"label\": \"no\", \"rationale\": \"This work clearly suggests that, following long term exposure to hypoxia, ET-1 and ET-1 receptors are not involved in the persistence of systemic hypertension in a rat model, and that chronic exposure to severe hypoxic stress was associated with a downregulation of the ET-A receptors response to ET-1.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 17669692, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Normal granulomas form in the presence of TNF in Zebrafish.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tumor necrosis factor signaling mediates resistance to mycobacteria by inhibiting bacterial growth and macrophage death.\nABSTRACT: Tumor necrosis factor (TNF), a key effector in controlling tuberculosis, is thought to exert protection by directing formation of granulomas, organized aggregates of macrophages and other immune cells. Loss of TNF signaling causes progression of tuberculosis in humans, and the increased mortality of Mycobacterium tuberculosis-infected mice is associated with disorganized necrotic granulomas, although the precise roles of TNF signaling preceding this endpoint remain undefined. We monitored transparent Mycobacterium marinum-infected zebrafish live to conduct a stepwise dissection of how TNF signaling operates in mycobacterial pathogenesis. We found that loss of TNF signaling caused increased mortality even when only innate immunity was operant. In the absence of TNF, intracellular bacterial growth and granuloma formation were accelerated and was followed by necrotic death of overladen macrophages and granuloma breakdown. Thus, TNF is not required for tuberculous granuloma formation, but maintains granuloma integrity indirectly by restricting mycobacterial growth within macrophages and preventing their necrosis.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In the absence of TNF, intracellular bacterial growth and granuloma formation were accelerated and was followed by necrotic death of overladen macrophages and granuloma breakdown.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 861, "doc_id": "16066726", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Cells undergoing methionine restriction may activate miRNAs.\n\nCANDIDATE_PASSAGE:\nInterferons: Success in anti-viral immunotherapy. The interferons (IFNs) are glycoproteins with strong antiviral activities that represent one of the first lines of host defense against invading pathogens. These proteins are classified into three groups, Type I, II and III IFNs, based on the structure of their receptors on the cell surface. Due to their ability to modulate immune responses, they have become attractive therapeutic options to control chronic virus infections. In combination with other drugs, Type I IFNs are considered as \"standard of care\" in suppressing Hepatitis C (HCV) and Hepatitis B (HBV) infections, while Type III IFN has generated encouraging results as a treatment for HCV infection in phase III clinical trials. However, though effective, using IFNs as a treatment is not without the need for caution. IFNs are such powerful cytokines that affect a wide array of cell types; as a result, patients usually experience unpleasant symptoms, with a percentage of patients suffering system wide effects. Thus, constant monitoring is required for patients treated with IFN in order to reach the treatment goals of suppressing virus infection and maintaining quality of life.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "238", "doc_id": "3308636", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: L3MBTL2 binds to H2AK119Ub marked chromatin to form a PRC1 complex.\n\nCANDIDATE_PASSAGE:\nMicroRNA-21 is Induced by Rapamycin in a Model of Tuberous Sclerosis (TSC) and Lymphangioleiomyomatosis (LAM) Lymphangioleiomyomatosis (LAM), a multisystem disease of women, is manifest by the proliferation of smooth muscle-like cells in the lung resulting in cystic lung destruction. Women with LAM can also develop renal angiomyolipomas. LAM is caused by mutations in the tuberous sclerosis complex genes (TSC1 or TSC2), resulting in hyperactive mammalian Target of Rapamycin (mTOR) signaling. The mTOR inhibitor, Rapamycin, stabilizes lung function in LAM and decreases the volume of renal angiomyolipomas, but lung function declines and angiomyolipomas regrow when treatment is discontinued, suggesting that factors induced by mTORC1 inhibition may promote the survival of TSC2-deficient cells. Whether microRNA (miRNA, miR) signaling is involved in the response of LAM to mTORC1 inhibition is unknown. We identified Rapamycin-dependent miRNA in LAM patient angiomyolipoma-derived cells using two separate screens. First, we assayed 132 miRNA of known significance to tumor biology. Using a cut-off of >1.5-fold change, 48 microRNA were Rapamycin-induced, while 4 miRs were downregulated. In a second screen encompassing 946 miRNA, 18 miRs were upregulated by Rapamycin, while eight were downregulated. Dysregulation of miRs 29b, 21, 24, 221, 106a and 199a were common to both platforms and were classified as candidate \"RapamiRs. \" Validation by qRT-PCR confirmed that these microRNA were increased. miR-21, a pro-survival miR, was the most significantly increased by mTOR-inhibition (p<0.01). The regulation of miR-21 by Rapamycin is cell type independent. mTOR inhibition promotes the processing of the miR-21 transcript (pri-miR-21) to a premature form (pre-miR-21). In conclusion [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "672", "doc_id": "2266471", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Decrease of p62 in prostate tumor stroma results in defective autophagy.\n\nCANDIDATE_PASSAGE:\np62/SQSTM1 by Binding to Vitamin D Receptor Inhibits Hepatic Stellate Cell Activity, Fibrosis, and Liver Cancer. Hepatic stellate cells (HSCs) play critical roles in liver fibrosis and hepatocellular carcinoma (HCC). Vitamin D receptor (VDR) activation in HSCs inhibits liver inflammation and fibrosis. We found that p62/SQSTM1, a protein upregulated in liver parenchymal cells but downregulated in HCC-associated HSCs, negatively controls HSC activation. Total body or HSC-specific p62 ablation potentiates HSCs and enhances inflammation, fibrosis, and HCC progression. p62 directly interacts with VDR and RXR promoting their heterodimerization, which is critical for VDR:RXR target gene recruitment. Loss of p62 in HSCs impairs the repression of fibrosis and inflammation by VDR agonists. This demonstrates that p62 is a negative regulator of liver inflammation and fibrosis through its ability to promote VDR signaling in HSCs, whose activation supports HCC.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "315", "doc_id": "3701541", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does dJ-1 modulate the expression of Cu/Zn-superoxide dismutase-1 through the Erk1/2-Elk1 pathway in neuroprotection?\n\nABSTRACT:\nLoss of function mutations of Park7/DJ-1 gene increase the susceptibility of dopaminergic cells to reactive oxygen species and cause early onset familial Parkinson disease (PD). However, the mechanisms underlying dopaminergic neuron loss related to DJ-1 mutation remain undefined. Therefore, it is important to find the new mechanisms underlying the antioxidative functions of DJ-1. DJ-1 knockdown cells and DJ-1 knockout mice were used to elucidate the mechanisms underlying the antioxidative stress of DJ-1. Preliminary study of the saliva from PD patients and controls was used to confirm our findings obtained from the above studies. Our experiments showed that DJ-1 interacted with Erk1/2 and was required for the nuclear translocation of Erk1/2 upon oxidative stimulation. The translocation of Erk1/2 activated Elk1 and sequentially promoted superoxide dismutase1 (SOD1) expression. The nuclear translocation of Erk1/2, the activation of Elk1, and the ensuing upregulation of SOD1 were all suppressed in DJ-1 knockdown cells and DJ-1 null mice treated with oxidative insult. Furthermore, reintroduction of SOD1 into DJ-1 knockdown cells protected them against oxidative stress. Finally, in the preliminary study, we found close correlation between the protein levels of DJ-1 and SOD1 in the saliva samples from different stages of PD patients.", "output": "{\"label\": \"yes\", \"rationale\": \"Our studies suggest that DJ-1 regulates SOD1 expression through Erk1/2-Elk1 pathway in its protective response to oxidative insult.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 21796667, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Ly6C hi monocytes have a higher inflammatory capacity than Ly6C lo monocytes.\n\nCANDIDATE_PASSAGE:\nPrevalence of Multiple Sclerosis in Isfahan, Iran Background: The prevalence of multiple sclerosis (MS) shows considerable variability all over the world. According to Kurtzke, Iran is considered to have a low prevalence. Objective: To estimate the period prevalence and risk factors of MS in Isfahan, central part of Iran. Methods: A cross-sectional case register study conducted between 2004 and 2005. In the province of Isfahan, Iran, all patients known to have definite MS during 2004 and 2005, being alive and resident within Isfahan as well as being a member of the Isfahan MS Association were included in the study. Demographic and case-related information was recorded. 1,391 definite MS patients (308 men and 1,083 women) from the Isfahan MS Association, Iran, have been identified. The disease was confirmed using clinical information and MRI findings by a neurologist and radiologist. The patients were evaluated by interview and a questionnaire. Population data were obtained from the year 1999 Iran Census. The mean (SD) age of the participants was 32.5 (9.3) years with a mean (SD) duration of the disease of 6.4 (5.1) years for men and 6.9 (5.3) years for women. Results: The period prevalence of MS was 35.5 per 100,000 [95% confidence interval (CI) 33.6–37.3] in a population of 3,923,255, with a higher rate in women than men [54.5 (95% CI: 51.1–57.8) for women and 14.9 (95% CI: 13.3–16.6) for men]. The female/male ratio was 3.6 (95% CI: 3.2–4.1). The direct age-adjusted period prevalence was 59.5 per 100,000 (95% CI: 44.8–75.2) for women and 17.0 per 100,000 (95% CI: 8.9–25.1) for men. MS rates were highest among 30- to 39-year-olds and decreased with increasing age. Sensory and visual disturbances were the most common initial presentations with a prevalence of [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "726", "doc_id": "24557631", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The innate immune response struggles to remove small numbers of parasites.\n\nCANDIDATE_ABSTRACT:\nTITLE: Partitioning regulatory mechanisms of within-host malaria dynamics using the effective propagation number.\nABSTRACT: Immune clearance and resource limitation (via red blood cell depletion) shape the peaks and troughs of malaria parasitemia, which in turn affect disease severity and transmission. Quantitatively partitioning the relative roles of these effects through time is challenging. Using data from rodent malaria, we estimated the effective propagation number, which reflects the relative importance of contrasting within-host control mechanisms through time and is sensitive to the inoculating parasite dose. Our analysis showed that the capacity of innate responses to restrict initial parasite growth saturates with parasite dose and that experimentally enhanced innate immunity can affect parasite density indirectly via resource depletion. Such a statistical approach offers a tool to improve targeting of drugs or vaccines for human therapy by revealing the dynamics and interactions of within-host regulatory mechanisms.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Our analysis showed that the capacity of innate responses to restrict initial parasite growth saturates with parasite dose and that experimentally enhanced innate immunity can affect parasite density indirectly via resource depletion.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1223, "doc_id": "5289038", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Antidepressants increase the severity of migraines.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tricyclic antidepressants and headaches: systematic review and meta-analysis\nABSTRACT: OBJECTIVE To evaluate the efficacy and relative adverse effects of tricyclic antidepressants in the treatment of migraine, tension-type, and mixed headaches. DESIGN Meta-analysis. DATA SOURCES Medline, Embase, the Cochrane Trials Registry, and PsycLIT. Studies reviewed Randomised trials of adults receiving tricyclics as only treatment for a minimum of four weeks. DATA EXTRACTION Frequency of headaches (number of headache attacks for migraine and number of days with headache for tension-type headaches), intensity of headache, and headache index. RESULTS 37 studies met the inclusion criteria. Tricyclics significantly reduced the number of days with tension-type headache and number of headache attacks from migraine than placebo (average standardised mean difference -1.29, 95% confidence interval -2.18 to -0.39 and -0.70, -0.93 to -0.48) but not compared with selective serotonin reuptake inhibitors (-0.80, -2.63 to 0.02 and -0.20, -0.60 to 0.19). The effect of tricyclics increased with longer duration of treatment (β=-0.11, 95% confidence interval -0.63 to -0.15; P<0.0005). Tricyclics were also more likely to reduce the intensity of headaches by at least 50% than either placebo (tension-type: relative risk 1.41, 95% confidence interval 1.02 to 1.89; migraine: 1.80, 1.24 to 2.62) or selective serotonin reuptake inhibitors (1.73, 1.34 to 2.22 and 1.72, 1.15 to 2.55). Tricyclics were more likely to cause adverse effects than placebo (1.53, 95% confidence interval 1.11 to 2.12) and selective serotonin reuptake inhibitors (2.22, 1.52 to 3.32), including dry mouth (P<0.0005 for both), drowsiness (P<0.0005 for both), and weight gain (P<0.001 for both), but did not increase dropout rates (placebo: 1.22, 0.83 to 1.80, selective serotonin reuptake inhibitors: 1.16, 0.81 t [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Tricyclics were also more likely to reduce the intensity of headaches by at least 50% than either placebo (tension-type: relative risk 1.41, 95% confidence interval 1.02 to 1.89; migraine: 1.80, 1.24 to 2.62) or selective serotonin reuptake inhibitors (1.73, 1.34 to 2.22 and 1.72, 1.15 to 2.55).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 119, "doc_id": "14606752", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: ALDH1 expression is associated with better breast cancer outcomes.\n\nCANDIDATE_PASSAGE:\nALDH1 is a marker of normal and malignant human mammary stem cells and a predictor of poor clinical outcome. Application of stem cell biology to breast cancer research has been limited by the lack of simple methods for identification and isolation of normal and malignant stem cells. Utilizing in vitro and in vivo experimental systems, we show that normal and cancer human mammary epithelial cells with increased aldehyde dehydrogenase activity (ALDH) have stem/progenitor properties. These cells contain the subpopulation of normal breast epithelium with the broadest lineage differentiation potential and greatest growth capacity in a xenotransplant model. In breast carcinomas, high ALDH activity identifies the tumorigenic cell fraction, capable of self-renewal and of generating tumors that recapitulate the heterogeneity of the parental tumor. In a series of 577 breast carcinomas, expression of ALDH1 detected by immunostaining correlated with poor prognosis. These findings offer an important new tool for the study of normal and malignant breast stem cells and facilitate the clinical application of stem cell concepts.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "51", "doc_id": "45638119", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Long chain polyunsaturated fatty acids supplementation is associated with lower rates of atopic eczema at 1 year.\n\nCANDIDATE_PASSAGE:\nLong-term effects of continuing adjuvant tamoxifen to 10 years versus stopping at 5 years after diagnosis of oestrogen receptor-positive breast cancer: ATLAS, a randomised trial BACKGROUND For women with oestrogen receptor (ER)-positive early breast cancer, treatment with tamoxifen for 5 years substantially reduces the breast cancer mortality rate throughout the first 15 years after diagnosis. We aimed to assess the further effects of continuing tamoxifen to 10 years instead of stopping at 5 years. METHODS In the worldwide Adjuvant Tamoxifen: Longer Against Shorter (ATLAS) trial, 12,894 women with early breast cancer who had completed 5 years of treatment with tamoxifen were randomly allocated to continue tamoxifen to 10 years or stop at 5 years (open control). Allocation (1:1) was by central computer, using minimisation. After entry (between 1996 and 2005), yearly follow-up forms recorded any recurrence, second cancer, hospital admission, or death. We report effects on breast cancer outcomes among the 6846 women with ER-positive disease, and side-effects among all women (with positive, negative, or unknown ER status). Long-term follow-up still continues. This study is registered, number ISRCTN19652633. FINDINGS Among women with ER-positive disease, allocation to continue tamoxifen reduced the risk of breast cancer recurrence (617 recurrences in 3428 women allocated to continue vs 711 in 3418 controls, p=0·002), reduced breast cancer mortality (331 deaths vs 397 deaths, p=0·01), and reduced overall mortality (639 deaths vs 722 deaths, p=0·01). The reductions in adverse breast cancer outcomes appeared to be less extreme before than after year 10 (recurrence rate ratio [RR] 0·90 [95% CI 0·79–1·02] during years 5–9 and 0·75 [0·62–0·90] in later years; breast ca [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "709", "doc_id": "12438901", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: TMEM27 is a marker for beta cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tmem27: a cleaved and shed plasma membrane protein that stimulates pancreatic beta cell proliferation.\nABSTRACT: The signals and molecular mechanisms that regulate the replication of terminally differentiated beta cells are unknown. Here, we report the identification and characterization of transmembrane protein 27 (Tmem27, collectrin) in pancreatic beta cells. Expression of Tmem27 is reduced in Tcf1(-/-) mice and is increased in islets of mouse models with hypertrophy of the endocrine pancreas. Tmem27 forms dimers and its extracellular domain is glycosylated, cleaved and shed from the plasma membrane of beta cells. This cleavage process is beta cell specific and does not occur in other cell types. Overexpression of full-length Tmem27, but not the truncated or soluble protein, leads to increased thymidine incorporation, whereas silencing of Tmem27 using RNAi results in a reduction of cell replication. Furthermore, transgenic mice with increased expression of Tmem27 in pancreatic beta cells exhibit increased beta cell mass. Our results identify a pancreatic beta cell transmembrane protein that regulates cell growth of pancreatic islets.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"This cleavage process is beta cell specific and does not occur in other cell types.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1133, "doc_id": "24142891", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: A diminished ovarian reserve is a very strong indicator of infertility, even in an a priori non-infertile population.\n\nCANDIDATE_PASSAGE:\nThe VTI family of SNARE proteins is necessary for plant viability and mediates different protein transport pathways. The Arabidopsis genome contains a family of v-SNAREs: VTI11, VTI12, and VTI13. Only VTI11 and VTI12 are expressed at appreciable levels. Although these two proteins are 60% identical, they complement different transport pathways when expressed in the yeast vti1 mutant. VTI11 was identified recently as the mutated gene in the shoot gravitropic mutant zig. Here, we show that the vti11 zig mutant has defects in vascular patterning and auxin transport. An Arabidopsis T-DNA insertion mutant, vti12, had a normal phenotype under nutrient-rich growth conditions. However, under nutrient-poor conditions, vti12 showed an accelerated senescence phenotype, suggesting that VTI12 may play a role in the plant autophagy pathway. VTI11 and VTI12 also were able to substitute for each other in their respective SNARE complexes, and a double-mutant cross between zig and vti12 was embryo lethal. These results suggest that some VTI1 protein was necessary for plant viability and that the two proteins were partially functionally redundant.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "40", "doc_id": "1669173", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Suboptimal nutrition is not predictive of chronic disease\n\nCANDIDATE_ABSTRACT:\nTITLE: Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015\nABSTRACT: BACKGROUND The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. METHODS We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors-the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. We characterised risk exposure in relation to a Socio-demographic Index (SDI). FINDINGS Between 1990 and 2015, global exposure to unsafe sanitation, household air pollution, childhood underweight, childhood stunting, and smoking [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In 2015, the ten largest contributors to global DALYs among Level 3 risks were high systolic blood pressure (211·8 million [192·7 million to 231·1 million] global DALYs), smoking (148·6 million [134·2 million to 163·1 million]), high fasting plasma glucose (143·1 million [125·1 million to 163·5 million]), high BMI (120·1 million [83·8 million to 158·4 million]), childhood undernutrition (113·3 million [103·9 million to 123·4 million]), ambient particulate matter (103·1 million [90·8 million to 115·1 million]), high total cholesterol (88·7 million [74·6 million to 105·7 million]), household air pollution (85·6 million [66·7 million to 106·1 million]), alcohol use (85·0 million [77·2 million to 93·0 million]), and diets high in sodium (83·0 million [49·3 million to 127·5 million]).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1110, "doc_id": "13770184", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Normal expression of RUNX1 causes tumorsupressing effects.\n\nCANDIDATE_PASSAGE:\nCOPD: epidemiology, prevalence, morbidity and mortality, and disease heterogeneity. COPD continues to cause a heavy health and economic burden both in the United States and around the world. Some of the risk factors for COPD are well-known and include smoking, occupational exposures, air pollution, airway hyperresponsiveness, asthma, and certain genetic variations, although many questions, such as why < 20% of smokers develop significant airway obstruction, remain. Precise definitions of COPD vary and are frequently dependent on an accurate diagnosis of the problem by a physician. These differences in the definition of COPD can have large effects on the estimates of COPD in the population. Furthermore, evidence that COPD represents several different disease processes with potentially different interventions continues to emerge. In most of the world, COPD prevalence and mortality are still increasing and likely will continue to rise in response to increases in smoking, particularly by women and adolescents. Resources aimed at smoking cessation and prevention, COPD education and early detection, and better treatment will be of the most benefit in our continuing efforts against this important cause of morbidity and mortality.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "858", "doc_id": "7285256", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Female carriers of the Apolipoprotein E4 (APOE4) allele have shorter lifetime exposure to estrogen due to a decreased reproductive period.\n\nCANDIDATE_PASSAGE:\nReproductive period and risk of dementia in postmenopausal women. CONTEXT Exogenous estrogen use may lower risk of dementia in postmenopausal women. A relationship between long-term exposure to endogenous estrogens and incident dementia has been hypothesized but not studied. OBJECTIVE To determine whether a longer reproductive period, as an indicator of longer exposure to endogenous estrogens, is associated with lower risk of dementia and Alzheimer disease (AD) in women who have natural menopause. DESIGN AND SETTING The Rotterdam Study, a population-based prospective cohort study conducted in the Netherlands. PARTICIPANTS A total of 3601 women aged 55 years or older who did not have dementia at baseline (1990-1993) and had information on age at menarche, age at menopause, and type of menopause. Participants were reexamined in 1993-1994 and 1997-1999 and were continuously monitored for development of dementia. MAIN OUTCOME MEASURES Incidence of dementia, based on Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition criteria, and AD, based on National Institute of Neurological Disorders and Stroke/Alzheimer's Disease and Related Disorders Association criteria, compared by quartiles of reproductive period among women with natural menopause. RESULTS During 21 046 person-years of follow-up (median follow-up, 6.3 years), 199 women developed dementia, including 159 who developed AD. After adjusting for age, dementia was not clearly associated with length of reproductive period. However, after adjusting for multiple covariates, women with natural menopause and more reproductive years had an increased risk of dementia (adjusted rate ratio [RR] for women with >39 reproductive years [highest quartile] compared with <34 reproductive years [lowest [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "417", "doc_id": "6309659", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Type 1 Diabetes is associated with subtle perturbations in T reg development.\n\nCANDIDATE_ABSTRACT:\nTITLE: Type 1 diabetes-associated IL2RA variation lowers IL-2 signaling and contributes to diminished CD4+CD25+ regulatory T cell function.\nABSTRACT: Numerous reports have demonstrated that CD4(+)CD25(+) regulatory T cells (Tregs) from individuals with a range of human autoimmune diseases, including type 1 diabetes, are deficient in their ability to control autologous proinflammatory responses when compared with nondiseased, control individuals. Treg dysfunction could be a primary, causal event or may result from perturbations in the immune system during disease development. Polymorphisms in genes associated with Treg function, such as IL2RA, confer a higher risk of autoimmune disease. Although this suggests a primary role for defective Tregs in autoimmunity, a link between IL2RA gene polymorphisms and Treg function has not been examined. We addressed this by examining the impact of an IL2RA haplotype associated with type 1 diabetes on Treg fitness and suppressive function. Studies were conducted using healthy human subjects to avoid any confounding effects of disease. We demonstrated that the presence of an autoimmune disease-associated IL2RA haplotype correlates with diminished IL-2 responsiveness in Ag-experienced CD4(+) T cells, as measured by phosphorylation of STAT5a, and is associated with lower levels of FOXP3 expression by Tregs and a reduction in their ability to suppress proliferation of autologous effector T cells. These data offer a rationale that contributes to the molecular and cellular mechanisms through which polymorphisms in the IL-2RA gene affect immune regulation, and consequently upon susceptibility to autoimmune and inflammatory diseases.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Numerous reports have demonstrated that CD4(+)CD25(+) regulatory T cells (Tregs) from individuals with a range of human autoimmune diseases, including type 1 diabetes, are deficient in their ability to control autologous proinflammatory responses when compared with nondiseased, control individuals.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1334, "doc_id": "11899391", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: A diminished ovarian reserve is a very strong indicator of infertility, even in an a priori non-infertile population.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\nABSTRACT: Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential. Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age. Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area. Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH. Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle). Conception was defined as a positive pregnancy test result. Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis. After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively). Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cy [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (63%; 95% CI, 50%-73%) compared with women (n = 654) with normal values (62%; 95% CI, 57%-66%) or after 12 cycles of attempt (82% [95% CI, 70%-89%] vs 75% [95% CI, 70%-78%], respectively).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 40, "doc_id": "13497630", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Ten percent (10%) of kidney cancers in the UK are attributable to excess weight.\n\nCANDIDATE_ABSTRACT:\nTITLE: Aberrant luminal progenitors as the candidate target population for basal tumor development in BRCA1 mutation carriers\nABSTRACT: Basal-like breast cancers arising in women carrying mutations in the BRCA1 gene, encoding the tumor suppressor protein BRCA1, are thought to develop from the mammary stem cell. To explore early cellular changes that occur in BRCA1 mutation carriers, we have prospectively isolated distinct epithelial subpopulations from normal mammary tissue and preneoplastic specimens from individuals heterozygous for a BRCA1 mutation. We describe three epithelial subsets including basal stem/progenitor, luminal progenitor and mature luminal cells. Unexpectedly, we found that breast tissue from BRCA1 mutation carriers harbors an expanded luminal progenitor population that shows factor-independent growth in vitro. Moreover, gene expression profiling revealed that breast tissue heterozygous for a BRCA1 mutation and basal breast tumors were more similar to normal luminal progenitor cells than any other subset, including the stem cell–enriched population. The c-KIT tyrosine kinase receptor (encoded by KIT) emerged as a key marker of luminal progenitor cells and was more highly expressed in BRCA1-associated preneoplastic tissue and tumors. Our findings suggest that an aberrant luminal progenitor population is a target for transformation in BRCA1-associated basal tumors .", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1148, "doc_id": "1866911", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Birth-weight is negatively associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Intrauterine factors and risk of breast cancer: a systematic review and meta-analysis of current evidence.\nABSTRACT: BACKGROUND Emerging evidence suggests an association between female prenatal experience and her subsequent risk of developing breast cancer. Potential underlying mechanisms include variation in amounts of maternal endogenous sex hormones and growth hormones, germ-cell mutations, formation of cancer stem-cells, and other genetic or epigenetic events. We reviewed and summarised quantitatively the available data on intrauterine exposures and risk of breast cancer. METHODS We systematically searched for studies that assessed association between perinatal factors and risk of breast cancer. We reviewed separately each of the perinatal factors, including birthweight, birth length, parental age at delivery, gestational age, intrauterine exposure to diethylstilbestrol, twin membership, maternal pre-eclampsia or eclampsia, and other factors. FINDINGS We identified 57 studies published between Oct 1, 1980, and June 21, 2007. Increased risk of breast cancer was noted with increased birthweight (relative risk [RR] 1.15 [95% CI 1.09-1.21]), birth length (1.28 [1.11-1.48]), higher maternal age (1.13 [1.02-1.25]), and paternal age (1.12 [1.05-1.19]). Decreased risk of breast cancer was noted for maternal pre-eclampsia and eclampsia (0.48 [0.30-0.78]) and twin membership (0.93 [0.87-1.00]). No association was noted between risk of breast cancer and gestational age at birth (0.95 [0.71-1.26]) or maternal diethylstilbestrol treatment (1.40 [0.86-2.28]). INTERPRETATION The intrauterine environment contributes to the predisposition of women to breast cancer in adulthood. The in-utero mechanisms responsible for such predisposition need to be elucidated.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Increased risk of breast cancer was noted with increased birthweight (relative risk [RR] 1.15 [95% CI 1.09-1.21]), birth length (1.28 [1.11-1.48]), higher maternal age (1.13 [1.02-1.25]), and paternal age (1.12 [1.05-1.19]).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 178, "doc_id": "23557241", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Angiotensin converting enzyme inhibitors are associated with decreased risk for functional renal insufficiency.\n\nCANDIDATE_ABSTRACT:\nTITLE: Once-a-day Concerta methylphenidate versus three-times-daily methylphenidate in laboratory and natural settings.\nABSTRACT: OBJECTIVE Methylphenidate (MPH), the most commonly prescribed drug for attention-deficit/hyperactivity disorder (ADHD), has a short half-life, which necessitates multiple daily doses. The need for multiple doses produces problems with medication administration during school and after-school hours, and therefore with compliance. Previous long-acting stimulants and preparations have shown effects equivalent to twice-daily dosing of MPH. This study tests the efficacy and duration of action, in natural and laboratory settings, of an extended-release MPH preparation designed to last 12 hours and therefore be equivalent to 3-times-daily dosing. METHODS Sixty-eight children with ADHD, 6 to 12 years old, participated in a within-subject, double-blind comparison of placebo, immediate-release (IR) MPH 3 times a day (tid), and Concerta, a once-daily MPH formulation. Three dosing levels of medication were used: 5 mg IR MPH tid/18 mg Concerta once a day (qd); 10 mg IR MPH tid/36 mg Concerta qd; and 15 mg IR MPH tid/54 mg Concerta qd. All children were currently medicated with MPH at enrollment, and each child's dose level was based on that child's MPH dosing before the study. The doses of Concerta were selected to be comparable to the daily doses of MPH that each child received. To achieve the ascending rate of MPH delivery determined by initial investigations to provide the necessary continuous coverage, Concerta doses were 20% higher on a daily basis than a comparable tid regimen of IR MPH. Children received each medication condition for 7 days. The investigation was conducted in the context of a background clinical behavioral intervention in both the natural environment and the laboratory setting. Parents received behavioral parent training and teachers were taught to [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 112, "doc_id": "2475059", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Major antigen-induced signals from the T cell receptor and secondary signals from costimulatory receptors are required for T cell activation.\n\nCANDIDATE_ABSTRACT:\nTITLE: CD28 Costimulation: From Mechanism to Therapy.\nABSTRACT: Ligation of the CD28 receptor on T cells provides a critical second signal alongside T cell receptor (TCR) ligation for naive T cell activation. Here, we discuss the expression, structure, and biochemistry of CD28 and its ligands. CD28 signals play a key role in many T cell processes, including cytoskeletal remodeling, production of cytokines, survival, and differentiation. CD28 ligation leads to unique epigenetic, transcriptional, and post-translational changes in T cells that cannot be recapitulated by TCR ligation alone. We discuss the function of CD28 and its ligands in both effector and regulatory T cells. CD28 is critical for regulatory T cell survival and the maintenance of immune homeostasis. We outline the roles that CD28 and its family members play in human disease and we review the clinical efficacy of drugs that block CD28 ligands. Despite the centrality of CD28 and its family members and ligands to immune function, many aspects of CD28 biology remain unclear. Translation of a basic understanding of CD28 function into immunomodulatory therapeutics has been uneven, with both successes and failures. Such real-world results might stem from multiple factors, including complex receptor-ligand interactions among CD28 family members, differences between the mouse and human CD28 families, and cell-type specific roles of CD28 family members.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Ligation of the CD28 receptor on T cells provides a critical second signal alongside T cell receptor (TCR) ligation for naive T cell activation.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 749, "doc_id": "13868795", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: A breast cancer patient's capacity to metabolize tamoxifen influences treatment outcome.\n\nCANDIDATE_PASSAGE:\nAssociation between the Medicare Modernization Act of 2003 and patient wait times and travel distance for chemotherapy. CONTEXT The Medicare Prescription Drug, Improvement, and Modernization Act of 2003 (MMA) altered reimbursements for outpatient chemotherapy drugs and drug administration services. Anecdotal reports suggest that these adjustments may have negatively affected access to chemotherapy for Medicare beneficiaries. OBJECTIVE To compare patient wait times and travel distances for chemotherapy before and after the enactment of the MMA. DESIGN, SETTING, AND PATIENTS Analysis of a nationally representative 5% sample of claims from the Centers for Medicare & Medicaid Services for the period 2003 through 2006. Patients were Medicare beneficiaries with incident breast cancer, colorectal cancer, leukemia, lung cancer, or lymphoma who received chemotherapy in inpatient hospital, institutional outpatient, or physician office settings. MAIN OUTCOME MEASURES Days from incident diagnosis to first chemotherapy visit and distance traveled for treatment, controlling for age, sex, race/ethnicity, cancer type, geographic region, comorbid conditions, and year of diagnosis and treatment. RESULTS There were 5082 incident cases of breast cancer, colorectal cancer, leukemia, lung cancer, or lymphoma in 2003; 5379 cases in 2004; 5116 cases in 2005; and 5288 cases in 2006. Approximately 70% of patients received treatment in physician office settings in each year. Although the distribution of treatment settings in 2004 and 2005 was not significantly different from 2003 (P = .24 and P = .72, respectively), there was a small but significant change from 2003 to 2006 (P = .02). The proportion of patients receiving chemotherapy in inpatient settings decreased from 10.2% in 2003 [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "30", "doc_id": "24575065", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: High levels of CRP lead to a higher risk of exacerbations in chronic obstructive pulmonary disease (COPD).\n\nCANDIDATE_PASSAGE:\nBullying in school: are short pupils at risk? Questionnaire study in a cohort. Bullying is still prevalent in schools and is clearly stressful for victims. 1 2 It may also have undesirable consequences for bullies, with antisocial behaviour persisting into adulthood. Victims are generally reported to be weaker than the bullies. 2 3 This would suggest that very short pupils are more likely to be victims and less likely to be the aggressors. The Wessex growth study allowed us to examine the prevalence of bullying, as experienced or perpetrated by pupils of different heights. Ninety two short normal adolescents who had been below the third centile for height at school entry4 and 117 controls matched for age and sex completed a bullying questionnaire, derived from work by Whitney and Smith.5 There were no refusals or any significant differences in sex or social class between the groups. Mean age (range) was 14.7 (13.4-15.7) years. Mean height SD scores were: short pupils −1.90 (−3.53 to −0.01), controls 0.31 (−1.41 …", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "515", "doc_id": "16855829", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: ATM and Rad3 related protein have no role in sensing DNA damage.\n\nCANDIDATE_PASSAGE:\nVisualization of recombination intermediates produced by RAD52-mediated single-strand annealing. Double-strand breaks (DSBs) occur frequently during DNA replication. They are also caused by ionizing radiation, chemical damage or as part of the series of programmed events that occur during meiosis. In yeast, DSB repair requires RAD52, a protein that plays a critical role in homologous recombination. Here we describe the actions of human RAD52 protein in a model system for single-strand annealing (SSA) using tailed (i.e. exonuclease resected) duplex DNA molecules. Purified human RAD52 protein binds resected DSBs and promotes associations between complementary DNA termini. Heteroduplex intermediates of these recombination reactions have been visualized by electron microscopy, revealing the specific binding of multiple rings of RAD52 to the resected termini and the formation of large protein complexes at heteroduplex joints formed by RAD52-mediated annealing.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "64", "doc_id": "7151961", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The extracellular domain of TMEM27 is cleaved in human beta cells.\n\nCANDIDATE_PASSAGE:\nTmem27: a cleaved and shed plasma membrane protein that stimulates pancreatic beta cell proliferation. The signals and molecular mechanisms that regulate the replication of terminally differentiated beta cells are unknown. Here, we report the identification and characterization of transmembrane protein 27 (Tmem27, collectrin) in pancreatic beta cells. Expression of Tmem27 is reduced in Tcf1(-/-) mice and is increased in islets of mouse models with hypertrophy of the endocrine pancreas. Tmem27 forms dimers and its extracellular domain is glycosylated, cleaved and shed from the plasma membrane of beta cells. This cleavage process is beta cell specific and does not occur in other cell types. Overexpression of full-length Tmem27, but not the truncated or soluble protein, leads to increased thymidine incorporation, whereas silencing of Tmem27 using RNAi results in a reduction of cell replication. Furthermore, transgenic mice with increased expression of Tmem27 in pancreatic beta cells exhibit increased beta cell mass. Our results identify a pancreatic beta cell transmembrane protein that regulates cell growth of pancreatic islets.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1216", "doc_id": "24142891", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Insomnia can be effectively treated with cognitive behavioral therapy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cognitive behavioral therapy vs zopiclone for treatment of chronic primary insomnia in older adults: a randomized controlled trial.\nABSTRACT: CONTEXT Insomnia is a common condition in older adults and is associated with a number of adverse medical, social, and psychological consequences. Previous research has suggested beneficial outcomes of both psychological and pharmacological treatments, but blinded placebo-controlled trials comparing the effects of these treatments are lacking. OBJECTIVE To examine short- and long-term clinical efficacy of cognitive behavioral therapy (CBT) and pharmacological treatment in older adults experiencing chronic primary insomnia. DESIGN, SETTING, AND PARTICIPANTS A randomized, double-blinded, placebo-controlled trial of 46 adults (mean age, 60.8 y; 22 women) with chronic primary insomnia conducted between January 2004 and December 2005 in a single Norwegian university-based outpatient clinic for adults and elderly patients. INTERVENTION CBT (sleep hygiene, sleep restriction, stimulus control, cognitive therapy, and relaxation; n = 18), sleep medication (7.5-mg zopiclone each night; n = 16), or placebo medication (n = 12). All treatment duration was 6 weeks, and the 2 active treatments were followed up at 6 months. MAIN OUTCOME MEASURES Ambulant clinical polysomnographic data and sleep diaries were used to determine total wake time, total sleep time, sleep efficiency, and slow-wave sleep (only assessed using polysomnography) on all 3 assessment points. RESULTS CBT resulted in improved short- and long-term outcomes compared with zopiclone on 3 out of 4 outcome measures. For most outcomes, zopiclone did not differ from placebo. Participants receiving CBT improved their sleep efficiency from 81.4% at pretreatment to 90.1% at 6-month follow-up compared with a decrease from 82.3% to 81.9% in the zopiclone group. Participants in the CBT group spent much more time in slow- [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Participants receiving CBT improved their sleep efficiency from 81.4% at pretreatment to 90.1% at 6-month follow-up compared with a decrease from 82.3% to 81.9% in the zopiclone group.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 641, "doc_id": "5912283", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: T regulatory cells (tTregs) lacking αvβ8 are more adept at suppressing pathogenic T-cell responses during active inflammation.\n\nCANDIDATE_PASSAGE:\nLocal, Efflux-Dependent Auxin Gradients as a Common Module for Plant Organ Formation Plants, compared to animals, exhibit an amazing adaptability and plasticity in their development. This is largely dependent on the ability of plants to form new organs, such as lateral roots, leaves, and flowers during postembryonic development. Organ primordia develop from founder cell populations into organs by coordinated cell division and differentiation. Here, we show that organ formation in Arabidopsis involves dynamic gradients of the signaling molecule auxin with maxima at the primordia tips. These gradients are mediated by cellular efflux requiring asymmetrically localized PIN proteins, which represent a functionally redundant network for auxin distribution in both aerial and underground organs. PIN1 polar localization undergoes a dynamic rearrangement, which correlates with establishment of auxin gradients and primordium development. Our results suggest that PIN-dependent, local auxin gradients represent a common module for formation of all plant organs, regardless of their mature morphology or developmental origin.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1130", "doc_id": "16557565", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does intraoperative MR imaging increase the extent of tumor resection in patients with high-grade gliomas?\n\nABSTRACT:\nMR is being used increasingly as an intraoperative imaging technique. The purpose of this study was to test the hypothesis that intraoperative MR imaging increases the extent of tumor resection, thus improving surgical results in patients with high-grade gliomas. Thirty-eight patients with intracranial high-grade gliomas underwent 41 operations. Using a neuronavigation system, tumors were resected in all patients to the point at which the neurosurgeon would have terminated the operation because he thought that all enhancing tumor had been removed. Intraoperative MR imaging (0.2 T) was performed, and surgery, if necessary and feasible, was continued. All patients underwent early postoperative MR imaging (1.5 T). By comparing the proportions of patients in whom complete resection of all enhancing tumor was shown by intraoperative and early postoperative MR imaging, respectively, the impact of intraoperative MR imaging on surgery was determined. Intraoperative MR imaging showed residual enhancing tumor in 22 cases (53.7%). In 15 patients (36.6%), no residual tumor was seen, whereas the results of the remaining four intraoperative MR examinations (9.7%) were inconclusive. In 17 of the 22 cases in which residual tumor was seen, surgery was continued. Early postoperative MR imaging showed residual tumor in eight patients (19.5%) and no residual tumor in 31 cases (75.6%); findings were uncertain in two patients (4.9%). The difference in the proportion of \"complete removals\" was statistically highly significant (P = .0004).", "output": "{\"label\": \"yes\", \"rationale\": \"Intraoperative MR imaging significantly increases the rate of complete tumor removal. The rate of complete removal of all enhancing tumor parts was only 36.6% when neuronavigation alone was used, which suggests the benefits of intraoperative imaging.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 10543634, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Bariatric surgery increases rates of colorectal cancer.\n\nCANDIDATE_PASSAGE:\nAspirin in the chemoprevention of colorectal neoplasia: an overview. Considerable evidence supports the effectiveness of aspirin for chemoprevention of colorectal cancer (CRC) in addition to its well-established benefits in the prevention of vascular disease. Epidemiologic studies have consistently observed an inverse association between aspirin use and risk of CRC. A recent pooled analysis of a long-term posttrial follow-up of nearly 14,000 patients from four randomized, cardiovascular disease prevention trials showed that daily aspirin treatment for about five years was associated with a 34% reduction in 20-year CRC mortality. A separate metaanalysis of nearly 3,000 patients with a history of colorectal adenoma or cancer in four randomized adenoma prevention trials showed that aspirin reduced the occurrence of advanced adenomas by 28% and any adenoma by 17%. Aspirin has also been shown to be beneficial in a clinical trial of patients with Lynch syndrome, a hereditary CRC syndrome; in those treated with aspirin for at least two years, there was a 50% or more reduction in the risk of CRC commencing five years after randomization and after aspirin had been discontinued. A few observational studies have shown an increase in survival among patients with CRC who use aspirin. Taken together, these findings strengthen the case for consideration of long-term aspirin use in CRC prevention. Despite these compelling data, there is a lack of consensus about the balance of risks and benefits associated with long-term aspirin use, particularly in low-risk populations. The optimal dose to use for cancer prevention and the precise mechanism underlying aspirin's anticancer effect require further investigation.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "164", "doc_id": "7613033", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Normal expression of RUNX1 has tumor-promoting effects.\n\nCANDIDATE_PASSAGE:\nLife and death of cardiac stem cells: a paradigm shift in cardiac biology. The recognition that myocyte mitosis occurs in the fetal, neonatal, adult, and hypertrophied heart and that a pool of primitive, undifferentiated cells is present in the myocardium has put forward a different view of the biology of the heart. The new paradigm suggests that myocyte formation is preserved during postnatal life, in adulthood or senescence, pointing to a remarkable growth reserve of the heart throughout the course of life of the organism. This article reviews a large body of novel information, which has been obtained in the last 2 decades, in favor of the notion that the mammalian heart has the inherent ability to continuously replace its parenchymal cells and that this unexpected characteristic has important implications in understanding myocardial homeostasis, cardiac aging, and tissue repair. The paradigm that the heart is a postmitotic organ incapable of regenerating parenchymal cells was established in the 1970s, and this dogma has profoundly conditioned basic and clinical research in cardiology for the last 3 decades. On the basis of this paradigm, cardiomyocytes undergo cellular hypertrophy1,2 but cannot be replaced either by entry into the cell cycle of a subpopulation of nonterminally differentiated myocytes or by activation of a pool of primitive cells that become committed to the myocyte lineage. The only response of cardiomyocytes to stress is hypertrophy and/or death. Therefore, a tremendous effort was made to identify the molecular mechanisms of myocyte hypertrophy and their genetic control. A sophisticated knowledge of various signaling pathways has been achieved, and our understanding of the biology of hypertrophic myocyte growth has advanced markedly.3 An [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "859", "doc_id": "14060030", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Progerin induces premature aging in stem cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Human iPSC-based modeling of late-onset disease via progerin-induced aging.\nABSTRACT: Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) resets their identity back to an embryonic age and, thus, presents a significant hurdle for modeling late-onset disorders. In this study, we describe a strategy for inducing aging-related features in human iPSC-derived lineages and apply it to the modeling of Parkinson's disease (PD). Our approach involves expression of progerin, a truncated form of lamin A associated with premature aging. We found that expression of progerin in iPSC-derived fibroblasts and neurons induces multiple aging-related markers and characteristics, including dopamine-specific phenotypes such as neuromelanin accumulation. Induced aging in PD iPSC-derived dopamine neurons revealed disease phenotypes that require both aging and genetic susceptibility, such as pronounced dendrite degeneration, progressive loss of tyrosine hydroxylase (TH) expression, and enlarged mitochondria or Lewy-body-precursor inclusions. Thus, our study suggests that progerin-induced aging can be used to reveal late-onset age-related disease features in hiPSC-based disease models.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Thus, our study suggests that progerin-induced aging can be used to reveal late-onset age-related disease features in hiPSC-based disease models.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 979, "doc_id": "11659421", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Polymeal nutrition increases cardiovascular mortality.\n\nCANDIDATE_ABSTRACT:\nTITLE: Case Management and Client Access to Health and Social Services in Outpatient Substance Abuse Treatment\nABSTRACT: A primary goal of case management is to coordinate services across treatment settings and to integrate substance abuse services with other types of services offered in the community, including housing, mental health, medical, and social services. However, case management is a global construct that consists of several key dimensions, which include extent of case management coverage, the degree of management of the referral process, and the location of case management activity (on-site, off-site, or both). This study examines the relationship between specific dimensions of case management and the utilization of health and ancillary social services in outpatient substance abuse treatment. In general, results suggest that more active case management during the referral process and providing case management both on-site and off-site are most consistent with our predictions of greater use of health and ancillary social services by substance abuse clients. However, these effects are specific to general health care and mental health services. Case management appears to have little effect on use of social services or aftercare plans.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 959, "doc_id": "485020", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: PRC1-bound plasmids sediment at a slower rate in unbound plasmids than in sucrose gradients.\n\nCANDIDATE_PASSAGE:\nThe role of alcohol in the Russian mortality crisis. AIMS Alcohol is believed to be an important factor behind the sharp rise in mortality during the period 1990-94 in Russia. However, the rise in the standard alcohol consumption proxy does not seem to be sufficient to explain all the increase in mortality. This study adopts a novel approach to exploring the role of the alcohol factor in the increased mortality by investigating whether the mismatch between trends in mortality and recorded alcohol consumption is due to an underestimation of the consumption increase. DESIGN AND MEASUREMENTS First, the alcohol effect on the male accident rate was estimated using data for the period 1959-89. Next, the estimated alcohol effect and the observed accident mortality rate for the period 1990-98 were used to backcast alcohol consumption during that period. Thirdly, the backcasted alcohol series was used to predict trajectories in alcohol poisoning mortality, the homicide rate and all-cause mortality during the period 1990-98. FINDINGS There was a markedly stronger increase in the backcasted consumption proxy than in the standard alcohol consumption proxy during the period 1990-98. There was a substantial gap between the observed mortality rates and the rates predicted from the standard alcohol consumption proxy, whereas the predictions from the backcasted alcohol proxy were much closer to the target. CONCLUSIONS Much of the rise in Russian mortality in 1990-94 appears to have been due to the increase in population drinking, but this increase is grossly underestimated by the commonly used consumption proxy combining alcohol sales, estimation of illicit alcohol production and proportion of alcohol-positive violent deaths.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "916", "doc_id": "46437558", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: A deficiency of vitamin B12 increases blood levels of homocysteine.\n\nCANDIDATE_PASSAGE:\nLong-term effect of aspirin on cancer risk in carriers of hereditary colorectal cancer: an analysis from the CAPP2 randomised controlled trial BACKGROUND Observational studies report reduced colorectal cancer in regular aspirin consumers. Randomised controlled trials have shown reduced risk of adenomas but none have employed prevention of colorectal cancer as a primary endpoint. The CAPP2 trial aimed to investigate the antineoplastic effects of aspirin and a resistant starch in carriers of Lynch syndrome, the major form of hereditary colorectal cancer; we now report long-term follow-up of participants randomly assigned to aspirin or placebo. METHODS In the CAPP2 randomised trial, carriers of Lynch syndrome were randomly assigned in a two-by-two factorial design to 600 mg aspirin or aspirin placebo or 30 g resistant starch or starch placebo, for up to 4 years. Randomisation was in blocks of 16 with provision for optional single-agent randomisation and extended postintervention double-blind follow-up; participants and investigators were masked to treatment allocation. The primary endpoint was development of colorectal cancer. Analysis was by intention to treat and per protocol. This trial is registered, ISRCTN59521990. RESULTS 861 participants were randomly assigned to aspirin or aspirin placebo. At a mean follow-up of 55·7 months, 48 participants had developed 53 primary colorectal cancers (18 of 427 randomly assigned to aspirin, 30 of 434 to aspirin placebo). Intention-to-treat analysis of time to first colorectal cancer showed a hazard ratio (HR) of 0·63 (95% CI 0·35-1·13, p=0·12). Poisson regression taking account of multiple primary events gave an incidence rate ratio (IRR) of 0·56 (95% CI 0·32-0·99, p=0·05). For participants completing 2 years of interve [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "36", "doc_id": "15648443", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Scapular stabilizer exercises are more effective than general exercise therapy in reducing pain and improving function of the shoulder.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effect of specific exercise strategy on need for surgery in patients with subacromial impingement syndrome: randomised controlled study\nABSTRACT: OBJECTIVE To evaluate if a specific exercise strategy, targeting the rotator cuff and scapula stabilisers, improves shoulder function and pain more than unspecific exercises in patients with subacromial impingement syndrome, thereby decreasing the need for arthroscopic subacromial decompression. DESIGN Randomised, participant and single assessor blinded, controlled study. SETTING Department of orthopaedics in a Swedish university hospital. PARTICIPANTS 102 patients with long standing (over six months) persistent subacromial impingement syndrome in whom earlier conservative treatment had failed, recruited through orthopaedic specialists. INTERVENTIONS The specific exercise strategy consisted of strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers in combination with manual mobilisation. The control exercise programme consisted of unspecific movement exercises for the neck and shoulder. Patients in both groups received five to six individual guided treatment sessions during 12 weeks. In between these supervised sessions the participants performed home exercises once or twice a day for 12 weeks. MAIN OUTCOME MEASURES The primary outcome was the Constant-Murley shoulder assessment score evaluating shoulder function and pain. Secondary outcomes were patients' global impression of change because of treatment and decision regarding surgery. RESULTS Most (97, 95%) participants completed the 12 week study. There was a significantly greater improvement in the Constant-Murley score in the specific exercise group than in the control exercise group (24 points (95% confidence interval 19 to 28.0) v 9 points (5 to 13); mean difference between group: 15 points (8.5 to 20.6)). Significantly more patients in the [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSION A specific exercise strategy, focusing on strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers, is effective in reducing pain and improving shoulder function in patients with persistent subacromial impingement syndrome.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1069, "doc_id": "4200695", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: One in two surgical randomized controlled trials are discontinued early.\n\nCANDIDATE_ABSTRACT:\nTITLE: Discontinuation and non-publication of surgical randomised controlled trials: observational study\nABSTRACT: OBJECTIVE To determine the rate of early discontinuation and non-publication of randomised controlled trials involving patients undergoing surgery. DESIGN Cross sectional observational study of registered and published trials. SETTING Randomised controlled trials of interventions in patients undergoing a surgical procedure. DATA SOURCES The ClinicalTrials.gov database was searched for interventional trials registered between January 2008 and December 2009 using the keyword \"surgery\". Recruitment status was extracted from the ClinicalTrials.gov database. A systematic search for studies published in peer reviewed journals was performed; if they were not found, results posted on the ClinicalTrials.gov results database were sought. Email queries were sent to trial investigators of discontinued and unpublished completed trials if no reason for the respective status was disclosed. MAIN OUTCOME MEASURES Trial discontinuation before completion and non-publication after completion. Logistic regression was used to determine the effect of funding source on publication status, with adjustment for intervention type and trial size. RESULTS Of 818 registered trials found using the keyword \"surgery\", 395 met the inclusion criteria. Of these, 21% (81/395) were discontinued early, most commonly owing to poor recruitment (44%, 36/81). The remaining 314 (79%) trials proceeded to completion, with a publication rate of 66% (208/314) at a median time of 4.9 (interquartile range 4.0-6.0) years from study completion to publication search. A further 6% (20/314) of studies presented results on ClinicalTrials.gov without a corresponding peer reviewed publication. Industry funding did not affect the rate of discontinuation (adjusted odds ratio 0.91, 95% confidence interval 0.54 to 1.55) [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Of these, 21% (81/395) were discontinued early, most commonly owing to poor recruitment (44%, 36/81).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 886, "doc_id": "6477536", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Physical activity level is associated with the difference in maximal oxygen consumption between black and white youth.\n\nCANDIDATE_ABSTRACT:\nTITLE: Relationship of physical activity and television watching with body weight and level of fatness among children: results from the Third National Health and Nutrition Examination Survey.\nABSTRACT: CONTEXT Physical inactivity contributes to weight gain in adults, but whether this relationship is true for children of different ethnic groups is not well established. OBJECTIVE To assess participation in vigorous activity and television watching habits and their relationship to body weight and fatness in US children. DESIGN Nationally representative cross-sectional survey with an in-person interview and medical examination. SETTING AND PARTICIPANTS Between 1988 and 1994, 4063 children aged 8 through 16 years were examined as part of the National Health and Nutrition Examination Survey III. Mexican Americans and non-Hispanic blacks were oversampled to produce reliable estimates for these groups. MAIN OUTCOME MEASURES Episodes of weekly vigorous activity and daily hours of television watched, and their relationship to body mass index and body fatness. RESULTS Eighty percent of US children reported performing 3 or more bouts of vigorous activity each week. This rate was lower in non-Hispanic black and Mexican American girls (69% and 73%, respectively). Twenty percent of US children participated in 2 or fewer bouts of vigorous activity perweek, and the rate was higher in girls (26%) than in boys (17%). Overall, 26% of US children watched 4 or more hours of television per day and 67% watched at least 2 hours per day. Non-Hispanic black children had the highest rates of watching 4 or more hours of television per day (42%). Boys and girls who watch 4 or more hours of television each day had greater body fat (P<.001) and had a greater body mass index (P<.001) than those who watched less than 2 hours per day. CONCLUSIONS Many US children watch a great deal of television and are inadequately vigorously active. Vigorous activity levels are lowest among girls, non-His [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 946, "doc_id": "8428935", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: High levels of CRP reduces the risk of exacerbations in chronic obstructive pulmonary disease (COPD).\n\nCANDIDATE_PASSAGE:\nChronic variable stress activates hematopoietic stem cells Exposure to psychosocial stress is a risk factor for many diseases, including atherosclerosis. Although incompletely understood, interaction between the psyche and the immune system provides one potential mechanism linking stress and disease inception and progression. Known cross-talk between the brain and immune system includes the hypothalamic-pituitary-adrenal axis, which centrally drives glucocorticoid production in the adrenal cortex, and the sympathetic-adrenal-medullary axis, which controls stress-induced catecholamine release in support of the fight-or-flight reflex. It remains unknown, however, whether chronic stress changes hematopoietic stem cell activity. Here we show that stress increases proliferation of these most primitive hematopoietic progenitors, giving rise to higher levels of disease-promoting inflammatory leukocytes. We found that chronic stress induced monocytosis and neutrophilia in humans. While investigating the source of leukocytosis in mice, we discovered that stress activates upstream hematopoietic stem cells. Under conditions of chronic variable stress in mice, sympathetic nerve fibers released surplus noradrenaline, which signaled bone marrow niche cells to decrease CXCL12 levels through the β3-adrenergic receptor. Consequently, hematopoietic stem cell proliferation was elevated, leading to an increased output of neutrophils and inflammatory monocytes. When atherosclerosis-prone Apoe(-/-) mice were subjected to chronic stress, accelerated hematopoiesis promoted plaque features associated with vulnerable lesions that cause myocardial infarction and stroke in humans.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "516", "doc_id": "5107861", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: LRBA promotes CTLA - 4 recycling.\n\nCANDIDATE_ABSTRACT:\nTITLE: Autosomal dominant immune dysregulation syndrome in humans with CTLA4 mutations\nABSTRACT: The protein cytotoxic T lymphocyte antigen-4 (CTLA-4) is an essential negative regulator of immune responses, and its loss causes fatal autoimmunity in mice. We studied a large family in which five individuals presented with a complex, autosomal dominant immune dysregulation syndrome characterized by hypogammaglobulinemia, recurrent infections and multiple autoimmune clinical features. We identified a heterozygous nonsense mutation in exon 1 of CTLA4. Screening of 71 unrelated patients with comparable clinical phenotypes identified five additional families (nine individuals) with previously undescribed splice site and missense mutations in CTLA4. Clinical penetrance was incomplete (eight adults of a total of 19 genetically proven CTLA4 mutation carriers were considered unaffected). However, CTLA-4 protein expression was decreased in regulatory T cells (Treg cells) in both patients and carriers with CTLA4 mutations. Whereas Treg cells were generally present at elevated numbers in these individuals, their suppressive function, CTLA-4 ligand binding and transendocytosis of CD80 were impaired. Mutations in CTLA4 were also associated with decreased circulating B cell numbers. Taken together, mutations in CTLA4 resulting in CTLA-4 haploinsufficiency or impaired ligand binding result in disrupted T and B cell homeostasis and a complex immune dysregulation syndrome.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 677, "doc_id": "857189", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: 70% of burn patients are admitted for hospitalization and further treatment after appearing at hospital emergency wards or outpatient clinics.\n\nCANDIDATE_PASSAGE:\nAcute respiratory failure in patients with severe community-acquired pneumonia: a prospective randomized evaluation of noninvasive ventilation. In uncontrolled studies, noninvasive positive pressure ventilation (NPPV) was found useful in avoiding endotracheal intubation in patients with acute respiratory failure (ARF) caused by severe community-acquired pneumonia (CAP). We conducted a prospective, randomized study comparing standard treatment plus NPPV delivered through a face mask to standard treatment alone in patients with severe CAP and ARF. Patients fitting the American Thoracic Society criteria for severe CAP were included in presence of ARF (refractory hypoxemia and/or hypercapnia with acidosis). Exclusion criteria were: severe hemodynamic instability, requirement for emergent cardiopulmonary resuscitation, home mechanical ventilation or oxygen long-term supplementation, concomitant severe disease with a low expectation of life, inability to expectorate or contraindications to the use of the mask. Fifty-six consecutive patients (28 in each arm) were enrolled, and the two groups were similar at study entry. The use of NPPV was well tolerated, safe, and associated with a significant reduction in respiratory rate, need for endotracheal intubation (21% versus 50%; p = 0.03), and duration of intensive care unit (ICU) stay (1.8 ± 0.7 d versus 6 ± 1.8 d; p = 0.04). The two groups had a similar intensity of nursing care workload, time interval from study entry to endotracheal intubation, duration of hospitalization, and hospital mortality. Among patients with chronic obstructive pulmonary disease (COPD), those randomized to NPPV had a lower intensity of nursing care workload (p = 0.04) and improved 2-mo survival (88.9% versus 37.5%; p = 0.05). We conclude tha [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "21", "doc_id": "40867854", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Articles published in open access format are less likely to be cited than traditional journals.\n\nCANDIDATE_ABSTRACT:\nTITLE: Open Access Increases Citation Rate\nABSTRACT: PLoS Biology publishes today a research article by Gunther Eysenbach that is not about biology. It is about citations. It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles. As such, it adds objective support to the belief we have always held that open-access publication speeds up scientific dialog between researchers and, consequently, should be extended to the whole scientific literature as quickly as possible. It is therefore fitting that we publish such a paper. We have long argued that papers freely available in a journal will be more often read and cited than those behind a subscription barrier. However, solid evidence to support or refute such a claim has been surprisingly hard to find. Since most open-access journals are new, comparisons of the effects of open access with established subscription-based journals are easily confounded by age and reputation. In the current study, Eysenbach compared citations compiled by Thomson Scientific (formerly Thomson ISI) to individual articles published between June 2004 and December 2004 in the same journal—namely, Proceedings of the National Academy of Sciences (PNAS), which announced its open-access option for authors on June 8 of that year, with an associated publication charge of US$1,000. Non-OA articles in PNAS are subject to a six-month “toll-access” delay before the article becomes publicly available. The results of this natural experiment are clear: in the 4 to 16 months following publication, OA articles gained a significant citation advantage over non-OA articles during the same period. They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely between 10 and 16 months. Given that P [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely between 10 and 16 months.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 129, "doc_id": "27768226", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Klf4 is not required for proper myeloid cell differentiation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Kruppel-like factor 4 is essential for inflammatory monocyte differentiation in vivo.\nABSTRACT: Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types. We demonstrate in this study that hematopoietic cells from KLF4(-/-) fetal livers (FL) contained normal numbers of functional hematopoietic progenitor cells, were radioprotective, and performed as well as KLF4(+/+) cells in competitive repopulation assays. However, hematopoietic \"KLF4(-/-) chimeras\" generated by transplantation of KLF4(-/-) fetal livers cells into lethally irradiated wild-type mice completely lacked circulating inflammatory (CD115(+)Gr1(+)) monocytes, and had reduced numbers of resident (CD115(+)Gr1(-)) monocytes. Although the numbers and function of peritoneal macrophages were normal in KLF4(-/-) chimeras, bone marrow monocytic cells from KLF4(-/-) chimeras expressed lower levels of key trafficking molecules and were more apoptotic. Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes. In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells. The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 669, "doc_id": "25148216", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: CR is associated with higher methylation age.\n\nCANDIDATE_ABSTRACT:\nTITLE: A neuroimaging investigation of the association between aerobic fitness, hippocampal volume, and memory performance in preadolescent children.\nABSTRACT: Because children are becoming overweight, unhealthy, and unfit, understanding the neurocognitive benefits of an active lifestyle in childhood has important public health and educational implications. Animal research has indicated that aerobic exercise is related to increased cell proliferation and survival in the hippocampus as well as enhanced hippocampal-dependent learning and memory. Recent evidence extends this relationship to elderly humans by suggesting that high aerobic fitness levels in older adults are associated with increased hippocampal volume and superior memory performance. The present study aimed to further extend the link between fitness, hippocampal volume, and memory to a sample of preadolescent children. To this end, magnetic resonance imaging was employed to investigate whether higher- and lower-fit 9- and 10-year-old children showed differences in hippocampal volume and if the differences were related to performance on an item and relational memory task. Relational but not item memory is primarily supported by the hippocampus. Consistent with predictions, higher-fit children showed greater bilateral hippocampal volumes and superior relational memory task performance compared to lower-fit children. Hippocampal volume was also positively associated with performance on the relational but not the item memory task. Furthermore, bilateral hippocampal volume was found to mediate the relationship between fitness level (VO(2) max) and relational memory. No relationship between aerobic fitness, nucleus accumbens volume, and memory was reported, which strengthens the hypothesized specific effect of fitness on the hippocampus. The findings are the first to indicate that aerobic fitness may relate to the structure and function of the preadolescent human brain.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 212, "doc_id": "2424794", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The minor G allele of FOXO3 is related to less severe symptoms of Crohn's Disease.\n\nCANDIDATE_ABSTRACT:\nTITLE: Common Carotid Intima Media Thickness and Ankle-Brachial Pressure Index Correlate with Local but Not Global Atheroma Burden: A Cross Sectional Study Using Whole Body Magnetic Resonance Angiography\nABSTRACT: BACKGROUND Common carotid intima media thickness (CIMT) and ankle brachial pressure index (ABPI) are used as surrogate marker of atherosclerosis, and have been shown to correlate with arterial stiffness, however their correlation with global atherosclerotic burden has not been previously assessed. We compare CIMT and ABPI with atheroma burden as measured by whole body magnetic resonance angiography (WB-MRA). METHODS 50 patients with symptomatic peripheral arterial disease were recruited. CIMT was measured using ultrasound while rest and exercise ABPI were performed. WB-MRA was performed in a 1.5T MRI scanner using 4 volume acquisitions with a divided dose of intravenous gadolinium gadoterate meglumine (Dotarem, Guerbet, FR). The WB-MRA data was divided into 31 anatomical arterial segments with each scored according to degree of luminal narrowing: 0 = normal, 1 = <50%, 2 = 50-70%, 3 = 70-99%, 4 = vessel occlusion. The segment scores were summed and from this a standardized atheroma score was calculated. RESULTS The atherosclerotic burden was high with a standardised atheroma score of 39.5±11. Common CIMT showed a positive correlation with the whole body atheroma score (β 0.32, p = 0.045), however this was due to its strong correlation with the neck and thoracic segments (β 0.42 p = 0.01) with no correlation with the rest of the body. ABPI correlated with the whole body atheroma score (β -0.39, p = 0.012), which was due to a strong correlation with the ilio-femoral vessels with no correlation with the thoracic or neck vessels. On multiple linear regression, no correlation between CIMT and global atheroma burden was present (β 0.13 p = 0.45), while the correlation between ABPI and atheroma burden persisted (β -0.45 p = 0.005). CONCLUSION ABPI but not CIMT corre [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1231, "doc_id": "87758", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Activator-inhibitor pairs are provided dorsally by Admpchordin.\n\nCANDIDATE_PASSAGE:\nSirtuin-1 is a nutrient-dependent modulator of inflammation Inflammation accompanies obesity and its comorbidities-type 2 diabetes, non-alcoholic fatty liver disease and atherosclerosis, among others-and may contribute to their pathogenesis. Yet the cellular machinery that links nutrient sensing to inflammation remains incompletely characterized. The protein deacetylase sirtuin-1 (SirT1) is activated by energy depletion and plays a critical role in the mammalian response to fasting. More recently it has been implicated in the repression of inflammation. SirT1 mRNA and protein expression are suppressed in obese rodent and human white adipose tissue, while experimental reduction of SirT1 in adipocytes and macrophages causes low-grade inflammation that mimics that observed in obesity. Thus suppression of SirT1 during overnutrition may be critical to the development of obesity-associated inflammation. This effect is attributable to multiple actions of SirT1, including direct deacetylation of NFκB and chromatin remodeling at inflammatory gene promoters. In this work, we report that SirT1 is also suppressed by diet-induced obesity in macrophages, which are key contributors to the ontogeny of metabolic inflammation. Thus, SirT1 may be a common mechanism by which cells sense nutrient status and modulate inflammatory signaling networks in accordance with organismal energy availability.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "72", "doc_id": "6171953", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Are aBCB1 gene polymorphisms associated with treatment outcome in elderly acute myeloid leukemia patients?\n\nABSTRACT:\nThe classical multidrug resistance (MDR) gene MDR1 (ABCB1) encodes for the drug efflux pump P-glycoprotein (P-gp). P-gp expression is an adverse prognostic factor for treatment outcome in acute myeloid leukemia (AML) and is more frequently observed in older patients. Single-nucleotide polymorphisms of the ABCB1 gene, C1236T, G2677T, and C3435T, have been associated with altered drug metabolism and treatment outcome. We prospectively determined these single-nucleotide polymorphisms in AML blasts in a cohort of patients aged 60 years or older with AML and evaluated their relevance with regard to P-gp function and expression, ABCB1 messenger ribonucleic acid (mRNA) expression, and clinical outcome. We have analyzed purified bone marrow-derived leukemic blasts, obtained at diagnosis, in 150 patients who were treated within a multicenter, randomized, phase 3 trial of elderly patients with AML. The significance of the allelic ABCB1 variants of C1236T, G2677T, and C3435T was evaluated with respect to P-gp expression and function in leukemic blasts and ABCB1 mRNA expression levels, and these values were correlated with treatment outcome. P-gp function and expression in leukemic blasts and ABCB1 mRNA levels in patients with AML did not vary significantly among any of the allelic variants of ABCB1. None of these allelic variations predicted a difference in complete response rate and survival endpoints.", "output": "{\"label\": \"no\", \"rationale\": \"In AML patients aged 60 years or older, allelic ABCB1 variations of C1236T, G2677T, or C3435T are not associated with altered P-gp function or with MDR1 expression at the transcriptional or translational level in leukemic blasts, and they do not significantly affect clinical prognosis.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 17112800, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Ethanol stress lowers the expression of PSP in bacteria.\n\nCANDIDATE_PASSAGE:\nRegulation of Serum Amyloid A3 (SAA3) in Mouse Colonic Epithelium and Adipose Tissue by the Intestinal Microbiota The gut microbiota has been proposed as an environmental factor that affects the development of metabolic and inflammatory diseases in mammals. Recent reports indicate that gut bacteria-derived lipopolysaccharide (LPS) can initiate obesity and insulin resistance in mice; however, the molecular interactions responsible for microbial regulation of host metabolism and mediators of inflammation have not been studied in detail. Hepatic serum amyloid A (SAA) proteins are markers and proposed mediators of inflammation that exhibit increased levels in serum of insulin-resistant mice. Adipose tissue-derived SAA3 displays monocyte chemotactic activity and may play a role in metabolic inflammation associated with obesity and insulin resistance. To investigate a potential mechanistic link between the intestinal microbiota and induction of proinflammatory host factors, we performed molecular analyses of germ-free, conventionally raised and genetically modified Myd88-/- mouse models. SAA3 expression was determined to be significantly augmented in adipose (9.9+/-1.9-fold; P<0.001) and colonic tissue (7.0+/-2.3-fold; P<0.05) by the presence of intestinal microbes. In the colon, we provided evidence that SAA3 is partially regulated through the Toll-like receptor (TLR)/MyD88/NF-kappaB signaling axis. We identified epithelial cells and macrophages as cellular sources of SAA3 in the colon and found that colonic epithelial expression of SAA3 may be part of an NF-kappaB-dependent response to LPS from gut bacteria. In vitro experiments showed that LPS treatments of both epithelial cells and macrophages induced SAA3 expression (27.1+/-2.5-fold vs. 1.6+/-0.1-fold, respec [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "392", "doc_id": "12658073", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does limb-salvage surgery offer patients better quality of life and functional capacity than amputation?\n\nABSTRACT:\nPatients with aggressive lower extremity musculoskeletal tumors may be candidates for either above-knee amputation or limb-salvage surgery. However, the subjective and objective benefits of limb-salvage surgery compared with amputation are not fully clear.QUESTIONS/ We therefore compared functional status and quality of life for patients treated with above-knee amputation versus limb-salvage surgery. We reviewed 20 of 51 patients aged 15 years and older treated with above-knee amputation or limb-salvage surgery for aggressive musculoskeletal tumors around the knee between 1994 and 2004 as a retrospective cohort study. At last followup we obtained the Physiological Cost Index, the Reintegration to Normal Living Index, SF-36, and the Toronto Extremity Salvage Score questionnaires. The minimum followup was 12 months (median, 56 months; range, 12-108 months). Compared with patients having above-knee amputation, patients undergoing limb-salvage surgery had superior Physiological Cost Index scores and Reintegration to Normal Living Index. The Toronto Extremity Salvage scores and SF-36 scores were similar in the two groups.", "output": "{\"label\": \"maybe\", \"rationale\": \"These data suggest that limb-salvage surgery offers better gait efficiency and return to normal living compared with above-knee amputation, but does not improve the patient's perception of quality of life.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 22302658, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Gene expression does not vary appreciably across genetically identical cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Nature, Nurture, or Chance: Stochastic Gene Expression and Its Consequences\nABSTRACT: Gene expression is a fundamentally stochastic process, with randomness in transcription and translation leading to cell-to-cell variations in mRNA and protein levels. This variation appears in organisms ranging from microbes to metazoans, and its characteristics depend both on the biophysical parameters governing gene expression and on gene network structure. Stochastic gene expression has important consequences for cellular function, being beneficial in some contexts and harmful in others. These situations include the stress response, metabolism, development, the cell cycle, circadian rhythms, and aging.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Gene expression is a fundamentally stochastic process, with randomness in transcription and translation leading to cell-to-cell variations in mRNA and protein levels.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 452, "doc_id": "12804937", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Mitochondria play a trivial role in calcium homeostasis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Targeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth\nABSTRACT: Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs). GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets. We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels. To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA). Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis. The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays. The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts. In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival. Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation. Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may funct [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 798, "doc_id": "33370", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Consumption of whole fruits increases the risk of type 2 diabetes.\n\nCANDIDATE_PASSAGE:\nThe histone acetyltransferase MOF is a key regulator of the embryonic stem cell core transcriptional network. Pluripotent embryonic stem cells (ESCs) maintain self-renewal and the potential for rapid response to differentiation cues. Both ESC features are subject to epigenetic regulation. Here we show that the histone acetyltransferase Mof plays an essential role in the maintenance of ESC self-renewal and pluripotency. ESCs with Mof deletion lose characteristic morphology, alkaline phosphatase (AP) staining, and differentiation potential. They also have aberrant expression of the core transcription factors Nanog, Oct4, and Sox2. Importantly, the phenotypes of Mof null ESCs can be partially suppressed by Nanog overexpression, supporting the idea that Mof functions as an upstream regulator of Nanog in ESCs. Genome-wide ChIP-sequencing and transcriptome analyses further demonstrate that Mof is an integral component of the ESC core transcriptional network and that Mof primes genes for diverse developmental programs. Mof is also required for Wdr5 recruitment and H3K4 methylation at key regulatory loci, highlighting the complexity and interconnectivity of various chromatin regulators in ESCs.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "283", "doc_id": "12040627", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does food affect the pharmacokinetics of solifenacin , a new muscarinic receptor antagonist : results of a randomized crossover trial?\n\nABSTRACT:\nTo determine the effect of food ingestion on the pharmacokinetic profile of solifenacin succinate (YM905; Vesicare, a new bladder selective muscarinic receptor antagonist for the treatment of overactive bladder, a chronic disease usually caused by involuntary detrusor muscle contractions during bladder filling. A randomized, two-period, crossover study in two groups of 12 healthy men (aged 18-45 years, body weight 60-100 kg, body mass index < or =30). A single 10-mg dose of solifenacin was administered to the first group in the fasting state during period 1 and in the fed state during period 2, and to the second group in the fed state during period 1 and in the fasting state during period 2 (10 mg is two times the suggested starting dose). There was a 14-day washout between treatment periods. Parameters obtained included C(max), AUC(last), and AUC(0-inf), as well as t(1/2), t(max), and t(lag). One subject withdrew during the first period for personal reasons. No statistically or clinically significant pharmacokinetic differences occurred between subjects in the fed and fasting states. All geometric mean ratios were close to 1 (C(max), 1.033; AUC(last), 1.068; AUC(0-inf), 1.040). The 90% confidence intervals (CIs) fell in the predefined no-food-effect boundaries of 0.8-1.25 (C(max), 0.953-1.120; AUC(last), 0.990-1.153; AUC(0-inf), 0.976-1.109). The mean difference in t(1/2) was -3.8 h (90% CI 7.6-0.0). There were no significant differences between the fed and fasting states with regard to t(max) and t(lag) (P > 0.05).", "output": "{\"label\": \"no\", \"rationale\": \"The pharmacokinetics of oral solifenacin was not affected by food ingestion, suggesting that this drug may be administered with or without food. The results observed in this investigation are consistent with those of previous studies of solifenacin.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 15206986, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Mitochondria play a major role in energy production.\n\nCANDIDATE_ABSTRACT:\nTITLE: Targeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth\nABSTRACT: Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs). GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets. We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels. To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA). Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis. The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays. The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts. In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival. Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation. Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may funct [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 797, "doc_id": "33370", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The C-type lectin receptor (CLEC-2) rearranges the actin cytoskeleton in dendritic cells to promote efficient motility along stromal surfaces.\n\nCANDIDATE_ABSTRACT:\nTITLE: Podoplanin-Rich Stromal Networks Induce Dendritic Cell Motility via Activation of the C-type Lectin Receptor CLEC-2\nABSTRACT: To initiate adaptive immunity, dendritic cells (DCs) move from parenchymal tissues to lymphoid organs by migrating along stromal scaffolds that display the glycoprotein podoplanin (PDPN). PDPN is expressed by lymphatic endothelial and fibroblastic reticular cells and promotes blood-lymph separation during development by activating the C-type lectin receptor, CLEC-2, on platelets. Here, we describe a role for CLEC-2 in the morphodynamic behavior and motility of DCs. CLEC-2 deficiency in DCs impaired their entry into lymphatics and trafficking to and within lymph nodes, thereby reducing T cell priming. CLEC-2 engagement of PDPN was necessary for DCs to spread and migrate along stromal surfaces and sufficient to induce membrane protrusions. CLEC-2 activation triggered cell spreading via downregulation of RhoA activity and myosin light-chain phosphorylation and triggered F-actin-rich protrusions via Vav signaling and Rac1 activation. Thus, activation of CLEC-2 by PDPN rearranges the actin cytoskeleton in DCs to promote efficient motility along stromal surfaces.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Thus, activation of CLEC-2 by PDPN rearranges the actin cytoskeleton in DCs to promote efficient motility along stromal surfaces.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1153, "doc_id": "7370282", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Suboptimal nutrition is a leading cause of premature death\n\nCANDIDATE_PASSAGE:\nFunctional inhibition of osteoblastic cells in an in vivo mouse model of myeloid leukemia. Pancytopenia is a major cause of morbidity in acute myeloid leukemia (AML), yet its cause is unclear. Normal osteoblastic cells have been shown to support hematopoiesis. To define the effects of leukemia on osteoblastic cells, we used an immunocompetent murine model of AML. Leukemic mice had inhibition of osteoblastic cells, with decreased serum levels of the bone formation marker osteocalcin. Osteoprogenitor cells and endosteal-lining osteopontin(+) cells were reduced, and osteocalcin mRNA in CD45(-) marrow cells was diminished. This resulted in severe loss of mineralized bone. Osteoclasts were only transiently increased without significant increases in bone resorption, and their inhibition only partially rescued leukemia-induced bone loss. In vitro data suggested that a leukemia-derived secreted factor inhibited osteoblastic cells. Because the chemokine CCL-3 was recently reported to inhibit osteoblastic function in myeloma, we tested its expression in our model and in AML patients. Consistent with its potential novel role in leukemic-dependent bone loss, CCL-3 mRNA was significantly increased in malignant marrow cells from leukemic mice and from samples from AML patients. Based on these results, we propose that therapeutic mitigation of leukemia-induced uncoupling of osteoblastic and osteoclastic cells may represent a novel approach to promote normal hematopoiesis in patients with myeloid neoplasms.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1109", "doc_id": "10795340", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The one-child policy has created a hospitable environment for female infants.\n\nCANDIDATE_ABSTRACT:\nTITLE: Perinatal mortality in rural China: retrospective cohort study.\nABSTRACT: OBJECTIVES To explore the use of local civil registration data to assess the perinatal mortality in a typical rural county in a less developed province in China, 1999-2000. DESIGN Retrospective cohort study. Pregnancies in a cohort of women followed from registration of pregnancy to outcome of infant seven days after birth. SETTING Routine family planning records in 20 rural townships in eastern China. SUBJECTS 3697 pregnancies registered by the local family planning system during 1999. MAIN OUTCOME MEASURES Abortions, stillbirths, early neonatal mortality, perinatal mortality. RESULTS Only three cases were lost to follow up. The average age of the women at pregnancy was 25.9 years. Three hundred and twelve pregnancies were aborted and 240 ended in miscarriage (total 552, 15%). The perinatal mortality rate was 69 per 1000 births, the rate of stillbirth was 24 per 1000 births, and the early neonatal mortality was 46 per 1000 live births. The early neonatal mortality was 29 in boys and 69 in girls per 1000 live births. The perinatal mortality rate increased notably with parity and was higher in townships having lower income per capita. CONCLUSIONS The family planning system at the most local level is a useful data source for studying perinatal mortality in rural China. The perinatal mortality rate in the study county was higher than previously reported for both rural and urban areas in China. The results by parity and sex of the infant raise concern over the impact of the one child policy.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The early neonatal mortality was 29 in boys and 69 in girls per 1000 live births.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1246, "doc_id": "7662395", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: NR5A2 does not play a role in development of endometrial tissues.\n\nCANDIDATE_PASSAGE:\nLiver receptor homolog-1 is essential for pregnancy Successful pregnancy requires coordination of an array of signals and factors from multiple tissues. One such element, liver receptor homolog-1 (Lrh-1), is an orphan nuclear receptor that regulates metabolism and hormone synthesis. It is strongly expressed in granulosa cells of ovarian follicles and in the corpus luteum of rodents and humans. Germline ablation of Nr5a2 (also called Lrh-1), the gene coding for Lrh-1, in mice is embryonically lethal at gastrulation. Depletion of Lrh-1 in the ovarian follicle shows that it regulates genes required for both steroid synthesis and ovulation. To study the effects of Lrh-1 on mouse gestation, we genetically disrupted its expression in the corpus luteum, resulting in luteal insufficiency. Hormone replacement permitted embryo implantation but was followed by gestational failure with impaired endometrial decidualization, compromised placental formation, fetal growth retardation and fetal death. Lrh-1 is also expressed in the mouse and human endometrium, and in a primary culture of human endometrial stromal cells, reduction of NR5A2 transcript abundance by RNA interference abrogated decidualization. These findings show that Lrh-1 is necessary for maintenance of the corpus luteum, for promotion of decidualization and for formation of the placenta. It therefore has multiple, indispensible roles in establishing and sustaining pregnancy.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "835", "doc_id": "15928989", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Reduced responsiveness to interleukin-2 in regulatory T cells is associated with greater resistance to autoimmune diseases such as Type 1 Diabetes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Large-scale genetic fine mapping and genotype-phenotype associations implicate polymorphism in the IL2RA region in type 1 diabetes\nABSTRACT: Genome-wide association studies are now identifying disease-associated chromosome regions. However, even after convincing replication, the localization of the causal variant(s) requires comprehensive resequencing, extensive genotyping and statistical analyses in large sample sets leading to targeted functional studies. Here, we have localized the type 1 diabetes (T1D) association in the interleukin 2 receptor alpha (IL2RA) gene region to two independent groups of SNPs, spanning overlapping regions of 14 and 40 kb, encompassing IL2RA intron 1 and the 5′ regions of IL2RA and RBM17 (odds ratio = 2.04, 95% confidence interval = 1.70–2.45; P = 1.92 × 10−28; control frequency = 0.635). Furthermore, we have associated IL2RA T1D susceptibility genotypes with lower circulating levels of the biomarker, soluble IL-2RA (P = 6.28 × 10−28), suggesting that an inherited lower immune responsiveness predisposes to T1D.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Furthermore, we have associated IL2RA T1D susceptibility genotypes with lower circulating levels of the biomarker, soluble IL-2RA (P = 6.28 × 10−28), suggesting that an inherited lower immune responsiveness predisposes to T1D.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1029, "doc_id": "13940200", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Normal expression of RUNX1 has tumor-promoting effects.\n\nCANDIDATE_PASSAGE:\nModulation of cancer chemotherapy by green tea. Biochemical modulation has played an important role in the development of cancer chemotherapy. We have directed our attention to the intake of common beverages and investigated the effects of green tea and tea components on the antitumor activity of doxorubicin. We carried out the combined treatment of toxorubicin and green tea on Ehrlich ascites carcinoma tumor-bearing mice. The oral administration of green tea enhanced 2.5-fold the inhibitory effects of doxorubicin on tumor growth. The Doxorubicin concentration in the tumor was increased by the combination of green tea with doxorubicin. In contrast, the increase in doxorubicin concentration was not observed in normal tissues after green tea combination. Furthermore, the enhancement of antitumor activity of doxorubicin induced by green tea was observed in M5076 ovarian sarcoma, which has low sensitivity to doxorubicin. These results suggest that drinking green tea can encourage cancer chemotherapy and may improve the quality of life of clinical patients.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "859", "doc_id": "2296264", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: In rhesus macaques, daily subcutaneous injections of emtricitabine are ineffective at protecting against rectally transmitted simian-human immunodeficiency virus.\n\nCANDIDATE_PASSAGE:\nHuman Cytomegalovirus Latency-Associated Proteins Elicit Immune-Suppressive IL-10 Producing CD4+ T Cells Human cytomegalovirus (HCMV) is a widely prevalent human herpesvirus, which, after primary infection, persists in the host for life. In healthy individuals, the virus is well controlled by the HCMV-specific T cell response. A key feature of this persistence, in the face of a normally robust host immune response, is the establishment of viral latency. In contrast to lytic infection, which is characterised by extensive viral gene expression and virus production, long-term latency in cells of the myeloid lineage is characterised by highly restricted expression of viral genes, including UL138 and LUNA. Here we report that both UL138 and LUNA-specific T cells were detectable directly ex vivo in healthy HCMV seropositive subjects and that this response is principally CD4⁺ T cell mediated. These UL138-specific CD4⁺ T cells are able to mediate MHC class II restricted cytotoxicity and, importantly, show IFNγ effector function in the context of both lytic and latent infection. Furthermore, in contrast to CDCD4⁺ T cells specific to antigens expressed solely during lytic infection, both the UL138 and LUNA-specific CD4⁺ T cell responses included CD4⁺ T cells that secreted the immunosuppressive cytokine cIL-10. We also show that cIL-10 expressing CD4⁺ T-cells are directed against latently expressed US28 and UL111A. Taken together, our data show that latency-associated gene products of HCMV generate CD4⁺ T cell responses in vivo, which are able to elicit effector function in response to both lytic and latently infected cells. Importantly and in contrast to CD4⁺ T cell populations, which recognise antigens solely expressed during lytic infection, include a subset of cell [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "582", "doc_id": "10450300", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Vitamin D is an important factor in the relationship between calcium and parathyroid hormone.\n\nCANDIDATE_ABSTRACT:\nTITLE: Relationship between serum parathyroid hormone levels, vitamin D sufficiency, and calcium intake.\nABSTRACT: CONTEXT Adequate vitamin D status for optimum bone health has received increased recognition in recent years; however, the ideal intake is not known. Serum 25-hydroxyvitamin D is the generally accepted indicator of vitamin D status, but no universal reference level has been reached. OBJECTIVE To investigate the relative importance of high calcium intake and serum 25-hydroxyvitamin D for calcium homeostasis, as determined by serum intact parathyroid hormone (PTH). DESIGN, SETTING, AND PARTICIPANTS Cross-sectional study of 2310 healthy Icelandic adults who were divided equally into 3 age groups (30-45 years, 50-65 years, or 70-85 years) and recruited from February 2001 to January 2003. They were administered a semi-quantitative food frequency questionnaire, which assessed vitamin D and calcium intake. Participants were further divided into groups according to calcium intake (<800 mg/d, 800-1200 mg/d, and >1200 mg/d) and serum 25-hydroxyvitamin D level (<10 ng/mL, 10-18 ng/mL, and >18 ng/mL). MAIN OUTCOME MEASURE Serum intact PTH as determined by calcium intake and vitamin D. RESULTS A total of 944 healthy participants completed all parts of the study. After adjusting for relevant factors, serum PTH was lowest in the group with a serum 25-hydroxyvitamin D level of more than 18 ng/mL but highest in the group with a serum 25-hydroxyvitamin D level of less than 10 ng/mL. At the low serum 25-hydroxyvitamin D level (<10 ng/mL), calcium intake of less than 800 mg/d vs more than 1200 mg/d was significantly associated with higher serum PTH (P = .04); and at a calcium intake of more than 1200 mg/d, there was a significant difference between the lowest and highest vitamin D groups (P = .04). CONCLUSIONS As long as vitamin D status is ensured, calcium intake levels of mor [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS As long as vitamin D status is ensured, calcium intake levels of more than 800 mg/d may be unnecessary for maintaining calcium metabolism.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1371, "doc_id": "16256507", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Recognition of start codons depends on the translation initiation factor IF3.\n\nCANDIDATE_ABSTRACT:\nTITLE: High Km soluble 5'-nucleotidase from human placenta. Properties and allosteric regulation by IMP and ATP.\nABSTRACT: A human placental soluble \"high Km\" 5'-nucleotidase has been separated from \"low Km\" 5'-nucleotidase and nonspecific phosphatase by AMP-Sepharose affinity chromatography. The enzyme was purified 8000-fold to a specific activity of 25.6 mumol/min/mg. The subunit molecular mass is 53 kDa, and the native molecular mass is 210 kDa, suggesting a tetrameric structure. Soluble high Km 5'-nucleotidase is most active with IMP and GMP and their deoxy derivatives. IMP is hydrolyzed 15 times faster than AMP. The enzyme has a virtually absolute requirement for magnesium ions and is regulated by them. Purine nucleoside 5'-triphosphates strongly activate the enzyme with the potency order dATP greater than ATP greater than GTP. 2,3-Diphosphoglycerate activates the enzyme as potently as ATP. Three millimolar ATP decreased the Km for IMP from 0.33 to 0.09 mM and increased the Vmax 12-fold. ATP activation was modified by the IMP concentration. At 20 microM IMP the ATP-dependent activation curve was sigmoidal, while at 2 mM IMP it was hyperbolic. The A0.5 values for ATP were 2.26 and 0.70 mM, and the relative maximal velocities were 32.9 and 126.0 nmol/min, respectively. Inorganic phosphate shifts the hyperbolic substrate velocity relationship for IMP to a sigmoidal one. With physiological concentrations of cofactors (3 mM ATP, 1-4 mM Pi, 150 mM KCl) at pH 7.4, the enzyme is 25-35 times more active toward 100 microM IMP than 100 microM AMP. These data show that: (a) soluble human placental high Km 5'-nucleotidase coexists in human placenta with the low Km enzyme; (b) under physiological conditions the enzyme favors the hydrolysis of IMP and is critically regulated by IMP, ATP, and Pi levels; and (c) kinetic properties of ATP and IMP are each modified by the other compound sugge [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1023, "doc_id": "393001", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: 32% of liver transplantation programs required patients to discontinue methadone treatment in 2001.\n\nCANDIDATE_ABSTRACT:\nTITLE: Liver transplantation and opioid dependence.\nABSTRACT: ContextChronic hepatitis C is the leading cause for liver transplantation in the United States. Intravenous drug use, the major risk factor, accounts for approximately 60% of hepatitis C virus transmission. Information from the United Network of Organ Sharing (UNOS) does not address substance use among liver transplantation patients. ObjectiveTo identify addiction-related criteria for admission to the UNOS liver transplantation waiting list and posttransplantation problems experienced by patients who are prescribed maintenance methadone. Design, Setting, and ParticipantsMail survey of all 97 adult US liver transplantation programs (belonging to UNOS) in March 2000 with telephone follow-up conducted in May and June 2000.Main Outcome MeasuresPrograms' acceptance and management of patients with past or present substance use disorder. ResultsOf the 97 programs surveyed, 87 (90%) responded. All accept applicants with a history of alcoholism or other addictions, including heroin dependence. Eighty-eight percent of the responding programs require at least 6 months of abstinence from alcohol; 83% from illicit drugs. Ninety-four percent have addiction treatment requirements. Consultations from substance abuse specialists are obtained by 86%. Patients receiving methadone maintenance are accepted by 56% of the responding programs. Approximately 180 patients receiving methadone maintenance are reported to have undergone liver transplantation. ConclusionsMost liver transplantation programs have established policies for patients with substance use disorders. Opiate-dependent patients receiving opiate replacement therapy seem underrepresented in transplantation programs. Little anecdotal evidence for negative impact of opiate replacement therapy on liver transplantation ou [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Policies requiring discontinuation of methadone in 32% of all programs contradict the evidence base for efficacy of long-term replacement therapies and potentially result in relapse of previously stable patients.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 9, "doc_id": "44265107", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Golli-deficient T-cells prefer to differentiate into an anergic phenotype in the adaptive immune response when there are increased levels of Ca2+ in the cytosol.\n\nCANDIDATE_PASSAGE:\nIsolated liver perfusion for non-resectable liver tumours: a review. Many treatments have been proposed for non-resectable primary or secondary hepatic cancer but the results have generally been disappointing. Isolated Hepatic Perfusion (IHP) was first attempted four decades ago but it gained acceptance only recently, after spectacular tumour responses were obtained by isolated limb perfusion with melphalan and tumour necrosis factor (TNF) for melanomas and sarcomas. Surgical isolation of the liver is a technically demanding operation that allows the safe administration of high doses of chemotherapeutics and TNF. Percutaneous techniques using balloon occlusion catheters are simpler but result in higher leakage rates from the perfusion circuit into the systemic circulation. Several phase I-II trials indicate that IHP can yield high tumour response rates, even when there is resistance to systemic chemotherapy. However, no significant advantage in overall survival has been demonstrated so far. IHP offers unique pharmacokinetic advantages for locoregional chemotherapy and biotherapy. It might also allow gene therapy with limited systemic exposure and toxicity. At present, IHP nevertheless remains an experimental treatment modality which should therefore be used in controlled trials only.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "478", "doc_id": "13380980", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Incidence of sepsis has fallen substantially from 2009 to 2014.\n\nCANDIDATE_PASSAGE:\nTherapeutic equivalence of alendronate 70 mg once-weekly and alendronate 10 mg daily in the treatment of osteoporosis. Alendronate Once-Weekly Study Group. Dosing convenience is a key element in the effective management of any chronic disease, and is particularly important in the long-term management of osteoporosis. Less frequent dosing with any medication may enhance compliance, thereby maximizing the effectiveness of therapy. Animal data support the rationale that once-weekly dosing with alendronate 70 mg (7 times the daily oral treatment dose) could provide similar efficacy to daily dosing with alendronate 10 mg due to its long duration of effect in bone. In addition, dog studies suggest that the potential for esophageal irritation, observed with daily oral bisphosphonates, may be substantially reduced with once-weekly dosing. This dosing regimen would provide patients with increased convenience and would be likely to enhance patient compliance. We compared the efficacy and safety of treatment with oral once-weekly alendronate 70 mg (N=519), twice-weekly alendronate 35 mg (N=369), and daily alendronate 10 mg (N=370) in a one-year, double-blind, multicenter study of postmenopausal women (ages 42 to 95) with osteoporosis (bone mineral density [BMD] of either lumbar spine or femoral neck at least 2.5 SDs below peak premenopausal mean, or prior vertebral or hip fracture). The primary efficacy endpoint was the comparability of increases in lumbar spine BMD, using strict pre-defined equivalence criteria. Secondary endpoints included changes in BMD at the hip and total body and rate of bone turnover, as assessed by biochemical markers. Both of the new regimens fully satisfied the equivalence criteria relative to daily therapy. Mean increases in lumbar spine BMD [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "595", "doc_id": "3613041", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Do endocannabinoids acting at cannabinoid-1 receptors regulate cardiovascular function in hypertension?\n\nABSTRACT:\nEndocannabinoids are novel lipid mediators with hypotensive and cardiodepressor activity. Here, we examined the possible role of the endocannabinergic system in cardiovascular regulation in hypertension. In spontaneously hypertensive rats (SHR), cannabinoid-1 receptor (CB1) antagonists increase blood pressure and left ventricular contractile performance. Conversely, preventing the degradation of the endocannabinoid anandamide by an inhibitor of fatty acid amidohydrolase reduces blood pressure, cardiac contractility, and vascular resistance to levels in normotensive rats, and these effects are prevented by CB1 antagonists. Similar changes are observed in 2 additional models of hypertension, whereas in normotensive control rats, the same parameters remain unaffected by any of these treatments. CB1 agonists lower blood pressure much more in SHR than in normotensive Wistar-Kyoto rats, and the expression of CB1 is increased in heart and aortic endothelium of SHR compared with Wistar-Kyoto rats.", "output": "{\"label\": \"yes\", \"rationale\": \"We conclude that endocannabinoids tonically suppress cardiac contractility in hypertension and that enhancing the CB1-mediated cardiodepressor and vasodilator effects of endogenous anandamide by blocking its hydrolysis can normalize blood pressure. Targeting the endocannabinoid system offers novel therapeutic strategies in the treatment of hypertension.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 15451779, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Genes regulated by Esrrb transcription factor are sensitive to Mbd3 function.\n\nCANDIDATE_PASSAGE:\nRNA sequencing identifies dysregulation of the human pancreatic islet transcriptome by the saturated fatty acid palmitate. Pancreatic β-cell dysfunction and death are central in the pathogenesis of type 2 diabetes (T2D). Saturated fatty acids cause β-cell failure and contribute to diabetes development in genetically predisposed individuals. Here we used RNA sequencing to map transcripts expressed in five palmitate-treated human islet preparations, observing 1,325 modified genes. Palmitate induced fatty acid metabolism and endoplasmic reticulum (ER) stress. Functional studies identified novel mediators of adaptive ER stress signaling. Palmitate modified genes regulating ubiquitin and proteasome function, autophagy, and apoptosis. Inhibition of autophagic flux and lysosome function contributed to lipotoxicity. Palmitate inhibited transcription factors controlling β-cell phenotype, including PAX4 and GATA6. Fifty-nine T2D candidate genes were expressed in human islets, and 11 were modified by palmitate. Palmitate modified expression of 17 splicing factors and shifted alternative splicing of 3,525 transcripts. Ingenuity Pathway Analysis of modified transcripts and genes confirmed that top changed functions related to cell death. Database for Annotation, Visualization and Integrated Discovery (DAVID) analysis of transcription factor binding sites in palmitate-modified transcripts revealed a role for PAX4, GATA, and the ER stress response regulators XBP1 and ATF6. This human islet transcriptome study identified novel mechanisms of palmitate-induced β-cell dysfunction and death. The data point to cross talk between metabolic stress and candidate genes at the β-cell level.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "456", "doc_id": "13958154", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Deregulation of HAND2 is a crucial step in endometrial carcinogenesis in mice.\n\nCANDIDATE_ABSTRACT:\nTITLE: Advantages of larval control for African malaria vectors: Low mobility and behavioural responsiveness of immature mosquito stages allow high effective coverage\nABSTRACT: Based on sensitivity analysis of the MacDonald-Ross model, it has long been argued that the best way to reduce malaria transmission is to target adult female mosquitoes with insecticides that can reduce the longevity and human-feeding frequency of vectors. However, these analyses have ignored a fundamental biological difference between mosquito adults and the immature stages that precede them: adults are highly mobile flying insects that can readily detect and avoid many intervention measures whereas mosquito eggs, larvae and pupae are confined within relatively small aquatic habitats and cannot readily escape control measures. We hypothesize that the control of adult but not immature mosquitoes is compromised by their ability to avoid interventions such as excito-repellant insecticides. We apply a simple model of intervention avoidance by mosquitoes and demonstrate that this can substantially reduce effective coverage, in terms of the proportion of the vector population that is covered, and overall impact on malaria transmission. We review historical evidence that larval control of African malaria vectors can be effective and conclude that the only limitations to the effective coverage of larval control are practical rather than fundamental. Larval control strategies against the vectors of malaria in sub-Saharan Africa could be highly effective, complementary to adult control interventions, and should be prioritized for further development, evaluation and implementation as an integral part of Rolling Back Malaria.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 335, "doc_id": "1349033", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Klf4 is important for proper myeloid cell differentiation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Kruppel-like factor 4 is essential for inflammatory monocyte differentiation in vivo.\nABSTRACT: Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types. We demonstrate in this study that hematopoietic cells from KLF4(-/-) fetal livers (FL) contained normal numbers of functional hematopoietic progenitor cells, were radioprotective, and performed as well as KLF4(+/+) cells in competitive repopulation assays. However, hematopoietic \"KLF4(-/-) chimeras\" generated by transplantation of KLF4(-/-) fetal livers cells into lethally irradiated wild-type mice completely lacked circulating inflammatory (CD115(+)Gr1(+)) monocytes, and had reduced numbers of resident (CD115(+)Gr1(-)) monocytes. Although the numbers and function of peritoneal macrophages were normal in KLF4(-/-) chimeras, bone marrow monocytic cells from KLF4(-/-) chimeras expressed lower levels of key trafficking molecules and were more apoptotic. Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes. In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells. The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 668, "doc_id": "25148216", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: COPI coatmer is involved in viral replication.\n\nCANDIDATE_ABSTRACT:\nTITLE: COPI Complex Is a Regulator of Lipid Homeostasis\nABSTRACT: Lipid droplets are ubiquitous triglyceride and sterol ester storage organelles required for energy storage homeostasis and biosynthesis. Although little is known about lipid droplet formation and regulation, it is clear that members of the PAT (perilipin, adipocyte differentiation related protein, tail interacting protein of 47 kDa) protein family coat the droplet surface and mediate interactions with lipases that remobilize the stored lipids. We identified key Drosophila candidate genes for lipid droplet regulation by RNA interference (RNAi) screening with an image segmentation-based optical read-out system, and show that these regulatory functions are conserved in the mouse. Those include the vesicle-mediated Coat Protein Complex I (COPI) transport complex, which is required for limiting lipid storage. We found that COPI components regulate the PAT protein composition at the lipid droplet surface, and promote the association of adipocyte triglyceride lipase (ATGL) with the lipid droplet surface to mediate lipolysis. Two compounds known to inhibit COPI function, Exo1 and Brefeldin A, phenocopy COPI knockdowns. Furthermore, RNAi inhibition of ATGL and simultaneous drug treatment indicate that COPI and ATGL function in the same pathway. These data indicate that the COPI complex is an evolutionarily conserved regulator of lipid homeostasis, and highlight an interaction between vesicle transport systems and lipid droplets.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 211, "doc_id": "13794374", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Surgical treatment is not superior to non-surgical in treating adults with displaced fractures of the proximal humerus.\n\nCANDIDATE_PASSAGE:\nSurgical vs nonsurgical treatment of adults with displaced fractures of the proximal humerus: the PROFHER randomized clinical trial. IMPORTANCE The need for surgery for the majority of patients with displaced proximal humeral fractures is unclear, but its use is increasing. OBJECTIVE To evaluate the clinical effectiveness of surgical vs nonsurgical treatment for adults with displaced fractures of the proximal humerus involving the surgical neck. DESIGN, SETTING, AND PARTICIPANTS A pragmatic, multicenter, parallel-group, randomized clinical trial, the Proximal Fracture of the Humerus Evaluation by Randomization (PROFHER) trial, recruited 250 patients aged 16 years or older (mean age, 66 years [range, 24-92 years]; 192 [77%] were female; and 249 [99.6%] were white) who presented at the orthopedic departments of 32 acute UK National Health Service hospitals between September 2008 and April 2011 within 3 weeks after sustaining a displaced fracture of the proximal humerus involving the surgical neck. Patients were followed up for 2 years (up to April 2013) and 215 had complete follow-up data. The data for 231 patients (114 in surgical group and 117 in nonsurgical group) were included in the primary analysis. INTERVENTIONS Fracture fixation or humeral head replacement were performed by surgeons experienced in these techniques. Nonsurgical treatment was sling immobilization. Standardized outpatient and community-based rehabilitation was provided to both groups. MAIN OUTCOMES AND MEASURES Primary outcome was the Oxford Shoulder Score (range, 0-48; higher scores indicate better outcomes) assessed during a 2-year period, with assessment and data collection at 6, 12, and 24 months. Sample size was based on a minimal clinically important difference of 5 points for the O [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1115", "doc_id": "44048701", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: De novo assembly of sequence data has fewer specific contigs than unassembled sequence data.\n\nCANDIDATE_PASSAGE:\nIdentification of T6SS-dependent effector and immunity proteins by Tn-seq in Vibrio cholerae. Type VI protein secretion system (T6SS) is important for bacterial competition through contact-dependent killing of competitors. T6SS delivers effectors to neighboring cells and corresponding antagonistic proteins confer immunity against effectors that are delivered by sister cells. Although T6SS has been found in more than 100 gram-negative bacteria including many important human pathogens, few T6SS-dependent effector and immunity proteins have been experimentally determined. Here we report a high-throughput approach using transposon mutagenesis and deep sequencing (Tn-seq) to identify T6SS immunity proteins in Vibrio cholerae. Saturating transposon mutagenesis was performed in wild type and a T6SS null mutant. Genes encoding immunity proteins were predicted to be essential in the wild type but dispensable in the T6SS mutant. By comparing the relative abundance of each transposon mutant in the mutant library using deep sequencing, we identified three immunity proteins that render protection against killing by T6SS predatory cells. We also identified their three cognate T6SS-secreted effectors and show these are important for not only antibacterial and antieukaryotic activities but also assembly of T6SS apparatus. The lipase and muramidase T6SS effectors identified in this study underscore the diversity of T6SS-secreted substrates and the distinctly different mechanisms that target these for secretion by the dynamic T6SS organelle.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "310", "doc_id": "22632303", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Diminished ovarian reserve is a reliable indicator of infertility in a non-infertile population.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\nABSTRACT: Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential. Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age. Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area. Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH. Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle). Conception was defined as a positive pregnancy test result. Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis. After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively). Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cy [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 349, "doc_id": "13497630", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Hypothalamic glutamate neurotransmission is crucial to energy balance.\n\nCANDIDATE_PASSAGE:\nDefining early lineage specification of human embryonic stem cells by the orchestrated balance of canonical Wnt/beta-catenin, Activin/Nodal and BMP signaling. The canonical Wnt/beta-catenin signaling has remarkably diverse roles in embryonic development, stem cell self-renewal and cancer progression. Here, we show that stabilized expression of beta-catenin perturbed human embryonic stem (hES)-cell self-renewal, such that up to 80% of the hES cells developed into the primitive streak (PS)/mesoderm progenitors, reminiscent of early mammalian embryogenesis. The formation of the PS/mesoderm progenitors essentially depended on the cooperative action of beta-catenin together with Activin/Nodal and BMP signaling pathways. Intriguingly, blockade of BMP signaling completely abolished mesoderm generation, and induced a cell fate change towards the anterior PS progenitors. The PI3-kinase/Akt, but not MAPK, signaling pathway had a crucial role in the anterior PS specification, at least in part, by enhancing beta-catenin stability. In addition, Activin/Nodal and Wnt/beta-catenin signaling synergistically induced the generation and specification of the anterior PS/endoderm. Taken together, our findings clearly demonstrate that the orchestrated balance of Activin/Nodal and BMP signaling defines the cell fate of the nascent PS induced by canonical Wnt/beta-catenin signaling in hES cells.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "540", "doc_id": "43661837", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Auditory entrainment is strengthened when people see congruent visual and auditory information.\n\nCANDIDATE_PASSAGE:\np53 induces formation of NEAT1 lncRNA-containing paraspeckles that modulate replication stress response and chemosensitivity In a search for mediators of the p53 tumor suppressor pathway, which induces pleiotropic and often antagonistic cellular responses, we identified the long noncoding RNA (lncRNA) NEAT1. NEAT1 is an essential architectural component of paraspeckle nuclear bodies, whose pathophysiological relevance remains unclear. Activation of p53, pharmacologically or by oncogene-induced replication stress, stimulated the formation of paraspeckles in mouse and human cells. Silencing Neat1 expression in mice, which prevents paraspeckle formation, sensitized preneoplastic cells to DNA-damage-induced cell death and impaired skin tumorigenesis. We provide mechanistic evidence that NEAT1 promotes ATR signaling in response to replication stress and is thereby engaged in a negative feedback loop that attenuates oncogene-dependent activation of p53. NEAT1 targeting in established human cancer cell lines induced synthetic lethality with genotoxic chemotherapeutics, including PARP inhibitors, and nongenotoxic activation of p53. This study establishes a key genetic link between NEAT1 paraspeckles, p53 biology and tumorigenesis and identifies NEAT1 as a promising target to enhance sensitivity of cancer cells to both chemotherapy and p53 reactivation therapy.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "141", "doc_id": "21521236", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Stroke patients with prior use of direct oral anticoagulants have a higher risk of in-hospital mortality than stroke patients with prior use of warfarin.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association of Intracerebral Hemorrhage Among Patients Taking Non–Vitamin K Antagonist vs Vitamin K Antagonist Oral Anticoagulants With In-Hospital Mortality\nABSTRACT: Importance Although non–vitamin K antagonist oral anticoagulants (NOACs) are increasingly used to prevent thromboembolic disease, there are limited data on NOAC-related intracerebral hemorrhage (ICH). Objective To assess the association between preceding oral anticoagulant use (warfarin, NOACs, and no oral anticoagulants [OACs]) and in-hospital mortality among patients with ICH. Design, Setting, and Participants Retrospective cohort study of 141 311 patients with ICH admitted from October 2013 to December 2016 to 1662 Get With The Guidelines–Stroke hospitals. Exposures Anticoagulation therapy before ICH, defined as any use of OACs within 7 days prior to hospital arrival. Main Outcomes and Measures In-hospital mortality. Results Among 141 311 patients with ICH (mean [SD] age, 68.3 [15.3] years; 48.1% women), 15 036 (10.6%) were taking warfarin and 4918 (3.5%) were taking NOACs preceding ICH, and 39 585 (28.0%) and 5783 (4.1%) were taking concomitant single and dual antiplatelet agents, respectively. Patients with prior use of warfarin or NOACs were older and had higher prevalence of atrial fibrillation and prior stroke. Acute ICH stroke severity (measured by the National Institutes of Health Stroke Scale) was not significantly different across the 3 groups (median, 9 [interquartile range, 2-21] for warfarin, 8 [2-20] for NOACs, and 8 [2-19] for no OACs). The unadjusted in-hospital mortality rates were 32.6% for warfarin, 26.5% for NOACs, and 22.5% for no OACs. Compared with patients without prior use of OACs, the risk of in-hospital mortality was higher among patients with prior use of warfarin (adjusted risk difference [ARD], 9.0% [97.5% CI, 7.9% to 10.1%]; adjusted odds ratio [AOR], 1.62 [97.5% CI, 1.53 to 1.71]) and higher among patients with prior use of [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Compared with patients with prior use of warfarin, patients with prior use of NOACs had a lower risk of in-hospital mortality (ARD, −5.7% [97.5% CI, −7.3% to −4.2%]; AOR, 0.75 [97.5% CI, 0.69 to 0.81]).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1103, "doc_id": "3898784", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Klf4 is important for proper myeloid cell differentiation.\n\nCANDIDATE_PASSAGE:\nKruppel-like factor 4 is essential for inflammatory monocyte differentiation in vivo. Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types. We demonstrate in this study that hematopoietic cells from KLF4(-/-) fetal livers (FL) contained normal numbers of functional hematopoietic progenitor cells, were radioprotective, and performed as well as KLF4(+/+) cells in competitive repopulation assays. However, hematopoietic \"KLF4(-/-) chimeras\" generated by transplantation of KLF4(-/-) fetal livers cells into lethally irradiated wild-type mice completely lacked circulating inflammatory (CD115(+)Gr1(+)) monocytes, and had reduced numbers of resident (CD115(+)Gr1(-)) monocytes. Although the numbers and function of peritoneal macrophages were normal in KLF4(-/-) chimeras, bone marrow monocytic cells from KLF4(-/-) chimeras expressed lower levels of key trafficking molecules and were more apoptotic. Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes. In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells. The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiat [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "668", "doc_id": "25148216", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Pure neural progenitor cell (NPC) populations can only be obtained from cell cultures that undergo passaging, filtration, or other isolation and cell sorting methods.\n\nCANDIDATE_PASSAGE:\nNiche-Independent Symmetrical Self-Renewal of a Mammalian Tissue Stem Cell Pluripotent mouse embryonic stem (ES) cells multiply in simple monoculture by symmetrical divisions. In vivo, however, stem cells are generally thought to depend on specialised cellular microenvironments and to undergo predominantly asymmetric divisions. Ex vivo expansion of pure populations of tissue stem cells has proven elusive. Neural progenitor cells are propagated in combination with differentiating progeny in floating clusters called neurospheres. The proportion of stem cells in neurospheres is low, however, and they cannot be directly observed or interrogated. Here we demonstrate that the complex neurosphere environment is dispensable for stem cell maintenance, and that the combination of fibroblast growth factor 2 (FGF-2) and epidermal growth factor (EGF) is sufficient for derivation and continuous expansion by symmetrical division of pure cultures of neural stem (NS) cells. NS cells were derived first from mouse ES cells. Neural lineage induction was followed by growth factor addition in basal culture media. In the presence of only EGF and FGF-2, resulting NS cells proliferate continuously, are diploid, and clonogenic. After prolonged expansion, they remain able to differentiate efficiently into neurons and astrocytes in vitro and upon transplantation into the adult brain. Colonies generated from single NS cells all produce neurons upon growth factor withdrawal. NS cells uniformly express morphological, cell biological, and molecular features of radial glia, developmental precursors of neurons and glia. Consistent with this profile, adherent NS cell lines can readily be established from foetal mouse brain. Similar NS cells can be generated from human ES cells and human foeta [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "989", "doc_id": "9988425", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Algerian physicians constitue the largest component of sub-Saharan Africa-trained physicians in the United States.\n\nCANDIDATE_PASSAGE:\nPhysician Emigration from Sub-Saharan Africa to the United States: Analysis of the 2011 AMA Physician Masterfile BACKGROUND The large-scale emigration of physicians from sub-Saharan Africa (SSA) to high-income nations is a serious development concern. Our objective was to determine current emigration trends of SSA physicians found in the physician workforce of the United States. METHODS AND FINDINGS We analyzed physician data from the World Health Organization (WHO) Global Health Workforce Statistics along with graduation and residency data from the 2011 American Medical Association Physician Masterfile (AMA-PM) on physicians trained or born in SSA countries who currently practice in the US. We estimated emigration proportions, year of US entry, years of practice before emigration, and length of time in the US. According to the 2011 AMA-PM, 10,819 physicians were born or trained in 28 SSA countries. Sixty-eight percent (n = 7,370) were SSA-trained, 20% (n = 2,126) were US-trained, and 12% (n = 1,323) were trained outside both SSA and the US. We estimated active physicians (age ≤ 70 years) to represent 96% (n = 10,377) of the total. Migration trends among SSA-trained physicians increased from 2002 to 2011 for all but one principal source country; the exception was South Africa whose physician migration to the US decreased by 8% (-156). The increase in last-decade migration was >50% in Nigeria (+1,113) and Ghana (+243), >100% in Ethiopia (+274), and >200% (+244) in Sudan. Liberia was the most affected by migration to the US with 77% (n = 175) of its estimated physicians in the 2011 AMA-PM. On average, SSA-trained physicians have been in the US for 18 years. They practiced for 6.5 years before US entry, and nearly half emigrated during the implementation years [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "96", "doc_id": "14500725", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Rhythmic expression of Cry1 translates directly into a circadian regulation of cAMP signaling in gluconeogenesis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Hyaluronan impairs vascular function and drug delivery in a mouse model of pancreatic cancer\nABSTRACT: OBJECTIVE Pancreatic ductal adenocarcinoma (PDA) is characterised by stromal desmoplasia and vascular dysfunction, which critically impair drug delivery. This study examines the role of an abundant extracellular matrix component, the megadalton glycosaminoglycan hyaluronan (HA), as a novel therapeutic target in PDA. METHODS Using a genetically engineered mouse model of PDA, the authors enzymatically depleted HA by a clinically formulated PEGylated human recombinant PH20 hyaluronidase (PEGPH20) and examined tumour perfusion, vascular permeability and drug delivery. The preclinical utility of PEGPH20 in combination with gemcitabine was assessed by short-term and survival studies. RESULTS PEGPH20 rapidly and sustainably depleted HA, inducing the re-expansion of PDA blood vessels and increasing the intratumoral delivery of two chemotherapeutic agents, doxorubicin and gemcitabine. Moreover, PEGPH20 triggered fenestrations and interendothelial junctional gaps in PDA tumour endothelia and promoted a tumour-specific increase in macromolecular permeability. Finally, combination therapy with PEGPH20 and gemcitabine led to inhibition of PDA tumour growth and prolonged survival over gemcitabine monotherapy, suggesting immediate clinical utility. CONCLUSIONS The authors demonstrate that HA impedes the intratumoral vasculature in PDA and propose that its enzymatic depletion be explored as a means to improve drug delivery and response in patients with pancreatic cancer.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1044, "doc_id": "2565138", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Birth-weight is negatively associated with breast cancer.\n\nCANDIDATE_PASSAGE:\nMammographic density, plasma vitamin D levels and risk of breast cancer in postmenopausal women. Mammographic density is a strong risk factor for breast cancer, but the underlying biology for this association is unknown. Studies suggest that vitamin D may reduce breast cancer risk and dietary vitamin D intake has been associated with reduced breast density. We conducted a case-control study nested within the Nurses' Health Study cohort consisting of 463 and 497 postmenopausal cases and controls, respectively. We examined the association between mammographic density and plasma levels of 25-hydroxyvitamin D [25(OH)D] and 1,25-dihydroxyvitamin D [1,25(OH)(2)D]. We assessed whether plasma vitamin D metabolites modify the association between breast density and breast cancer. Percent mammographic density was measured from digitized film mammograms. Generalized linear models were used to determine mean percent breast density per quartile of vitamin D metabolite. Logistic regression models were used to calculate relative risks and confidence intervals. All models were adjusted for matching variables and potential confounders. We found no cross-sectional association between circulating levels of 25(OH)D or 1,25(OH)(2)D with mammographic density. Women in the highest tertile of mammographic density and lowest tertile of plasma 25(OH)D had 4 times greater risk of breast cancer than women with the lowest mammographic density and highest plasma 25(OH)D levels (RR = 3.8; 95% CI: 2.0-7.3). The overall interaction between mammographic density and plasma 25(OH)D was nonsignificant (p-het = 0.20). These results indicate that the association between mammographic density and breast cancer is independent of plasma vitamin D metabolites in postmenopausal women. Further research e [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "178", "doc_id": "38551172", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Nanoparticles can be targeted against specific cell types by incorporating aptamers into lipid nanoparticles.\n\nCANDIDATE_PASSAGE:\nA mathematical investigation of the effects of inhibitor therapy on three putative phosphorylation cascades governing the two-component system of the agr operon. Two-component systems (TCSs) are widely employed by bacteria to sense specific external signals and conduct an appropriate response via a phosphorylation cascade within the cell. The TCS of the agr operon in the bacterium Staphylococcus aureus forms part of a regulatory process termed quorum sensing, a cell-to-cell communication mechanism used to assess population density. Since S. aureus manipulates this \"knowledge\" in order to co-ordinate production of its armoury of exotoxin virulence factors required to promote infection, it is important to understand fully how this process works. We present three models of the agr operon, each incorporating a different phosphorylation cascade for the TCS since the precise nature of the cascade is not fully understood. Using numerical and asymptotic techniques we examine the effects of inhibitor therapy, a novel approach to controlling bacterial infection through the attenuation of virulence, on each of these three cascades. We present results which, if evaluated against appropriate experimental data, provide insights into the potential effectiveness of such therapy. Moreover, the TCS models presented here are of broad relevance given that TCSs are widely conserved throughout the bacterial kingdom.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "839", "doc_id": "31844040", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Microcin J25 inhibits nucleoside triphosphate (NTP) binding.\n\nCANDIDATE_PASSAGE:\nDual Regulation of miRNA Biogenesis Generates Target Specificity in Neurotrophin-Induced Protein Synthesis Control of translation is a fundamental source of regulation in gene expression. The induction of protein synthesis by brain-derived neurotrophic factor (BDNF) critically contributes to enduring modifications of synaptic function, but how BDNF selectively affects only a minority of expressed mRNAs is poorly understood. We report that BDNF rapidly elevates Dicer, increasing mature miRNA levels and inducing RNA processing bodies in neurons. BDNF also rapidly induces Lin28, causing selective loss of Lin28-regulated miRNAs and a corresponding upregulation in translation of their target mRNAs. Binding sites for Lin28-regulated miRNAs are necessary and sufficient to confer BDNF responsiveness to a transcript. Lin28 deficiency, or expression of a Lin28-resistant Let-7 precursor miRNA, inhibits BDNF translation specificity and BDNF-dependent dendrite arborization. Our data establish that specificity in BDNF-regulated translation depends upon a two-part posttranscriptional control of miRNA biogenesis that generally enhances mRNA repression in association with GW182 while selectively derepressing and increasing translation of specific mRNAs.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "788", "doc_id": "15590539", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: DUSP4 downregulation deactivates the Ras-ERK pathway\n\nCANDIDATE_ABSTRACT:\nTITLE: Alcohol Sales and Risk of Serious Assault\nABSTRACT: BACKGROUND Alcohol is a contributing cause of unintentional injuries, such as motor vehicle crashes. Prior research on the association between alcohol use and violent injury was limited to survey-based data, and the inclusion of cases from a single trauma centre, without adequate controls. Beyond these limitations was the inability of prior researchers to comprehensively capture most alcohol sales. In Ontario, most alcohol is sold through retail outlets run by the provincial government, and hospitals are financed under a provincial health care system. We assessed the risk of being hospitalized due to assault in association with retail alcohol sales across Ontario. METHODS AND FINDINGS We performed a population-based case-crossover analysis of all persons aged 13 years and older hospitalized for assault in Ontario from 1 April 2002 to 1 December 2004. On the day prior to each assault case's hospitalization, the volume of alcohol sold at the store in closest proximity to the victim's home was compared to the volume of alcohol sold at the same store 7 d earlier. Conditional logistic regression analysis was used to determine the associated relative risk (RR) of assault per 1,000 l higher daily sales of alcohol. Of the 3,212 persons admitted to hospital for assault, nearly 25% were between the ages of 13 and 20 y, and 83% were male. A total of 1,150 assaults (36%) involved the use of a sharp or blunt weapon, and 1,532 (48%) arose during an unarmed brawl or fight. For every 1,000 l more of alcohol sold per store per day, the relative risk of being hospitalized for assault was 1.13 (95% confidence interval [CI] 1.02-1.26). The risk was accentuated for males (1.18, 95% CI 1.05-1.33), youth aged 13 to 20 y (1.21, 95% CI 0.99-1.46), and those in urban areas (1.19, 95% [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 308, "doc_id": "980196", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Cost effectiveness evaluations based on cRCT data accurately reflect prices for patients in actual clinical practice.\n\nCANDIDATE_PASSAGE:\nA Comparison of Cost Effectiveness Using Data from Randomized Trials or Actual Clinical Practice: Selective Cox-2 Inhibitors as an Example BACKGROUND Data on absolute risks of outcomes and patterns of drug use in cost-effectiveness analyses are often based on randomised clinical trials (RCTs). The objective of this study was to evaluate the external validity of published cost-effectiveness studies by comparing the data used in these studies (typically based on RCTs) to observational data from actual clinical practice. Selective Cox-2 inhibitors (coxibs) were used as an example. METHODS AND FINDINGS The UK General Practice Research Database (GPRD) was used to estimate the exposure characteristics and individual probabilities of upper gastrointestinal (GI) events during current exposure to nonsteroidal anti-inflammatory drugs (NSAIDs) or coxibs. A basic cost-effectiveness model was developed evaluating two alternative strategies: prescription of a conventional NSAID or coxib. Outcomes included upper GI events as recorded in GPRD and hospitalisation for upper GI events recorded in the national registry of hospitalisations (Hospital Episode Statistics) linked to GPRD. Prescription costs were based on the prescribed number of tables as recorded in GPRD and the 2006 cost data from the British National Formulary. The study population included over 1 million patients prescribed conventional NSAIDs or coxibs. Only a minority of patients used the drugs long-term and daily (34.5% of conventional NSAIDs and 44.2% of coxibs), whereas coxib RCTs required daily use for at least 6-9 months. The mean cost of preventing one upper GI event as recorded in GPRD was US$104k (ranging from US$64k with long-term daily use to US$182k with intermittent use) and US$298k for hospitaliza [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "290", "doc_id": "15048300", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: mTORC2 regulates intracellular cysteine levels through xCT inhibition.\n\nCANDIDATE_ABSTRACT:\nTITLE: mTORC2 Regulates Amino Acid Metabolism in Cancer by Phosphorylation of the Cystine-Glutamate Antiporter xCT.\nABSTRACT: Mutations in cancer reprogram amino acid metabolism to drive tumor growth, but the molecular mechanisms are not well understood. Using an unbiased proteomic screen, we identified mTORC2 as a critical regulator of amino acid metabolism in cancer via phosphorylation of the cystine-glutamate antiporter xCT. mTORC2 phosphorylates serine 26 at the cytosolic N terminus of xCT, inhibiting its activity. Genetic inhibition of mTORC2, or pharmacologic inhibition of the mammalian target of rapamycin (mTOR) kinase, promotes glutamate secretion, cystine uptake, and incorporation into glutathione, linking growth factor receptor signaling with amino acid uptake and utilization. These results identify an unanticipated mechanism regulating amino acid metabolism in cancer, enabling tumor cells to adapt to changing environmental conditions.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"mTORC2 phosphorylates serine 26 at the cytosolic N terminus of xCT, inhibiting its activity. Genetic inhibition of mTORC2, or pharmacologic inhibition of the mammalian target of rapamycin (mTOR) kinase, promotes glutamate secretion, cystine uptake, and incorporation into glutathione, linking growth factor receptor signaling with amino acid uptake and utilization.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1389, "doc_id": "23895668", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: N-terminal cleavage reduces success identifying transcription start sites.\n\nCANDIDATE_ABSTRACT:\nTITLE: Identification and Functional Characterization of N-Terminally Acetylated Proteins in Drosophila melanogaster\nABSTRACT: Protein modifications play a major role for most biological processes in living organisms. Amino-terminal acetylation of proteins is a common modification found throughout the tree of life: the N-terminus of a nascent polypeptide chain becomes co-translationally acetylated, often after the removal of the initiating methionine residue. While the enzymes and protein complexes involved in these processes have been extensively studied, only little is known about the biological function of such N-terminal modification events. To identify common principles of N-terminal acetylation, we analyzed the amino-terminal peptides from proteins extracted from Drosophila Kc167 cells. We detected more than 1,200 mature protein N-termini and could show that N-terminal acetylation occurs in insects with a similar frequency as in humans. As the sole true determinant for N-terminal acetylation we could extract the (X)PX rule that indicates the prevention of acetylation under all circumstances. We could show that this rule can be used to genetically engineer a protein to study the biological relevance of the presence or absence of an acetyl group, thereby generating a generic assay to probe the functional importance of N-terminal acetylation. We applied the assay by expressing mutated proteins as transgenes in cell lines and in flies. Here, we present a straightforward strategy to systematically study the functional relevance of N-terminal acetylations in cells and whole organisms. Since the (X)PX rule seems to be of general validity in lower as well as higher eukaryotes, we propose that it can be used to study the function of N-terminal acetylation in all species.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 821, "doc_id": "8646760", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Omnivores produce more trimethylamine N-oxide from dietary I-carnitine than vegetarians.\n\nCANDIDATE_PASSAGE:\nIntestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis Intestinal microbiota metabolism of choline and phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO). We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice. Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism. The presence of specific bacterial taxa in human feces was associated with both plasma TMAO concentration and dietary status. Plasma L-carnitine levels in subjects undergoing cardiac evaluation (n = 2,595) predicted increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels. Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed. In mice with an intact intestinal microbiota, dietary supplementation with TMAO or either carnitine or choline reduced in vivo reverse cholesterol transport. Intestinal microbiota may thus contribute to the well-established link between high levels of red meat consumption and CVD risk.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "884", "doc_id": "14803797", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Ly6C hi monocytes have a lower inflammatory capacity than Ly6C lo monocytes.\n\nCANDIDATE_PASSAGE:\nSubpopulations of mouse blood monocytes differ in maturation stage and inflammatory response. Blood monocytes are well-characterized precursors for macrophages and dendritic cells. Subsets of human monocytes with differential representation in various disease states are well known. In contrast, mouse monocyte subsets have been characterized minimally. In this study we identify three subpopulations of mouse monocytes that can be distinguished by differential expression of Ly-6C, CD43, CD11c, MBR, and CD62L. The subsets share the characteristics of extensive phagocytosis, similar expression of M-CSF receptor (CD115), and development into macrophages upon M-CSF stimulation. By eliminating blood monocytes with dichloromethylene-bisphosphonate-loaded liposomes and monitoring their repopulation, we showed a developmental relationship between the subsets. Monocytes were maximally depleted 18 h after liposome application and subsequently reappeared in the circulation. These cells were exclusively of the Ly-6C(high) subset, resembling bone marrow monocytes. Serial flow cytometric analyses of newly released Ly-6C(high) monocytes showed that Ly-6C expression on these cells was down-regulated while in circulation. Under inflammatory conditions elicited either by acute infection with Listeria monocytogenes or chronic infection with Leishmania major, there was a significant increase in immature Ly-6C(high) monocytes, resembling the inflammatory left shift of granulocytes. In addition, acute peritoneal inflammation recruited preferentially Ly-6C(med-high) monocytes. Taken together, these data identify distinct subpopulations of mouse blood monocytes that differ in maturation stage and capacity to become recruited to inflammatory sites.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "728", "doc_id": "36444198", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: B cells go though plasmablast differentiation and antibody production by continuous expression of EBI2.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cost-effectiveness of 10-Year Risk Thresholds for Initiation of Statin Therapy for Primary Prevention of Cardiovascular Disease.\nABSTRACT: IMPORTANCE The American College of Cardiology and the American Heart Association (ACC/AHA) cholesterol treatment guidelines have wide-scale implications for treating adults without history of atherosclerotic cardiovascular disease (ASCVD) with statins. OBJECTIVE To estimate the cost-effectiveness of various 10-year ASCVD risk thresholds that could be used in the ACC/AHA cholesterol treatment guidelines. DESIGN, SETTING, AND PARTICIPANTS Microsimulation model, including lifetime time horizon, US societal perspective, 3% discount rate for costs, and health outcomes. In the model, hypothetical individuals from a representative US population aged 40 to 75 years received statin treatment, experienced ASCVD events, and died from ASCVD-related or non-ASCVD-related causes based on ASCVD natural history and statin treatment parameters. Data sources for model parameters included National Health and Nutrition Examination Surveys, large clinical trials and meta-analyses for statin benefits and treatment, and other published sources. MAIN OUTCOMES AND MEASURES Estimated ASCVD events prevented and incremental costs per quality-adjusted life-year (QALY) gained. RESULTS In the base-case scenario, the current ASCVD threshold of 7.5% or higher, which was estimated to be associated with 48% of adults treated with statins, had an incremental cost-effectiveness ratio (ICER) of $37,000/QALY compared with a 10% or higher threshold. More lenient ASCVD thresholds of 4.0% or higher (61% of adults treated) and 3.0% or higher (67% of adults treated) had ICERs of $81,000/QALY and $140,000/QALY, respectively. Shifting from a 7.5% or higher ASCVD risk threshold to a 3.0% or higher ASCVD risk threshold was estimated to be associated with an additional 161,560 cardiovascular disease events [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 152, "doc_id": "1287809", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Hyperfibrinogenemia decreases rates of femoropopliteal bypass thrombosis.\n\nCANDIDATE_PASSAGE:\nSputum inflammation predicts exacerbations after cessation of inhaled corticosteroids in COPD. INTRODUCTION The GOLD guidelines advocate not to institute inhaled corticosteroids (ICS) in patients with mild-to-moderate COPD. However, many patients do use ICS and in some patients, withdrawal is associated with deteriorating lung function and increased exacerbation rates. Unfortunately, physicians do not know in which patients they can stop ICS treatment safely. AIM To identify predictors of COPD exacerbations after ICS withdrawal. METHODS During ICS treatment, post-bronchodilator spirometry, body plethysmography, and health status assessment were performed in 68 COPD patients using ICS. Additionally, sputum cell differentials, supernatant leukotriene B(4), eosinophilic cationic protein, and myeloperoxidase, serum C-reactive protein and soluble intracellular adhesion molecule, and urinary desmosine were assessed. Sputum was also analysed for mRNA levels of haemoxygenase-1, tumour necrosis factor-α, RANTES, interleukin 5(IL-5), IL-10, IL-12, IL-13, transforming growth factor-β, and interferon-γ. STATISTICS Cox regression analyses were performed using time to exacerbation as outcome variable to identify significant hazards for a COPD exacerbation after ICS withdrawal. RESULTS Higher sputum % eosinophils, higher sputum MPO/neutrophil level, longer duration of COPD symptoms, <40 packyears smoking, and ICS withdrawal in November, December or January were significant hazards (all p<0.05) for experiencing a COPD exacerbation after ICS withdrawal in a monovariate model. In a multivariate model, all factors proved independent predictors except for sputum MPO/neutrophil level. CONCLUSIONS Decisions on whether or not inhaled corticosteroids can be safely withdrawn in mild [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "532", "doc_id": "25319221", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Incidence of 10/66 dementia is higher than the incidence of DSM-IV dementia.\n\nCANDIDATE_ABSTRACT:\nTITLE: Rapamycin passes the torch: a new generation of mTOR inhibitors\nABSTRACT: Mammalian target of rapamycin (mTOR) is an atypical protein kinase that controls growth and metabolism in response to nutrients, growth factors and cellular energy levels, and it is frequently dysregulated in cancer and metabolic disorders. Rapamycin is an allosteric inhibitor of mTOR, and was approved as an immuno-suppressant in 1999. In recent years, interest has focused on its potential as an anticancer drug. However, the performance of rapamycin and its analogues (rapalogues) has been undistinguished despite isolated successes in subsets of cancer, suggesting that the full therapeutic potential of targeting mTOR has yet to be exploited. A new generation of ATP-competitive inhibitors that directly target the mTOR catalytic site display potent and comprehensive mTOR inhibition and are in early clinical trials.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 591, "doc_id": "1227277", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Charcoal is an effective treatment for acute paraquat poisoning.\n\nCANDIDATE_PASSAGE:\nFailure of continuous venovenous hemofiltration to prevent death in paraquat poisoning. Paraquat poisoning is characterized by multiorgan failure and pulmonary fibrosis with respiratory failure. Multiorgan failure with circulatory collapse is a major cause of early death within 3 days of paraquat ingestion. Recent studies suggested that continuous venovenous hemofiltration (CVVH) had a role in the treatment of multiorgan failure by promoting hemodynamic stability. We therefore evaluated the effect of prophylactic CVVH in 80 patients with paraquat poisoning (August 1996 to February 1999). The amount ingested was 2.1 +/- 1.0 mouthfuls (as 20% concentrate). All patients were treated with hemoperfusion (HP; duration, 6.4 +/- 3.0 hours) within 24 hours of ingestion and then randomly assigned to the HP-alone or HP-CVVH group. Forty-four patients underwent HP only, and 36 patients underwent CVVH (duration, 57.4 +/- 31.3 hours; ultrafiltration volume, 40.2 +/- 4.8 L/d) after HP. Although time to death after ingestion was significantly longer in the HP-CVVH than HP group (5.0 +/- 5.0 versus 2.5 +/- 2.1 days; P < 0.05), there was no difference in mortality rates between the two groups (66.7% versus 63.6%; P = 0.82). In the HP group, early circulatory collapse was a major cause of death compared with the HP-CVVH group, in which late respiratory failure was a major cause of death. In conclusion, prophylactic CVVH after HP prevented early death caused by circulatory collapse and prolonged survival time. However, it could not prevent late death caused by respiratory failure and did not provide a survival benefit in acute paraquat poisoning.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "245", "doc_id": "24097933", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Decreased diastolic blood pressure (DBP) is associated with abdominal aortic aneurysm.\n\nCANDIDATE_ABSTRACT:\nTITLE: Blood pressure and incidence of twelve cardiovascular diseases: lifetime risks, healthy life-years lost, and age-specific associations in 1·25 million people\nABSTRACT: BACKGROUND The associations of blood pressure with the different manifestations of incident cardiovascular disease in a contemporary population have not been compared. In this study, we aimed to analyse the associations of blood pressure with 12 different presentations of cardiovascular disease. METHODS We used linked electronic health records from 1997 to 2010 in the CALIBER (CArdiovascular research using LInked Bespoke studies and Electronic health Records) programme to assemble a cohort of 1·25 million patients, 30 years of age or older and initially free from cardiovascular disease, a fifth of whom received blood pressure-lowering treatments. We studied the heterogeneity in the age-specific associations of clinically measured blood pressure with 12 acute and chronic cardiovascular diseases, and estimated the lifetime risks (up to 95 years of age) and cardiovascular disease-free life-years lost adjusted for other risk factors at index ages 30, 60, and 80 years. This study is registered at ClinicalTrials.gov, number NCT01164371. FINDINGS During 5·2 years median follow-up, we recorded 83,098 initial cardiovascular disease presentations. In each age group, the lowest risk for cardiovascular disease was in people with systolic blood pressure of 90-114 mm Hg and diastolic blood pressure of 60-74 mm Hg, with no evidence of a J-shaped increased risk at lower blood pressures. The effect of high blood pressure varied by cardiovascular disease endpoint, from strongly positive to no effect. Associations with high systolic blood pressure were strongest for intracerebral haemorrhage (hazard ratio 1·44 [95% CI 1·32-1·58]), subarachnoid haemorrhage (1·43 [1·25-1·63]), and stable angina (1·41 [1·36-1·46]), and weakest for abdominal aortic aneurysm (1·08 [1·00-1·17]). Com [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Compared with diastolic blood pressure, raised systolic blood pressure had a greater effect on angina, myocardial infarction, and peripheral arterial disease, whereas raised diastolic blood pressure had a greater effect on abdominal aortic aneurysm than did raised systolic pressure.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 317, "doc_id": "4506414", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Monoclonal antibody targeting of N-cadherin encourages castration resistance.\n\nCANDIDATE_ABSTRACT:\nTITLE: Monoclonal antibody targeting of N-cadherin inhibits prostate cancer growth, metastasis and castration resistance\nABSTRACT: The transition from androgen-dependent to castration-resistant prostate cancer (CRPC) is a lethal event of uncertain molecular etiology. Comparing gene expression in isogenic androgen-dependent and CRPC xenografts, we found a reproducible increase in N-cadherin expression, which was also elevated in primary and metastatic tumors of individuals with CRPC. Ectopic expression of N-cadherin in nonmetastatic, androgen-dependent prostate cancer models caused castration resistance, invasion and metastasis. Monoclonal antibodies against the ectodomain of N-cadherin reduced proliferation, adhesion and invasion of prostate cancer cells in vitro. In vivo, these antibodies slowed the growth of multiple established CRPC xenografts, blocked local invasion and metastasis and, at higher doses, led to complete regression. N-cadherin–specific antibodies markedly delayed the time to emergence of castration resistance, markedly affected tumor histology and angiogenesis, and reduced both AKT serine-threonine kinase activity and serum interleukin-8 (IL-8) secretion. These data indicate that N-cadherin is a major cause of both prostate cancer metastasis and castration resistance. Therapeutic targeting of this factor with monoclonal antibodies may have considerable clinical benefit.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"N-cadherin–specific antibodies markedly delayed the time to emergence of castration resistance, markedly affected tumor histology and angiogenesis, and reduced both AKT serine-threonine kinase activity and serum interleukin-8 (IL-8) secretion.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 801, "doc_id": "22180793", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Pre-mRNAs associated with spliceosomal components are more stable than unassociated splicing substrates.\n\nCANDIDATE_PASSAGE:\nCryo-EM structures of Tau filaments from Alzheimer’s disease brain Alzheimer's disease is the most common neurodegenerative disease, and there are no mechanism-based therapies. The disease is defined by the presence of abundant neurofibrillary lesions and neuritic plaques in the cerebral cortex. Neurofibrillary lesions comprise paired helical and straight tau filaments, whereas tau filaments with different morphologies characterize other neurodegenerative diseases. No high-resolution structures of tau filaments are available. Here we present cryo-electron microscopy (cryo-EM) maps at 3.4-3.5 Å resolution and corresponding atomic models of paired helical and straight filaments from the brain of an individual with Alzheimer's disease. Filament cores are made of two identical protofilaments comprising residues 306-378 of tau protein, which adopt a combined cross-β/β-helix structure and define the seed for tau aggregation. Paired helical and straight filaments differ in their inter-protofilament packing, showing that they are ultrastructural polymorphs. These findings demonstrate that cryo-EM allows atomic characterization of amyloid filaments from patient-derived material, and pave the way for investigation of a range of neurodegenerative diseases.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "964", "doc_id": "4446814", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Most termination events in Okazaki fragments are sequence specific.\n\nCANDIDATE_ABSTRACT:\nTITLE: Activin/Nodal signalling in stem cells.\nABSTRACT: Activin/Nodal growth factors control a broad range of biological processes, including early cell fate decisions, organogenesis and adult tissue homeostasis. Here, we provide an overview of the mechanisms by which the Activin/Nodal signalling pathway governs stem cell function in these different stages of development. We describe recent findings that associate Activin/Nodal signalling to pathological conditions, focusing on cancer stem cells in tumorigenesis and its potential as a target for therapies. Moreover, we will discuss future directions and questions that currently remain unanswered on the role of Activin/Nodal signalling in stem cell self-renewal, differentiation and proliferation.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 808, "doc_id": "226488", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does advanced qRT-PCR technology allow detection of the cholecystokinin 1 receptor ( CCK1R ) expression in human pancreas?\n\nABSTRACT:\nTo help clarify the controversy over the detection of expression of the cholecystokinin 1 receptor (CCK1R; CCKAR) in human pancreas. Applied qRT-PCR to detect CCK1R expression using the SYBR green/Smart Cycler II and the QZyme oligonucleotide/ABI PRISM 7500 systems to detect CCK1R expressed message in highly purified cDNAs from human pancreas and other tissues. Samples of normal pancreas were obtained at operation (pancreaticoduodenectomy; Whipple's procedure) and used to ascertain the expression of CCK1R in human tissue and investigate donor individual variability in expression levels by semi-quantitative RT-PCR and scanning densitometry. We present molecular evidence obtained with advanced qRT-PCR technology that clearly establishes CCK1R expression in human pancreas. Amplification variation in individual human samples is documented here. By targeting different stretches of the sequence with several primer pairs, it was observed that SYBR green qRT-PCR failed to amplify efficiently over GGA-and GAA-rich nucleotide triplet regions, leading to false negative results. The QZyme system quantified the expression with the following distribution: stomach > small intestine approximately colon > brain approximately kidney > pancreas. CCK1R expression levels varied from undetectable, to high levels of expression, in individual samples collected from surgical specimens.", "output": "{\"label\": \"yes\", \"rationale\": \"CCK1R message can be conclusively detected and quantified in human pancreas cDNA by targeting the appropriate nucleotide sequence regions of this gene.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 16258365, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Higher plasma levels of I-carnitine, when associated with trimethylamine N-oxide, are positively correlated with cardiovascular events in humans.\n\nCANDIDATE_PASSAGE:\nIntestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis Intestinal microbiota metabolism of choline and phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO). We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice. Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism. The presence of specific bacterial taxa in human feces was associated with both plasma TMAO concentration and dietary status. Plasma L-carnitine levels in subjects undergoing cardiac evaluation (n = 2,595) predicted increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels. Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed. In mice with an intact intestinal microbiota, dietary supplementation with TMAO or either carnitine or choline reduced in vivo reverse cholesterol transport. Intestinal microbiota may thus contribute to the well-established link between high levels of red meat consumption and CVD risk.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "524", "doc_id": "14803797", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The HSV-2 infection is typically asymptomatic.\n\nCANDIDATE_PASSAGE:\nViral Infection of Engrafted Human Islets Leads to Diabetes Type 1 diabetes (T1D) is characterized by the destruction of the insulin-producing β-cells of pancreatic islets. Genetic and environmental factors both contribute to T1D development. Viral infection with enteroviruses is a suspected trigger for T1D, but a causal role remains unproven and controversial. Studies in animals are problematic because of species-specific differences in host cell susceptibility and immune responses to candidate viral pathogens such as coxsackievirus B (CVB). In order to resolve the controversial role of viruses in human T1D, we developed a viral infection model in immunodeficient mice bearing human islet grafts. Hyperglycemia was induced in mice by specific ablation of native β-cells. Human islets, which are naturally susceptible to CVB infection, were transplanted to restore normoglycemia. Transplanted mice were infected with CVB4 and monitored for hyperglycemia. Forty-seven percent of CVB4-infected mice developed hyperglycemia. Human islet grafts from infected mice contained viral RNA, expressed viral protein, and had reduced insulin levels compared with grafts from uninfected mice. Human-specific gene expression profiles in grafts from infected mice revealed the induction of multiple interferon-stimulated genes. Thus, human islets can become severely dysfunctional with diminished insulin production after CVB infection of β-cells, resulting in diabetes.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1168", "doc_id": "16572581", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Artefacts in 24-h pharyngeal and oesophageal pH monitoring: is simplification of pH data analysis feasible?\n\nABSTRACT:\nAmbulatory 24-h dual-channel pharyngeal and oesophageal pH monitoring is the standard test for measuring gastro-oesophageal and gastropharyngeal reflux. Artefacts caused by the intake of food may result in falsely positive gastropharyngeal reflux, which necessitates a manual review of 24-h pH data. The purpose of the study was to investigate the influence of meals and whether leaving out meals affected the reliability of the test. Patients referred for otolaryngological complaints, suspected to have been caused by gastro-oesophageal reflux, underwent 24-h dual-channel pH monitoring. The raw unprocessed pH data were corrected by visual inspection of the 24-h tracings (corrected data), by leaving out meals or meals plus a 2-h postprandrial period. The raw pH data were substantially influenced by artefacts of food intake and pseudoreflux. Data obtained by leaving out meals agreed best with manually corrected data. Many of the falsely positive reflux episodes could be removed, thereby inducing a 9%-18% chance of undetected reflux. When examining the fraction of time supine, manually corrected data and data leaving out meals were fully concordant and detected 79% of patients with gastropharyngeal reflux. However, leaving out meals plus a 2-h postprandrial period resulted in 21%-50% falsely negative tests.", "output": "{\"label\": \"maybe\", \"rationale\": \"Leaving out the period of intake of meals and beverages from the raw pH data might be the second best test after the time-consuming visual correction with a small chance of undetected gastropharyngeal reflux. For scientific purposes and when in doubt, it remains necessary to review the computer-generated data manually to discover every gastropharyngeal reflux event.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 14992556, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Tuberculosis incidence occurs at higher rates in more sparsely populated areas in the UK.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tuberculosis mortality in England and Wales during 1982-1992: its association with poverty, ethnicity and AIDS.\nABSTRACT: This paper seeks to establish the strength of association between contemporary tuberculosis (TB) in England and Wales and several potential aetiological factors. It presents an ecological analysis of standardised annual TB mortality rates for the 403 local authority districts between 1982 and 1992, disaggregated by age and sex. Social, demographic and ethnicity measures from the 1981 and 1991 censuses and standardised annual AIDS-related mortality rates for young men are used to calculate Poisson regression models. A strong association was found between all TB mortality groups and overcrowding at the household level. For women, no other measures improved the explanatory power of the models. In multiple regressions, both poverty and AIDS-related mortality explained additional variation in the model for younger men. The link between ethnicity and tuberculosis notifications was not reflected in this analysis of mortality. For all groups no evidence of a positive relationship with ethnicity was found, once overcrowding had been accounted for. The significance of household as opposed to district level crowding suggests that prolonged contact is required for disease transmission. Regression analysis indicates that it is the overcrowding and poverty among ethnic populations that is significant for their tuberculosis mortality. The fact that the relationship between AIDS and TB is confined to the group most typical of AIDS patients provides evidence that AIDS has little influence on the level of tuberculosis mortality in the wider population. Explanations for the observed relationship include preferential certification, migration for treatment and shortcomings in health care provision.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"A strong association was found between all TB mortality groups and overcrowding at the household level.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1327, "doc_id": "22194407", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Replacement of OCT4 and SOX2 genes with GATA3 is not capable of reprogramming human cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Reprogramming of human fibroblasts to pluripotency with lineage specifiers.\nABSTRACT: Since the initial discovery that OCT4, SOX2, KLF4, and c-MYC overexpression sufficed for the induction of pluripotency in somatic cells, methodologies replacing the original factors have enhanced our understanding of the reprogramming process. However, unlike in mouse, OCT4 has not been replaced successfully during reprogramming of human cells. Here we report on a strategy to accomplish this replacement. Through a combination of transcriptome and bioinformatic analysis we have identified factors previously characterized as being lineage specifiers that are able to replace OCT4 and SOX2 in the reprogramming of human fibroblasts. Our results show that it is possible to replace OCT4 and SOX2 simultaneously with alternative lineage specifiers in the reprogramming of human cells. At a broader level, they also support a model in which counteracting lineage specification networks underlies the induction of pluripotency.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1038, "doc_id": "16287725", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Radioiodine treatment of non-toxic multinodular goitre increases thyroid volume.\n\nCANDIDATE_PASSAGE:\nRadioiodine treatment of multinodular non-toxic goitre. OBJECTIVE To investigate the long term effect of radioactive iodine on thyroid function and size in patients with non-toxic multinodular goitre. DESIGN Consecutive patients with multinodular non-toxic goitre selected for radioactive iodine treatment and followed for a minimum of 12 months (median 48 months) after an intended dose of 3.7 MBq/g thyroid tissue corrected to a 100% uptake of iodine-131 in 24 hours. PATIENTS 69 patients with a growing multinodular non-toxic goitre causing local compression symptoms or cosmetic inconveniences. The treatment was chosen because of a high operative risk, previous thyroidectomy, or refusal to be operated on. MAIN OUTCOME MEASUREMENTS Standard thyroid function variables and ultrasonically determined thyroid volume before treatment as well as 1, 2, 3, 6, and 12 months after treatment and then once a year. RESULTS 56 patients were treated with a single dose of 131I, 12 with two doses, and one with four doses. In 45 patients treated with one dose and remaining euthyroid the median thyroid volume was reduced from 73 (interquartile range 50-106) ml to 29 (23-48) ml at 24 months in the 39 patients in whom this was measured during follow up. The median reduction was 40 (22-48) ml (60% reduction, p < 0.0001), half of which occurred within three months. Patients treated with two doses as well as those developing hypothyroidism and hyperthyroidism had a significant reduction in thyroid volume. Eleven patients developed hypothyroidism (cumulative five year risk 22%, 95% confidence interval 4.8% to 38.4%). Side effects were few: three cases of hyperthyroidism and two cases of radiation thyroiditis. Only one patient was dissatisfied with the result; she was referred for operati [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1011", "doc_id": "9745001", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Elevated cell-free mitochondrial DNA levels are associated with mortality.\n\nCANDIDATE_ABSTRACT:\nTITLE: The cytidine deaminase CEM15 induces hypermutation in newly synthesized HIV-1 DNA\nABSTRACT: High mutation frequency during reverse transcription has a principal role in the genetic variation of primate lentiviral populations. It is the main driving force for the generation of drug resistance and the escape from immune surveillance. G to A hypermutation is one of the characteristics of primate lentiviruses, as well as other retroviruses, during replication in vivo and in cell culture. The molecular mechanisms of this process, however, remain to be clarified. Here, we demonstrate that CEM15 (also known as apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3G; APOBEC3G), an endogenous inhibitor of human immunodeficiency virus type 1 (HIV-1) replication, is a cytidine deaminase and is able to induce G to A hypermutation in newly synthesized viral DNA. This effect can be counteracted by the HIV-1 virion infectivity factor (Vif). It seems that this viral DNA mutator is a viral defence mechanism in host cells that may induce either lethal hypermutation or instability of the incoming nascent viral reverse transcripts, which could account for the Vif-defective phenotype. Importantly, the accumulation of CEM15-mediated non-lethal hypermutation in the replicating viral genome could potently contribute to the genetic variation of primate lentiviral populations.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 375, "doc_id": "2638387", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Articles published in open access format are more likely to be cited than traditional journals.\n\nCANDIDATE_ABSTRACT:\nTITLE: Open Access Increases Citation Rate\nABSTRACT: PLoS Biology publishes today a research article by Gunther Eysenbach that is not about biology. It is about citations. It provides robust evidence that open-access articles (OA articles) are more immediately recognized and cited than non-OA articles. As such, it adds objective support to the belief we have always held that open-access publication speeds up scientific dialog between researchers and, consequently, should be extended to the whole scientific literature as quickly as possible. It is therefore fitting that we publish such a paper. We have long argued that papers freely available in a journal will be more often read and cited than those behind a subscription barrier. However, solid evidence to support or refute such a claim has been surprisingly hard to find. Since most open-access journals are new, comparisons of the effects of open access with established subscription-based journals are easily confounded by age and reputation. In the current study, Eysenbach compared citations compiled by Thomson Scientific (formerly Thomson ISI) to individual articles published between June 2004 and December 2004 in the same journal—namely, Proceedings of the National Academy of Sciences (PNAS), which announced its open-access option for authors on June 8 of that year, with an associated publication charge of US$1,000. Non-OA articles in PNAS are subject to a six-month “toll-access” delay before the article becomes publicly available. The results of this natural experiment are clear: in the 4 to 16 months following publication, OA articles gained a significant citation advantage over non-OA articles during the same period. They are twice as likely to be cited 4 to 10 months after publication and almost three times as likely between 10 and 16 months. Given that P [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The results of this natural experiment are clear: in the 4 to 16 months following publication, OA articles gained a significant citation advantage over non-OA articles during the same period.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 130, "doc_id": "27768226", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: ART has no effect on the infectiveness of HIV-positive people.\n\nCANDIDATE_ABSTRACT:\nTITLE: HIV Treatment as Prevention: Systematic Comparison of Mathematical Models of the Potential Impact of Antiretroviral Therapy on HIV Incidence in South Africa\nABSTRACT: BACKGROUND Many mathematical models have investigated the impact of expanding access to antiretroviral therapy (ART) on new HIV infections. Comparing results and conclusions across models is challenging because models have addressed slightly different questions and have reported different outcome metrics. This study compares the predictions of several mathematical models simulating the same ART intervention programmes to determine the extent to which models agree about the epidemiological impact of expanded ART. METHODS AND FINDINGS Twelve independent mathematical models evaluated a set of standardised ART intervention scenarios in South Africa and reported a common set of outputs. Intervention scenarios systematically varied the CD4 count threshold for treatment eligibility, access to treatment, and programme retention. For a scenario in which 80% of HIV-infected individuals start treatment on average 1 y after their CD4 count drops below 350 cells/µl and 85% remain on treatment after 3 y, the models projected that HIV incidence would be 35% to 54% lower 8 y after the introduction of ART, compared to a counterfactual scenario in which there is no ART. More variation existed in the estimated long-term (38 y) reductions in incidence. The impact of optimistic interventions including immediate ART initiation varied widely across models, maintaining substantial uncertainty about the theoretical prospect for elimination of HIV from the population using ART alone over the next four decades. The number of person-years of ART per infection averted over 8 y ranged between 5.8 and 18.7. Considering the actual scale-up of ART in South Africa, seven models estimated that current HIV incidence is 17% to 32% lower than it would have been in the absence of ART. Differences [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Considering the actual scale-up of ART in South Africa, seven models estimated that current HIV incidence is 17% to 32% lower than it would have been in the absence of ART.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 60, "doc_id": "13899137", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: ERAP1 SNPs are epistatic to HLA alleles for ankylosing spondylitis.\n\nCANDIDATE_PASSAGE:\nNetting neutrophils in autoimmune small-vessel vasculitis Small-vessel vasculitis (SVV) is a chronic autoinflammatory condition linked to antineutrophil cytoplasm autoantibodies (ANCAs). Here we show that chromatin fibers, so-called neutrophil extracellular traps (NETs), are released by ANCA-stimulated neutrophils and contain the targeted autoantigens proteinase-3 (PR3) and myeloperoxidase (MPO). Deposition of NETs in inflamed kidneys and circulating MPO-DNA complexes suggest that NET formation triggers vasculitis and promotes the autoimmune response against neutrophil components in individuals with SVV.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "366", "doc_id": "17741440", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Bariatric surgery has a positive impact on mental health.\n\nCANDIDATE_PASSAGE:\nEpidemiology of Staphylococcus aureus blood and skin and soft tissue infections in the US military health system, 2005-2010. CONTEXT Rates of hospital-onset methicillin-resistant Staphylococcus aureus (MRSA) infections are reported as decreasing, but recent rates of community-onset S. aureus infections are less known. OBJECTIVES To characterize the overall and annual incidence rates of community-onset and hospital-onset S. aureus bacteremia and skin and soft tissue infections (SSTIs) in a national health care system and to evaluate trends in the incidence rates of S. aureus bacteremia and SSTIs and the proportion due to MRSA. DESIGN, SETTING, AND PARTICIPANTS Observational study of all Department of Defense TRICARE beneficiaries from January 2005 through December 2010. Medical record databases were used to identify and classify all annual first-positive S. aureus blood and wound or abscess cultures as methicillin-susceptible S. aureus or MRSA, and as community-onset or hospital-onset infections (isolates collected >3 days after hospital admission). MAIN OUTCOME MEASURES Unadjusted incidence rates per 100,000 person-years of observation, the proportion of infections that was due to MRSA, and annual trends for 2005 through 2010 (examined using the Spearman rank correlation test or the Mantel-Haenszel χ2 test for linear trend). RESULTS During 56 million person-years (nonactive duty: 47 million person-years; active duty: 9 million person-years), there were 2643 blood and 80,281 wound or abscess annual first-positive S. aureus cultures. Annual incidence rates varied from 3.6 to 6.0 per 100,000 person-years for S. aureus bacteremia and 122.7 to 168.9 per 100,000 person-years for S. aureus SSTIs. The annual incidence rates for community-onset MRSA bacteremia decrea [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "163", "doc_id": "14408200", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Cellular clocks are associated with mitosis timing in NIH 3T3 cells.\n\nCANDIDATE_PASSAGE:\nRobust synchronization of coupled circadian and cell cycle oscillators in single mammalian cells Circadian cycles and cell cycles are two fundamental periodic processes with a period in the range of 1 day. Consequently, coupling between such cycles can lead to synchronization. Here, we estimated the mutual interactions between the two oscillators by time-lapse imaging of single mammalian NIH3T3 fibroblasts during several days. The analysis of thousands of circadian cycles in dividing cells clearly indicated that both oscillators tick in a 1:1 mode-locked state, with cell divisions occurring tightly 5 h before the peak in circadian Rev-Erbα-YFP reporter expression. In principle, such synchrony may be caused by either unidirectional or bidirectional coupling. While gating of cell division by the circadian cycle has been most studied, our data combined with stochastic modeling unambiguously show that the reverse coupling is predominant in NIH3T3 cells. Moreover, temperature, genetic, and pharmacological perturbations showed that the two interacting cellular oscillators adopt a synchronized state that is highly robust over a wide range of parameters. These findings have implications for circadian function in proliferative tissues, including epidermis, immune cells, and cancer.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "241", "doc_id": "2212067", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pioglitazone use is significantly associated with an increased risk of prostate cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pioglitazone Use and Risk of Bladder Cancer and Other Common Cancers in Persons With Diabetes.\nABSTRACT: IMPORTANCE Studies suggest pioglitazone use may increase risk of cancers. OBJECTIVE To examine whether pioglitazone use for diabetes is associated with risk of bladder and 10 additional cancers. DESIGN, SETTING, AND PARTICIPANTS Cohort and nested case-control analyses among persons with diabetes. A bladder cancer cohort followed 193,099 persons aged 40 years or older in 1997-2002 until December 2012; 464 case patients and 464 matched controls were surveyed about additional confounders. A cohort analysis of 10 additional cancers included 236,507 persons aged 40 years or older in 1997-2005 and followed until June 2012. Cohorts were from Kaiser Permanente Northern California. EXPOSURES Ever use, duration, cumulative dose, and time since initiation of pioglitazone as time dependent. MAIN OUTCOMES AND MEASURES Incident cancer, including bladder, prostate, female breast, lung/bronchus, endometrial, colon, non-Hodgkin lymphoma, pancreas, kidney/renal pelvis, rectum, and melanoma. RESULTS Among 193,099 persons in the bladder cancer cohort, 34,181 (18%) received pioglitazone (median duration, 2.8 years; range, 0.2-13.2 years) and 1261 had incident bladder cancer. Crude incidences of bladder cancer in pioglitazone users and nonusers were 89.8 and 75.9 per 100,000 person-years, respectively. Ever use of pioglitazone was not associated with bladder cancer risk (adjusted hazard ratio [HR], 1.06; 95% CI, 0.89-1.26). Results were similar in case-control analyses (pioglitazone use: 19.6% among case patients and 17.5% among controls; adjusted odds ratio, 1.18; 95% CI, 0.78-1.80). In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95% CI, 1.02-1.26) and p [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The increased prostate and pancreatic cancer risks associated with ever use of pioglitazone merit further investigation to assess whether they are causal or are due to chance, residual confounding, or reverse causality.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 954, "doc_id": "3355397", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: eRNAs influence is linked to senescence, aging, and carcinogenesis.\n\nCANDIDATE_ABSTRACT:\nTITLE: eRNAs are required for p53-dependent enhancer activity and gene transcription.\nABSTRACT: Binding within or nearby target genes involved in cell proliferation and survival enables the p53 tumor suppressor gene to regulate their transcription and cell-cycle progression. Using genome-wide chromatin-binding profiles, we describe binding of p53 also to regions located distantly from any known p53 target gene. Interestingly, many of these regions possess conserved p53-binding sites and all known hallmarks of enhancer regions. We demonstrate that these p53-bound enhancer regions (p53BERs) indeed contain enhancer activity and interact intrachromosomally with multiple neighboring genes to convey long-distance p53-dependent transcription regulation. Furthermore, p53BERs produce, in a p53-dependent manner, enhancer RNAs (eRNAs) that are required for efficient transcriptional enhancement of interacting target genes and induction of a p53-dependent cell-cycle arrest. Thus, our results ascribe transcription enhancement activity to p53 with the capacity to regulate multiple genes from a single genomic binding site. Moreover, eRNA production from p53BERs is required for efficient p53 transcription enhancement.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1387, "doc_id": "9669099", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The DESMOND program demonstrates no significant impact on biochemical outcomes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effectiveness of a diabetes education and self management programme (DESMOND) for people with newly diagnosed type 2 diabetes mellitus: three year follow-up of a cluster randomised controlled trial in primary care\nABSTRACT: OBJECTIVE To measure whether the benefits of a single education and self management structured programme for people with newly diagnosed type 2 diabetes mellitus are sustained at three years. DESIGN Three year follow-up of a multicentre cluster randomised controlled trial in primary care, with randomisation at practice level. SETTING 207 general practices in 13 primary care sites in the United Kingdom. PARTICIPANTS 731 of the 824 participants included in the original trial were eligible for follow-up. Biomedical data were collected on 604 (82.6%) and questionnaire data on 513 (70.1%) participants. INTERVENTION A structured group education programme for six hours delivered in the community by two trained healthcare professional educators compared with usual care. MAIN OUTCOME MEASURES The primary outcome was glycated haemoglobin (HbA(1c)) levels. The secondary outcomes were blood pressure, weight, blood lipid levels, smoking status, physical activity, quality of life, beliefs about illness, depression, emotional impact of diabetes, and drug use at three years. RESULTS HbA(1c) levels at three years had decreased in both groups. After adjusting for baseline and cluster the difference was not significant (difference -0.02, 95% confidence interval -0.22 to 0.17). The groups did not differ for the other biomedical and lifestyle outcomes and drug use. The significant benefits in the intervention group across four out of five health beliefs seen at 12 months were sustained at three years (P<0.01). Depression scores and quality of life did not differ at three years. CONCLUSION A single programme for people with newly diagnosed type 2 diabetes mellitus showed no difference in biomedical or lifestyle outcomes at three years although there were sustained improvements in [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"After adjusting for baseline and cluster the difference was not significant (difference -0.02, 95% confidence interval -0.22 to 0.17).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1157, "doc_id": "12584053", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Functional consequences of genomic alterations due to Myelodysplastic syndrome (MDS) are poorly understood due to the lack of an animal model.\n\nCANDIDATE_PASSAGE:\nDealing with substantial heterogeneity in Cochrane reviews. Cross-sectional study BACKGROUND Dealing with heterogeneity in meta-analyses is often tricky, and there is only limited advice for authors on what to do. We investigated how authors addressed different degrees of heterogeneity, in particular whether they used a fixed effect model, which assumes that all the included studies are estimating the same true effect, or a random effects model where this is not assumed. METHODS We sampled randomly 60 Cochrane reviews from 2008, which presented a result in its first meta-analysis with substantial heterogeneity (I2 greater than 50%, i.e. more than 50% of the variation is due to heterogeneity rather than chance). We extracted information on choice of statistical model, how the authors had handled the heterogeneity, and assessed the methodological quality of the reviews in relation to this. RESULTS The distribution of heterogeneity was rather uniform in the whole I2 interval, 50-100%. A fixed effect model was used in 33 reviews (55%), but there was no correlation between I2 and choice of model (P = 0.79). We considered that 20 reviews (33%), 16 of which had used a fixed effect model, had major problems. The most common problems were: use of a fixed effect model and lack of rationale for choice of that model, lack of comment on even severe heterogeneity and of reservations and explanations of its likely causes. The problematic reviews had significantly fewer included trials than other reviews (4.3 vs. 8.0, P = 0.024). The problems became less pronounced with time, as those reviews that were most recently updated more often used a random effects model. CONCLUSION One-third of Cochrane reviews with substantial heterogeneity had major problems in relation to their [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "437", "doc_id": "7547329", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is second metatarsal length positively correlated with increased pressure and medial deviation of the second toe in a robotic cadaveric simulation of gait?\n\nABSTRACT:\nThe term `crossover second toe' has been used to describe a deformity of the second metatarsophalangeal joint (MTPJ) that includes a progressive migration of the second toe in a dorsal and medial direction. The long onset and complex anatomy of the deformity has led to uncertainty about its etiology and treatment. The purpose of this study was to investigate the relationship between second metatarsal length and second MTPJ plantar pressure and joint angles during gait. We hypothesized that elongation of the second metatarsal would increase the plantar pressure underneath the second MTPJ and be associated with a deviation of the MTPJ angles in a dorsal and medial direction. Incremental surgical elongation of the second metatarsal was performed on six cadaveric feet. A robotic gait simulator (RGS) simulated physiologic tibial motion, tendon loading, and ground reaction forces (GRF) on the cadaveric feet. We determined the peak pressure and pressure-time integral under the second MTPJ during gait, as well as the transverse and sagittal MTPJ angles. Second metatarsal peak pressure and pressure-time integral were positively correlated with an increase in second metatarsal length. First metatarsal peak pressure and pressure-time integral were significantly negatively associated with second metatarsal length. MTPJ transverse plane angle was positively associated with second metatarsal length but sagittal angle was not.", "output": "{\"label\": \"yes\", \"rationale\": \"Our results support the hypothesis that second metatarsal length is positively associated with medial deviation of the second toe and increased plantar pressure underneath the second MTPJ.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 22735203, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: IRG1 has antiviral effects against neurotropic viruses.\n\nCANDIDATE_PASSAGE:\nDifferential innate immune response programs in neuronal subtypes determine susceptibility to infection in the brain by positive stranded RNA viruses Although susceptibility of neurons in the brain to microbial infection is a major determinant of clinical outcome, little is known about the molecular factors governing this vulnerability. Here we show that two types of neurons from distinct brain regions showed differential permissivity to replication of several positive-stranded RNA viruses. Granule cell neurons of the cerebellum and cortical neurons from the cerebral cortex have unique innate immune programs that confer differential susceptibility to viral infection ex vivo and in vivo. By transducing cortical neurons with genes that were expressed more highly in granule cell neurons, we identified three interferon-stimulated genes (ISGs; Ifi27, Irg1 and Rsad2 (also known as Viperin)) that mediated the antiviral effects against different neurotropic viruses. Moreover, we found that the epigenetic state and microRNA (miRNA)-mediated regulation of ISGs correlates with enhanced antiviral response in granule cell neurons. Thus, neurons from evolutionarily distinct brain regions have unique innate immune signatures, which probably contribute to their relative permissiveness to infection.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "549", "doc_id": "9433958", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is myocardial contractility constant during spontaneous atrial fibrillation in patients?\n\nABSTRACT:\nThe variation in stroke volume and pulse pressure characteristic of atrial fibrillation is usually ascribed to time-dependent ventricular filling, implying a single positive relationship between end-systolic pressure and volume, which defines a single state of myocardial contractility. We tested the hypothesis that contractility also varies. We measured the left ventricular pressure and volume continuously with a conductance catheter with catheter-tip micromanometer introduced retrogradely into the left ventricle. The end-systolic pressure-volume relationship was determined in 6 patients in atrial fibrillation undergoing cardiac catheterization for diagnostic purposes and 4 control patients in sinus rhythm undergoing coronary artery bypass graft surgery. The normal positive relationship between end-systolic pressure and volume was found in the control patients, but no such positive relationship was found in any patient in atrial fibrillation. In the latter, the slopes of the linear regressions were either not significantly different from zero or significantly negative (r values <0.08), both results indicating a change in contractility from beat to beat. Significantly negative relationships were found between end-systolic volume and preceding R-R interval (-0.82", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: PGE 2 suppresss intestinal tumor growth by altering the expression of tumor suppressing and DNA repair genes.\n\nCANDIDATE_PASSAGE:\nControl of Nutrient Stress-Induced Metabolic Reprogramming by PKCζ in Tumorigenesis Tumor cells have high-energetic and anabolic needs and are known to adapt their metabolism to be able to survive and keep proliferating under conditions of nutrient stress. We show that PKCζ deficiency promotes the plasticity necessary for cancer cells to reprogram their metabolism to utilize glutamine through the serine biosynthetic pathway in the absence of glucose. PKCζ represses the expression of two key enzymes of the pathway, PHGDH and PSAT1, and phosphorylates PHGDH at key residues to inhibit its enzymatic activity. Interestingly, the loss of PKCζ in mice results in enhanced intestinal tumorigenesis and increased levels of these two metabolic enzymes, whereas patients with low levels of PKCζ have a poor prognosis. Furthermore, PKCζ and caspase-3 activities are correlated with PHGDH levels in human intestinal tumors. Taken together, this demonstrates that PKCζ is a critical metabolic tumor suppressor in mouse and human cancer.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "908", "doc_id": "17755060", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The NF-κB essential modulator gene prevents intestinal inflammation by inhibiting receptor-interacting protein (RIP) kinase 1 kinase activity-mediated epithelial cell death.\n\nCANDIDATE_ABSTRACT:\nTITLE: Fruit consumption and risk of type 2 diabetes: results from three prospective longitudinal cohort studies\nABSTRACT: OBJECTIVE To determine whether individual fruits are differentially associated with risk of type 2 diabetes. DESIGN Prospective longitudinal cohort study. SETTING Health professionals in the United States. PARTICIPANTS 66,105 women from the Nurses' Health Study (1984-2008), 85,104 women from the Nurses' Health Study II (1991-2009), and 36,173 men from the Health Professionals Follow-up Study (1986-2008) who were free of major chronic diseases at baseline in these studies. MAIN OUTCOME MEASURE Incident cases of type 2 diabetes, identified through self report and confirmed by supplementary questionnaires. RESULTS During 3,464,641 person years of follow-up, 12,198 participants developed type 2 diabetes. After adjustment for personal, lifestyle, and dietary risk factors of diabetes, the pooled hazard ratio of type 2 diabetes for every three servings/week of total whole fruit consumption was 0.98 (95% confidence interval 0.97 [corrected] to 0.99). With mutual adjustment of individual fruits, the pooled hazard ratios of type 2 diabetes for every three servings/week were 0.74 (0.66 to 0.83) for blueberries, 0.88 (0.83 to 0.93) for grapes and raisins, 0.89 (0.79 to 1.01) for prunes, 0.93 (0.90 to 0.96) for apples and pears, 0.95 (0.91 to 0.98) for bananas, 0.95 (0.91 to 0.99) for grapefruit, 0.97 (0.92 to 1.02) for peaches, plums, and apricots, 0.99 (0.95 to 1.03) for oranges, 1.03 (0.96 to 1.10) for strawberries, and 1.10 (1.02 to 1.18) for cantaloupe. The pooled hazard ratio for the same increment in fruit juice consumption was 1.08 (1.05 to 1.11). The associations with risk of type 2 diabetes differed significantly among individual fruits (P<0.001 in all cohorts). CONCLUSION Our findings suggest the presence of heterogeneity in the associations between individual [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1171, "doc_id": "1974176", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: AMP-activated protein kinase (AMPK) activation reduces inflammation-related fibrosis in the lungs.\n\nCANDIDATE_ABSTRACT:\nTITLE: Metformin reverses established lung fibrosis in a bleomycin model\nABSTRACT: Fibrosis is a pathological result of a dysfunctional repair response to tissue injury and occurs in a number of organs, including the lungs1. Cellular metabolism regulates tissue repair and remodelling responses to injury2-4. AMPK is a critical sensor of cellular bioenergetics and controls the switch from anabolic to catabolic metabolism5. However, the role of AMPK in fibrosis is not well understood. Here, we demonstrate that in humans with idiopathic pulmonary fibrosis (IPF) and in an experimental mouse model of lung fibrosis, AMPK activity is lower in fibrotic regions associated with metabolically active and apoptosis-resistant myofibroblasts. Pharmacological activation of AMPK in myofibroblasts from lungs of humans with IPF display lower fibrotic activity, along with enhanced mitochondrial biogenesis and normalization of sensitivity to apoptosis. In a bleomycin model of lung fibrosis in mice, metformin therapeutically accelerates the resolution of well-established fibrosis in an AMPK-dependent manner. These studies implicate deficient AMPK activation in non-resolving, pathologic fibrotic processes, and support a role for metformin (or other AMPK activators) to reverse established fibrosis by facilitating deactivation and apoptosis of myofibroblasts.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"These studies implicate deficient AMPK activation in non-resolving, pathologic fibrotic processes, and support a role for metformin (or other AMPK activators) to reverse established fibrosis by facilitating deactivation and apoptosis of myofibroblasts.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 55, "doc_id": "49556906", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: PGE 2 suppresss intestinal tumor growth by altering the expression of tumor suppressing and DNA repair genes.\n\nCANDIDATE_PASSAGE:\nForces in Tissue Morphogenesis and Patterning During development, mechanical forces cause changes in size, shape, number, position, and gene expression of cells. They are therefore integral to any morphogenetic processes. Force generation by actin-myosin networks and force transmission through adhesive complexes are two self-organizing phenomena driving tissue morphogenesis. Coordination and integration of forces by long-range force transmission and mechanosensing of cells within tissues produce large-scale tissue shape changes. Extrinsic mechanical forces also control tissue patterning by modulating cell fate specification and differentiation. Thus, the interplay between tissue mechanics and biochemical signaling orchestrates tissue morphogenesis and patterning in development.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "908", "doc_id": "1922901", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Approximately 250,000 people are infected with human T-cell lymphotropic virus type 1 in the United Kingdom.\n\nCANDIDATE_ABSTRACT:\nTITLE: HTLV-I/II associated disease in England and Wales, 1993-7: retrospective review of serology requests.\nABSTRACT: Apart from HIV two exogenous retroviruses (human T cell leukaemia viruses type I (HTLV-I) and type II (HTLV-II)) infect humans. HTLV-I infection is endemic in Japan, the Caribbean, Africa, and Melanesia and is found among immigrants from these regions in Europe. HTLV-I infection is associated with a 1-5% lifetime risk of adult T cell leukaemia/lymphoma, 1 a 0.25% lifetime risk of HTLV-I associated myelopathy, 2 and other inflammatory conditions (uveitis, alveolitis, and arthritis).1 HTLV-II infection is endemic in some native American and African peoples and among injecting drug users and has been associated with neurological disease.1 Between 1986 and 1992, 100 cases of HTLV-I associated myelopathy and 44 cases of adult T cell leukaemia/lymphoma were diagnosed in the United Kingdom.3 Adult T cell leukaemia/lymphoma was first described in 1977 and patients with it have a mean life expectancy of only six months, so most of the 44 cases were probably incident cases. …", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 126, "doc_id": "24512064", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: 40mg/day dosage of folic acid and 2mg/day dosage of vitamin B12 does not affect chronic kidney disease (CKD) progression.\n\nCANDIDATE_PASSAGE:\nInterleukin 18 function in atherosclerosis is mediated by the interleukin 18 receptor and the Na-Cl co-transporter Interleukin-18 (IL18) participates in atherogenesis through several putative mechanisms. Interruption of IL18 action reduces atherosclerosis in mice. Here, we show that absence of the IL18 receptor (IL18r) does not affect atherosclerosis in apolipoprotein E–deficient (Apoe−/−) mice, nor does it affect IL18 cell surface binding to or signaling in endothelial cells. As identified initially by co-immunoprecipitation with IL18, we found that IL18 interacts with the Na-Cl co-transporter (NCC; also known as SLC12A3), a 12-transmembrane-domain ion transporter protein preferentially expressed in the kidney. NCC is expressed in atherosclerotic lesions, where it colocalizes with IL18r. In Apoe−/− mice, combined deficiency of IL18r and NCC, but not single deficiency of either protein, protects mice from atherosclerosis. Peritoneal macrophages from Apoe−/− mice or from Apoe−/− mice lacking IL18r or NCC show IL18 binding and induction of cell signaling and cytokine and chemokine expression, but macrophages from Apoe−/− mice with combined deficiency of IL18r and NCC have a blunted response. An interaction between NCC and IL18r on macrophages was detected by co-immunoprecipitation. IL18 binds to the cell surface of NCC-transfected COS-7 cells, which do not express IL18r, and induces cell signaling and cytokine expression. This study identifies NCC as an IL18-binding protein that collaborates with IL18r in cell signaling, inflammatory molecule expression, and experimental atherogenesis.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "12", "doc_id": "24384587", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Physical activity does not improve cognitive function in individuals with Alzheimers.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effect of physical activity on cognitive function in older adults at risk for Alzheimer disease: a randomized trial.\nABSTRACT: CONTEXT Many observational studies have shown that physical activity reduces the risk of cognitive decline; however, evidence from randomized trials is lacking. OBJECTIVE To determine whether physical activity reduces the rate of cognitive decline among older adults at risk. DESIGN AND SETTING Randomized controlled trial of a 24-week physical activity intervention conducted between 2004 and 2007 in metropolitan Perth, Western Australia. Assessors of cognitive function were blinded to group membership. PARTICIPANTS We recruited volunteers who reported memory problems but did not meet criteria for dementia. Three hundred eleven individuals aged 50 years or older were screened for eligibility, 89 were not eligible, and 52 refused to participate. A total of 170 participants were randomized and 138 participants completed the 18-month assessment. INTERVENTION Participants were randomly allocated to an education and usual care group or to a 24-week home-based program of physical activity. MAIN OUTCOME MEASURE Change in Alzheimer Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) scores (possible range, 0-70) over 18 months. RESULTS In an intent-to-treat analysis, participants in the intervention group improved 0.26 points (95% confidence interval, -0.89 to 0.54) and those in the usual care group deteriorated 1.04 points (95% confidence interval, 0.32 to 1.82) on the ADAS-Cog at the end of the intervention. The absolute difference of the outcome measure between the intervention and control groups was -1.3 points (95% confidence interval,-2.38 to -0.22) at the end of the intervention. At 18 months, participants in the intervention group improved 0.73 points (95% confidence interval, -1.27 to 0.03) on the ADAS-Cog, and those in the usual care group improved 0.04 p [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS In this study of adults with subjective memory impairment, a 6-month program of physical activity provided a modest improvement in cognition over an 18-month follow-up period.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 944, "doc_id": "1642727", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Immune complex triggered cell death leads to extracellular release of nuclear DNA.\n\nCANDIDATE_PASSAGE:\nNeutrophil extracellular traps enriched in oxidized mitochondrial DNA are interferogenic and contribute to lupus-like disease Neutrophil extracellular traps (NETs) are implicated in autoimmunity, but how they are generated and their roles in sterile inflammation remain unclear. Ribonucleoprotein immune complexes (RNP ICs), inducers of NETosis, require mitochondrial reactive oxygen species (ROS) for maximal NET stimulation. After RNP IC stimulation of neutrophils, mitochondria become hypopolarized and translocate to the cell surface. Extracellular release of oxidized mitochondrial DNA is proinflammatory in vitro, and when this DNA is injected into mice, it stimulates type I interferon (IFN) signaling through a pathway dependent on the DNA sensor STING. Mitochondrial ROS are also necessary for spontaneous NETosis of low-density granulocytes from individuals with systemic lupus erythematosus. This was also observed in individuals with chronic granulomatous disease, who lack NADPH oxidase activity but still develop autoimmunity and type I IFN signatures. Mitochondrial ROS inhibition in vivo reduces disease severity and type I IFN responses in a mouse model of lupus. Together, these findings highlight a role for mitochondria in the generation not only of NETs but also of pro-inflammatory oxidized mitochondrial DNA in autoimmune diseases.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "555", "doc_id": "1049501", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: TMEM27 is a marker for beta cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tmem27: a cleaved and shed plasma membrane protein that stimulates pancreatic beta cell proliferation.\nABSTRACT: The signals and molecular mechanisms that regulate the replication of terminally differentiated beta cells are unknown. Here, we report the identification and characterization of transmembrane protein 27 (Tmem27, collectrin) in pancreatic beta cells. Expression of Tmem27 is reduced in Tcf1(-/-) mice and is increased in islets of mouse models with hypertrophy of the endocrine pancreas. Tmem27 forms dimers and its extracellular domain is glycosylated, cleaved and shed from the plasma membrane of beta cells. This cleavage process is beta cell specific and does not occur in other cell types. Overexpression of full-length Tmem27, but not the truncated or soluble protein, leads to increased thymidine incorporation, whereas silencing of Tmem27 using RNAi results in a reduction of cell replication. Furthermore, transgenic mice with increased expression of Tmem27 in pancreatic beta cells exhibit increased beta cell mass. Our results identify a pancreatic beta cell transmembrane protein that regulates cell growth of pancreatic islets.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here, we report the identification and characterization of transmembrane protein 27 (Tmem27, collectrin) in pancreatic beta cells.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1133, "doc_id": "24142891", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Alirocumab treatment reduces apo(a) fractional clearance rate.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effects of PCSK9 Inhibition With Alirocumab on Lipoprotein Metabolism in Healthy Humans\nABSTRACT: BACKGROUND Alirocumab, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), lowers plasma low-density lipoprotein (LDL) cholesterol and apolipoprotein B100 (apoB). Although studies in mice and cells have identified increased hepatic LDL receptors as the basis for LDL lowering by PCSK9 inhibitors, there have been no human studies characterizing the effects of PCSK9 inhibitors on lipoprotein metabolism. In particular, it is not known whether inhibition of PCSK9 has any effects on very low-density lipoprotein or intermediate-density lipoprotein (IDL) metabolism. Inhibition of PCSK9 also results in reductions of plasma lipoprotein (a) levels. The regulation of plasma Lp(a) levels, including the role of LDL receptors in the clearance of Lp(a), is poorly defined, and no mechanistic studies of the Lp(a) lowering by alirocumab in humans have been published to date. METHODS Eighteen (10 F, 8 mol/L) participants completed a placebo-controlled, 2-period study. They received 2 doses of placebo, 2 weeks apart, followed by 5 doses of 150 mg of alirocumab, 2 weeks apart. At the end of each period, fractional clearance rates (FCRs) and production rates (PRs) of apoB and apo(a) were determined. In 10 participants, postprandial triglycerides and apoB48 levels were measured. RESULTS Alirocumab reduced ultracentrifugally isolated LDL-C by 55.1%, LDL-apoB by 56.3%, and plasma Lp(a) by 18.7%. The fall in LDL-apoB was caused by an 80.4% increase in LDL-apoB FCR and a 23.9% reduction in LDL-apoB PR. The latter was due to a 46.1% increase in IDL-apoB FCR coupled with a 27.2% decrease in conversion of IDL to LDL. The FCR of apo(a) tended to increase (24.6%) without any change in apo(a) PR. Alirocumab had no effects on FCRs or PRs of very low-density lipopro [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Alirocumab decreased LDL-C and LDL-apoB by increasing IDL- and LDL-apoB FCRs and decreasing LDL-apoB PR.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 98, "doc_id": "6540064", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Long chain polyunsaturated fatty acids supplementation has no significant effects on wheezing or asthma at 3 and 6 years.\n\nCANDIDATE_PASSAGE:\nMultiple mechanisms disrupt the let-7 microRNA family in neuroblastoma Poor prognosis in neuroblastoma is associated with genetic amplification of MYCN. MYCN is itself a target of let-7, a tumour suppressor family of microRNAs implicated in numerous cancers. LIN28B, an inhibitor of let-7 biogenesis, is overexpressed in neuroblastoma and has been reported to regulate MYCN. Here we show, however, that LIN28B is dispensable in MYCN-amplified neuroblastoma cell lines, despite de-repression of let-7. We further demonstrate that MYCN messenger RNA levels in amplified disease are exceptionally high and sufficient to sponge let-7, which reconciles the dispensability of LIN28B. We found that genetic loss of let-7 is common in neuroblastoma, inversely associated with MYCN amplification, and independently associated with poor outcomes, providing a rationale for chromosomal loss patterns in neuroblastoma. We propose that let-7 disruption by LIN28B, MYCN sponging, or genetic loss is a unifying mechanism of neuroblastoma development with broad implications for cancer pathogenesis.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "705", "doc_id": "4467129", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Induction of urokinase receptor signaling in podocytes causes foot process effacement and proteinuria.\n\nCANDIDATE_ABSTRACT:\nTITLE: Fra-1 protooncogene regulates IL-6 expression in macrophages and promotes the generation of M2d macrophages\nABSTRACT: The tumor microenvironment (TME) plays a prominent role in the growth of tumor cells. As the major inflammatory component of the TME, M2d macrophages are educated by the TME such that they adopt an immunosuppressive role that promotes tumor metastasis and progression. Fra-1 forms activator protein-1 heterodimers with Jun partners and drives gene transcription. Fra-1 is thought to drastically induce tumorigenesis and progression. However, the functional role of Fra-1 in the generation of M2d macrophages is poorly understood to date. Here, we demonstrate that 4T1 mammary carcinoma cells, when co-cultured with RAW264.7 macrophage cells, skew the RAW264.7 macrophage cell differentiation into M2d macrophages. The 4T1 cells stimulate de novo overexpression of Fra-1 in RAW264.7 cells, and then Fra-1 binds to the interleukin 6 (IL-6) promoter to increase the production of the cytokine IL-6 in RAW264.7 cells. IL-6 acts in an autocrine fashion to skew RAW264.7 macrophage cell differentiation into M2d macrophages. These findings open new insights into how to reverse M2d macrophage-induced immune tolerance to improve the efficacy of immunotherapeutic approaches.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 626, "doc_id": "164985", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: In transgenic mice harboring green florescent protein under the control of the Sox2 promoter, more than 50 percent of the cells with green florescent colocalize with cell proliferation markers.\n\nCANDIDATE_PASSAGE:\nCardiac neural crest cells contribute to the dormant multipotent stem cell in the mammalian heart Arodent cardiac side population cell fraction formed clonal spheroids in serum-free medium, which expressed nestin, Musashi-1, and multi-drug resistance transporter gene 1, markers of undifferentiated neural precursor cells. These markers were lost following differentiation, and were replaced by the expression of neuron-, glial-, smooth muscle cell–, or cardiomyocyte-specific proteins. Cardiosphere-derived cells transplanted into chick embryos migrated to the truncus arteriosus and cardiac outflow tract and contributed to dorsal root ganglia, spinal nerves, and aortic smooth muscle cells. Lineage studies using double transgenic mice encoding protein 0–Cre/Floxed-EGFP revealed undifferentiated and differentiated neural crest-derived cells in the fetal myocardium. Undifferentiated cells expressed GATA-binding protein 4 and nestin, but not actinin, whereas the differentiated cells were identified as cardiomyocytes. These results suggest that cardiac neural crest-derived cells migrate into the heart, remain there as dormant multipotent stem cells—and under the right conditions—differentiate into cardiomyocytes and typical neural crest-derived cells, including neurons, glia, and smooth muscle.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "588", "doc_id": "106301", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The tip of the inner tube of the toxic type VI secretion system (T6SS) antibacterial effector in Escherichia coli (E. coli) carries toxic effector proteins.\n\nCANDIDATE_ABSTRACT:\nTITLE: PAAR-repeat proteins sharpen and diversify the Type VI secretion system spike\nABSTRACT: The bacterial type VI secretion system (T6SS) is a large multicomponent, dynamic macromolecular machine that has an important role in the ecology of many Gram-negative bacteria. T6SS is responsible for translocation of a wide range of toxic effector molecules, allowing predatory cells to kill both prokaryotic as well as eukaryotic prey cells. The T6SS organelle is functionally analogous to contractile tails of bacteriophages and is thought to attack cells by initially penetrating them with a trimeric protein complex called the VgrG spike. Neither the exact protein composition of the T6SS organelle nor the mechanisms of effector selection and delivery are known. Here we report that proteins from the PAAR (proline-alanine-alanine-arginine) repeat superfamily form a sharp conical extension on the VgrG spike, which is further involved in attaching effector domains to the spike. The crystal structures of two PAAR-repeat proteins bound to VgrG-like partners show that these proteins sharpen the tip of the T6SS spike complex. We demonstrate that PAAR proteins are essential for T6SS-mediated secretion and target cell killing by Vibrio cholerae and Acinetobacter baylyi. Our results indicate a new model of the T6SS organelle in which the VgrG-PAAR spike complex is decorated with multiple effectors that are delivered simultaneously into target cells in a single contraction-driven translocation event.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here we report that proteins from the PAAR (proline-alanine-alanine-arginine) repeat superfamily form a sharp conical extension on the VgrG spike, which is further involved in attaching effector domains to the spike. The crystal structures of two PAAR-repeat proteins bound to VgrG-like partners show that these proteins sharpen the tip of the T6SS spike complex.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1274, "doc_id": "4406819", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: N-terminal cleavage increases success identifying transcription start sites.\n\nCANDIDATE_PASSAGE:\nIdentification and Functional Characterization of N-Terminally Acetylated Proteins in Drosophila melanogaster Protein modifications play a major role for most biological processes in living organisms. Amino-terminal acetylation of proteins is a common modification found throughout the tree of life: the N-terminus of a nascent polypeptide chain becomes co-translationally acetylated, often after the removal of the initiating methionine residue. While the enzymes and protein complexes involved in these processes have been extensively studied, only little is known about the biological function of such N-terminal modification events. To identify common principles of N-terminal acetylation, we analyzed the amino-terminal peptides from proteins extracted from Drosophila Kc167 cells. We detected more than 1,200 mature protein N-termini and could show that N-terminal acetylation occurs in insects with a similar frequency as in humans. As the sole true determinant for N-terminal acetylation we could extract the (X)PX rule that indicates the prevention of acetylation under all circumstances. We could show that this rule can be used to genetically engineer a protein to study the biological relevance of the presence or absence of an acetyl group, thereby generating a generic assay to probe the functional importance of N-terminal acetylation. We applied the assay by expressing mutated proteins as transgenes in cell lines and in flies. Here, we present a straightforward strategy to systematically study the functional relevance of N-terminal acetylations in cells and whole organisms. Since the (X)PX rule seems to be of general validity in lower as well as higher eukaryotes, we propose that it can be used to study the function of N-terminal acetylation in all species.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "820", "doc_id": "8646760", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: A mutation in HNF4A leads to an increased risk of diabetes by the age of 14 years.\n\nCANDIDATE_PASSAGE:\nMalignancies, prothrombotic mutations, and the risk of venous thrombosis. CONTEXT Venous thrombosis is a common complication in patients with cancer, leading to additional morbidity and compromising quality of life. OBJECTIVE To identify individuals with cancer with an increased thrombotic risk, evaluating different tumor sites, the presence of distant metastases, and carrier status of prothrombotic mutations. DESIGN, SETTING, AND PATIENTS A large population-based, case-control (Multiple Environmental and Genetic Assessment [MEGA] of risk factors for venous thrombosis) study of 3220 consecutive patients aged 18 to 70 years, with a first deep venous thrombosis of the leg or pulmonary embolism, between March 1, 1999, and May 31, 2002, at 6 anticoagulation clinics in the Netherlands, and separate 2131 control participants (partners of the patients) reported via a questionnaire on acquired risk factors for venous thrombosis. Three months after discontinuation of the anticoagulant therapy, all patients and controls were interviewed, a blood sample was taken, and DNA was isolated to ascertain the factor V Leiden and prothrombin 20210A mutations. MAIN OUTCOME MEASURE Risk of venous thrombosis. RESULTS The overall risk of venous thrombosis was increased 7-fold in patients with a malignancy (odds ratio [OR], 6.7; 95% confidence interval [CI], 5.2-8.6) vs persons without malignancy. Patients with hematological malignancies had the highest risk of venous thrombosis, adjusted for age and sex (adjusted OR, 28.0; 95% CI, 4.0-199.7), followed by lung cancer and gastrointestinal cancer. The risk of venous thrombosis was highest in the first few months after the diagnosis of malignancy (adjusted OR, 53.5; 95% CI, 8.6-334.3). Patients with cancer with distant metastases had a [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "45", "doc_id": "1387104", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Mice that lack Interferon-γ or its receptor exhibit high resistance to experimental autoimmune myocarditis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Lethal autoimmune myocarditis in interferon-gamma receptor-deficient mice: enhanced disease severity by impaired inducible nitric oxide synthase induction.\nABSTRACT: BACKGROUND Interferon-gamma (IFN-gamma) is an essential cytokine in the regulation of inflammatory responses in autoimmune diseases. Little is known about its role in inflammatory heart disease. METHODS AND RESULTS We showed that IFN-gamma receptor-deficient mice (IFN-gammaR(-/-)) on a BALB/c background immunized with a peptide derived from cardiac alpha-myosin heavy chain develop severe myocarditis with high mortality. Although myocarditis subsided in wild-type mice after 3 weeks, IFN-gammaR(-/-) mice showed persistent disease. The persistent inflammation was accompanied by vigorous in vitro CD4 T-cell responses and impaired inducible nitric oxide synthase expression, together with evidence of impaired nitric oxide production in IFN-gammaR(-/-) hearts. Treatment of wild-type mice with the nitric oxide synthetase inhibitor N:-nitro-l-arginine-methyl-ester enhanced in vitro CD4 T-cell proliferation and prevented healing of myocarditis. CONCLUSIONS Our data provide evidence that IFN-gamma protects mice from lethal autoimmune myocarditis by inducing the expression of inducible nitric oxide synthase followed by the downregulation of T-cell responses.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Our data provide evidence that IFN-gamma protects mice from lethal autoimmune myocarditis by inducing the expression of inducible nitric oxide synthase followed by the downregulation of T-cell responses.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 781, "doc_id": "24338780", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: N-terminal cleavage increases success identifying transcription start sites.\n\nCANDIDATE_PASSAGE:\nThe DNA Methylome of Human Peripheral Blood Mononuclear Cells DNA methylation plays an important role in biological processes in human health and disease. Recent technological advances allow unbiased whole-genome DNA methylation (methylome) analysis to be carried out on human cells. Using whole-genome bisulfite sequencing at 24.7-fold coverage (12.3-fold per strand), we report a comprehensive (92.62%) methylome and analysis of the unique sequences in human peripheral blood mononuclear cells (PBMC) from the same Asian individual whose genome was deciphered in the YH project. PBMC constitute an important source for clinical blood tests world-wide. We found that 68.4% of CpG sites and <0.2% of non-CpG sites were methylated, demonstrating that non-CpG cytosine methylation is minor in human PBMC. Analysis of the PBMC methylome revealed a rich epigenomic landscape for 20 distinct genomic features, including regulatory, protein-coding, non-coding, RNA-coding, and repeat sequences. Integration of our methylome data with the YH genome sequence enabled a first comprehensive assessment of allele-specific methylation (ASM) between the two haploid methylomes of any individual and allowed the identification of 599 haploid differentially methylated regions (hDMRs) covering 287 genes. Of these, 76 genes had hDMRs within 2 kb of their transcriptional start sites of which >80% displayed allele-specific expression (ASE). These data demonstrate that ASM is a recurrent phenomenon and is highly correlated with ASE in human PBMCs. Together with recently reported similar studies, our study provides a comprehensive resource for future epigenomic research and confirms new sequencing technology as a paradigm for large-scale epigenomics studies.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "820", "doc_id": "18670", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Cost effectiveness evaluations based on cRCT data lack external validity.\n\nCANDIDATE_PASSAGE:\nThe Danish prescription registries. The extensive computerisation of Danish pharmacies has permitted the establishment of two large prescription registries: The Odense University Pharmacoepidemiological Database (OPED) and the Pharmacoepidemiological Prescription Database of North Jutland (PDNJ). The Danish prescription registries content, coverage, completeness and the quality of the data are discussed in this article. Furthermore, conditions for access to the data are presented. The two prescription registries cover a background population of approximately one million or 18% of the Danish population. The populations covered by the registries are stable and representative of the Danish population in general. The registries cover all reimbursed medicine at the level of the individual user. Registration of a unique and permanent personal identifier enables the compilation of longitudinal drug histories and allows the linking of prescription data to other population-based Danish registries. The degree of completeness of the Danish prescription registries is excellent for reimbursed prescription drugs. A small number of comparison studies also indicate high validity of the register information. The Danish prescription registries represent a useful new data source for pharmacoepidemiological studies.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "292", "doc_id": "23841828", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: H4 G94P proteins induce chromatin assembly, which increases free histones.\n\nCANDIDATE_PASSAGE:\nHistone levels are regulated by phosphorylation and ubiquitylation dependent proteolysis Histone levels are tightly regulated to prevent harmful effects such as genomic instability and hypersensitivity to DNA-damaging agents due to the accumulation of these highly basic proteins when DNA replication slows down or stops. Although chromosomal histones are stable, excess (non-chromatin bound) histones are rapidly degraded in a Rad53 (radiation sensitive 53) kinase-dependent manner in Saccharomyces cerevisiae. Here we demonstrate that excess histones associate with Rad53 in vivo and seem to undergo modifications such as tyrosine phosphorylation and polyubiquitylation, before their proteolysis by the proteasome. We have identified the Tyr 99 residue of histone H3 as being critical for the efficient ubiquitylation and degradation of this histone. We have also identified the ubiquitin conjugating enzymes (E2) Ubc4 and Ubc5, as well as the ubiquitin ligase (E3) Tom1 (temperature dependent organization in mitotic nucleus 1), as enzymes involved in the ubiquitylation of excess histones. Regulated histone proteolysis has major implications for the maintenance of epigenetic marks on chromatin, genomic stability and the packaging of sperm DNA.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "484", "doc_id": "14637235", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Exhaustion of B cells contributes to poor Ab response in HIV-infected individuals.\n\nCANDIDATE_PASSAGE:\nNatural history of adult T-cell leukemia/lymphoma and approaches to therapy After cell-to-cell transmission, HTLV-I increases its viral genome by de novo infection and proliferation of infected cells. Proliferation of infected cells is clonal and persistent in vivo. During the carrier state, infected cells are selected in vivo by the host's immune system, the genetic and epigenetic environment of proviral integration sites, and other factors. In leukemic cells, tax gene expression is frequently impaired by genetic and epigenetic mechanisms. Such loss of Tax expression enables ATL cells to escape the host immune system. On the other hand, ATL cells acquire the ability to proliferate without Tax by intracellular genetic and epigenetic changes. Despite advances in support and the development of novel treatment agents, the prognosis for ATLL remains poor. A number of therapies, however, do appear to improve prognosis compared to CHOP (VEPA). These include interferon-α plus zidovudine (probably after 1–2 cycles of CHOP), intensive chemotherapy as in LSG-15 with G-CSF support and Allo-SCT (which includes the potential for cure). Emerging novel approaches include HDAC inhibitors, monoclonal antibodies, and proteasome inhibitors. Comparison between different therapeutic approaches is complicated by the range of natural history of ATLL, different recruitments of naïve-to-therapy, refractory or relapsed patients, and variations in the reporting of outcome that frequently excludes difficult-to-evaluate patients. Moreover, results from relatively small proof-of-principle studies have not been extended with randomized, controlled trials. As a result, currently, there is no clear evidence to support the value of any particular treatment approach over others. To avoid furt [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "398", "doc_id": "20754359", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Sympathetic nerve activity is reduced throughout normal pregnancy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Regulation of sympathetic nerve activity during the cold pressor test in normotensive pregnant and nonpregnant women.\nABSTRACT: Baseline neurovascular transduction is reduced in normotensive pregnancy; however, little is known about changes to neurovascular transduction during periods of heightened sympathetic activation. We tested the hypothesis that, despite an exacerbated muscle sympathetic nerve activity (microneurography) response to cold pressor stimulation, the blunting of neurovascular transduction in normotensive pregnant women would result in similar changes in vascular resistance and mean arterial pressure (Finometer) relative to nonpregnant controls. Baseline neurovascular transduction was reduced in pregnant women relative to controls when expressed as the quotient of both total resistance and mean arterial pressure and sympathetic burst frequency (0.32±0.07 versus 0.58±0.16 mm Hg/L/min/bursts/min, P<0.001 and 2.4±0.7 versus 3.6±0.8 mm Hg/bursts/min, P=0.001). Sympathetic activation was greater across all 3 minutes of cold pressor stimulation in the pregnant women relative to the nonpregnant controls. Peak sympathoexcitation was also greater in pregnant than in nonpregnant women, whether expressed as sympathetic burst frequency (+17±13 versus +7±8 bursts/min, P=0.049), burst incidence (+17±9 versus +6±11 bursts/100 hb, P=0.03), or total activity (+950±660 versus +363±414 arbitrary units, P=0.04). However, neurovascular transduction during peak cold pressor-induced sympathoexcitation remained blunted in pregnant women (0.25±0.11 versus 0.45±0.08 mm Hg/L/min/bursts/min, P<0.001 and 1.9±1.0 versus 3.2±0.9 mm Hg/bursts/min, P=0.006). Therefore, mean arterial pressure (93±21 versus 99±6 mm Hg, P=0.4) and total peripheral resistance (12±3 versus 14±3 mm Hg/L/min) were not different between pregnant and nonpregnant women during peak sympathoexcitation. These data indicate that [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Peak sympathoexcitation was also greater in pregnant than in nonpregnant women, whether expressed as sympathetic burst frequency (+17±13 versus +7±8 bursts/min, P=0.049), burst incidence (+17±9 versus +6±11 bursts/100 hb, P=0.03), or total activity (+950±660 versus +363±414 arbitrary units, P=0.04).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1120, "doc_id": "13907928", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Chronic aerobic exercise alters endothelial function, improving vasodilating mechanisms mediated by NO.\n\nCANDIDATE_ABSTRACT:\nTITLE: Endothelium-mediated relaxation of porcine collateral-dependent arterioles is improved by exercise training.\nABSTRACT: BACKGROUND Endothelium-dependent modulation of coronary tone is impaired in the collateral-dependent coronary microcirculation. We used a porcine model of chronic coronary occlusion and collateral development to evaluate the hypothesis that exercise training enhances endothelium-mediated relaxation and increases endothelial nitric oxide synthase (ecNOS) mRNA levels of collateral-dependent microvasculature. METHODS AND RESULTS Adult female miniature swine were subjected to chronic, progressive ameroid occlusion of the proximal left circumflex coronary artery (LCx); after 2 months, animals were randomly exposed to 16-week exercise-training (EX group; treadmill running) or sedentary (SED group; cage confinement) protocols. After completion of EX or SED programs, coronary arterioles ( approximately 100 microm in diameter) were isolated from collateral-dependent LCx (distal to occlusion) and nonoccluded left anterior descending coronary artery (LAD) regions of each heart. Arterioles were studied by in vitro videomicroscopy or frozen for ecNOS mRNA analysis (RT-PCR techniques). Relaxation to the endothelium-dependent vasodilator bradykinin was decreased (P<0.05) in arterioles isolated from collateral-dependent LCx versus nonoccluded LAD regions of SED animals. Bradykinin-mediated relaxation, however, was not different in LCx versus LAD arterioles isolated from EX animals. Nitroprusside-induced relaxation was unaffected by either chronic occlusion or exercise. Importantly, ecNOS mRNA expression was significantly decreased in arterioles isolated from LCx versus LAD regions of SED animals. After training, ecNOS mRNA expression was not different between LAD and LCx arterioles. CONCLUSIONS These data indicate that exercise training enhances bradykinin-mediated relaxati [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Relaxation to the endothelium-dependent vasodilator bradykinin was decreased (P<0.05) in arterioles isolated from collateral-dependent LCx versus nonoccluded LAD regions of SED animals. CONCLUSIONS These data indicate that exercise training enhances bradykinin-mediated relaxation of collateral-dependent LCx arterioles isolated after chronic coronary occlusion, most likely because of effects on ecNOS mRNA expression and increased production of NO.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 261, "doc_id": "1122279", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Patients in stable partnerships progress from HIV to death at the same rate as patients not in partnerships.\n\nCANDIDATE_PASSAGE:\nStable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study. OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART). DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study). SETTING Seven outpatient clinics throughout Switzerland. PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years). MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound. RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion. When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership. In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without. Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression. CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patien [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "925", "doc_id": "17077004", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does tertiary Gleason pattern 5 on needle biopsy predict greater tumour volume on radical prostatectomy?\n\nABSTRACT:\nThe modified Gleason system of 2005 recommends incorporating higher grade tertiary patterns on needle biopsy into final Gleason scores to better correlate with radical prostatectomy findings. However, limited literature exists on the validity of this practice and the significance of tertiary Gleason patterns in needle biopsy. Over a 20 month period there were 25 cases of Gleason score 7 with tertiary pattern 5 on needle biopsy with follow-up radical prostatectomy reported at our institution. Pathological findings at radical prostatectomy from these cases were compared with those from patients with Gleason score 4 + 3 = 7 tumours (50 cases) and Gleason score 4 + 5 = 9 tumours (63 cases) on needle biopsy. Comparison of Gleason score 4 + 3 = 7 with 4 + 3 = 7(+5) tumours on needle biopsy, showed a significant difference in tumour volume in the corresponding radical prostatectomy specimen (p = 0.02). Differences in patient age, serum prostate specific antigen levels at diagnosis, positive surgical margins, extraprostatic extension, seminal vesicle invasion and lymph node metastases were not statistically significant between the two patient groups or when Gleason score 4 + 3 = 7(+5) and Gleason score 9 tumours were compared.", "output": "{\"label\": \"yes\", \"rationale\": \"Tertiary pattern 5 on needle biopsy predicts greater tumour volume. This suggests that for thin core biopsies, if tertiary pattern 5 is present this should be incorporated into the final Gleason score.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 22002115, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Active caspase-11 participate in regulating phagosome-lysosome fusion.\n\nCANDIDATE_PASSAGE:\n6-phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumor growth by inhibiting LKB1-AMPK signaling The oxidative pentose phosphate pathway (PPP) contributes to tumour growth, but the precise contribution of 6-phosphogluconate dehydrogenase (6PGD), the third enzyme in this pathway, to tumorigenesis remains unclear. We found that suppression of 6PGD decreased lipogenesis and RNA biosynthesis and elevated ROS levels in cancer cells, attenuating cell proliferation and tumour growth. 6PGD-mediated production of ribulose-5-phosphate (Ru-5-P) inhibits AMPK activation by disrupting the active LKB1 complex, thereby activating acetyl-CoA carboxylase 1 and lipogenesis. Ru-5-P and NADPH are thought to be precursors in RNA biosynthesis and lipogenesis, respectively; thus, our findings provide an additional link between the oxidative PPP and lipogenesis through Ru-5-P-dependent inhibition of LKB1-AMPK signalling. Moreover, we identified and developed 6PGD inhibitors, physcion and its derivative S3, that effectively inhibited 6PGD, cancer cell proliferation and tumour growth in nude mice xenografts without obvious toxicity, suggesting that 6PGD could be an anticancer target.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "78", "doc_id": "1686997", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Patients with common epithelial cancers are more likely to have an emergency event as their first hospital admission if they live in resource-deprived areas.\n\nCANDIDATE_ABSTRACT:\nTITLE: Social variations in access to hospital care for patients with colorectal, breast, and lung cancer between 1999 and 2006: retrospective analysis of hospital episode statistics\nABSTRACT: OBJECTIVES To determine the extent to which type of hospital admission (emergency compared with elective) and surgical procedure varied by socioeconomic circumstances, age, sex, and year of admission for colorectal, breast, and lung cancer. DESIGN Repeated cross sectional study with data from individual patients, 1 April 1999 to 31 March 2006. SETTING Hospital episode statistics (HES) dataset. PARTICIPANTS 564 821 patients aged 50 and over admitted with a diagnosis of colorectal, breast, or lung cancer. MAIN OUTCOME MEASURES Proportion of patients admitted as emergencies, and the proportion receiving the recommended surgical treatment. RESULTS Patients from deprived areas, older people, and women were more likely to be admitted as emergencies. For example, the adjusted odds ratio for patients with breast cancer in the least compared with most deprived fifth of deprivation was 0.63 (95% confidence interval 0.60 to 0.66) and the adjusted odds ratio for patients with lung cancer aged 80-89 compared with those aged 50-59 was 3.13 (2.93 to 3.34). There were some improvements in disparities between age groups but not for patients living in deprived areas over time. Patients from deprived areas were less likely to receive preferred procedures for rectal, breast, and lung cancer. These findings did not improve with time. For example, 67.4% (3529/5237) of patients in the most deprived fifth of deprivation had anterior resection for rectal cancer compared with 75.5% (4497/5959) of patients in the least deprived fifth (1.34, 1.22 to 1.47). Over half (54.0%, 11 256/20 849) of patients in the most deprived fifth of deprivation had breast conserving surgery compared with 63.7% (18 445/28 960) of patients in the least deprived fifth (1.21, 1.16 to 1.26). Men were less like [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"For example, the adjusted odds ratio for patients with breast cancer in the least compared with most deprived fifth of deprivation was 0.63 (95% confidence interval 0.60 to 0.66) and the adjusted odds ratio for patients with lung cancer aged 80-89 compared with those aged 50-59 was 3.13 (2.93 to 3.34). There were some improvements in disparities between age groups but not for patients living in deprived areas over time.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 926, "doc_id": "16390264", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Long chain polyunsaturated fatty acids supplementation reduces wheezing and asthma.\n\nCANDIDATE_PASSAGE:\nSerum plant and other noncholesterol sterols, cholesterol metabolism and 22-year mortality among middle-aged men. OBJECTIVE To evaluate long-term prognostic effect of serum noncholesterol sterols, including plant sterols, in middle-aged men with high cardiovascular disease (CVD) risk, without statins at baseline. METHODS This was a prospective study of 232 men (mean age 60 years) at high risk of CVD in 1985-1986. Most were hypercholesterolemic, 29 (12%) had a history of CVD or cancer, 6 (3%) had diabetes, and 46 (20%) had metabolic syndrome (MS). Measured noncholesterol sterols (expressed as absolute concentrations or ratios to serum cholesterol to standardize for cholesterol concentrations) included lathosterol and desmosterol (reflect cholesterol synthesis), and plant sterols (campesterol and sitosterol) and cholestanol (reflect cholesterol absorption). Main outcome measure was total mortality. RESULTS At baseline, markers of cholesterol synthesis and absorption showed expected inverse associations. During the 22-year follow-up 101 men (43%) died. At baseline, nonsurvivors smoked more, exercised less and had more components of MS (although not filling strict criteria), whereas traditional risk factors of CVD were not significantly different. Of the noncholesterol sterols (either absolute or ratio), only sitosterol was significantly higher in survivors than in nonsurvivors (P=0.02). In multivariable analyses, highest sitosterol-to-cholesterol tertile was associated with significantly lower mortality risk (HR 0.51, 95% CI 0.30-0.87) as compared to lowest tertile. Other associations were nonsignificant, although a \"global\" index of cholesterol metabolism (desmosterol-to-sitosterol ratio) suggested higher cholesterol synthesis and lower absorption to be associ [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "710", "doc_id": "9617381", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: LSD1-positive promoters are associated with RNA polymerase II\n\nCANDIDATE_PASSAGE:\nChoosing appropriate substitution models for the phylogenetic analysis of protein-coding sequences. Although phylogenetic inference of protein-coding sequences continues to dominate the literature, few analyses incorporate evolutionary models that consider the genetic code. This problem is exacerbated by the exclusion of codon-based models from commonly employed model selection techniques, presumably due to the computational cost associated with codon models. We investigated an efficient alternative to standard nucleotide substitution models, in which codon position (CP) is incorporated into the model. We determined the most appropriate model for alignments of 177 RNA virus genes and 106 yeast genes, using 11 substitution models including one codon model and four CP models. The majority of analyzed gene alignments are best described by CP substitution models, rather than by standard nucleotide models, and without the computational cost of full codon models. These results have significant implications for phylogenetic inference of coding sequences as they make it clear that substitution models incorporating CPs not only are a computationally realistic alternative to standard models but may also frequently be statistically superior.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "679", "doc_id": "18027063", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: BCL-2 activation antagonizes the apoptotic effects of c-Myc.\n\nCANDIDATE_ABSTRACT:\nTITLE: Antiapoptotic BCL-2 is required for maintenance of a model leukemia.\nABSTRACT: Resistance to apoptosis, often achieved by the overexpression of antiapoptotic proteins, is common and perhaps required in the genesis of cancer. However, it remains uncertain whether apoptotic defects are essential for tumor maintenance. To test this, we generated mice expressing a conditional BCL-2 gene and constitutive c-myc that develop lymphoblastic leukemia. Eliminating BCL-2 yielded rapid loss of leukemic cells and significantly prolonged survival, formally validating BCL-2 as a rational target for cancer therapy. Loss of this single molecule resulted in cell death, despite or perhaps attributable to the presence of other oncogenic events. This suggests a generalizable model in which aberrations inherent to cancer generate tonic death signals that would otherwise kill the cell if not opposed by a requisite apoptotic defect(s).", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Eliminating BCL-2 yielded rapid loss of leukemic cells and significantly prolonged survival, formally validating BCL-2 as a rational target for cancer therapy.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 155, "doc_id": "37549932", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Incidence rates of cervical cancer have increased due to nationwide screening programs based primarily on cytology to detect uterine cervical cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mass screening programmes and trends in cervical cancer in Finland and the Netherlands.\nABSTRACT: With respect to cervical cancer management, Finland and the Netherlands are comparable in relevant characteristics, e.g., fertility rate, age-of-mother at first birth and a national screening programme for several years. The aim of this study is to compare trends in incidence of and mortality from cervical cancer in Finland and the Netherlands in relation to the introduction and intensity of the screening programmes. Therefore, incidence and mortality rates were calculated using the Cancer Registries of Finland and the Netherlands. Data on screening intensity were obtained from the Finnish Cancer Registry and the Dutch evaluation centre at ErasmusMC-Rotterdam. Women aged 30-60 have been screened every 5 years, in Finland since 1992 and in the Netherlands since 1996. Screening protocols for smear taking and referral to the gynaecologist are comparable. Incidence and mortality rates have declined more in Finland. In 2003, age-adjusted incidence and mortality in Finland were 4.0 and 0.9 and in the Netherlands 4.9 and 1.4 per 100,000 woman-years, respectively. Excess smear use in the Netherlands was estimated to be 24 per 1,000 women during a 5-year interval compared to 121 in Finland. The decline in mortality in Finland seems to be almost completely related to the screening programme whereas in the Netherlands it was initially considered to be a natural decline. Differences in risk factors might also play a role: the Netherlands has higher population density and higher percentages of immigrants and (female) smokers. The greater excess smear use in Finland might also have affected incidence.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Incidence and mortality rates have declined more in Finland.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 598, "doc_id": "25742130", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: DUSP4 increases apoptosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Profiling of residual breast cancers after neoadjuvant chemotherapy identifies DUSP4 deficiency as a mechanism of drug resistance\nABSTRACT: Neoadjuvant chemotherapy (NAC) induces a pathological complete response (pCR) in ∼30% of patients with breast cancer. However, many patients have residual cancer after chemotherapy, which correlates with a higher risk of metastatic recurrence and poorer outcome than those who achieve a pCR. We hypothesized that molecular profiling of tumors after NAC would identify genes associated with drug resistance. Digital transcript counting was used to profile surgically resected breast cancers after NAC. Low concentrations of dual specificity protein phosphatase 4 (DUSP4), an ERK phosphatase, correlated with high post-NAC tumor cell proliferation and with basal-like breast cancer (BLBC) status. BLBC had higher DUSP4 promoter methylation and gene expression patterns of Ras-ERK pathway activation relative to other breast cancer subtypes. DUSP4 overexpression increased chemotherapy-induced apoptosis, whereas DUSP4 depletion dampened the response to chemotherapy. Reduced DUSP4 expression in primary tumors after NAC was associated with treatment-refractory high Ki-67 scores and shorter recurrence-free survival. Finally, inhibition of mitogen-activated protein kinase kinase (MEK) synergized with docetaxel treatment in BLBC xenografts. Thus, DUSP4 downregulation activates the Ras-ERK pathway in BLBC, resulting in an attenuated response to anti-cancer chemotherapy.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"DUSP4 overexpression increased chemotherapy-induced apoptosis, whereas DUSP4 depletion dampened the response to chemotherapy.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 309, "doc_id": "7821634", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The origin of the CRF01_1b2k protein occurred between 1923 and 1956.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Global Spread of Hepatitis C Virus 1a and 1b: A Phylodynamic and Phylogeographic Analysis\nABSTRACT: BACKGROUND Hepatitis C virus (HCV) is estimated to affect 130-180 million people worldwide. Although its origin is unknown, patterns of viral diversity suggest that HCV genotype 1 probably originated from West Africa. Previous attempts to estimate the spatiotemporal parameters of the virus, both globally and regionally, have suggested that epidemic HCV transmission began in 1900 and grew steadily until the late 1980s. However, epidemiological data suggest that the expansion of HCV may have occurred after the Second World War. The aim of our study was to elucidate the timescale and route of the global spread of HCV. METHODS AND FINDINGS We show that the rarely sequenced HCV region (E2P7NS2) is more informative for molecular epidemiology studies than the more commonly used NS5B region. We applied phylodynamic methods to a substantial set of new E2P7NS2 and NS5B sequences, together with all available global HCV sequences with information in both of these genomic regions, in order to estimate the timescale and nature of the global expansion of the most prevalent HCV subtypes, 1a and 1b. We showed that transmission of subtypes 1a and 1b \"exploded\" between 1940 and 1980, with the spread of 1b preceding that of 1a by at least 16 y (95% confidence interval 15-17). Phylogeographic analysis of all available NS5B sequences suggests that HCV subtypes 1a and 1b disseminated from the developed world to the developing countries. CONCLUSIONS The evolutionary rate of HCV appears faster than previously suggested. The global spread of HCV coincided with the widespread use of transfused blood and blood products and with the expansion of intravenous drug use but slowed prior to the wide implementation of anti-HCV screening. Differences in the transmission routes associated with [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1247, "doc_id": "5114282", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Auditory entrainment is strengthened when people see congruent visual and auditory information.\n\nCANDIDATE_PASSAGE:\nThe association between common physical impairments and dementia in low and middle income countries, and, among people with dementia, their association with cognitive function and disability. A 10/66 Dementia Research Group population-based study. OBJECTIVE Chronic physical comorbidity is common in dementia. However, there is an absence of evidence to support good practice guidelines for attention to these problems. We aimed to study the extent of this comorbidity and its impact on cognitive function and disability in population-based studies in low and middle income countries, where chronic diseases and impairments are likely to be both common and undertreated. METHODS A multicentre cross-sectional survey of all over 65 year old residents (n = 15 022) in 11 catchment areas in China, India, Cuba, Dominican Republic, Venezuela, Mexico and Peru. We estimated the prevalence of pain, incontinence, hearing and visual impairments, mobility impairment and undernutrition according to the presence of dementia and its severity, and, among those with dementia, the independent contribution of these impairments to cognitive function and disability, adjusting for age, gender, education and dementia severity. RESULTS Incontinence, hearing impairment, mobility impairment and undernutrition were consistently linearly associated with the presence of dementia and its severity across regions. Among people with dementia, incontinence, hearing impairment and mobility impairment were independently associated with disability in all regions while the contributions of pain, visual impairment and undernutrition were inconsistent. Only hearing impairment made a notable independent contribution to cognitive impairment. CONCLUSIONS There is an urgent need for clinical trials of the feasi [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "141", "doc_id": "21274919", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: NR5A2 is important in reverse cholesterol transport in humans.\n\nCANDIDATE_PASSAGE:\nSEROSURVEY FOR FELINE LEUKEMIA VIRUS AND LENTIVIRUSES IN CAPTIVE SMALL NEOTROPIC FELIDS IN SÃO PAULO STATE, BRAZIL Abstract Feline leukemia virus (FeLV), Gammaretrovirus, and feline immunodeficiency virus, a Lentivirus, are members of the family Retroviridae, and may establish persistent infections in the domestic cat (Felis catus). Cytoproliferative and cytosuppressive disorders may result from infection with these viruses. Morbidity and mortality rates are high in domestic cats worldwide. Infection of endangered neotropic small felids with these viruses could be devastating. To investigate the prevalence of FeLV and feline lentiviruses in neotropic small felids kept in captivity in São Paulo state, Brazil, serum samples from 104 animals belonging to the species Leopardus pardalis, Leopardus tigrinus, Leopardus wiedii, Herpailurus yaguarondi, and Oncifelis geoffroyi were tested for FeLV and feline lentiviruses by commercially available immunoassays. All results were negative, suggesting that retrovirus infection is not an important clinical problem in these populations. Because domestic cats in São Paulo city are naturally infected with these pathogens, and feral cats are commonly found in zoologic facilities in Brazil, preventive measures should be taken to avoid transmission of retroviruses to naive populations of wild and captive neotropic felids in Brazil.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "838", "doc_id": "34074902", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Normal granulomas form in the absence of TNF in Zebrafish.\n\nCANDIDATE_ABSTRACT:\nTITLE: A rapid method for extraction of cotton (Gossypium spp.) genomic DNA suitable for RFLP or PCR analysis\nABSTRACT: Extraction of high-quality genomic DNA fromGossypium (cotton) species is difficult due to high levels of polysaccharide, oxidizable quinones, and other interfering substances. We describe a procedure that consistently permits isolation of cotton genomic DNA of satisfactory size and quality for RFLP and PCR analysis, as well as for most routine cloning applications. Several antioxidants, phenol-binding reagents, and phenol oxidase inhibitors are used throughout the procedure, and most polysaccharides are eliminated early in the procedure by isolation of nuclei.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 860, "doc_id": "102662", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Androgenetic haploid mouse embryonic stem cells (ESCs) can be derived and genetically manipulated in vitro.\n\nCANDIDATE_PASSAGE:\nAn RNA-sequencing transcriptome and splicing database of glia, neurons, and vascular cells of the cerebral cortex. The major cell classes of the brain differ in their developmental processes, metabolism, signaling, and function. To better understand the functions and interactions of the cell types that comprise these classes, we acutely purified representative populations of neurons, astrocytes, oligodendrocyte precursor cells, newly formed oligodendrocytes, myelinating oligodendrocytes, microglia, endothelial cells, and pericytes from mouse cerebral cortex. We generated a transcriptome database for these eight cell types by RNA sequencing and used a sensitive algorithm to detect alternative splicing events in each cell type. Bioinformatic analyses identified thousands of new cell type-enriched genes and splicing isoforms that will provide novel markers for cell identification, tools for genetic manipulation, and insights into the biology of the brain. For example, our data provide clues as to how neurons and astrocytes differ in their ability to dynamically regulate glycolytic flux and lactate generation attributable to unique splicing of PKM2, the gene encoding the glycolytic enzyme pyruvate kinase. This dataset will provide a powerful new resource for understanding the development and function of the brain. To ensure the widespread distribution of these datasets, we have created a user-friendly website (http://web.stanford.edu/group/barres_lab/brain_rnaseq.html) that provides a platform for analyzing and comparing transciption and alternative splicing profiles for various cell classes in the brain.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "111", "doc_id": "13921526", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Tirasemtiv has no effect on cardiac muscle.\n\nCANDIDATE_PASSAGE:\nActivation of fast skeletal muscle troponin as a potential therapeutic approach for treating neuromuscular diseases Limited neural input results in muscle weakness in neuromuscular disease because of a reduction in the density of muscle innervation, the rate of neuromuscular junction activation or the efficiency of synaptic transmission. We developed a small-molecule fast-skeletal-troponin activator, CK-2017357, as a means to increase muscle strength by amplifying the response of muscle when neural input is otherwise diminished secondary to neuromuscular disease. Binding selectively to the fast-skeletal-troponin complex, CK-2017357 slows the rate of calcium release from troponin C and sensitizes muscle to calcium. As a consequence, the force-calcium relationship of muscle fibers shifts leftwards, as does the force-frequency relationship of a nerve-muscle pair, so that CK-2017357 increases the production of muscle force in situ at sub-maximal nerve stimulation rates. Notably, we show that sensitization of the fast-skeletal-troponin complex to calcium improves muscle force and grip strength immediately after administration of single doses of CK-2017357 in a model of the neuromuscular disease myasthenia gravis. Troponin activation may provide a new therapeutic approach to improve physical activity in diseases where neuromuscular function is compromised.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1302", "doc_id": "12631697", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Inhibiting focal adhesion formation increases the rate at which cells convert mechanical strain into inflammation and fibrosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Focal adhesion kinase links mechanical force to skin fibrosis via inflammatory signaling\nABSTRACT: Exuberant fibroproliferation is a common complication after injury for reasons that are not well understood. One key component of wound repair that is often overlooked is mechanical force, which regulates cell-matrix interactions through intracellular focal adhesion components, including focal adhesion kinase (FAK). Here we report that FAK is activated after cutaneous injury and that this process is potentiated by mechanical loading. Fibroblast-specific FAK knockout mice have substantially less inflammation and fibrosis than control mice in a model of hypertrophic scar formation. We show that FAK acts through extracellular-related kinase (ERK) to mechanically trigger the secretion of monocyte chemoattractant protein-1 (MCP-1, also known as CCL2), a potent chemokine that is linked to human fibrotic disorders. Similarly, MCP-1 knockout mice form minimal scars, indicating that inflammatory chemokine pathways are a major mechanism by which FAK mechanotransduction induces fibrosis. Small-molecule inhibition of FAK blocks these effects in human cells and reduces scar formation in vivo through attenuated MCP-1 signaling and inflammatory cell recruitment. These findings collectively indicate that physical force regulates fibrosis through inflammatory FAK–ERK–MCP-1 pathways and that molecular strategies targeting FAK can effectively uncouple mechanical force from pathologic scar formation.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"These findings collectively indicate that physical force regulates fibrosis through inflammatory FAK–ERK–MCP-1 pathways and that molecular strategies targeting FAK can effectively uncouple mechanical force from pathologic scar formation.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 633, "doc_id": "5172048", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Gpr124 increases BBB breakdown in mouse models of ischemic stroke.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pleiotropy as a mechanism to stabilize cooperation\nABSTRACT: Most genes affect many traits. This phenomenon, known as pleiotropy, is a major constraint on evolution because adaptive change in one trait may be prevented because it would compromise other traits affected by the same genes. Here we show that pleiotropy can have an unexpected effect and benefit one of the most enigmatic of adaptations—cooperation. A spectacular act of cooperation occurs in the social amoeba Dictyostelium discoideum, in which some cells die to form a stalk that holds the other cells aloft as reproductive spores. We have identified a gene, dimA, in D. discoideum that has two contrasting effects. It is required to receive the signalling molecule DIF-1 that causes differentiation into prestalk cells. Ignoring DIF-1 and not becoming prestalk should allow cells to cheat by avoiding the stalk. However, we find that in aggregations containing the wild-type cells, lack of the dimA gene results in exclusion from spores. This pleiotropic linkage of stalk and spore formation limits the potential for cheating in D. discoideum because defecting on prestalk cell production results in an even greater reduction in spores. We propose that the evolution of pleiotropic links between cheating and personal costs can stabilize cooperative adaptations.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 479, "doc_id": "2140513", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Antimicrobial agents are less effective due to the pressure of antimicrobial usage.\n\nCANDIDATE_PASSAGE:\nAssociation between infection with Helicobacter pylori and risk of gastric cancer: evidence from a prospective investigation. OBJECTIVE To investigate the association between gastric cancer and prior infection with Helicobacter pylori. DESIGN Case-control comparison of prevalence of IgG antibodies to H pylori in blood samples collected prospectively, before diagnosis of gastric cancer in the cases. Presence of H pylori antibody (greater than 10 micrograms IgG/ml) determined by enzyme linked immunosorbent assay (ELISA). SUBJECTS 29 men with a subsequent diagnosis of gastric cancer and 116 aged matched controls selected from over 22,000 middle aged men participating in two ongoing cohort studies (the British United Provident Association study and the Caerphilly collaborative heart disease study), who had provided blood samples during 1975-1982. RESULTS 20 of the 29 cases (69%) and 54 of the 116 controls (47%) were positive for H pylori specific antibody. The median specific IgG concentration was significantly higher in the cases than controls (90 micrograms/ml v 3.6 micrograms/ml, p less than 0.01). The estimated odds ratio for the risk of gastric cancer in those with a history of infection with H pylori was 2.77 (95% confidence interval 1.04 to 7.97, 2p = 0.039). CONCLUSIONS H pylori infection may be an important cause of gastric cancer; between 35% and 55% of all cases may be associated with such an infection.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "121", "doc_id": "2052720", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Birth-weight is negatively associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Role of birthweight in the etiology of breast cancer.\nABSTRACT: Breast cancer may originate in utero. We reviewed the available evidence on the association between birthweight and the risk of breast cancer. To date, 26 research papers addressing this issue have been published. The majority of studies identified a positive link between birthweight and premenopausal, but not postmenopausal, breast cancer. The relative risk estimate for breast cancer comparing women with high birthweight to women with low birthweight combining all studies including both pre- and postmenopausal breast cancer was 1.23 (95% confidence interval 1.13-1.34). The mechanisms underlying this association likely include elevated levels of growth factors that may increase the number of susceptible stem cells in the mammary gland or initiate tumors through DNA mutations. Loss of imprinting (LOI) of growth hormone genes relevant for intrauterine growth, such as insulin-like growth factor 2 (IGF2), leads to abnormally high levels of these hormones evidenced by high birthweight. LOI of IGF2 has also been found in mammary tumor tissue. The role of environmental factors that stimulate such epigenetic regulation of gene expression remains to be elucidated.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The relative risk estimate for breast cancer comparing women with high birthweight to women with low birthweight combining all studies including both pre- and postmenopausal breast cancer was 1.23 (95% confidence interval 1.13-1.34).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 178, "doc_id": "27123743", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Anthrax spores remain deadly until affected areas are decontaminated.\n\nCANDIDATE_ABSTRACT:\nTITLE: Gender-dependent differences in outcome after the treatment of infection in hospitalized patients.\nABSTRACT: CONTEXT While it is established that management strategies and outcomes differ by gender for many diseases, its effect on infection has not been adequately studied. OBJECTIVE To investigate the role of gender among hospitalized patients treated for infection. DESIGN Observational cohort study conducted during a 26-month period from December 1996 through January 1999. SETTING University-affiliated hospital. PARTICIPANTS A total of 892 patients in the surgical units of the hospital with 1470 consecutive infectious episodes (782 in men and 688 in women). MAIN OUTCOME MEASURES Mortality during hospitalization by gender for infection episodes overall and for specific infectious sites, including lung, peritoneum, bloodstream, catheter, urine, surgical site, and skin/soft tissue. RESULTS Among all infections, there was no significant difference in mortality based on gender (men, 11.1% vs women, 14.2%; P = .07). After logistic regression analysis, factors independently associated with mortality included higher APACHE (Acute Physiology and Chronic Health Evaluation) II score, older age, malignancy, blood transfusion, and diagnosis of infection more than 7 days after admission, but not gender (female odds ratio [OR] for death, 1.32; 95% confidence interval [CI], 0.90-1.94; P = .16). Mortality was higher in women for lung (men, 18% vs women, 34%; P = .002) and soft tissue (men, 2% vs women, 10%; P < or = .05) infection; for other infectious sites, mortality did not differ by gender. Factors associated with mortality due to pneumonia by logistic regression included higher APACHE II score, malignancy, diabetes mellitus, diagnosis of infection more than 7 days after admission, older age, transplantation, and female gender (OR for death, 2.25; 95% CI, 1.17-4.32; P = .02). [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 116, "doc_id": "2488880", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Obesity raises life quality.\n\nCANDIDATE_PASSAGE:\nCollective trauma in northern Sri Lanka: a qualitative psychosocial-ecological study BACKGROUND Complex situations that follow war and natural disasters have a psychosocial impact on not only the individual but also on the family, community and society. Just as the mental health effects on the individual psyche can result in non pathological distress as well as a variety of psychiatric disorders; massive and widespread trauma and loss can impact on family and social processes causing changes at the family, community and societal levels. METHOD This qualitative, ecological study is a naturalistic, psychosocial ethnography in Northern Sri Lanka, while actively involved in psychosocial and community mental health programmes among the Tamil community. Participatory observation, key informant interviews and focus group discussion with community level relief and rehabilitation workers and government and non-governmental officials were used to gather data. The effects on the community of the chronic, man-made disaster, war, in Northern Sri Lanka were compared with the contexts found before the war and after the tsunami. RESULTS Fundamental changes in the functioning of the family and the community were observed. While the changes after the tsunami were not so prominent, the chronic war situation caused more fundamental social transformations. At the family level, the dynamics of single parent families, lack of trust among members, and changes in significant relationships, and child rearing practices were seen. Communities tended to be more dependent, passive, silent, without leadership, mistrustful, and suspicious. Additional adverse effects included the breakdown in traditional structures, institutions and familiar ways of life, and deterioration in social norms a [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "876", "doc_id": "15780826", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Major vault protein regulates sorting of tumor suppressive miR-193a into EVs.\n\nCANDIDATE_PASSAGE:\nA SUMO-Dependent Protein Network Regulates Chromosome Congression during Oocyte Meiosis During Caenorhabditis elegans oocyte meiosis, a multi-protein ring complex (RC) localized between homologous chromosomes, promotes chromosome congression through the action of the chromokinesin KLP-19. While some RC components are known, the mechanism of RC assembly has remained obscure. We show that SUMO E3 ligase GEI-17/PIAS is required for KLP-19 recruitment to the RC, and proteomic analysis identified KLP-19 as a SUMO substrate in vivo. In vitro analysis revealed that KLP-19 is efficiently sumoylated in a GEI-17-dependent manner, while GEI-17 undergoes extensive auto-sumoylation. GEI-17 and another RC component, the kinase BUB-1, contain functional SUMO interaction motifs (SIMs), allowing them to recruit SUMO modified proteins, including KLP-19, into the RC. Thus, dynamic SUMO modification and the presence of SIMs in RC components generate a SUMO-SIM network that facilitates assembly of the RC. Our results highlight the importance of SUMO-SIM networks in regulating the assembly of dynamic protein complexes.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "752", "doc_id": "23577014", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: 4-PBA treatment decreases endoplasmic reticulum stress in response to general endoplasmic reticulum stress markers.\n\nCANDIDATE_PASSAGE:\nAntimicrobial peptide pleurocidin synergizes with antibiotics through hydroxyl radical formation and membrane damage, and exerts antibiofilm activity. BACKGROUND Pleurocidin, a 25-mer antimicrobial peptide (AMP), is known to exert bactericidal activity. However, the synergistic activity and mechanism(s) of pleurocidin in combination with conventional antibiotics, and the antibiofilm effect of the peptide are poorly understood. METHODS The interaction between pleurocidin and antibiotics was evaluated using checkerboard assay. To study the mechanism(s) involved in their synergism, we detected hydroxyl radical formation using 3'-(p-hydroxyphenyl) fluorescein, measured the NAD(+)/NADH ratio by NAD(+) cycling assay, observed change in bacterial viability with the hydroxyl radical scavenger thiourea, and investigated cytoplasmic membrane damage using propidium iodide. Also, the antibiofilm effect of pleurocidin was examined with the tissue culture plate method. RESULTS All combinations of pleurocidin and antibiotics showed synergistic interaction against bacterial strains (fractional inhibitory concentration index (FICI)≤0.5) except for Enterococcus faecium treated with a combination of the peptide and ampicillin (FICI=0.75). We identified that pleurocidin alone and in combinations with antibiotics induced formation of hydroxyl radicals. The oxidative stress was caused by a transient NADH depletion and the addition of thiourea prevented bacterial death, especially in the case of the combined treatment of pleurocidin and ampicillin showing synergisms. The combination of pleurocidin and erythromycin increased permeability of bacterial cytoplasmic membrane. Additionally, pleurocidin exhibited a potent inhibitory effect on preformed biofilm of bacterial organisms. In [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "10", "doc_id": "350542", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Intra-cerebroventricular infusion of amyloid-β oligomers reduces expression of fibronectin type-III domain-containing protein 5 mRNA in mice hippocampi.\n\nCANDIDATE_PASSAGE:\nEpigenetic therapy activates type I interferon signaling in murine ovarian cancer to reduce immunosuppression and tumor burden. Ovarian cancer is the most lethal of all gynecological cancers, and there is an urgent unmet need to develop new therapies. Epithelial ovarian cancer (EOC) is characterized by an immune suppressive microenvironment, and response of ovarian cancers to immune therapies has thus far been disappointing. We now find, in a mouse model of EOC, that clinically relevant doses of DNA methyltransferase and histone deacetylase inhibitors (DNMTi and HDACi, respectively) reduce the immune suppressive microenvironment through type I IFN signaling and improve response to immune checkpoint therapy. These data indicate that the type I IFN response is required for effective in vivo antitumorigenic actions of the DNMTi 5-azacytidine (AZA). Through type I IFN signaling, AZA increases the numbers of CD45+ immune cells and the percentage of active CD8+ T and natural killer (NK) cells in the tumor microenvironment, while reducing tumor burden and extending survival. AZA also increases viral defense gene expression in both tumor and immune cells, and reduces the percentage of macrophages and myeloid-derived suppressor cells in the tumor microenvironment. The addition of an HDACi to AZA enhances the modulation of the immune microenvironment, specifically increasing T and NK cell activation and reducing macrophages over AZA treatment alone, while further increasing the survival of the mice. Finally, a triple combination of DNMTi/HDACi plus the immune checkpoint inhibitor α-PD-1 provides the best antitumor effect and longest overall survival, and may be an attractive candidate for future clinical trials in ovarian cancer.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "655", "doc_id": "9767444", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The risk of breast cancer among parous women increases with placental weight of pregnancies, and this association is strongest for premenopausal breast cancer.\n\nCANDIDATE_PASSAGE:\nResponses of primate frontal cortex neurons during natural vocal communication. The role of primate frontal cortex in vocal communication and its significance in language evolution have a controversial history. While evidence indicates that vocalization processing occurs in ventrolateral prefrontal cortex neurons, vocal-motor activity has been conjectured to be primarily subcortical and suggestive of a distinctly different neural architecture from humans. Direct evidence of neural activity during natural vocal communication is limited, as previous studies were performed in chair-restrained animals. Here we recorded the activity of single neurons across multiple regions of prefrontal and premotor cortex while freely moving marmosets engaged in a natural vocal behavior known as antiphonal calling. Our aim was to test whether neurons in marmoset frontal cortex exhibited responses during vocal-signal processing and/or vocal-motor production in the context of active, natural communication. We observed motor-related changes in single neuron activity during vocal production, but relatively weak sensory responses for vocalization processing during this natural behavior. Vocal-motor responses occurred both prior to and during call production and were typically coupled to the timing of each vocalization pulse. Despite the relatively weak sensory responses a population classifier was able to distinguish between neural activity that occurred during presentations of vocalization stimuli that elicited an antiphonal response and those that did not. These findings are suggestive of the role that nonhuman primate frontal cortex neurons play in natural communication and provide an important foundation for more explicit tests of the functional contributions of these neocortica [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1266", "doc_id": "14195528", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Cholesterol loading induces KLF4 expression in VSMCs, resulting in the expression of pro-inflammatory cytokines.\n\nCANDIDATE_PASSAGE:\nIL-23–responsive innate lymphoid cells are increased in inflammatory bowel disease Results of experimental and genetic studies have highlighted the role of the IL-23/IL-17 axis in the pathogenesis of inflammatory bowel disease (IBD). IL-23-driven inflammation has been primarily linked to Th17 cells; however, we have recently identified a novel population of innate lymphoid cells (ILCs) in mice that produces IL-17, IL-22, and IFN-γ in response to IL-23 and mediates innate colitis. The relevance of ILC populations in human health and disease is currently poorly understood. In this study, we have analyzed the role of IL-23-responsive ILCs in the human intestine in control and IBD patients. Our results show increased expression of the Th17-associated cytokine genes IL17A and IL17F among intestinal CD3⁻ cells in IBD. IL17A and IL17F expression is restricted to CD56⁻ ILCs, whereas IL-23 induces IL22 and IL26 in the CD56⁺ ILC compartment. Furthermore, we observed a significant and selective increase in CD127⁺CD56⁻ ILCs in the inflamed intestine in Crohn's disease (CD) patients but not in ulcerative colitis patients. These results indicate that IL-23-responsive ILCs are present in the human intestine and that intestinal inflammation in CD is associated with the selective accumulation of a phenotypically distinct ILC population characterized by inflammatory cytokine expression. ILCs may contribute to intestinal inflammation through cytokine production, lymphocyte recruitment, and organization of the inflammatory tissue and may represent a novel tissue-specific target for subtypes of IBD.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "258", "doc_id": "1022115", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Early patent ductus ateriosus (PDA) screening increases in-hospital mortality.\n\nCANDIDATE_PASSAGE:\nUp-regulation of PPAR-gamma mRNA expression in the liver of obese patients: an additional reinforcing lipogenic mechanism to SREBP-1c induction. INTRODUCTION Triglyceride accumulation in the liver is an early feature in the development of nonalcoholic fatty liver disease (NAFLD) associated with human obesity, which is a multifactorial syndrome and whose underlying mechanisms are beginning to be understood. OBJECTIVES Liver peroxisome proliferator-activated receptor-γ (PPAR-γ) mRNA expression was measured as a signaling mechanism related to steatosis in obese patients with NAFLD. METHODS Liver PPAR-γ and sterol receptor element-binding protein 1c (SREBP-1c) mRNA (real-time RT-PCR), serum total adiponectin (RIA), and high molecular weight (HMW)-adiponectin (ELISA) levels, and insulin resistance (IR) evolution (homeostasis model assessment-IR) were determined in 22 obese NAFLD patients (16 with steatosis and six with steatohepatitis) who underwent subtotal gastrectomy with gastrojejunal anastomosis in Roux-en-Y and 16 nonobese subjects who underwent laparoscopic cholecystectomy (controls). RESULTS Liver PPAR-γ mRNA levels were 112 and 188% higher (P < 0.05) than control values in obese patients with steatosis and steatohepatitis, respectively, who also exhibited 70 and 62% increases in those of SREBP-1c, concomitantly with IR and lower levels of serum total adiponectin and HMW-adiponectin (P < 0.05). Liver PPAR-γ expression showed positive associations with SREBP-1c mRNA levels (r = 0.86; P < 0.0001), serum insulin levels (r = 0.39; P < 0.01), and homeostasis model assessment-IR (r = 0.60; P < 0.0001), and negative correlations with total adiponectin (r = -0.37; P < 0.01) and HMW-adiponectin (r = -0.51; P < 0.001) levels in serum. CONCLUSIONS PPAR-γ is up-regul [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "368", "doc_id": "22478394", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: IRG1 has antiviral effects against neurotropic viruses.\n\nCANDIDATE_ABSTRACT:\nTITLE: Murine Dishevelled 3 Functions in Redundant Pathways with Dishevelled 1 and 2 in Normal Cardiac Outflow Tract, Cochlea, and Neural Tube Development\nABSTRACT: Dishevelled (Dvl) proteins are important signaling components of both the canonical beta-catenin/Wnt pathway, which controls cell proliferation and patterning, and the planar cell polarity (PCP) pathway, which coordinates cell polarity within a sheet of cells and also directs convergent extension cell (CE) movements that produce narrowing and elongation of the tissue. Three mammalian Dvl genes have been identified and the developmental roles of Dvl1 and Dvl2 were previously determined. Here, we identify the functions of Dvl3 in development and provide evidence of functional redundancy among the three murine Dvls. Dvl3(-/-) mice died perinatally with cardiac outflow tract abnormalities, including double outlet right ventricle and persistent truncus arteriosis. These mutants also displayed a misorientated stereocilia in the organ of Corti, a phenotype that was enhanced with the additional loss of a single allele of the PCP component Vangl2/Ltap (LtapLp/+). Although neurulation appeared normal in both Dvl3(-/-) and LtapLp/+ mutants, Dvl3(+/-);LtapLp/+ combined mutants displayed incomplete neural tube closure. Importantly, we show that many of the roles of Dvl3 are also shared by Dvl1 and Dvl2. More severe phenotypes were observed in Dvl3 mutants with the deficiency of another Dvl, and increasing Dvl dosage genetically with Dvl transgenes demonstrated the ability of Dvls to compensate for each other to enable normal development. Interestingly, global canonical Wnt signaling appeared largely unaffected in the double Dvl mutants, suggesting that low Dvl levels are sufficient for functional canonical Wnt signals. In summary, we demonstrate that Dvl3 is required for cardiac outflow tract development and describe its importance in the PCP pathway during neurulation a [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 549, "doc_id": "317204", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Varenicline monotherapy is more effective after 26 weeks of treatment compared to combination nicotine replacement therapies with varenicline or bupropion.\n\nCANDIDATE_PASSAGE:\nCoordinate regulation of the IL-4, IL-13, and IL-5 cytokine cluster in Th2 clones revealed by allelic expression patterns. The cytokines IL-4, IL-13, and IL-5 are markers for the Th2 subset of effector T cells and are often expressed together. These cytokine genes are organized within 140 kb of orthologous DNA in both mouse and human. Using IL-4-expressing CD4+ T cell clones derived from F1 mice, we identified allelic polymorphisms for each of these cytokines and assessed the parental identity of the cytokine mRNAs. Both monoallelic and biallelic expression occurred for each gene and for an additional gene, IL-3, that lies with GM-CSF over 450 kb telomeric on the same chromosome. When coexpressed in T cell clones, IL-4 was expressed from the same allele as IL-13 or IL-5 in 81% of instances. In contrast, there was only 52% concordance of these three cytokines at the allelic level among clones that expressed IL-3. Independent expression of the cytokine alleles occurs commonly in T cells, but the clustered locus encompassing IL-4, IL-13, and IL-5 is subject to coordinate regulation.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1360", "doc_id": "36242796", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: RTEL1 interacts with TRF2 through a C4C4 motif\n\nCANDIDATE_ABSTRACT:\nTITLE: TRF2 Recruits RTEL1 to Telomeres in S Phase to Promote T-Loop Unwinding\nABSTRACT: The helicase RTEL1 promotes t-loop unwinding and suppresses telomere fragility to maintain the integrity of vertebrate telomeres. An interaction between RTEL1 and PCNA is important to prevent telomere fragility, but how RTEL1 engages with the telomere to promote t-loop unwinding is unclear. Here, we establish that the shelterin protein TRF2 recruits RTEL1 to telomeres in S phase, which is required to prevent catastrophic t-loop processing by structure-specific nucleases. We show that the TRF2-RTEL1 interaction is mediated by a metal-coordinating C4C4 motif in RTEL1, which is compromised by the Hoyeraal-Hreidarsson syndrome (HHS) mutation, RTEL1(R1264H). Conversely, we define a TRF2(I124D) substitution mutation within the TRFH domain of TRF2, which eliminates RTEL1 binding and phenocopies the RTEL1(R1264H) mutation, giving rise to aberrant t-loop excision, telomere length heterogeneity, and loss of the telomere as a circle. These results implicate TRF2 in the recruitment of RTEL1 to facilitate t-loop disassembly at telomeres in S phase.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We show that the TRF2-RTEL1 interaction is mediated by a metal-coordinating C4C4 motif in RTEL1, which is compromised by the Hoyeraal-Hreidarsson syndrome (HHS) mutation, RTEL1(R1264H).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1006, "doc_id": "4926049", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Sildenafil worsens erectile function in men who experience sexual dysfunction as a result of the use of SSRI antidepressants.\n\nCANDIDATE_ABSTRACT:\nTITLE: Treatment of antidepressant-associated sexual dysfunction with sildenafil: a randomized controlled trial.\nABSTRACT: CONTEXT Sexual dysfunction is a common adverse effect of antidepressants that frequently results in treatment noncompliance. OBJECTIVE To assess the efficacy of sildenafil citrate in men with sexual dysfunction associated with the use of selective and nonselective serotonin reuptake inhibitor (SRI) antidepressants. DESIGN, SETTING, AND PATIENTS Prospective, parallel-group, randomized, double-blind, placebo-controlled trial conducted between November 1, 2000, and January 1, 2001, at 3 US university medical centers among 90 male outpatients (mean [SD] age, 45 [8] years) with major depression in remission and sexual dysfunction associated with SRI antidepressant treatment. INTERVENTION Patients were randomly assigned to take sildenafil (n = 45) or placebo (n = 45) at a flexible dose starting at 50 mg and adjustable to 100 mg before sexual activity for 6 weeks. MAIN OUTCOME MEASURES The primary outcome measure was score on the Clinical Global Impression-Sexual Function (CGI-SF); secondary measures were scores on the International Index of Erectile Function, Arizona Sexual Experience Scale, Massachusetts General Hospital-Sexual Functioning Questionnaire, and Hamilton Rating Scale for Depression (HAM-D). RESULTS Among the 90 randomized patients, 93% (83/89) of patients treated per protocol took at least 1 dose of study drug and 85% (76/89) completed week 6 end-point assessments with last observation carried forward analyses. At a CGI-SF score of 2 or lower, 54.5% (24/44) of sildenafil compared with 4.4% (2/45) of placebo patients were much or very much improved (P<.001). Erectile function, arousal, ejaculation, orgasm, and overall satisfaction domain measures improved significantly in sildenafil compared with placebo patients. Mean depression scores remained consi [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Erectile function, arousal, ejaculation, orgasm, and overall satisfaction domain measures improved significantly in sildenafil compared with placebo patients.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1087, "doc_id": "39281140", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Birth-weight is positively associated with breast cancer.\n\nCANDIDATE_PASSAGE:\nIntrauterine environments and breast cancer risk: meta-analysis and systematic review INTRODUCTION Various perinatal factors, including birth weight, birth order, maternal age, gestational age, twin status, and parental smoking, have been postulated to affect breast cancer risk in daughters by altering the hormonal environment of the developing fetal mammary glands. Despite ample biologic plausibility, epidemiologic studies to date have yielded conflicting results. We investigated the associations between perinatal factors and subsequent breast cancer risk through meta-analyses. METHODS We reviewed breast cancer studies published from January 1966 to February 2007 that included data on birth weight, birth order, maternal age, gestational age, twin status, and maternal or paternal smoking. Meta-analyses using random effect models were employed to summarize the results. RESULTS We found that heavier birth weights were associated with increased breast cancer risk, with studies involving five categories of birth weight identifying odds ratios (ORs) of 1.24 (95% confidence interval [CI] 1.04 to 1.48) for 4,000 g or more and 1.15 (95% CI 1.04 to 1.26) for 3,500 g to 3,999 g, relative to a birth weight of 2,500 to 2,599 g. These studies provided no support for a J-shaped relationship of birthweight to risk. Support for an association with birthweight was also derived from studies based on three birth weight categories (OR 1.15 [95% CI 1.01 to 1.31] for > or =4,000 g relative to <3,000 g) and two birth weight categories (OR 1.09 [95% CI 1.02 to 1.18] for > or =3,000 g relative to <3,000 g). Women born to older mothers and twins were also at some increased risk, but the results were heterogeneous across studies and publication years. Birth order, prematurity, and mat [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "179", "doc_id": "17450673", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Expression of MSX2 is induced 3 hours after the addition of BMP4, which is earlier than T and CDX2.\n\nCANDIDATE_PASSAGE:\nMembrane estrogen receptor-α levels in MCF-7 breast cancer cells predict cAMP and proliferation responses 17β-estradiol (E2) can rapidly induce cAMP production, but the conditions under which these cAMP levels are best measured and the signaling pathways responsible for the consequent proliferative effects on breast cancer cells are not fully understood. To help resolve these issues, we compared cAMP mechanistic responses in MCF-7 cell lines selected for low (mERlow) and high (mERhigh) expression of the membrane form of estrogen receptor (mER)-α, and thus addressed the receptor subform involved in cAMP signaling. MCF-7 cells were immunopanned and subsequently separated by fluorescence activated cell sorting into mERhigh (mER-α-enriched) and mERlow (mER-α-depleted) populations. Unique (compared with previously reported) incubation conditions at 4°C were found to be optimal for demonstrating E2-induced cAMP production. Time-dependent and dose-dependent effects of E2 on cAMP production were determined for both cell subpopulations. The effects of forskolin, 8-CPT cAMP, protein kinase A inhibitor (H-89), and adenylyl cyclase inhibitor (SQ 22,536) on E2-induced cell proliferation were assessed using the crystal violet assay. We demonstrated a rapid and transient cAMP increase after 1 pmol/l E2 stimulation in mERhigh cells; at 4°C these responses were much more reliable and robust than at 37°C (the condition most often used). The loss of cAMP at 37°C was not due to export. 3-Isobutyl-1-methylxanthine (IBMX; 1 mmol/l) only partially preserved cAMP, suggesting that multiple phosphodiesterases modulate its level. The accumulated cAMP was consistently much higher in mERhigh cells than in mERlow cells, implicating mER-α levels in the process. ICI172,780 blocked the E2-i [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "401", "doc_id": "4999633", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: There is no known interaction between Pioneer factor OCT3/4 and major chromatin remodeling factors.\n\nCANDIDATE_ABSTRACT:\nTITLE: An Oct4-Centered Protein Interaction Network in Embryonic Stem Cells\nABSTRACT: Transcription factors, such as Oct4, are critical for establishing and maintaining pluripotent cell identity. Whereas the genomic locations of several pluripotency transcription factors have been reported, the spectrum of their interaction partners is underexplored. Here, we use an improved affinity protocol to purify Oct4-interacting proteins from mouse embryonic stem cells (ESCs). Subsequent purification of Oct4 partners Sall4, Tcfcp2l1, Dax1, and Esrrb resulted in an Oct4 interactome of 166 proteins, including transcription factors and chromatin-modifying complexes with documented roles in self-renewal, but also many factors not previously associated with the ESC network. We find that Esrrb associated with the basal transcription machinery and also detect interactions between transcription factors and components of the TGF-beta, Notch, and Wnt signaling pathways. Acute depletion of Oct4 reduced binding of Tcfcp2l1, Dax1, and Esrrb to several target genes. In conclusion, our purification protocol allowed us to bring greater definition to the circuitry controlling pluripotent cell identity.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Subsequent purification of Oct4 partners Sall4, Tcfcp2l1, Dax1, and Esrrb resulted in an Oct4 interactome of 166 proteins, including transcription factors and chromatin-modifying complexes with documented roles in self-renewal, but also many factors not previously associated with the ESC network.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1294, "doc_id": "30507607", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: IL-6 signaling plays a major role in atherosclerotic cardiovascular disease.\n\nCANDIDATE_ABSTRACT:\nTITLE: Interleukin-6 receptor pathways in coronary heart disease: a collaborative meta-analysis of 82 studies\nABSTRACT: BACKGROUND Persistent inflammation has been proposed to contribute to various stages in the pathogenesis of cardiovascular disease. Interleukin-6 receptor (IL6R) signalling propagates downstream inflammation cascades. To assess whether this pathway is causally relevant to coronary heart disease, we studied a functional genetic variant known to affect IL6R signalling. METHODS In a collaborative meta-analysis, we studied Asp358Ala (rs2228145) in IL6R in relation to a panel of conventional risk factors and inflammation biomarkers in 125,222 participants. We also compared the frequency of Asp358Ala in 51,441 patients with coronary heart disease and in 136,226 controls. To gain insight into possible mechanisms, we assessed Asp358Ala in relation to localised gene expression and to postlipopolysaccharide stimulation of interleukin 6. FINDINGS The minor allele frequency of Asp358Ala was 39%. Asp358Ala was not associated with lipid concentrations, blood pressure, adiposity, dysglycaemia, or smoking (p value for association per minor allele ≥0·04 for each). By contrast, for every copy of 358Ala inherited, mean concentration of IL6R increased by 34·3% (95% CI 30·4-38·2) and of interleukin 6 by 14·6% (10·7-18·4), and mean concentration of C-reactive protein was reduced by 7·5% (5·9-9·1) and of fibrinogen by 1·0% (0·7-1·3). For every copy of 358Ala inherited, risk of coronary heart disease was reduced by 3·4% (1·8-5·0). Asp358Ala was not related to IL6R mRNA levels or interleukin-6 production in monocytes. INTERPRETATION Large-scale human genetic and biomarker data are consistent with a causal association between IL6R-related pathways and coronary heart disease. FUNDING British Heart Foundation; UK Medical Research Council; UK National Institute of Health Research, Cambr [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"By contrast, for every copy of 358Ala inherited, mean concentration of IL6R increased by 34·3% (95% CI 30·4-38·2) and of interleukin 6 by 14·6% (10·7-18·4), and mean concentration of C-reactive protein was reduced by 7·5% (5·9-9·1) and of fibrinogen by 1·0% (0·7-1·3). For every copy of 358Ala inherited, risk of coronary heart disease was reduced by 3·4% (1·8-5·0).\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 548, "doc_id": "18199839", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The density of cytokine receptor bearing cells affects the distance over which cytokines act.\n\nCANDIDATE_PASSAGE:\nSurgical Resection for Patients with Solid Brain Metastases: Current Status Brain metastases occur in up to 40% of patients with cancer. Their management has been revolutionized in the last decade by three developments: improved imaging and detection of metastases, better treatment of systemic disease with the result that metastases occur more often; and improved surgical techniques including image-guided surgery to treat metastatic lesions. Class 1 data suggest that surgery is a better treatment for metastases than whole brain radiation. Other data suggest that metastases even in eloquent cortex can be removed safely. The complication rate is low and the recurrence rate is less than 10%. In general, indications for surgery include a mass with an unknown primary; a symptomatic mass including one in eloquent areas; a mass with considerable edema requiring high dose steroids; a mass greater than 3 cm; or patient preference when radiosurgery may also be an option. The question of radiosurgery or whole brain radiation as adjunct to surgical removal requires further evaluation.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1210", "doc_id": "23639838", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Female carriers of the Apolipoprotein E4 (APOE4) allele have decreased risk for dementia.\n\nCANDIDATE_ABSTRACT:\nTITLE: Control of immunity by the TNFR-related molecule OX40 (CD134).\nABSTRACT: TNFR/TNF superfamily members can control diverse aspects of immune function. Research over the past 10 years has shown that one of the most important and prominent interactions in this family is that between OX40 (CD134) and its partner OX40L (CD252). These molecules strongly regulate conventional CD4 and CD8 T cells, and more recent data are highlighting their ability to modulate NKT cell and NK cell function as well as to mediate cross-talk with professional antigen-presenting cells and diverse cell types such as mast cells, smooth muscle cells, and endothelial cells. Additionally, OX40-OX40L interactions alter the differentiation and activity of regulatory T cells. Blocking OX40L has produced strong therapeutic effects in multiple animal models of autoimmune and inflammatory disease, and, in line with a prospective clinical future, reagents that stimulate OX40 signaling are showing promise as adjuvants for vaccination as well as for treatment of cancer.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 413, "doc_id": "2417551", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pyridostatin prevents double-strand breaks accumulation.\n\nCANDIDATE_ABSTRACT:\nTITLE: The mitochondrial RNA-binding protein GRSF1 localizes to RNA granules and is required for posttranscriptional mitochondrial gene expression.\nABSTRACT: RNA-binding proteins are at the heart of posttranscriptional gene regulation, coordinating the processing, storage, and handling of cellular RNAs. We show here that GRSF1, previously implicated in the binding and selective translation of influenza mRNAs, is targeted to mitochondria where it forms granules that colocalize with foci of newly synthesized mtRNA next to mitochondrial nucleoids. GRSF1 preferentially binds RNAs transcribed from three contiguous genes on the light strand of mtDNA, the ND6 mRNA, and the long noncoding RNAs for cytb and ND5, each of which contains multiple consensus binding sequences. RNAi-mediated knockdown of GRSF1 leads to alterations in mitochondrial RNA stability, abnormal loading of mRNAs and lncRNAs on the mitochondrial ribosome, and impaired ribosome assembly. This results in a specific protein synthesis defect and a failure to assemble normal amounts of the oxidative phosphorylation complexes. These data implicate GRSF1 as a key regulator of posttranscriptional mitochondrial gene expression.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 998, "doc_id": "935538", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does vitamin A deficiency alter the pulmonary parenchymal elastic modulus and elastic fiber concentration in rats?\n\nABSTRACT:\nBronchial hyperreactivity is influenced by properties of the conducting airways and the surrounding pulmonary parenchyma, which is tethered to the conducting airways. Vitamin A deficiency (VAD) is associated with an increase in airway hyperreactivity in rats and a decrease in the volume density of alveoli and alveolar ducts. To better define the effects of VAD on the mechanical properties of the pulmonary parenchyma, we have studied the elastic modulus, elastic fibers and elastin gene-expression in rats with VAD, which were supplemented with retinoic acid (RA) or remained unsupplemented. Parenchymal mechanics were assessed before and after the administration of carbamylcholine (CCh) by determining the bulk and shear moduli of lungs that that had been removed from rats which were vitamin A deficient or received a control diet. Elastin mRNA and insoluble elastin were quantified and elastic fibers were enumerated using morphometric methods. Additional morphometric studies were performed to assess airway contraction and alveolar distortion. VAD produced an approximately 2-fold augmentation in the CCh-mediated increase of the bulk modulus and a significant dampening of the increase in shear modulus after CCh, compared to vitamin A sufficient (VAS) rats. RA-supplementation for up to 21 days did not reverse the effects of VAD on the elastic modulus. VAD was also associated with a decrease in the concentration of parenchymal elastic fibers, which was restored and was accompanied by an increase in tropoelastin mRNA after 12 days of RA-treatment. Lung elastin, which was resistant to 0.1 N NaOH at 98 degrees, decreased in VAD and was not restored after 21 days of RA-treatment.", "output": "{\"label\": \"yes\", \"rationale\": \"Alterations in parenchymal mechanics and structure contribute to bronchial hyperreactivity in VAD but they are not reversed by RA-treatment, in contrast to the VAD-related alterations in the airways.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 16033655, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Early patent ductus ateriosus (PDA) screening increases in-hospital mortality.\n\nCANDIDATE_PASSAGE:\nAssociation Between Early Screening for Patent Ductus Arteriosus and In-Hospital Mortality Among Extremely Preterm Infants. IMPORTANCE There is currently no consensus for the screening and treatment of patent ductus arteriosus (PDA) in extremely preterm infants. Less pharmacological closure and more supportive management have been observed without evidence to support these changes. OBJECTIVE To evaluate the association between early screening echocardiography for PDA and in-hospital mortality. DESIGN, SETTING, AND PARTICIPANTS Comparison of screened and not screened preterm infants enrolled in the EPIPAGE 2 national prospective population-based cohort study that included all preterm infants born at less than 29 weeks of gestation and hospitalized in 68 neonatal intensive care units in France from April through December 2011. Two main analyses were performed to adjust for potential selection bias, one using propensity score matching and one using neonatal unit preference for early screening echocardiography as an instrumental variable. EXPOSURES Early screening echocardiography before day 3 of life. MAIN OUTCOMES AND MEASURES The primary outcome was death between day 3 and discharge. The secondary outcomes were major neonatal morbidities (pulmonary hemorrhage, severe bronchopulmonary dysplasia, severe cerebral lesions, and necrotizing enterocolitis). RESULTS Among the 1513 preterm infants with data available to determine exposure, 847 were screened for PDA and 666 were not; 605 infants from each group could be paired. Exposed infants were treated for PDA more frequently during their hospitalization than nonexposed infants (55.1% vs 43.1%; odds ratio [OR], 1.62 [95% CI, 1.31 to 2.00]; absolute risk reduction [ARR] in events per 100 infants, -12.0 [95% CI, -17. [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "368", "doc_id": "27099731", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Medications to treat obesity do not have side effects.\n\nCANDIDATE_PASSAGE:\nLong term pharmacotherapy for obesity and overweight: updated meta-analysis. OBJECTIVE To summarise the long term efficacy of anti-obesity drugs in reducing weight and improving health status. DESIGN Updated meta-analysis of randomised trials. DATA SOURCES Medline, Embase, the Cochrane controlled trials register, the Current Science meta-register of controlled trials, and reference lists of identified articles. All data sources were searched from December 2002 (end date of last search) to December 2006. STUDIES REVIEWED Double blind randomised placebo controlled trials of approved anti-obesity drugs used in adults (age over 18) for one year or longer. RESULTS 30 trials of one to four years' duration met the inclusion criteria: 16 orlistat (n=10 631 participants), 10 sibutramine (n=2623), and four rimonabant (n=6365). Of these, 14 trials were new and 16 had previously been identified. Attrition rates averaged 30-40%. Compared with placebo, orlistat reduced weight by 2.9 kg (95% confidence interval 2.5 kg to 3.2 kg), sibutramine by 4.2 kg (3.6 kg to 4.7 kg), and rimonabant by 4.7 kg (4.1 kg to 5.3 kg). Patients receiving active drug treatment were significantly more likely to achieve 5% and 10% weight loss thresholds. Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein. Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glyca [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "765", "doc_id": "7552215", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: PD-1 triggering on monocytes reduces IL-10 production by monocytes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Programmed death-1–induced interleukin-10 production by monocytes impairs CD4+ T cell activation during HIV infection\nABSTRACT: Viral replication and microbial translocation from the gut to the blood during HIV infection lead to hyperimmune activation, which contributes to the decline in CD4+ T cell numbers during HIV infection. Programmed death-1 (PD-1) and interleukin-10 (IL-10) are both upregulated during HIV infection. Blocking interactions between PD-1 and programmed death ligand-1 (PD-L1) and between IL-10 and IL-10 receptor (IL-10R) results in viral clearance and improves T cell function in animal models of chronic viral infections. Here we show that high amounts of microbial products and inflammatory cytokines in the plasma of HIV-infected subjects lead to upregulation of PD-1 expression on monocytes that correlates with high plasma concentrations of IL-10. Triggering of PD-1 expressed on monocytes by PD-L1 expressed on various cell types induced IL-10 production and led to reversible CD4+ T cell dysfunction. We describe a new function for PD-1 whereby microbial products inhibit T cell expansion and function by upregulating PD-1 levels and IL-10 production by monocytes after binding of PD-1 by PD-L1.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We describe a new function for PD-1 whereby microbial products inhibit T cell expansion and function by upregulating PD-1 levels and IL-10 production by monocytes after binding of PD-1 by PD-L1.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 903, "doc_id": "10648422", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Glucose restriction to 0.05% reduces RLS (replicative life span) by 20-40% in S. cerevisiae.\n\nCANDIDATE_PASSAGE:\nSir2-Independent Life Span Extension by Calorie Restriction in Yeast Calorie restriction slows aging and increases life span in many organisms. In yeast, a mechanistic explanation has been proposed whereby calorie restriction slows aging by activating Sir2. Here we report the identification of a Sir2-independent pathway responsible for a majority of the longevity benefit associated with calorie restriction. Deletion of FOB1 and overexpression of SIR2 have been previously found to increase life span by reducing the levels of toxic rDNA circles in aged mother cells. We find that combining calorie restriction with either of these genetic interventions dramatically enhances longevity, resulting in the longest-lived yeast strain reported thus far. Further, calorie restriction results in a greater life span extension in cells lacking both Sir2 and Fob1 than in cells where Sir2 is present. These findings indicate that Sir2 and calorie restriction act in parallel pathways to promote longevity in yeast and, perhaps, higher eukaryotes.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "472", "doc_id": "7185591", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: cSMAC formation enhances weak ligand signalling.\n\nCANDIDATE_PASSAGE:\nPituitary adenylate cyclase-activating polypeptide (PACAP(1-38)) enhances N-methyl-D-aspartate receptor function and brain-derived neurotrophic factor expression via RACK1. We recently identified a novel mechanism for modulation of the phosphorylation state and function of the N-methyl-d-aspartate (NMDA) receptor via the scaffolding protein RACK1. We found that RACK1 binds both the NR2B subunit of the NMDA receptor and the nonreceptor protein-tyrosine kinase, Fyn. RACK1 inhibits Fyn phosphorylation of NR2B and decreases NMDA receptor-mediated currents in CA1 hippocampal slices (Yaka, R., Thornton, C., Vagts, A. J., Phamluong, K., Bonci, A., and Ron, D. (2002) Proc. Natl. Acad. Sci. U. S. A. 99, 5710-5715). Here, we identified the signaling cascade by which RACK1 is released from the NMDA receptor complex and identified the consequences of the dissociation. We found that activation of the cAMP/protein kinase A pathway in hippocampal slices induced the release of RACK1 from NR2B and Fyn. This resulted in the induction of NR2B phosphorylation and the enhancement of NMDA receptor-mediated activity via Fyn. We identified the neuropeptide, pituitary adenylate cyclase activating polypeptide (PACAP(1-38)), as a ligand that induced phosphorylation of NR2B and enhanced NMDA receptor potentials. Finally, we found that activation of the cAMP/protein kinase A pathway induced the movement of RACK1 to the nuclear compartment in dissociated hippocampal neurons. Nuclear RACK1 in turn was found to regulate the expression of brain-derived neurotrophic factor induced by PACAP(1-38). Taken together our results suggest that activation of adenylate cyclase by PACAP(1-38) results in the release of RACK1 from the NMDA receptor and Fyn. This in turn leads to NMDA receptor phosphoryla [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1385", "doc_id": "23076291", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Chlamydia trachomatis is most prevalent in the UK among sexually-experienced individuals aged 16 to 24.\n\nCANDIDATE_ABSTRACT:\nTITLE: Prevalence, risk factors, and uptake of interventions for sexually transmitted infections in Britain: findings from the National Surveys of Sexual Attitudes and Lifestyles (Natsal)\nABSTRACT: BACKGROUND Population-based estimates of prevalence, risk distribution, and intervention uptake inform delivery of control programmes for sexually transmitted infections (STIs). We undertook the third National Survey of Sexual Attitudes and Lifestyles (Natsal-3) after implementation of national sexual health strategies, and describe the epidemiology of four STIs in Britain (England, Scotland, and Wales) and the uptake of interventions. METHODS Between Sept 6, 2010 and Aug 31, 2012 , we did a probability sample survey of 15,162 women and men aged 16-74 years in Britain. Participants were interviewed with computer-assisted face-to-face and self-completion questionnaires. Urine from a sample of participants aged 16-44 years who reported at least one sexual partner over the lifetime was tested for the presence of Chlamydia trachomatis, type-specific human papillomavirus (HPV), Neisseria gonorrhoeae, and HIV antibody. We describe age-specific and sex-specific prevalences of infection and intervention uptake, in relation to demographic and behavioural factors, and explore changes since Natsal-1 (1990-91) and Natsal-2 (1999-2001). FINDINGS Of 8047 eligible participants invited to provide a urine sample, 4828 (60%) agreed. We excluded 278 samples, leaving 4550 (94%) participants with STI test results. Chlamydia prevalence was 1·5% (95% CI 1·1-2·0) in women and 1·1% (0·7-1·6) in men. Prevalences in individuals aged 16-24 years were 3·1% (2·2-4·3) in women and 2·3% (1·5-3·4) in men. Area-level deprivation and higher numbers of partners, especially without use of condoms, were risk factors. However, 60·4% (45·5-73·7) of chlamydia in women and 43·3% (25·9-62·5) in men was in individuals who had had one partner in the past year. Among sexually active 16-24-year-olds, 54· [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Prevalences in individuals aged 16-24 years were 3·1% (2·2-4·3) in women and 2·3% (1·5-3·4) in men.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 256, "doc_id": "5850219", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Cytochrome c is transferred from cytosol to the mitochondrial intermembrane space during apoptosis.\n\nCANDIDATE_PASSAGE:\nUse of a targeted oncolytic poxvirus, JX-594, in patients with refractory primary or metastatic liver cancer: a phase I trial. BACKGROUND JX-594 is a targeted oncolytic poxvirus designed to selectively replicate in and destroy cancer cells with cell-cycle abnormalities and epidermal growth factor receptor (EGFR)-ras pathway activation. Direct oncolysis plus granulocyte-macrophage colony-stimulating factor (GM-CSF) expression also stimulates shutdown of tumour vasculature and antitumoral immunity. We aimed to assess intratumoral injection of JX-594 in patients with refractory primary or metastatic liver cancer. METHODS Between Jan 4, 2006, and July 4, 2007, 14 patients with histologically confirmed refractory primary or metastatic liver tumours (up to 10.9 cm total diameter) that were amenable to image-guided intratumoral injections were enrolled into this non-comparative, open-label, phase I dose-escalation trial (standard 3x3 design; two to six patients for each dose with 12-18 estimated total patients). Patients received one of four doses of intratumoral JX-594 (10(8) plaque-forming units [pfu], 3x10(8) pfu, 10(9) pfu, or 3x10(9) pfu) every 3 weeks at Dong-A University Hospital (Busan, South Korea). Patients were monitored after treatment for at least 48 h in hospital and for at least 4 weeks as out-patients. Adverse event-monitoring according to the National Cancer Institute Common Toxicity Criteria (version 3) and standard laboratory toxicity grading for haematology, liver and renal function, coagulation studies, serum chemistry, and urinalysis were done. The primary aims were to ascertain the maximum-tolerated dose (MTD) and safety of JX-594 treatment. Data were also collected on pharmacokinetics, pharmacodynamics, and efficacy. Analysis was per protoco [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "299", "doc_id": "38886345", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Podocytes are motile and migrate in the presence of injury.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tracking the fate of glomerular epithelial cells in vivo using serial multiphoton imaging in novel mouse models with fluorescent lineage tags\nABSTRACT: Podocytes are critical in the maintenance of a healthy glomerular filter; however, they have been difficult to study in the intact kidney because of technical limitations. Here we report the development of serial multiphoton microscopy (MPM) of the same glomeruli over several days to visualize the motility of podocytes and parietal epithelial cells (PECs) in vivo. In podocin-GFP mice, podocytes formed sporadic multicellular clusters after unilateral ureteral ligation and migrated into the parietal Bowman's capsule. The tracking of single cells in podocin-confetti mice featuring cell-specific expression of CFP, GFP, YFP or RFP revealed the simultaneous migration of multiple podocytes. In phosphoenolpyruvate carboxykinase (PEPCK)-GFP mice, serial MPM found PEC-to-podocyte migration and nanotubule connections. Our data support a highly dynamic rather than a static nature of the glomerular environment and cellular composition. Future application of this new approach should advance our understanding of the mechanisms of glomerular injury and regeneration.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In podocin-GFP mice, podocytes formed sporadic multicellular clusters after unilateral ureteral ligation and migrated into the parietal Bowman's capsule.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 957, "doc_id": "123859", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Energy balance requires hypothalamic glutamate neurotransmission.\n\nCANDIDATE_PASSAGE:\nControl of glutamate clearance and synaptic efficacy by glial coverage of neurons. Analysis of excitatory synaptic transmission in the rat hypothalamic supraoptic nucleus revealed that glutamate clearance and, as a consequence, glutamate concentration and diffusion in the extracellular space, is associated with the degree of astrocytic coverage of its neurons. Reduction in glutamate clearance, whether induced pharmacologically or associated with a relative decrease of glial coverage in the vicinity of synapses, affected transmitter release through modulation of presynaptic metabotropic glutamate receptors. Astrocytic wrapping of neurons, therefore, contributes to the regulation of synaptic efficacy in the central nervous system.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "378", "doc_id": "306311", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Basophils counteract disease development in patients with systemic lupus erythematosus (SLE).\n\nCANDIDATE_PASSAGE:\nBASOPHILS AND THE T HELPER 2 ENVIRONMENT CAN PROMOTE THE DEVELOPMENT OF LUPUS NEPHRITIS In systemic lupus erythematosus (SLE), self-reactive antibodies can target the kidney (lupus nephritis), leading to functional failure and possible mortality. We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice). Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis. Basophils were also present in the lymph nodes and spleen of subjects with SLE. Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "171", "doc_id": "12670680", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Increased microtubule acetylation repairs LRRK2 Roc-COR domain mutation induced locomotor deficits.\n\nCANDIDATE_PASSAGE:\nNef is physically recruited into the immunological synapse and potentiates T cell activation early after TCR engagement. The HIV-1 protein Nef enhances viral pathogenicity and accelerates disease progression in vivo. Nef potentiates T cell activation by an unknown mechanism, probably by optimizing the intracellular environment for HIV replication. Using a new T cell reporter system, we have found that Nef more than doubles the number of cells expressing the transcription factors NF-kappaB and NFAT after TCR stimulation. This Nef-induced priming of TCR signaling pathways occurred independently of calcium signaling and involved a very proximal step before protein kinase C activation. Engagement of the TCR by MHC-bound Ag triggers the formation of the immunological synapse by recruiting detergent-resistant membrane microdomains, termed lipid rafts. Approximately 5-10% of the total cellular pool of Nef is localized within lipid rafts. Using confocal and real-time microscopy, we found that Nef in lipid rafts was recruited into the immunological synapse within minutes after Ab engagement of the TCR/CD3 and CD28 receptors. This recruitment was dependent on the N-terminal domain of Nef encompassing its myristoylation. Nef did not increase the number of cell surface lipid rafts or immunological synapses. Recently, studies have shown a specific interaction of Nef with an active subpopulation of p21-activated kinase-2 found only in the lipid rafts. Thus, the corecruitment of Nef and key cellular partners (e.g., activated p21-activated kinase-2) into the immunological synapse may underlie the increased frequency of cells expressing transcriptionally active forms of NF-kappaB and NFAT and the resultant changes in T cell activation.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "613", "doc_id": "6936141", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: ALDH1 expression is associated with better breast cancer outcomes.\n\nCANDIDATE_PASSAGE:\nALDH1 is a marker of normal and malignant human mammary stem cells and a predictor of poor clinical outcome. Application of stem cell biology to breast cancer research has been limited by the lack of simple methods for identification and isolation of normal and malignant stem cells. Utilizing in vitro and in vivo experimental systems, we show that normal and cancer human mammary epithelial cells with increased aldehyde dehydrogenase activity (ALDH) have stem/progenitor properties. These cells contain the subpopulation of normal breast epithelium with the broadest lineage differentiation potential and greatest growth capacity in a xenotransplant model. In breast carcinomas, high ALDH activity identifies the tumorigenic cell fraction, capable of self-renewal and of generating tumors that recapitulate the heterogeneity of the parental tumor. In a series of 577 breast carcinomas, expression of ALDH1 detected by immunostaining correlated with poor prognosis. These findings offer an important new tool for the study of normal and malignant breast stem cells and facilitate the clinical application of stem cell concepts.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "51", "doc_id": "45638119", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Mice that lack Interferon-γ or its receptor exhibit high resistance to experimental autoimmune myocarditis.\n\nCANDIDATE_PASSAGE:\nLethal autoimmune myocarditis in interferon-gamma receptor-deficient mice: enhanced disease severity by impaired inducible nitric oxide synthase induction. BACKGROUND Interferon-gamma (IFN-gamma) is an essential cytokine in the regulation of inflammatory responses in autoimmune diseases. Little is known about its role in inflammatory heart disease. METHODS AND RESULTS We showed that IFN-gamma receptor-deficient mice (IFN-gammaR(-/-)) on a BALB/c background immunized with a peptide derived from cardiac alpha-myosin heavy chain develop severe myocarditis with high mortality. Although myocarditis subsided in wild-type mice after 3 weeks, IFN-gammaR(-/-) mice showed persistent disease. The persistent inflammation was accompanied by vigorous in vitro CD4 T-cell responses and impaired inducible nitric oxide synthase expression, together with evidence of impaired nitric oxide production in IFN-gammaR(-/-) hearts. Treatment of wild-type mice with the nitric oxide synthetase inhibitor N:-nitro-l-arginine-methyl-ester enhanced in vitro CD4 T-cell proliferation and prevented healing of myocarditis. CONCLUSIONS Our data provide evidence that IFN-gamma protects mice from lethal autoimmune myocarditis by inducing the expression of inducible nitric oxide synthase followed by the downregulation of T-cell responses.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "781", "doc_id": "24338780", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does limb-salvage surgery offer patients better quality of life and functional capacity than amputation?\n\nABSTRACT:\nPatients with aggressive lower extremity musculoskeletal tumors may be candidates for either above-knee amputation or limb-salvage surgery. However, the subjective and objective benefits of limb-salvage surgery compared with amputation are not fully clear.QUESTIONS/ We therefore compared functional status and quality of life for patients treated with above-knee amputation versus limb-salvage surgery. We reviewed 20 of 51 patients aged 15 years and older treated with above-knee amputation or limb-salvage surgery for aggressive musculoskeletal tumors around the knee between 1994 and 2004 as a retrospective cohort study. At last followup we obtained the Physiological Cost Index, the Reintegration to Normal Living Index, SF-36, and the Toronto Extremity Salvage Score questionnaires. The minimum followup was 12 months (median, 56 months; range, 12-108 months). Compared with patients having above-knee amputation, patients undergoing limb-salvage surgery had superior Physiological Cost Index scores and Reintegration to Normal Living Index. The Toronto Extremity Salvage scores and SF-36 scores were similar in the two groups.", "output": "{\"label\": \"maybe\", \"rationale\": \"These data suggest that limb-salvage surgery offers better gait efficiency and return to normal living compared with above-knee amputation, but does not improve the patient's perception of quality of life.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 22302658, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does 18-Fluorodeoxyglucose positron emission tomography aid in diagnosis of pancreatic ductal adenocarcinoma?\n\nABSTRACT:\nThere are no accurate and reliable tools for diagnosis of early stage pancreatic ductal adenocarcinoma (PDA) or small metastatic lesions. It is also a challenge to differentiate PDA from focal mass-forming pancreatitis (FMP). There is controversy regarding the efficacy of 18-fluorodeoxyglucose positron-emission tomography (FDG-PET) in the diagnosis of PDA. We investigated whether FDG-PET provides information that, combined with data from other imaging techniques, can aid in decision making for patients with suspected PDA. We performed a retrospective analysis of data collected from 232 consecutive patients with suspected PDA at Kobe University Hospital from January 2006 through June 2012. All patients underwent a diagnostic imaging protocol that included multidetector row computed tomography, superparamagnetic iron oxide-enhanced magnetic resonance imaging, and FDG-PET. Based on endoscopic ultrasonography, fine-needle aspiration biopsy, or endoscopic retrograde cholangiopancreatography analyses, 218 patients had PDA (89 underwent resection and 129 did not) and 14 patients had FMP (8 had focal mass-forming chronic pancreatitis and 6 had focal mass-forming autoimmune pancreatitis). FDG-PET detected 50% of stages 0 and I, 91.9% of stage II, 100% of stage III, and 96.8% of stage IV tumors. Detection was affected significantly by tumor size (P = .024) and T stage (P = .023) in resected tumors. Multidetector row computed tomography detected significantly more liver metastases than FDG-PET. Few para-aortic lymph node or peritoneal metastases were detected by FDG-PET. FDG-PET correctly identified 11 of the 14 patients with FMP (5 of 8 with focal mass-forming chronic pancreatitis and 6 of 6 with focal mass-forming autoimmune pancreatitis).", "output": "{\"label\": \"no\", \"rationale\": \"FDG-PET is not effective in detecting early stage PDA and small metastases, or in differentiating PDA from FMP. Combining FDG-PET with current diagnostic techniques for PDA did not provide any decisive information, therefore it should not be included in this analysis.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 23353642, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: BCL-2 activation antagonizes the apoptotic effects of c-Myc.\n\nCANDIDATE_ABSTRACT:\nTITLE: Antiapoptotic BCL-2 is required for maintenance of a model leukemia.\nABSTRACT: Resistance to apoptosis, often achieved by the overexpression of antiapoptotic proteins, is common and perhaps required in the genesis of cancer. However, it remains uncertain whether apoptotic defects are essential for tumor maintenance. To test this, we generated mice expressing a conditional BCL-2 gene and constitutive c-myc that develop lymphoblastic leukemia. Eliminating BCL-2 yielded rapid loss of leukemic cells and significantly prolonged survival, formally validating BCL-2 as a rational target for cancer therapy. Loss of this single molecule resulted in cell death, despite or perhaps attributable to the presence of other oncogenic events. This suggests a generalizable model in which aberrations inherent to cancer generate tonic death signals that would otherwise kill the cell if not opposed by a requisite apoptotic defect(s).", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Eliminating BCL-2 yielded rapid loss of leukemic cells and significantly prolonged survival, formally validating BCL-2 as a rational target for cancer therapy.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 155, "doc_id": "37549932", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Women with a lower birth weight are more likely to develop breast cancer later in life.\n\nCANDIDATE_ABSTRACT:\nTITLE: Birth Size and Breast Cancer Risk: Re-analysis of Individual Participant Data from 32 Studies\nABSTRACT: BACKGROUND Birth size, perhaps a proxy for prenatal environment, might be a correlate of subsequent breast cancer risk, but findings from epidemiological studies have been inconsistent. We re-analysed individual participant data from published and unpublished studies to obtain more precise estimates of the magnitude and shape of the birth size-breast cancer association. METHODS AND FINDINGS Studies were identified through computer-assisted and manual searches, and personal communication with investigators. Individual participant data from 32 studies, comprising 22,058 breast cancer cases, were obtained. Random effect models were used, if appropriate, to combine study-specific estimates of effect. Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003). Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data. Birth length and head circumference from birth records were also positively associated with breast cancer risk (pooled RR per one SD increment: 1.06 [95% CI 1.03-1.10] and 1.09 [95% CI 1.03-1.15], respectively). Simultaneous adjustment for these three birth size variables showed that length was the strongest independent predictor of risk. The birth size effec [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1380, "doc_id": "16322674", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Insomnia can be effectively treated with cognitive behavioral therapy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cognitive behavioral therapy vs zopiclone for treatment of chronic primary insomnia in older adults: a randomized controlled trial.\nABSTRACT: CONTEXT Insomnia is a common condition in older adults and is associated with a number of adverse medical, social, and psychological consequences. Previous research has suggested beneficial outcomes of both psychological and pharmacological treatments, but blinded placebo-controlled trials comparing the effects of these treatments are lacking. OBJECTIVE To examine short- and long-term clinical efficacy of cognitive behavioral therapy (CBT) and pharmacological treatment in older adults experiencing chronic primary insomnia. DESIGN, SETTING, AND PARTICIPANTS A randomized, double-blinded, placebo-controlled trial of 46 adults (mean age, 60.8 y; 22 women) with chronic primary insomnia conducted between January 2004 and December 2005 in a single Norwegian university-based outpatient clinic for adults and elderly patients. INTERVENTION CBT (sleep hygiene, sleep restriction, stimulus control, cognitive therapy, and relaxation; n = 18), sleep medication (7.5-mg zopiclone each night; n = 16), or placebo medication (n = 12). All treatment duration was 6 weeks, and the 2 active treatments were followed up at 6 months. MAIN OUTCOME MEASURES Ambulant clinical polysomnographic data and sleep diaries were used to determine total wake time, total sleep time, sleep efficiency, and slow-wave sleep (only assessed using polysomnography) on all 3 assessment points. RESULTS CBT resulted in improved short- and long-term outcomes compared with zopiclone on 3 out of 4 outcome measures. For most outcomes, zopiclone did not differ from placebo. Participants receiving CBT improved their sleep efficiency from 81.4% at pretreatment to 90.1% at 6-month follow-up compared with a decrease from 82.3% to 81.9% in the zopiclone group. Participants in the CBT group spent much more time in slow- [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Participants in the CBT group spent much more time in slow-wave sleep (stages 3 and 4) compared with those in other groups, and spent less time awake during the night.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 641, "doc_id": "5912283", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Pioneer factor OCT3/4 interacts with major chromatin remodeling factors.\n\nCANDIDATE_PASSAGE:\nGlobal, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015 BACKGROUND The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. METHODS We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors-the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "955", "doc_id": "13770184", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Cell autonomous sex determination in somatic cells occurs in Galliformes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Somatic sex identity is cell-autonomous in the chicken\nABSTRACT: In the mammalian model of sex determination, embryos are considered to be sexually indifferent until the transient action of a sex-determining gene initiates gonadal differentiation. Although this model is thought to apply to all vertebrates, this has yet to be established. Here we have examined three lateral gynandromorph chickens (a rare, naturally occurring phenomenon in which one side of the animal appears male and the other female) to investigate the sex-determining mechanism in birds. These studies demonstrated that gynandromorph birds are genuine male:female chimaeras, and indicated that male and female avian somatic cells may have an inherent sex identity. To test this hypothesis, we transplanted presumptive mesoderm between embryos of reciprocal sexes to generate embryos containing male:female chimaeric gonads. In contrast to the outcome for mammalian mixed-sex chimaeras, in chicken mixed-sex chimaeras the donor cells were excluded from the functional structures of the host gonad. In an example where female tissue was transplanted into a male host, donor cells contributing to the developing testis retained a female identity and expressed a marker of female function. Our study demonstrates that avian somatic cells possess an inherent sex identity and that, in birds, sexual differentiation is substantively cell autonomous.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"These studies demonstrated that gynandromorph birds are genuine male:female chimaeras, and indicated that male and female avian somatic cells may have an inherent sex identity.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 235, "doc_id": "4388470", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Patients in stable partnerships progress from HIV to death at the same rate as patients not in partnerships.\n\nCANDIDATE_ABSTRACT:\nTITLE: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\nABSTRACT: OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART). DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study). SETTING Seven outpatient clinics throughout Switzerland. PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years). MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound. RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion. When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership. In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without. Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression. CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 925, "doc_id": "17077004", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Chenodeoxycholic acid treatment decreases brown adipose tissue activity.\n\nCANDIDATE_PASSAGE:\nSIRT1 is required for long-term growth of human mesenchymal stem cells Human mesenchymal stem cells (MSCs) have therapeutic potential because of their ability to self-renew and differentiate into multiple tissues. However, senescence often occurs in MSCs when they are cultured in vitro and the molecular mechanisms underlying this effect remain unclear. In this study, we found that NAD-dependent protein deacetylase SIRT1 is differentially expressed in both human bone marrow-derived MSCs (B-MSCs) and adipose tissue-derived MSCs after increasing passages of cell culture. Using lentiviral shRNA we demonstrated that selective knockdown of SIRT1 in human MSCs at early passage slows down cell growth and accelerates cellular senescence. Conversely, overexpression of SIRT1 delays senescence in B-MSCs that have undergone prolonged in vitro culturing and the cells do not lose adipogenic and osteogenic potential. In addition, we found that the delayed accumulation of the protein p16 is involved in the effect of SIRT1. However, resveratrol, which has been used as an activator of SIRT1 deacetylase activity, only transiently promotes proliferation of B-MSCs. Our findings will help us understand the role of SIRT1 in the aging of normal diploid cells and may contribute to the prevention of human MSCs senescence thus benefiting MSCs-based tissue engineering and therapies.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "250", "doc_id": "15491308", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Glucose restriction to 0.05% reduces RLS (replicative life span) by 20-40% in S. cerevisiae.\n\nCANDIDATE_ABSTRACT:\nTITLE: Calorie restriction extends Saccharomyces cerevisiae lifespan by increasing respiration\nABSTRACT: Calorie restriction (CR) extends lifespan in a wide spectrum of organisms and is the only regimen known to lengthen the lifespan of mammals. We established a model of CR in budding yeast Saccharomyces cerevisiae. In this system, lifespan can be extended by limiting glucose or by reducing the activity of the glucose-sensing cyclic-AMP-dependent kinase (PKA). Lifespan extension in a mutant with reduced PKA activity requires Sir2 and NAD (nicotinamide adenine dinucleotide). In this study we explore how CR activates Sir2 to extend lifespan. Here we show that the shunting of carbon metabolism toward the mitochondrial tricarboxylic acid cycle and the concomitant increase in respiration play a central part in this process. We discuss how this metabolic strategy may apply to CR in animals.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 472, "doc_id": "4414481", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Marmosets have a brain region homologous to Broca's area.\n\nCANDIDATE_PASSAGE:\nDecreased neurogenesis after cholinergic forebrain lesion in the adult rat. Adult neurogenesis has been shown to be regulated by a multitude of extracellular cues, including hormones, growth factors, and neurotransmitters. The cholinergic system of the basal forebrain is one of the key transmitter systems for learning and memory. Because adult neurogenesis has been implicated in cognitive performance, the present work aims at defining the role of cholinergic input for adult neurogenesis by using an immunotoxic lesion approach. The immunotoxin 192IgG-saporin was infused into the lateral ventricle of adult rats to selectively lesion cholinergic neurons of the cholinergic basal forebrain (CBF), which project to the two main regions of adult neurogenesis: the dentate gyrus and the olfactory bulb. Five weeks after lesioning, neurogenesis, defined by the number of cells colocalized for bromodeoxyuridine (BrdU) and the neuronal nuclei marker NeuN, declined significantly in the granule cell layers of the dentate gyrus and olfactory bulb. Furthermore, immunotoxic lesions to the CBF led to increased numbers of apoptotic cells specifically in the subgranular zone, the progenitor region of the dentate gyrus, and within the periglomerular layer of the olfactory bulb. We propose that the cholinergic system plays a survival-promoting role for neuronal progenitors and immature neurons within regions of adult neurogenesis, similar to effects observed previously during brain development. As a working hypothesis, neuronal loss within the CBF system leads not only to cognitive deficits but may also alter on a cellular level the functionality of the dentate gyrus, which in turn may aggravate cognitive deficits.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "758", "doc_id": "22549449", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Normal granulomas form in the absence of TNF in Zebrafish.\n\nCANDIDATE_PASSAGE:\nEstablishment and in vitro differentiation of a new embryonic stem cell line from human blastocyst. Embryonic stem cells have the ability to remain undifferentiated and proliferate indefinitely in vitro while maintaining the potential to differentiate into derivatives of all three embryonic germ layers. These cells have, therefore, potential for in vitro differentiation studies, gene function, and so on. The aim of this study was to produce a human embryonic stem cell line. An inner cell mass of a human blastocyst was separated and cultured on mouse embryonic fibroblasts in embryonic stem cell medium with related additives. The established line was evaluated by morphology; passaging; freezing and thawing; alkaline phosphatase; Oct-4 expression; anti-surface markers including Tra-1-60 and Tra-1-81; and karyotype and spontaneous differentiation. Differentiated cardiomyocytes and neurons were evaluated by transmission electron microscopy and immunocytochemistry. Here, we report the derivation of a new embryonic stem cell line (Royan H1) from a human blastocyst that remains undifferentiated in morphology during continuous passaging for more than 30 passages, maintains a normal XX karyotype, is viable after freezing and thawing, and expresses alkaline phosphatase, Oct-4, Tra-1-60, and Tra-1-81. These cells remain undifferentiated when grown on mouse embryonic fibroblast feeder layers in the presence or absence of recombinant human leukemia inhibitory factor. Royan H1 cells can differentiate in vitro in the absence of feeder cells and can produce embryoid bodies that can further differentiate into beating cardiomyocytes as well as neurons. These results define Royan H1 cells as a new human embryonic stem cell line.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "860", "doc_id": "36651210", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Therapeutic use of the drug Dapsone to treat pyoderma gangrenous is based on anecdotal evidence.\n\nCANDIDATE_PASSAGE:\nInteraction between broad-spectrum antibiotics and the combined oral contraceptive pill. A literature review. There is considerable variation in opinion about the importance of drug interactions between the combined oral contraceptive pill (COCP) and broad-spectrum antibiotics. Clinical practice varies widely, especially between doctors in Europe and those in the US. Rifampicin and griseofulvin induce hepatic enzymes and do appear to have a genuine interaction with the COCP, leading to reduced efficacy. The situation with the broad-spectrum antibiotics is less clear. There are relatively few prospective studies of the pharmacokinetics of concurrent COCP and antibiotic use and few, if any, demonstrate a convincing basis for any reduced contraceptive efficacy. There is evidence, however, that variable contraceptive steroid handling could make some women, at some times, more susceptible to COCP failure. Given the serious consequences of unwanted pregnancy, the cautious approach of using additional or alternative contraception during short courses of broad-spectrum antibiotics and the initial weeks of long-term antibiotic administration may be justified to safeguard the few unidentifiable women who may be at risk. Conflicting opinion and advice is potentially confusing to both professionals and patients, and instructions for additional precautions during and after concurrent COCP and antibiotic use are complicated. Many women are ignorant of, or confused about, the circumstances that can cause OC to fail. Health professionals who prescribe the COCP must continue to strive to educate women about the mode of action and about the times when there is the greatest danger of failure. Professionals who feel that concurrent antibiotic use represents a real threat to con [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1282", "doc_id": "35186640", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Chenodeoxycholic acid treatment decreases brown adipose tissue activity.\n\nCANDIDATE_ABSTRACT:\nTITLE: Generation of mice with a conditional allele for the p75(NTR) neurotrophin receptor gene.\nABSTRACT: The p75(NTR) neurotrophin receptor has been implicated in multiple biological and pathological processes. While significant advances have recently been made in understanding the physiologic role of p75(NTR) , many details and aspects remain to be determined. This is in part because the two existing knockout mouse models (Exons 3 or 4 deleted, respectively), both display features that defy definitive conclusions. Here we describe the generation of mice that carry a conditional p75(NTR) (p75(NTR-FX) ) allele made by flanking Exons 4-6, which encode the transmembrane and all cytoplasmic domains, by loxP sites. To validate this novel conditional allele, both neural crest-specific p75(NTR) /Wnt1-Cre mutants and conventional p75(NTR) null mutants were generated. Both mutants displayed abnormal hind limb reflexes, implying that loss of p75(NTR) in neural crest-derived cells causes a peripheral neuropathy similar to that seen in conventional p75(NTR) mutants. This novel conditional p75(NTR) allele will offer new opportunities to investigate the role of p75(NTR) in specific tissues and cells.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 250, "doc_id": "368506", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: In chronic viral infections or tumors, peptides that selectively inhibit PTPRS can be utilized to boost insufficient activity of pDCs.\n\nCANDIDATE_PASSAGE:\nThe carboxyl terminus of human cytomegalovirus-encoded 7 transmembrane receptor US28 camouflages agonism by mediating constitutive endocytosis. US28 is one of four 7 transmembrane (7TM) chemokine receptors encoded by human cytomegalovirus and has been shown to both signal and endocytose in a ligand-independent, constitutively active manner. Here we show that the constitutive activity and constitutive endocytosis properties of US28 are separable entities in this viral chemokine receptor. We generated chimeric and mutant US28 proteins that were altered in either their constitutive endocytic (US28 Delta 300, US28 Delta 317, US28-NK1-ctail, and US28-ORF74-ctail) or signaling properties (US28R129A). By using this series of mutants, we show that the cytoplasmic tail domain of US28 per se regulates receptor endocytosis, independent of the signaling ability of the core domain of US28. The constitutive endocytic property of the US28 c-tail was transposable to other 7TM receptors, the herpes virus 8-encoded ORF74 and the tachykinin NK1 receptor (ORF74-US28-ctail and NK1-US28-ctail). Deletion of the US28 C terminus resulted in reduced constitutive endocytosis and consequently enhanced signaling capacity of all receptors tested as assessed by inositol phosphate turnover, NF-kappa B, and cAMP-responsive element-binding protein transcription assays. We further show that the constitutive endocytic property of US28 affects the action of its chemokine ligand fractalkine/CX3CL1 and show that in the absence of the US28 C terminus, fractalkine/CX3CL1 acts as an agonist on US28. This demonstrates for the first time that the endocytic properties of a 7TM receptor can camouflage the agonist properties of a ligand.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "572", "doc_id": "10906636", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Replacement of histone H2A with H2A.Z slows gene activation in yeasts by stabilizing +1 nucleosomes.\n\nCANDIDATE_PASSAGE:\nHistones are incorporated in trans during reassembly of the yeast PHO5 promoter. In yeast, remodeling of PHO5 promoter chromatin upon activation is accompanied by transient hyperacetylation and subsequent eviction of histones from the promoter in trans. In the course of rerepression, nucleosomes have to be reassembled on the promoter. We have analyzed where the histones for reassembly of the inactive promoter chromatin come from. The use of a strain with two differently tagged and differently regulated versions of histone H3 allowed us to discriminate between histones originating from the chromatin fraction and histones arising from the soluble histone pool. In this way, we show that the incorporated histones originate from a source in trans. Promoter closure occurs very rapidly, and the histone chaperones Asf1 and Hir1 as well as the SWI/SNF nucleosome remodeling complex appear to be important for rapid reassembly of nucleosomes at the PHO5 promoter.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1041", "doc_id": "406733", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Non-invasive ventilation use should be decreased if there is inadequate response to conventional treatment.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cost effectiveness of ward based non-invasive ventilation for acute exacerbations of chronic obstructive pulmonary disease: economic analysis of randomised controlled trial.\nABSTRACT: OBJECTIVE To evaluate the cost effectiveness of standard treatment with and without the addition of ward based non-invasive ventilation in patients admitted to hospital with an acute exacerbation of chronic obstructive pulmonary disease. DESIGN Incremental cost effectiveness analysis of a randomised controlled trial. SETTING Medical wards in 14 hospitals in the United Kingdom. PARTICIPANTS The trial comprised 236 patients admitted to hospital with an acute exacerbation of chronic obstructive pulmonary disease and mild to moderate acidosis (pH 7.25-7.35) secondary to respiratory failure. The economic analysis compared the costs of treatment that these patients received after randomisation. MAIN OUTCOME MEASURE Incremental cost per in-hospital death. RESULTS 24/118 died in the group receiving standard treatment and 12/118 in the group receiving non-invasive ventilation (P=0.05). Allocation to the group receiving non-invasive ventilation was associated with a reduction in costs of 49362 pounds sterling (78741 dollars; 73109 euros), mainly through reduced use of intensive care units. The incremental cost effectiveness ratio was -645 pounds sterling per death avoided (95% confidence interval -2310 pounds sterling to 386 pounds sterling), indicating a dominant (more effective and less costly) strategy. Modelling of these data indicates that a typical UK hospital providing a non-invasive ventilation service will avoid six deaths and three to nine admissions to intensive care units per year, with an associated cost reduction of 12000-53000 pounds sterling per year. CONCLUSIONS Non-invasive ventilation is a highly cost effective treatment that both reduced total costs and improved mortality in hospital.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Modelling of these data indicates that a typical UK hospital providing a non-invasive ventilation service will avoid six deaths and three to nine admissions to intensive care units per year, with an associated cost reduction of 12000-53000 pounds sterling per year.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 852, "doc_id": "13843341", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Insulin increases risk of severe kidney failure.\n\nCANDIDATE_ABSTRACT:\nTITLE: Diabetes treatments and risk of amputation, blindness, severe kidney failure, hyperglycaemia, and hypoglycaemia: open cohort study in primary care\nABSTRACT: OBJECTIVE To assess the risks of amputation, blindness, severe kidney failure, hyperglycaemia, and hypoglycaemia in patients with type 2 diabetes associated with prescribed diabetes drugs, particularly newer agents including gliptins or glitazones (thiazolidinediones). DESIGN Open cohort study in primary care. SETTING 1243 practices contributing data to the QResearch database in England. PARTICIPANTS 469,688 patients with type 2 diabetes aged 25-84 years between 1 April 2007 and 31 January 2015. EXPOSURES Hypoglycaemic agents (glitazones, gliptins, metformin, sulphonylureas, insulin, and other) alone and in combination. MAIN OUTCOME MEASURES First recorded diagnoses of amputation, blindness, severe kidney failure, hyperglycaemia, and hypoglycaemia recorded on patients' primary care, mortality, or hospital records. Cox models estimated hazard ratios for diabetes treatments adjusting for potential confounders. RESULTS 21,308 (4.5%) and 32,533 (6.9%) patients received prescriptions for glitazones and gliptins during follow-up, respectively. Compared with non-use, glitazones were associated with a decreased risk of blindness (adjusted hazard ratio 0.71, 95% confidence interval 0.57 to 0.89; rate 14.4 per 10,000 person years of exposure) and an increased risk of hypoglycaemia (1.22, 1.10 to 1.37; 65.1); gliptins were associated with a decreased risk of hypoglycaemia (0.86, 0.77 to 0.96; 45.8). Although the numbers of patients prescribed gliptin monotherapy or glitazones monotherapy were relatively low, there were significantly increased risks of severe kidney failure compared with metformin monotherapy (adjusted hazard ratio 2.55, 95% confidence interval 1.13 to 5.74). We found significantly lower risks of hyperglycaemia among patients prescribed dual therapy inv [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 644, "doc_id": "13619127", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: A single nucleotide variant the gene DGKK is strongly associated with increased risk of hypospadias.\n\nCANDIDATE_PASSAGE:\nACAM2000™: The new smallpox vaccine for United States Strategic National Stockpile Smallpox was eradicated more than 30 years ago, but heightened concerns over bioterrorism have brought smallpox and smallpox vaccination back to the forefront. The previously licensed smallpox vaccine in the United States, Dryvax (Wyeth Laboratories, Inc.), was highly effective, but the supply was insufficient to vaccinate the entire current US population. Additionally, Dryvax had a questionable safety profile since it consisted of a pool of vaccinia virus strains with varying degrees of virulence, and was grown on the skin of calves, an outdated technique that poses an unnecessary risk of contamination. The US government has therefore recently supported development of an improved live vaccinia virus smallpox vaccine. This initiative has resulted in the development of ACAM2000 (Acambis, Inc.), a single plaque-purified vaccinia virus derivative of Dryvax, aseptically propagated in cell culture. Preclinical and clinical trials reported in 2008 demonstrated that ACAM2000 has comparable immunogenicity to that of Dryvax, and causes a similar frequency of adverse events. Furthermore, like Dryvax, ACAM2000 vaccination has been shown by careful cardiac screening to result in an unexpectedly high rate of myocarditis and pericarditis. ACAM2000 received US Food and Drug Administration (FDA) approval in August 2007, and replaced Dryvax for all smallpox vaccinations in February 2008. Currently, over 200 million doses of ACAM2000 have been produced for the US Strategic National Stockpile. This review of ACAM2000 addresses the production, characterization, clinical trials, and adverse events associated with this new smallpox vaccine.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "46", "doc_id": "8069939", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: LDL cholesterol has no involvement in the development of cardiovascular disease.\n\nCANDIDATE_ABSTRACT:\nTITLE: LDL-cholesterol concentrations: a genome-wide association study\nABSTRACT: BACKGROUND LDL cholesterol has a causal role in the development of cardiovascular disease. Improved understanding of the biological mechanisms that underlie the metabolism and regulation of LDL cholesterol might help to identify novel therapeutic targets. We therefore did a genome-wide association study of LDL-cholesterol concentrations. METHODS We used genome-wide association data from up to 11,685 participants with measures of circulating LDL-cholesterol concentrations across five studies, including data for 293 461 autosomal single nucleotide polymorphisms (SNPs) with a minor allele frequency of 5% or more that passed our quality control criteria. We also used data from a second genome-wide array in up to 4337 participants from three of these five studies, with data for 290,140 SNPs. We did replication studies in two independent populations consisting of up to 4979 participants. Statistical approaches, including meta-analysis and linkage disequilibrium plots, were used to refine association signals; we analysed pooled data from all seven populations to determine the effect of each SNP on variations in circulating LDL-cholesterol concentrations. FINDINGS In our initial scan, we found two SNPs (rs599839 [p=1.7x10(-15)] and rs4970834 [p=3.0x10(-11)]) that showed genome-wide statistical association with LDL cholesterol at chromosomal locus 1p13.3. The second genome screen found a third statistically associated SNP at the same locus (rs646776 [p=4.3x10(-9)]). Meta-analysis of data from all studies showed an association of SNPs rs599839 (combined p=1.2x10(-33)) and rs646776 (p=4.8x10(-20)) with LDL-cholesterol concentrations. SNPs rs599839 and rs646776 both explained around 1% of the variation in circulating LDL-cholesterol concentrations and were associated wi [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"BACKGROUND LDL cholesterol has a causal role in the development of cardiovascular disease.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 674, "doc_id": "2095573", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Mice defective for deoxyribonucleic acid (DNA) polymerase m (polm) reveal increased sensitivity to ionizing radiation (IR).\n\nCANDIDATE_PASSAGE:\nAssociation of Intracerebral Hemorrhage Among Patients Taking Non–Vitamin K Antagonist vs Vitamin K Antagonist Oral Anticoagulants With In-Hospital Mortality Importance Although non–vitamin K antagonist oral anticoagulants (NOACs) are increasingly used to prevent thromboembolic disease, there are limited data on NOAC-related intracerebral hemorrhage (ICH). Objective To assess the association between preceding oral anticoagulant use (warfarin, NOACs, and no oral anticoagulants [OACs]) and in-hospital mortality among patients with ICH. Design, Setting, and Participants Retrospective cohort study of 141 311 patients with ICH admitted from October 2013 to December 2016 to 1662 Get With The Guidelines–Stroke hospitals. Exposures Anticoagulation therapy before ICH, defined as any use of OACs within 7 days prior to hospital arrival. Main Outcomes and Measures In-hospital mortality. Results Among 141 311 patients with ICH (mean [SD] age, 68.3 [15.3] years; 48.1% women), 15 036 (10.6%) were taking warfarin and 4918 (3.5%) were taking NOACs preceding ICH, and 39 585 (28.0%) and 5783 (4.1%) were taking concomitant single and dual antiplatelet agents, respectively. Patients with prior use of warfarin or NOACs were older and had higher prevalence of atrial fibrillation and prior stroke. Acute ICH stroke severity (measured by the National Institutes of Health Stroke Scale) was not significantly different across the 3 groups (median, 9 [interquartile range, 2-21] for warfarin, 8 [2-20] for NOACs, and 8 [2-19] for no OACs). The unadjusted in-hospital mortality rates were 32.6% for warfarin, 26.5% for NOACs, and 22.5% for no OACs. Compared with patients without prior use of OACs, the risk of in-hospital mortality was higher among patients with prior use of warfarin (adjusted [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "777", "doc_id": "3898784", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does physician team management affect goal achievement in the intensive care unit?\n\nABSTRACT:\nThere are few investigations evaluating the impact of physician management and leadership skills on patient care. Our objective was to determine whether there were perceived differences in management and leadership performance within a group of intensivists and to correlate these differences with processes of care outcomes. Prospective cohort from January 31 to June 30, 2005. Pediatric intensive care unit in an urban, academic children's hospital. Pediatric intensive care unit staff intensivists were the primary participants. None. The intensivists' management and leadership performances were assessed by residents and fellows using the Physician Management Index. The primary outcome attributable to the staff was the accomplishment of daily patient goals. A total of 827 resident and fellow assessments of the management and leadership performance of attendings (n = 8) were collected over 2077 patient days (103.4 +/- 39.0 surveys/attending). The mean Physician Management Index was 78.1 +/- 6.2 and differed significantly among the attendings (p < .001). There was excellent agreement by the raters concerning attending performance (intraclass correlation = 0.801). The attendings' Physician Management Indexes were correlated with age (r = 0.594, p < .001) and experience (r = 0.656, p < .001) but not other personal or environmental factors. An average of 3.3 +/- 0.6 goals per patient were written each day, and 86.0% +/- 7.0% were accomplished. Accomplishment of patient goals was correlated with the Physician Management Index (r = 0.306, p < .001) and length of rounds (r = -0.341, p < .001). Other variables, including midnight census, numbers of admissions and discharges, codes, and consultations, did not correlate with the Physician Management Index.", "output": "{\"label\": \"yes\", \"rationale\": \"Management and leadership performance of attending intensivists can be measured and is associated with efficiency of care as assessed by accomplishment of daily patient goals. Attendings differ in their management and leadership performances.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 17906596, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Healthy volunteers exhibit rapid and transient increase of cellular ATP after being bolus-injected with fructose.\n\nCANDIDATE_PASSAGE:\nIonic mechanism of ouabain-induced concurrent apoptosis and necrosis in individual cultured cortical neurons Energy deficiency and dysfunction of the Na+, K+-ATPase are common consequences of many pathological insults. The nature and mechanism of cell injury induced by impaired Na+, K+-ATPase, however, are not well defined. We used cultured cortical neurons to examine the hypothesis that blocking the Na+, K+-ATPase induces apoptosis by depleting cellular K+ and, concurrently, induces necrotic injury in the same cells by increasing intracellular Ca2+ and Na+. The Na+, K+-ATPase inhibitor ouabain induced concentration-dependent neuronal death. Ouabain triggered transient neuronal cell swelling followed by cell shrinkage, accompanied by intracellular Ca2+ and Na+ increase, K+ decrease, cytochrome c release, caspase-3 activation, and DNA laddering. Electron microscopy revealed the coexistence of ultrastructural features of both apoptosis and necrosis in individual cells. The caspase inhibitor Z-Val-Ala-Asp(OMe)-fluoromethyl ketone (Z-VAD-FMK) blocked >50% of ouabain-induced neuronal death. Potassium channel blockers or high K+ medium, but not Ca2+ channel blockade, prevented cytochrome c release, caspase activation, and DNA damage. Blocking of K+, Ca2+, or Na+ channels or high K+ medium each attenuated the ouabain-induced cell death; combined inhibition of K+ channels and Ca2+ or Na+ channels resulted in additional protection. Moreover, coapplication of Z-VAD-FMK and nifedipine produced virtually complete neuroprotection. These results suggest that the neuronal death associated with Na+, K+-pump failure consists of concurrent apoptotic and necrotic components, mediated by intracellular depletion of K+ and accumulation of Ca2+ and Na+, respectively. The ouabain-i [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "504", "doc_id": "17231273", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Converting apoE4 to apoE3 by gene editing worsens the pathology associated with apoE4 in human iPSCderived neurons.\n\nCANDIDATE_PASSAGE:\nIdentification of secreted proteins that mediate cell-cell interactions in an in vitro model of the lung cancer microenvironment. Non-small cell lung cancer (NSCLC) cells with somatic mutations in K-ras recruit to the tumor a variety of cell types (hereafter collectively termed \"stromal cells\") that can promote or inhibit tumorigenesis by mechanisms that have not been fully elucidated. Here, we postulated that stromal cells in the tumor microenvironment alter the tumor cell secretome, including those proteins required for tumor growth and dissemination, and we developed an in vitro model to test this hypothesis. Coculturing a murine K-ras mutant lung adenocarcinoma cell line (LKR-13) with a murine lung stromal cell (macrophage, endothelial cell, or fibroblast) enhanced stromal cell migration, induced endothelial tube formation, increased LKR-13 cell proliferation, and regulated the secretion of proteins involved in angiogenesis, inflammation, cell proliferation, and epithelial-to-mesenchymal transition. Among these proteins, CXCL1 has been reported to promote NSCLC development, whereas interleukin-18 (IL-18) has an undefined role. Genetic and pharmacologic strategies to inhibit CXCL1 and IL-18 revealed that stromal cell migration, LKR-13 cell proliferation, and LKR-13 cell tumorigenicity required one or both of these proteins. We conclude that stromal cells enhanced LKR-13 cell tumorigenicity partly through their effects on the secretome of LKR-13 cells. Strategies to inhibit tumor/stromal cell interactions may be useful as therapeutic approaches in NSCLC patients.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "287", "doc_id": "15727984", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Participants who quit smoking reduce lung cancer risk by approximately 50%.\n\nCANDIDATE_PASSAGE:\nEffect of smoking reduction on lung cancer risk. CONTEXT Many smokers are unable or unwilling to completely quit smoking. A proposed means of harm reduction is to reduce the number of cigarettes smoked per day. However, it is not clear whether this strategy decreases the risk for tobacco-related diseases. OBJECTIVE To assess the effects of smoking reduction on lung cancer incidence. DESIGN, SETTING, AND PARTICIPANTS Observational population-based cohort study with up to 31 years of follow-up from the Copenhagen Centre for Prospective Population Studies, which administrates data from 3 longitudinal studies conducted in Copenhagen and suburbs, the Copenhagen City Heart Study, the Copenhagen Male Study, and the Glostrup Population Studies, Denmark. Participants were 11,151 men and 8563 women (N = 19,714) aged 20 to 93 years, who attended 2 consecutive examinations with a 5- to 10-year interval between 1964 and 1988. Participants underwent a physical examination and completed self-filled questionnaires about lifestyle habits. The study population was divided into 6 groups according to smoking habits: continued heavy smokers (> or =15 cigarettes/d), reducers (reduced from > or =15 cigarettes/d by minimum of 50% without quitting), continued light smokers (1-14 cigarettes/d), quitters (stopped between first and second examination), stable ex-smokers, and never smokers. MAIN OUTCOME MEASURE Incident primary lung cancer cases assessed by record linkage with the National Cancer Registry until December 31, 2003. RESULTS There were 864 incident lung cancers during follow-up. Using Cox regression, the adjusted hazard ratio (HR) for lung cancer in reducers was 0.73 (95% confidence interval [CI], 0.54-0.98) compared with persistent heavy smokers. The HR for light smokers w [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "919", "doc_id": "16422880", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Incidence of heart failure increased by 10% in women since 1979.\n\nCANDIDATE_PASSAGE:\nThioredoxin mediates oxidation-dependent phosphorylation of CRMP2 and growth cone collapse. Semaphorin3A (Sema3A) is a repulsive guidance molecule for axons, which acts by inducing growth cone collapse through phosphorylation of CRMP2 (collapsin response mediator protein 2). Here, we show a role for CRMP2 oxidation and thioredoxin (TRX) in the regulation of CRMP2 phosphorylation and growth cone collapse. Sema3A stimulation generated hydrogen peroxide (H2O2) through MICAL (molecule interacting with CasL) and oxidized CRMP2, enabling it to form a disulfide-linked homodimer through cysteine-504. Oxidized CRMP2 then formed a transient disulfide-linked complex with TRX, which stimulated CRMP2 phosphorylation by glycogen synthase kinase-3, leading to growth cone collapse. We also reconstituted oxidation-dependent phosphorylation of CRMP2 in vitro, using a limited set of purified proteins. Our results not only clarify the importance of H2O2 and CRMP2 oxidation in Sema3A-induced growth cone collapse but also indicate an unappreciated role for TRX in linking CRMP2 oxidation to phosphorylation.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "594", "doc_id": "33912020", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The availability of safe places to study is not effective at decreasing homelessness.\n\nCANDIDATE_PASSAGE:\nCollective trauma in northern Sri Lanka: a qualitative psychosocial-ecological study BACKGROUND Complex situations that follow war and natural disasters have a psychosocial impact on not only the individual but also on the family, community and society. Just as the mental health effects on the individual psyche can result in non pathological distress as well as a variety of psychiatric disorders; massive and widespread trauma and loss can impact on family and social processes causing changes at the family, community and societal levels. METHOD This qualitative, ecological study is a naturalistic, psychosocial ethnography in Northern Sri Lanka, while actively involved in psychosocial and community mental health programmes among the Tamil community. Participatory observation, key informant interviews and focus group discussion with community level relief and rehabilitation workers and government and non-governmental officials were used to gather data. The effects on the community of the chronic, man-made disaster, war, in Northern Sri Lanka were compared with the contexts found before the war and after the tsunami. RESULTS Fundamental changes in the functioning of the family and the community were observed. While the changes after the tsunami were not so prominent, the chronic war situation caused more fundamental social transformations. At the family level, the dynamics of single parent families, lack of trust among members, and changes in significant relationships, and child rearing practices were seen. Communities tended to be more dependent, passive, silent, without leadership, mistrustful, and suspicious. Additional adverse effects included the breakdown in traditional structures, institutions and familiar ways of life, and deterioration in social norms a [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1197", "doc_id": "15780826", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: PKG-la plays an essential role in expression of pain hypersensitivity in PGK-la knockout mice.\n\nCANDIDATE_PASSAGE:\nHistone deacetylase 5 interacts with Krüppel-like factor 2 and inhibits its transcriptional activity in endothelium. AIMS Vascular endothelial dysfunction and inflammation are hallmarks of atherosclerosis. Krüppel-like factor 2 (KLF2) is a key mediator of anti-inflammatory and anti-atherosclerotic properties of the endothelium. However, little is known of the molecular mechanisms for regulating KLF2 transcriptional activation. METHODS AND RESULTS Here, we found that histone deacetylase 5 (HDAC5) associates with KLF2 and represses KLF2 transcriptional activation. HDAC5 resided with KLF2 in the nuclei of human umbilical cord vein endothelial cells (HUVECs). Steady laminar flow attenuated the association of HDAC5 with KLF2 via stimulating HDAC5 phosphorylation-dependent nuclear export in HUVEC. We also mapped the KLF2-HDAC5-interacting domains and found that the N-terminal region of HDAC5 interacts with the C-terminal domain of KLF2. Chromatin immunoprecipitation and luciferase reporter assays showed that HDAC5 through a direct association with KLF2 suppressed KLF2 transcriptional activation. HDAC5 overexpression inhibited KLF2-dependent endothelial nitric oxide synthesis (eNOS) promoter activity in COS7 cell and gene expression in both HUVECs and bovine aortic endothelial cells (BAECs). Conversely, HDAC5 silencing enhanced KLF2 transcription and hence eNOS expression in HUVEC. Moreover, we observed that the level of eNOS protein in the thoracic aorta isolated from HDAC5 knockout mice was higher, whereas expression of pro-inflammatory vascular cell adhesion molecule 1 was lower, compared with those of HDAC5 wild-type mice. CONCLUSIONS We reveal a novel role of HDAC5 in modulating the KLF2 transcriptional activation and eNOS expression. These findings suggest th [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "911", "doc_id": "2316374", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Cognitive behavioral therapy is an ineffective treatment for insomnia\n\nCANDIDATE_PASSAGE:\nThe HMG-CoA reductase inhibitor simvastatin activates the protein kinase Akt and promotes angiogenesis in normocholesterolemic animals. Recent studies suggest that statins can function to protect the vasculature in a manner that is independent of their lipid-lowering activity. We show here that statins rapidly activate the protein kinase Akt/PKB in endothelial cells. Accordingly, simvastatin enhanced phosphorylation of the endogenous Akt substrate endothelial nitric oxide synthase (eNOS), inhibited apoptosis and accelerated vascular structure formation in vitro in an Akt-dependent manner. Similar to vascular endothelial growth factor (VEGF) treatment, both simvastatin administration and enhanced Akt signaling in the endothelium promoted angiogenesis in ischemic limbs of normocholesterolemic rabbits. Therefore, activation of Akt represents a mechanism that can account for some of the beneficial side effects of statins, including the promotion of new blood vessel growth.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "267", "doc_id": "24005548", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In mouse models, the loss of CSF1R facilitates MOZ-TIF2-induced leuekmogenesis.\n\nCANDIDATE_ABSTRACT:\nTITLE: PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2\nABSTRACT: Leukemias and other cancers possess self-renewing stem cells that help to maintain the cancer. Cancer stem cell eradication is thought to be crucial for successful anticancer therapy. Using an acute myeloid leukemia (AML) model induced by the leukemia-associated monocytic leukemia zinc finger (MOZ)-TIF2 fusion protein, we show here that AML can be cured by the ablation of leukemia stem cells. The MOZ fusion proteins MOZ-TIF2 and MOZ-CBP interacted with the transcription factor PU.1 to stimulate the expression of macrophage colony–stimulating factor receptor (CSF1R, also known as M-CSFR, c-FMS or CD115). Studies using PU.1-deficient mice showed that PU.1 is essential for the ability of MOZ-TIF2 to establish and maintain AML stem cells. Cells expressing high amounts of CSF1R (CSF1Rhigh cells), but not those expressing low amounts of CSF1R (CSF1Rlow cells), showed potent leukemia-initiating activity. Using transgenic mice expressing a drug-inducible suicide gene controlled by the CSF1R promoter, we cured AML by ablation of CSF1Rhigh cells. Moreover, induction of AML was suppressed in CSF1R-deficient mice and CSF1R inhibitors slowed the progression of MOZ-TIF2–induced leukemia. Thus, in this subtype of AML, leukemia stem cells are contained within the CSF1Rhigh cell population, and we suggest that targeting of PU.1-mediated upregulation of CSF1R expression might be a useful therapeutic approach.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Cells expressing high amounts of CSF1R (CSF1Rhigh cells), but not those expressing low amounts of CSF1R (CSF1Rlow cells), showed potent leukemia-initiating activity.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 578, "doc_id": "8764879", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Adult tissue-resident macrophages are seeded before birth.\n\nCANDIDATE_PASSAGE:\nInnate lymphoid cells mediate influenza-induced airway hyper-reactivity independently of adaptive immunity Patients with asthma, a major public health problem, are at high risk for serious disease from influenza virus infection, but the pathogenic mechanisms by which influenza A causes airway disease and asthma are not fully known. We show here in a mouse model that influenza infection acutely induced airway hyper-reactivity (AHR), a cardinal feature of asthma, independently of T helper type 2 (TH2) cells and adaptive immunity. Instead, influenza infection induced AHR through a previously unknown pathway that required the interleukin 13 (IL-13)–IL-33 axis and cells of the non-T cell, non-B cell innate lymphoid type called 'natural helper cells'. Infection with influenza A virus, which activates the NLRP3 inflammasome, resulted in much more production of IL-33 by alveolar macrophages, which in turn activated natural helper cells producing substantial IL-13.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "86", "doc_id": "696006", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Walking in traffic areas in London improves lung function in elderly adults.\n\nCANDIDATE_ABSTRACT:\nTITLE: Respiratory and cardiovascular responses to walking down a traffic-polluted road compared with walking in a traffic-free area in participants aged 60 years and older with chronic lung or heart disease and age-matched healthy controls: a randomised, crossover study\nABSTRACT: BACKGROUND Long-term exposure to pollution can lead to an increase in the rate of decline of lung function, especially in older individuals and in those with chronic obstructive pulmonary disease (COPD), whereas shorter-term exposure at higher pollution levels has been implicated in causing excess deaths from ischaemic heart disease and exacerbations of COPD. We aimed to assess the effects on respiratory and cardiovascular responses of walking down a busy street with high levels of pollution compared with walking in a traffic-free area with lower pollution levels in older adults. METHODS In this randomised, crossover study, we recruited men and women aged 60 years and older with angiographically proven stable ischaemic heart disease or stage 2 Global initiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable for 6 months, and age-matched healthy volunteers. Individuals with ischaemic heart disease or COPD were recruited from existing databases or outpatient respiratory and cardiology clinics at the Royal Brompton & Harefield NHS Foundation Trust and age-matched healthy volunteers using advertising and existing databases. All participants had abstained from smoking for at least 12 months and medications were taken as recommended by participants' doctors during the study. Participants were randomly assigned by drawing numbered disks at random from a bag to do a 2 h walk either along a commercial street in London (Oxford Street) or in an urban park (Hyde Park). Baseline measurements of participants were taken before the walk in the hospital laboratory. During each walk session, black carbon, particulate matter (PM) concentrations, ultrafine particles, and nitrogen dioxide (NO2) concentrations were measured. FINDINGS Between October, 2012 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Participants with COPD reported more cough (odds ratio [OR] 1·95, 95% CI 0·96-3·95; p<0·1), sputum (3·15, 1·39-7·13; p<0·05), shortness of breath (1·86, 0·97-3·57; p<0·1), and wheeze (4·00, 1·52-10·50; p<0·05) after walking down Oxford Street compared with Hyde Park.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1373, "doc_id": "21003930", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is perforation of the appendix a risk factor for tubal infertility and ectopic pregnancy?\n\nABSTRACT:\nTo critically assess the evidence that appendiceal perforation is a risk factor for subsequent tubal infertility or ectopic pregnancy. Epidemiologic studies investigating the relationship between appendectomy and infertility or ectopic pregnancy were identified by searching the MEDLINE database from 1966 to 1997. Appropriate citations were also extracted from a manual search of the bibliographies of selected papers. Twenty-three articles were retrieved. Only 4 presented original data including comparisons to a nonexposed control group and they form the basis for this study. Because the raw data or specific techniques of data analysis were not always explicitly described, indices of risk for exposure were extracted from the data as presented and were analysed without attempting to convert them to a common measure. Articles were assessed according to the criteria of the Evidence-Based Medicine Working Group for evaluating articles on harm. Review of the literature yielded estimates of the risk of adverse fertility outcomes ranging from 1.6 (95% confidence interval [CI] 1.1 to 2.5) for ectopic pregnancy after an appendectomy to 4.8 (95% CI 1.5 to 14.9) for tubal infertility from perforation of the appendix. Recall bias, and poor adjustment for confounding variables in some reports, weakened the validity of the studies.", "output": "{\"label\": \"maybe\", \"rationale\": \"The methodologic weaknesses of the studies do not permit acceptance of increased risk of tubal pregnancy or infertility as a consequence of perforation of the appendix, so a causal relationship cannot be supported by the data currently available. Only a well-designed case-control study with unbiased ascertainment of exposure and adjustment for confounding variables will provide a definitive answer.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 10223070, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Depletion of T-helper 17 (Th17) cells during simian immunodeficiency virus (SIV) infection decreases dissemination of Salmonella Typhimurium from the gut.\n\nCANDIDATE_PASSAGE:\nUnmet need for mental health care among U.S. children: variation by ethnicity and insurance status. OBJECTIVE Policy discussions regarding the mental health needs of children and adolescents emphasize a lack of use of mental health services among youth, but few national estimates are available. The authors use three national data sets and examine ethnic disparities in unmet need (defined as having a need for mental health evaluation but not using any services in a 1-year period) to provide such estimates. METHOD The authors conducted secondary data analyses in three nationally representative household surveys fielded in 1996-1998: the National Health Interview Survey, the National Survey of American Families, and the Community Tracking Survey. They determined rates of mental health service use by children and adolescents 3-17 years of age and differences by ethnicity and insurance status. Among the children defined as in need of mental health services, defined by an estimator of mental health problems (selected items from the Child Behavior Checklist), they examined the association of unmet need with ethnicity and insurance status. RESULTS In a 12-month period, 2%-3% of children 3-5 years old and 6%-9% of children and adolescents 6-17 years old used mental health services. Of children and adolescents 6-17 years old who were defined as needing mental health services, nearly 80% did not receive mental health care. Controlling for other factors, the authors determined that the rate of unmet need was greater among Latino than white children and among uninsured than publicly insured children. CONCLUSIONS These findings reveal that most children who need a mental health evaluation do not receive services and that Latinos and the uninsured have especially high rate [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "332", "doc_id": "45548062", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: 10% of sudden infant death syndrome (SIDS) deaths happen in newborns aged less than 6 months.\n\nCANDIDATE_PASSAGE:\nPrognostic Accuracy of the SOFA Score, SIRS Criteria, and qSOFA Score for In-Hospital Mortality Among Adults With Suspected Infection Admitted to the Intensive Care Unit Importance The Sepsis-3 Criteria emphasized the value of a change of 2 or more points in the Sequential [Sepsis-related] Organ Failure Assessment (SOFA) score, introduced quick SOFA (qSOFA), and removed the systemic inflammatory response syndrome (SIRS) criteria from the sepsis definition. Objective Externally validate and assess the discriminatory capacities of an increase in SOFA score by 2 or more points, 2 or more SIRS criteria, or a qSOFA score of 2 or more points for outcomes among patients who are critically ill with suspected infection. Design, Setting, and Participants Retrospective cohort analysis of 184 875 patients with an infection-related primary admission diagnosis in 182 Australian and New Zealand intensive care units (ICUs) from 2000 through 2015. Exposures SOFA, qSOFA, and SIRS criteria applied to data collected within 24 hours of ICU admission. Main Outcomes and Measures The primary outcome was in-hospital mortality. In-hospital mortality or ICU length of stay (LOS) of 3 days or more was a composite secondary outcome. Discrimination was assessed using the area under the receiver operating characteristic curve (AUROC). Adjusted analyses were performed using a model of baseline risk determined using variables independent of the scoring systems. Results Among 184 875 patients (mean age, 62.9 years [SD, 17.4]; women, 82 540 [44.6%]; most common diagnosis bacterial pneumonia, 32 634 [17.7%]), a total of 34 578 patients (18.7%) died in the hospital, and 102 976 patients (55.7%) died or experienced an ICU LOS of 3 days or more. SOFA score increased by 2 or more points in 90.1%; 8 [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "6", "doc_id": "5185871", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Beta-band coherence is diminished for visible stimuli over invisible stimuli.\n\nCANDIDATE_ABSTRACT:\nTITLE: Converging Intracranial Markers of Conscious Access\nABSTRACT: We compared conscious and nonconscious processing of briefly flashed words using a visual masking procedure while recording intracranial electroencephalogram (iEEG) in ten patients. Nonconscious processing of masked words was observed in multiple cortical areas, mostly within an early time window (<300 ms), accompanied by induced gamma-band activity, but without coherent long-distance neural activity, suggesting a quickly dissipating feedforward wave. In contrast, conscious processing of unmasked words was characterized by the convergence of four distinct neurophysiological markers: sustained voltage changes, particularly in prefrontal cortex, large increases in spectral power in the gamma band, increases in long-distance phase synchrony in the beta range, and increases in long-range Granger causality. We argue that all of those measures provide distinct windows into the same distributed state of conscious processing. These results have a direct impact on current theoretical discussions concerning the neural correlates of conscious access.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 174, "doc_id": "1710116", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Students who perform poorly in the early years of medical school are at increased risk for professional misconduct later in their careers.\n\nCANDIDATE_PASSAGE:\nVariables Affecting Kinetics of Minimal Residual Disease Clearance in Children with Lymphoblastic Leukaemia; Results of the United Kingdom Medical Research Council (UK MRC) Protocols ALL97, ALL97/99 and ALL2003. We studied the influence of patient, leukaemia and treatment characteristics on the kinetics of Minimal Residual Disease (MRD) clearance in children with lymphoblastic leukaemia treated using an intensive risk stratified approach. UK MRC protocol ALL97 (1997–1999), and its amended version ALL 97/99 (1999–2002), compared the efficacy and toxicity of dexamethasone (DEX) with prednisolone (PRED), and 6-thioguanine (TG) with 6-Mercaptopurine (MP) in a randomised fashion. The trial produced a 5 year event-free survival (EFS) of 80%, with better systemic and Central Nervous System outcomes in DEX compared with PRED recipients but no difference between TG and MP recipients. Several changes to the risk stratification and treatment regimens during the period of the trial provided an opportunity to determine their impact on MRD clearance. We compared this with clearance in those treated on the successor trial ALL 2003 (more intensive induction containing DEX and Pegylated Asparaginase). The variables investigated for their potential influence on MRD status at the end of induction (EOI) were: NCI Risk; Asparaginase intensity (Erwinia Asparaginase [ERW] in ALL 97 and early part of ALL97/99 vs native or Pegylated E. Coli Asparaginase [E. Coli] in later part of ALL 97/99 and ALL2003); DEX vs PRED; and marrow response at day 8/15 of induction (Slow Early Response [SER] >25% blasts vs Rapid Early Response [RER] ⩽ 25% blasts). MRD was assessed using either a semi-quantitative sequence-specific PCR (ALL97) or Real-Time Quantitative PCR (ALL99 and ALL 2003) of antigen [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1105", "doc_id": "80522346", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Propriospinal interneurons that play a role in the plastic reorganization of spinal circuits are integral for recovery from spinal cord injury.\n\nCANDIDATE_PASSAGE:\nImmune reconstitution after cord blood transplantation: peculiarities, clinical implications and management strategies. Umbilical cord blood (UCB) is now widely used as an alternative hematopoietic stem cell source for patients lacking closely matched related or unrelated adult donors. UCB transplantation has traditionally been associated with delayed engraftment, poor immune reconstitution and consequent increased risk of infection. More recent clinical studies, however, suggest that conditioning regimens and in particular the omission of in vivo T-cell depletion may play a crucial role in post-transplant T-cell expansion, facilitating a uniquely rapid immune recovery after UCB transplantation. The peculiar characteristics of UCB cells, the importance of thymic function and the role of conditioning regimens and graft-versus-host disease influencing immune reconstitution are described. The last part of the review reports available data on UCB, as well as third-party peripheral blood derived anti-viral cell therapy, which provides a novel approach to rescue UCB recipients with viral complications in the post-transplant period.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "980", "doc_id": "27243019", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: High levels of copeptin decrease risk of diabetes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mendelian Randomization Study of B-Type Natriuretic Peptide and Type 2 Diabetes: Evidence of Causal Association from Population Studies\nABSTRACT: BACKGROUND Genetic and epidemiological evidence suggests an inverse association between B-type natriuretic peptide (BNP) levels in blood and risk of type 2 diabetes (T2D), but the prospective association of BNP with T2D is uncertain, and it is unclear whether the association is confounded. METHODS AND FINDINGS We analysed the association between levels of the N-terminal fragment of pro-BNP (NT-pro-BNP) in blood and risk of incident T2D in a prospective case-cohort study and genotyped the variant rs198389 within the BNP locus in three T2D case-control studies. We combined our results with existing data in a meta-analysis of 11 case-control studies. Using a Mendelian randomization approach, we compared the observed association between rs198389 and T2D to that expected from the NT-pro-BNP level to T2D association and the NT-pro-BNP difference per C allele of rs198389. In participants of our case-cohort study who were free of T2D and cardiovascular disease at baseline, we observed a 21% (95% CI 3%-36%) decreased risk of incident T2D per one standard deviation (SD) higher log-transformed NT-pro-BNP levels in analysis adjusted for age, sex, body mass index, systolic blood pressure, smoking, family history of T2D, history of hypertension, and levels of triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. The association between rs198389 and T2D observed in case-control studies (odds ratio = 0.94 per C allele, 95% CI 0.91-0.97) was similar to that expected (0.96, 0.93-0.98) based on the pooled estimate for the log-NT-pro-BNP level to T2D association derived from a meta-analysis of our study and published data (hazard ratio = 0.82 per SD, 0.74-0.90) and the difference in NT-pro-BNP levels (0.22 SD, 0.15-0.29) per C allele of r [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 517, "doc_id": "15663829", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: In transgenic mice harboring green florescent protein under the control of the Sox2 promoter, less than ten percent of the cells with green florescent colocalize with cell proliferation markers.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cell Stem Cell Article In Vivo Fate Analysis Reveals the Multipotent and Self-Renewal Capacities of Sox2 + Neural Stem Cells in the Adult Hippocampus\nABSTRACT: To characterize the properties of adult neural stem cells (NSCs), we generated and analyzed Sox2-GFP transgenic mice. Sox2-GFP cells in the subgranular zone (SGZ) express markers specific for progenitors, but they represent two morphologically distinct populations that differ in proliferation levels. Lentivirus- and retrovirus-mediated fate-tracing studies showed that Sox2+ cells in the SGZ have potential to give rise to neurons and astrocytes, revealing their multipotency at the population as well as at a single-cell level. A subpopulation of Sox2+ cells gives rise to cells that retain Sox2, highlighting Sox2+ cells as a primary source for adult NSCs. In response to mitotic signals, increased proliferation of Sox2+ cells is coupled with the generation of Sox2+ NSCs as well as neuronal precursors. An asymmetric contribution of Sox2+ NSCs may play an important role in maintaining the constant size of the NSC pool and producing newly born neurons during adult neurogenesis.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 587, "doc_id": "16999023", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Deletion of ATM and Rad3 related protein is not predictive of acute tissue loss.\n\nCANDIDATE_PASSAGE:\nGolgi Export of the Kir2.1 Channel Is Driven by a Trafficking Signal Located within Its Tertiary Structure Mechanisms that are responsible for sorting newly synthesized proteins for traffic to the cell surface from the Golgi are poorly understood. Here, we show that the potassium channel Kir2.1, mutations in which are associated with Andersen-Tawil syndrome, is selected as cargo into Golgi export carriers in an unusual signal-dependent manner. Unlike conventional trafficking signals, which are typically comprised of short linear peptide sequences, Golgi exit of Kir2.1 is dictated by residues that are embedded within the confluence of two separate domains. This signal patch forms a recognition site for interaction with the AP1 adaptor complex, thereby marking Kir2.1 for incorporation into clathrin-coated vesicles at the trans-Golgi. The identification of a trafficking signal in the tertiary structure of Kir2.1 reveals a quality control step that couples protein conformation to Golgi export and provides molecular insight into how mutations in Kir2.1 arrest the channels at the Golgi.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "325", "doc_id": "18078750", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Noninvasive positive pressure ventilation is not predictive of acute respiratory failure after solid organ transplantation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Noninvasive ventilation for treatment of acute respiratory failure in patients undergoing solid organ transplantation: a randomized trial.\nABSTRACT: CONTEXT Noninvasive ventilation (NIV) has been associated with lower rates of endotracheal intubation in populations of patients with acute respiratory failure. OBJECTIVE To compare NIV with standard treatment using supplemental oxygen administration to avoid endotracheal intubation in recipients of solid organ transplantation with acute hypoxemic respiratory failure. DESIGN AND SETTING Prospective randomized study conducted at a 14-bed, general intensive care unit of a university hospital. PATIENTS Of 238 patients who underwent solid organ transplantation from December 1995 to October 1997, 51 were treated for acute respiratory failure. Of these, 40 were eligible and 20 were randomized to each group. INTERVENTION Noninvasive ventilation vs standard treatment with supplemental oxygen administration. MAIN OUTCOME MEASURES The need for endotracheal intubation and mechanical ventilation at any time during the study, complications not present on admission, duration of ventilatory assistance, length of hospital stay, and intensive care unit mortality. RESULTS The 2 groups were similar at study entry. Within the first hour of treatment, 14 patients (70%) in the NIV group, and 5 patients (25%) in the standard treatment group improved their ratio of the PaO2 to the fraction of inspired oxygen (FIO2). Over time, a sustained improvement in PaO2 to FIO2 was noted in 12 patients (60%) in the NIV group, and in 5 patients (25%) randomized to standard treatment (P = .03). The use of NIV was associated with a significant reduction in the rate of endotracheal intubation (20% vs 70%; P = .002), rate of fatal complications (20% vs 50%; P = .05), length of stay in the intensive care unit by survivors (mean [SD] days, 5.5 [3] vs 9 [4]; P = .03), and intensive care unit mortality [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Within the first hour of treatment, 14 patients (70%) in the NIV group, and 5 patients (25%) in the standard treatment group improved their ratio of the PaO2 to the fraction of inspired oxygen (FIO2).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 855, "doc_id": "8190282", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is procalcitonin a predictor for high-grade vesicoureteral reflux in children : meta-analysis of individual patient data?\n\nABSTRACT:\nTo assess the predictive value of procalcitonin, a serum inflammatory marker, in the identification of children with first urinary tract infection (UTI) who might have high-grade (≥3) vesicoureteral reflux (VUR). We conducted a meta-analysis of individual data, including all series of children aged 1 month to 4 years with a first UTI, a procalcitonin (PCT) level measurement, cystograms, and an early dimercaptosuccinic acid scan. Of the 152 relevant identified articles, 12 studies representing 526 patients (10% with VUR ≥3) were included. PCT level was associated with VUR ≥3 as a continuous (P = .001), and as a binary variable, with a 0.5 ng/mL preferred threshold (adjusted OR, 2.5; 95% CI, 1.1 to 5.4). The sensitivity of PCT ≥0.5 ng/mL was 83% (95% CI, 71 to 91) with 43% specificity rate (95% CI, 38 to 47). In the subgroup of children with a positive results on dimercaptosuccinic acid scan, PCT ≥0.5 ng/mL was also associated with high-grade VUR (adjusted OR, 4.8; 95% CI, 1.3 to 17.6).", "output": "{\"label\": \"yes\", \"rationale\": \"We confirmed that PCT is a sensitive and validated predictor strongly associated with VUR ≥3, regardless of the presence of early renal parenchymal involvement in children with a first UTI.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 21511275, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: 4-PBA treatment raises endoplasmic reticulum stress in response to general endoplasmic reticulum stress markers.\n\nCANDIDATE_PASSAGE:\nComparative determinants of 4-year cardiovascular event rates in stable outpatients at risk of or with atherothrombosis. CONTEXT Clinicians and trialists have difficulty with identifying which patients are highest risk for cardiovascular events. Prior ischemic events, polyvascular disease, and diabetes mellitus have all been identified as predictors of ischemic events, but their comparative contributions to future risk remain unclear. OBJECTIVE To categorize the risk of cardiovascular events in stable outpatients with various initial manifestations of atherothrombosis using simple clinical descriptors. DESIGN, SETTING, AND PATIENTS Outpatients with coronary artery disease, cerebrovascular disease, or peripheral arterial disease or with multiple risk factors for atherothrombosis were enrolled in the global Reduction of Atherothrombosis for Continued Health (REACH) Registry and were followed up for as long as 4 years. Patients from 3647 centers in 29 countries were enrolled between 2003 and 2004 and followed up until 2008. Final database lock was in April 2009. MAIN OUTCOME MEASURES Rates of cardiovascular death, myocardial infarction, and stroke. RESULTS A total of 45,227 patients with baseline data were included in this 4-year analysis. During the follow-up period, a total of 5481 patients experienced at least 1 event, including 2315 with cardiovascular death, 1228 with myocardial infarction, 1898 with stroke, and 40 with both a myocardial infarction and stroke on the same day. Among patients with atherothrombosis, those with a prior history of ischemic events at baseline (n = 21,890) had the highest rate of subsequent ischemic events (18.3%; 95% confidence interval [CI], 17.4%-19.1%); patients with stable coronary, cerebrovascular, or peripheral artery dise [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "11", "doc_id": "16760369", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The NF-κB essential modulator gene induces intestinal inflammation by promoting receptor-interacting protein (RIP) kinase 1 kinase activity-mediated epithelial cell death.\n\nCANDIDATE_PASSAGE:\nNEMO Prevents RIP Kinase 1-Mediated Epithelial Cell Death and Chronic Intestinal Inflammation by NF-κB-Dependent and -Independent Functions Intestinal epithelial cells (IECs) regulate gut immune homeostasis, and impaired epithelial responses are implicated in the pathogenesis of inflammatory bowel diseases (IBD). IEC-specific ablation of nuclear factor κB (NF-κB) essential modulator (NEMO) caused Paneth cell apoptosis and impaired antimicrobial factor expression in the ileum, as well as colonocyte apoptosis and microbiota-driven chronic inflammation in the colon. Combined RelA, c-Rel, and RelB deficiency in IECs caused Paneth cell apoptosis but not colitis, suggesting that NEMO prevents colon inflammation by NF-κB-independent functions. Inhibition of receptor-interacting protein kinase 1 (RIPK1) kinase activity or combined deficiency of Fas-associated via death domain protein (FADD) and RIPK3 prevented epithelial cell death, Paneth cell loss, and colitis development in mice with epithelial NEMO deficiency. Therefore, NEMO prevents intestinal inflammation by inhibiting RIPK1 kinase activity-mediated IEC death, suggesting that RIPK1 inhibitors could be effective in the treatment of colitis in patients with NEMO mutations and possibly in IBD.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1170", "doc_id": "18956141", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Are glucose intolerance and diabetes observed in the long-term follow-up of nonpancreatectomized patients with persistent hyperinsulinemic hypoglycemia of infancy due to mutations in the ABCC8 gene?\n\nABSTRACT:\nTo report the long-term follow-up of three nonpancreatectomized patients with persistent hyperinsulinemic hypoglycemia of infancy due to mutations in the ABCC8 gene. Oral glucose tolerance test (OGTT) and venous 24-h glucose-insulin profile were performed yearly from adolescence. Patient 1 (now aged 31 years) developed insulin-dependent diabetes at the age of 25 years. In patient 2 (now aged 17 years), impaired fasting glucose and a diabetic OGTT response with normal A1C values have been observed since the age of 10 years. In patient 3 (now aged 24 years), intolerant OGTT response and hyperglycemic episodes with normal A1C have been observed since the age of 16 years. All patients presented relatively low insulin levels during hyperglycemia, normal BMI, and negative autoantibodies (GAD antibody, insulinoma-associated protein 2, and islet cell antibody).", "output": "{\"label\": \"yes\", \"rationale\": \"Development of glucose metabolism impairment ranging from glucose intolerance to insulin-dependent diabetes is observed in the evolution of these patients.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 18339976, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: RAD52 is involved in break-induced DNA replication (BIR).\n\nCANDIDATE_ABSTRACT:\nTITLE: Alternative Lengthening of Telomeres Mediated by Mitotic DNA Synthesis Engages Break-Induced Replication Processes.\nABSTRACT: Alternative lengthening of telomeres (ALT) is a telomerase-independent telomere maintenance mechanism that occurs in a subset of cancers. By analyzing telomerase-positive cells and their human TERC knockout-derived ALT human cell lines, we show that ALT cells harbor more fragile telomeres representing telomere replication problems. ALT-associated replication defects trigger mitotic DNA synthesis (MiDAS) at telomeres in a RAD52-dependent, but RAD51-independent, manner. Telomeric MiDAS is a conservative DNA synthesis process, potentially mediated by break-induced replication, similar to type II ALT survivors in Saccharomyces cerevisiae Replication stresses induced by ectopic oncogenic expression of cyclin E, G-quadruplexes, or R-loop formation facilitate the ALT pathway and lead to telomere clustering, a hallmark of ALT cancers. The TIMELESS/TIPIN complex suppresses telomere clustering and telomeric MiDAS, whereas the SMC5/6 complex promotes them. In summary, ALT cells exhibit more telomere replication defects that result in persistent DNA damage responses at telomeres, leading to the engagement of telomeric MiDAS (spontaneous mitotic telomere synthesis) that is triggered by DNA replication stress, a potential driver of genomic duplications in cancer.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"ALT-associated replication defects trigger mitotic DNA synthesis (MiDAS) at telomeres in a RAD52-dependent, but RAD51-independent, manner.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1003, "doc_id": "4319844", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Walking in traffic areas in London improves lung function in elderly adults.\n\nCANDIDATE_ABSTRACT:\nTITLE: Respiratory and cardiovascular responses to walking down a traffic-polluted road compared with walking in a traffic-free area in participants aged 60 years and older with chronic lung or heart disease and age-matched healthy controls: a randomised, crossover study\nABSTRACT: BACKGROUND Long-term exposure to pollution can lead to an increase in the rate of decline of lung function, especially in older individuals and in those with chronic obstructive pulmonary disease (COPD), whereas shorter-term exposure at higher pollution levels has been implicated in causing excess deaths from ischaemic heart disease and exacerbations of COPD. We aimed to assess the effects on respiratory and cardiovascular responses of walking down a busy street with high levels of pollution compared with walking in a traffic-free area with lower pollution levels in older adults. METHODS In this randomised, crossover study, we recruited men and women aged 60 years and older with angiographically proven stable ischaemic heart disease or stage 2 Global initiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable for 6 months, and age-matched healthy volunteers. Individuals with ischaemic heart disease or COPD were recruited from existing databases or outpatient respiratory and cardiology clinics at the Royal Brompton & Harefield NHS Foundation Trust and age-matched healthy volunteers using advertising and existing databases. All participants had abstained from smoking for at least 12 months and medications were taken as recommended by participants' doctors during the study. Participants were randomly assigned by drawing numbered disks at random from a bag to do a 2 h walk either along a commercial street in London (Oxford Street) or in an urban park (Hyde Park). Baseline measurements of participants were taken before the walk in the hospital laboratory. During each walk session, black carbon, particulate matter (PM) concentrations, ultrafine particles, and nitrogen dioxide (NO2) concentrations were measured. FINDINGS Between October, 2012 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Participants with COPD reported more cough (odds ratio [OR] 1·95, 95% CI 0·96-3·95; p<0·1), sputum (3·15, 1·39-7·13; p<0·05), shortness of breath (1·86, 0·97-3·57; p<0·1), and wheeze (4·00, 1·52-10·50; p<0·05) after walking down Oxford Street compared with Hyde Park.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1373, "doc_id": "21003930", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Mice lacking Sirt1 in Sf1-expressing neurons have increased susceptibility to diet-induced obesity and insulin resistance.\n\nCANDIDATE_PASSAGE:\nSIRT1 deacetylase in SF1 neurons protects against metabolic imbalance. Chronic feeding on high-calorie diets causes obesity and type 2 diabetes mellitus (T2DM), illnesses that affect hundreds of millions. Thus, understanding the pathways protecting against diet-induced metabolic imbalance is of paramount medical importance. Here, we show that mice lacking SIRT1 in steroidogenic factor 1 (SF1) neurons are hypersensitive to dietary obesity owing to maladaptive energy expenditure. Also, mutant mice have increased susceptibility to developing dietary T2DM due to insulin resistance in skeletal muscle. Mechanistically, these aberrations arise, in part, from impaired metabolic actions of the neuropeptide orexin-A and the hormone leptin. Conversely, mice overexpressing SIRT1 in SF1 neurons are more resistant to diet-induced obesity and insulin resistance due to increased energy expenditure and enhanced skeletal muscle insulin sensitivity. Our results unveil important protective roles of SIRT1 in SF1 neurons against dietary metabolic imbalance.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "779", "doc_id": "13001323", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The sliding activity of kinesin-8 protein Kip3 promotes bipolar spindle assembly.\n\nCANDIDATE_PASSAGE:\nMicrotubule sliding activity of a kinesin-8 promotes spindle assembly and spindle length control Molecular motors play critical roles in the formation of mitotic spindles, either through controlling the stability of individual microtubules, or by crosslinking and sliding microtubule arrays. Kinesin-8 motors are best known for their regulatory roles in controlling microtubule dynamics. They contain microtubule-destabilizing activities, and restrict spindle length in a wide variety of cell types and organisms. Here, we report an antiparallel microtubule-sliding activity of the budding yeast kinesin-8, Kip3. The in vivo importance of this sliding activity was established through the identification of complementary Kip3 mutants that separate the sliding activity and microtubule-destabilizing activity. In conjunction with Cin8, a kinesin-5 family member, the sliding activity of Kip3 promotes bipolar spindle assembly and the maintenance of genome stability. We propose a slide-disassemble model where the sliding and destabilizing activity of Kip3 balance during pre-anaphase. This facilitates normal spindle assembly. However, the destabilizing activity of Kip3 dominates in late anaphase, inhibiting spindle elongation and ultimately promoting spindle disassembly.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1273", "doc_id": "11041152", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Basophils promote disease development in patients with systemic lupus erythematosus (SLE).\n\nCANDIDATE_ABSTRACT:\nTITLE: Involvement of CB1 cannabinoid receptors in emotional behaviour\nABSTRACT: Rationale: Endogenous and exogenous cannabinoids acting through the CB1 cannabinoid receptors are implicated in the control of a variety of behavioural and neuroendocrine functions, including emotional responses, and learning and memory processes. Recently, knockout mice deficient in the CB1 cannabinoid receptor have been generated, and these animals result in an excellent tool to evaluate the neurophysiology of the endogenous cannabinoid system. Objectives: To establish the role of the CB1 cannabinoid receptor in several emotional-related behavioural responses, including aggressiveness, anxiety, depression and learning models, using CB1 knockout mice. Methods: We evaluated the spontaneous responses of CB1 knockout mice and wild-type controls under different behavioural paradigms, including the light/dark box, the chronic unpredictable mild stress, the resident–intruder test and the active avoidance paradigm. Results: Our findings showed that CB1 knockout mice presented an increase in the aggressive response measured in the resident–intruder test and an anxiogenic-like response in the light/dark box. Furthermore, a higher sensitivity to exhibit depressive-like responses in the chronic unpredictable mild stress procedure was observed in CB1 knockout mice, suggesting an increased susceptibility to develop an anhedonic state in these animals. Finally, CB1 knockout mice showed a significant increase in the conditioned responses produced in the active avoidance model, suggesting an improvement of learning and memory processes. Conclusions: Taken together these findings demonstrate that endogenous cannabinoids through the activation of CB1 receptors are implicated in the control of emotional behaviour and participate in the physiological processes of learning and memory.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 172, "doc_id": "649951", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Commelina yellow mottle virus' (ComYMV) genome consists of 2140 baise pairs.\n\nCANDIDATE_ABSTRACT:\nTITLE: Properties of Commelina yellow mottle virus's complete DNA sequence, genomic discontinuities and transcript suggest that it is a pararetrovirus.\nABSTRACT: The non-enveloped bacilliform viruses are the second group of plant viruses known to possess a genome consisting of circular double-stranded DNA. We have characterized the viral transcript and determined the complete sequence of the genome of Commelina mellow mottle virus (CoYMV), a member of this group. Analysis of the viral transcript indicates that the virus encodes a single terminally-redundant genome-length plus 120 nucleotide transcript. A fraction of the transcripts is polyadenylated, although the majority of the transcript is not polyadenylated. Analysis of the genome sequence indicates that the genome is 7489 bp in size and that the transcribed strand contains three open reading frames capable of encoding proteins of 23, 15 and 216 kd. The function of the 25 and 15 kd proteins is unknown. Similarities between the 216 kd polypeptide and the cauliflower mosaic virus coat protein and protease/reverse transcriptase polyprotein suggest that the 216 kd polypeptide is a polyprotein that is proteolytically processed to yield the virion coat protein, a protease, and replicase (reverse transcriptase and ribonuclease H). Each strand of the CoYMV genome is interrupted by site-specific discontinuities. The locations of the 5'-ends of these discontinuities, and the presence and location of a region on the CoYMV transcript capable of annealing with the 3'-end of cytosolic initiator methionine tRNA are consistent with replication by reverse transcription. We have demonstrated that a construct containing 1.3 CoYMV genomes is infective when introduced into Commelina diffusa, the host for CoYMV, using Agrobacterium-mediated infection.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Analysis of the genome sequence indicates that the genome is 7489 bp in size and that the transcribed strand contains three open reading frames capable of encoding proteins of 23, 15 and 216 kd.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 278, "doc_id": "14376683", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Cardiac tissue-resident macrophages directly contribute to electrical activity.\n\nCANDIDATE_ABSTRACT:\nTITLE: Macrophages Facilitate Electrical Conduction in the Heart\nABSTRACT: Organ-specific functions of tissue-resident macrophages in the steady-state heart are unknown. Here, we show that cardiac macrophages facilitate electrical conduction through the distal atrioventricular node, where conducting cells densely intersperse with elongated macrophages expressing connexin 43. When coupled to spontaneously beating cardiomyocytes via connexin-43-containing gap junctions, cardiac macrophages have a negative resting membrane potential and depolarize in synchrony with cardiomyocytes. Conversely, macrophages render the resting membrane potential of cardiomyocytes more positive and, according to computational modeling, accelerate their repolarization. Photostimulation of channelrhodopsin-2-expressing macrophages improves atrioventricular conduction, whereas conditional deletion of connexin 43 in macrophages and congenital lack of macrophages delay atrioventricular conduction. In the Cd11bDTR mouse, macrophage ablation induces progressive atrioventricular block. These observations implicate macrophages in normal and aberrant cardiac conduction.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here, we show that cardiac macrophages facilitate electrical conduction through the distal atrioventricular node, where conducting cells densely intersperse with elongated macrophages expressing connexin 43.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 228, "doc_id": "4928057", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The deregulated and prolonged activation of monocytes has deleterious effects in chronic infectious conditions.\n\nCANDIDATE_PASSAGE:\nHypothermic preservation up-regulates calpain expression and increases ubiquitination in cultured vascular endothelial cells: influence of dopamine pretreatment. BACKGROUND Prolonged hypothermia, as occurs during solid organ transplantation, negatively influences transplantation outcome. Proteolysis is one of the deleterious events implicated in preservation injury of organ allografts. This strongly affects graft quality and hence immediate organ function. Since donor catecholamine treatment improves transplantation outcome after renal transplantation, the present study was conducted to examine the influence of dopamine (DA) pretreatment on hypothermia induced proteolysis in endothelial cells subjected to prolonged cold storage. MATERIALS AND METHODS Lactate dehydrogenase (LDH) assay, two-dimensional electrophoresis, ubiquitination analysis, intracellular calcium measurement, and Western blot analysis were performed on human umbilical vein endothelial cells (HUVEC) subjected to hypothermic preservation or not. RESULTS HUVEC were highly susceptible to cold storage, which was reflected by morphological changes, loss of viability, and by significant changes in cellular proteome. DA pretreatment prevented cell death during cold storage. Western blot analysis demonstrated a time dependent up-regulation of calpain 1 and 2 during cold storage, which could be prevented by addition of EDTA. DA pretreatment abolished autoproteolysis of calpain 1. Analysis of ubiquitination revealed a significant increase in ubiquitinated conjugates after cold storage. This was not prevented by DA pretreatment. Neither proteasome nor calpain inhibitors prevented cell death during cold storage. CONCLUSION In endothelial cells subjected to cold preservation, activation of the calpain pat [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1212", "doc_id": "25817686", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Certain immunomodulator-human dialyzable leukocyte extract (hDLE) peptides are recognized by toll-like receptors (TLRs) on macrophages and dendritic cells.\n\nCANDIDATE_PASSAGE:\ninduction of early IFN-inducible genes in the absence of type On recognition of influenza virus (Flu) by TLR7, plasmacytoid dendritic cells (pDCs) produce type I IFN in significant amounts. Synthetic TLR7 ligands induce the maturation of pDCs, as evidenced by the expression of costimulatory molecules and the production of proinflammatory cytokines; however, they induce only low-level production of IFN-alpha. To dissect the TLR7 signaling in pDCs and how these different profiles are induced, we studied the effects of 2 TLR7 ligands (Flu and CL097) on the activation of blood-isolated pDCs and the human GEN2.2 pDC cell line. Type I IFN production by pDCs correlates with differential interferon regulatory factor 7 (IRF7) translocation into the nucleus induced by the 2 TLR7 ligands. Surprisingly, with both activators we nevertheless observed the rapid expression of the IFN-inducible genes mxa, cxcl10, and trail within 4 hours of stimulation. This expression, controlled by STAT1 phosphorylation, was independent of type I IFN. STAT1 activation was found to be strictly dependent on the PI3K-p38MAPK pathway, showing a new signaling pathway leading to rapid expression of IFN-inducible genes after TLR7 triggering. Thus, pDCs, through this unusual TLR7 signaling, have the capacity to promptly respond to viral infection during the early phases of the innate immune response.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "244", "doc_id": "72159", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Autologous transplantation of mesenchymal stem cells has lower rates of rejection than induction therapy with anti-interleukin-2 receptor antibodies.\n\nCANDIDATE_ABSTRACT:\nTITLE: TECHNICAL ADVANCE Floral dip: a simplified method for Agrobacterium-mediated\nABSTRACT: The Agrobacterium vacuum infiltration method has made it possible to transform Arabidopsis thaliana without plant tissue culture or regeneration. In the present study, this method was evaluated and a substantially modified transformation method was developed. The labor-intensive vacuum infiltration process was eliminated in favor of simple dipping of developing floral tissues into a solution containing Agrobacterium tumefaciens, 5% sucrose and 500 microliters per litre of surfactant Silwet L-77. Sucrose and surfactant were critical to the success of the floral dip method. Plants inoculated when numerous immature floral buds and few siliques were present produced transformed progeny at the highest rate. Plant tissue culture media, the hormone benzylamino purine and pH adjustment were unnecessary, and Agrobacterium could be applied to plants at a range of cell densities. Repeated application of Agrobacterium improved transformation rates and overall yield of transformants approximately twofold. Covering plants for 1 day to retain humidity after inoculation also raised transformation rates twofold. Multiple ecotypes were transformable by this method. The modified method should facilitate high-throughput transformation of Arabidopsis for efforts such as T-DNA gene tagging, positional cloning, or attempts at targeted gene replacement.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 146, "doc_id": "410286", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Low expression of miR7a exerts a biological function in testis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Assessing the ceRNA hypothesis with quantitative measurements of miRNA and target abundance.\nABSTRACT: Recent studies have reported that competitive endogenous RNAs (ceRNAs) can act as sponges for a microRNA (miRNA) through their binding sites and that changes in ceRNA abundances from individual genes can modulate the activity of miRNAs. Consideration of this hypothesis would benefit from knowing the quantitative relationship between a miRNA and its endogenous target sites. Here, we altered intracellular target site abundance through expression of an miR-122 target in hepatocytes and livers and analyzed the effects on miR-122 target genes. Target repression was released in a threshold-like manner at high target site abundance (≥1.5 × 10(5) added target sites per cell), and this threshold was insensitive to the effective levels of the miRNA. Furthermore, in response to extreme metabolic liver disease models, global target site abundance of hepatocytes did not change sufficiently to affect miRNA-mediated repression. Thus, modulation of miRNA target abundance is unlikely to cause significant effects on gene expression and metabolism through a ceRNA effect.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 716, "doc_id": "18421962", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Suboptimal nutrition is a leading cause of premature death\n\nCANDIDATE_PASSAGE:\nMechanisms of pancreatic beta-cell death in type 1 and type 2 diabetes: many differences, few similarities. Type 1 and type 2 diabetes are characterized by progressive beta-cell failure. Apoptosis is probably the main form of beta-cell death in both forms of the disease. It has been suggested that the mechanisms leading to nutrient- and cytokine-induced beta-cell death in type 2 and type 1 diabetes, respectively, share the activation of a final common pathway involving interleukin (IL)-1beta, nuclear factor (NF)-kappaB, and Fas. We review herein the similarities and differences between the mechanisms of beta-cell death in type 1 and type 2 diabetes. In the insulitis lesion in type 1 diabetes, invading immune cells produce cytokines, such as IL-1beta, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma. IL-1beta and/or TNF-alpha plus IFN-gamma induce beta-cell apoptosis via the activation of beta-cell gene networks under the control of the transcription factors NF-kappaB and STAT-1. NF-kappaB activation leads to production of nitric oxide (NO) and chemokines and depletion of endoplasmic reticulum (ER) calcium. The execution of beta-cell death occurs through activation of mitogen-activated protein kinases, via triggering of ER stress and by the release of mitochondrial death signals. Chronic exposure to elevated levels of glucose and free fatty acids (FFAs) causes beta-cell dysfunction and may induce beta-cell apoptosis in type 2 diabetes. Exposure to high glucose has dual effects, triggering initially \"glucose hypersensitization\" and later apoptosis, via different mechanisms. High glucose, however, does not induce or activate IL-1beta, NF-kappaB, or inducible nitric oxide synthase in rat or human beta-cells in vitro or in vivo in Psammomys obesus. F [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1109", "doc_id": "42873134", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: De novo assembly of sequence data has more specific contigs than unassembled sequence data.\n\nCANDIDATE_PASSAGE:\nA culture-independent sequence-based metagenomics approach to the investigation of an outbreak of Shiga-toxigenic Escherichia coli O104:H4. IMPORTANCE Identification of the bacterium responsible for an outbreak can aid in disease management. However, traditional culture-based diagnosis can be difficult, particularly if no specific diagnostic test is available for an outbreak strain. OBJECTIVE To explore the potential of metagenomics, which is the direct sequencing of DNA extracted from microbiologically complex samples, as an open-ended clinical discovery platform capable of identifying and characterizing bacterial strains from an outbreak without laboratory culture. DESIGN, SETTING, AND PATIENTS In a retrospective investigation, 45 samples were selected from fecal specimens obtained from patients with diarrhea during the 2011 outbreak of Shiga-toxigenic Escherichia coli (STEC) O104:H4 in Germany. Samples were subjected to high-throughput sequencing (August-September 2012), followed by a 3-phase analysis (November 2012-February 2013). In phase 1, a de novo assembly approach was developed to obtain a draft genome of the outbreak strain. In phase 2, the depth of coverage of the outbreak strain genome was determined in each sample. In phase 3, sequences from each sample were compared with sequences from known bacteria to identify pathogens other than the outbreak strain. MAIN OUTCOMES AND MEASURES The recovery of genome sequence data for the purposes of identification and characterization of the outbreak strain and other pathogens from fecal samples. RESULTS During phase 1, a draft genome of the STEC outbreak strain was obtained. During phase 2, the outbreak strain genome was recovered from 10 samples at greater than 10-fold coverage and from 26 samples at grea [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "312", "doc_id": "6173523", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Hematopoietic Stem Cell purification reaches purity rates above 90%.\n\nCANDIDATE_ABSTRACT:\nTITLE: Combined Single-Cell Functional and Gene Expression Analysis Resolves Heterogeneity within Stem Cell Populations\nABSTRACT: Heterogeneity within the self-renewal durability of adult hematopoietic stem cells (HSCs) challenges our understanding of the molecular framework underlying HSC function. Gene expression studies have been hampered by the presence of multiple HSC subtypes and contaminating non-HSCs in bulk HSC populations. To gain deeper insight into the gene expression program of murine HSCs, we combined single-cell functional assays with flow cytometric index sorting and single-cell gene expression assays. Through bioinformatic integration of these datasets, we designed an unbiased sorting strategy that separates non-HSCs away from HSCs, and single-cell transplantation experiments using the enriched population were combined with RNA-seq data to identify key molecules that associate with long-term durable self-renewal, producing a single-cell molecular dataset that is linked to functional stem cell activity. Finally, we demonstrated the broader applicability of this approach for linking key molecules with defined cellular functions in another stem cell system.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 509, "doc_id": "13980338", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: There is no association between HNF4A mutations and diabetes risks.\n\nCANDIDATE_PASSAGE:\nMacrosomia and Hyperinsulinaemic Hypoglycaemia in Patients with Heterozygous Mutations in the HNF4A Gene Background Macrosomia is associated with considerable neonatal and maternal morbidity. Factors that predict macrosomia are poorly understood. The increased rate of macrosomia in the offspring of pregnant women with diabetes and in congenital hyperinsulinaemia is mediated by increased foetal insulin secretion. We assessed the in utero and neonatal role of two key regulators of pancreatic insulin secretion by studying birthweight and the incidence of neonatal hypoglycaemia in patients with heterozygous mutations in the maturity-onset diabetes of the young (MODY) genes HNF4A (encoding HNF-4α) and HNF1A/TCF1 (encoding HNF-1α), and the effect of pancreatic deletion of Hnf4a on foetal and neonatal insulin secretion in mice.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1292", "doc_id": "56893404", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Students who perform poorly in the early years of medical school are at increased risk for professional misconduct later in their careers.\n\nCANDIDATE_PASSAGE:\nRisk factors at medical school for subsequent professional misconduct: multicentre retrospective case-control study OBJECTIVE To determine whether there are risk factors in a doctor's time at medical school that are associated with subsequent professional misconduct. DESIGN Matched case-control study. Setting Records from medical schools and the General Medical Council (GMC). PARTICIPANTS 59 doctors who had graduated from any one of eight medical schools in the United Kingdom in 1958-97 and had a proved finding of serious professional misconduct in GMC proceedings in 1999-2004 (cases); 236 controls (four for each case) were selected by systematic sampling from matching graduation cohorts. Case-control status was revealed by the GMC after completion of data entry. MAIN OUTCOME MEASURE Odds ratios for being a \"case,\" with multivariable conditional logistic regression of potential risk factors including pre-admission characteristics and progress during the course. These data were obtained from anonymised copies of the students' progress files held by their original medical schools. RESULTS Univariate conditional logistic regression analysis found that cases were more likely to be men, to be of lower estimated social class, and to have had academic difficulties during their medical course, especially in the early years. Multivariable analysis showed that male sex (odds ratio 9.80, 95% confidence interval 2.43 to 39.44, P=0.001), lower social class (4.28, 1.52 to 12.09, P=0.006), and failure of early or preclinical examinations (5.47, 2.17 to 13.79, P<0.001) were independently associated with being a case. CONCLUSIONS This small study suggests that male sex, a lower socioeconomic background, and early academic difficulties at medical school could be risk factors [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1105", "doc_id": "6710713", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Decreased conversion of PGE 2 to PPARy ligand 15-ket-PGE 2 causes accumulation of PGE.\n\nCANDIDATE_PASSAGE:\nHaematopoietic stem cells and early lymphoid progenitors occupy distinct bone marrow niches Although haematopoietic stem cells (HSCs) are commonly assumed to reside within a specialized microenvironment, or niche, most published experimental manipulations of the HSC niche have affected the function of diverse restricted progenitors. This raises the fundamental question of whether HSCs and restricted progenitors reside within distinct, specialized niches or whether they share a common niche. Here we assess the physiological sources of the chemokine CXCL12 for HSC and restricted progenitor maintenance. Cxcl12(DsRed) knock-in mice (DsRed-Express2 recombined into the Cxcl12 locus) showed that Cxcl12 was primarily expressed by perivascular stromal cells and, at lower levels, by endothelial cells, osteoblasts and some haematopoietic cells. Conditional deletion of Cxcl12 from haematopoietic cells or nestin-cre-expressing cells had little or no effect on HSCs or restricted progenitors. Deletion of Cxcl12 from endothelial cells depleted HSCs but not myeloerythroid or lymphoid progenitors. Deletion of Cxcl12 from perivascular stromal cells depleted HSCs and certain restricted progenitors and mobilized these cells into circulation. Deletion of Cxcl12 from osteoblasts depleted certain early lymphoid progenitors but not HSCs or myeloerythroid progenitors, and did not mobilize these cells into circulation. Different stem and progenitor cells thus reside in distinct cellular niches in bone marrow: HSCs occupy a perivascular niche and early lymphoid progenitors occupy an endosteal niche.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "316", "doc_id": "4366738", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Fz/PCP-dependent Pk localizes to the anterior membrane of neuroectoderm cells during zebrafish neuralation\n\nCANDIDATE_PASSAGE:\nLocal Ca2+ influx through Ca2+ release-activated Ca2+ (CRAC) channels stimulates production of an intracellular messenger and an intercellular pro-inflammatory signal. Ca2+ entry through store-operated Ca2+ channels drives the production of the pro-inflammatory molecule leukotriene C4 (LTC4) from mast cells through a pathway involving Ca2+-dependent protein kinase C, mitogen-activated protein kinases ERK1/2, phospholipase A2, and 5-lipoxygenase. Here we examine whether local Ca2+ influx through store-operated Ca2+ release-activated Ca2+ (CRAC) channels in the plasma membrane stimulates this signaling pathway. Manipulating the amplitude and spatial extent of Ca2+ entry by altering chemical and electrical gradients for Ca2+ influx or changing the Ca2+ buffering of the cytoplasm all impacted on protein kinase C and ERK activation, generation of arachidonic acid and LTC4 secretion, with little change in the bulk cytoplasmic Ca2+ rise. Similar bulk cytoplasmic Ca2+ concentrations were achieved when CRAC channels were activated in 0.25 mm external Ca2+ versus 2 mm Ca2+ and 100 nm La3+, an inhibitor of CRAC channels. However, despite similar bulk cytoplasmic Ca2+, protein kinase C activation and LTC4 secretion were larger in 2 mm Ca2+ and La3+ than in 0.25 mm Ca2+, consistent with the central involvement of a subplasmalemmal Ca2+ rise. The nonreceptor tyrosine kinase Syk coupled CRAC channel opening to protein kinase C and ERK activation. Recombinant TRPC3 channels also activated protein kinase C, suggesting that subplasmalemmal Ca2+ rather than a microdomain exclusive to CRAC channels is the trigger. Hence a subplasmalemmal Ca2+ increase in mast cells is highly versatile in that it triggers cytoplasmic responses through generation of intracellular messengers as we [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "439", "doc_id": "37964706", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Walking in traffic areas in London improves lung function in elderly adults.\n\nCANDIDATE_ABSTRACT:\nTITLE: Respiratory and cardiovascular responses to walking down a traffic-polluted road compared with walking in a traffic-free area in participants aged 60 years and older with chronic lung or heart disease and age-matched healthy controls: a randomised, crossover study\nABSTRACT: BACKGROUND Long-term exposure to pollution can lead to an increase in the rate of decline of lung function, especially in older individuals and in those with chronic obstructive pulmonary disease (COPD), whereas shorter-term exposure at higher pollution levels has been implicated in causing excess deaths from ischaemic heart disease and exacerbations of COPD. We aimed to assess the effects on respiratory and cardiovascular responses of walking down a busy street with high levels of pollution compared with walking in a traffic-free area with lower pollution levels in older adults. METHODS In this randomised, crossover study, we recruited men and women aged 60 years and older with angiographically proven stable ischaemic heart disease or stage 2 Global initiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable for 6 months, and age-matched healthy volunteers. Individuals with ischaemic heart disease or COPD were recruited from existing databases or outpatient respiratory and cardiology clinics at the Royal Brompton & Harefield NHS Foundation Trust and age-matched healthy volunteers using advertising and existing databases. All participants had abstained from smoking for at least 12 months and medications were taken as recommended by participants' doctors during the study. Participants were randomly assigned by drawing numbered disks at random from a bag to do a 2 h walk either along a commercial street in London (Oxford Street) or in an urban park (Hyde Park). Baseline measurements of participants were taken before the walk in the hospital laboratory. During each walk session, black carbon, particulate matter (PM) concentrations, ultrafine particles, and nitrogen dioxide (NO2) concentrations were measured. FINDINGS Between October, 2012 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Participants with COPD reported more cough (odds ratio [OR] 1·95, 95% CI 0·96-3·95; p<0·1), sputum (3·15, 1·39-7·13; p<0·05), shortness of breath (1·86, 0·97-3·57; p<0·1), and wheeze (4·00, 1·52-10·50; p<0·05) after walking down Oxford Street compared with Hyde Park.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1373, "doc_id": "21003930", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The artifactual C-terminal helix swapping in the StART domain is observed in the Ups1-Mdm35 heterodimer of the StARkin superfamily.\n\nCANDIDATE_PASSAGE:\nA diffusion tensor magnetic resonance imaging study of corpus callosum from adult patients with migraine complicated with depressive/anxious disorder. OBJECTIVE The aim of this study was to investigate the possible microstructural abnormalities of the corpus callosum (CC) in adult patients with migraine without aura complicated with depressive/anxious disorder. BACKGROUND Emotional disorders, especially depression and anxiety, are with relatively higher incidence in migraine population. However, the mechanism of migraine complicated with depressive/anxious disorder remains unclear. METHODS Diffusion tensor magnetic resonance imaging was carried out in 12 adult patients with simple migraine (without aura and without depressive/anxious disorder) (S-M group), 12 adult patients with complicated migraine (without aura but complicated with depressive/anxious disorder) (Co-M group), and 12 age- and sex-matched healthy subjects (Control group). Fractional anisotropy (FA) and apparent diffusion coefficient were measured at genu, body, and splenium of the CC, respectively. RESULTS There were significant differences in FA values at all locations of the CC among the 3 groups. The FA values from both the SM and Co-M groups were significantly lower than the control (P < .05 and P < .01, respectively). The FA values from Co-M group were significantly lower than the SM group (P < .01). The apparent diffusion coefficient values of the above regions had no significant differences among these groups (P > .05). There were negative correlations between FA value of genu of the CC and disease course as well as FA value of genu and body of the CC and headache frequency (P < .05). Negative correlations were also found between FA values at all locations of the CC and Hamilton anxiety [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1195", "doc_id": "24148722", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: 90% of sudden infant death syndrome (SIDS) deaths happen in newborns aged less than 6 months.\n\nCANDIDATE_PASSAGE:\nEIF2AK3, encoding translation initiation factor 2-α kinase 3, is mutated in patients with Wolcott-Rallison syndrome Wolcott-Rallison syndrome (WRS) is a rare, autosomal recessive disorder characterized by permanent neonatal or early infancy insulin-dependent diabetes. Epiphyseal dysplasia, osteoporosis and growth retardation occur at a later age. Other frequent multisystemic manifestations include hepatic and renal dysfunction, mental retardation and cardiovascular abnormalities. On the basis of two consanguineous families, we mapped WRS to a region of less than 3 cM on chromosome 2p12, with maximal evidence of linkage and homozygosity at 4 microsatellite markers within an interval of approximately 1 cM. The gene encoding the eukaryotic translation initiation factor 2-α kinase 3 (EIF2AK3) resides in this interval; thus we explored it as a candidate. We identified distinct mutations of EIF2AK3 that segregated with the disorder in each of the families. The first mutation produces a truncated protein in which the entire catalytic domain is missing. The other changes an amino acid, located in the catalytic domain of the protein, that is highly conserved among kinases from the same subfamily. Our results provide evidence for the role of EIF2AK3 in WRS. The identification of this gene may provide insight into the understanding of the more common forms of diabetes and other pathologic manifestations of WRS.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "25", "doc_id": "24521894", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Women with a higher birth weight are more likely to develop breast cancer later in life.\n\nCANDIDATE_PASSAGE:\nMagnesium sulphate for women at risk of preterm birth for neuroprotection of the fetus. BACKGROUND Epidemiological and basic science evidence suggests that magnesium sulphate before birth may be neuroprotective for the fetus. OBJECTIVES To assess the effects of magnesium sulphate as a neuroprotective agent when given to women considered at risk of preterm birth. SEARCH STRATEGY We searched the Cochrane Pregnancy and Childbirth Group's Trials Register (31 August 2008). SELECTION CRITERIA Randomised controlled trials of antenatal magnesium sulphate therapy in women threatening or likely to give birth at less than 37 weeks' gestational age. For one subgroup analysis, studies were broadly categorised by the primary intent of the study into \"neuroprotective intent\", or \"other intent (maternal neuroprotective - pre-eclampsia)\", or \"other intent (tocolytic)\". DATA COLLECTION AND ANALYSIS At least two authors assessed trial eligibility and quality, and extracted data. MAIN RESULTS Five trials (6145 babies) were eligible for this review. Antenatal magnesium sulphate therapy given to women at risk of preterm birth substantially reduced the risk of cerebral palsy in their child (Relative Risk (RR) 0.68; 95% Confidence interval (CI) 0.54 to 0.87; five trials; 6145 infants). There was also a significant reduction in the rate of substantial gross motor dysfunction (RR 0.61; 95% CI 0.44 to 0.85; four trials; 5980 infants). No statistically significant effect of antenatal magnesium sulphate therapy was detected on paediatric mortality (RR 1.04; 95% CI 0.92 to 1.17; five trials; 6145 infants), or on other neurological impairments or disabilities in the first few years of life. Overall there were no significant effects of antenatal magnesium therapy on combined rates of morta [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1379", "doc_id": "27129115", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: MICAL redox enzymes regulate actin dynamics in many cell types.\n\nCANDIDATE_ABSTRACT:\nTITLE: Drosophila MICAL regulates myofilament organization and synaptic structure\nABSTRACT: The overall size and structure of a synaptic terminal is an important determinant of its function. In a large-scale mutagenesis screen, designed to identify Drosophila mutants with abnormally structured neuromuscular junctions (NMJs), we discovered mutations in Drosophila mical, a conserved gene encoding a multi-domain protein with a N-terminal monooxygenase domain. In mical mutants, synaptic boutons do not sprout normally over the muscle surface and tend to form clusters along synaptic branches and at nerve entry sites. Consistent with high expression of MICAL in somatic muscles, immunohistochemical stainings reveal that the subcellular localization and architecture of contractile muscle filaments are dramatically disturbed in mical mutants. Instead of being integrated into a regular sarcomeric pattern, actin and myosin filaments are disorganized and accumulate beneath the plasmamembrane. Whereas contractile elements are strongly deranged, the proposed organizer of sarcomeric structure, D-Titin, is much less affected. Transgenic expression of interfering RNA molecules demonstrates that MICAL is required in muscles for the higher order arrangement of myofilaments. Ultrastructural analysis confirms that myosin-rich thick filaments enter submembranous regions and interfere with synaptic development, indicating that the disorganized myofilaments may cause the synaptic growth phenotype. As a model, we suggest that the filamentous network around synaptic boutons restrains the spreading of synaptic branches.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Instead of being integrated into a regular sarcomeric pattern, actin and myosin filaments are disorganized and accumulate beneath the plasmamembrane.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 737, "doc_id": "16562534", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: FACT and other histone chaperone(s) compensate for Histone 2A (H2A)-histone 2B (H2B) dimer eviction during the histone exchange process.\n\nCANDIDATE_PASSAGE:\nHistone Methylation-Dependent Mechanisms Impose Ligand Dependency for Gene Activation by Nuclear Receptors Nuclear receptors undergo ligand-dependent conformational changes that are required for corepressor-coactivator exchange, but whether there is an actual requirement for specific epigenetic landmarks to impose ligand dependency for gene activation remains unknown. Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases (HMTs) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals. This strategy, based at least in part on an HMT-dependent inhibitory histone code, imposes a requirement for specific histone demethylases, including LSD1, to permit ligand- and signal-dependent activation of regulated gene expression. These events link an inhibitory methylation component of the histone code to a broadly used strategy that circumvents pathological constitutive gene induction by physiologically regulated transcription factors.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "407", "doc_id": "13639330", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Inhibiting focal adhesion formation enables cells to convert mechanical strain into eventual scarring.\n\nCANDIDATE_ABSTRACT:\nTITLE: Focal adhesion kinase links mechanical force to skin fibrosis via inflammatory signaling\nABSTRACT: Exuberant fibroproliferation is a common complication after injury for reasons that are not well understood. One key component of wound repair that is often overlooked is mechanical force, which regulates cell-matrix interactions through intracellular focal adhesion components, including focal adhesion kinase (FAK). Here we report that FAK is activated after cutaneous injury and that this process is potentiated by mechanical loading. Fibroblast-specific FAK knockout mice have substantially less inflammation and fibrosis than control mice in a model of hypertrophic scar formation. We show that FAK acts through extracellular-related kinase (ERK) to mechanically trigger the secretion of monocyte chemoattractant protein-1 (MCP-1, also known as CCL2), a potent chemokine that is linked to human fibrotic disorders. Similarly, MCP-1 knockout mice form minimal scars, indicating that inflammatory chemokine pathways are a major mechanism by which FAK mechanotransduction induces fibrosis. Small-molecule inhibition of FAK blocks these effects in human cells and reduces scar formation in vivo through attenuated MCP-1 signaling and inflammatory cell recruitment. These findings collectively indicate that physical force regulates fibrosis through inflammatory FAK–ERK–MCP-1 pathways and that molecular strategies targeting FAK can effectively uncouple mechanical force from pathologic scar formation.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Small-molecule inhibition of FAK blocks these effects in human cells and reduces scar formation in vivo through attenuated MCP-1 signaling and inflammatory cell recruitment.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 632, "doc_id": "5172048", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: RUNX is not expressed in skin tissue.\n\nCANDIDATE_PASSAGE:\nThe Bone and Joint Decade 2000-2010. The World Health Organisation has declared the period 2000 to 2010 the Bone and Joint Decade. This is indeed timely and appropriate. Hundreds of millions of people in the world today are beset with a host of disabilities caused by trauma, ageing and degeneration and other affections of the musculo-skeletal system. With the state of art of orthopaedic surgery and rheumatology, sufferers of bone and joint disabilities have benefited a great deal from advances in pharmacology, newer techniques of imaging, surgery and man-made materials to replace diseased or damaged bone and cartilage. However, man-made materials, being non-living, are subject to wear and tear and loosening in the host bone. As we advance into the Bone and Joint Decade, further improvement in the treatment of bone and joint diseases lies in more basic cartilage and bone research. The Human Genome Project has provided us with a better understanding of disease genes and the possibility of gene manipulation to prevent and treat specific diseases. Cartilage cells culture and transplant are already a reality. Tissue engineering, i.e. growing cells in three-dimensional substrates of collagen or synthetic biodegradable polymers, started in the 1980s, will in future be used to replace damaged bone and cartilage parts with living and bone and cartilaginous tissues, respectively. The first steps have been taken; more research needs to be done. And it is not unreasonable to expect a significant breakthrough in the treatment of bone and joint diseases at the end of this decade. Ann Acad Med Singapore 2002; 31:621-2", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1008", "doc_id": "58050905", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Upregulation of PD1 causes the upregulation of Satb1.\n\nCANDIDATE_ABSTRACT:\nTITLE: SATB1 Expression Governs Epigenetic Repression of PD‐1 in Tumor‐Reactive T Cells\nABSTRACT: &NA; Despite the importance of programmed cell death‐1 (PD‐1) in inhibiting T cell effector activity, the mechanisms regulating its expression remain poorly defined. We found that the chromatin organizer special AT‐rich sequence‐binding protein‐1 (Satb1) restrains PD‐1 expression induced upon T cell activation by recruiting a nucleosome remodeling deacetylase (NuRD) complex to Pdcd1 regulatory regions. Satb1 deficienct T cells exhibited a 40‐fold increase in PD‐1 expression. Tumor‐derived transforming growth factor &bgr; (Tgf‐&bgr;) decreased Satb1 expression through binding of Smad proteins to the Satb1 promoter. Smad proteins also competed with the Satb1‐NuRD complex for binding to Pdcd1 enhancers, releasing Pdcd1 expression from Satb1‐mediated repression, Satb1‐deficient tumor‐reactive T cells lost effector activity more rapidly than wild‐type lymphocytes at tumor beds expressing PD‐1 ligand (CD274), and these differences were abrogated by sustained CD274 blockade. Our findings suggest that Satb1 functions to prevent premature T cell exhaustion by regulating Pdcd1 expression upon T cell activation. Dysregulation of this pathway in tumor‐infiltrating T cells results in diminished anti‐tumor immunity. Graphical Abstract Figure. No caption available. HighlightsT cell activation increased the expression of Satb1 in mature CD8+ and CD4+ T cellsRecruitment of the NuRD repression complex by Satb1 inhibits expression of Pdcd1In tumors, TGF‐&bgr; inhibits Satb1 expression in T cells, increasing Pdcd1 expressionSatb1−/− T cells express high amounts of PD‐1 and have decreased anti‐tumor activity &NA; Stephen et al. show that the chromatin organizer Satb1 controls expression levels of PD‐1 upon T cell activation through the recruitment of a de‐acetylase complex to re [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1350, "doc_id": "5377642", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Increased lipolysis leads to higher P38 phosphorylation in adipose tissue.\n\nCANDIDATE_PASSAGE:\nMurine embryonic stem cell differentiation is promoted by SOCS-3 and inhibited by the zinc finger transcription factor Klf4. Embryonic stem (ES) cells homozygous for a Shp-2 mutation (Shp-2(Delta46-110)) demonstrate leukemia inhibitory factor (LIF) hypersensitivity and increased LIF-stimulated phosphorylation of signal transducer and activator of transcription (STAT3). We hypothesized that LIF-responsive genes in Shp-2(Delta46-110) cells would represent potential candidates for molecules vital for ES cell self-renewal. Using microarray analysis, we detected 41 genes whose expression was modified by LIF in Shp-2(Delta46-110) ES cells. Induction of 2 significantly up-regulated genes, suppressor of cytokine signaling-3 (SOCS-3) and Kruppel-like factor 4 (Klf4), was verified using Northern blotting. ES cells overexpressing SOCS-3 had an increased capacity to differentiate to hematopoietic progenitors, rather than to self-renew. In contrast, ES cells overexpressing Klf4 had a greater capacity to self-renew based on secondary embryoid body (EB) formation. Klf4-transduced d6 EBs expressed higher levels of Oct-4, consistent with the notion that Klf4 promotes ES cell self-renewal. These findings verify the negative role of SOCS-3 on LIF signaling and provide a novel role for Klf4 in ES cell function.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "611", "doc_id": "18489989", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The availability of safe places to study is not effective at decreasing homelessness.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mental health problems of homeless children and families: longitudinal study.\nABSTRACT: OBJECTIVE To establish the mental health needs of homeless children and families before and after rehousing. DESIGN Cross sectional, longitudinal study. SETTING City of Birmingham. SUBJECTS 58 rehoused families with 103 children aged 2-16 years and 21 comparison families of low socioeconomic status in stable housing, with 54 children. MAIN OUTCOME MEASURES Children's mental health problems and level of communication; mothers' mental health problems and social support one year after rehousing. RESULTS Mental health problems remained significantly higher in rehoused mothers and their children than in the comparison group (mothers 26% v 5%, P = 0.04; children 39% v 11%, P = 0.0003). Homeless mothers continued to have significantly less social support at follow up. Mothers with a history of abuse and poor social integration were more likely to have children with persistent mental health problems. CONCLUSIONS Homeless families have a high level of complex needs that cannot be met by conventional health services and arrangements. Local strategies for rapid rehousing into permanent accommodation, effective social support and health care for parents and children, and protection from violence and intimidation should be developed and implemented.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1197, "doc_id": "25649714", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Artefacts in 24-h pharyngeal and oesophageal pH monitoring: is simplification of pH data analysis feasible?\n\nABSTRACT:\nAmbulatory 24-h dual-channel pharyngeal and oesophageal pH monitoring is the standard test for measuring gastro-oesophageal and gastropharyngeal reflux. Artefacts caused by the intake of food may result in falsely positive gastropharyngeal reflux, which necessitates a manual review of 24-h pH data. The purpose of the study was to investigate the influence of meals and whether leaving out meals affected the reliability of the test. Patients referred for otolaryngological complaints, suspected to have been caused by gastro-oesophageal reflux, underwent 24-h dual-channel pH monitoring. The raw unprocessed pH data were corrected by visual inspection of the 24-h tracings (corrected data), by leaving out meals or meals plus a 2-h postprandrial period. The raw pH data were substantially influenced by artefacts of food intake and pseudoreflux. Data obtained by leaving out meals agreed best with manually corrected data. Many of the falsely positive reflux episodes could be removed, thereby inducing a 9%-18% chance of undetected reflux. When examining the fraction of time supine, manually corrected data and data leaving out meals were fully concordant and detected 79% of patients with gastropharyngeal reflux. However, leaving out meals plus a 2-h postprandrial period resulted in 21%-50% falsely negative tests.", "output": "{\"label\": \"maybe\", \"rationale\": \"Leaving out the period of intake of meals and beverages from the raw pH data might be the second best test after the time-consuming visual correction with a small chance of undetected gastropharyngeal reflux. For scientific purposes and when in doubt, it remains necessary to review the computer-generated data manually to discover every gastropharyngeal reflux event.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 14992556, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Risedronate increases risk of vertebral and non-vertebral fractures.\n\nCANDIDATE_PASSAGE:\nCatch and release: how do kinetochores hook the right microtubules during mitosis? Sport fishermen keep tension on their lines to prevent hooked fish from releasing. A molecular version of this angler's trick, operating at kinetochores, ensures accuracy during mitosis: the mitotic spindle attaches randomly to chromosomes and then correctly bioriented attachments are stabilized due to the tension exerted on them by opposing microtubules. Incorrect attachments, which lack tension, are unstable and release quickly, allowing another chance for biorientation. Stabilization of molecular interactions by tension also occurs in other physiological contexts, such as cell adhesion, motility, hemostasis, and tissue morphogenesis. Here, we review models for the stabilization of kinetochore attachments with an eye toward emerging models for other force-activated systems. Although attention in the mitosis field has focused mainly on one kinase-based mechanism, multiple mechanisms may act together to stabilize properly bioriented kinetochores and some principles governing other tension-sensitive systems may also apply to kinetochores.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1050", "doc_id": "17805221", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Pyridostatin decreases telomere fragility in BRCA2-deficient cells.\n\nCANDIDATE_PASSAGE:\nThe BLM helicase contributes to telomere maintenance through processing of late-replicating intermediate structures Werner's syndrome (WS) and Bloom's syndrome (BS) are cancer predisposition disorders caused by loss of function of the RecQ helicases WRN or BLM, respectively. BS and WS are characterized by replication defects, hyperrecombination events and chromosomal aberrations, which are hallmarks of cancer. Inefficient replication of the G-rich telomeric strand contributes to chromosome aberrations in WS cells, demonstrating a link between WRN, telomeres and genomic stability. Herein, we provide evidence that BLM also contributes to chromosome-end maintenance. Telomere defects (TDs) are observed in BLM-deficient cells at an elevated frequency, which is similar to cells lacking a functional WRN helicase. Loss of both helicases exacerbates TDs and chromosome aberrations, indicating that BLM and WRN function independently in telomere maintenance. BLM localization, particularly its recruitment to telomeres, changes in response to replication dysfunction, such as in WRN-deficient cells or after aphidicolin treatment. Exposure to replication challenge causes an increase in decatenated deoxyribonucleic acid (DNA) structures and late-replicating intermediates (LRIs), which are visible as BLM-covered ultra-fine bridges (UFBs) in anaphase. A subset of UFBs originates from telomeric DNA and their frequency correlates with telomere replication defects. We propose that the BLM complex contributes to telomere maintenance through its activity in resolving LRIs.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "990", "doc_id": "2679511", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does perspective-taking increase patient satisfaction in medical encounters?\n\nABSTRACT:\nTo assess whether perspective-taking, which researchers in other fields have shown to induce empathy, improves patient satisfaction in encounters between student-clinicians and standardized patients (SPs). In three studies, randomly assigned students (N = 608) received either a perspective-taking instruction or a neutral instruction prior to a clinical skills examination in 2006-2007. SP satisfaction was the main outcome in all three studies. Study 1 involved 245 third-year medical students from two universities. Studies 2 and 3 extended Study 1 to examine generalizability across student and SP subpopulations. Study 2 (105 physician assistant students, one university) explored the effect of perspective-taking on African American SPs' satisfaction. Study 3 (258 third-year medical students, two universities) examined the intervention's effect on students with high and low baseline perspective-taking tendencies. Intervention students outscored controls in patient satisfaction in all studies: Study 1: P = .01, standardized effect size = 0.16; Study 2: P = .001, standardized effect size = 0.31; Study 3: P = .009, standardized effect size = 0.13. In Study 2, perspective-taking improved African American SPs' satisfaction. In Study 3, intervention students with high baseline perspective-taking tendencies outscored controls (P = .0004, standardized effect size = 0.25), whereas those with low perspective-taking tendencies did not (P = .72, standardized effect size = 0.00).", "output": "{\"label\": \"maybe\", \"rationale\": \"Perspective-taking increased patient satisfaction in all three studies, across medical schools, clinical disciplines, and racially diverse students and SPs. Perspective-taking as a means for improving patient satisfaction deserves further exploration in clinical training and practice.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 20736672, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: LSD1-positive promoters are associated with RNA polymerase II\n\nCANDIDATE_PASSAGE:\nHistone Methylation-Dependent Mechanisms Impose Ligand Dependency for Gene Activation by Nuclear Receptors Nuclear receptors undergo ligand-dependent conformational changes that are required for corepressor-coactivator exchange, but whether there is an actual requirement for specific epigenetic landmarks to impose ligand dependency for gene activation remains unknown. Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases (HMTs) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals. This strategy, based at least in part on an HMT-dependent inhibitory histone code, imposes a requirement for specific histone demethylases, including LSD1, to permit ligand- and signal-dependent activation of regulated gene expression. These events link an inhibitory methylation component of the histone code to a broadly used strategy that circumvents pathological constitutive gene induction by physiologically regulated transcription factors.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "679", "doc_id": "13639330", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Converting apoE4 to apoE3 by gene editing prevents the pathology associated with apoE4 in human iPSCderived neurons.\n\nCANDIDATE_PASSAGE:\nAmyloid accumulation is a late event in sporadic Alzheimer's disease-like pathology in nontransgenic rats The amyloid cascade hypothesis posits that deposition of the amyloid β (Aβ) peptide in the brain is a key event in the initiation of Alzheimer's disease (AD). Nonetheless, it now seems increasingly unlikely that amyloid toxicity is the cause of sporadic AD, which leads to cognitive decline. Here, using accelerated-senescence nontransgenic OXYS rats, we confirmed that aggregation of Aβ is a later event in AD-like pathology. We showed that an age-dependent increase in the levels of Aβ₁₋₄₂ and extracellular Aβ deposits in the brain of OXYS rats occur later than do synaptic losses, neuronal cell death, mitochondrial structural abnormalities, and hyperphosphorylation of the tau protein. We identified the variants of the genes that are strongly associated with the risk of either late-onset or early-onset AD, including App, Apoe4, Bace1, Psen1, Psen2, and Picalm. We found that in OXYS rats nonsynonymous SNPs were located only in the genes Casp3 and Sorl1. Thus, we present proof that OXYS rats may be a model of sporadic AD. It is possible that multiple age-associated pathological processes may precede the toxic amyloid accumulation, which in turn triggers the final stage of the sporadic form of AD and becomes a hallmark event of the disease.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "286", "doc_id": "15347087", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: H4 G94P proteins induce degradation of free histones via Rad53-dependent mechanisms.\n\nCANDIDATE_PASSAGE:\nIncreased lipid peroxidation as a mechanism of methionine-induced atherosclerosis in rabbits. Methionine is converted by the transmethylation/transsulfuration pathway to homocysteine which may exert atherogenic effects by several mechanisms, including lipid peroxidation. Therefore, the excessive dietary methionine may induce the development of atherosclerosis. To test this hypothesis, plasma and aortic thiobarbituric acid reactive substances (TBARS), as well as activities of aortic and erythrocyte superoxide dismutase (SOD), catalase and selenium-dependent glutathione peroxidase (GPX) were measured in rabbits fed a diet enriched with 0.3% methionine for 6 or 9 months. Histological examinations of aortas also were performed. Feeding rabbits a methionine-enriched diet for 6 or 9 months resulted in significant increases in plasma and aortic TBARS levels and aortic antioxidant enzyme activities. However, a decrease in plasma antioxidant activity (AOA) was observed. In erythrocytes, SOD activity increased, catalase remained normal and GPX decreased in the treated animals. Histological examination of aortas showed typical atherosclerotic changes, such as intimal thickening, deposition of cholesterol, and calcification in methionine-fed rabbits. These results confirm that high-methionine diet may induce atherosclerosis in rabbits and indicate disturbances in lipid peroxidation and antioxidant processes as possible mechanisms of its atherogenic influence.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "485", "doc_id": "36654066", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does shaving the incision site increase the infection rate after spinal surgery?\n\nABSTRACT:\nA prospective randomized clinical study. To determine whether shaving the incision site before spinal surgery causes postsurgical infection. Spine surgeons usually shave the skin of the incision site immediately before surgery is performed. However, evidence from some surgical series suggests that presurgical shaving may increase the postsurgical infection rate. To our knowledge, no previously published studies have addressed this issue. A total of 789 patients scheduled to undergo spinal surgery were randomly allocated into 2 groups: those in whom the site of operation was shaved immediately before surgery (shaved group; 371 patients) and the patients in whom presurgical shaving was not performed (unshaved group; 418 patients). The mean duration of anesthesia and the infection rates in both groups were recorded and compared. The duration of anesthesia did not differ in the 2 groups (P>0.05). A postoperative infection developed in 4 patients in the shaved group and in 1 patient in the nonshaved group (P<0.01).", "output": "{\"label\": \"maybe\", \"rationale\": \"The shaving of the incision site immediately before spinal surgery may increase the rate of postoperative infection.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 17621202, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Ca2+ cycling controls whole-body energy homeostasis in beige fat.\n\nCANDIDATE_PASSAGE:\nRelationship between activity levels, aerobic fitness, and body fat in 8- to 10-yr-old children. The relationships between children's activity, aerobic fitness, and fatness are unclear. Indirect estimates of activity, e.g., heart rate (HR) and recall, may mask any associations. The purpose of this study was to assess these relationships by using the Tritrac-R3D, a pedometer, and heart rate. Thirty-four children, ages 8-10 yr, participated in the study. The Tritrac and pedometer were worn for up to 6 days. HR was measured for 1 day. Activity measured by Tritrac or pedometer correlated positively to fitness in the whole group (Tritrac, r = 0.66; pedometer, r = 0.59; P < 0.01) and in boys and girls separately (P < 0.05) and correlated negatively to fatness in the whole group (r = -0.42, P < 0.05). In contrast, HR did not correlate significantly to fitness, and HR of >139 beats/min correlated positively to fatness in girls (r = 0.64, P < 0.05). This suggests that HR is misleading as a measure of activity. This study supports a positive relationship between activity and fitness and suggests a negative relationship between fatness and activity.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "220", "doc_id": "2575938", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The severity of cardiac involvement in amyloidosis can be described by the degree of transmurality of late gadolinium enhancement in MRI.\n\nCANDIDATE_ABSTRACT:\nTITLE: Prognostic Value of Late Gadolinium Enhancement Cardiovascular Magnetic Resonance in Cardiac Amyloidosis\nABSTRACT: BACKGROUND The prognosis and treatment of the 2 main types of cardiac amyloidosis, immunoglobulin light chain (AL) and transthyretin (ATTR) amyloidosis, are substantially influenced by cardiac involvement. Cardiovascular magnetic resonance with late gadolinium enhancement (LGE) is a reference standard for the diagnosis of cardiac amyloidosis, but its potential for stratifying risk is unknown. METHODS AND RESULTS Two hundred fifty prospectively recruited subjects, 122 patients with ATTR amyloid, 9 asymptomatic mutation carriers, and 119 patients with AL amyloidosis, underwent LGE cardiovascular magnetic resonance. Subjects were followed up for a mean of 24±13 months. LGE was performed with phase-sensitive inversion recovery (PSIR) and without (magnitude only). These were compared with extracellular volume measured with T1 mapping. PSIR was superior to magnitude-only inversion recovery LGE because PSIR always nulled the tissue (blood or myocardium) with the longest T1 (least gadolinium). LGE was classified into 3 patterns: none, subendocardial, and transmural, which were associated with increasing amyloid burden as defined by extracellular volume (P<0.0001), with transitions from none to subendocardial LGE at an extracellular volume of 0.40 to 0.43 (AL) and 0.39 to 0.40 (ATTR) and to transmural at 0.48 to 0.55 (AL) and 0.47 to 0.59 (ATTR). Sixty-seven patients (27%) died. Transmural LGE predicted death (hazard ratio, 5.4; 95% confidence interval, 2.1-13.7; P<0.0001) and remained independent after adjustment for N-terminal pro-brain natriuretic peptide, ejection fraction, stroke volume index, E/E', and left ventricular mass index (hazard ratio, 4.1; 95% confidence interval, 1.3-13.1; P<0.05). CONCLUSIONS There is a continuum of cardiac involvement in systemic A [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"LGE was classified into 3 patterns: none, subendocardial, and transmural, which were associated with increasing amyloid burden as defined by extracellular volume (P<0.0001), with transitions from none to subendocardial LGE at an extracellular volume of 0.40 to 0.43 (AL) and 0.39 to 0.40 (ATTR) and to transmural at 0.48 to 0.55 (AL) and 0.47 to 0.59 (ATTR).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1271, "doc_id": "13768432", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Type 1 Diabetes is associated with subtle perturbations in T reg development.\n\nCANDIDATE_ABSTRACT:\nTITLE: Large-scale genetic fine mapping and genotype-phenotype associations implicate polymorphism in the IL2RA region in type 1 diabetes\nABSTRACT: Genome-wide association studies are now identifying disease-associated chromosome regions. However, even after convincing replication, the localization of the causal variant(s) requires comprehensive resequencing, extensive genotyping and statistical analyses in large sample sets leading to targeted functional studies. Here, we have localized the type 1 diabetes (T1D) association in the interleukin 2 receptor alpha (IL2RA) gene region to two independent groups of SNPs, spanning overlapping regions of 14 and 40 kb, encompassing IL2RA intron 1 and the 5′ regions of IL2RA and RBM17 (odds ratio = 2.04, 95% confidence interval = 1.70–2.45; P = 1.92 × 10−28; control frequency = 0.635). Furthermore, we have associated IL2RA T1D susceptibility genotypes with lower circulating levels of the biomarker, soluble IL-2RA (P = 6.28 × 10−28), suggesting that an inherited lower immune responsiveness predisposes to T1D.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here, we have localized the type 1 diabetes (T1D) association in the interleukin 2 receptor alpha (IL2RA) gene region to two independent groups of SNPs, spanning overlapping regions of 14 and 40 kb, encompassing IL2RA intron 1 and the 5′ regions of IL2RA and RBM17 (odds ratio = 2.04, 95% confidence interval = 1.70–2.45; P = 1.92 × 10−28; control frequency = 0.635).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1334, "doc_id": "13940200", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The minor G allele of FOXO3 is related to less severe symptoms of Crohn's Disease.\n\nCANDIDATE_ABSTRACT:\nTITLE: Molecular Basis for Target RNA Recognition and Cleavage by Human RISC\nABSTRACT: The RNA-Induced Silencing Complex (RISC) is a ribonucleoprotein particle composed of a single-stranded short interfering RNA (siRNA) and an endonucleolytically active Argonaute protein, capable of cleaving mRNAs complementary to the siRNA. The mechanism by which RISC cleaves a target RNA is well understood, however it remains enigmatic how RISC finds its target RNA. Here, we show, both in vitro and in vivo, that the accessibility of the target site correlates directly with the efficiency of cleavage, demonstrating that RISC is unable to unfold structured RNA. In the course of target recognition, RISC transiently contacts single-stranded RNA nonspecifically and promotes siRNA-target RNA annealing. Furthermore, the 5' part of the siRNA within RISC creates a thermodynamic threshold that determines the stable association of RISC and the target RNA. We therefore provide mechanistic insights by revealing features of RISC and target RNAs that are crucial to achieve efficiency and specificity in RNA interference.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1231, "doc_id": "950306", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Hypothalamic glutamate neurotransmission is crucial to energy balance.\n\nCANDIDATE_PASSAGE:\nLactate Metabolism in Human Lung Tumors Cancer cells consume glucose and secrete lactate in culture. It is unknown whether lactate contributes to energy metabolism in living tumors. We previously reported that human non-small-cell lung cancers (NSCLCs) oxidize glucose in the tricarboxylic acid (TCA) cycle. Here, we show that lactate is also a TCA cycle carbon source for NSCLC. In human NSCLC, evidence of lactate utilization was most apparent in tumors with high 18fluorodeoxyglucose uptake and aggressive oncological behavior. Infusing human NSCLC patients with 13C-lactate revealed extensive labeling of TCA cycle metabolites. In mice, deleting monocarboxylate transporter-1 (MCT1) from tumor cells eliminated lactate-dependent metabolite labeling, confirming tumor-cell-autonomous lactate uptake. Strikingly, directly comparing lactate and glucose metabolism in vivo indicated that lactate's contribution to the TCA cycle predominates. The data indicate that tumors, including bona fide human NSCLC, can use lactate as a fuel in vivo.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "540", "doc_id": "36653415", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The DEXI promoter region is bound by multiple transcription factors in a murine haematopoietic progenitor cell line.\n\nCANDIDATE_PASSAGE:\nLoss of imprinting in colorectal cancer linked to hypomethylation of H19 and IGF2. Epigenetic alterations in human cancers include global DNA hypomethylation,gene hypomethylation and promoter hypermethylation, and loss of imprinting (LOI) of the insulin-like growth factor-II gene (IGF2). A mechanism for LOI described previously is hypermethylation of a differentially methylated region (DMR) upstream of the H19 gene, allowing activation of the normally silent maternal allele of IGF2. Here we show that this mechanism does not apply to colorectal cancers, which show hypomethylation of the H19 DMR as well as a DMR upstream of exon 3 of IGF2. This hypomethylation is found in both colorectal cancers and normal mucosa from the same patients, and in cell lines with somatic cell knockout of DNA methyltransferases DNMT1 and DNMT3B. These data suggest that hypomethylation is a mechanism for LOI, that the popular IGF2-H19 enhancer competition model for IGF2 imprinting does not apply to the human colon, and that an alternative model for LOI would involve a transcriptional repressor acting on the normally silent maternal allele of IGF2.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1161", "doc_id": "17775228", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Lysine histone demethylase inhibitor JIB 04 is inactive against KDM5A.\n\nCANDIDATE_PASSAGE:\nExosomes in Plasma of Patients with Ovarian Carcinoma: Potential Biomarkers of Tumor Progression and Response to Therapy. BACKGROUND In patients with Ovarian Cancer (OvCa) exosomes released by tumor cells are present in the plasma and could be involved in tumor progression. This study examines the association between the exosome presence/protein content in plasma of OvCa patients and disease outcome, response to standard therapy and/or tumorresistance to therapies in patients studied at diagnosis and also serially during and after therapy. DESIGN AND METHODS Exosomes were purified from OvCa patients' plasma (n=22), patients with benign tumors (n=10) or (n=10) healthy controls (NC) using ultracentrifugation. Exosomes were visualized by scanning electron microscopy. Their protein content was measured. The presence of MAGE 3/6 and TGF-β1 in exosomes was evaluated in Western blots. RESULTS The OvCa patients' plasma contained higher levels of exosomal proteins (p<0.05) compared to those isolated from plasma of patients with benign tumors or NC. Exosomes isolated from OvCa patients's plasma carried TGF-β1 and MAGE3/6, which distinguished OvCa patients from those with benign tumors and NC. High protein levels of exosomes were seen in newly diagnosed patients; however in advanced stages of OvCa patients the protein content of isolated exosomes was significantly higher than that of early stages. The exosome levels variably changed during/after chemotherapy, and correlations between the changes in exosomal protein levels and clinical data suggested that the protein content of exosomes might be useful in predicting responses to therapy and prognosis in OvCa patients. CONCLUSION Analysis of plasma exosomes levels offers a novel approach to diagnosis and monitoring respo [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "730", "doc_id": "9095943", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Vitamin D is an important factor in the relationship between calcium and parathyroid hormone.\n\nCANDIDATE_PASSAGE:\nRAS genes in Saccharomyces cerevisiae: signal transduction in search of a pathway. Ras proteins in budding yeasts initially appeared to regulate initiation of the cell cycle in response to nutrient availability. More recent work, while clarifying the mechanism of Ras-mediated signal transduction, has undermined our notion of the signal Ras transmits. We now suspect that Ras helps to coordinate cellular metabolism and mass accumulation, but what Ras responds to is not clear.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1371", "doc_id": "8210189", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nCANDIDATE_PASSAGE:\nRare and common variants: twenty arguments Genome-wide association studies have greatly improved our understanding of the genetic basis of disease risk. The fact that they tend not to identify more than a fraction of the specific causal loci has led to divergence of opinion over whether most of the variance is hidden as numerous rare variants of large effect or as common variants of very small effect. Here I review 20 arguments for and against each of these models of the genetic basis of complex traits and conclude that both classes of effect can be readily reconciled.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1004", "doc_id": "2739854", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: HNF4A mutations are associated with macrosomia in infancy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Macrosomia and Hyperinsulinaemic Hypoglycaemia in Patients with Heterozygous Mutations in the HNF4A Gene\nABSTRACT: Background Macrosomia is associated with considerable neonatal and maternal morbidity. Factors that predict macrosomia are poorly understood. The increased rate of macrosomia in the offspring of pregnant women with diabetes and in congenital hyperinsulinaemia is mediated by increased foetal insulin secretion. We assessed the in utero and neonatal role of two key regulators of pancreatic insulin secretion by studying birthweight and the incidence of neonatal hypoglycaemia in patients with heterozygous mutations in the maturity-onset diabetes of the young (MODY) genes HNF4A (encoding HNF-4α) and HNF1A/TCF1 (encoding HNF-1α), and the effect of pancreatic deletion of Hnf4a on foetal and neonatal insulin secretion in mice.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 490, "doc_id": "56893404", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Medications to treat obesity have unwanted side effects.\n\nCANDIDATE_ABSTRACT:\nTITLE: Long term pharmacotherapy for obesity and overweight: updated meta-analysis.\nABSTRACT: OBJECTIVE To summarise the long term efficacy of anti-obesity drugs in reducing weight and improving health status. DESIGN Updated meta-analysis of randomised trials. DATA SOURCES Medline, Embase, the Cochrane controlled trials register, the Current Science meta-register of controlled trials, and reference lists of identified articles. All data sources were searched from December 2002 (end date of last search) to December 2006. STUDIES REVIEWED Double blind randomised placebo controlled trials of approved anti-obesity drugs used in adults (age over 18) for one year or longer. RESULTS 30 trials of one to four years' duration met the inclusion criteria: 16 orlistat (n=10 631 participants), 10 sibutramine (n=2623), and four rimonabant (n=6365). Of these, 14 trials were new and 16 had previously been identified. Attrition rates averaged 30-40%. Compared with placebo, orlistat reduced weight by 2.9 kg (95% confidence interval 2.5 kg to 3.2 kg), sibutramine by 4.2 kg (3.6 kg to 4.7 kg), and rimonabant by 4.7 kg (4.1 kg to 5.3 kg). Patients receiving active drug treatment were significantly more likely to achieve 5% and 10% weight loss thresholds. Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein. Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorde [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorders.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 766, "doc_id": "7552215", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: During the primary early antibody response activated B cells migrate toward the inner-and outer follicular areas where oxysterol accumulation is generated by stromal cells.\n\nCANDIDATE_PASSAGE:\nOverexpression of the circadian clock gene Bmal1 increases sensitivity to oxaliplatin in colorectal cancer. PURPOSE The circadian clock gene Bmal1 is involved in cancer cell proliferation and DNA damage sensitivity. The aim of this study was to explore the effect of Bmal1 on oxaliplatin sensitivity and to determine its clinical significance in colorectal cancer. EXPERIMENTAL DESIGN Three colorectal cancer cell lines, HCT116, THC8307 and HT29, were used. The Bmal1-mediated control of colorectal cancer cell proliferation was tested in vitro and in vivo. MTT and colony formation assays were performed to determine the sensitivity of colorectal cancer cells to oxaliplatin. Flow cytometry was used to examine changes in the cell-cycle distribution and apoptosis rate. Proteins expressed downstream of Bmal1 upon its overexpression were determined by Western blotting. Immunohistochemistry was used to analyze Bmal1 expression in 82 archived colorectal cancer tumors from patients treated with oxaliplatin-based regimens. RESULTS Bmal1 overexpression inhibited colorectal cancer cell proliferation and increased colorectal cancer sensitivity to oxaliplatin in three colorectal cancer cell lines and HCT116 cells model in vivo. Furthermore, the overall survival of patients with colorectal cancer with high Bmal1 levels in their primary tumors was significantly longer than that of patients with low Bmal1 levels (27 vs. 19 months; P = 0.043). The progression-free survival of patients with high Bmal1 expression was also significantly longer than that of patients with low Bmal1 expression (11 vs. 5 months; P = 0.015). Mechanistically, the effect of Bmal1 was associated with its ability to regulate G2-M arrest by activating the ATM pathway. CONCLUSION Bmal1 shows the potential as a [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "361", "doc_id": "7165938", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: General exercise therapy is more effective than rotator cuff exercises in reducing pain and improving function of the shoulder.\n\nCANDIDATE_PASSAGE:\nEffect of specific exercise strategy on need for surgery in patients with subacromial impingement syndrome: randomised controlled study OBJECTIVE To evaluate if a specific exercise strategy, targeting the rotator cuff and scapula stabilisers, improves shoulder function and pain more than unspecific exercises in patients with subacromial impingement syndrome, thereby decreasing the need for arthroscopic subacromial decompression. DESIGN Randomised, participant and single assessor blinded, controlled study. SETTING Department of orthopaedics in a Swedish university hospital. PARTICIPANTS 102 patients with long standing (over six months) persistent subacromial impingement syndrome in whom earlier conservative treatment had failed, recruited through orthopaedic specialists. INTERVENTIONS The specific exercise strategy consisted of strengthening eccentric exercises for the rotator cuff and concentric/eccentric exercises for the scapula stabilisers in combination with manual mobilisation. The control exercise programme consisted of unspecific movement exercises for the neck and shoulder. Patients in both groups received five to six individual guided treatment sessions during 12 weeks. In between these supervised sessions the participants performed home exercises once or twice a day for 12 weeks. MAIN OUTCOME MEASURES The primary outcome was the Constant-Murley shoulder assessment score evaluating shoulder function and pain. Secondary outcomes were patients' global impression of change because of treatment and decision regarding surgery. RESULTS Most (97, 95%) participants completed the 12 week study. There was a significantly greater improvement in the Constant-Murley score in the specific exercise group than in the control exercise group (24 points (95% confidenc [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "453", "doc_id": "4200695", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Synaptic activity enhances local release of brain derived neurotrophic factor from postsynaptic dendrites.\n\nCANDIDATE_ABSTRACT:\nTITLE: BC1 RNA, the transcript from a master gene for ID element amplification, is able to prime its own reverse transcription.\nABSTRACT: ID elements are short interspersed elements (SINEs) found in high copy number in many rodent genomes. BC1 RNA, an ID-related transcript, is derived from the single copy BC1 RNA gene. The BC1 RNA gene has been shown to be a master gene for ID element amplification in rodent genomes. ID elements are dispersed through a process termed retroposition. The retroposition process involves a number of potential regulatory steps. These regulatory steps may include transcription in the appropriate tissue, transcript stability, priming of the RNA transcript for reverse transcription and integration. This study focuses on priming of the RNA transcript for reverse transcription. BC1 RNA gene transcripts are shown to be able to prime their own reverse transcription in an efficient intramolecular and site-specific fashion. This self-priming ability is a consequence of the secondary structure of the 3'-unique region. The observation that a gene actively amplified throughout rodent evolution makes a RNA capable of efficient self-primed reverse transcription strongly suggests that self-priming is at least one feature establishing the BC1 RNA gene as a master gene for amplification of ID elements.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1121, "doc_id": "7912", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In S. cerevisiae, the absence of RNA surveillance pathways reduces sensitivity to high iron conditions.\n\nCANDIDATE_ABSTRACT:\nTITLE: Empirical Bayesian models for analysing molecular serotyping microarrays\nABSTRACT: BACKGROUND Microarrays offer great potential as a platform for molecular diagnostics, testing clinical samples for the presence of numerous biomarkers in highly multiplexed assays. In this study applied to infectious diseases, data from a microarray designed for molecular serotyping of Streptococcus pneumoniae was used, identifying the presence of any one of 91 known pneumococcal serotypes from DNA extracts. This microarray incorporated oligonucleotide probes for all known capsular polysaccharide synthesis genes and required a statistical analysis of the microarray intensity data to determine which serotype, or combination of serotypes, were present within a sample based on the combination of genes detected. RESULTS We propose an empirical Bayesian model for calculating the probabilities of combinations of serotypes from the microarray data. The model takes into consideration the dependencies between serotypes, induced by genes they have in common, and by homologous genes which, although not identical, are similar to each other in sequence. For serotypes which are very similar in capsular gene composition, extra probes are included on the microarray, providing additional information which is integrated into the Bayesian model. For each serotype combination with high probability, a second model, a Bayesian random effects model is applied to determine the relative abundance of each serotype. CONCLUSIONS To assess the accuracy of the proposed analysis we applied our methods to experimental data from samples containing individual serotypes and samples containing combinations of serotypes with known levels of abundance. All but two of the known serotypes of S. pneumoniae that were tested as individual samples could be uniquely determined by the Bayesian model. Th [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 566, "doc_id": "54440", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Rising temperatures caused by global warming lowers the risk of dengue fever transmission.\n\nCANDIDATE_PASSAGE:\nHigh spatial resolution mapping of malaria transmission risk in the Gambia, west Africa, using LANDSAT TM satellite imagery. Understanding local variability in malaria transmission risk is critically important when designing intervention or vaccine trials. Using a combination of field data, satellite image analysis, and GIS modeling, we developed a high-resolution map of malaria entomological inoculation rates (EIR) in The Gambia, West Africa. The analyses are based on the variation in exposure to malaria parasites experienced in 48 villages in 1996 and 21 villages in 1997. The entomological inoculation rate (EIR) varied from 0 to 166 infective bites per person per rainy season. Detailed field surveys identified the major Anopheles gambiae s.l. breeding habitats. These habitats were mapped by classification of a LANDSAT TM satellite image with an overall accuracy of 85%. Village EIRs decreased as a power function based on the breeding areas size and proximity. We use this relationship and the breeding habitats to map the variation in EIR over the entire 2500-km(2) study area.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1053", "doc_id": "20931483", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: T regulatory cells (tTregs) lacking αvβ8 are more adept at suppressing pathogenic T-cell responses during active inflammation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Integrin αvβ8-Mediated TGF-β Activation by Effector Regulatory T Cells Is Essential for Suppression of T-Cell-Mediated Inflammation\nABSTRACT: Regulatory T (Treg) cells play a pivotal role in suppressing self-harmful T cell responses, but how Treg cells mediate suppression to maintain immune homeostasis and limit responses during inflammation is unclear. Here we show that effector Treg cells express high amounts of the integrin αvβ8, which enables them to activate latent transforming growth factor-β (TGF-β). Treg-cell-specific deletion of integrin αvβ8 did not result in a spontaneous inflammatory phenotype, suggesting that this pathway is not important in Treg-cell-mediated maintenance of immune homeostasis. However, Treg cells lacking expression of integrin αvβ8 were unable to suppress pathogenic T cell responses during active inflammation. Thus, our results identify a mechanism by which Treg cells suppress exuberant immune responses, highlighting a key role for effector Treg-cell-mediated activation of latent TGF-β in suppression of self-harmful T cell responses during active inflammation.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"However, Treg cells lacking expression of integrin αvβ8 were unable to suppress pathogenic T cell responses during active inflammation.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1130, "doc_id": "17997584", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Macropinocytosis contributes to a cell's supply of amino acids via the intracellular uptake of protein.\n\nCANDIDATE_PASSAGE:\nA direct role for IFN-gamma in regulation of Th1 cell development. IL-12 has been identified as a major cytokine influencing the differentiation of CD4 cells to a Th1 phenotype, whereas a role for IFN-gamma is controversial. We investigated the interrelationship between IL-12 and IFN-gamma in promoting Th1 responses using naive CD4 cells reactive with pigeon cytochrome c from TCR transgenics and memory CD4 cells derived by in vivo priming with KLH. Without exogenous rIL-12 or rIFN-gamma, primary and memory effectors induced by Ag or anti-CD3 and anti-CD28 secreted variable levels of IL-2 and IFN-gamma. The level of IFN-gamma secreted by effectors correlated with endogenous IFN-gamma produced in primary cultures, and anti-IFN-gamma largely inhibited the development of effectors producing IFN-gamma. With optimal TCR stimulation and costimulation, endogenous IFN-gamma, without IL-12, was sufficient to elicit Th1 cells via an autocrine mechanism, whereas with suboptimal stimulation, exogenous rIFN-gamma or rIL-12 was required for Th1 development. However, rIL-12 was more effective than rIFN-gamma, partially because rIL-12 greatly enhanced autocrine production of IFN-gamma, and optimal development of the Th1 phenotype was mediated by the synergistic actions of both cytokines. Thus, both IFN-gamma and IL-12 can independently regulate Th1 development, but because of IFN-gamma-mediated feedback, their relative contributions are determined by the conditions of T cell stimulation. The extent of differentiation to a Th1 phenotype may, therefore, depend on the availability of both APC-derived IL-12 and autocrine IFN-gamma consequent to the overall strength of T cell stimulation.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "744", "doc_id": "39539647", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: VgrG (Tssl) protein punctures membranes by forming a spike at the tip of the tube apparatus.\n\nCANDIDATE_ABSTRACT:\nTITLE: Statin prophylaxis and inflammatory mediators following cardiopulmonary bypass: a systematic review\nABSTRACT: INTRODUCTION Induction of an inflammatory response is thought to have a significant role in the complications that follow cardiopulmonary bypass (CPB). The statin drugs are increasingly being recognized as having potent anti-inflammatory effects and hence have potential to influence an important mechanism of injury in CPB, although there is no current confirmation that this is indeed the case. Our objective was to systematically review if pre-operative prophylactic statin therapy, compared with placebo or standard of care, can decrease the inflammatory response in people undergoing heart surgery with CPB. METHODS We performed a systematic and comprehensive literature search for all randomized controlled trials (RCTs) of open heart surgery with CPB in adults or children who received prophylactic statin treatment prior to CPB, with reported outcomes which included markers of inflammation. Two authors independently identified eligible studies, extracted data, and assessed study quality using standardized instruments. Weighted mean difference (WMD) was the primary summary statistic with data pooled using a random effects model. Descriptive analysis was used when data could not be pooled. RESULTS Eight RCTs were included in the review, with the number of trials for each inflammatory outcome being even more limited. Pooled data demonstrated benefit with the use of statin to attenuate the post-CPB increase in interleukins 6 and 8 (IL-6, IL-8), peak high sensitivity C-reactive protein (hsCRP), and tumor necrosis factor-alpha (TNF-alpha) post-CPB (WMD [95% confidence interval (CI)] -23.5 pg/ml [-36.6 to -10.5]; -23.4 pg/ml [-35.8 to -11.0]; -15.3 mg/L [CI -26.9 to -3.7]; -2.10 pg/ml [-3.83 to -0.37] respectively). Very limited RCT evidence suggests that prophylactic [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1366, "doc_id": "2391552", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is immediate affective motivation impaired in schizophrenia?\n\nABSTRACT:\nAmong the various cognitive and affective evaluations that contribute to decisions about whether to engage in a future activity, three affective evaluations are particularly relevant: 1) interest in the activity itself, 2) the pleasure anticipated from the activity and 3) the excitement experienced while looking forward to the activity. In addition to these pre-activity evaluations, affective evaluations that are done after the activity is completed impact people's motivation to repeat the same activity. Although extant research suggests that these affective processes may be impaired in schizophrenia, it is not clear whether these impairments are mostly secondary to cognitive deficits. In three independent studies utilizing simple laboratory tasks with minimal cognitive demands, patients with schizophrenia or schizoaffective disorder and healthy control subjects evaluated their pleasure, interest, and excitement immediately before and after completing the tasks. Patients' anticipated pleasure and posttest evaluations of pleasure and interest were significantly greater than controls'. No group differences were found for excitement. In patients, there were significant negative correlations between anticipated pleasure, pretest excitement and depression scores, and between pretest interest and negative symptoms.", "output": "{\"label\": \"no\", \"rationale\": \"In these experiments, immediate affective evaluations reported by participants with schizophrenia or schizoaffective disorder were greater or similar to controls'. This finding is consistent with recent affective research showing that experiences of pleasure are intact in schizophrenia. These results emphasize the need to disentangle affective from cognitive processes in order to better understand the complex impairments present in schizophrenia spectrum disorders.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25159096, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Tuberculosis incidence occurs at higher rates in more sparsely populated areas in the UK.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tuberculosis mortality in England and Wales during 1982-1992: its association with poverty, ethnicity and AIDS.\nABSTRACT: This paper seeks to establish the strength of association between contemporary tuberculosis (TB) in England and Wales and several potential aetiological factors. It presents an ecological analysis of standardised annual TB mortality rates for the 403 local authority districts between 1982 and 1992, disaggregated by age and sex. Social, demographic and ethnicity measures from the 1981 and 1991 censuses and standardised annual AIDS-related mortality rates for young men are used to calculate Poisson regression models. A strong association was found between all TB mortality groups and overcrowding at the household level. For women, no other measures improved the explanatory power of the models. In multiple regressions, both poverty and AIDS-related mortality explained additional variation in the model for younger men. The link between ethnicity and tuberculosis notifications was not reflected in this analysis of mortality. For all groups no evidence of a positive relationship with ethnicity was found, once overcrowding had been accounted for. The significance of household as opposed to district level crowding suggests that prolonged contact is required for disease transmission. Regression analysis indicates that it is the overcrowding and poverty among ethnic populations that is significant for their tuberculosis mortality. The fact that the relationship between AIDS and TB is confined to the group most typical of AIDS patients provides evidence that AIDS has little influence on the level of tuberculosis mortality in the wider population. Explanations for the observed relationship include preferential certification, migration for treatment and shortcomings in health care provision.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"A strong association was found between all TB mortality groups and overcrowding at the household level.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1327, "doc_id": "22194407", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Homozygous deletion of murine Sbds gene from osterix-expressing mesenchymal stem and progenitor cells (MPCs) induces oxidative stress.\n\nCANDIDATE_PASSAGE:\nEndogenous bone marrow MSCs are dynamic, fate-restricted participants in bone maintenance and regeneration. Mesenchymal stem cells (MSCs) commonly defined by in vitro functions have entered clinical application despite little definition of their function in residence. Here, we report genetic pulse-chase experiments that define osteoblastic cells as short-lived and nonreplicative, requiring replenishment from bone-marrow-derived, Mx1(+) stromal cells with \"MSC\" features. These cells respond to tissue stress and migrate to sites of injury, supplying new osteoblasts during fracture healing. Single cell transplantation yielded progeny that both preserve progenitor function and differentiate into osteoblasts, producing new bone. They are capable of local and systemic translocation and serial transplantation. While these cells meet current definitions of MSCs in vitro, they are osteolineage restricted in vivo in growing and adult animals. Therefore, bone-marrow-derived MSCs may be a heterogeneous population with the Mx1(+) population, representing a highly dynamic and stress responsive stem/progenitor cell population of fate-restricted potential that feeds the high cell replacement demands of the adult skeleton.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "526", "doc_id": "9412420", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Tumor development occurs in conjunction with suppression of pro-inflammatory cytokines.\n\nCANDIDATE_PASSAGE:\nCD8+ T cells are activated in an antigen-independent manner in HIV-infected individuals. Hyperactivation of T cells, particularly of CD8(+) T cells, is a hallmark of chronic HIV 1 (HIV-1) infection. Little is known about the antigenic specificities and the mechanisms by which HIV-1 causes activation of CD8(+) T cells during chronic infection. We report that CD8(+) T cells were activated during in vivo HIV-1 replication irrespective of their Ag specificity. Cytokines present during untreated HIV-1 infection, most prominently IL-15, triggered proliferation and expression of activation markers in CD8(+) T cells, but not CD4(+) T cells, in the absence of TCR stimulation. Moreover, LPS or HIV-1-activated dendritic cells (DCs) stimulated CD8(+) T cells in an IL-15-dependent but Ag-independent manner, and IL-15 expression was highly increased in DCs isolated from viremic HIV-1 patients, suggesting that CD8(+) T cells are activated by inflammatory cytokines in untreated HIV-1 patients independent of Ag specificity. This finding contrasts with CD4(+) T cells whose in vivo activation seems biased toward specificities for persistent Ags. These observations explain the higher abundance of activated CD8(+) T cells compared with CD4(+) T cells in untreated HIV-1 infection.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1330", "doc_id": "35987381", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Chinese individuals with TT homozygosity in the MTHFR gene are more vulnerable to strokes caused by low levels of folate intake.\n\nCANDIDATE_ABSTRACT:\nTITLE: The effect of folate fortification on folic acid-based homocysteine-lowering intervention and stroke risk: a meta-analysis.\nABSTRACT: OBJECTIVE Folate and vitamin B12 are two vital regulators in the metabolic process of homocysteine, which is a risk factor of atherothrombotic events. Low folate intake or low plasma folate concentration is associated with increased stroke risk. Previous randomized controlled trials presented discordant findings in the effect of folic acid supplementation-based homocysteine lowering on stroke risk. The aim of the present review was to perform a meta-analysis of relevant randomized controlled trials to check the how different folate fortification status might affect the effects of folic acid supplementation in lowering homocysteine and reducing stroke risk. DESIGN Relevant randomized controlled trials were identified through formal literature search. Homocysteine reduction was compared in subgroups stratified by folate fortification status. Relative risks with 95 % confidence intervals were used as a measure to assess the association between folic acid supplementation and stroke risk. SETTING The meta-analysis included fourteen randomized controlled trials, SUBJECTS A total of 39 420 patients. RESULTS Homocysteine reductions were 26·99 (sd 1·91) %, 18·38 (sd 3·82) % and 21·30 (sd 1·98) %, respectively, in the subgroups without folate fortification, with folate fortification and with partial folate fortification. Significant difference was observed between the subgroups with folate fortification and without folate fortification (P=0·05). The relative risk of stroke was 0·88 (95 % CI 0·77, 1·00, P=0·05) in the subgroup without folate fortification, 0·94 (95 % CI 0·58, 1·54, P=0·82) in the subgroup with folate fortification and 0·91 (95 % CI 0·82, 1·01, P=0·09) in the subgroup with partial folate fortification. CONCLUSIONS Folic acid supplementation might have a [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 254, "doc_id": "37424881", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Surfactin producing cells and exopolymer producing cells cooperate to generate \"Van Gogh\" bundles that have sliding abilities on specialized media.\n\nCANDIDATE_ABSTRACT:\nTITLE: Host–Parasite Interactions and the Evolution of Gene Expression\nABSTRACT: Interactions between hosts and parasites provide an ongoing source of selection that promotes the evolution of a variety of features in the interacting species. Here, we use a genetically explicit mathematical model to explore how patterns of gene expression evolve at genetic loci responsible for host resistance and parasite infection. Our results reveal the striking yet intuitive conclusion that gene expression should evolve along very different trajectories in the two interacting species. Specifically, host resistance loci should frequently evolve to co-express alleles, whereas parasite infection loci should evolve to express only a single allele. This result arises because hosts that co-express resistance alleles are able to recognize and clear a greater diversity of parasite genotypes. By the same token, parasites that co-express antigen or elicitor alleles are more likely to be recognized and cleared by the host, and this favours the expression of only a single allele. Our model provides testable predictions that can help interpret accumulating data on expression levels for genes relevant to host−parasite interactions.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1114, "doc_id": "1852826", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Autologous transplantation of mesenchymal stem cells has better graft function than induction therapy with anti-interleukin-2 receptor antibodies.\n\nCANDIDATE_ABSTRACT:\nTITLE: Induction therapy with autologous mesenchymal stem cells in living-related kidney transplants: a randomized controlled trial.\nABSTRACT: CONTEXT Antibody-based induction therapy plus calcineurin inhibitors (CNIs) reduce acute rejection rates in kidney recipients; however, opportunistic infections and toxic CNI effects remain challenging. Reportedly, mesenchymal stem cells (MSCs) have successfully treated graft-vs-host disease. OBJECTIVE To assess autologous MSCs as replacement of antibody induction for patients with end-stage renal disease who undergo ABO-compatible, cross-match-negative kidney transplants from a living-related donor. DESIGN, SETTING, AND PATIENTS One hundred fifty-nine patients were enrolled in this single-site, prospective, open-label, randomized study from February 2008-May 2009, when recruitment was completed. INTERVENTION Patients were inoculated with marrow-derived autologous MSC (1-2 x 10(6)/kg) at kidney reperfusion and two weeks later. Fifty-three patients received standard-dose and 52 patients received low-dose CNIs (80% of standard); 51 patients in the control group received anti-IL-2 receptor antibody plus standard-dose CNIs. MAIN OUTCOME MEASURES The primary measure was 1-year incidence of acute rejection and renal function (estimated glomerular filtration rate [eGFR]); the secondary measure was patient and graft survival and incidence of adverse events. RESULTS Patient and graft survival at 13 to 30 months was similar in all groups. After 6 months, 4 of 53 patients (7.5%) in the autologous MSC plus standard-dose CNI group (95% CI, 0.4%-14.7%; P = .04) and 4 of 52 patients (7.7%) in the low-dose group (95% CI, 0.5%-14.9%; P = .046) compared with 11 of 51 controls (21.6%; 95% CI, 10.5%-32.6%) had biopsy-confirmed acute rejection. None of the patients in either autologous MSC group had glucorticoid-resistant rejection, whereas 4 patients (7.8%) in the control group [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"After 6 months, 4 of 53 patients (7.5%) in the autologous MSC plus standard-dose CNI group (95% CI, 0.4%-14.7%; P = .04) and 4 of 52 patients (7.7%) in the low-dose group (95% CI, 0.5%-14.9%; P = .046) compared with 11 of 51 controls (21.6%; 95% CI, 10.5%-32.6%) had biopsy-confirmed acute rejection.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 144, "doc_id": "10582939", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Upregulation of mosGCTL-1 is induced upon infection with West Nile virus.\n\nCANDIDATE_PASSAGE:\nA C-Type Lectin Collaborates with a CD45 Phosphatase Homolog to Facilitate West Nile Virus Infection of Mosquitoes West Nile virus (WNV) is the most common arthropod-borne flavivirus in the United States; however, the vector ligand(s) that participate in infection are not known. We now show that an Aedes aegypti C-type lectin, mosGCTL-1, is induced by WNV, interacts with WNV in a calcium-dependent manner, and facilitates infection in vivo and in vitro. A mosquito homolog of human CD45 in A. aegypti, designated mosPTP-1, recruits mosGCTL-1 to enable viral attachment to cells and to enhance viral entry. In vivo experiments show that mosGCTL-1 and mosPTP-1 function as part of the same pathway and are critical for WNV infection of mosquitoes. A similar phenomenon was also observed in Culex quinquefasciatus, a natural vector of WNV, further demonstrating that these genes participate in WNV infection. During the mosquito blood-feeding process, WNV infection was blocked in vivo with mosGCTL-1 antibodies. A molecular understanding of flaviviral-arthropod interactions may lead to strategies to control viral dissemination in nature.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1352", "doc_id": "12885341", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: A mutation in HNF4A leads to an increased risk of developing diabetes by the age of 14 years.\n\nCANDIDATE_ABSTRACT:\nTITLE: Macrosomia and Hyperinsulinaemic Hypoglycaemia in Patients with Heterozygous Mutations in the HNF4A Gene\nABSTRACT: Background Macrosomia is associated with considerable neonatal and maternal morbidity. Factors that predict macrosomia are poorly understood. The increased rate of macrosomia in the offspring of pregnant women with diabetes and in congenital hyperinsulinaemia is mediated by increased foetal insulin secretion. We assessed the in utero and neonatal role of two key regulators of pancreatic insulin secretion by studying birthweight and the incidence of neonatal hypoglycaemia in patients with heterozygous mutations in the maturity-onset diabetes of the young (MODY) genes HNF4A (encoding HNF-4α) and HNF1A/TCF1 (encoding HNF-1α), and the effect of pancreatic deletion of Hnf4a on foetal and neonatal insulin secretion in mice.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We assessed the in utero and neonatal role of two key regulators of pancreatic insulin secretion by studying birthweight and the incidence of neonatal hypoglycaemia in patients with heterozygous mutations in the maturity-onset diabetes of the young (MODY) genes HNF4A (encoding HNF-4α) and HNF1A/TCF1 (encoding HNF-1α), and the effect of pancreatic deletion of Hnf4a on foetal and neonatal insulin secretion in mice.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 44, "doc_id": "56893404", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Toll-like receptor (TLR) signaling is involved in the pathogenesis of human MDS.\n\nCANDIDATE_PASSAGE:\nA multiple indicators multiple causes model of late-life depression in Latin American countries BACKGROUND The Euro-D depression scale consists of symptom clusters that may be differentially related to demographic and cognitive characteristics in older adults. This hypothesis needs further investigation and the role of measurement bias on substantive conclusions remains to be established. METHOD The study sample comprised 10,405 community-dwelling older adults from six Latin American countries. We applied a Multiple Indicators Multiple Causes (MIMIC) model for a concurrent investigation of measurement bias and of the association between Euro-D symptom clusters and background variables. RESULTS The factorial validity of Euro-D, with a two-dimensional structure--affective suffering and motivation disturbance, was consistently supported in all countries. Although complete measurement invariance could not be assumed across countries, measurement bias was minor. Both Euro-D factors were unrelated to age, but related to gender, as well as to impairment in memory and verbal fluency. Gender differences were larger for affective suffering than for motivation disturbance, whereas differences in verbal fluency impairment were more strongly related to motivation disturbance. LIMITATIONS Our analytic strategies could only examine invariance at the level of indicator thresholds. The generalisability of current findings needs to be examined in clinical populations. A wider set of cognitive tests is needed. We did not examine the compositional factors that could have accounted for the variation in Euro-D scores across countries, as this was beyond the aims of the paper. CONCLUSION The current study adds evidence for the construct validity of Euro-D and for the possible diff [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1306", "doc_id": "12899460", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: A total of 1,000 people in the UK are asymptomatic carriers of vCJD infection.\n\nCANDIDATE_PASSAGE:\nIntegrin αvβ3/c-src “Oncogenic Unit” Promotes Anchorage-independence and Tumor Progression Integrins regulate adhesion-dependent growth, survival and invasion of tumor cells. In particular, expression of integrin alpha(v)beta(3) is associated with progression of a variety of human tumors. Here we reveal a previously undescribed adhesion-independent role for integrin alpha(v)beta(3) in pancreatic cancer and other carcinomas. Specifically, alpha(v)beta(3) expressed in carcinoma cells enhanced anchorage-independent tumor growth in vitro and increased lymph node metastases in vivo. These effects required recruitment of c-Src to the beta(3) integrin cytoplasmic tail, leading to c-Src activation, Crk-associated substrate (CAS) phosphorylation and tumor cell survival that, unexpectedly, was independent of cell adhesion or focal adhesion kinase (FAK) activation. Pharmacological blockade of c-Src kinase activity or decreased expression of endogenous alpha(v)beta(3) integrin or c-Src not only inhibited anchorage-independent growth but also suppressed metastasis in vivo, yet these manipulations did not affect tumor cell migration or invasion. These data define an unexpected role for an integrin as a mediator of anchorage independence, suggesting that an alpha(v)beta(3)-c-Src signaling module may account for the aggressive behavior of integrin alpha(v)beta(3)-expressing tumors in humans.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "48", "doc_id": "1782201", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Integrated care is successful at tackling multiple comorbidities.\n\nCANDIDATE_PASSAGE:\nControlling nuclear receptors: the circular logic of cofactor cycles Nuclear receptors regulate many biologically important processes in development and homeostasis by their bimodal function as repressors and activators of gene transcription. A finely tuned modulation of the transcriptional activities of nuclear receptors is crucial for determining highly specific and diversified programmes of gene expression. Recent studies have provided insights into the molecular mechanisms that are required to switch between repression and activation functions, the combinatorial roles of the multiple cofactor complexes that are required for mediating transcriptional regulation, and the central question of how several different signalling pathways can be integrated at the nuclear level to achieve specific profiles of gene expression.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "648", "doc_id": "20028729", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Notch signaling occurs between tumor cells and stromal cells.\n\nCANDIDATE_PASSAGE:\nCrosstalk between tumor and endothelial cells promotes tumor angiogenesis by MAPK activation of Notch signaling. While significant progress has been made in understanding the induction of tumor vasculature by secreted angiogenic factors, little is known regarding contact-dependent signals that promote tumor angiogenesis. Here, we report that the Notch ligand Jagged1 induced by growth factors via mitogen-activating protein kinase (MAPK) in head and neck squamous cell carcinoma (HNSCC) cells triggered Notch activation in neighboring endothelial cells (ECs) and promoted capillary-like sprout formation. Jagged1-expressing HNSCC cells significantly enhanced neovascularization and tumor growth in vivo. Moreover, the level of Jagged1 was significantly correlated with tumor blood vessel content and associated with HNSCC development. Our results elucidate a novel mechanism by which the direct interplay between tumor cells and ECs promotes angiogenesis through MAPK and Notch signaling pathways.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "863", "doc_id": "20568364", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The latent infection of myeloid cells with human cytomegalovirus induces a number of changes in gene expression.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mouse Spermatogenic Stem Cells Continually Interconvert between Equipotent Singly Isolated and Syncytial States\nABSTRACT: The identity and behavior of mouse spermatogenic stem cells have been a long-standing focus of interest. In the prevailing \"As model,\" stem cell function is restricted to singly isolated (As) spermatogonia. By examining single-cell dynamics of GFRα1+ stem cells in vivo, we evaluate an alternative hypothesis that, through fragmentation, syncytial spermatogonia also contribute to stem cell function in homeostasis. We use live imaging and pulse labeling to quantitatively determine the fates of individual GFRα1+ cells and find that, during steady-state spermatogenesis, the entire GFRα1+ population comprises a single stem cell pool, in which cells continually interconvert between As and syncytial states. A minimal biophysical model, relying only on the rates of incomplete cell division and syncytial fragmentation, precisely predicts the stochastic fates of GFRα1+ cells during steady state and postinsult regeneration. Thus, our results define an alternative and dynamic model for spermatogenic stem cell function in the mouse testis.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1224, "doc_id": "1381673", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Post-transcriptional handling of mitochondrial transcripts occurs in mitochondrial RNA granules.\n\nCANDIDATE_ABSTRACT:\nTITLE: GRSF1 Regulates RNA Processing in Mitochondrial RNA Granules\nABSTRACT: Various specialized domains have been described in the cytosol and the nucleus; however, little is known about compartmentalization within the mitochondrial matrix. GRSF1 (G-rich sequence factor 1) is an RNA binding protein that was previously reported to localize in the cytosol. We found that an isoform of GRSF1 accumulates in discrete foci in the mitochondrial matrix. These foci are composed of nascent mitochondrial RNA and also contain RNase P, an enzyme that participates in mitochondrial RNA processing. GRSF1 was found to interact with RNase P and to be required for processing of both classical and tRNA-less RNA precursors. In its absence, cleavage of primary RNA transcripts is abnormal, leading to decreased expression of mitochondrially encoded proteins and mitochondrial dysfunction. Our findings suggest that the foci containing GRSF1 and RNase P correspond to sites where primary RNA transcripts converge to be processed. We have termed these large ribonucleoprotein structures \"mitochondrial RNA granules. \"", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Our findings suggest that the foci containing GRSF1 and RNase P correspond to sites where primary RNA transcripts converge to be processed.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 962, "doc_id": "13931771", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does perspective-taking increase patient satisfaction in medical encounters?\n\nABSTRACT:\nTo assess whether perspective-taking, which researchers in other fields have shown to induce empathy, improves patient satisfaction in encounters between student-clinicians and standardized patients (SPs). In three studies, randomly assigned students (N = 608) received either a perspective-taking instruction or a neutral instruction prior to a clinical skills examination in 2006-2007. SP satisfaction was the main outcome in all three studies. Study 1 involved 245 third-year medical students from two universities. Studies 2 and 3 extended Study 1 to examine generalizability across student and SP subpopulations. Study 2 (105 physician assistant students, one university) explored the effect of perspective-taking on African American SPs' satisfaction. Study 3 (258 third-year medical students, two universities) examined the intervention's effect on students with high and low baseline perspective-taking tendencies. Intervention students outscored controls in patient satisfaction in all studies: Study 1: P = .01, standardized effect size = 0.16; Study 2: P = .001, standardized effect size = 0.31; Study 3: P = .009, standardized effect size = 0.13. In Study 2, perspective-taking improved African American SPs' satisfaction. In Study 3, intervention students with high baseline perspective-taking tendencies outscored controls (P = .0004, standardized effect size = 0.25), whereas those with low perspective-taking tendencies did not (P = .72, standardized effect size = 0.00).", "output": "{\"label\": \"maybe\", \"rationale\": \"Perspective-taking increased patient satisfaction in all three studies, across medical schools, clinical disciplines, and racially diverse students and SPs. Perspective-taking as a means for improving patient satisfaction deserves further exploration in clinical training and practice.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 20736672, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Adult tissue-resident macrophages are seeded before birth.\n\nCANDIDATE_PASSAGE:\nOrigin and functions of tissue macrophages. Macrophages are distributed in tissues throughout the body and contribute to both homeostasis and disease. Recently, it has become evident that most adult tissue macrophages originate during embryonic development and not from circulating monocytes. Each tissue has its own composition of embryonically derived and adult-derived macrophages, but it is unclear whether macrophages of distinct origins are functionally interchangeable or have unique roles at steady state. This new understanding also prompts reconsideration of the function of circulating monocytes. Classical Ly6c(hi) monocytes patrol the extravascular space in resting organs, and Ly6c(lo) nonclassical monocytes patrol the vasculature. Inflammation triggers monocytes to differentiate into macrophages, but whether resident and newly recruited macrophages possess similar functions during inflammation is unclear. Here, we define the tools used for identifying the complex origin of tissue macrophages and discuss the relative contributions of tissue niche versus ontological origin to the regulation of macrophage functions during steady state and inflammation.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "86", "doc_id": "22406695", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Tetraspanin-3 is a causative factor in the development of acute myelogenous leukemia\n\nCANDIDATE_ABSTRACT:\nTITLE: Tetraspanin 3 Is Required for the Development and Propagation of Acute Myelogenous Leukemia.\nABSTRACT: Acute Myelogenous Leukemia (AML) is an aggressive cancer that strikes both adults and children and is frequently resistant to therapy. Thus, identifying signals needed for AML propagation is a critical step toward developing new approaches for treating this disease. Here, we show that Tetraspanin 3 is a target of the RNA binding protein Musashi 2, which plays a key role in AML. We generated Tspan3 knockout mice that were born without overt defects. However, Tspan3 deletion impaired leukemia stem cell self-renewal and disease propagation and markedly improved survival in mouse models of AML. Additionally, Tspan3 inhibition blocked growth of AML patient samples, suggesting that Tspan3 is also important in human disease. As part of the mechanism, we show that Tspan3 deficiency disabled responses to CXCL12/SDF-1 and led to defects in AML localization within the niche. These identify Tspan3 as an important regulator of aggressive leukemias and highlight a role for Tspan3 in oncogenesis.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"However, Tspan3 deletion impaired leukemia stem cell self-renewal and disease propagation and markedly improved survival in mouse models of AML.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1150, "doc_id": "11369420", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In young and middle-aged adults, current or remote uses of ADHD medications do not increase the risk of serious cardiovascular events.\n\nCANDIDATE_ABSTRACT:\nTITLE: ADHD medications and risk of serious cardiovascular events in young and middle-aged adults.\nABSTRACT: CONTEXT More than 1.5 million US adults use stimulants and other medications labeled for treatment of attention-deficit/hyperactivity disorder (ADHD). These agents can increase heart rate and blood pressure, raising concerns about their cardiovascular safety. OBJECTIVE To examine whether current use of medications prescribed primarily to treat ADHD is associated with increased risk of serious cardiovascular events in young and middle-aged adults. DESIGN, SETTING, AND PARTICIPANTS Retrospective, population-based cohort study using electronic health care records from 4 study sites (OptumInsight Epidemiology, Tennessee Medicaid, Kaiser Permanente California, and the HMO Research Network), starting in 1986 at 1 site and ending in 2005 at all sites, with additional covariate assessment using 2007 survey data. Participants were adults aged 25 through 64 years with dispensed prescriptions for methylphenidate, amphetamine, or atomoxetine at baseline. Each medication user (n = 150,359) was matched to 2 nonusers on study site, birth year, sex, and calendar year (443,198 total users and nonusers). MAIN OUTCOME MEASURES Serious cardiovascular events, including myocardial infarction (MI), sudden cardiac death (SCD), or stroke, with comparison between current or new users and remote users to account for potential healthy-user bias. RESULTS During 806,182 person-years of follow-up (median, 1.3 years per person), 1357 cases of MI, 296 cases of SCD, and 575 cases of stroke occurred. There were 107,322 person-years of current use (median, 0.33 years), with a crude incidence per 1000 person-years of 1.34 (95% CI, 1.14-1.57) for MI, 0.30 (95% CI, 0.20-0.42) for SCD, and 0.56 (95% CI, 0.43-0.72) for stroke. The multivariable-adjusted rate ratio (RR) of serious cardiovascular eve [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The multivariable-adjusted rate ratio (RR) of serious cardiovascular events for current use vs nonuse of ADHD medications was 0.83 (95% CI, 0.72-0.96). Among new users of ADHD medications, the adjusted RR was 0.77 (95% CI, 0.63-0.94).\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 589, "doc_id": "10984005", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does rugby headgear prevent concussion?\n\nABSTRACT:\nTo examine the attitudes of players and coaches to the use of protective headgear, particularly with respect to the prevention of concussion. A questionnaire designed to assess attitudes to headgear was administered to 63 players from four different Canadian teams, each representing a different level of play (high school, university, community club, national). In addition, coaches from all four levels were questioned about team policies and their personal opinions about the use of headgear to prevent concussion. Although the players tended to believe that the headgear could prevent concussion (62%), the coaches were less convinced (33%). Despite the players' belief that headgear offers protection against concussion, only a minority reported wearing headgear (27%) and few (24%) felt that its use should be made mandatory. Common reasons for not wearing headgear were \"its use is not mandatory\", \"it is uncomfortable\", and \"it costs too much\".", "output": "{\"label\": \"maybe\", \"rationale\": \"Although most players in the study believe that rugby headgear may prevent concussion, only a minority reported wearing it. Coaches tended to be less convinced than the players that rugby headgear can prevent concussion.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 11867487, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: V-9302 inhibits antitumor responses by decreasing cell death and oxidative stress.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pharmacological Blockade of ASCT2-dependent Glutamine Transport Leads To Anti-tumor Efficacy in Preclinical Models\nABSTRACT: The unique metabolic demands of cancer cells underscore potentially fruitful opportunities for drug discovery in the era of precision medicine. However, therapeutic targeting of cancer metabolism has led to surprisingly few new drugs to date. The neutral amino acid glutamine serves as a key intermediate in numerous metabolic processes leveraged by cancer cells, including biosynthesis, cell signaling, and oxidative protection. Herein we report the preclinical development of V-9302, a competitive small molecule antagonist of transmembrane glutamine flux that selectively and potently targets the amino acid transporter ASCT2. Pharmacological blockade of ASCT2 with V-9302 resulted in attenuated cancer cell growth and proliferation, increased cell death, and increased oxidative stress, which collectively contributed to antitumor responses in vitro and in vivo. This is the first study, to our knowledge, to demonstrate the utility of a pharmacological inhibitor of glutamine transport in oncology, representing a new class of targeted therapy and laying a framework for paradigm-shifting therapies targeting cancer cell metabolism.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Pharmacological blockade of ASCT2 with V-9302 resulted in attenuated cancer cell growth and proliferation, increased cell death, and increased oxidative stress, which collectively contributed to antitumor responses in vitro and in vivo.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1355, "doc_id": "5256564", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Omnivores produce more trimethylamine N-oxide from dietary I-carnitine than vegetarians.\n\nCANDIDATE_PASSAGE:\nMembrane topology of the 60-kDa Oxa1p homologue from Escherichia coli. We have characterized the membrane topology of a 60-kDa inner membrane protein from Escherichia coli that is homologous to the recently identified Oxa1p protein in Saccharomyces cerevisiae mitochondria implicated in the assembly of mitochondrial inner membrane proteins. Hydrophobicity and alkaline phosphatase fusion analyses suggest a membrane topology with six transmembrane segments, including an N-terminal signal-anchor sequence not present in mitochondrial Oxa1p. In contrast to partial N-terminal fusion protein constructs, the full-length protein folds into a protease-resistant conformation, suggesting that important folding determinants are present in the C-terminal part of the molecule.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "884", "doc_id": "7643848", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The DEXI promoter region is bound by multiple transcription factors in a murine haematopoietic progenitor cell line.\n\nCANDIDATE_PASSAGE:\nAtaxia, dementia, and hypogonadotropism caused by disordered ubiquitination. BACKGROUND The combination of ataxia and hypogonadism was first described more than a century ago, but its genetic basis has remained elusive. METHODS We performed whole-exome sequencing in a patient with ataxia and hypogonadotropic hypogonadism, followed by targeted sequencing of candidate genes in similarly affected patients. Neurologic and reproductive endocrine phenotypes were characterized in detail. The effects of sequence variants and the presence of an epistatic interaction were tested in a zebrafish model. RESULTS Digenic homozygous mutations in RNF216 and OTUD4, which encode a ubiquitin E3 ligase and a deubiquitinase, respectively, were found in three affected siblings in a consanguineous family. Additional screening identified compound heterozygous truncating mutations in RNF216 in an unrelated patient and single heterozygous deleterious mutations in four other patients. Knockdown of rnf216 or otud4 in zebrafish embryos induced defects in the eye, optic tectum, and cerebellum; combinatorial suppression of both genes exacerbated these phenotypes, which were rescued by nonmutant, but not mutant, human RNF216 or OTUD4 messenger RNA. All patients had progressive ataxia and dementia. Neuronal loss was observed in cerebellar pathways and the hippocampus; surviving hippocampal neurons contained ubiquitin-immunoreactive intranuclear inclusions. Defects were detected at the hypothalamic and pituitary levels of the reproductive endocrine axis. CONCLUSIONS The syndrome of hypogonadotropic hypogonadism, ataxia, and dementia can be caused by inactivating mutations in RNF216 or by the combination of mutations in RNF216 and OTUD4. These findings link disordered ubiquitination to neurode [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1161", "doc_id": "24725136", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is caecal pneumatosis an absolute contraindication for endoluminal stenting in patients with acute malignant large bowel obstruction?\n\nABSTRACT:\nThe computed tomographic (CT) finding of caecal pneumatosis in patients with malignant large bowel obstruction has been associated with ischaemia and impending perforation. Emergency surgery is then usually performed without consideration of endoluminal stenting. The aim of our study was to correlate caecal viability to the CT finding of caecal pneumatosis in patients with acute malignant large bowel obstruction. A retrospective review of the CT scans of all patients presenting with acute malignant large bowel obstruction was performed. Patients with CT evidence of caecal pneumatosis were identified and this was correlated with intraoperative and histopathological findings. There were 10 patients who had caecal pneumatosis on their CT scans between 2007 and 2010. Five underwent immediate surgery while the other five had emergency endoluminal stenting performed. One failed the stenting procedure and proceeded to emergency surgery. The other four were stented successfully and underwent interval surgery in an elective setting. In the six patients who underwent emergency surgery, four were found to have a viable caecum intra-operatively and underwent a segmental resection. The remaining two had an ischaemic caecum--one had curvilinear pneumatosis and the other had a predominantly bubbly pattern of pneumatosis on their CT scans.", "output": "{\"label\": \"no\", \"rationale\": \"Caecal pneumatosis alone is not a reliable predictor of caecal viability in patients with acute malignant large bowel obstruction. Such a finding on CT scan should be correlated clinically before excluding the role of endoluminal stenting.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 24529169, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Tumor development occurs in conjunction with upregulation of pro-inflammatory cytokines.\n\nCANDIDATE_PASSAGE:\nParaneoplastic thrombocytosis: the secrets of tumor self-promotion. Paraneoplastic thrombocytosis is associated with many solid tumors and often correlates with reduced survival. Recent studies suggest that a pathogenic feed back loop may be operative between platelets and tumor cells, with reciprocal interactions between tumor growth/metastasis and thrombocytosis/platelet activation. Specific molecular pathways have been identified in which tumors can stimulate platelet production and activation; activated platelets can, in turn, promote tumor growth and metastasis. Taken together, these findings provide exciting new potential targets for therapeutic intervention.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1331", "doc_id": "14075252", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Birth-weight is positively associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Role of birthweight in the etiology of breast cancer.\nABSTRACT: Breast cancer may originate in utero. We reviewed the available evidence on the association between birthweight and the risk of breast cancer. To date, 26 research papers addressing this issue have been published. The majority of studies identified a positive link between birthweight and premenopausal, but not postmenopausal, breast cancer. The relative risk estimate for breast cancer comparing women with high birthweight to women with low birthweight combining all studies including both pre- and postmenopausal breast cancer was 1.23 (95% confidence interval 1.13-1.34). The mechanisms underlying this association likely include elevated levels of growth factors that may increase the number of susceptible stem cells in the mammary gland or initiate tumors through DNA mutations. Loss of imprinting (LOI) of growth hormone genes relevant for intrauterine growth, such as insulin-like growth factor 2 (IGF2), leads to abnormally high levels of these hormones evidenced by high birthweight. LOI of IGF2 has also been found in mammary tumor tissue. The role of environmental factors that stimulate such epigenetic regulation of gene expression remains to be elucidated.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The majority of studies identified a positive link between birthweight and premenopausal, but not postmenopausal, breast cancer.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 179, "doc_id": "27123743", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Ca2+ cycling controls whole-body energy homeostasis in beige fat.\n\nCANDIDATE_PASSAGE:\nRelationship between activity levels, aerobic fitness, and body fat in 8- to 10-yr-old children. The relationships between children's activity, aerobic fitness, and fatness are unclear. Indirect estimates of activity, e.g., heart rate (HR) and recall, may mask any associations. The purpose of this study was to assess these relationships by using the Tritrac-R3D, a pedometer, and heart rate. Thirty-four children, ages 8-10 yr, participated in the study. The Tritrac and pedometer were worn for up to 6 days. HR was measured for 1 day. Activity measured by Tritrac or pedometer correlated positively to fitness in the whole group (Tritrac, r = 0.66; pedometer, r = 0.59; P < 0.01) and in boys and girls separately (P < 0.05) and correlated negatively to fatness in the whole group (r = -0.42, P < 0.05). In contrast, HR did not correlate significantly to fitness, and HR of >139 beats/min correlated positively to fatness in girls (r = 0.64, P < 0.05). This suggests that HR is misleading as a measure of activity. This study supports a positive relationship between activity and fitness and suggests a negative relationship between fatness and activity.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "220", "doc_id": "2575938", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Leuko-reduced blood reduces infectious complications in red blood cell transfusion.\n\nCANDIDATE_ABSTRACT:\nTITLE: Clinical outcomes following institution of the Canadian universal leukoreduction program for red blood cell transfusions.\nABSTRACT: CONTEXT A number of countries have implemented a policy of universal leukoreduction of their blood supply, but the potential role of leukoreduction in decreasing postoperative mortality and infection is unclear. OBJECTIVE To evaluate clinical outcomes following adoption of a national universal prestorage leukoreduction program for blood transfusions. DESIGN, SETTING, AND POPULATION Retrospective before-and-after cohort study conducted from August 1998 to August 2000 in 23 academic and community hospitals throughout Canada, enrolling 14 786 patients who received red blood cell transfusions following cardiac surgery or repair of hip fracture, or who required intensive care following a surgical intervention or multiple trauma. INTERVENTION Universal prestorage leukoreduction program introduced by 2 Canadian blood agencies. A total of 6982 patients were enrolled during the control period and 7804 patients were enrolled following prestorage leukoreduction. MAIN OUTCOME MEASURES All-cause in-hospital mortality and serious nosocomial infections (pneumonia, bacteremia, septic shock, all surgical site infections) occurring after first transfusion and at least 2 days after index procedure or intensive care unit admission. Secondary outcomes included rates of posttransfusion fever and antibiotic use. RESULTS Unadjusted in-hospital mortality rates were significantly lower following the introduction of leukoreduction compared with the control period (6.19% vs 7.03%, respectively; P =.04). Compared with the control period, the adjusted odds of death following leukoreduction were reduced (odds ratio [OR], 0.87; 95% confidence interval [CI], 0.75-0.99), but serious nosocomial infections did not decrease (adjusted OR, 0.97; 95% CI, 0.87-1.09). The frequency of posttransfusio [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Compared with the control period, the adjusted odds of death following leukoreduction were reduced (odds ratio [OR], 0.87; 95% confidence interval [CI], 0.75-0.99), but serious nosocomial infections did not decrease (adjusted OR, 0.97; 95% CI, 0.87-1.09).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 693, "doc_id": "24088502", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does phylogenomic analysis of carangimorph fishes reveal flatfish asymmetry arose in a blink of the evolutionary eye?\n\nABSTRACT:\nFlatfish cranial asymmetry represents one of the most remarkable morphological innovations among vertebrates, and has fueled vigorous debate on the manner and rate at which strikingly divergent phenotypes evolve. A surprising result of many recent molecular phylogenetic studies is the lack of support for flatfish monophyly, where increasingly larger DNA datasets of up to 23 loci have either yielded a weakly supported flatfish clade or indicated the group is polyphyletic. Lack of resolution for flatfish relationships has been attributed to analytical limitations for dealing with processes such as nucleotide non-stationarity and incomplete lineage sorting (ILS). We tackle this phylogenetic problem using a sequence dataset comprising more than 1,000 ultraconserved DNA element (UCE) loci covering 45 carangimorphs, the broader clade containing flatfishes and several other specialized lineages such as remoras, billfishes, and archerfishes. We present a phylogeny based on UCE loci that unequivocally supports flatfish monophyly and a single origin of asymmetry. We document similar levels of discordance among UCE loci as in previous, smaller molecular datasets. However, relationships among flatfishes and carangimorphs recovered from multilocus concatenated and species tree analyses of our data are robust to the analytical framework applied and size of data matrix used. By integrating the UCE data with a rich fossil record, we find that the most distinctive carangimorph bodyplans arose rapidly during the Paleogene (66.0-23.03 Ma). Flatfish asymmetry, for example, likely evolved over an interval of no more than 2.97 million years.", "output": "{\"label\": \"yes\", \"rationale\": \"The longstanding uncertainty in phylogenetic hypotheses for flatfishes and their carangimorph relatives highlights the limitations of smaller molecular datasets when applied to successive, rapid divergences. Here, we recovered significant support for flatfish monophyly and relationships among carangimorphs through analysis of over 1,000 UCE loci. The resulting time-calibrated phylogeny points to phenotypic divergence early within carangimorph history that broadly matches with the predictions of adaptive models of lineage diversification.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 27769164, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: KRT17 modulates the expression of the transcriptional regulator AIRE in diseased epithelia.\n\nCANDIDATE_ABSTRACT:\nTITLE: Keratin-dependent regulation of Aire and gene expression in skin tumor keratinocytes\nABSTRACT: Expression of the intermediate filament protein keratin 17 (K17) is robustly upregulated in inflammatory skin diseases and in many tumors originating in stratified and pseudostratified epithelia. We report that autoimmune regulator (Aire), a transcriptional regulator, is inducibly expressed in human and mouse tumor keratinocytes in a K17-dependent manner and is required for timely onset of Gli2-induced skin tumorigenesis in mice. The induction of Aire mRNA in keratinocytes depends on a functional interaction between K17 and the heterogeneous nuclear ribonucleoprotein hnRNP K. Further, K17 colocalizes with Aire protein in the nucleus of tumor-prone keratinocytes, and each factor is bound to a specific promoter region featuring an NF-κB consensus sequence in a relevant subset of K17- and Aire-dependent proinflammatory genes. These findings provide radically new insight into keratin intermediate filament and Aire function, along with a molecular basis for the K17-dependent amplification of inflammatory and immune responses in diseased epithelia.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The induction of Aire mRNA in keratinocytes depends on a functional interaction between K17 and the heterogeneous nuclear ribonucleoprotein hnRNP K. Further, K17 colocalizes with Aire protein in the nucleus of tumor-prone keratinocytes, and each factor is bound to a specific promoter region featuring an NF-κB consensus sequence in a relevant subset of K17- and Aire-dependent proinflammatory genes.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 665, "doc_id": "12580014", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Bone Marrow (BM) transplantation is used to treat acute myeloid leukemia (AML)\n\nCANDIDATE_ABSTRACT:\nTITLE: Tetraspanin 3 Is Required for the Development and Propagation of Acute Myelogenous Leukemia.\nABSTRACT: Acute Myelogenous Leukemia (AML) is an aggressive cancer that strikes both adults and children and is frequently resistant to therapy. Thus, identifying signals needed for AML propagation is a critical step toward developing new approaches for treating this disease. Here, we show that Tetraspanin 3 is a target of the RNA binding protein Musashi 2, which plays a key role in AML. We generated Tspan3 knockout mice that were born without overt defects. However, Tspan3 deletion impaired leukemia stem cell self-renewal and disease propagation and markedly improved survival in mouse models of AML. Additionally, Tspan3 inhibition blocked growth of AML patient samples, suggesting that Tspan3 is also important in human disease. As part of the mechanism, we show that Tspan3 deficiency disabled responses to CXCL12/SDF-1 and led to defects in AML localization within the niche. These identify Tspan3 as an important regulator of aggressive leukemias and highlight a role for Tspan3 in oncogenesis.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 182, "doc_id": "11369420", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does vaginal intraepithelial neoplasia have the same evolution as cervical intraepithelial neoplasia?\n\nABSTRACT:\nVaginal intraepithelial neoplasia is a little known disease which could be related to risk factors different from simple HPV infections. To ascertain wheter vaginal lesions have a natural history similar to cervical lesions.MATERIALS & A retrospective study to identify patients with vaginal lesions and synchronous cervical lesions through biopsy. The rate of mild cervical lesions (koilocytosis, warts, CIN I with and without koilocytosis) was compared with the rate of severe cervical lesions (CIN II and III, cervical carcinoma) in patients with mild vaginal lesions (warts and koilocytosis, and low-grade VAIN) and in patients with severe vaginal lesions (high-grade VAIN). Using koilocytosis as a marker, the rate of \"active\" cervical lesions was compared with the rate of \"non active\" cervical lesions in patients with \"active\" versus \"non active\" vaginal lesions. Finally, the rates of mild and severe cervical lesions were compared among each group of VAIN (low-grade, high-grade, with or without koilocytosis). In patients with mild vaginal lesions, mild cervical lesions were significantly more frequent than severe cervical lesions. In patients with \"active\" vaginal lesions the rate of \"active\" cervical lesions was significantly higher than \"non active\" cervical lesions. The differences in rates of mild cervical lesions and severe cervical lesions among patients with high-grade VAIN and low-grade VAIN (with and without koilocytosis) were not significant.", "output": "{\"label\": \"maybe\", \"rationale\": \"These data suggest that CIN and VAIN may have some common features in certain cases, i.e., if an HPV infection is proved.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 18714572, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Birth-weight is negatively associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Birth Size and Breast Cancer Risk: Re-analysis of Individual Participant Data from 32 Studies\nABSTRACT: BACKGROUND Birth size, perhaps a proxy for prenatal environment, might be a correlate of subsequent breast cancer risk, but findings from epidemiological studies have been inconsistent. We re-analysed individual participant data from published and unpublished studies to obtain more precise estimates of the magnitude and shape of the birth size-breast cancer association. METHODS AND FINDINGS Studies were identified through computer-assisted and manual searches, and personal communication with investigators. Individual participant data from 32 studies, comprising 22,058 breast cancer cases, were obtained. Random effect models were used, if appropriate, to combine study-specific estimates of effect. Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003). Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data. Birth length and head circumference from birth records were also positively associated with breast cancer risk (pooled RR per one SD increment: 1.06 [95% CI 1.03-1.10] and 1.09 [95% CI 1.03-1.15], respectively). Simultaneous adjustment for these three birth size variables showed that length was the strongest independent predictor of risk. The birth size effec [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 178, "doc_id": "16322674", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: A diminished ovarian reserve is a very strong indicator of infertility, even in an a priori non-infertile population.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\nABSTRACT: Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential. Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age. Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area. Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH. Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle). Conception was defined as a positive pregnancy test result. Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis. After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively). Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cy [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 40, "doc_id": "13497630", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The Snf1 complex regulates carbon and energy metabolism in baker's yeast (Saccharomyces cerevisiae).\n\nCANDIDATE_ABSTRACT:\nTITLE: Compound heterozygous ZMPSTE24 mutations reduce prelamin A processing and result in a severe progeroid phenotype.\nABSTRACT: Hutchinson–Gilford progeria syndrome (HGPS; OMIM 176670) is an extremely rare but devastating disorder that mimics premature aging.1–3 Affected children appear normal at birth but typically develop failure to thrive in the first two years. Other features include alopecia, micrognathia, loss of subcutaneous fat with prominent veins, abnormal dentition, sclerodermatous skin changes, and osteolysis of the clavicles and distal phalanges. The mean age of death is at age 13 years, most commonly due to atherosclerosis. HGPS is mainly sporadic in occurrence, but a genetic cause has now been implicated following the identification of de novo heterozygous mutations in the LMNA gene in the majority of HGPS patients.4,5 A single family showing autosomal recessive inheritance of homozygous LMNA mutations has also been reported.6 LMNA encodes lamins A and C, components of the nuclear lamina, a meshwork underlying the nuclear envelope that serves as a structural support and is also thought to contribute to chromatin organisation and the regulation of gene expression.7,8 Interestingly, mutations in LMNA have recently been associated with at least eight inherited disorders, known as laminopathies, with differential dystrophic effects on a variety of tissues including muscle, neurones, skin, bone, and adipose tissue (reviewed in Mounkes et al 9). However, the realisation that these disorders share common genetic defects has led to clinical re-evaluation, with emerging evidence of significant phenotypic overlap.10 Hence the laminopathies might reasonably be considered as a spectrum of related diseases. HGPS has phenotypic similarities to several other laminopathies, in particular the atypical Werner’s syndrome11 and mandibuloacral dysplasia (MAD; OMIM 248370 and 608612).12 The [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1182, "doc_id": "834336", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: HAND2 methylation is a key step in early endometrial carcinogenesis.\n\nCANDIDATE_PASSAGE:\nCatalytic-Independent Functions of PARP-1 Determine Sox2 Pioneer Activity at Intractable Genomic Loci. Pioneer transcription factors (TFs) function as genomic first responders, binding to inaccessible regions of chromatin to promote enhancer formation. The mechanism by which pioneer TFs gain access to chromatin remains an important unanswered question. Here we show that PARP-1, a nucleosome-binding protein, cooperates with intrinsic properties of the pioneer TF Sox2 to facilitate its binding to intractable genomic loci in embryonic stem cells. These actions of PARP-1 occur independently of its poly(ADP-ribosyl) transferase activity. PARP-1-dependent Sox2-binding sites reside in euchromatic regions of the genome with relatively high nucleosome occupancy and low co-occupancy by other transcription factors. PARP-1 stabilizes Sox2 binding to nucleosomes at suboptimal sites through cooperative interactions on DNA. Our results define intrinsic and extrinsic features that determine Sox2 pioneer activity. The conditional pioneer activity observed with Sox2 at a subset of binding sites may be a key feature of other pioneer TFs operating at intractable genomic loci.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "488", "doc_id": "23208167", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is anaemia a risk factor for progression of acute kidney injury : a retrospective analysis?\n\nABSTRACT:\nIn hospitalised patients, anaemia increases the risk of developing acute kidney injury (AKI). Our aim was to determine whether anaemia also has an impact on the risk of progression from early AKI to more severe AKI in critically ill patients. We retrospectively analysed the data of patients admitted to the adult intensive care unit between 2007 and 2009 who had AKI I as per the AKI Network classification, and who had undergone haemodynamic monitoring within 12 h of AKI I. We collected baseline characteristics, severity of illness, haemoglobin (Hb), and haemodynamic parameters in the first 12 h of AKI I and differentiated between patients who progressed to AKI III and those who did not. Univariate and multivariate logistic regression analyses were used to identify risk factors for progression. Associations between Hb, arterial oxygen saturation and cardiac index were explored by receiver operating characteristic curve analysis. Two hundred and ten patients (median age 70 years, 68% male) underwent haemodynamic monitoring within 12 h of AKI I; 85 (41.5%) progressed to AKI III. The proportion of patients with underlying cardiac disease was significantly higher among progressors versus non-progressors (58% vs 34%, respectively; p = 0.001). On the first day of AKI I, progressors had a significantly higher Sequential Organ Failure Assessment score (9 vs 8; p < 0.001), lower cardiac index (median 2.6 vs 3.3 L/min/m(2); p < 0.001), higher arterial lactate (2 vs 1.6 mmol/L; p < 0.001), higher central venous pressure (16 vs 13; p = 0.02), lower mean arterial blood pressure (median 71 vs 74 mmHg; p = 0.01) and significantly higher requirement for cardiovascular and respiratory support, but there was no difference in Hb concentration (median 96 g/L in both groups). Mult [TRUNCATED]", "output": "{\"label\": \"no\", \"rationale\": \"In critically ill patients with AKI stage 1, anaemia was not associated with an increased risk of progression to more severe AKI.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 26951090, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does repetitive paired-pulse transcranial magnetic stimulation affect corticospinal excitability and finger tapping in Parkinson 's disease?\n\nABSTRACT:\nTo study the effect of long trains of a recently established conditioning-test paired-pulse repetitive transcranial magnetic stimulation (rTMS) paradigm on corticospinal excitability and finger tapping speed. We applied 900 inhibiting or facilitating paired-pulses or 900 real or sham single stimuli at 1Hz over the motor cortex contralateral to the dominant hand of 9 healthy subjects and contralateral to the more affected hand of 11 patients with Parkinson's disease. In both groups, motor evoked potentials (MEPs) from suprathreshold pulses were larger after facilitating paired-pulses than after inhibiting paired-pulses. After real single-pulse rTMS and after either type of paired-pulse rTMS patients showed an increase in finger tapping frequency on the stimulated hand. Tapping was unchanged contralaterally, after sham stimuli, and in controls. Tremor and tapping frequencies were not correlated, nor was the change in MEP size correlated to the change in tapping frequency.", "output": "{\"label\": \"yes\", \"rationale\": \"Repetitive paired-pulses allow selective induction of corticospinal inhibition or facilitation, but do not enhance the transient improvement of finger motility induced by conventional single-pulse rTMS.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 12048055, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: GATA3 regulates self-renewal capacity in bone marrow hematopoietic stem cells.\n\nCANDIDATE_PASSAGE:\nGATA-3 regulates hematopoietic stem cell maintenance and cell-cycle entry. Maintaining hematopoietic stem cell (HSC) quiescence is a critical property for the life-long generation of blood cells. Approximately 75% of cells in a highly enriched long-term repopulating HSC (LT-HSC) pool (Lin(-)Sca1(+)c-Kit(hi)CD150(+)CD48(-)) are quiescent, with only a small percentage of the LT-HSCs in cycle. Transcription factor GATA-3 is known to be vital for the development of T cells at multiple stages in the thymus and for Th2 differentiation in the peripheral organs. Although it is well documented that GATA-3 is expressed in HSCs, a role for GATA-3 in any prethymic progenitor cell has not been established. In the present study, we show that Gata3-null mutant mice generate fewer LT-HSCs and that fewer Gata3-null LT-HSCs are in cycle. Furthermore, Gata3 mutant hematopoietic progenitor cells fail to be recruited into an increased cycling state after 5-fluorouracil-induced myelosuppression. Therefore, GATA-3 is required for the maintenance of a normal number of LT-HSCs and for their entry into the cell cycle.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "445", "doc_id": "10165258", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Side effects associated with antidepressants increases risk of stroke.\n\nCANDIDATE_PASSAGE:\nAntidepressant use and risk of adverse outcomes in older people: population based cohort study OBJECTIVES To investigate the association between antidepressant treatment and risk of several potential adverse outcomes in older people with depression and to examine risks by class of antidepressant, duration of use, and dose. DESIGN Cohort study of people aged 65 and over diagnosed as having depression. SETTING 570 general practices in the United Kingdom supplying data to the QResearch primary care database. PARTICIPANTS 60,746 patients diagnosed as having a new episode of depression between the ages of 65 and 100 years from 1 January 1996 to 31 December 2007 and followed up until 31 December 2008. MAIN OUTCOME MEASURES Hazard ratios associated with antidepressant use for all cause mortality, attempted suicide/self harm, myocardial infarction, stroke/transient ischaemic attack, falls, fractures, upper gastrointestinal bleeding, epilepsy/seizures, road traffic accidents, adverse drug reactions, and hyponatraemia, adjusted for a range of potential confounding variables. Hazard ratios were calculated for antidepressant class (tricyclic and related antidepressants, selective serotonin reuptake inhibitors, other antidepressants), dose, and duration of use and for commonly prescribed individual drugs. RESULTS 54,038 (89.0%) patients received at least one prescription for an antidepressant during follow-up. A total of 1,398,359 antidepressant prescriptions were issued: 764,659 (54.7%) for selective serotonin reuptake inhibitors, 442,192 (31.6%) for tricyclic antidepressants, 2203 (0.2%) for monoamine oxidase inhibitors, and 189,305 (13.5%) for the group of other antidepressants. The associations with the adverse outcomes differed significantly between the antidepressa [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1084", "doc_id": "5691302", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Patients in stable partnerships progress from HIV to death at the same rate as patients not in partnerships.\n\nCANDIDATE_ABSTRACT:\nTITLE: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\nABSTRACT: OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART). DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study). SETTING Seven outpatient clinics throughout Switzerland. PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years). MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound. RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion. When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership. In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without. Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression. CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 925, "doc_id": "17077004", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Hypocretin neurones suppress panicprone state in rats.\n\nCANDIDATE_ABSTRACT:\nTITLE: A KEY ROLE FOR OREXIN IN PANIC ANXIETY\nABSTRACT: Panic disorder is a severe anxiety disorder with recurrent, debilitating panic attacks. In individuals with panic disorder there is evidence of decreased central gamma-aminobutyric acid (GABA) activity as well as marked increases in autonomic and respiratory responses after intravenous infusions of hypertonic sodium lactate. In a rat model of panic disorder, chronic inhibition of GABA synthesis in the dorsomedial-perifornical hypothalamus of rats produces anxiety-like states and a similar vulnerability to sodium lactate-induced cardioexcitatory responses. The dorsomedial-perifornical hypothalamus is enriched in neurons containing orexin (ORX, also known as hypocretin), which have a crucial role in arousal, vigilance and central autonomic mobilization, all of which are key components of panic. Here we show that activation of ORX-synthesizing neurons is necessary for developing a panic-prone state in the rat panic model, and either silencing of the hypothalamic gene encoding ORX (Hcrt) with RNAi or systemic ORX-1 receptor antagonists blocks the panic responses. Moreover, we show that human subjects with panic anxiety have elevated levels of ORX in the cerebrospinal fluid compared to subjects without panic anxiety. Taken together, our results suggest that the ORX system may be involved in the pathophysiology of panic anxiety and that ORX antagonists constitute a potential new treatment strategy for panic disorder.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Here we show that activation of ORX-synthesizing neurons is necessary for developing a panic-prone state in the rat panic model, and either silencing of the hypothalamic gene encoding ORX (Hcrt) with RNAi or systemic ORX-1 receptor antagonists blocks the panic responses.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 537, "doc_id": "16056514", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The relationship between a breast cancer patient's capacity to metabolize tamoxifen and treatment outcome is dependent on the patient's genetic make-up.\n\nCANDIDATE_PASSAGE:\nEmbryonic stem cell lines from human blastocysts: somatic differentiation in vitro We describe the derivation of pluripotent embryonic stem (ES) cells from human blastocysts. Two diploid ES cell lines have been cultivated in vitro for extended periods while maintaining expression of markers characteristic of pluripotent primate cells. Human ES cells express the transcription factor Oct-4, essential for development of pluripotential cells in the mouse. When grafted into SCID mice, both lines give rise to teratomas containing derivatives of all three embryonic germ layers. Both cell lines differentiate in vitro into extraembryonic and somatic cell lineages. Neural progenitor cells may be isolated from differentiating ES cell cultures and induced to form mature neurons. Embryonic stem cells provide a model to study early human embryology, an investigational tool for discovery of novel growth factors and medicines, and a potential source of cells for use in transplantation therapy.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1259", "doc_id": "3360421", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Chenodeosycholic acid treatment increases whole-body energy expenditure.\n\nCANDIDATE_ABSTRACT:\nTITLE: Junctional actin assembly is mediated by Formin-like 2 downstream of Rac1\nABSTRACT: Epithelial integrity is vitally important, and its deregulation causes early stage cancer. De novo formation of an adherens junction (AJ) between single epithelial cells requires coordinated, spatial actin dynamics, but the mechanisms steering nascent actin polymerization for cell-cell adhesion initiation are not well understood. Here we investigated real-time actin assembly during daughter cell-cell adhesion formation in human breast epithelial cells in 3D environments. We identify formin-like 2 (FMNL2) as being specifically required for actin assembly and turnover at newly formed cell-cell contacts as well as for human epithelial lumen formation. FMNL2 associates with components of the AJ complex involving Rac1 activity and the FMNL2 C terminus. Optogenetic control of Rac1 in living cells rapidly drove FMNL2 to epithelial cell-cell contact zones. Furthermore, Rac1-induced actin assembly and subsequent AJ formation critically depends on FMNL2. These data uncover FMNL2 as a driver for human epithelial AJ formation downstream of Rac1.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 248, "doc_id": "2576811", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Deletion of ATM and Rad3 related protein leads to acute tissue loss.\n\nCANDIDATE_PASSAGE:\nThe Immune Response to Melanoma Is Limited by Thymic Selection of Self-Antigens The expression of melanoma-associated antigens (MAA) being limited to normal melanocytes and melanomas, MAAs are ideal targets for immunotherapy and melanoma vaccines. As MAAs are derived from self, immune responses to these may be limited by thymic tolerance. The extent to which self-tolerance prevents efficient immune responses to MAAs remains unknown. The autoimmune regulator (AIRE) controls the expression of tissue-specific self-antigens in thymic epithelial cells (TECs). The level of antigens expressed in the TECs determines the fate of auto-reactive thymocytes. Deficiency in AIRE leads in both humans (APECED patients) and mice to enlarged autoreactive immune repertoires. Here we show increased IgG levels to melanoma cells in APECED patients correlating with autoimmune skin features. Similarly, the enlarged T cell repertoire in AIRE(-/-) mice enables them to mount anti-MAA and anti-melanoma responses as shown by increased anti-melanoma antibodies, and enhanced CD4(+) and MAA-specific CD8(+) T cell responses after melanoma challenge. We show that thymic expression of gp100 is under the control of AIRE, leading to increased gp100-specific CD8(+) T cell frequencies in AIRE(-/-) mice. TRP-2 (tyrosinase-related protein), on the other hand, is absent from TECs and consequently TRP-2 specific CD8(+) T cells were found in both AIRE(-/-) and AIRE(+/+) mice. This study emphasizes the importance of investigating thymic expression of self-antigens prior to their inclusion in vaccination and immunotherapy strategies.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "326", "doc_id": "18488986", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: There is an inverse relationship between hip fractures and statin use.\n\nCANDIDATE_ABSTRACT:\nTITLE: HMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients.\nABSTRACT: CONTEXT Recent animal studies have found that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) lipid-lowering drugs (statins) substantially increase bone formation, but whether statin use in humans results in clinically meaningful bone formation or a reduction in the risk of osteoporotic fractures is not known. OBJECTIVE To determine whether the use of statins is associated with reduced hip fracture risk. DESIGN Case-control study. SETTING AND PATIENTS A total of 6110 New Jersey residents aged 65 years or older and enrolled in Medicare and either Medicaid or the Pharmacy Assistance for the Aged and Disabled program. Case patients (n=1222) underwent surgical repair of a hip fracture in 1994. Control patients (n=4888) were identified at a ratio of 4:1 and frequency-matched to case patients for age and sex. MAIN OUTCOME MEASURE Adjusted odds ratio (OR) of hip fracture by statin use in the 180 days and 3 years prior to the index date (the earliest date of admission for surgery), adjusted for demographic and clinical characteristics and health care utilization. RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus. No significant relationship was observed between use of nonstatin lipid-lowering agents and hip fracture risk. Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowe [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowering agents.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1290, "doc_id": "4687948", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: High levels of CRP reduces the risk of exacerbations in chronic obstructive pulmonary disease (COPD).\n\nCANDIDATE_PASSAGE:\nInflammatory biomarkers and exacerbations in chronic obstructive pulmonary disease. IMPORTANCE Exacerbations of respiratory symptoms in chronic obstructive pulmonary disease (COPD) have profound and long-lasting adverse effects on patients. OBJECTIVE To test the hypothesis that elevated levels of inflammatory biomarkers in individuals with stable COPD are associated with an increased risk of having exacerbations. DESIGN, SETTING, AND PARTICIPANTS Prospective cohort study examining 61,650 participants with spirometry measurements from the Copenhagen City Heart Study (2001-2003) and the Copenhagen General Population Study (2003-2008). Of these, 6574 had COPD, defined as a ratio between forced expiratory volume in 1 second (FEV1) and forced vital capacity below 0.7. MAIN OUTCOMES AND MEASURES Baseline levels of C-reactive protein (CRP) and fibrinogen and leukocyte count were measured in participants at a time when they were not experiencing symptoms of exacerbations. Exacerbations were recorded and defined as short-course treatment with oral corticosteroids alone or in combination with an antibiotic or as a hospital admission due to COPD. Levels of CRP and fibrinogen and leukocyte count were defined as high or low according to cut points of 3 mg/L, 14 μmol/L, and 9 ×10(9)/L, respectively. RESULTS During follow-up, 3083 exacerbations were recorded (mean, 0.5/participant). In the first year of follow-up, multivariable-adjusted odds ratios for having frequent exacerbations were 1.2 (95% CI, 0.7-2.2; 17 events/1000 person-years) for individuals with 1 high biomarker, 1.7 (95% CI, 0.9-3.2; 32 events/1000 person-years) for individuals with 2 high biomarkers, and 3.7 (95% CI, 1.9-7.4; 81 events/1000 person-years) for individuals with 3 high biomarkers compared with in [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "516", "doc_id": "29564505", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is biofilm formation a prerequisite for production of the antibacterial compound tropodithietic acid in Phaeobacter inhibens DSM17395?\n\nABSTRACT:\nThe goal of this study was to investigate if biofilm formation on population level is a physiological requirement for antagonism in Phaeobacter inhibens DSM17395, since the antibiotic compound tropodithietic acid (TDA) is produced by several Roseobacter clade species during growth as multicellular aggregates or biofilms at the air-liquid interface and is induced on single cell level upon attachment. A mutant library was created by Tn5 transposon insertion and 22 TDA-positive (brown) mutants with decreased biofilm formation or adhesion, and eight TDA-negative (white) mutants with increased biofilm formation or adhesion were selected. None of the selected biofilm-overproducing white mutants showed any antibiotic activity, while all brown mutants with reduced or disabled biofilm formation produced the antibacterial compound. Sequencing analysis indicated that genes that are likely involved in EPS/LPS production, motility and chemotaxis, and redox regulation play a role in biofilm formation and/or adhesion in P. inhibens DSM17395.", "output": "{\"label\": \"no\", \"rationale\": \"Cell aggregation and biofilm formation are not physiological prerequisites for TDA production.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25284322, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The NF-κB essential modulator gene induces intestinal inflammation by promoting receptor-interacting protein (RIP) kinase 1 kinase activity-mediated epithelial cell death.\n\nCANDIDATE_PASSAGE:\np62/SQSTM1 by Binding to Vitamin D Receptor Inhibits Hepatic Stellate Cell Activity, Fibrosis, and Liver Cancer. Hepatic stellate cells (HSCs) play critical roles in liver fibrosis and hepatocellular carcinoma (HCC). Vitamin D receptor (VDR) activation in HSCs inhibits liver inflammation and fibrosis. We found that p62/SQSTM1, a protein upregulated in liver parenchymal cells but downregulated in HCC-associated HSCs, negatively controls HSC activation. Total body or HSC-specific p62 ablation potentiates HSCs and enhances inflammation, fibrosis, and HCC progression. p62 directly interacts with VDR and RXR promoting their heterodimerization, which is critical for VDR:RXR target gene recruitment. Loss of p62 in HSCs impairs the repression of fibrosis and inflammation by VDR agonists. This demonstrates that p62 is a negative regulator of liver inflammation and fibrosis through its ability to promote VDR signaling in HSCs, whose activation supports HCC.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1170", "doc_id": "3701541", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Klf4 is not required for proper myeloid cell differentiation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Kruppel-like factor 4 is essential for inflammatory monocyte differentiation in vivo.\nABSTRACT: Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types. We demonstrate in this study that hematopoietic cells from KLF4(-/-) fetal livers (FL) contained normal numbers of functional hematopoietic progenitor cells, were radioprotective, and performed as well as KLF4(+/+) cells in competitive repopulation assays. However, hematopoietic \"KLF4(-/-) chimeras\" generated by transplantation of KLF4(-/-) fetal livers cells into lethally irradiated wild-type mice completely lacked circulating inflammatory (CD115(+)Gr1(+)) monocytes, and had reduced numbers of resident (CD115(+)Gr1(-)) monocytes. Although the numbers and function of peritoneal macrophages were normal in KLF4(-/-) chimeras, bone marrow monocytic cells from KLF4(-/-) chimeras expressed lower levels of key trafficking molecules and were more apoptotic. Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes. In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells. The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 669, "doc_id": "25148216", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Women with a lower birth weight are more likely to develop breast cancer later in life.\n\nCANDIDATE_PASSAGE:\nIntrauterine factors and risk of breast cancer: a systematic review and meta-analysis of current evidence. BACKGROUND Emerging evidence suggests an association between female prenatal experience and her subsequent risk of developing breast cancer. Potential underlying mechanisms include variation in amounts of maternal endogenous sex hormones and growth hormones, germ-cell mutations, formation of cancer stem-cells, and other genetic or epigenetic events. We reviewed and summarised quantitatively the available data on intrauterine exposures and risk of breast cancer. METHODS We systematically searched for studies that assessed association between perinatal factors and risk of breast cancer. We reviewed separately each of the perinatal factors, including birthweight, birth length, parental age at delivery, gestational age, intrauterine exposure to diethylstilbestrol, twin membership, maternal pre-eclampsia or eclampsia, and other factors. FINDINGS We identified 57 studies published between Oct 1, 1980, and June 21, 2007. Increased risk of breast cancer was noted with increased birthweight (relative risk [RR] 1.15 [95% CI 1.09-1.21]), birth length (1.28 [1.11-1.48]), higher maternal age (1.13 [1.02-1.25]), and paternal age (1.12 [1.05-1.19]). Decreased risk of breast cancer was noted for maternal pre-eclampsia and eclampsia (0.48 [0.30-0.78]) and twin membership (0.93 [0.87-1.00]). No association was noted between risk of breast cancer and gestational age at birth (0.95 [0.71-1.26]) or maternal diethylstilbestrol treatment (1.40 [0.86-2.28]). INTERPRETATION The intrauterine environment contributes to the predisposition of women to breast cancer in adulthood. The in-utero mechanisms responsible for such predisposition need to be elucidated.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1380", "doc_id": "23557241", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Mice that lack Interferon-γ or its receptor exhibit high resistance to experimental autoimmune myocarditis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Lethal autoimmune myocarditis in interferon-gamma receptor-deficient mice: enhanced disease severity by impaired inducible nitric oxide synthase induction.\nABSTRACT: BACKGROUND Interferon-gamma (IFN-gamma) is an essential cytokine in the regulation of inflammatory responses in autoimmune diseases. Little is known about its role in inflammatory heart disease. METHODS AND RESULTS We showed that IFN-gamma receptor-deficient mice (IFN-gammaR(-/-)) on a BALB/c background immunized with a peptide derived from cardiac alpha-myosin heavy chain develop severe myocarditis with high mortality. Although myocarditis subsided in wild-type mice after 3 weeks, IFN-gammaR(-/-) mice showed persistent disease. The persistent inflammation was accompanied by vigorous in vitro CD4 T-cell responses and impaired inducible nitric oxide synthase expression, together with evidence of impaired nitric oxide production in IFN-gammaR(-/-) hearts. Treatment of wild-type mice with the nitric oxide synthetase inhibitor N:-nitro-l-arginine-methyl-ester enhanced in vitro CD4 T-cell proliferation and prevented healing of myocarditis. CONCLUSIONS Our data provide evidence that IFN-gamma protects mice from lethal autoimmune myocarditis by inducing the expression of inducible nitric oxide synthase followed by the downregulation of T-cell responses.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Although myocarditis subsided in wild-type mice after 3 weeks, IFN-gammaR(-/-) mice showed persistent disease.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 781, "doc_id": "24338780", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Autophagy deficiency in the liver increases vulnerability to insulin resistance.\n\nCANDIDATE_ABSTRACT:\nTITLE: Autophagy deficiency leads to protection from obesity and insulin resistance by inducing Fgf21 as a mitokine\nABSTRACT: Despite growing interest and a recent surge in papers, the role of autophagy in glucose and lipid metabolism is unclear. We produced mice with skeletal muscle–specific deletion of Atg7 (encoding autophagy-related 7). Unexpectedly, these mice showed decreased fat mass and were protected from diet-induced obesity and insulin resistance; this phenotype was accompanied by increased fatty acid oxidation and browning of white adipose tissue (WAT) owing to induction of fibroblast growth factor 21 (Fgf21). Mitochondrial dysfunction induced by autophagy deficiency increased Fgf21 expression through induction of Atf4, a master regulator of the integrated stress response. Mitochondrial respiratory chain inhibitors also induced Fgf21 in an Atf4-dependent manner. We also observed induction of Fgf21, resistance to diet-induced obesity and amelioration of insulin resistance in mice with autophagy deficiency in the liver, another insulin target tissue. These findings suggest that autophagy deficiency and subsequent mitochondrial dysfunction promote Fgf21 expression, a hormone we consequently term a 'mitokine', and together these processes promote protection from diet-induced obesity and insulin resistance.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Unexpectedly, these mice showed decreased fat mass and were protected from diet-induced obesity and insulin resistance; this phenotype was accompanied by increased fatty acid oxidation and browning of white adipose tissue (WAT) owing to induction of fibroblast growth factor 21 (Fgf21).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 149, "doc_id": "6227220", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Cancers that initially benefit from epidermal growth factor receptor targeted therapies later become refractory through several mechanisms.\n\nCANDIDATE_PASSAGE:\nUncoupling of leading- and lagging-strand DNA replication during lesion bypass in vivo. Numerous agents attack DNA, forming lesions that impair normal replication. Specialized DNA polymerases transiently replace the replicative polymerase and copy past lesions, thus generating mutations, the major initiating cause of cancer. We monitored, in Escherichia coli, the kinetics of replication of both strands of DNA molecules containing a single replication block in either the leading or lagging strand. Despite a block in the leading strand, lagging-strand synthesis proceeded further, implying transient uncoupling of concurrent strand synthesis. Replication through the lesion requires specialized DNA polymerases and is achieved with similar kinetics and efficiencies in both strands.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "227", "doc_id": "41314611", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does shaving the incision site increase the infection rate after spinal surgery?\n\nABSTRACT:\nA prospective randomized clinical study. To determine whether shaving the incision site before spinal surgery causes postsurgical infection. Spine surgeons usually shave the skin of the incision site immediately before surgery is performed. However, evidence from some surgical series suggests that presurgical shaving may increase the postsurgical infection rate. To our knowledge, no previously published studies have addressed this issue. A total of 789 patients scheduled to undergo spinal surgery were randomly allocated into 2 groups: those in whom the site of operation was shaved immediately before surgery (shaved group; 371 patients) and the patients in whom presurgical shaving was not performed (unshaved group; 418 patients). The mean duration of anesthesia and the infection rates in both groups were recorded and compared. The duration of anesthesia did not differ in the 2 groups (P>0.05). A postoperative infection developed in 4 patients in the shaved group and in 1 patient in the nonshaved group (P<0.01).", "output": "{\"label\": \"maybe\", \"rationale\": \"The shaving of the incision site immediately before spinal surgery may increase the rate of postoperative infection.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 17621202, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: 4-PBA treatment raises endoplasmic reticulum stress in response to general endoplasmic reticulum stress markers.\n\nCANDIDATE_PASSAGE:\nComparative determinants of 4-year cardiovascular event rates in stable outpatients at risk of or with atherothrombosis. CONTEXT Clinicians and trialists have difficulty with identifying which patients are highest risk for cardiovascular events. Prior ischemic events, polyvascular disease, and diabetes mellitus have all been identified as predictors of ischemic events, but their comparative contributions to future risk remain unclear. OBJECTIVE To categorize the risk of cardiovascular events in stable outpatients with various initial manifestations of atherothrombosis using simple clinical descriptors. DESIGN, SETTING, AND PATIENTS Outpatients with coronary artery disease, cerebrovascular disease, or peripheral arterial disease or with multiple risk factors for atherothrombosis were enrolled in the global Reduction of Atherothrombosis for Continued Health (REACH) Registry and were followed up for as long as 4 years. Patients from 3647 centers in 29 countries were enrolled between 2003 and 2004 and followed up until 2008. Final database lock was in April 2009. MAIN OUTCOME MEASURES Rates of cardiovascular death, myocardial infarction, and stroke. RESULTS A total of 45,227 patients with baseline data were included in this 4-year analysis. During the follow-up period, a total of 5481 patients experienced at least 1 event, including 2315 with cardiovascular death, 1228 with myocardial infarction, 1898 with stroke, and 40 with both a myocardial infarction and stroke on the same day. Among patients with atherothrombosis, those with a prior history of ischemic events at baseline (n = 21,890) had the highest rate of subsequent ischemic events (18.3%; 95% confidence interval [CI], 17.4%-19.1%); patients with stable coronary, cerebrovascular, or peripheral artery dise [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "11", "doc_id": "16760369", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does use of hydrophilic guidewires significantly improve technical success rates of peripheral PTA?\n\nABSTRACT:\nTo determine whether the use of hydrophilic guidewires has increased the technical success rate of peripheral percutaneous transluminal angioplasty (PTA).MATERIAL/ We performed 125 procedures and analyzed the technical success rates of PTA using the conventional guidewire first and then if needed, the hydrophilic guidewire for iliac and SFA stenoses or occlusions. Angioplasty was performed on 25 stenosed, 25 occluded iliac arteries and 25 stenosed, 50 occluded femoral arteries. The result was defined as technical success when the lesion was crossed by a guidewire and balloon, then it was dilated with restoration of vessel lumen and less than 30% residual stenosis and the rise in ABI values was at least 0.15 after 24 hours. The technical success rate after PTA of stenosed iliac arteries was achieved in 96% (24/25) using conventional wires and 100% using hydrophilic guidewire; in iliac occlusions, the rates were 60% (15/25) and 96%, respectively; in femoral stenosis - 84% (21/25) and 100%; in occlusions in the first group: lesions<10 cm -64% (16/25) and 96%, in the second group: lesions>10 cm -48% (12/25) and 88%. In the iliac group, there was no significant difference in the success of iliac stenosis PTA. However, there were significant changes in the success rates of PTA performed for SFA stenosis and iliac and SFA occlusions.", "output": "{\"label\": \"maybe\", \"rationale\": \"In summary, we report an overall improvement and high technical success rate for peripherial PTA. The use of hydrophilic guidewires made significant difference to the technical success rate of PTA, especially in occlusion and more complicated lesions.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 16538201, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Medications to treat obesity do not have side effects.\n\nCANDIDATE_PASSAGE:\nA parasomnia overlap disorder involving sleepwalking, sleep terrors, and REM sleep behavior disorder in 33 polysomnographically confirmed cases. A series of 33 patients with combined (injurious) sleepwalking, sleep terrors, and rapid eye movement (REM) sleep behavior disorder (viz. \"parasomnia overlap disorder\") was gathered over an 8-year period. Patients underwent clinical and polysomnographic evaluations. Mean age was 34 +/- 14 (SD) years; mean age of parasomnia onset was 15 +/- 16 years (range 1-66); 70% (n = 23) were males. An idiopathic subgroup (n = 22) had a significantly earlier mean age of parasomnia onset (9 +/- 7 years) than a symptomatic subgroup (n = 11) (27 +/- 23 years, p = 0.002), whose parasomnia began with either of the following: neurologic disorders, n = 6 [congenital Mobius syndrome, narcolepsy, multiple sclerosis, brain tumor (and treatment), brain trauma, indeterminate disorder (exaggerated startle response/atypical cataplexy)]; nocturnal paroxysmal atrial fibrillation, n = 1; posttraumatic stress disorder/major depression, n = 1; chronic ethanol/amphetamine abuse and withdrawal, n = 1; or mixed disorders (schizophrenia, brain trauma, substance abuse), n = 2. The rate of DSM-III-R (Diagnostic and Statistical Manual, 3rd edition, revised) Axis 1 psychiatric disorders was not elevated; group scores on various psychometric tests were not elevated. Forty-five percent (n = 15) had previously received psychologic or psychiatric therapy for their parasomnia, without benefit. Treatment outcome was available for n = 20 patients; 90% (n = 18) had substantial parasomnia control with bedtime clonazepam (n = 13), alprazolam and/or carbamazepine (n = 4), or self-hypnosis (n = 1). Thus, \"parasomnia overlap disorder\" is a treatable condition that eme [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "765", "doc_id": "21373821", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Febrile seizures reduce the threshold for development of epilepsy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Febrile seizures in the developing brain result in persistent modification of neuronal excitability in limbic circuits\nABSTRACT: Febrile (fever-induced) seizures affect 3–5% of infants and young children. Despite the high incidence of febrile seizures, their contribution to the development of epilepsy later in life has remained controversial. Combining a new rat model of complex febrile seizures and patch clamp techniques, we determined that hyperthermia-induced seizures in the immature rat cause a selective presynaptic increase in inhibitory synaptic transmission in the hippocampus that lasts into adulthood. The long-lasting nature of these potent alterations in synaptic communication after febrile seizures does not support the prevalent view of the 'benign' nature of early-life febrile convulsions.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 411, "doc_id": "14924526", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Bariatric surgery leads to negative outcomes in mental health.\n\nCANDIDATE_ABSTRACT:\nTITLE: Host–Parasite Interactions and the Evolution of Gene Expression\nABSTRACT: Interactions between hosts and parasites provide an ongoing source of selection that promotes the evolution of a variety of features in the interacting species. Here, we use a genetically explicit mathematical model to explore how patterns of gene expression evolve at genetic loci responsible for host resistance and parasite infection. Our results reveal the striking yet intuitive conclusion that gene expression should evolve along very different trajectories in the two interacting species. Specifically, host resistance loci should frequently evolve to co-express alleles, whereas parasite infection loci should evolve to express only a single allele. This result arises because hosts that co-express resistance alleles are able to recognize and clear a greater diversity of parasite genotypes. By the same token, parasites that co-express antigen or elicitor alleles are more likely to be recognized and cleared by the host, and this favours the expression of only a single allele. Our model provides testable predictions that can help interpret accumulating data on expression levels for genes relevant to host−parasite interactions.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 166, "doc_id": "1852826", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Increased microtubule acetylation repairs interference of axonal transport caused by LRRK2 Roc-COR domain mutations.\n\nCANDIDATE_ABSTRACT:\nTITLE: 6-phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumor growth by inhibiting LKB1-AMPK signaling\nABSTRACT: The oxidative pentose phosphate pathway (PPP) contributes to tumour growth, but the precise contribution of 6-phosphogluconate dehydrogenase (6PGD), the third enzyme in this pathway, to tumorigenesis remains unclear. We found that suppression of 6PGD decreased lipogenesis and RNA biosynthesis and elevated ROS levels in cancer cells, attenuating cell proliferation and tumour growth. 6PGD-mediated production of ribulose-5-phosphate (Ru-5-P) inhibits AMPK activation by disrupting the active LKB1 complex, thereby activating acetyl-CoA carboxylase 1 and lipogenesis. Ru-5-P and NADPH are thought to be precursors in RNA biosynthesis and lipogenesis, respectively; thus, our findings provide an additional link between the oxidative PPP and lipogenesis through Ru-5-P-dependent inhibition of LKB1-AMPK signalling. Moreover, we identified and developed 6PGD inhibitors, physcion and its derivative S3, that effectively inhibited 6PGD, cancer cell proliferation and tumour growth in nude mice xenografts without obvious toxicity, suggesting that 6PGD could be an anticancer target.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 614, "doc_id": "1686997", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does carbohydrate supplementation blunt the prolonged exercise-induced reduction of in vivo immunity?\n\nABSTRACT:\nCarbohydrate (CHO) supplementation during prolonged exercise is widely acknowledged to blunt in vitro immunoendocrine responses, but no study has investigated in vivo immunity. To determine the effect of CHO supplementation during prolonged exercise on in vivo immune induction using experimental contact hypersensitivity with the novel antigen diphenylcyclopropenone (DPCP). In a double-blind design, 32 subjects were randomly assigned to 120 min of treadmill exercise at 60 % [Formula: see text] with CHO (Ex-CHO) or placebo (Ex-PLA) supplementation. Responses were also compared to 16 resting control (CON) subjects from a previous study (for additional comparison with a resting non-exercise condition). Standardised diets (24 h pre-trial) and breakfasts (3.5 h pre-trial) were provided. Subjects received a primary DPCP exposure (sensitisation) 20 min after trial completion, and exactly 28 days later the strength of immune reactivity was quantified by magnitude of the cutaneous response (skin-fold thickness and erythema) to a low dose-series DPCP challenge. Stress hormones and leucocyte trafficking were also monitored. CHO supplementation blunted the cortisol and leucocyte trafficking responses, but there was no difference (P > 0.05) between Ex-CHO and Ex-PLA in the in vivo immune responses (e.g. both ~46 % lower than CON for skin-fold response).", "output": "{\"label\": \"no\", \"rationale\": \"CHO supplementation does not influence the decrease in in vivo immunity seen after prolonged exercise. The effects with more stressful (or fasted) exercise remain to be determined. However, there appears to be no benefit under the conditions of the present study, which have practical relevance to what many athletes do in training or competition.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 26163337, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Sepsis related mortality has remained stable between 2009-2014.\n\nCANDIDATE_ABSTRACT:\nTITLE: Incidence and Trends of Sepsis in US Hospitals Using Clinical vs Claims Data, 2009-2014\nABSTRACT: Importance Estimates from claims-based analyses suggest that the incidence of sepsis is increasing and mortality rates from sepsis are decreasing. However, estimates from claims data may lack clinical fidelity and can be affected by changing diagnosis and coding practices over time. Objective To estimate the US national incidence of sepsis and trends using detailed clinical data from the electronic health record (EHR) systems of diverse hospitals. Design, Setting, and Population Retrospective cohort study of adult patients admitted to 409 academic, community, and federal hospitals from 2009-2014. Exposures Sepsis was identified using clinical indicators of presumed infection and concurrent acute organ dysfunction, adapting Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) criteria for objective and consistent EHR-based surveillance. Main Outcomes and Measures Sepsis incidence, outcomes, and trends from 2009-2014 were calculated using regression models and compared with claims-based estimates using International Classification of Diseases, Ninth Revision, Clinical Modification codes for severe sepsis or septic shock. Case-finding criteria were validated against Sepsis-3 criteria using medical record reviews. Results A total of 173 690 sepsis cases (mean age, 66.5 [SD, 15.5] y; 77 660 [42.4%] women) were identified using clinical criteria among 2 901 019 adults admitted to study hospitals in 2014 (6.0% incidence). Of these, 26 061 (15.0%) died in the hospital and 10 731 (6.2%) were discharged to hospice. From 2009-2014, sepsis incidence using clinical criteria was stable (+0.6% relative change/y [95% CI, −2.3% to 3.5%], P = .67) whereas incidence per claims increased (+10.3%/y [95% CI, 7.2% to 13.3%], P < .001). In-hospital morta [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Conclusions and Relevance In clinical data from 409 hospitals, sepsis was present in 6% of adult hospitalizations, and in contrast to claims-based analyses, neither the incidence of sepsis nor the combined outcome of death or discharge to hospice changed significantly between 2009-2014.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1072, "doc_id": "4824840", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Trans-acting factors, such as lncRNAs, influence mRNA translation.\n\nCANDIDATE_ABSTRACT:\nTITLE: LincRNA-p21 suppresses target mRNA translation.\nABSTRACT: Mammalian long intergenic noncoding RNAs (lincRNAs) are best known for modulating transcription. Here we report a posttranscriptional function for lincRNA-p21 as a modulator of translation. Association of the RNA-binding protein HuR with lincRNA-p21 favored the recruitment of let-7/Ago2 to lincRNA-p21, leading to lower lincRNA-p21 stability. Under reduced HuR levels, lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and β-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1311, "doc_id": "13763195", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Reducing H3k4me3 methylation induces mouse epiblast stem cells to naive pluripotency efficiently.\n\nCANDIDATE_PASSAGE:\nAnaphase-Promoting Complex/Cyclosome–Dependent Proteolysis of Human Cyclin a Starts at the Beginning of Mitosis and Is Not Subject to the Spindle Assembly Checkpoint Cyclin A is a stable protein in S and G2 phases, but is destabilized when cells enter mitosis and is almost completely degraded before the metaphase to anaphase transition. Microinjection of antibodies against subunits of the anaphase-promoting complex/cyclosome (APC/C) or against human Cdc20 (fizzy) arrested cells at metaphase and stabilized both cyclins A and B1. Cyclin A was efficiently polyubiquitylated by Cdc20 or Cdh1-activated APC/C in vitro, but in contrast to cyclin B1, the proteolysis of cyclin A was not delayed by the spindle assembly checkpoint. The degradation of cyclin B1 was accelerated by inhibition of the spindle assembly checkpoint. These data suggest that the APC/C is activated as cells enter mitosis and immediately targets cyclin A for degradation, whereas the spindle assembly checkpoint delays the degradation of cyclin B1 until the metaphase to anaphase transition. The “destruction box” (D-box) of cyclin A is 10–20 residues longer than that of cyclin B. Overexpression of wild-type cyclin A delayed the metaphase to anaphase transition, whereas expression of cyclin A mutants lacking a D-box arrested cells in anaphase.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1030", "doc_id": "600808", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Higher plasma levels of I-carnitine, when associated with trimethylamine N-oxide, are negatively correlated with cardiovascular events in humans.\n\nCANDIDATE_ABSTRACT:\nTITLE: Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis\nABSTRACT: Intestinal microbiota metabolism of choline and phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO). We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice. Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism. The presence of specific bacterial taxa in human feces was associated with both plasma TMAO concentration and dietary status. Plasma L-carnitine levels in subjects undergoing cardiac evaluation (n = 2,595) predicted increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels. Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed. In mice with an intact intestinal microbiota, dietary supplementation with TMAO or either carnitine or choline reduced in vivo reverse cholesterol transport. Intestinal microbiota may thus contribute to the well-established link between high levels of red meat consumption and CVD risk.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 523, "doc_id": "14803797", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Beta-band coherence is diminished for visible stimuli over invisible stimuli.\n\nCANDIDATE_PASSAGE:\nA transition in brain state during propofol-induced unconsciousness. Rhythmic oscillations shape cortical dynamics during active behavior, sleep, and general anesthesia. Cross-frequency phase-amplitude coupling is a prominent feature of cortical oscillations, but its role in organizing conscious and unconscious brain states is poorly understood. Using high-density EEG and intracranial electrocorticography during gradual induction of propofol general anesthesia in humans, we discovered a rapid drug-induced transition between distinct states with opposite phase-amplitude coupling and different cortical source distributions. One state occurs during unconsciousness and may be similar to sleep slow oscillations. A second state occurs at the loss or recovery of consciousness and resembles an enhanced slow cortical potential. These results provide objective electrophysiological landmarks of distinct unconscious brain states, and could be used to help improve EEG-based monitoring for general anesthesia.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "174", "doc_id": "8734695", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Combination nicotine replacement therapies with varenicline or bupropion lead to significantly higher long-term abstinence rates at 52 weeks than varenicline monotherapy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Combination varenicline and bupropion SR for tobacco-dependence treatment in cigarette smokers: a randomized trial.\nABSTRACT: IMPORTANCE Combining pharmacotherapies for tobacco-dependence treatment may increase smoking abstinence. OBJECTIVE To determine efficacy and safety of varenicline and bupropion sustained-release (SR; combination therapy) compared with varenicline (monotherapy) in cigarette smokers. DESIGN, SETTING, AND PARTICIPANTS Randomized, blinded, placebo-controlled multicenter clinical trial with a 12-week treatment period and follow-up through week 52 conducted between October 2009 and April 2013 at 3 midwestern clinical research sites. Five hundred six adult (≥18 years) cigarette smokers were randomly assigned and 315 (62%) completed the study. INTERVENTIONS Twelve weeks of varenicline and bupropion SR or varenicline and placebo. MAIN OUTCOMES AND MEASURES Primary outcome was abstinence rates at week 12, defined as prolonged (no smoking from 2 weeks after the target quit date) abstinence and 7-day point-prevalence (no smoking past 7 days) abstinence. Secondary outcomes were prolonged and point-prevalence smoking abstinence rates at weeks 26 and 52. Outcomes were biochemically confirmed. RESULTS At 12 weeks, 53.0% of the combination therapy group achieved prolonged smoking abstinence and 56.2% achieved 7-day point-prevalence smoking abstinence compared with 43.2% and 48.6% in varenicline monotherapy (odds ratio [OR], 1.49; 95% CI, 1.05-2.12; P = .03 and OR, 1.36; 95% CI, 0.95-1.93; P = .09, respectively). At 26 weeks, 36.6% of the combination therapy group achieved prolonged and 38.2% achieved 7-day point-prevalence smoking abstinence compared with 27.6% and 31.9% in varenicline monotherapy (OR, 1.52; 95% CI, 1.04-2.22; P = .03 and OR, 1.32; 95% CI, 0.91-1.91; P = .14, respectively). At 52 weeks, 30.9% of the combination therapy group achieved prolonged and 36.6% achi [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Neither outcome was significantly different at 52 weeks.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 274, "doc_id": "11614737", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Ly6C hi monocytes have a higher inflammatory capacity than Ly6C lo monocytes.\n\nCANDIDATE_PASSAGE:\nFate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis. Mononuclear phagocytes, including monocytes, macrophages, and dendritic cells, contribute to tissue integrity as well as to innate and adaptive immune defense. Emerging evidence for labor division indicates that manipulation of these cells could bear therapeutic potential. However, specific ontogenies of individual populations and the overall functional organization of this cellular network are not well defined. Here we report a fate-mapping study of the murine monocyte and macrophage compartment taking advantage of constitutive and conditional CX(3)CR1 promoter-driven Cre recombinase expression. We have demonstrated that major tissue-resident macrophage populations, including liver Kupffer cells and lung alveolar, splenic, and peritoneal macrophages, are established prior to birth and maintain themselves subsequently during adulthood independent of replenishment by blood monocytes. Furthermore, we have established that short-lived Ly6C(+) monocytes constitute obligatory steady-state precursors of blood-resident Ly6C(-) cells and that the abundance of Ly6C(+) blood monocytes dynamically controls the circulation lifespan of their progeny.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "726", "doc_id": "7521113", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Bactericidal activity of 3 cutaneous/mucosal antiseptic solutions in the presence of interfering substances: Improvement of the NF EN 13727 European Standard?\n\nABSTRACT:\nThere is no standard protocol for the evaluation of antiseptics used for skin and mucous membranes in the presence of interfering substances. Our objective was to suggest trial conditions adapted from the NF EN 13727 standard, for the evaluation of antiseptics used in gynecology and dermatology. Three antiseptic solutions were tested in vitro: a chlorhexidine-benzalkonium (CB) combination, a hexamidine-chlorhexidine-chlorocresol (HCC) combination, and povidone iodine (P). The adaptation of trial conditions to the standard involved choosing dilutions, solvent, and interfering substances. The activity of solutions was assessed on the recommended strains at concentrations of 97% (pure solution), 50%, and 10% (diluted solution), and 1%. A logarithmic reduction ≥ 5 was expected after 60seconds of contact, to meet requirements of bactericidal activity. HCC did not present any bactericidal activity except on P. aeruginosa at a concentration of 97%. P was not bactericidal on E. hirae at any concentration and on S. aureus at 97%. CB had the most homogeneous bactericidal activity with a reduction>5 log on the 4 bacterial strains at concentrations of 97%, 50% and 10%.", "output": "{\"label\": \"maybe\", \"rationale\": \"Adapting the NF EN 13727 standard allowed assessing the 3 tested solutions: only CB was bactericidal in dirty conditions. This study proved the possibility of validating antiseptic choice in vitro, in current practice conditions, for adjunctive treatment of skin and mucous membranes disorders, primarily of bacterial origin or with a potential of superinfection.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 25779009, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The minor G allele of FOXO3 is related to more severe symptoms of Crohn's Disease.\n\nCANDIDATE_PASSAGE:\nResponse to self antigen imprints regulatory memory in tissues Immune homeostasis in tissues is achieved through a delicate balance between pathogenic T-cell responses directed at tissue-specific antigens and the ability of the tissue to inhibit these responses. The mechanisms by which tissues and the immune system communicate to establish and maintain immune homeostasis are currently unknown. Clinical evidence suggests that chronic or repeated exposure to self antigen within tissues leads to an attenuation of pathological autoimmune responses, possibly as a means to mitigate inflammatory damage and preserve function. Many human organ-specific autoimmune diseases are characterized by the initial presentation of the disease being the most severe, with subsequent flares being of lesser severity and duration. In fact, these diseases often spontaneously resolve, despite persistent tissue autoantigen expression. In the practice of antigen-specific immunotherapy, allergens or self antigens are repeatedly injected in the skin, with a diminution of the inflammatory response occurring after each successive exposure. Although these findings indicate that tissues acquire the ability to attenuate autoimmune reactions upon repeated responses to antigens, the mechanism by which this occurs is unknown. Here we show that upon expression of self antigen in a peripheral tissue, thymus-derived regulatory T cells (Treg cells) become activated, proliferate and differentiate into more potent suppressors, which mediate resolution of organ-specific autoimmunity in mice. After resolution of the inflammatory response, activated Treg cells are maintained in the target tissue and are primed to attenuate subsequent autoimmune reactions when antigen is re-expressed. Thus, Treg cells func [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1232", "doc_id": "4380287", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Reduction of Rpl38 alters the composition of the Hox gene mRNAs translation in mice without lowering overall protein synthesis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Ribosome-Mediated Specificity in Hox mRNA Translation and Vertebrate Tissue Patterning\nABSTRACT: Historically, the ribosome has been viewed as a complex ribozyme with constitutive rather than regulatory capacity in mRNA translation. Here we identify mutations of the Ribosomal Protein L38 (Rpl38) gene in mice exhibiting surprising tissue-specific patterning defects, including pronounced homeotic transformations of the axial skeleton. In Rpl38 mutant embryos, global protein synthesis is unchanged; however the translation of a select subset of Homeobox mRNAs is perturbed. Our data reveal that RPL38 facilitates 80S complex formation on these mRNAs as a regulatory component of the ribosome to confer transcript-specific translational control. We further show that Rpl38 expression is markedly enriched in regions of the embryo where loss-of-function phenotypes occur. Unexpectedly, a ribosomal protein (RP) expression screen reveals dynamic regulation of individual RPs within the vertebrate embryo. Collectively, these findings suggest that RP activity may be highly regulated to impart a new layer of specificity in the control of gene expression and mammalian development.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In Rpl38 mutant embryos, global protein synthesis is unchanged; however the translation of a select subset of Homeobox mRNAs is perturbed.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1031, "doc_id": "12486491", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Ambulatory blood pressure monitoring is inaccurate at diagnosing hypertension.\n\nCANDIDATE_PASSAGE:\nRenal outcomes with different fixed-dose combination therapies in patients with hypertension at high risk for cardiovascular events (ACCOMPLISH): a prespecified secondary analysis of a randomised controlled trial. BACKGROUND The Avoiding Cardiovascular Events through Combination Therapy in Patients Living with Systolic Hypertension (ACCOMPLISH) trial showed that initial antihypertensive therapy with benazepril plus amlodipine was superior to benazepril plus hydrochlorothiazide in reducing cardiovascular morbidity and mortality. We assessed the effects of these drug combinations on progression of chronic kidney disease. METHODS ACCOMPLISH was a double-blind, randomised trial undertaken in five countries (USA, Sweden, Norway, Denmark, and Finland). 11 506 patients with hypertension who were at high risk for cardiovascular events were randomly assigned via a central, telephone-based interactive voice response system in a 1:1 ratio to receive benazepril (20 mg) plus amlodipine (5 mg; n=5744) or benazepril (20 mg) plus hydrochlorothiazide (12.5 mg; n=5762), orally once daily. Drug doses were force-titrated for patients to attain recommended blood pressure goals. Progression of chronic kidney disease, a prespecified endpoint, was defined as doubling of serum creatinine concentration or end-stage renal disease (estimated glomerular filtration rate <15 mL/min/1.73 m(2) or need for dialysis). Analysis was by intention to treat (ITT). This trial is registered with ClinicalTrials.gov, number NCT00170950. FINDINGS The trial was terminated early (mean follow-up 2.9 years [SD 0.4]) because of superior efficacy of benazepril plus amlodipine compared with benazepril plus hydrochlorothiazide. At trial completion, vital status was not known for 143 (1%) patients who were lost [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "106", "doc_id": "40790033", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Sepsis related mortality has remained stable between 2009-2014.\n\nCANDIDATE_ABSTRACT:\nTITLE: Incidence and Trends of Sepsis in US Hospitals Using Clinical vs Claims Data, 2009-2014\nABSTRACT: Importance Estimates from claims-based analyses suggest that the incidence of sepsis is increasing and mortality rates from sepsis are decreasing. However, estimates from claims data may lack clinical fidelity and can be affected by changing diagnosis and coding practices over time. Objective To estimate the US national incidence of sepsis and trends using detailed clinical data from the electronic health record (EHR) systems of diverse hospitals. Design, Setting, and Population Retrospective cohort study of adult patients admitted to 409 academic, community, and federal hospitals from 2009-2014. Exposures Sepsis was identified using clinical indicators of presumed infection and concurrent acute organ dysfunction, adapting Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) criteria for objective and consistent EHR-based surveillance. Main Outcomes and Measures Sepsis incidence, outcomes, and trends from 2009-2014 were calculated using regression models and compared with claims-based estimates using International Classification of Diseases, Ninth Revision, Clinical Modification codes for severe sepsis or septic shock. Case-finding criteria were validated against Sepsis-3 criteria using medical record reviews. Results A total of 173 690 sepsis cases (mean age, 66.5 [SD, 15.5] y; 77 660 [42.4%] women) were identified using clinical criteria among 2 901 019 adults admitted to study hospitals in 2014 (6.0% incidence). Of these, 26 061 (15.0%) died in the hospital and 10 731 (6.2%) were discharged to hospice. From 2009-2014, sepsis incidence using clinical criteria was stable (+0.6% relative change/y [95% CI, −2.3% to 3.5%], P = .67) whereas incidence per claims increased (+10.3%/y [95% CI, 7.2% to 13.3%], P < .001). In-hospital morta [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In-hospital mortality using clinical criteria declined (−3.3%/y [95% CI, −5.6% to −1.0%], P = .004), but there was no significant change in the combined outcome of death or discharge to hospice (−1.3%/y [95% CI, −3.2% to 0.6%], P = .19).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1072, "doc_id": "4824840", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: There is a positive correlation between hip fractures and statin use.\n\nCANDIDATE_ABSTRACT:\nTITLE: HMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients.\nABSTRACT: CONTEXT Recent animal studies have found that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) lipid-lowering drugs (statins) substantially increase bone formation, but whether statin use in humans results in clinically meaningful bone formation or a reduction in the risk of osteoporotic fractures is not known. OBJECTIVE To determine whether the use of statins is associated with reduced hip fracture risk. DESIGN Case-control study. SETTING AND PATIENTS A total of 6110 New Jersey residents aged 65 years or older and enrolled in Medicare and either Medicaid or the Pharmacy Assistance for the Aged and Disabled program. Case patients (n=1222) underwent surgical repair of a hip fracture in 1994. Control patients (n=4888) were identified at a ratio of 4:1 and frequency-matched to case patients for age and sex. MAIN OUTCOME MEASURE Adjusted odds ratio (OR) of hip fracture by statin use in the 180 days and 3 years prior to the index date (the earliest date of admission for surgery), adjusted for demographic and clinical characteristics and health care utilization. RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus. No significant relationship was observed between use of nonstatin lipid-lowering agents and hip fracture risk. Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowe [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowering agents.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1288, "doc_id": "4687948", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: TNFAIP3 is a tumor suppressor in glioblastoma.\n\nCANDIDATE_PASSAGE:\nPremature chromosome condensation: evidence for in vivo cell fusion in human malignant tumours. Premature chromosome condensation (PCC) was studied in direct preparations of tissues from patients with haematological diseases and carcinomas of various histological types. PCC was found in 6 out of 166 malignancies (128 haematological cases, 35 carcinomas and 3 malignant effusions) analysed with the GTG-technique. Chromosome analysis revealed S-phase and G1-phase PCC in each case; the frequency of PCC varied between 1, 4 and 8.6% of the metaphases analysed. It is suggested that PCC chromosomes, which represent cell fusion in vivo, are not very rare in naturally-occurring human malignancies, and that cell fusion may affect the malignant phenotype. In conjunction with other factors they may also explain the heterogeneity of tumour cell populations.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1137", "doc_id": "26182390", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Immune responses result in the development of inflammatory Th17 cells and anti-inflammatory iTregs.\n\nCANDIDATE_PASSAGE:\nRecent developments and complexities in neutrophil transmigration. PURPOSE OF REVIEW As the migration of neutrophils from blood to inflamed tissues is an essential component of innate immunity and a key contributing factor to the pathogenesis of inflammatory disorders, this aspect of leukocyte biology continues to be a highly dynamic field of research. This review summarizes recent findings in this area, focusing on the mechanisms that mediate neutrophil transmigration, an area where significant progress has been made. RECENT FINDINGS The topics to be covered will include responses that are prerequisite to neutrophil migration through venular walls, such as leukocyte luminal crawling and cellular and molecular changes in leukocytes and endothelial cells (e.g. formation of protrusions) that collectively support leukocyte transendothelial cell migration. Advances in both paracellular and transcellular neutrophil migration through endothelial cells will be discussed, addressing the associated roles and regulation of expression of endothelial cell luminal and junctional adhesion molecules. Beyond the endothelium, migration through the vascular pericyte coverage and basement membrane will be reviewed. SUMMARY The unquestionable role of neutrophils in the development and progression of inflammatory conditions suggests that a better understanding of the tissue-specific and stimulus-specific mechanisms that mediate this response may identify novel pathways that could be exploited for the development of more specific anti-inflammatory interventions.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "560", "doc_id": "20608982", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does normothermic normokalemic simultaneous antegrade/retrograde perfusion improve myocardial oxygenation and energy metabolism for hypertrophied hearts?\n\nABSTRACT:\nBeating-heart valve surgery appears to be a promising technique for protection of hypertrophied hearts. Normothermic normokalemic simultaneous antegrade/retrograde perfusion (NNSP) may improve myocardial perfusion. However, its effects on myocardial oxygenation and energy metabolism remain unclear. The present study was to determine whether NNSP improved myocardial oxygenation and energy metabolism of hypertrophied hearts relative to normothermic normokalemic antegrade perfusion (NNAP). Twelve hypertrophied pig hearts underwent a protocol consisting of three 20-minute perfusion episodes (10 minutes NNAP and 10 minutes NNSP in a random order) with each conducted at a different blood flow in the left anterior descending coronary artery (LAD [100%, 50%, and 20% of its initial control]). Myocardial oxygenation was assessed using near-infrared spectroscopic imaging. Myocardial energy metabolism was monitored using localized phosphorus-31 magnetic resonance spectroscopy. With 100% LAD flow, both NNAP and NNSP maintained myocardial oxygenation, adenosine triphosphate, phosphocreatine, and inorganic phosphate at normal levels. When LAD flow was reduced to 50% of its control level, NNSP resulted in a small but significant decrease in myocardial oxygenation and phosphocreatine, whereas those measurements did not change significantly during NNAP. With LAD flow further reduced to 20% of its control level, both NNAP and NNSP caused a substantial decrease in myocardial oxygenation, adenosine triphosphate, and phosphocreatine with an increase in inorganic phosphate. However, the changes were significantly greater during NNSP than during NNAP.", "output": "{\"label\": \"no\", \"rationale\": \"Normothermic normokalemic simultaneous antegrade/retrograde perfusion did not improve, but slightly impaired myocardial oxygenation and energy metabolism of beating hypertrophied hearts relative to NNAP. Therefore, NNSP for protection of beating hypertrophied hearts during valve surgery should be used with extra caution.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 17462393, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Activated Cdk5 regulates DNA damage-induced neuronal death.\n\nCANDIDATE_PASSAGE:\nGreen tea polyphenol causes differential oxidative environments in tumor versus normal epithelial cells. Green tea polyphenols (GTPPs) are considered beneficial to human health, especially as chemopreventive agents. Recently, cytotoxic reactive oxygen species (ROS) were identified in tumor and certain normal cell cultures incubated with high concentrations of the most abundant GTPP, (-)-epigallocatechin-3-gallate (EGCG). If EGCG also provokes the production of ROS in normal epithelial cells, it may preclude the topical use of EGCG at higher doses. The current study examined the oxidative status of normal epithelial, normal salivary gland, and oral carcinoma cells treated with EGCG, using ROS measurement and catalase and superoxide dismutase activity assays. The results demonstrated that high concentrations of EGCG induced oxidative stress only in tumor cells. In contrast, EGCG reduced ROS in normal cells to background levels. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and 5-bromodeoxyuridine incorporation data were also compared between the two oral carcinoma cell lines treated by EGCG, which suggest that a difference in the levels of endogenous catalase activity may play an important role in reducing oxidative stress provoked by EGCG in tumor cells. It is concluded that pathways activated by GTPPs or EGCG in normal epithelial versus tumor cells create different oxidative environments, favoring either normal cell survival or tumor cell destruction. This finding may lead to applications of naturally occurring polyphenols to enhance the effectiveness of chemo/radiation therapy to promote cancer cell death while protecting normal cells.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "68", "doc_id": "6650933", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Whole brain radiotherapy increases the occurrence of new brain metastases.\n\nCANDIDATE_ABSTRACT:\nTITLE: Stereotactic radiosurgery plus whole-brain radiation therapy vs stereotactic radiosurgery alone for treatment of brain metastases: a randomized controlled trial.\nABSTRACT: CONTEXT In patients with brain metastases, it is unclear whether adding up-front whole-brain radiation therapy (WBRT) to stereotactic radiosurgery (SRS) has beneficial effects on mortality or neurologic function compared with SRS alone. OBJECTIVE To determine if WBRT combined with SRS results in improvements in survival, brain tumor control, functional preservation rate, and frequency of neurologic death. DESIGN, SETTING, AND PATIENTS Randomized controlled trial of 132 patients with 1 to 4 brain metastases, each less than 3 cm in diameter, enrolled at 11 hospitals in Japan between October 1999 and December 2003. INTERVENTIONS Patients were randomly assigned to receive WBRT plus SRS (65 patients) or SRS alone (67 patients). MAIN OUTCOME MEASURES The primary end point was overall survival; secondary end points were brain tumor recurrence, salvage brain treatment, functional preservation, toxic effects of radiation, and cause of death. RESULTS The median survival time and the 1-year actuarial survival rate were 7.5 months and 38.5% (95% confidence interval, 26.7%-50.3%) in the WBRT + SRS group and 8.0 months and 28.4% (95% confidence interval, 17.6%-39.2%) for SRS alone (P = .42). The 12-month brain tumor recurrence rate was 46.8% in the WBRT + SRS group and 76.4% for SRS alone group (P<.001). Salvage brain treatment was less frequently required in the WBRT + SRS group (n = 10) than with SRS alone (n = 29) (P<.001). Death was attributed to neurologic causes in 22.8% of patients in the WBRT + SRS group and in 19.3% of those treated with SRS alone (P = .64). There were no significant differences in systemic and neurologic functional preservation and toxic effects of radiation. CONCLUSIONS Compared with SRS alone, the use of WBRT plus SRS did not improve survival [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Compared with SRS alone, the use of WBRT plus SRS did not improve survival for patients with 1 to 4 brain metastases, but intracranial relapse occurred considerably more frequently in those who did not receive WBRT.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1376, "doc_id": "3944632", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Medications to treat obesity do not have side effects.\n\nCANDIDATE_ABSTRACT:\nTITLE: Long term pharmacotherapy for obesity and overweight: updated meta-analysis.\nABSTRACT: OBJECTIVE To summarise the long term efficacy of anti-obesity drugs in reducing weight and improving health status. DESIGN Updated meta-analysis of randomised trials. DATA SOURCES Medline, Embase, the Cochrane controlled trials register, the Current Science meta-register of controlled trials, and reference lists of identified articles. All data sources were searched from December 2002 (end date of last search) to December 2006. STUDIES REVIEWED Double blind randomised placebo controlled trials of approved anti-obesity drugs used in adults (age over 18) for one year or longer. RESULTS 30 trials of one to four years' duration met the inclusion criteria: 16 orlistat (n=10 631 participants), 10 sibutramine (n=2623), and four rimonabant (n=6365). Of these, 14 trials were new and 16 had previously been identified. Attrition rates averaged 30-40%. Compared with placebo, orlistat reduced weight by 2.9 kg (95% confidence interval 2.5 kg to 3.2 kg), sibutramine by 4.2 kg (3.6 kg to 4.7 kg), and rimonabant by 4.7 kg (4.1 kg to 5.3 kg). Patients receiving active drug treatment were significantly more likely to achieve 5% and 10% weight loss thresholds. Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein. Sibutramine improved [corrected] concentrations of high density lipoprotein cholesterol and triglycerides [corrected] Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorde [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Orlistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 765, "doc_id": "7552215", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does bRAF V600E predict aggressive features of pediatric papillary thyroid carcinoma?\n\nABSTRACT:\nThis study aimed to review the prevalence of the BRAF V600E mutation in pediatric papillary thyroid carcinoma (PTC) and any possible association with aggressive tumor behavior. A retrospective chart review and post hoc BRAF V600E mutational analysis of archived tumor tissue. Patients 0 to 18 years old who underwent surgery for PTC from 1999 to 2012 were selected for a retrospective chart review to assess for aggressive disease characteristics. Microdissection was performed on archived tumor tissue, which was analyzed for the BRAF V600E mutation by pyrosequencing. Archived tumor specimens were available for 19/27 pediatric patients who fit the inclusion criteria. Ages ranged from 2.8 to 18 years (median, 13.7 years). Thirteen patients (68.4%) had central neck metastases, eight (42.1%) had lateral neck metastases, and five (26.3%) had pulmonary metastases. The BRAF V600E mutation was present in seven patients (36.8%). There were 11 patients with classic PTC, seven with a follicular variant of PTC, and one with an oncocytic variant. Seven (63.6%) with classical PTC were BRAF V600E positive. All histologic variants were wild type. PTC histology significantly correlated with the BRAF mutation (P = .013). The BRAF mutation was associated with a lower metastases, age at diagnosis, completeness of resection, invasion, and size of the tumor score, which trended toward significance (P = .087). Presence of lymphatic or pulmonary metastases, tumor size, overall age, lymphovascular invasion, or extrathyroidal extension were not associated with BRAF V600E. Our results are combined with existing studies for a combined incidence of 28.4%.", "output": "{\"label\": \"no\", \"rationale\": \"BRAF V600E mutations may be more prevalent than previously thought in pediatric patients with PTC, but do not correlate with aggressive disease characteristics.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 24604709, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Blocking the interaction between TDP-43 and respiratory complex I proteins ND3 and ND6 leads to increased TDP-43-induced neuronal loss.\n\nCANDIDATE_PASSAGE:\nInteraction of Helicobacter pylori with gastric epithelial cells is mediated by the p53 protein family. BACKGROUND & AIMS Although the p53 tumor suppressor has been extensively studied, many critical questions remain unanswered about the biological functions of p53 homologs, p73 and p63. Accumulating evidence suggests that both p73 and p63 play important roles in regulation of apoptosis, cell differentiation, and therapeutic drug sensitivity. METHODS Gastric epithelial cells were cocultured with Helicobacter pylori, and the roles of p63 and p73 proteins were assessed by luciferase reporter, real-time polymerase chain reaction, immunoblotting, and cell survival assays. Short hairpin RNA and dominant-negative mutants were used to inhibit activity of p73 and p63 isoforms. Human and murine gastric tissues were analyzed by immunohistochemistry with p73 and p63 antibodies and modified Steiner's silver method. RESULTS Interaction of H pylori with gastric epithelial cells leads to robust up-regulation of p73 protein in vitro and in vivo in human gastritis specimens and H pylori-infected mice. The p73 increase resulted in up-regulation of pro-apoptotic genes, NOXA, PUMA, and FAS receptor in gastric epithelial cells. Down-regulation of p73 activity suppressed cell death and Fas receptor induced by H pylori. Bacterial virulence factors within the cag pathogenicity island, c-Abl tyrosine kinase, and interaction with p63 isoforms control the activity of p73. CONCLUSION Our findings implicate p73 in H pylori-induced apoptosis and more generally suggest that the p53 family may play a role in the epithelial cell response to H pylori infection.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "180", "doc_id": "29367554", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Active caspase-11 protein promotes pyroptosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Caspase-11 promotes the fusion of phagosomes harboring pathogenic bacteria with lysosomes by modulating actin polymerization.\nABSTRACT: Inflammasomes are multiprotein complexes that include members of the NLR (nucleotide-binding domain leucine-rich repeat containing) family and caspase-1. Once bacterial molecules are sensed within the macrophage, the inflammasome is assembled, mediating the activation of caspase-1. Caspase-11 mediates caspase-1 activation in response to lipopolysaccharide and bacterial toxins, and yet its role during bacterial infection is unknown. Here, we demonstrated that caspase-11 was dispensable for caspase-1 activation in response to Legionella, Salmonella, Francisella, and Listeria. We also determined that active mouse caspase-11 was required for restriction of L. pneumophila infection. Similarly, human caspase-4 and caspase-5, homologs of mouse caspase-11, cooperated to restrict L. pneumophila infection in human macrophages. Caspase-11 promoted the fusion of the L. pneumophila vacuole with lysosomes by modulating actin polymerization through cofilin. However, caspase-11 was dispensable for the fusion of lysosomes with phagosomes containing nonpathogenic bacteria, uncovering a fundamental difference in the trafficking of phagosomes according to their cargo.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Here, we demonstrated that caspase-11 was dispensable for caspase-1 activation in response to Legionella, Salmonella, Francisella, and Listeria.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 79, "doc_id": "5099266", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Mice that lack Interferon-γ or its receptor are highly susceptible to experimental autoimmune myocarditis.\n\nCANDIDATE_PASSAGE:\nGene regulation in the immune system by long noncoding RNAs Long noncoding RNAs (lncRNAs) are emerging as critical regulators of gene expression in the immune system. Studies have shown that lncRNAs are expressed in a highly lineage-specific manner and control the differentiation and function of innate and adaptive cell types. In this Review, we focus on mechanisms used by lncRNAs to regulate genes encoding products involved in the immune response, including direct interactions with chromatin, RNA and proteins. In addition, we address new areas of lncRNA biology, such as the functions of enhancer RNAs, circular RNAs and chemical modifications to RNA in cellular processes. We emphasize critical gaps in knowledge and future prospects for the roles of lncRNAs in the immune system and autoimmune disease.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "780", "doc_id": "5519177", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Activation of PPM1D suppresses p53 function.\n\nCANDIDATE_ABSTRACT:\nTITLE: Generation of large numbers of dendritic cells from mouse bone marrow cultures supplemented with granulocyte/macrophage colony-stimulating factor\nABSTRACT: Antigen-presenting, major histocompatibility complex (MHC) class II-rich dendritic cells are known to arise from bone marrow. However, marrow lacks mature dendritic cells, and substantial numbers of proliferating less-mature cells have yet to be identified. The methodology for inducing dendritic cell growth that was recently described for mouse blood now has been modified to MHC class II-negative precursors in marrow. A key step is to remove the majority of nonadherent, newly formed granulocytes by gentle washes during the first 2-4 d of culture. This leaves behind proliferating clusters that are loosely attached to a more firmly adherent \"stroma. \" At days 4-6 the clusters can be dislodged, isolated by 1-g sedimentation, and upon reculture, large numbers of dendritic cells are released. The latter are readily identified on the basis of their distinct cell shape, ultrastructure, and repertoire of antigens, as detected with a panel of monoclonal antibodies. The dendritic cells express high levels of MHC class II products and act as powerful accessory cells for initiating the mixed leukocyte reaction. Neither the clusters nor mature dendritic cells are generated if macrophage colony-stimulating factor rather than granulocyte/macrophage colony-stimulating factor (GM-CSF) is applied. Therefore, GM-CSF generates all three lineages of myeloid cells (granulocytes, macrophages, and dendritic cells). Since > 5 x 10(6) dendritic cells develop in 1 wk from precursors within the large hind limb bones of a single animal, marrow progenitors can act as a major source of dendritic cells. This feature should prove useful for future molecular and clinical studies of this otherwise trace cell type.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 70, "doc_id": "188911", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The risk of cancer rises with level of alcohol consumption.\n\nCANDIDATE_ABSTRACT:\nTITLE: Alcohol use and burden for 195 countries and territories, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016\nABSTRACT: Summary Background Alcohol use is a leading risk factor for death and disability, but its overall association with health remains complex given the possible protective effects of moderate alcohol consumption on some conditions. With our comprehensive approach to health accounting within the Global Burden of Diseases, Injuries, and Risk Factors Study 2016, we generated improved estimates of alcohol use and alcohol-attributable deaths and disability-adjusted life-years (DALYs) for 195 locations from 1990 to 2016, for both sexes and for 5-year age groups between the ages of 15 years and 95 years and older. Methods Using 694 data sources of individual and population-level alcohol consumption, along with 592 prospective and retrospective studies on the risk of alcohol use, we produced estimates of the prevalence of current drinking, abstention, the distribution of alcohol consumption among current drinkers in standard drinks daily (defined as 10 g of pure ethyl alcohol), and alcohol-attributable deaths and DALYs. We made several methodological improvements compared with previous estimates: first, we adjusted alcohol sales estimates to take into account tourist and unrecorded consumption; second, we did a new meta-analysis of relative risks for 23 health outcomes associated with alcohol use; and third, we developed a new method to quantify the level of alcohol consumption that minimises the overall risk to individual health. Findings Globally, alcohol use was the seventh leading risk factor for both deaths and DALYs in 2016, accounting for 2·2% (95% uncertainty interval [UI] 1·5–3·0) of age-standardised female deaths and 6·8% (5·8–8·0) of age-standardised male deaths. Among the population aged 15–49 years, alcohol use was the leading risk factor globally in 2016, [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"For populations aged 50 years and older, cancers accounted for a large proportion of total alcohol-attributable deaths in 2016, constituting 27·1% (95% UI 21·2–33·3) of total alcohol-attributable female deaths and 18·9% (15·3–22·6) of male deaths.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1268, "doc_id": "52072815", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Pioneer factor OCT3/4 interacts with major chromatin remodeling factors.\n\nCANDIDATE_PASSAGE:\nImpact of aortic stiffness on survival in end-stage renal disease. BACKGROUND Damage to large arteries is a major factor in the high cardiovascular morbidity and mortality of patients with end-stage renal disease (ESRD). Increased arterial stiffness and intima-media thickness, together with increased pulse pressure, are the principal arterial alterations. Whether increased aortic pulse-wave velocity (PWV), a classic marker of increased arterial stiffness, may predict all-cause and/or cardiovascular mortality has never been investigated. METHODS AND RESULTS A cohort of 241 patients with ESRD undergoing hemodialysis was studied between April 1987 and April 1998. The mean duration of follow-up was 72+/-41 months (mean+/-SD). Mean age at entry was 51.5+/-16.3 years. Seventy-three deaths occurred, including 48 cardiovascular and 25 noncardiovascular fatal events. At entry, together with standard clinical and biochemical analyses, patients underwent echocardiography and aortic PWV measured by Doppler ultrasonography. On the basis of Cox analyses, 2 factors emerged as predictors of all-cause and cardiovascular mortality: age and aortic PWV. Hemoglobin and low diastolic pressure interfered to a smaller extent. After adjustment for all the confounding factors, an OR for PWV >12. 0 versus <9.4 m/s was 5.4 (95% CI, 2.4 to 11.9) for all-cause mortality and 5.9 (95% CI, 2.3 to 15.5) for cardiovascular mortality. For each PWV increase of 1 m/s in our study population, all-cause mortality-adjusted OR was 1.39 (95% CI, 1.19 to 1.62). CONCLUSIONS These results provide the first direct evidence that in patients with ESRD, increased aortic stiffness determined by measurement of aortic PWV is a strong independent predictor of all-cause and mainly cardiovascular mortality.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "955", "doc_id": "6525844", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Genetic deletion of JAM-A increases gut permeability.\n\nCANDIDATE_PASSAGE:\nMechanisms of Renal Cell Apoptosis Induced by Cyclosporine A: A Systematic Review of in vitro Studies Background:Chronic cyclosporine A (CsA) nephrotoxicity (CCN) is a major cause of chronic renal dysfunction and has no effective clinical interventions yet. Objective: To reveal the mechanisms of renal cell apoptosis in CCN, we analyzed all in vitro studies of such mechanisms. Methods: We collected all in vitro studies about the mechanisms of renal cell apoptosis induced by CsA in Medline (1966 to July 2010), Embase (1980 to July 2010) and ISI (1986 to July 2010), evaluated their quality according to in vitro standards and extracted data following the PICOS principles and synthesized the data. Results: First,CsA could upregulate Fas and Fas-L expression, increase FADD and apoptosis enzymes (caspase-2, -3, -4, -7, -8, -9 and -10) and downregulate the Bcl-2 and Bcl-xL. Second, CsA could induce oxidative stress and damage the antioxidant defense system. Third, CsA could increase the expression of HERP, GRP78 and CHOP. Fourth, CsA could induce renal cell apoptosis and increase their iNOS and p53 expression in cultured cells. Conclusions: At least four pathways are involved in renal cell apoptosis induced by CsA in different cell species. Caspases might be their final common pathway in vitro. They might all provide potential points for interventions, but these need to be confirmed in vivo.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "461", "doc_id": "238409", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Gene expression does not vary appreciably across genetically identical cells.\n\nCANDIDATE_PASSAGE:\nMemory and Modularity in Cell-Fate Decision Making Genetically identical cells sharing an environment can display markedly different phenotypes. It is often unclear how much of this variation derives from chance, external signals, or attempts by individual cells to exert autonomous phenotypic programs. By observing thousands of cells for hundreds of consecutive generations under constant conditions, we dissect the stochastic decision between a solitary, motile state and a chained, sessile state in Bacillus subtilis. We show that the motile state is 'memoryless', exhibiting no autonomous control over the time spent in the state. In contrast, the time spent as connected chains of cells is tightly controlled, enforcing coordination among related cells in the multicellular state. We show that the three-protein regulatory circuit governing the decision is modular, as initiation and maintenance of chaining are genetically separable functions. As stimulation of the same initiating pathway triggers biofilm formation, we argue that autonomous timing allows a trial commitment to multicellularity that external signals could extend.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "452", "doc_id": "464511", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Bariatric surgery increases rates of colorectal cancer.\n\nCANDIDATE_PASSAGE:\nPathogenesis of diseases associated with antineutrophil cytoplasm autoantibodies. Little is known about the etiologies of diseases associated with circulating antineutrophil cytoplasm autoantibodies (ANCA), such as primary vasculitides and inflammatory bowel diseases. However, the understanding of immune mechanisms supposedly involved in the pathogenesis of these diseases is still growing. In the present review, we first focus on the mechanisms triggering the development of ANCA, including the potential role of microbial superantigens and the possible defect(s) in the progression of apoptosis or in the removal of apoptotic cells. We next concentrate on the contribution of ANCA to the clinical symptoms and on the pathogenic role of ANCA, including the accessibility of ANCA antigens as targets for circulating antibodies and the mode of action of ANCA. Mechanisms of neutrophil activation by ANCA include the engagement of Fcgamma receptors, the possible mechanisms of neutrophil-mediated tissue damage, and the neutrophil-endothelial interaction.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "164", "doc_id": "27789588", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The PRDM1 gene, when combined with the PRDM14 gene, plays an important role during primordial germ cell specification.\n\nCANDIDATE_PASSAGE:\nRelationship between Sloan-Kettering virus expression and mouse follicular development Sloan-Kettering virus gene product (Ski) is an unique nuclear pro-oncoprotein and belongs to the ski/sno proto-oncogene family. Ski plays multiple roles in a variety of cell types, it can induce both oncogenic transformation and terminal muscle differentiation when expressed at high levels. Ski/SnoN are important transcription regulators of the transforming growth factor-β (TGF-β) superfamily and function mainly through heterodimers. Since TGF-β superfamily are key regulators of follicle development and it has been previously shown that SnoN is also vital to follicle development, this research was conducted to clarify the relationship between Ski expression and mouse follicular development, in ovaries of neonatal and gonadotropin-induced immature mice by immunohistochemical and real-time PCR techniques. In postnatal mice, positive staining for Ski was highly detected in oocyte nuclei at postnatal day 1. With follicular development, the localization moved gradually from oocyte nuclei to perinuclear space and the total levels decreased. During the estrous cycle, Ski expression was apparent at proestrus and estrus, faint at metestrus, highest at diestrus. After injection of gonadotropin, Ski was found in perinuclear space and weak in oocyte nuclei. Following the initiation of luteinization, the expression of Ski was found in corpus luteum. Real-time PCR results also showed that Ski mRNA expression was opposite to ovulation-related genes during the cumulus expansion, with the development of the follicles, its expression level decreased. Ski is expressed in a specific manner during follicle development, ovulation and luteinization. So Ski might play essential roles in these pro [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1177", "doc_id": "643765", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Taxation of sugar-sweetened beverages had no effect on the incidence rate of type II diabetes in India.\n\nCANDIDATE_ABSTRACT:\nTITLE: Averting Obesity and Type 2 Diabetes in India through Sugar-Sweetened Beverage Taxation: An Economic-Epidemiologic Modeling Study\nABSTRACT: BACKGROUND Taxing sugar-sweetened beverages (SSBs) has been proposed in high-income countries to reduce obesity and type 2 diabetes. We sought to estimate the potential health effects of such a fiscal strategy in the middle-income country of India, where there is heterogeneity in SSB consumption, patterns of substitution between SSBs and other beverages after tax increases, and vast differences in chronic disease risk within the population. METHODS AND FINDINGS Using consumption and price variations data from a nationally representative survey of 100,855 Indian households, we first calculated how changes in SSB price alter per capita consumption of SSBs and substitution with other beverages. We then incorporated SSB sales trends, body mass index (BMI), and diabetes incidence data stratified by age, sex, income, and urban/rural residence into a validated microsimulation of caloric consumption, glycemic load, overweight/obesity prevalence, and type 2 diabetes incidence among Indian subpopulations facing a 20% SSB excise tax. The 20% SSB tax was anticipated to reduce overweight and obesity prevalence by 3.0% (95% CI 1.6%-5.9%) and type 2 diabetes incidence by 1.6% (95% CI 1.2%-1.9%) among various Indian subpopulations over the period 2014-2023, if SSB consumption continued to increase linearly in accordance with secular trends. However, acceleration in SSB consumption trends consistent with industry marketing models would be expected to increase the impact efficacy of taxation, averting 4.2% of prevalent overweight/obesity (95% CI 2.5-10.0%) and 2.5% (95% CI 1.0-2.8%) of incident type 2 diabetes from 2014-2023. Given current consumption and BMI distributions, our results suggest the largest relative effect would be expected among young rural men, refuting our a [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The 20% SSB tax was anticipated to reduce overweight and obesity prevalence by 3.0% (95% CI 1.6%-5.9%) and type 2 diabetes incidence by 1.6% (95% CI 1.2%-1.9%) among various Indian subpopulations over the period 2014-2023, if SSB consumption continued to increase linearly in accordance with secular trends.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1144, "doc_id": "10071552", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Primary cervical cytology screening with HPV detection has higher longitudinal sensitivity to detect severe cervical intraepithelial neoplasia than conventional cytology.\n\nCANDIDATE_ABSTRACT:\nTITLE: Efficacy of human papillomavirus testing for the detection of invasive cervical cancers and cervical intraepithelial neoplasia: a randomised controlled trial.\nABSTRACT: BACKGROUND Human papillomavirus (HPV) testing is known to be more sensitive, but less specific than cytology for detecting cervical intraepithelial neoplasia (CIN). We assessed the efficacy of cervical-cancer screening policies that are based on HPV testing. METHODS Between March, 2004, and December, 2004, in two separate recruitment phases, women aged 25-60 years were randomly assigned to conventional cytology or to HPV testing in combination with liquid-based cytology (first phase) or alone (second phase). Randomisation was done by computer in two screening centres and by sequential opening of numbered sealed envelopes in the remaining seven centres. During phase one, women who were HPV-positive and aged 35-60 years were referred to colposcopy, whereas women aged 25-34 years were referred to colposcopy only if cytology was also abnormal or HPV testing was persistently positive. During phase two, women in the HPV group were referred for colposcopy if the HPV test was positive. Two rounds of screening occurred in each phase, and all women had cytology testing only at the second round. The primary endpoint was the detection of grade 2 and 3 CIN, and of invasive cervical cancers during the first and second screening rounds. Analysis was done by intention to screen. This trial is registered, number ISRCTN81678807. FINDINGS In total for both phases, 47,001 women were randomly assigned to the cytology group and 47,369 to HPV testing. 33,851 women from the cytology group and 32,998 from the HPV-testing group had a second round of screening. We also retrieved the histological diagnoses from screening done elsewhere. The detection of invasive cervical cancers was similar for the two groups in the first round of screening (nine in the cytology group vs seven in the H [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"INTERPRETATION HPV-based screening is more effective than cytology in preventing invasive cervical cancer, by detecting persistent high-grade lesions earlier and providing a longer low-risk period.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 973, "doc_id": "27873158", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: A diminished ovarian reserve is a very strong indicator of infertility, even in an a priori non-infertile population.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\nABSTRACT: Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential. Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age. Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area. Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH. Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle). Conception was defined as a positive pregnancy test result. Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis. After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively). Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cy [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 40, "doc_id": "13497630", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Lack of FGF21 in mice leads to atherosclerotic plaque formation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Fibroblast Growth Factor 21 Prevents Atherosclerosis by Suppression of Hepatic Sterol Regulatory Element-Binding Protein-2 and Induction of Adiponectin in Mice\nABSTRACT: BACKGROUND Fibroblast growth factor 21 (FGF21) is a metabolic hormone with pleiotropic effects on glucose and lipid metabolism and insulin sensitivity. It acts as a key downstream target of both peroxisome proliferator-activated receptor α and γ, the agonists of which have been used for lipid lowering and insulin sensitization, respectively. However, the role of FGF21 in the cardiovascular system remains elusive. METHODS AND RESULTS The roles of FGF21 in atherosclerosis were investigated by evaluating the impact of FGF21 deficiency and replenishment with recombinant FGF21 in apolipoprotein E(-/-) mice. FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia. Replenishment of FGF21 protects against atherosclerosis in apolipoprotein E(-/-)mice via 2 independent mechanisms, inducing the adipocyte production of adiponectin, which in turn acts on the blood vessels to inhibit neointima formation and macrophage inflammation, and suppressing the hepatic expression of the transcription factor sterol regulatory element-binding protein-2, thereby leading to reduced cholesterol synthesis and attenuation of hypercholesterolemia. Chronic treatment with adiponectin partially reverses atherosclerosis without obvious effects on hypercholesterolemia in FGF21-deficient apolipoprotein E(-/-) mice. By contrast, the cholesterol-lowering effects of FGF21 are abrogated by hepatic expression of sterol regulatory element-binding protein-2. CONCLUSIONS FGF21 protects against atherosclerosis via fine tuning the multiorgan crosstalk among liver, adipose tissue, and blood vessels.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"FGF21 deficiency causes a marked exacerbation of atherosclerotic plaque formation and premature death in apolipoprotein E(-/-) mice, which is accompanied by hypoadiponectinemia and severe hypercholesterolemia.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 681, "doc_id": "9315213", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Women with a lower birth weight are more likely to develop breast cancer later in life.\n\nCANDIDATE_ABSTRACT:\nTITLE: Birth Size and Breast Cancer Risk: Re-analysis of Individual Participant Data from 32 Studies\nABSTRACT: BACKGROUND Birth size, perhaps a proxy for prenatal environment, might be a correlate of subsequent breast cancer risk, but findings from epidemiological studies have been inconsistent. We re-analysed individual participant data from published and unpublished studies to obtain more precise estimates of the magnitude and shape of the birth size-breast cancer association. METHODS AND FINDINGS Studies were identified through computer-assisted and manual searches, and personal communication with investigators. Individual participant data from 32 studies, comprising 22,058 breast cancer cases, were obtained. Random effect models were used, if appropriate, to combine study-specific estimates of effect. Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003). Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data. Birth length and head circumference from birth records were also positively associated with breast cancer risk (pooled RR per one SD increment: 1.06 [95% CI 1.03-1.10] and 1.09 [95% CI 1.03-1.15], respectively). Simultaneous adjustment for these three birth size variables showed that length was the strongest independent predictor of risk. The birth size effec [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1380, "doc_id": "16322674", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Primary cervical cancer screening with HPV detection has higher longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_ABSTRACT:\nTITLE: Evidence regarding human papillomavirus testing in secondary prevention of cervical cancer.\nABSTRACT: More than ever, clinicians need regularly updated reviews given the continuously increasing amount of new information regarding innovative cervical cancer prevention methods. A summary is given from recent meta-analyses and systematic reviews on 3 possible clinical applications of human papillomavirus (HPV) testing: triage of women with equivocal or low-grade cytologic abnormalities; prediction of the therapeutic outcome after treatment of cervical intraepithelial neoplasia (CIN) lesions, and last not but not least, primary screening for cervical cancer and pre-cancer. Consistent evidence is available indicating that HPV-triage with the Hybrid Capture(®) 2 assay (Qiagen Gaithersburg, Inc., MD, USA [previously Digene Corp.] (HC2) is more accurate (higher sensitivity, similar specificity) than repeat cytology to triage women with equivocal Pap smear results. Several other tests show at least similar accuracy but mRNA testing with the APTIMA(®) (Gen-Probe Inc., San Diego, CA, USA) test is similarly sensitive but more specific compared to HC2. In triage of low-grade squamous intraepithelial lesions (LSIL), HC2 is more sensitive but its specificity is substantially lower compared to repeat cytology. The APTIMA(®) test is more specific than HC2 without showing a loss in sensitivity. Identification of DNA of HPV types 16 and/or 18, or RNA from the five most carcinogenic HPV types allow selecting women at highest risk for CIN3+ but the sensitivity and negative predictive value of these markers are lower than full-range high-risk HPV (hrHPV) testing. After conservative treatment of cervical pre-cancer, HPV testing picks up more quickly, with higher sensitivity and not lower specificity, residual or recurrent high-grade CIN than follow-up cytology. Primary screening f [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Primary screening for hrHPV generally detects more CIN2, CIN3 or cancer compared to cytology at cut-off atypical squamous cells of undetermined significance (ASC-US) or LSIL, but is less specific.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 971, "doc_id": "28617573", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Microglia are an innate immune cell type of the peripheral nervous system.\n\nCANDIDATE_ABSTRACT:\nTITLE: Sublime Microglia: Expanding Roles for the Guardians of the CNS\nABSTRACT: Recent findings challenge the concept that microglia solely function in disease states in the central nervous system (CNS). Rather than simply reacting to CNS injury, infection, or pathology, emerging lines of evidence indicate that microglia sculpt the structure of the CNS, refine neuronal circuitry and network connectivity, and contribute to plasticity. These physiological functions of microglia in the normal CNS begin during development and persist into maturity. Here, we develop a conceptual framework for functions of microglia beyond neuroinflammation and discuss the rich repertoire of signaling and communication motifs in microglia that are critical both in pathology and for the normal physiology of the CNS.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"These physiological functions of microglia in the normal CNS begin during development and persist into maturity.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 790, "doc_id": "15493354", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Do kaurane diterpenes protect against apoptosis and inhibition of phagocytosis in activated macrophages?\n\nABSTRACT:\nThe kaurane diterpenes foliol and linearol are inhibitors of the activation of nuclear factor kappaB, a transcription factor involved in the inflammatory response. Effects of these diterpenes on apoptosis and phagocytosis have been analysed in cultured peritoneal macrophages and in the mouse macrophage cell line, RAW 264.7. Macrophages were maintained in culture and activated with pro-inflammatory stimuli in the absence or presence of diterpenes. Apoptosis and the phagocytosis in these cells under these conditions were determined. Incubation of macrophages with a mixture of bacterial lipopolysaccharide (LPS)/interferon-gamma (IFN-gamma) induced apoptosis through a NO-dependent pathway, an effect significantly inhibited by foliol and linearol in the low muM range, without cytotoxic effects. Apoptosis in macrophages induced by NO donors was also inhibited. The diterpenes prevented apoptosis through a mechanism compatible with the inhibition of caspase-3 activation, release of cytochrome c to the cytosol and p53 overexpression, as well as an alteration in the levels of proteins of the Bcl-2 family, in particular, the levels of Bax. Cleavage of poly(ADP-ribose) polymerase, a well-established caspase substrate, was reduced by these diterpenes. Treatment of cells with foliol and linearol decreased phagocytosis of zymosan bioparticles by RAW 264.7 cells and to a greater extent by peritoneal macrophages.", "output": "{\"label\": \"yes\", \"rationale\": \"Both diterpenes protected macrophages from apoptosis and inhibited phagocytosis, resulting in a paradoxical control of macrophage function, as viability was prolonged but inflammatory and phagocytic functions were impaired.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 17618303, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is tumor size a determinant of the rate of stage T1 renal cell cancer synchronous metastasis?\n\nABSTRACT:\nA recent multi-institutional analysis of 995 patients treated for renal cell cancer questioned the relationship between tumor size and the synchronous metastasis rate. We revisited the hypothesis that metastatic potential is unrelated to tumor size. We tested the relationship between tumor size and synchronous metastasis in 22,204 patients with T1a and T1b renal cell cancer diagnosed and/or treated with nephrectomy for clear cell, papillary or chromophobe histological subtypes in 1 of 9 Surveillance, Epidemiology and End Results registries between 1988 and 2004. In the study population the synchronous metastasis rate was 9.6%, including 5.6% vs 14.2% for T1a vs T1b. Stratification by 1 cm tumor size intervals revealed that the rate increased with increasing tumor size, that is 4.8% at 1.0 cm or less, 4.2% at 1.1 to 2.0 cm, 4.9% at 2.1 to 3.0 cm, 7.1% at 3.1 to 4.0 cm, 12.1% at 4.1 to 5.0 cm, 13.3% at 5.1 to 6.0 cm and 18.4% 6.1 to 7.0 cm (chi-square trend p <0.001). Cubic spline analysis showed that tumor size was virtually linearly related to the synchronous metastasis rate. Stratification by histological subtype in patients treated with nephrectomy revealed that clear cell renal cell cancer was most frequently associated with synchronous metastasis. Finally, tumor size was an independent predictor of synchronous metastasis in multivariate regression models adjusted for age, gender, histological subtype and year of diagnosis quartiles.", "output": "{\"label\": \"yes\", \"rationale\": \"Our study confirms that tumor size is an important determinant of the likelihood of synchronous metastasis in patients with T1a and T1b renal cell cancer. The synchronous metastasis rate directly increases with increasing tumor size. Even patients with small renal masses are at risk for synchronous metastasis and patients with clear cell renal cell cancer are at highest risk.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 19683281, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does adrenal insufficiency predict early mortality in patients with cirrhosis?\n\nABSTRACT:\nAdrenal insufficiency (AI), also known as hepato-adrenal syndrome, is a well-known entity in cirrhotic patients. However, factors associated with AI and its effect on survival are still not clear. We determined the prevalence of AI in patients with cirrhosis who had no hemodynamic instability or any acute deterioration, and studied its influence on short-term survival. In consecutive cirrhotic patients, presence of AI was determined either by total serum cortisol <18 µg/dl, 60 minutes after 250 µg synacthen injection, or when the delta-fraction (post-synacthen serum cortisol minus basal serum cortisol) was <9 µg/dl. A total of 120 patients were included in the study (median age 50 years (range 27-73), males 87%). The median CTP and MELD scores were 10 (range 6-13) and 20 (range 6-40). The etiology of cirrhosis was alcohol (51%), cryptogenic (28%), viral (19%) and autoimmune (2%). Sixty-nine patients (58%) had AI and the remaining 51 (42%) had normal adrenal function. Serum bilirubin was significantly higher (p < 0.05) in the AI group, and total cholesterol, HDL, LDL and hemoglobin were significantly lower (p < 0.05) in the AI group. CTP score, MELD score, and basal cortisol levels were not different between those with and without AI (p = NS). By 120 days of follow-up, 41 patients had died. Thus, the 120-day survival was 66%, and this was higher in patients without AI than in patients with AI (78% vs 56%; p = 0.019). On multivariate analysis absence of AI, low WBC and low CTP score independently predicted 120-day survival.", "output": "{\"label\": \"yes\", \"rationale\": \"AI is present in more than half of cirrhotic patients but does not parallel the severity scores of cirrhosis. Its presence predicts early mortality in these patients, and this prediction is independent of CTP or MELD scores.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 26668746, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cardiac tissue-resident macrophages directly contribute to electrical activity.\n\nCANDIDATE_ABSTRACT:\nTITLE: Macrophages Facilitate Electrical Conduction in the Heart\nABSTRACT: Organ-specific functions of tissue-resident macrophages in the steady-state heart are unknown. Here, we show that cardiac macrophages facilitate electrical conduction through the distal atrioventricular node, where conducting cells densely intersperse with elongated macrophages expressing connexin 43. When coupled to spontaneously beating cardiomyocytes via connexin-43-containing gap junctions, cardiac macrophages have a negative resting membrane potential and depolarize in synchrony with cardiomyocytes. Conversely, macrophages render the resting membrane potential of cardiomyocytes more positive and, according to computational modeling, accelerate their repolarization. Photostimulation of channelrhodopsin-2-expressing macrophages improves atrioventricular conduction, whereas conditional deletion of connexin 43 in macrophages and congenital lack of macrophages delay atrioventricular conduction. In the Cd11bDTR mouse, macrophage ablation induces progressive atrioventricular block. These observations implicate macrophages in normal and aberrant cardiac conduction.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"These observations implicate macrophages in normal and aberrant cardiac conduction.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 228, "doc_id": "4928057", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Medications to treat obesity have unwanted side effects.\n\nCANDIDATE_ABSTRACT:\nTITLE: Probable person to person transmission of novel avian influenza A (H7N9) virus in Eastern China, 2013: epidemiological investigation\nABSTRACT: OBJECTIVE To determine whether the novel avian influenza H7N9 virus can transmit from person to person and its efficiency. DESIGN Epidemiological investigations conducted after a family cluster of two patients with avian H7N9 in March 2013. SETTING Wuxi, Eastern China. PARTICIPANTS Two patients, their close contacts, and relevant environments. Samples from the patients and environments were collected and tested by real time reverse transcriptase-polymerase chain reaction (rRT-PCR), viral culture, and haemagglutination inhibition assay. Any contacts who became ill had samples tested for avian H7N9 by rRT-PCR. Paired serum samples were obtained from contacts for serological testing by haemagglutination inhibition assays. MAIN OUTCOMES MEASURES Clinical data, history of exposure before the onset of illnesses, and results of laboratory testing of pathogens and further analysis of sequences and phylogenetic tree to isolated strains. RESULTS The index patient became ill five to six days after his last exposure to poultry. The second patient, his daughter aged 32, who provided unprotected bedside care in the hospital, had no known exposure to poultry. She developed symptoms six days after her last contact with her father. Two strains were isolated successfully from the two patients. Genome sequence and analyses of phylogenetic trees showed that both viruses were almost genetically identical. Forty three close contacts of both patients were identified. One had mild illness but had negative results for avian H7N9 by rRT-PCR. All 43 close contacts tested negative for haemagglutination inhibition antibodies specific for avian H7N9. CONCLUSIONS The infection of the daughter probably resulted from contact with her father (the index patient) during unprotected exposure, s [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 766, "doc_id": "253672", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Vitamin D is an important factor in the relationship between calcium and parathyroid hormone.\n\nCANDIDATE_ABSTRACT:\nTITLE: Relationship between serum parathyroid hormone levels, vitamin D sufficiency, and calcium intake.\nABSTRACT: CONTEXT Adequate vitamin D status for optimum bone health has received increased recognition in recent years; however, the ideal intake is not known. Serum 25-hydroxyvitamin D is the generally accepted indicator of vitamin D status, but no universal reference level has been reached. OBJECTIVE To investigate the relative importance of high calcium intake and serum 25-hydroxyvitamin D for calcium homeostasis, as determined by serum intact parathyroid hormone (PTH). DESIGN, SETTING, AND PARTICIPANTS Cross-sectional study of 2310 healthy Icelandic adults who were divided equally into 3 age groups (30-45 years, 50-65 years, or 70-85 years) and recruited from February 2001 to January 2003. They were administered a semi-quantitative food frequency questionnaire, which assessed vitamin D and calcium intake. Participants were further divided into groups according to calcium intake (<800 mg/d, 800-1200 mg/d, and >1200 mg/d) and serum 25-hydroxyvitamin D level (<10 ng/mL, 10-18 ng/mL, and >18 ng/mL). MAIN OUTCOME MEASURE Serum intact PTH as determined by calcium intake and vitamin D. RESULTS A total of 944 healthy participants completed all parts of the study. After adjusting for relevant factors, serum PTH was lowest in the group with a serum 25-hydroxyvitamin D level of more than 18 ng/mL but highest in the group with a serum 25-hydroxyvitamin D level of less than 10 ng/mL. At the low serum 25-hydroxyvitamin D level (<10 ng/mL), calcium intake of less than 800 mg/d vs more than 1200 mg/d was significantly associated with higher serum PTH (P = .04); and at a calcium intake of more than 1200 mg/d, there was a significant difference between the lowest and highest vitamin D groups (P = .04). CONCLUSIONS As long as vitamin D status is ensured, calcium intake levels of mor [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS As long as vitamin D status is ensured, calcium intake levels of more than 800 mg/d may be unnecessary for maintaining calcium metabolism.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1371, "doc_id": "16256507", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Ribosomopathies have a low degree of cell and tissue specific pathology.\n\nCANDIDATE_ABSTRACT:\nTITLE: Ribosome-Mediated Specificity in Hox mRNA Translation and Vertebrate Tissue Patterning\nABSTRACT: Historically, the ribosome has been viewed as a complex ribozyme with constitutive rather than regulatory capacity in mRNA translation. Here we identify mutations of the Ribosomal Protein L38 (Rpl38) gene in mice exhibiting surprising tissue-specific patterning defects, including pronounced homeotic transformations of the axial skeleton. In Rpl38 mutant embryos, global protein synthesis is unchanged; however the translation of a select subset of Homeobox mRNAs is perturbed. Our data reveal that RPL38 facilitates 80S complex formation on these mRNAs as a regulatory component of the ribosome to confer transcript-specific translational control. We further show that Rpl38 expression is markedly enriched in regions of the embryo where loss-of-function phenotypes occur. Unexpectedly, a ribosomal protein (RP) expression screen reveals dynamic regulation of individual RPs within the vertebrate embryo. Collectively, these findings suggest that RP activity may be highly regulated to impart a new layer of specificity in the control of gene expression and mammalian development.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Unexpectedly, a ribosomal protein (RP) expression screen reveals dynamic regulation of individual RPs within the vertebrate embryo. Collectively, these findings suggest that RP activity may be highly regulated to impart a new layer of specificity in the control of gene expression and mammalian development.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1049, "doc_id": "12486491", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Genomic sequences involved in alternative splicing responsible for Hutchinson-Gilford progeria syndrome (HGPS) are abundant in the ''progerinonly'' allele of Lmna knock-in models.\n\nCANDIDATE_PASSAGE:\nComputational analysis of 3'-ends of ESTs shows four classes of alternative polyadenylation in human, mouse, and rat. Alternative initiation, splicing, and polyadenylation are key mechanisms used by many organisms to generate diversity among mature mRNA transcripts originating from the same transcription unit. While previous computational analyses of alternative polyadenylation have focused on polyadenylation activities within or downstream of the normal 3'-terminal exons, we present the results of the first genome-wide analysis of patterns of alternative polyadenylation in the human, mouse, and rat genomes occurring over the entire transcribed regions of mRNAs using 3'-ESTs with poly(A) tails aligned to genomic sequences. Four distinct classes of patterns of alternative polyadenylation result from this analysis: tandem poly(A) sites, composite exons, hidden exons, and truncated exons. We estimate that at least 49% (human), 31% (mouse), and 28% (rat) of polyadenylated transcription units have alternative polyadenylation. A portion of these alternative polyadenylation events result in new protein isoforms.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "466", "doc_id": "21853444", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Increased diastolic blood pressure (DBP) is associated with abdominal aortic aneurysm.\n\nCANDIDATE_ABSTRACT:\nTITLE: CD169+ MACROPHAGES PRESENT LIPID ANTIGENS TO MEDIATE EARLY ACTIVATION OF INVARIANT NKT CELLS IN LYMPH NODES\nABSTRACT: Invariant natural killer T cells (iNKT cells) are involved in the host defense against microbial infection. Although it is known that iNKT cells recognize glycolipids presented by CD1d, how and where they encounter antigen in vivo remains unclear. Here we used multiphoton microscopy to visualize the dynamics and activation of iNKT cells in lymph nodes. After antigen administration, iNKT cells became confined in a CD1d-dependent manner in close proximity to subcapsular sinus CD169(+) macrophages. These macrophages retained, internalized and presented lipid antigen and were required for iNKT cell activation, cytokine production and population expansion. Thus, CD169(+) macrophages can act as true antigen-presenting cells controlling early iNKT cell activation and favoring the fast initiation of immune responses.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 607, "doc_id": "1933281", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Female carriers of the Apolipoprotein E4 (APOE4) allele have increased risk for dementia.\n\nCANDIDATE_PASSAGE:\nReproductive period and risk of dementia in postmenopausal women. CONTEXT Exogenous estrogen use may lower risk of dementia in postmenopausal women. A relationship between long-term exposure to endogenous estrogens and incident dementia has been hypothesized but not studied. OBJECTIVE To determine whether a longer reproductive period, as an indicator of longer exposure to endogenous estrogens, is associated with lower risk of dementia and Alzheimer disease (AD) in women who have natural menopause. DESIGN AND SETTING The Rotterdam Study, a population-based prospective cohort study conducted in the Netherlands. PARTICIPANTS A total of 3601 women aged 55 years or older who did not have dementia at baseline (1990-1993) and had information on age at menarche, age at menopause, and type of menopause. Participants were reexamined in 1993-1994 and 1997-1999 and were continuously monitored for development of dementia. MAIN OUTCOME MEASURES Incidence of dementia, based on Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition criteria, and AD, based on National Institute of Neurological Disorders and Stroke/Alzheimer's Disease and Related Disorders Association criteria, compared by quartiles of reproductive period among women with natural menopause. RESULTS During 21 046 person-years of follow-up (median follow-up, 6.3 years), 199 women developed dementia, including 159 who developed AD. After adjusting for age, dementia was not clearly associated with length of reproductive period. However, after adjusting for multiple covariates, women with natural menopause and more reproductive years had an increased risk of dementia (adjusted rate ratio [RR] for women with >39 reproductive years [highest quartile] compared with <34 reproductive years [lowest [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "415", "doc_id": "6309659", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Binding of p53 to enhancer regions (p53BERs) regulates the activity of p53 transcription and cell cycle arrest through the production of p53-dependent eRNAs.\n\nCANDIDATE_ABSTRACT:\nTITLE: eRNAs are required for p53-dependent enhancer activity and gene transcription.\nABSTRACT: Binding within or nearby target genes involved in cell proliferation and survival enables the p53 tumor suppressor gene to regulate their transcription and cell-cycle progression. Using genome-wide chromatin-binding profiles, we describe binding of p53 also to regions located distantly from any known p53 target gene. Interestingly, many of these regions possess conserved p53-binding sites and all known hallmarks of enhancer regions. We demonstrate that these p53-bound enhancer regions (p53BERs) indeed contain enhancer activity and interact intrachromosomally with multiple neighboring genes to convey long-distance p53-dependent transcription regulation. Furthermore, p53BERs produce, in a p53-dependent manner, enhancer RNAs (eRNAs) that are required for efficient transcriptional enhancement of interacting target genes and induction of a p53-dependent cell-cycle arrest. Thus, our results ascribe transcription enhancement activity to p53 with the capacity to regulate multiple genes from a single genomic binding site. Moreover, eRNA production from p53BERs is required for efficient p53 transcription enhancement.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Furthermore, p53BERs produce, in a p53-dependent manner, enhancer RNAs (eRNAs) that are required for efficient transcriptional enhancement of interacting target genes and induction of a p53-dependent cell-cycle arrest.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 177, "doc_id": "9669099", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Ethanol stress increases the expression of PSP in bacteria.\n\nCANDIDATE_ABSTRACT:\nTITLE: Regulatory and metabolic rewiring during laboratory evolution of ethanol tolerance in E. coli\nABSTRACT: Understanding the genetic basis of adaptation is a central problem in biology. However, revealing the underlying molecular mechanisms has been challenging as changes in fitness may result from perturbations to many pathways, any of which may contribute relatively little. We have developed a combined experimental/computational framework to address this problem and used it to understand the genetic basis of ethanol tolerance in Escherichia coli. We used fitness profiling to measure the consequences of single-locus perturbations in the context of ethanol exposure. A module-level computational analysis was then used to reveal the organization of the contributing loci into cellular processes and regulatory pathways (e.g. osmoregulation and cell-wall biogenesis) whose modifications significantly affect ethanol tolerance. Strikingly, we discovered that a dominant component of adaptation involves metabolic rewiring that boosts intracellular ethanol degradation and assimilation. Through phenotypic and metabolomic analysis of laboratory-evolved ethanol-tolerant strains, we investigated naturally accessible pathways of ethanol tolerance. Remarkably, these laboratory-evolved strains, by and large, follow the same adaptive paths as inferred from our coarse-grained search of the fitness landscape.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 390, "doc_id": "1148122", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Suboptimal nutrition is not predictive of chronic disease\n\nCANDIDATE_ABSTRACT:\nTITLE: The Impact of the New WHO Antiretroviral Treatment Guidelines on HIV Epidemic Dynamics and Cost in South Africa\nABSTRACT: BACKGROUND Since November 2009, WHO recommends that adults infected with HIV should initiate antiretroviral therapy (ART) at CD4+ cell counts of ≤350 cells/µl rather than ≤200 cells/µl. South Africa decided to adopt this strategy for pregnant and TB co-infected patients only. We estimated the impact of fully adopting the new WHO guidelines on HIV epidemic dynamics and associated costs. METHODS AND FINDING We used an established model of the transmission and control of HIV in specified sexual networks and healthcare settings. We quantified the model to represent Hlabisa subdistrict, KwaZulu-Natal, South Africa. We predicted the HIV epidemic dynamics, number on ART and program costs under the new guidelines relative to treating patients at ≤200 cells/µl for the next 30 years. During the first five years, the new WHO treatment guidelines require about 7% extra annual investments, whereas 28% more patients receive treatment. Furthermore, there will be a more profound impact on HIV incidence, leading to relatively less annual costs after seven years. The resulting cumulative net costs reach a break-even point after on average 16 years. CONCLUSIONS Our study strengthens the WHO recommendation of starting ART at ≤350 cells/µl for all HIV-infected patients. Apart from the benefits associated with many life-years saved, a modest frontloading appears to lead to net savings within a limited time-horizon. This finding is robust to alternative assumptions and foreseeable changes in ART prices and effectiveness. Therefore, South Africa should aim at rapidly expanding its healthcare infrastructure to fully embrace the new WHO guidelines.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1110, "doc_id": "1986482", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Stiff substrates inhibit mesodermal differentiation by degrading beta-catenin in an integrin-dependent manner.\n\nCANDIDATE_PASSAGE:\nDorsomorphin, a Selective Small Molecule Inhibitor of BMP Signaling, Promotes Cardiomyogenesis in Embryonic Stem Cells BACKGROUND Pluripotent embryonic stem (ES) cells, which have the capacity to give rise to all tissue types in the body, show great promise as a versatile source of cells for regenerative therapy. However, the basic mechanisms of lineage specification of pluripotent stem cells are largely unknown, and generating sufficient quantities of desired cell types remains a formidable challenge. Small molecules, particularly those that modulate key developmental pathways like the bone morphogenetic protein (BMP) signaling cascade, hold promise as tools to study in vitro lineage specification and to direct differentiation of stem cells toward particular cell types. METHODOLOGY/ PRINCIPAL FINDINGS We describe the use of dorsomorphin, a selective small molecule inhibitor of BMP signaling, to induce myocardial differentiation in mouse ES cells. Cardiac induction is very robust, increasing the yield of spontaneously beating cardiomyocytes by at least 20 fold. Dorsomorphin, unlike the endogenous BMP antagonist Noggin, robustly induces cardiomyogenesis when treatment is limited to the initial 24-hours of ES cell differentiation. Quantitative-PCR analyses of differentiating ES cells indicate that pharmacological inhibition of BMP signaling during the early critical stage promotes the development of the cardiomyocyte lineage, but reduces the differentiation of endothelial, smooth muscle, and hematopoietic cells. CONCLUSIONS/ SIGNIFICANCE Administration of a selective small molecule BMP inhibitor during the initial stages of ES cell differentiation substantially promotes the differentiation of primitive pluripotent cells toward the cardiomyocytic lineage, appar [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1102", "doc_id": "14296612", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Patients with panic anxiety show decreased CSF levels of hypocretin.\n\nCANDIDATE_PASSAGE:\nOlanzapine depot exposure in male rats: Dose-dependent lipogenic effects without concomitant weight gain. Treatment with second-generation antipsychotic agents such as olanzapine frequently results in metabolic adverse effects, e.g. hyperphagia, weight gain and dyslipidaemia in patients of both genders. The molecular mechanisms underlying metabolic adverse effects are still largely unknown, and studies in rodents represent an important approach in their exploration. However, the validity of the rodent model is hampered by the fact that antipsychotics induce weight gain in female, but not male, rats. When administered orally, the short half-life of olanzapine in rats prevents stable plasma concentrations of the drug. We recently showed that a single intramuscular injection of long-acting olanzapine formulation yields clinically relevant plasma concentrations accompanied by several dysmetabolic features in the female rat. In the current study, we show that depot injections of 100-250 mg/kg olanzapine yielded clinically relevant plasma olanzapine concentrations also in male rats. In spite of transient hyperphagia, however, olanzapine resulted in weight loss rather than weight gain. The resultant negative feed efficiency was accompanied by a slight elevation of thermogenesis markers in brown adipose tissue for the highest olanzapine dose, but the olanzapine-related reduction in weight gain remains to be explained. In spite of the absence of weight gain, an olanzapine dose of 200mg/kg or above induced significantly elevated plasma cholesterol levels and pronounced activation of lipogenic gene expression in the liver. These results confirm that olanzapine stimulates lipogenic effects, independent of weight gain, and raise the possibility that endocrine factors may [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "930", "doc_id": "45153864", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: APOE4 expression in iPSC-derived neurons results in decreased tau phosphorylation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Gain of toxic Apolipoprotein E4 effects in Human iPSC-Derived Neurons Is Ameliorated by a Small-Molecule Structure Corrector\nABSTRACT: Efforts to develop drugs for Alzheimer's disease (AD) have shown promise in animal studies, only to fail in human trials, suggesting a pressing need to study AD in human model systems. Using human neurons derived from induced pluripotent stem cells that expressed apolipoprotein E4 (ApoE4), a variant of the APOE gene product and the major genetic risk factor for AD, we demonstrated that ApoE4-expressing neurons had higher levels of tau phosphorylation, unrelated to their increased production of amyloid-β (Aβ) peptides, and that they displayed GABAergic neuron degeneration. ApoE4 increased Aβ production in human, but not in mouse, neurons. Converting ApoE4 to ApoE3 by gene editing rescued these phenotypes, indicating the specific effects of ApoE4. Neurons that lacked APOE behaved similarly to those expressing ApoE3, and the introduction of ApoE4 expression recapitulated the pathological phenotypes, suggesting a gain of toxic effects from ApoE4. Treatment of ApoE4-expressing neurons with a small-molecule structure corrector ameliorated the detrimental effects, thus showing that correcting the pathogenic conformation of ApoE4 is a viable therapeutic approach for ApoE4-related AD.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Using human neurons derived from induced pluripotent stem cells that expressed apolipoprotein E4 (ApoE4), a variant of the APOE gene product and the major genetic risk factor for AD, we demonstrated that ApoE4-expressing neurons had higher levels of tau phosphorylation, unrelated to their increased production of amyloid-β (Aβ) peptides, and that they displayed GABAergic neuron degeneration.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 58, "doc_id": "4709641", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Persistor cells are one reason for incomplete responses to Tyrosine kinase inhibitor (TKI) therapy in cancer patients.\n\nCANDIDATE_PASSAGE:\nInterferon alpha and zidovudine therapy in adult T-cell leukaemia lymphoma: response and outcome in 15 patients. Adult T-cell leukaemia lymphoma (ATLL) is an aggressive disease caused by the human T-lymphotropic virus 1 (HTLV-I) with a short survival. Responses to interferon alpha (IFN-alpha) and zidovudine (AZT) have been documented but not with long-term follow-up. We treated 15 ATLL patients with IFN and AZT. Eleven patients had acute ATLL, two had lymphoma and two smouldering ATLL, with progression. The main features were: organomegaly (14), skin lesions (10), high white blood cell (WBC) count (11) and hypercalcaemia (9). Eleven patients had previously received chemotherapy and one had received an autograft. At the time of the study, seven patients had progressive disease and eight were in partial or complete clinical remission. Responses (PR) lasting 2+ to 44+ months were seen in 67%; 26% did not respond (NR) and one patient was not evaluable. Hypercalcaemia predicted a poor outcome but differences were not significant. Eight of the 15 patients have died 3-41 months from diagnosis. Median survival for the 15 patients was 18 months. Survival of the NR ranged from 4 to 20 months; six PR patients are alive 8-82 months from diagnosis. The differences in survival between NR (median: 6 months) and PR (55% of patients alive at 4 years) were statistically significant (P = 0.002). In conclusion, IFN and AZT improves the outcome of ATLL patients and helps maintain responses.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "939", "doc_id": "39443128", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Whole brain radiotherapy increases the occurrence of new brain metastases.\n\nCANDIDATE_ABSTRACT:\nTITLE: Stereotactic radiosurgery plus whole-brain radiation therapy vs stereotactic radiosurgery alone for treatment of brain metastases: a randomized controlled trial.\nABSTRACT: CONTEXT In patients with brain metastases, it is unclear whether adding up-front whole-brain radiation therapy (WBRT) to stereotactic radiosurgery (SRS) has beneficial effects on mortality or neurologic function compared with SRS alone. OBJECTIVE To determine if WBRT combined with SRS results in improvements in survival, brain tumor control, functional preservation rate, and frequency of neurologic death. DESIGN, SETTING, AND PATIENTS Randomized controlled trial of 132 patients with 1 to 4 brain metastases, each less than 3 cm in diameter, enrolled at 11 hospitals in Japan between October 1999 and December 2003. INTERVENTIONS Patients were randomly assigned to receive WBRT plus SRS (65 patients) or SRS alone (67 patients). MAIN OUTCOME MEASURES The primary end point was overall survival; secondary end points were brain tumor recurrence, salvage brain treatment, functional preservation, toxic effects of radiation, and cause of death. RESULTS The median survival time and the 1-year actuarial survival rate were 7.5 months and 38.5% (95% confidence interval, 26.7%-50.3%) in the WBRT + SRS group and 8.0 months and 28.4% (95% confidence interval, 17.6%-39.2%) for SRS alone (P = .42). The 12-month brain tumor recurrence rate was 46.8% in the WBRT + SRS group and 76.4% for SRS alone group (P<.001). Salvage brain treatment was less frequently required in the WBRT + SRS group (n = 10) than with SRS alone (n = 29) (P<.001). Death was attributed to neurologic causes in 22.8% of patients in the WBRT + SRS group and in 19.3% of those treated with SRS alone (P = .64). There were no significant differences in systemic and neurologic functional preservation and toxic effects of radiation. CONCLUSIONS Compared with SRS alone, the use of WBRT plus SRS did not improve survival [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Compared with SRS alone, the use of WBRT plus SRS did not improve survival for patients with 1 to 4 brain metastases, but intracranial relapse occurred considerably more frequently in those who did not receive WBRT.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1376, "doc_id": "3944632", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Vitamin D is an important factor in the relationship between calcium and parathyroid hormone.\n\nCANDIDATE_PASSAGE:\nRAS genes in Saccharomyces cerevisiae: signal transduction in search of a pathway. Ras proteins in budding yeasts initially appeared to regulate initiation of the cell cycle in response to nutrient availability. More recent work, while clarifying the mechanism of Ras-mediated signal transduction, has undermined our notion of the signal Ras transmits. We now suspect that Ras helps to coordinate cellular metabolism and mass accumulation, but what Ras responds to is not clear.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1371", "doc_id": "8210189", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: 5'-nucleotidase metabolizes 6MP.\n\nCANDIDATE_PASSAGE:\nNovel proteinaceous infectious particles cause scrapie. After infection and a prolonged incubation period, the scrapie agent causes a degenerative disease of the central nervous system in sheep and goats. Six lines of evidence including sensitivity to proteases demonstrate that this agent contains a protein that is required for infectivity. Although the scrapie agent is irreversibly inactivated by alkali, five procedures with more specificity for modifying nucleic acids failed to cause inactivation. The agent shows heterogeneity with respect to size, apparently a result of its hydrophobicity; the smallest form may have a molecular weight of 50,000 or less. Because the novel properties of the scrapie agent distinguish it from viruses, plasmids, and viroids, a new term \"prion\" is proposed to denote a small proteinaceous infectious particle which is resistant to inactivation by most procedures that modify nucleic acids. Knowledge of the scrapie agent structure may have significance for understanding the causes of several degenerative diseases.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "14", "doc_id": "7447120", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Exercise reduces cancer mortality rates among Chinese citizens.\n\nCANDIDATE_ABSTRACT:\nTITLE: Combined Impact of Lifestyle-Related Factors on Total and Cause-Specific Mortality among Chinese Women: Prospective Cohort Study\nABSTRACT: BACKGROUND Although cigarette smoking, excessive alcohol drinking, obesity, and several other well-studied unhealthy lifestyle-related factors each have been linked to the risk of multiple chronic diseases and premature death, little is known about the combined impact on mortality outcomes, in particular among Chinese and other non-Western populations. The objective of this study was to quantify the overall impact of lifestyle-related factors beyond that of active cigarette smoking and alcohol consumption on all-cause and cause-specific mortality in Chinese women. METHODS AND FINDINGS We used data from the Shanghai Women's Health Study, an ongoing population-based prospective cohort study in China. Participants included 71,243 women aged 40 to 70 years enrolled during 1996-2000 who never smoked or drank alcohol regularly. A healthy lifestyle score was created on the basis of five lifestyle-related factors shown to be independently associated with mortality outcomes (normal weight, lower waist-hip ratio, daily exercise, never exposed to spouse's smoking, higher daily fruit and vegetable intake). The score ranged from zero (least healthy) to five (most healthy) points. During an average follow-up of 9 years, 2,860 deaths occurred, including 775 from cardiovascular disease (CVD) and 1,351 from cancer. Adjusted hazard ratios for mortality decreased progressively with an increasing number of healthy lifestyle factors. Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality. The inverse association between the healthy lifestyle score and mortality was seen consistently regardless of ch [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The population attributable risks for not having 4-5 healthy lifestyle factors were 33% for total deaths, 59% for CVD deaths, and 19% for cancer deaths.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 397, "doc_id": "1456068", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does single dose propranolol affect physiologic or emotional reactivity to smoking cues?\n\nABSTRACT:\nSmoking cue exposure reactivates salient smoking-related memories, triggering craving to smoke, a phenomenon associated with maintenance of smoking behavior and relapse after periods of abstinence. Acute β-adrenergic blockade with propranolol reduces physiologic reactivity during subsequent recollection of traumatic events by inhibiting reconsolidation of reactivated memories in a process called memory reconsolidation blockade. The objective of this study is to determine whether a single dose of propranolol prior to retrieval of smoking-related memories reduces subsequent physiologic reactivity to personally salient smoking imagery scripts in current smokers. Fifty-four overnight-abstinent, adult smokers received a single-dose propranolol or placebo prior to reactivation of smoking-related memories in a randomized, double-blind, placebo-controlled trial and resumed smoking afterward. One week later, skin conductance (SC), heart rate (HR), left corrugator electromyogram (EMG), self-reported emotional state, and craving were assessed following script-driven imagery with neutral and personalized smoking-related scripts. Smoking scripts were associated with increased physiologic activation (SC, HR, EMG), craving, and negative emotional state compared with neutral scripts. Propranolol did not moderate the effect of script type on any outcome.", "output": "{\"label\": \"no\", \"rationale\": \"Personalized smoking script-driven imagery robustly increased physiologic activation, negative emotional state, and craving, and a single dose of propranolol prior to memory reactivation did not moderate this effect.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25413896, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The gene daf-16, which encodes forkhead Box O (FOXO), is required for all phenotypes associated with reduced insulin/insulin-like growth factor (Igf) signaling.\n\nCANDIDATE_PASSAGE:\nMutation spectrum in the nephrin gene (NPHS1) in congenital nephrotic syndrome. Congenital nephrotic syndrome, Finnish type (CNF or NPHS1), is an autosomal recessive disease characterized by massive proteinuria and development of nephrotic syndrome shortly after birth. The disease is most common in Finland, but many patients have been identified in other populations. The disease is caused by mutations in the gene for nephrin which is a key component of the glomerual ultrafilter, the podocyte slit diaphragm. A total of 30 mutations have been reported in the nephrin gene in patients with congenital nephrotic syndrome worldwide. In the Finnish population, two main mutations have been found. These two nonsense mutations account for over 94% of all mutations in Finland. Most mutations found in non-Finnish patients are missense mutations, but they include also nonsense and splice site mutations, as well as deletions and insertions. This mutation update summarizes the nature of all previously reported nephrin mutations and, additionally, describes 20 novel mutations recently identified in our laboratory.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1219", "doc_id": "41599676", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Cellular clocks are not predictive of mitosis timing in NIH 3T3 cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Robust synchronization of coupled circadian and cell cycle oscillators in single mammalian cells\nABSTRACT: Circadian cycles and cell cycles are two fundamental periodic processes with a period in the range of 1 day. Consequently, coupling between such cycles can lead to synchronization. Here, we estimated the mutual interactions between the two oscillators by time-lapse imaging of single mammalian NIH3T3 fibroblasts during several days. The analysis of thousands of circadian cycles in dividing cells clearly indicated that both oscillators tick in a 1:1 mode-locked state, with cell divisions occurring tightly 5 h before the peak in circadian Rev-Erbα-YFP reporter expression. In principle, such synchrony may be caused by either unidirectional or bidirectional coupling. While gating of cell division by the circadian cycle has been most studied, our data combined with stochastic modeling unambiguously show that the reverse coupling is predominant in NIH3T3 cells. Moreover, temperature, genetic, and pharmacological perturbations showed that the two interacting cellular oscillators adopt a synchronized state that is highly robust over a wide range of parameters. These findings have implications for circadian function in proliferative tissues, including epidermis, immune cells, and cancer.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The analysis of thousands of circadian cycles in dividing cells clearly indicated that both oscillators tick in a 1:1 mode-locked state, with cell divisions occurring tightly 5 h before the peak in circadian Rev-Erbα-YFP reporter expression.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 242, "doc_id": "2212067", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does longitudinal myocardial contraction improve early during titration with metoprolol CR/XL in patients with heart failure?\n\nABSTRACT:\nTo investigate diastolic and systolic left ventricular recovery during titration with metoprolol CR/XL (controlled release/extended release). Placebo run in, followed by an open study. University hospital. 14 patients with chronic heart failure. Metoprolol CR/XL titrated from 12.5 mg once daily to 200 mg once daily. M mode recordings of atrioventricular (AV) plane displacement, Doppler measurement of transmitral flow and pulmonary venous flow, two dimensional ejection fraction, and measurement of venous plasma concentration of noradrenaline. Patients were investigated after 2, 4, 6, and 24 weeks of treatment. A reduction of heart rate was observed on the first dose (12.5 mg once daily), from a mean (SD) of 74 (11) to 67 (11) beats/min, p < 0.05. This was accompanied by prominent effects on AV plane filling parameters, including an increase in early diastolic filling period from 87 (28) to 105 (33) ms (p < 0.05), and in the lateral AV plane fractional shortening from 8.7 (2.7)% to 10.2 (2.8)% (p < 0.05). An early trend towards improvement in global systolic left ventricular function was also seen, although this was not significant until six weeks. Ejection fraction increased from 33 (7.5)% to 38 (11)% (p < 0.05).", "output": "{\"label\": \"yes\", \"rationale\": \"First effects of left ventricular recovery during beta blocker treatment were seen in recordings of longitudinal performance, as expressed by AV plane displacement. Doppler flow dynamics as well as global systolic recovery appeared several weeks later, emphasising the importance of longitudinal performance in evaluating left ventricular function.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 11751658, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Commelina yellow mottle virus (ComYMV) has three typical badnavirus ORFs, capable of encoding proteins 23, 15, and 216 kD.\n\nCANDIDATE_PASSAGE:\nCytomegalovirus US2 destroys two components of the MHC class II pathway, preventing recognition by CD4+ T cells Human cytomegalovirus (HCMV) is a ubiquitous herpesvirus that causes life-threatening disease in patients who are immunosuppressed for bone marrow or tissue transplantation or who have AIDS (ref. 1). HCMV establishes lifelong latent infections and, after periodic reactivation from latency, uses a panel of immune evasion proteins to survive and replicate in the face of robust, fully primed host immunity. Monocyte/macrophages are important host cells for HCMV, serving as a latent reservoir and as a means of dissemination throughout the body. Macrophages and other HCMV-permissive cells, such as endothelial and glial cells, can express MHC class II proteins and present antigens to CD4+ T lymphocytes. Here, we show that the HCMV protein US2 causes degradation of two essential proteins in the MHC class II antigen presentation pathway: HLA-DR-α and DM-α. This was unexpected, as US2 has been shown to cause degradation of MHC class I (refs. 5,6), which has only limited homology with class II proteins. Expression of US2 in cells reduced or abolished their ability to present antigen to CD4+ T lymphocytes. Thus, US2 may allow HCMV-infected macrophages to remain relatively 'invisible' to CD4+ T cells, a property that would be important after virus reactivation.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "277", "doc_id": "27555165", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Women are more susceptible to death due to pneumonia when compared to men.\n\nCANDIDATE_ABSTRACT:\nTITLE: Gender-dependent differences in outcome after the treatment of infection in hospitalized patients.\nABSTRACT: CONTEXT While it is established that management strategies and outcomes differ by gender for many diseases, its effect on infection has not been adequately studied. OBJECTIVE To investigate the role of gender among hospitalized patients treated for infection. DESIGN Observational cohort study conducted during a 26-month period from December 1996 through January 1999. SETTING University-affiliated hospital. PARTICIPANTS A total of 892 patients in the surgical units of the hospital with 1470 consecutive infectious episodes (782 in men and 688 in women). MAIN OUTCOME MEASURES Mortality during hospitalization by gender for infection episodes overall and for specific infectious sites, including lung, peritoneum, bloodstream, catheter, urine, surgical site, and skin/soft tissue. RESULTS Among all infections, there was no significant difference in mortality based on gender (men, 11.1% vs women, 14.2%; P = .07). After logistic regression analysis, factors independently associated with mortality included higher APACHE (Acute Physiology and Chronic Health Evaluation) II score, older age, malignancy, blood transfusion, and diagnosis of infection more than 7 days after admission, but not gender (female odds ratio [OR] for death, 1.32; 95% confidence interval [CI], 0.90-1.94; P = .16). Mortality was higher in women for lung (men, 18% vs women, 34%; P = .002) and soft tissue (men, 2% vs women, 10%; P < or = .05) infection; for other infectious sites, mortality did not differ by gender. Factors associated with mortality due to pneumonia by logistic regression included higher APACHE II score, malignancy, diabetes mellitus, diagnosis of infection more than 7 days after admission, older age, transplantation, and female gender (OR for death, 2.25; 95% CI, 1.17-4.32; P = .02). [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Although gender may not be predictive of mortality among all infections, women appear to be at increased risk for death from hospital-acquired pneumonia, even after controlling for other comorbidities.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1378, "doc_id": "2488880", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pharmacist attendance at ward rounds increases adverse events in wards.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pharmacist participation on physician rounds and adverse drug events in the intensive care unit.\nABSTRACT: CONTEXT Pharmacist review of medication orders in the intensive care unit (ICU) has been shown to prevent errors, and pharmacist consultation has reduced drug costs. However, whether pharmacist participation in the ICU at the time of drug prescribing reduces adverse events has not been studied. OBJECTIVE To measure the effect of pharmacist participation on medical rounds in the ICU on the rate of preventable adverse drug events (ADEs) caused by ordering errors. DESIGN Before-after comparison between phase 1 (baseline) and phase 2 (after intervention implemented) and phase 2 comparison with a control unit that did not receive the intervention. SETTING A medical ICU (study unit) and a coronary care unit (control unit) in a large urban teaching hospital. PATIENTS Seventy-five patients randomly selected from each of 3 groups: all admissions to the study unit from February 1, 1993, through July 31, 1993 (baseline) and all admissions to the study unit (postintervention) and control unit from October 1, 1994, through July 7, 1995. In addition, 50 patients were selected at random from the control unit during the baseline period. INTERVENTION A senior pharmacist made rounds with the ICU team and remained in the ICU for consultation in the morning, and was available on call throughout the day. MAIN OUTCOME MEASURES Preventable ADEs due to ordering (prescribing) errors and the number, type, and acceptance of interventions made by the pharmacist. Preventable ADEs were identified by review of medical records of the randomly selected patients during both preintervention and postintervention phases. Pharmacists recorded all recommendations, which were then analyzed by type and acceptance. RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 pat [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS The presence of a pharmacist on rounds as a full member of the patient care team in a medical ICU was associated with a substantially lower rate of ADEs caused by prescribing errors.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 940, "doc_id": "12258338", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Self-advocacy training is effective at decreasing homelessness.\n\nCANDIDATE_PASSAGE:\nIn vitro antimicrobial activity of mangrove plant Sonneratia alba. OBJECTIVE To investigate the antimicrobial property of mangrove plant Sonneratia alba (S. alba). METHODS The antimicrobial activity was evaluated using disc diffusion and microdilution methods against six microorganisms. Soxhlet apparatus was used for extraction with a series of solvents, n-hexane, ethyl acetate and methanol in sequence of increasing polarity. RESULTS Methanol extract appeared to be the most effective extract while n-hexane extract showed no activity. The antimicrobial activities were observed against the gram positive bacteria Staphylococcus aureus (S. aureus) and Bacillus cereus (B. cereus), the gram negative Escherichia coli (E. coli) and the yeast Cryptococcus neoformans. Pseudomonas aeruginosa and Candida albicans appeared to be not sensitive to the concentrations tested since no inhibition zone was observed. E. coli (17.5 mm) appeared to be the most sensitive strain followed by S. aureus (12.5 mm) and B. cereus (12.5 mm). CONCLUSIONS From this study, it can be concluded that S. alba exhibits antimicrobial activities against certain microorganisms.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1070", "doc_id": "43165768", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Silencing of Bcl2 is important for the maintenance and progression of tumors.\n\nCANDIDATE_PASSAGE:\nLarge intestine-targeted nanoparticle-releasing oral vaccine to control genitorectal viral infection Both rectal and vaginal mucosal surfaces serve as transmission routes for pathogenic microorganisms. Vaccination through large intestinal mucosa, previously proven protective for both of these mucosal sites in animal studies, can be achieved successfully by direct intracolorectal (i.c.r.) administration, but this route is clinically impractical. Oral vaccine delivery seems preferable but runs the risk of the vaccine's destruction in the upper gastrointestinal tract. Therefore, we designed a large intestine-targeted oral delivery with pH-dependent microparticles containing vaccine nanoparticles, which induced colorectal immunity in mice comparably to colorectal vaccination and protected against rectal and vaginal viral challenge. Conversely, vaccine targeted to the small intestine induced only small intestinal immunity and provided no rectal or vaginal protection, demonstrating functional compartmentalization within the gut mucosal immune system. Therefore, using this oral vaccine delivery system to target the large intestine, but not the small intestine, may represent a feasible new strategy for immune protection of rectal and vaginal mucosa.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1088", "doc_id": "13764090", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: DUSP4 decreases apoptosis.\n\nCANDIDATE_PASSAGE:\nCongruent Visual Speech Enhances Cortical Entrainment to Continuous Auditory Speech in Noise-Free Conditions. UNLABELLED Congruent audiovisual speech enhances our ability to comprehend a speaker, even in noise-free conditions. When incongruent auditory and visual information is presented concurrently, it can hinder a listener's perception and even cause him or her to perceive information that was not presented in either modality. Efforts to investigate the neural basis of these effects have often focused on the special case of discrete audiovisual syllables that are spatially and temporally congruent, with less work done on the case of natural, continuous speech. Recent electrophysiological studies have demonstrated that cortical response measures to continuous auditory speech can be easily obtained using multivariate analysis methods. Here, we apply such methods to the case of audiovisual speech and, importantly, present a novel framework for indexing multisensory integration in the context of continuous speech. Specifically, we examine how the temporal and contextual congruency of ongoing audiovisual speech affects the cortical encoding of the speech envelope in humans using electroencephalography. We demonstrate that the cortical representation of the speech envelope is enhanced by the presentation of congruent audiovisual speech in noise-free conditions. Furthermore, we show that this is likely attributable to the contribution of neural generators that are not particularly active during unimodal stimulation and that it is most prominent at the temporal scale corresponding to syllabic rate (2-6 Hz). Finally, our data suggest that neural entrainment to the speech envelope is inhibited when the auditory and visual streams are incongruent both temporally and [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "306", "doc_id": "14437255", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Immune complex triggered cell death leads to extracellular release of nuclear DNA.\n\nCANDIDATE_PASSAGE:\nNeutrophil extracellular traps enriched in oxidized mitochondrial DNA are interferogenic and contribute to lupus-like disease Neutrophil extracellular traps (NETs) are implicated in autoimmunity, but how they are generated and their roles in sterile inflammation remain unclear. Ribonucleoprotein immune complexes (RNP ICs), inducers of NETosis, require mitochondrial reactive oxygen species (ROS) for maximal NET stimulation. After RNP IC stimulation of neutrophils, mitochondria become hypopolarized and translocate to the cell surface. Extracellular release of oxidized mitochondrial DNA is proinflammatory in vitro, and when this DNA is injected into mice, it stimulates type I interferon (IFN) signaling through a pathway dependent on the DNA sensor STING. Mitochondrial ROS are also necessary for spontaneous NETosis of low-density granulocytes from individuals with systemic lupus erythematosus. This was also observed in individuals with chronic granulomatous disease, who lack NADPH oxidase activity but still develop autoimmunity and type I IFN signatures. Mitochondrial ROS inhibition in vivo reduces disease severity and type I IFN responses in a mouse model of lupus. Together, these findings highlight a role for mitochondria in the generation not only of NETs but also of pro-inflammatory oxidized mitochondrial DNA in autoimmune diseases.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "555", "doc_id": "1049501", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Suboptimal nutrition is a leading cause of premature death\n\nCANDIDATE_PASSAGE:\nGlobal, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015 BACKGROUND The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. METHODS We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors-the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1109", "doc_id": "13770184", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pharmacist attendance at ward rounds increases adverse events in wards.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pharmacist participation on physician rounds and adverse drug events in the intensive care unit.\nABSTRACT: CONTEXT Pharmacist review of medication orders in the intensive care unit (ICU) has been shown to prevent errors, and pharmacist consultation has reduced drug costs. However, whether pharmacist participation in the ICU at the time of drug prescribing reduces adverse events has not been studied. OBJECTIVE To measure the effect of pharmacist participation on medical rounds in the ICU on the rate of preventable adverse drug events (ADEs) caused by ordering errors. DESIGN Before-after comparison between phase 1 (baseline) and phase 2 (after intervention implemented) and phase 2 comparison with a control unit that did not receive the intervention. SETTING A medical ICU (study unit) and a coronary care unit (control unit) in a large urban teaching hospital. PATIENTS Seventy-five patients randomly selected from each of 3 groups: all admissions to the study unit from February 1, 1993, through July 31, 1993 (baseline) and all admissions to the study unit (postintervention) and control unit from October 1, 1994, through July 7, 1995. In addition, 50 patients were selected at random from the control unit during the baseline period. INTERVENTION A senior pharmacist made rounds with the ICU team and remained in the ICU for consultation in the morning, and was available on call throughout the day. MAIN OUTCOME MEASURES Preventable ADEs due to ordering (prescribing) errors and the number, type, and acceptance of interventions made by the pharmacist. Preventable ADEs were identified by review of medical records of the randomly selected patients during both preintervention and postintervention phases. Pharmacists recorded all recommendations, which were then analyzed by type and acceptance. RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 pat [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"RESULTS The rate of preventable ordering ADEs decreased by 66% from 10.4 per 1000 patient-days (95% confidence interval [CI], 7-14) before the intervention to 3.5 (95% CI, 1-5; P<.001) after the intervention.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 940, "doc_id": "12258338", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The proliferative capacity of progenitors is regulated cell-autonomously.\n\nCANDIDATE_PASSAGE:\nFrontal stroke syndromes. The frontal lobe is the largest lobe of the brain, and it is thus commonly involved in stroke. Moreover, almost one in five strokes is limited to the prerolandic areas. This high frequency of anatomical involvement is in sharp contrast with the apparent rarity of clinical frontal dysfunction in stroke. It is remarkable that frontal behavioral syndromes have been rather uncommonly reported in patients with stroke as compared to patients with other diseases, such as brain tumor. This fact is paradoxical, because an acute process (stroke) is expected to yield more clinical dysfunction than a more chronic disease (tumor). A volume effect may be the main factor leading to this phenomenon. Another interesting aspect of frontal strokes is the contribution of so-called 'silent' strokes, the recurrence of which may nevertheless lead to intellectual decline and compromise recovery from another stroke with more specific neurologic dysfunction. The contribution of stroke to understanding of frontal lobe dysfunction is important, because of the focal nature of this disease, and great opportunity for clinical-topographic classification correlations. One of the first modern attempts to develop a clinical-topographic classification of frontal lobe lesions came from the school of Luria, who tried to delineate three main types of frontal lobe syndromes (premotor syndrome, prefrontal syndrome, medial-frontal syndrome). Recent anatomic correlates using MRI make it possible to improve this classification. We suggest considering six main clinical-anatomic frontal stroke syndromes: (1) prefrontal; (2) premotor; (3) superior medial; (4) orbital-medial; (5) basal forebrain; (6) white matter. Finally, another fascinating topic relates to frontal lobe symptom [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1255", "doc_id": "46764350", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Women with a higher birth weight are more likely to develop breast cancer later in life.\n\nCANDIDATE_ABSTRACT:\nTITLE: Intrauterine environments and breast cancer risk: meta-analysis and systematic review\nABSTRACT: INTRODUCTION Various perinatal factors, including birth weight, birth order, maternal age, gestational age, twin status, and parental smoking, have been postulated to affect breast cancer risk in daughters by altering the hormonal environment of the developing fetal mammary glands. Despite ample biologic plausibility, epidemiologic studies to date have yielded conflicting results. We investigated the associations between perinatal factors and subsequent breast cancer risk through meta-analyses. METHODS We reviewed breast cancer studies published from January 1966 to February 2007 that included data on birth weight, birth order, maternal age, gestational age, twin status, and maternal or paternal smoking. Meta-analyses using random effect models were employed to summarize the results. RESULTS We found that heavier birth weights were associated with increased breast cancer risk, with studies involving five categories of birth weight identifying odds ratios (ORs) of 1.24 (95% confidence interval [CI] 1.04 to 1.48) for 4,000 g or more and 1.15 (95% CI 1.04 to 1.26) for 3,500 g to 3,999 g, relative to a birth weight of 2,500 to 2,599 g. These studies provided no support for a J-shaped relationship of birthweight to risk. Support for an association with birthweight was also derived from studies based on three birth weight categories (OR 1.15 [95% CI 1.01 to 1.31] for > or =4,000 g relative to <3,000 g) and two birth weight categories (OR 1.09 [95% CI 1.02 to 1.18] for > or =3,000 g relative to <3,000 g). Women born to older mothers and twins were also at some increased risk, but the results were heterogeneous across studies and publication years. Birth order, prematurity, and maternal smoking were unrelated to breast cancer risk. CONCLUSION Our findings provide so [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"RESULTS We found that heavier birth weights were associated with increased breast cancer risk, with studies involving five categories of birth weight identifying odds ratios (ORs) of 1.24 (95% confidence interval [CI] 1.04 to 1.48) for 4,000 g or more and 1.15 (95% CI 1.04 to 1.26) for 3,500 g to 3,999 g, relative to a birth weight of 2,500 to 2,599 g. These studies provided no support for a J-shaped relationship of birthweight to risk.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1379, "doc_id": "17450673", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nCANDIDATE_ABSTRACT:\nTITLE: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\nABSTRACT: Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens. However, signals underlying mTEC development remain largely unclear. Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals. Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment. Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner. These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1181, "doc_id": "2734421", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Physical activity level has no association with the difference in maximal oxygen consumption between black and white youth.\n\nCANDIDATE_PASSAGE:\nBreast cancer and obesity: an update. Obesity has a complicated relationship to both breast cancer risk and the clinical behavior of the established disease. In postmenopausal women, particularly the elderly, various measures of obesity have been positively associated with risk. However, before menopause increased body weight is inversely related to breast cancer risk. In both premenopausal and postmenopausal breast cancer, the mechanisms by which body weight and obesity affect risk have been related to estrogenic activity. Obesity has also been related to advanced disease at diagnosis and with a poor prognosis in both premenopausal and postmenopausal breast cancer. Breast cancer in African-American women, considering its relationship to obesity, exhibits some important differences from those described in white women, although the high prevalence of obesity in African-American women may contribute to the relatively poor prognosis compared with white American women. Despite the emphasis on estrogens to explain the effects of obesity on breast cancer, other factors may prove to be equally or more important, particularly as they relate to expression of an aggressive tumor phenotype. Among these, this review serves to stress insulin, insulin-like growth factor-I, and leptin, and their relationship to angiogenesis, and transcriptional factors.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "945", "doc_id": "25973484", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: LRBA promotes CTLA - 4 recycling.\n\nCANDIDATE_ABSTRACT:\nTITLE: Autosomal dominant immune dysregulation syndrome in humans with CTLA4 mutations\nABSTRACT: The protein cytotoxic T lymphocyte antigen-4 (CTLA-4) is an essential negative regulator of immune responses, and its loss causes fatal autoimmunity in mice. We studied a large family in which five individuals presented with a complex, autosomal dominant immune dysregulation syndrome characterized by hypogammaglobulinemia, recurrent infections and multiple autoimmune clinical features. We identified a heterozygous nonsense mutation in exon 1 of CTLA4. Screening of 71 unrelated patients with comparable clinical phenotypes identified five additional families (nine individuals) with previously undescribed splice site and missense mutations in CTLA4. Clinical penetrance was incomplete (eight adults of a total of 19 genetically proven CTLA4 mutation carriers were considered unaffected). However, CTLA-4 protein expression was decreased in regulatory T cells (Treg cells) in both patients and carriers with CTLA4 mutations. Whereas Treg cells were generally present at elevated numbers in these individuals, their suppressive function, CTLA-4 ligand binding and transendocytosis of CD80 were impaired. Mutations in CTLA4 were also associated with decreased circulating B cell numbers. Taken together, mutations in CTLA4 resulting in CTLA-4 haploinsufficiency or impaired ligand binding result in disrupted T and B cell homeostasis and a complex immune dysregulation syndrome.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 677, "doc_id": "857189", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: In patients with congenital heart defects, β-blockers significantly improve clinical heart failure outcomes.\n\nCANDIDATE_PASSAGE:\nCarvedilol for children and adolescents with heart failure: a randomized controlled trial. CONTEXT Although beta-blockers improve symptoms and survival in adults with heart failure, little is known about these medications in children and adolescents. OBJECTIVE To prospectively evaluate the effects of carvedilol in children and adolescents with symptomatic systemic ventricular systolic dysfunction. DESIGN, SETTING, AND PARTICIPANTS A multicenter, randomized, double-blind, placebo-controlled study of 161 children and adolescents with symptomatic systolic heart failure from 26 US centers. In addition to treatment with conventional heart failure medications, patients were assigned to receive placebo or carvedilol. Enrollment began in June 2000 and the last dose was given in May 2005 (each patient received medication for 8 months). INTERVENTIONS Patients were randomized in a 1:1:1 ratio to twice-daily dosing with placebo, low-dose carvedilol (0.2 mg/kg per dose if weight <62.5 kg or 12.5 mg per dose if weight > or =62.5 kg), or high-dose carvedilol (0.4 mg/kg per dose if weight <62.5 kg or 25 mg per dose if weight > or =62.5 kg) and were stratified according to whether each patient's systemic ventricle was a left ventricle or not. MAIN OUTCOME MEASURES The primary outcome was a composite measure of heart failure outcomes in patients receiving carvedilol (low- and high-dose combined) vs placebo. Secondary efficacy variables included individual components of this composite, echocardiographic measures, and plasma b-type natriuretic peptide levels. RESULTS There was no statistically significant difference between groups for the composite end point based on the percentage of patients who improved, worsened, or were unchanged. Among 54 patients assigned to placebo, 30 [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "579", "doc_id": "34139429", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Genomic sequences involved in alternative splicing responsible for Hutchinson-Gilford progeria syndrome (HGPS) are abundant in the ''progerinonly'' allele of Lmna knock-in models.\n\nCANDIDATE_PASSAGE:\nShort-term medical service trips: a systematic review of the evidence. Short-term medical service trips (MSTs) aim to address unmet health care needs of low- and middle-income countries. The lack of critically reviewed empirical evidence of activities and outcomes is a concern. Developing evidence-based recommendations for health care delivery requires systematic research review. I focused on MST publications with empirical results. Searches in May 2013 identified 67 studies published since 1993, only 6% of the published articles on the topic in the past 20 years. Nearly 80% reported on surgical trips. Although the MST field is growing, its medical literature lags behind, with nearly all of the scholarly publications lacking significant data collection. By incorporating data collection into service trips, groups can validate practices and provide information about areas needing improvement.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "466", "doc_id": "38180456", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: RAD52 is involved in break-induced DNA replication (BIR).\n\nCANDIDATE_PASSAGE:\nDistinct roles for DNA-PK, ATM and ATR in RPA phosphorylation and checkpoint activation in response to replication stress DNA damage encountered by DNA replication forks poses risks of genome destabilization, a precursor to carcinogenesis. Damage checkpoint systems cause cell cycle arrest, promote repair and induce programed cell death when damage is severe. Checkpoints are critical parts of the DNA damage response network that act to suppress cancer. DNA damage and perturbation of replication machinery causes replication stress, characterized by accumulation of single-stranded DNA bound by replication protein A (RPA), which triggers activation of ataxia telangiectasia and Rad3 related (ATR) and phosphorylation of the RPA32, subunit of RPA, leading to Chk1 activation and arrest. DNA-dependent protein kinase catalytic subunit (DNA-PKcs) [a kinase related to ataxia telangiectasia mutated (ATM) and ATR] has well characterized roles in DNA double-strand break repair, but poorly understood roles in replication stress-induced RPA phosphorylation. We show that DNA-PKcs mutant cells fail to arrest replication following stress, and mutations in RPA32 phosphorylation sites targeted by DNA-PKcs increase the proportion of cells in mitosis, impair ATR signaling to Chk1 and confer a G2/M arrest defect. Inhibition of ATR and DNA-PK (but not ATM), mimic the defects observed in cells expressing mutant RPA32. Cells expressing mutant RPA32 or DNA-PKcs show sustained H2AX phosphorylation in response to replication stress that persists in cells entering mitosis, indicating inappropriate mitotic entry with unrepaired damage.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1003", "doc_id": "12909503", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does naltrexone affect isoflurane minimum alveolar concentration in cats?\n\nABSTRACT:\nTo test whether naltrexone, an opioid receptor antagonist, affects the minimum alveolar concentration (MAC) of isoflurane in cats, a species that is relatively resistant to the general anesthetic sparing effects of most opioids. Randomized, crossover, placebo-controlled, blinded experimental design. Six healthy adult cats weighing 4.9 ± 0.7 kg. The cats were studied twice. In the first study, baseline isoflurane MAC was measured in duplicate. The drug (saline control or 0.6 mg kg(-1) naltrexone) was administered IV every 40-60 minutes, and isoflurane MAC was re-measured. In the second study, cats received the second drug treatment using identical methods 2 weeks later. Isoflurane MAC was 2.03 ± 0.12% and was unchanged from baseline following saline or naltrexone administration.", "output": "{\"label\": \"no\", \"rationale\": \"Minimum alveolar concentration was unaffected by naltrexone. Because MAC in cats is unaffected by at least some mu-opioid agonists and antagonists, spinal neurons that are directly modulated by mu-opioid receptors in this species cannot be the neuroanatomic sites responsible for immobility from inhaled anesthetics.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 23279646, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is tachysystole Following Cervical Ripening and Induction of Labor Associated with Adverse Outcomes?\n\nABSTRACT:\nThis study was aimed at determining if significant uterine tachysystole was associated with adverse fetal or neonatal outcomes during cervical ripening and induction of labor. Women undergoing cervical ripening and subsequent labor induction (n = 905) were assessed for tachysystole, defined as ≥6 contractions in each of 2 consecutive 10-minute windows. Women with ≥3 episodes of tachysystole were compared to women with no tachysystole. Over a 5-year period, 70% of the 905 participants (n = 631) had no tachysystole, 143 had 1 or 2 episodes whereas 131 or 15% had ≥3 episodes (p = 0.991). The cesarean delivery rate was lower among those with tachysystole (28.2 vs. 34.1%), but the difference was not significant (p = 0.197). Non-reassuring fetal tracings were more common in the tachysystole group (14.4 vs. 21.4%, p = 0.017), but the Apgar scores at 5 min and the umbilical cord pH and base excess were similar between the 2 groups (p = 0.502, p = 0.435, and p = 0.535, respectively).", "output": "{\"label\": \"no\", \"rationale\": \"Tachysystole was not associated with adverse perinatal outcomes when compared to women with no tachysystole during cervical ripening and induction of labor.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 27816973, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is abdominal wall thickness useful to predict appendix visualization on sonography in adult patients with suspected appendicitis?\n\nABSTRACT:\nTo evaluate clinical and imaging factors for potential use in predicting appendix visualization on sonography (US) of adult patients with suspected appendicitis. All adult patients who underwent appendiceal US from January through June 2010 were included in this retrospective study. Clinicopathological records were reviewed for age, sex, weight, body mass index, symptom duration, Alvarado score, surgicopathologic diagnosis, and disposition. Imaging records were collated for abdominal thicknesses, appendix visualization, and impression. The definitive diagnosis was made on pathologic evaluation. Eighty-six patients (68 women; median age, 35.5 years; age range, 16-86 years) met the inclusion criteria. The patients' mean weight was 56 kg; body mass index, 22.4; duration of symptoms, 24 hours; and Alvarado score, 6.5. Of the 86 patients, 37 (43%) had appendicitis. The appendix was visualized on US in 27 patients, of whom 25 had appendicitis; the appendix was not visualized in 59 patients, of whom 12 had appendicitis. There was no correlation between the clinical factors studied, the abdominal fat thickness (10.9 versus 10.7 mm; p = 0.90), or the abdominal wall thickness (16.9 versus 17.3 mm; p = 0.76) between patients with a US-visualized appendix and those whose appendix was not visualized on US.", "output": "{\"label\": \"no\", \"rationale\": \"Abdominal thicknesses and other factors are not predictive of appendix visualization on US examination of adults with suspected appendicitis.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25338515, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Inositol lipid 3-phosphatase PTEN converts Ptdlns(3,4)P 2 into phosphatidylinositol 4-phosphate.\n\nCANDIDATE_ABSTRACT:\nTITLE: Naringenin inhibits allergen-induced airway inflammation and airway responsiveness and inhibits NF-kappaB activity in a murine model of asthma.\nABSTRACT: Naringenin, a flavonoid, has antiinflammatory and immunomodulatory properties. We investigated whether naringenin could attenuate allergen-induced airway inflammation and its possible mechanism in a murine model of asthma. Mice were sensitized and challenged with ovalbumin. Some mice were administered with naringenin before ovalbumin challenge. We evaluated the development of airway inflammation and airway reactivity. Interleukin (IL)4, IL13, chemokine (C-C motif) ligand (CCL)5, and CCL11 in bronchoalveolar lavage fluid and serum total IgE were detected by ELISA. IkappaBalpha degradation and inducible nitric oxide synthase (iNOS) in lungs were measured by Western blot. We also tested NF-kappaB binding activity by electrophoretic mobility shift assay. The mRNA levels of iNOS, CCL5, and CCL11 were detected by real-time PCR. Naringenin attenuated ovalbumin-induced airway inflammation and airway reactivity in experimental mice. The naringenin-treated mice had lower levels of IL4 and IL13 in the bronchoalveolar lavage fluid and lower serum total IgE. Furthermore, naringenin inhibited pulmonary IkappaBalpha degradation and NF-kappaB DNA-binding activity. The levels of CCL5, CCL11, and iNOS were also significantly reduced. The results indicated that naringenin may play protective roles in the asthma process. The inhibition of NF-kappaB and the decreased expression of its target genes may account for this phenomenon.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 636, "doc_id": "888896", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Suboptimal nutrition is not predictive of chronic disease\n\nCANDIDATE_ABSTRACT:\nTITLE: Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015\nABSTRACT: BACKGROUND The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. METHODS We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors-the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. We characterised risk exposure in relation to a Socio-demographic Index (SDI). FINDINGS Between 1990 and 2015, global exposure to unsafe sanitation, household air pollution, childhood underweight, childhood stunting, and smoking [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In 2015, the ten largest contributors to global DALYs among Level 3 risks were high systolic blood pressure (211·8 million [192·7 million to 231·1 million] global DALYs), smoking (148·6 million [134·2 million to 163·1 million]), high fasting plasma glucose (143·1 million [125·1 million to 163·5 million]), high BMI (120·1 million [83·8 million to 158·4 million]), childhood undernutrition (113·3 million [103·9 million to 123·4 million]), ambient particulate matter (103·1 million [90·8 million to 115·1 million]), high total cholesterol (88·7 million [74·6 million to 105·7 million]), household air pollution (85·6 million [66·7 million to 106·1 million]), alcohol use (85·0 million [77·2 million to 93·0 million]), and diets high in sodium (83·0 million [49·3 million to 127·5 million]).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1110, "doc_id": "13770184", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Individuals with low serum vitamin D concentrations have increased risk of multiple sclerosis.\n\nCANDIDATE_PASSAGE:\nCholesteryl Ester Transfer Protein (CETP) Polymorphisms Affect mRNA Splicing, HDL Levels, and Sex-Dependent Cardiovascular Risk Polymorphisms in and around the Cholesteryl Ester Transfer Protein (CETP) gene have been associated with HDL levels, risk for coronary artery disease (CAD), and response to therapy. The mechanism of action of these polymorphisms has yet to be defined. We used mRNA allelic expression and splice isoform measurements in human liver tissues to identify the genetic variants affecting CETP levels. Allelic CETP mRNA expression ratios in 56 human livers were strongly associated with several variants 2.5-7 kb upstream of the transcription start site (e.g., rs247616 p = 6.4 × 10(-5), allele frequency 33%). In addition, a common alternatively spliced CETP isoform lacking exon 9 (Δ9), has been shown to prevent CETP secretion in a dominant-negative manner. The Δ 9 expression ranged from 10 to 48% of total CETP mRNA in 94 livers. Increased formation of this isoform was exclusively associated with an exon 9 polymorphism rs5883-C>T (p = 6.8 × 10(-10)) and intron 8 polymorphism rs9930761-T>C (5.6 × 10(-8)) (in high linkage disequilibrium with allele frequencies 6-7%). rs9930761 changes a key splicing branch point nucleotide in intron 8, while rs5883 alters an exonic splicing enhancer sequence in exon 9.The effect of these polymorphisms was evaluated in two clinical studies. In the Whitehall II study of 4745 subjects, both rs247616 and rs5883T/rs9930761C were independently associated with increased HDL-C levels in males with similar effect size (rs247616 p = 9.6 × 10(-28) and rs5883 p = 8.6 × 10(-10), adjusted for rs247616). In an independent multiethnic US cohort of hypertensive subjects with CAD (INVEST-GENE), rs5883T/rs9930761C alone were signific [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "623", "doc_id": "3868322", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does rugby headgear prevent concussion?\n\nABSTRACT:\nTo examine the attitudes of players and coaches to the use of protective headgear, particularly with respect to the prevention of concussion. A questionnaire designed to assess attitudes to headgear was administered to 63 players from four different Canadian teams, each representing a different level of play (high school, university, community club, national). In addition, coaches from all four levels were questioned about team policies and their personal opinions about the use of headgear to prevent concussion. Although the players tended to believe that the headgear could prevent concussion (62%), the coaches were less convinced (33%). Despite the players' belief that headgear offers protection against concussion, only a minority reported wearing headgear (27%) and few (24%) felt that its use should be made mandatory. Common reasons for not wearing headgear were \"its use is not mandatory\", \"it is uncomfortable\", and \"it costs too much\".", "output": "{\"label\": \"maybe\", \"rationale\": \"Although most players in the study believe that rugby headgear may prevent concussion, only a minority reported wearing it. Coaches tended to be less convinced than the players that rugby headgear can prevent concussion.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 11867487, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Amitriptyline is an effective treatment for chronic tension-type headaches.\n\nCANDIDATE_PASSAGE:\nMechanisms of astrocytogenesis in the mammalian brain. In the mammalian central nervous system, astrocytes are the most abundant cell type and play crucial roles in brain development and function. Astrocytes are known to be produced from multipotent neural stem cells (NSCs) at the late gestational stage during brain development, and accumulating evidence indicates that this stage-dependent generation of astrocytes from NSCs is achieved by systematic cooperation between environmental cues and cell-intrinsic programs. Exemplifying the former is cytokine signaling through the gp130-Janus kinase/signal transducer and activator of transcription 3 pathway, and exemplifying the latter is epigenetic modification of astrocyte-specific genes. Here, we introduce recent advances in our understanding of the mechanisms that coordinate astrocytogenesis from NSCs by modulating signaling pathways and epigenetic programs, with a particular focus on the developing mammalian forebrain.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "108", "doc_id": "6559201", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: 53% of perinatal mortality is due to low birth weight.\n\nCANDIDATE_ABSTRACT:\nTITLE: Estimates of global prevalence of childhood underweight in 1990 and 2015.\nABSTRACT: CONTEXT One key target of the United Nations Millennium Development goals is to reduce the prevalence of underweight among children younger than 5 years by half between 1990 and 2015. OBJECTIVE To estimate trends in childhood underweight by geographic regions of the world. DESIGN, SETTING, AND PARTICIPANTS Time series study of prevalence of underweight, defined as weight 2 SDs below the mean weight for age of the National Center for Health Statistics and World Health Organization (WHO) reference population. National prevalence rates derived from the WHO Global Database on Child Growth and Malnutrition, which includes data on approximately 31 million children younger than 5 years who participated in 419 national nutritional surveys in 139 countries from 1965 through 2002. MAIN OUTCOME MEASURES Linear mixed-effects modeling was used to estimate prevalence rates and numbers of underweight children by region in 1990 and 2015 and to calculate the changes (ie, increase or decrease) to these values between 1990 and 2015. RESULTS Worldwide, underweight prevalence was projected to decline from 26.5% in 1990 to 17.6% in 2015, a change of -34% (95% confidence interval [CI], -43% to -23%). In developed countries, the prevalence was estimated to decrease from 1.6% to 0.9%, a change of -41% (95% CI, -92% to 343%). In developing regions, the prevalence was forecasted to decline from 30.2% to 19.3%, a change of -36% (95% CI, -45% to -26%). In Africa, the prevalence of underweight was forecasted to increase from 24.0% to 26.8%, a change of 12% (95% CI, 8%-16%). In Asia, the prevalence was estimated to decrease from 35.1% to 18.5%, a change of -47% (95% CI, -58% to -34%). Worldwide, the number of underweight children was projected to decline from 163.8 million in 1990 to 113. [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 17, "doc_id": "1606628", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: De novo assembly of sequence data has more specific contigs than unassembled sequence data.\n\nCANDIDATE_PASSAGE:\nHuman artificial chromosomes with alpha satellite-based de novo centromeres show increased frequency of nondisjunction and anaphase lag. Human artificial chromosomes have been used to model requirements for human chromosome segregation and to explore the nature of sequences competent for centromere function. Normal human centromeres require specialized chromatin that consists of alpha satellite DNA complexed with epigenetically modified histones and centromere-specific proteins. While several types of alpha satellite DNA have been used to assemble de novo centromeres in artificial chromosome assays, the extent to which they fully recapitulate normal centromere function has not been explored. Here, we have used two kinds of alpha satellite DNA, DXZ1 (from the X chromosome) and D17Z1 (from chromosome 17), to generate human artificial chromosomes. Although artificial chromosomes are mitotically stable over many months in culture, when we examined their segregation in individual cell divisions using an anaphase assay, artificial chromosomes exhibited more segregation errors than natural human chromosomes (P < 0.001). Naturally occurring, but abnormal small ring chromosomes derived from chromosome 17 and the X chromosome also missegregate more than normal chromosomes, implicating overall chromosome size and/or structure in the fidelity of chromosome segregation. As different artificial chromosomes missegregate over a fivefold range, the data suggest that variable centromeric DNA content and/or epigenetic assembly can influence the mitotic behavior of artificial chromosomes.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "312", "doc_id": "25041967", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Most termination events in Okazaki fragments are sequence specific.\n\nCANDIDATE_PASSAGE:\nThe First Myriapod Genome Sequence Reveals Conservative Arthropod Gene Content and Genome Organisation in the Centipede Strigamia maritima Myriapods (e.g., centipedes and millipedes) display a simple homonomous body plan relative to other arthropods. All members of the class are terrestrial, but they attained terrestriality independently of insects. Myriapoda is the only arthropod class not represented by a sequenced genome. We present an analysis of the genome of the centipede Strigamia maritima. It retains a compact genome that has undergone less gene loss and shuffling than previously sequenced arthropods, and many orthologues of genes conserved from the bilaterian ancestor that have been lost in insects. Our analysis locates many genes in conserved macro-synteny contexts, and many small-scale examples of gene clustering. We describe several examples where S. maritima shows different solutions from insects to similar problems. The insect olfactory receptor gene family is absent from S. maritima, and olfaction in air is likely effected by expansion of other receptor gene families. For some genes S. maritima has evolved paralogues to generate coding sequence diversity, where insects use alternate splicing. This is most striking for the Dscam gene, which in Drosophila generates more than 100,000 alternate splice forms, but in S. maritima is encoded by over 100 paralogues. We see an intriguing linkage between the absence of any known photosensory proteins in a blind organism and the additional absence of canonical circadian clock genes. The phylogenetic position of myriapods allows us to identify where in arthropod phylogeny several particular molecular mechanisms and traits emerged. For example, we conclude that juvenile hormone signalling evolved with the e [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "808", "doc_id": "1332250", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: IFIT1 restricts viral replication by sequestrating mis-capped viral RNAs.\n\nCANDIDATE_PASSAGE:\nNeutrophilic infiltration within the airway smooth muscle in patients with COPD. BACKGROUND COPD is an inflammatory disorder characterised by chronic airflow limitation, but the extent to which airway inflammation is related to functional abnormalities is still uncertain. The interaction between inflammatory cells and airway smooth muscle may have a crucial role. METHODS To investigate the microlocalisation of inflammatory cells within the airway smooth muscle in COPD, surgical specimens obtained from 26 subjects undergoing thoracotomy (eight smokers with COPD, 10 smokers with normal lung function, and eight non-smoking controls) were examined. Immunohistochemical analysis was used to quantify the number of neutrophils, macrophages, mast cells, CD4+ and CD8+ cells localised within the smooth muscle of peripheral airways. RESULTS Smokers with COPD had an increased number of neutrophils and CD8+ cells in the airway smooth muscle compared with non-smokers. Smokers with normal lung function also had a neutrophilic infiltration in the airway smooth muscle, but to a lesser extent. When all the subjects were analysed as one group, neutrophilic infiltration was inversely related to forced expiratory volume in 1 second (% predicted). CONCLUSIONS Microlocalisation of neutrophils and CD8+ cells in the airway smooth muscle in smokers with COPD suggests a possible role for these cells in the pathogenesis of smoking induced airflow limitation.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "544", "doc_id": "6417632", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Birth-weight is negatively associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Birth Size and Breast Cancer Risk: Re-analysis of Individual Participant Data from 32 Studies\nABSTRACT: BACKGROUND Birth size, perhaps a proxy for prenatal environment, might be a correlate of subsequent breast cancer risk, but findings from epidemiological studies have been inconsistent. We re-analysed individual participant data from published and unpublished studies to obtain more precise estimates of the magnitude and shape of the birth size-breast cancer association. METHODS AND FINDINGS Studies were identified through computer-assisted and manual searches, and personal communication with investigators. Individual participant data from 32 studies, comprising 22,058 breast cancer cases, were obtained. Random effect models were used, if appropriate, to combine study-specific estimates of effect. Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003). Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data. Birth length and head circumference from birth records were also positively associated with breast cancer risk (pooled RR per one SD increment: 1.06 [95% CI 1.03-1.10] and 1.09 [95% CI 1.03-1.15], respectively). Simultaneous adjustment for these three birth size variables showed that length was the strongest independent predictor of risk. The birth size effec [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 178, "doc_id": "16322674", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Gpr124 suppresses BBB breakdown in mouse models of ischemic stroke.\n\nCANDIDATE_PASSAGE:\nGpr124 is essential for blood–brain barrier integrity in central nervous system disease Although blood–brain barrier (BBB) compromise is central to the etiology of diverse central nervous system (CNS) disorders, endothelial receptor proteins that control BBB function are poorly defined. The endothelial G-protein-coupled receptor (GPCR) Gpr124 has been reported to be required for normal forebrain angiogenesis and BBB function in mouse embryos, but the role of this receptor in adult animals is unknown. Here Gpr124 conditional knockout (CKO) in the endothelia of adult mice did not affect homeostatic BBB integrity, but resulted in BBB disruption and microvascular hemorrhage in mouse models of both ischemic stroke and glioblastoma, accompanied by reduced cerebrovascular canonical Wnt–β-catenin signaling. Constitutive activation of Wnt–β-catenin signaling fully corrected the BBB disruption and hemorrhage defects of Gpr124-CKO mice, with rescue of the endothelial gene tight junction, pericyte coverage and extracellular-matrix deficits. We thus identify Gpr124 as an endothelial GPCR specifically required for endothelial Wnt signaling and BBB integrity under pathological conditions in adult mice. This finding implicates Gpr124 as a potential therapeutic target for human CNS disorders characterized by BBB disruption.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "480", "doc_id": "6325527", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: A diminished ovarian reserve does not solely indicate infertility in an a priori non-infertile population.\n\nCANDIDATE_ABSTRACT:\nTITLE: Deficiency and pharmacological stabilization of mast cells reduce diet-induced obesity and diabetes in mice\nABSTRACT: Although mast cell functions have classically been related to allergic responses, recent studies indicate that these cells contribute to other common diseases such as multiple sclerosis, rheumatoid arthritis, atherosclerosis, aortic aneurysm and cancer. This study presents evidence that mast cells also contribute to diet-induced obesity and diabetes. For example, white adipose tissue (WAT) from obese humans and mice contain more mast cells than WAT from their lean counterparts. Furthermore, in the context of mice on a Western diet, genetically induced deficiency of mast cells, or their pharmacological stabilization, reduces body weight gain and levels of inflammatory cytokines, chemokines and proteases in serum and WAT, in concert with improved glucose homeostasis and energy expenditure. Mechanistic studies reveal that mast cells contribute to WAT and muscle angiogenesis and associated cell apoptosis and cathepsin activity. Adoptive transfer experiments of cytokine-deficient mast cells show that these cells, by producing interleukin-6 (IL-6) and interferon-gamma (IFN-gamma), contribute to mouse adipose tissue cysteine protease cathepsin expression, apoptosis and angiogenesis, thereby promoting diet-induced obesity and glucose intolerance. Our results showing reduced obesity and diabetes in mice treated with clinically available mast cell-stabilizing agents suggest the potential of developing new therapies for these common human metabolic disorders.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 39, "doc_id": "597790", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Transcription factor EB induces transcription of pro-inflammatory cytokines in macrophages infected with Staphylococcus aureus.\n\nCANDIDATE_ABSTRACT:\nTITLE: TECHNICAL ADVANCE Floral dip: a simplified method for Agrobacterium-mediated\nABSTRACT: The Agrobacterium vacuum infiltration method has made it possible to transform Arabidopsis thaliana without plant tissue culture or regeneration. In the present study, this method was evaluated and a substantially modified transformation method was developed. The labor-intensive vacuum infiltration process was eliminated in favor of simple dipping of developing floral tissues into a solution containing Agrobacterium tumefaciens, 5% sucrose and 500 microliters per litre of surfactant Silwet L-77. Sucrose and surfactant were critical to the success of the floral dip method. Plants inoculated when numerous immature floral buds and few siliques were present produced transformed progeny at the highest rate. Plant tissue culture media, the hormone benzylamino purine and pH adjustment were unnecessary, and Agrobacterium could be applied to plants at a range of cell densities. Repeated application of Agrobacterium improved transformation rates and overall yield of transformants approximately twofold. Covering plants for 1 day to retain humidity after inoculation also raised transformation rates twofold. Multiple ecotypes were transformable by this method. The modified method should facilitate high-throughput transformation of Arabidopsis for efforts such as T-DNA gene tagging, positional cloning, or attempts at targeted gene replacement.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1312, "doc_id": "410286", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Ca2+ cycling controls whole-body energy homeostasis in beige fat.\n\nCANDIDATE_PASSAGE:\nUCP1-independent signaling involving SERCA2b-mediated calcium cycling regulates beige fat thermogenesis and systemic glucose homeostasis Uncoupling protein 1 (UCP1) plays a central role in nonshivering thermogenesis in brown fat; however, its role in beige fat remains unclear. Here we report a robust UCP1-independent thermogenic mechanism in beige fat that involves enhanced ATP-dependent Ca2+ cycling by sarco/endoplasmic reticulum Ca2+-ATPase 2b (SERCA2b) and ryanodine receptor 2 (RyR2). Inhibition of SERCA2b impairs UCP1-independent beige fat thermogenesis in humans and mice as well as in pigs, a species that lacks a functional UCP1 protein. Conversely, enhanced Ca2+ cycling by activation of α1- and/or β3-adrenergic receptors or the SERCA2b-RyR2 pathway stimulates UCP1-independent thermogenesis in beige adipocytes. In the absence of UCP1, beige fat dynamically expends glucose through enhanced glycolysis, tricarboxylic acid metabolism and pyruvate dehydrogenase activity for ATP-dependent thermogenesis through the SERCA2b pathway; beige fat thereby functions as a 'glucose sink' and improves glucose tolerance independently of body weight loss. Our study uncovers a noncanonical thermogenic mechanism through which beige fat controls whole-body energy homeostasis via Ca2+ cycling.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "220", "doc_id": "19205437", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: CD44v6 is not associated with constitutive and reprogrammed cancer stem cells driving cancer metastasis.\n\nCANDIDATE_PASSAGE:\nBest--worst scaling: What it can do for health care research and how to do it. Statements like \"quality of care is more highly valued than waiting time\" can neither be supported nor refuted by comparisons of utility parameters from a traditional discrete choice experiment (DCE). Best--worst scaling can overcome this problem because it asks respondents to perform a different choice task. However, whilst the nature of the best--worst task is generally understood, there are a number of issues relating to the design and analysis of a best--worst choice experiment that require further exposition. This paper illustrates how to aggregate and analyse such data and using a quality of life pilot study demonstrates how richer insights can be drawn by the use of best--worst tasks.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "203", "doc_id": "3222122", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Splenomegaly is observed in knockin mouse lacking the SHP-2 MAPK pathway.\n\nCANDIDATE_ABSTRACT:\nTITLE: Dissection of signaling cascades through gp130 in vivo: reciprocal roles for STAT3- and SHP2-mediated signals in immune responses.\nABSTRACT: We generated a series of knockin mouse lines, in which the cytokine receptor gp130-dependent STAT3 and/or SHP2 signals were disrupted, by replacing the mouse gp130 gene with human gp130 mutant cDNAs. The SHP2 signal-deficient mice (gp130F759/F759 were born normal but displayed splenomegaly and lymphadenopathy and an enhanced acute phase reaction. In contrast, the STAT3 signal-deficient mice (gp130FXQ/FXXQ) died perinatally, like the gp130-deficient mice (gp130D/D). The gp130F759/F759 mice showed prolonged gp130-induced STAT3 activation, indicating a negative regulatory role for SHP2. Th1-type cytokine production and IgG2a and IgG2b production were increased in the gp130F759/F759 mice, while they were decreased in the gp130FXXQ/FXXQ immune system. These results indicate that the balance of positive and negative signals generated through gp130 regulates the immune responses.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The SHP2 signal-deficient mice (gp130F759/F759 were born normal but displayed splenomegaly and lymphadenopathy and an enhanced acute phase reaction.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1097, "doc_id": "26851674", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Repressing IL-18 has negative effects on atherosclerotic lesion composition and progression.\n\nCANDIDATE_PASSAGE:\nCycling Quiescence in Temozolomide Resistant Glioblastoma Cells Is Partly Explained by microRNA-93 and -193-Mediated Decrease of Cyclin D Glioblastoma multiforme (GBM) is a fatal malignancy of the central nervous system, commonly associated with chemoresistance. The alkylating agent Temozolomide (TMZ) is the front-line chemotherapeutic agent and has undergone intense studies on resistance. These studies reported on mismatch repair gene upregulation, ABC-targeted drug efflux, and cell cycle alterations. The mechanism by which TMZ induces cell cycle arrest has not been well-established. TMZ-resistant GBM cells have been linked to microRNA (miRNA) and exosomes. A cell cycle miRNA array identified distinct miRNAs only in exosomes from TMZ-resistant GBM cell lines and primary spheres. We narrowed the miRs to miR-93 and -193 and showed in computational analyses that they could target Cyclin D1. Since Cyclin D1 is a major regulator of cell cycle progression, we performed cause-effect studies and showed a blunting effects of miR-93 and -193 in Cyclin D1 expression. These two miRs also decreased cell cycling quiescence and induced resistance to TMZ. Taken together, our data provide a mechanism by which GBM cells can exhibit TMZ-induced resistance through miRNA targeting of Cyclin D1. The data provide a number of therapeutic approaches to reverse chemoresistance at the miRNA, exosomal and cell cycle points.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1042", "doc_id": "67787658", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: β1/Ketel is able to bind microtubules.\n\nCANDIDATE_PASSAGE:\nP446L-importin-beta inhibits nuclear envelope assembly by sequestering nuclear envelope assembly factors to the microtubules. The P446L mutant Drosophila importin-beta (P446L-imp-beta) has been reported to prohibit--in dominant negative fashion--nuclear envelope (NE) assembly. Along elucidating the mode of action of P446L-imp-beta we studied in vitro NE assembly on Sepharose beads. While Drosophila embryo extracts support NE assembly over Sepharose beads coated with Ran, NE assembly does not take place in extracts supplied with exogenous P446L-imp-beta. A NE also forms over importin-beta-coated beads. Surprisingly, when immobilized to Sepharose beads P446L-imp-beta as efficiently recruits NE vesicles as normal importin-beta. The discrepancy in behavior of cytoplasmic and bead-bound P446L-imp-beta appears to be related to icreased--as compared to normal importin-beta--microtubule (MT) binding ability of P446L-imp-beta. While wild-type importin-beta is able to bind MTs and the binding decreases upon RanGTP interaction, P446L-imp-beta cannot be removed from the MTs by RanGTP. P446L-imp-beta, like normal importin-beta, binds some types of the nucleoporins that have been known to be required for NE assembly at the end of mitosis. It appears that the inhibitory effect of P446L-imp-beta on NE assembly is caused by sequestering some of the nucleoporins required for NE assembly to the MTs.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1407", "doc_id": "29863668", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Assembly of invadopodia is triggered by focal generation of phosphatidylinositol-3,4-biphosphate and the activation of the nonreceptor tyrosine kinase Src.\n\nCANDIDATE_PASSAGE:\nT cell receptor ligation induces the formation of dynamically regulated signaling assemblies Tcell antigen receptor (TCR) ligation initiates tyrosine kinase activation, signaling complex assembly, and immune synapse formation. Here, we studied the kinetics and mechanics of signaling complex formation in live Jurkat leukemic T cells using signaling proteins fluorescently tagged with variants of enhanced GFP (EGFP). Within seconds of contacting coverslips coated with stimulatory antibodies, T cells developed small, dynamically regulated clusters which were enriched in the TCR, phosphotyrosine, ZAP-70, LAT, Grb2, Gads, and SLP-76, excluded the lipid raft marker enhanced yellow fluorescent protein–GPI, and were competent to induce calcium elevations. LAT, Grb2, and Gads were transiently associated with the TCR. Although ZAP-70–containing clusters persisted for more than 20 min, photobleaching studies revealed that ZAP-70 continuously dissociated from and returned to these complexes. Strikingly, SLP-76 translocated to a perinuclear structure after clustering with the TCR. Our results emphasize the dynamically changing composition of signaling complexes and indicate that these complexes can form within seconds of TCR engagement, in the absence of either lipid raft aggregation or the formation of a central TCR-rich cluster.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "133", "doc_id": "2825380", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: aPKCz causes tumour suppression by affecting glutamine metabolism.\n\nCANDIDATE_PASSAGE:\nCOMMD proteins, a novel family of structural and functional homologs of MURR1. MURR1 is a multifunctional protein that inhibits nuclear factor kappaB (NF-kappaB), a transcription factor with pleiotropic functions affecting innate and adaptive immunity, apoptosis, cell cycle regulation, and oncogenesis. Here we report the discovery of a new family of proteins with homology to MURR1. These proteins form multimeric complexes and were identified in a biochemical screen for MURR1-associated factors. The family is defined by the presence of a conserved and unique motif termed the COMM (copper metabolism gene MURR1) domain, which functions as an interface for protein-protein interactions. Like MURR1, several of these factors also associate with and inhibit NF-kappaB. The proteins designated as COMMD or COMM domain containing 1-10 are extensively conserved in multicellular eukaryotic organisms and define a novel family of structural and functional homologs of MURR1. The prototype of this family, MURR1/COMMD1, suppresses NF-kappaB not by affecting nuclear translocation or binding of NF-kappaB to cognate motifs; rather, it functions in the nucleus by affecting the association of NF-kappaB with chromatin.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1383", "doc_id": "11844826", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The risk of male prisoners harming themselves is ten times that of female prisoners.\n\nCANDIDATE_ABSTRACT:\nTITLE: Self-harm in prisons in England and Wales: an epidemiological study of prevalence, risk factors, clustering, and subsequent suicide\nABSTRACT: BACKGROUND Self-harm and suicide are common in prisoners, yet robust information on the full extent and characteristics of people at risk of self-harm is scant. Furthermore, understanding how frequently self-harm is followed by suicide, and in which prisoners this progression is most likely to happen, is important. We did a case-control study of all prisoners in England and Wales to ascertain the prevalence of self-harm in this population, associated risk factors, clustering effects, and risk of subsequent suicide after self-harm. METHODS Records of self-harm incidents in all prisons in England and Wales were gathered routinely between January, 2004, and December, 2009. We did a case-control comparison of prisoners who self-harmed and those who did not between January, 2006, and December, 2009. We also used a Bayesian approach to look at clustering of people who self-harmed. Prisoners who self-harmed and subsequently died by suicide in prison were compared with other inmates who self-harmed. FINDINGS 139,195 self-harm incidents were recorded in 26,510 individual prisoners between 2004 and 2009; 5-6% of male prisoners and 20-24% of female inmates self-harmed every year. Self-harm rates were more than ten times higher in female prisoners than in male inmates. Repetition of self-harm was common, particularly in women and teenage girls, in whom a subgroup of 102 prisoners accounted for 17,307 episodes. In both sexes, self-harm was associated with younger age, white ethnic origin, prison type, and a life sentence or being unsentenced; in female inmates, committing a violent offence against an individual was also a factor. Substantial evidence was noted of clustering in time and location of prisoners who self-harmed (adjusted intra-class correlation 0·15, 95% CI 0 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"FINDINGS 139,195 self-harm incidents were recorded in 26,510 individual prisoners between 2004 and 2009; 5-6% of male prisoners and 20-24% of female inmates self-harmed every year.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1270, "doc_id": "13900610", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: RANK-RANKL pathway signalling is linked to development of Aire-expressing medullary thymic epithelial cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: RANK signals from CD4+3− inducer cells regulate development of Aire-expressing epithelial cells in the thymic medulla\nABSTRACT: Aire-expressing medullary thymic epithelial cells (mTECs) play a key role in preventing autoimmunity by expressing tissue-restricted antigens to help purge the emerging T cell receptor repertoire of self-reactive specificities. Here we demonstrate a novel role for a CD4+3− inducer cell population, previously linked to development of organized secondary lymphoid structures and maintenance of T cell memory in the functional regulation of Aire-mediated promiscuous gene expression in the thymus. CD4+3− cells are closely associated with mTECs in adult thymus, and in fetal thymus their appearance is temporally linked with the appearance of Aire+ mTECs. We show that RANKL signals from this cell promote the maturation of RANK-expressing CD80−Aire− mTEC progenitors into CD80+Aire+ mTECs, and that transplantation of RANK-deficient thymic stroma into immunodeficient hosts induces autoimmunity. Collectively, our data reveal cellular and molecular mechanisms leading to the generation of Aire+ mTECs and highlight a previously unrecognized role for CD4+3−RANKL+ inducer cells in intrathymic self-tolerance.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Collectively, our data reveal cellular and molecular mechanisms leading to the generation of Aire+ mTECs and highlight a previously unrecognized role for CD4+3−RANKL+ inducer cells in intrathymic self-tolerance.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1005, "doc_id": "3952288", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Do younger women have a better prognosis among patients with esophageal squamous cell carcinoma after esophagectomy?\n\nABSTRACT:\nEpidemiological studies have suggested a potential role for sex hormones in esophageal squamous cell carcinoma (ESCC) etiology. However, the significance of gender as an independent prognostic factor remains uncertain. Our retrospective study was designed to investigate the prognostic role of gender for survival after esophagectomy. Data from 674 patients with ESCC who underwent surgical resection were retrospectively analysed. Age 55 years was selected as a surrogate for menopause. Patients were assigned to age-gender groups: A (female younger than age 55 years), B (female age 55 years and older), C (male younger than age 55 years) and D (male age 55 years and older). Univariate and multivariate analyses were performed to identify prognostic factors for survival. There were 520 males and 154 females with median age was 58 years. The 1-, 3-, 5-year survival rates of group A, B, C and D were 93.6%, 70.2%, 61.7% vs. 86.9%, 47.7%, 40.2% vs. 77.8%, 43.9%, 37.0% and 80.3%, 47.9%, 36.6%, respectively (P=0.003). Multivariate analysis suggested that age-gender groups and pTNM staging were independent prognostic factors.", "output": "{\"label\": \"yes\", \"rationale\": \"Among patients with ESCC after esophagectomy, women younger than age 55 years attained a favorable prognosis.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 27162661, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: B cells go though plasmablast differentiation and antibody production by continuous expression of EBI2.\n\nCANDIDATE_ABSTRACT:\nTITLE: Guidance of B cells by the orphan G protein-coupled receptor EBI2 shapes humoral immune responses.\nABSTRACT: Humoral immunity depends on both rapid and long-term antibody production against invading pathogens. This is achieved by the generation of spatially distinct extrafollicular plasmablast and follicular germinal center (GC) B cell populations, but the signals that guide responding B cells to these alternative compartments have not been fully elucidated. Here, we show that expression of the orphan G protein-coupled receptor Epstein-Barr virus-induced gene 2 (EBI2, also known as GPR183) by activated B cells was essential for their movement to extrafollicular sites and induction of early plasmablast responses. Conversely, downregulation of EBI2 enabled B cells to access the center of follicles and promoted efficient GC formation. EBI2 therefore provides a previously uncharacterized dimension to B cell migration that is crucial for coordinating rapid versus long-term antibody responses.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"EBI2 therefore provides a previously uncharacterized dimension to B cell migration that is crucial for coordinating rapid versus long-term antibody responses.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 152, "doc_id": "15488881", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Mutations in G-Beta protein GNB2 are present in many cancers, resulting in loss of interaction with G-alpha subunits and concomitant activation of AKT pathway.\n\nCANDIDATE_PASSAGE:\nMutations in G protein beta subunits promote transformation and kinase inhibitor resistance Activating mutations in genes encoding G protein α (Gα) subunits occur in 4-5% of all human cancers, but oncogenic alterations in Gβ subunits have not been defined. Here we demonstrate that recurrent mutations in the Gβ proteins GNB1 and GNB2 confer cytokine-independent growth and activate canonical G protein signaling. Multiple mutations in GNB1 affect the protein interface that binds Gα subunits as well as downstream effectors and disrupt Gα interactions with the Gβγ dimer. Different mutations in Gβ proteins clustered partly on the basis of lineage; for example, all 11 GNB1 K57 mutations were in myeloid neoplasms, and seven of eight GNB1 I80 mutations were in B cell neoplasms. Expression of patient-derived GNB1 variants in Cdkn2a-deficient mouse bone marrow followed by transplantation resulted in either myeloid or B cell malignancies. In vivo treatment with the dual PI3K-mTOR inhibitor BEZ235 suppressed GNB1-induced signaling and markedly increased survival. In several human tumors, mutations in the gene encoding GNB1 co-occurred with oncogenic kinase alterations, including the BCR-ABL fusion protein, the V617F substitution in JAK2 and the V600K substitution in BRAF. Coexpression of patient-derived GNB1 variants with these mutant kinases resulted in inhibitor resistance in each context. Thus, GNB1 and GNB2 alterations confer transformed and resistance phenotypes across a range of human tumors and may be targetable with inhibitors of G protein signaling.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "814", "doc_id": "33387953", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The deamination of cytidine to uridine on the minus strand of viral DNA can inactivate the viral genome by inducing G-to-A mutations.\n\nCANDIDATE_PASSAGE:\nBroad antiretroviral defence by human APOBEC3G through lethal editing of nascent reverse transcripts Viral replication usually requires that innate intracellular lines of defence be overcome, a task usually accomplished by specialized viral gene products. The virion infectivity factor (Vif) protein of human immunodeficiency virus (HIV) is required during the late stages of viral production to counter the antiviral activity of APOBEC3G (apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G; also known as CEM15), a protein expressed notably in human T lymphocytes. When produced in the presence of APOBEC3G, vif-defective virus is non-infectious. APOBEC3G is closely related to APOBEC1, the central component of an RNA-editing complex that deaminates a cytosine residue in apoB messenger RNA. APOBEC family members also have potent DNA mutator activity through dC deamination; however, whether the editing potential of APOBEC3G has any relevance to HIV inhibition is unknown. Here, we demonstrate that it does, as APOBEC3G exerts its antiviral effect during reverse transcription to trigger G-to-A hypermutation in the nascent retroviral DNA. We also find that APOBEC3G can act on a broad range of retroviruses in addition to HIV, suggesting that hypermutation by editing is a general innate defence mechanism against this important group of pathogens.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1209", "doc_id": "4347374", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Gluten tolerance in adult patients with celiac disease 20 years after diagnosis?\n\nABSTRACT:\nCeliac disease (CD) is believed to be a permanent intolerance to gluten. A number of patients, however, discontinue the gluten-free diet (GFD) without developing symptoms or signs. The aim of our study was to investigate whether CD patients are capable of developing tolerance to gluten. All 77 adult patients from our hospital known to have biopsy-proven CD for more than 10 years were invited to participate. We investigated symptoms, gluten consumption, antibodies for CD and other autoimmunity, human leukocyte antigen (HLA)-typing, bone mineral density, and performed small bowel biopsies. Tolerance was defined as no immunological or histological signs of CD while consuming gluten. Sixty-six patients accepted participation, but after review of the diagnostic biopsies 53 were found to have true CD. Twenty-three percent of patients had a gluten-containing diet, 15% admitted gluten transgression and 62% followed the GFD. Patients on a GFD had significantly more osteoporosis. Normal small bowel mucosa was found in four of eight on gluten-containing diet and in four of four with gluten transgression. Two patients were considered to have developed tolerance to gluten. One of them was HLA-DQ2/DQ8 negative.", "output": "{\"label\": \"maybe\", \"rationale\": \"Development of tolerance to gluten seems possible in some patients with CD. Further follow-up will show whether this tolerance is permanent or only a long-term return to latency. This feature may be associated with genetic characteristics, especially with HLA genotypes that differ from DQ2 or DQ8.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 18403944, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: HbA1c consistently overestimates glycemic control in black individuals with Sickle cell trait (SCT).\n\nCANDIDATE_ABSTRACT:\nTITLE: Association of Sickle Cell Trait With Hemoglobin A1c in African Americans\nABSTRACT: Importance Hemoglobin A1c (HbA1c) reflects past glucose concentrations, but this relationship may differ between those with sickle cell trait (SCT) and those without it. Objective To evaluate the association between SCT and HbA1c for given levels of fasting or 2-hour glucose levels among African Americans. Design, Setting, and Participants Retrospective cohort study using data collected from 7938 participants in 2 community-based cohorts, the Coronary Artery Risk Development in Young Adults (CARDIA) study and the Jackson Heart Study (JHS). From the CARDIA study, 2637 patients contributed a maximum of 2 visits (2005-2011); from the JHS, 5301 participants contributed a maximum of 3 visits (2000-2013). All visits were scheduled at approximately 5-year intervals. Participants without SCT data, those without any concurrent HbA1c and glucose measurements, and those with hemoglobin variants HbSS, HbCC, or HbAC were excluded. Analysis of the primary outcome was conducted using generalized estimating equations (GEE) to examine the association of SCT with HbA1c levels, controlling for fasting or 2-hour glucose measures. Exposures Presence of SCT. Main Outcomes and Measures Hemoglobin A1c stratified by the presence or absence of SCT was the primary outcome measure. Results The analytic sample included 4620 participants (mean age, 52.3 [SD, 11.8] years; 2835 women [61.3%]; 367 [7.9%] with SCT) with 9062 concurrent measures of fasting glucose and HbA1c levels. In unadjusted GEE analyses, for a given fasting glucose, HbA1c values were statistically significantly lower in those with (5.72%) vs those without (6.01%) SCT (mean HbA1c difference, −0.29%; 95% CI, −0.35% to −0.23%). Findings were similar in models adjusted for key risk factors and in analyses using 2001 concurre [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The prevalence of prediabetes and diabetes was statistically significantly lower among participants with SCT when defined using HbA1c values (29.2% vs 48.6% for prediabetes and 3.8% vs 7.3% for diabetes in 572 observations from participants with SCT and 6877 observations from participants without SCT; P<.001 for both comparisons).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 499, "doc_id": "26064662", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: A low percentage of hematopoietic progenitor cells are susceptible to HIV-1 infection ex vivo.\n\nCANDIDATE_PASSAGE:\nHIV–1 Infects Multipotent Progenitor Cells Causing Cell Death and Establishing Latent Cellular Reservoirs HIV causes a chronic infection characterized by depletion of CD4(+) T lymphocytes and the development of opportunistic infections. Despite drugs that inhibit viral spread, HIV infection has been difficult to cure because of uncharacterized reservoirs of infected cells that are resistant to highly active antiretroviral therapy (HAART) and the immune response. Here we used CD34(+) cells from infected people as well as in vitro studies of wild-type HIV to show infection and killing of CD34(+) multipotent hematopoietic progenitor cells (HPCs). In some HPCs, we detected latent infection that stably persisted in cell culture until viral gene expression was activated by differentiation factors. A unique reporter HIV that directly detects latently infected cells in vitro confirmed the presence of distinct populations of active and latently infected HPCs. These findings have major implications for understanding HIV bone marrow pathology and the mechanisms by which HIV causes persistent infection.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "43", "doc_id": "7224723", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Cancer cells can stimulate the accumulation of intra-tumoural myeloid-derived suppressor cells by promoting granulocyte colony stimulating factor production.\n\nCANDIDATE_PASSAGE:\nDiscovery of endothelial to mesenchymal transition as a source for carcinoma-associated fibroblasts. Activated fibroblasts are associated with many different tumors. Myofibroblasts, activated fibroblasts, and perivascular mesenchymal cells such as pericytes play a role in cancer progression. Many studies suggest that myofibroblasts facilitate tumor growth and cancer progression. The source for myofibroblasts and other activated fibroblasts within the tumors is still debated. Although de novo activation of quiescent fibroblasts into alpha-smooth muscle actin (alpha SMA)-positive myofibroblasts is one likely source, epithelial to mesenchymal transition and bone marrow recruitment are also evolving as possible mechanisms for the emergence of a heterogeneous population of carcinoma-associated fibroblasts. Here, we show that transforming growth factor-beta1 could induce proliferating endothelial cells to undergo a phenotypic conversion into fibroblast-like cells. Such endothelial to mesenchymal transition (EndMT) is associated with the emergence of mesenchymal marker fibroblast-specific protein-1 (FSP1) and down-regulation of CD31/PECAM. Additionally, we show EndMT in tumors using the B16F10 melanoma model and the Rip-Tag2 spontaneous pancreatic carcinoma model. Crossing Tie2-Cre mice with R26Rosa-lox-Stop-lox-LacZ mice allows for irreversible tagging of endothelial cells. We provide unequivocal evidence for EndMT at the invasive front of the tumors in these transgenic mice. Collectively, our results show that EndMT is a unique mechanism for the accumulation of carcinoma-associated fibroblasts and suggest that antiangiogenic treatment of tumors may have a direct effect in decreasing activated fibroblasts that likely facilitate cancer progression.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "223", "doc_id": "6807122", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Cis-acting lncRNAs control the expression of genes that are positioned in the vicinity of their transcription sites.\n\nCANDIDATE_PASSAGE:\nRibosome biogenesis: Achilles heel of cancer? It is long been known that cancer and non-cancer cells can be distinguished on the basis of their nucleolar morphologies. As early as the 19th century, it was reported that cancer cells have larger and more irregularly shaped nucleoli. Since then, pathologists have used nucleolar morphology to predict the clinical outcome [1]. Nucleolar morphology is altered due to the up-regulation of ribosomal gene transcription. Within nucleoli, ribosomal genes (rDNA) are transcribed by RNA polymerase I (pol I). The pre-ribosomal RNA (pre-rRNA) transcripts are subsequently modified and processed into the mature 18S, 5.8S and 28S rRNAs. 5S rRNA is transcribed by RNA polymerase III in the nucleoplasm. Together with the ribosomal proteins, the 5S rRNA is imported into the nucleolus where 40S and 60S ribosomal subunits are assembled prior to export to the cytoplasm [1, 2]. Oncogenes such as c-Myc can both directly and indirectly upregulate rDNA transcription, while tumour suppressors like p53 and Rb suppress ribosome biogenesis. Mutations in these genes not only result in deregulated cell cycle control, but also upregulated ribosome biogenesis. In addition to ribosome biogenesis, the nucleolus is a key cellular stress sensor and plays a central role in p53 activation [1, 2]. The increased translational capacity of cancer cells enables them to maintain higher proliferation rates. As stated by Ruggero, “compared with normal cells, cancer cells may be addicted to increases in ribosome biogenesis and number” [1]. This provides new therapeutic opportunities. As it turns out many chemotherapeutic drugs used in cancer treatment already inhibit ribosome biogenesis. In one recent survey it was shown that 20 out of 36 drugs in clinical use [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "262", "doc_id": "6670101", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Systemic lupus erythematosus is a risk factor for cardiovascular disease.\n\nCANDIDATE_ABSTRACT:\nTITLE: Synaptic islands defined by the territory of a single astrocyte.\nABSTRACT: In the mammalian brain, astrocytes modulate neuronal function, in part, by synchronizing neuronal firing and coordinating synaptic networks. Little, however, is known about how this is accomplished from a structural standpoint. To investigate the structural basis of astrocyte-mediated neuronal synchrony and synaptic coordination, the three-dimensional relationships between cortical astrocytes and neurons was investigated. Using a transgenic and viral approach to label astrocytes with enhanced green fluorescent protein, we performed a three-dimensional reconstruction of astrocytes from tissue sections or live animals in vivo. We found that cortical astrocytes occupy nonoverlapping territories similar to those described in the hippocampus. Using immunofluorescence labeling of neuronal somata, a single astrocyte enwraps on average four neuronal somata with an upper limit of eight. Single-neuron dye-fills allowed us to estimate that one astrocyte contacts 300-600 neuronal dendrites. Together with the recent findings showing that glial Ca2+ signaling is restricted to individual astrocytes in vivo, and that Ca2+ signaling leads to gliotransmission, we propose the concept of functional islands of synapses in which groups of synapses confined within the boundaries of an individual astrocyte are modulated by the gliotransmitter environment controlled by that astrocyte. Our description offers a new structurally based conceptual framework to evaluate functional data involving interactions between neurons and astrocytes in the mammalian brain.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1127, "doc_id": "1771079", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Ambulatory blood pressure monitoring is inaccurate at diagnosing hypertension.\n\nCANDIDATE_ABSTRACT:\nTITLE: Relative effectiveness of clinic and home blood pressure monitoring compared with ambulatory blood pressure monitoring in diagnosis of hypertension: systematic review\nABSTRACT: OBJECTIVE To determine the relative accuracy of clinic measurements and home blood pressure monitoring compared with ambulatory blood pressure monitoring as a reference standard for the diagnosis of hypertension. DESIGN Systematic review with meta-analysis with hierarchical summary receiver operating characteristic models. Methodological quality was appraised, including evidence of validation of blood pressure measurement equipment. DATA SOURCES Medline (from 1966), Embase (from 1980), Cochrane Database of Systematic Reviews, DARE, Medion, ARIF, and TRIP up to May 2010. Eligibility criteria for selecting studies Eligible studies examined diagnosis of hypertension in adults of all ages using home and/or clinic blood pressure measurement compared with those made using ambulatory monitoring that clearly defined thresholds to diagnose hypertension. RESULTS The 20 eligible studies used various thresholds for the diagnosis of hypertension, and only seven studies (clinic) and three studies (home) could be directly compared with ambulatory monitoring. Compared with ambulatory monitoring thresholds of 135/85 mm Hg, clinic measurements over 140/90 mm Hg had mean sensitivity and specificity of 74.6% (95% confidence interval 60.7% to 84.8%) and 74.6% (47.9% to 90.4%), respectively, whereas home measurements over 135/85 mm Hg had mean sensitivity and specificity of 85.7% (78.0% to 91.0%) and 62.4% (48.0% to 75.0%). CONCLUSIONS Neither clinic nor home measurement had sufficient sensitivity or specificity to be recommended as a single diagnostic test. If ambulatory monitoring is taken as the reference standard, then treatment decisions based on clinic or home blood pressure alone might result in substantial overdiagnosis. Ambulatory monitoring before the start of lifelong [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Ambulatory monitoring before the start of lifelong drug treatment might lead to more appropriate targeting of treatment, particularly around the diagnostic threshold.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 106, "doc_id": "25515907", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does facial primer provide immediate and long-term improvements in mild-to-moderate facial hyperpigmentation and fine lines associated with photoaging?\n\nABSTRACT:\nPhotoaged skin results from various environmental factors, most importantly chronic sun exposure. Dyschromia and fine lines/wrinkles are common clinical manifestations of photodamaged skin. This single-center clinical trial was conducted to assess the efficacy and tolerability of a new multifunctional facial primer (camouflage, broad-spectrum SPF 50, and a treatment for hyperpigmentation) when used by females with mild-to-moderate facial hyperpigmentation and fine lines due to photoaging over a course of 12 weeks. Subjects were provided test material (Even Up-Clinical Pigment Perfector) and supporting products to use on their face and neck. Products were used according to specific application instructions. Clinical grading for efficacy and tolerability assessments were performed by an expert grader at baseline, baseline (post-application primer), week 4, week 8, week 12, and week 12 (post-application primer). Standardized digital photographs were taken, and self-assessment questionnaires were conducted. Twenty-eight female subjects completed the 12-week trial. The facial primer improved scores for the appearance of hyperpigmentation and other photoaging parameters immediately after the first application. The treatment also showed a progressive improvement in the clinical assessment of hyperpigmentation and other photoaging parameters over the 12-week trial. These long-term benefits can be attributed to an improvement in the underlying skin condition. The facial primer was well tolerated. Subject questionnaires showed that the product was highly rated at all visits.", "output": "{\"label\": \"yes\", \"rationale\": \"The facial primer was shown to be effective and well tolerated for immediate and long-term improvement in the appearance of mild-to-moderate hyperpigmentation and fine lines associated with photodamage when used over a 12-week period.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 26366102, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Autologous transplantation of mesenchymal stem cells has better graft function than induction therapy with anti-interleukin-2 receptor antibodies.\n\nCANDIDATE_PASSAGE:\n53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress Completion of genome duplication is challenged by structural and topological barriers that impede progression of replication forks. Although this can seriously undermine genome integrity, the fate of DNA with unresolved replication intermediates is not known. Here, we show that mild replication stress increases the frequency of chromosomal lesions that are transmitted to daughter cells. Throughout G1, these lesions are sequestered in nuclear compartments marked by p53-binding protein 1 (53BP1) and other chromatin-associated genome caretakers. We show that the number of such 53BP1 nuclear bodies increases after genetic ablation of BLM, a DNA helicase associated with dissolution of entangled DNA. Conversely, 53BP1 nuclear bodies are partially suppressed by knocking down SMC2, a condensin subunit required for mechanical stability of mitotic chromosomes. Finally, we provide evidence that 53BP1 nuclear bodies shield chromosomal fragile sites sequestered in these compartments against erosion. Together, these data indicate that restoration of DNA or chromatin integrity at loci prone to replication problems requires mitotic transmission to the next cell generations.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "144", "doc_id": "28271439", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: There is no known interaction between Pioneer factor OCT3/4 and major chromatin remodeling factors.\n\nCANDIDATE_PASSAGE:\nMeasuring adherence to highly active antiretroviral therapy: implications for research and practice. Highly active antiretroviral therapy (HAART) has radically changed the course of HIV disease, producing substantial reductions in both HIV-related morbidity and mortality. However, the complexity of the typical daily HAART regimen is substantial, and high levels of adherence are essential for complete and long-term viral suppression and the avoidance of drug resistance. The complexity of HAART has made the assessment of medication adherence of paramount importance. Even though various methods are in use, each measures only a subset of adherence behaviors, and each measure has limited predictive validity. Given the individual and public health concerns associated with adherence to HAART, there is a need for the continued development and validation of measures of medication adherence.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1294", "doc_id": "35087728", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Lupus-prone mice infected with curliproducing bacteria have higher autoantibody titers compared to controls.\n\nCANDIDATE_PASSAGE:\nAmyloid-DNA Composites of Bacterial Biofilms Stimulate Autoimmunity. Research on the human microbiome has established that commensal and pathogenic bacteria can influence obesity, cancer, and autoimmunity through mechanisms mostly unknown. We found that a component of bacterial biofilms, the amyloid protein curli, irreversibly formed fibers with bacterial DNA during biofilm formation. This interaction accelerated amyloid polymerization and created potent immunogenic complexes that activated immune cells, including dendritic cells, to produce cytokines such as type I interferons, which are pathogenic in systemic lupus erythematosus (SLE). When given systemically, curli-DNA composites triggered immune activation and production of autoantibodies in lupus-prone and wild-type mice. We also found that the infection of lupus-prone mice with curli-producing bacteria triggered higher autoantibody titers compared to curli-deficient bacteria. These data provide a mechanism by which the microbiome and biofilm-producing enteric infections may contribute to the progression of SLE and point to a potential molecular target for treatment of autoimmunity.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "721", "doc_id": "1834762", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Hypothalamic glutamate neurotransmission is unrelated to energy balance.\n\nCANDIDATE_ABSTRACT:\nTITLE: Synaptic glutamate release by ventromedial hypothalamic neurons is part of the neurocircuitry that prevents hypoglycemia.\nABSTRACT: The importance of neuropeptides in the hypothalamus has been experimentally established. Due to difficulties in assessing function in vivo, the roles of the fast-acting neurotransmitters glutamate and GABA are largely unknown. Synaptic vesicular transporters (VGLUTs for glutamate and VGAT for GABA) are required for vesicular uptake and, consequently, synaptic release of neurotransmitters. Ventromedial hypothalamic (VMH) neurons are predominantly glutamatergic and express VGLUT2. To evaluate the role of glutamate release from VMH neurons, we generated mice lacking VGLUT2 selectively in SF1 neurons (a major subset of VMH neurons). These mice have hypoglycemia during fasting secondary to impaired fasting-induced increases in the glucose-raising pancreatic hormone glucagon and impaired induction in liver of mRNAs encoding PGC-1alpha and the gluconeogenic enzymes PEPCK and G6Pase. Similarly, these mice have defective counterregulatory responses to insulin-induced hypoglycemia and 2-deoxyglucose (an antimetabolite). Thus, glutamate release from VMH neurons is an important component of the neurocircuitry that functions to prevent hypoglycemia.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"These mice have hypoglycemia during fasting secondary to impaired fasting-induced increases in the glucose-raising pancreatic hormone glucagon and impaired induction in liver of mRNAs encoding PGC-1alpha and the gluconeogenic enzymes PEPCK and G6Pase.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 541, "doc_id": "11886686", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: MICAL redox enzymes regulate actin dynamics.\n\nCANDIDATE_ABSTRACT:\nTITLE: Differential regulation of actin microfilaments by human MICAL proteins.\nABSTRACT: The Drosophila melanogaster MICAL protein is essential for the neuronal growth cone machinery that functions through plexin- and semaphorin-mediated axonal signaling. Drosophila MICAL is also involved in regulating myofilament organization and synaptic structures, and serves as an actin disassembly factor downstream of plexin-mediated axonal repulsion. In mammalian cells there are three known isoforms, MICAL1, MICAL2 and MICAL3, as well as the MICAL-like proteins MICAL-L1 and MICAL-L2, but little is known of their function, and information comes almost exclusively from neural cells. In this study we show that in non-neural cells human MICALs are required for normal actin organization, and all three MICALs regulate actin stress fibers. Moreover, we provide evidence that the generation of reactive oxygen species by MICAL proteins is crucial for their actin-regulatory function. However, although MICAL1 is auto-inhibited by its C-terminal coiled-coil region, MICAL2 remains constitutively active and affects stress fibers. These data suggest differential but complementary roles for MICAL1 and MICAL2 in actin microfilament regulation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In this study we show that in non-neural cells human MICALs are required for normal actin organization, and all three MICALs regulate actin stress fibers.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 738, "doc_id": "6609935", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: During the primary early antibody response activated B cells migrate toward the inner-and outer paracortical areas where oxysterol accumulation is generated by stromal cells.\n\nCANDIDATE_PASSAGE:\nFinding the right niche: B-cell migration in the early phases of T-dependent antibody responses. Humoral immune responses depend on B cells encountering antigen, interacting with helper T cells, proliferating and differentiating into low-affinity plasma cells or, after organizing into a germinal center (GC), high-affinity plasma cells and memory B cells. Remarkably, each of these events occurs in association with distinct stromal cells in separate subcompartments of the lymphoid tissue. B cells must migrate from niche to niche in a rapid and highly regulated manner to successfully mount a response. The chemokine, CXCL13, plays a central role in guiding B cells to follicles whereas T-zone chemokines guide activated B cells to the T zone. Sphingosine-1-phosphate (S1P) promotes cell egress from the tissue, as well as marginal-zone B-cell positioning in the spleen. Recent studies have identified a role for the orphan receptor, EBV-induced molecule 2 (EBI2; GPR183), in guiding activated B cells to inter and outer follicular niche(s) and down-regulation of this receptor is essential for organizing cells into GCs. In this review, we discuss current understanding of the roles played by chemokines, S1P and EBI2 in the migration events that underlie humoral immune responses.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "362", "doc_id": "38587347", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Macrolides protect against myocardial infarction.\n\nCANDIDATE_ABSTRACT:\nTITLE: Antibiotics and risk of subsequent first-time acute myocardial infarction.\nABSTRACT: CONTEXT Increasing evidence supports the hypothesis of a causal association between certain bacterial infections and increased risk of developing acute myocardial infarction. If such a causal association exists, subjects who used antibiotics active against the bacteria, regardless of indication, might be at lower risk of developing acute myocardial infarction than nonusers. OBJECTIVE To determine whether previous use of antibiotics decreases the risk of developing a first-time acute myocardial infarction. DESIGN Population-based case-control analysis. SETTING The United Kingdom-based General Practice Research Database comprising 350 general practices. PATIENTS A total of 3315 case patients aged 75 years or younger with a diagnosis of first-time acute myocardial infarction between 1992 and 1997 and 13139 controls without myocardial infarction matched to cases for age, sex, general practice attended, and calendar time. MAIN OUTCOME MEASURES Use of antibiotics among those who did or did not have a first-time acute myocardial infarction. RESULTS Cases were significantly less likely to have used tetracycline antibiotics (adjusted odds ratio [OR], 0.70; 95% confidence interval [CI], 0.55-0.90) or quinolones (adjusted OR, 0.45; 95% CI, 0.21-0.95). No effect was found for previous use of macrolides (primarily erythromycin), sulfonamides, penicillins, or cephalosporins. CONCLUSIONS The findings from this large case-control analysis provide further, albeit indirect, evidence for an association between bacterial infections with organisms susceptible to tetracycline or quinolone antibiotics and the risk of acute myocardial infarction. These results of preliminary nature should stimulate more research to further explore the role of infections in the etiology of acute myo [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"No effect was found for previous use of macrolides (primarily erythromycin), sulfonamides, penicillins, or cephalosporins.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 743, "doc_id": "32159283", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Macrolides protect against myocardial infarction.\n\nCANDIDATE_ABSTRACT:\nTITLE: Helicobacter pylori induces AGS cell motility and elongation via independent signaling pathways.\nABSTRACT: Helicobacter pylori induces motogenic and cytoskeletal responses in gastric epithelial cells. We demonstrate that these responses can be induced via independent signaling pathways that often occur in parallel. The cag pathogenicity island appears to be nonessential for induction of motility, whereas the elongation phenotype depends on translocation and phosphorylation of CagA.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 743, "doc_id": "2099400", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Active H. pylori urease has a polymeric structure that compromises two subunits, UreA and UreB.\n\nCANDIDATE_PASSAGE:\nGeneration and characterization of methyl-lysine histone antibodies. Publisher Summary This chapter summarizes the development and characterization of rabbit polyclonal antibodies named histone that are directed against the methylated H3-K9 position. It provides protocols for peptide design, rabbit immunizations, and quality controls of methyl-lysine histone antibodies, followed by their in vivo characterization using indirect IF of inter-and metaphase chromatin in wild-type (wt) and mutant mouse cells that are deficient for the Suv39h histone methyltransferases (HMTases). Histone amino-termini (tails) protrude from the nucleosome core and are subject to a variety of post-translational modifications, including acetylation (on lysine residues), phosphorylation (on serine and threonine residues), methylation (on lysine and arginine residues), ubiquitination (on lysine residues), and ADP-ribosylation (on glutamic acid residues). In addition to their structural roles, histones play important functions in the control of gene expression by regulating access to the underlying nucleosomal template. It is without doubt that the development of high-quality, position-specific methyl-lysine histone antibodies can provide important tools for the further decoding of the epigenetic information, which is in part, indexed by distinct methylation states of selective lysine residues in the histone amino-termini. A comparative analysis indicates significant discrepancies in the specificity and avidity of the available methyl-lysine histone antibodies and highlights the need for extensive quality controls, such that experimental data can be correctly interpreted despite the exquisite complexity of histone lysine methylation.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "75", "doc_id": "3230361", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Diabetes remission occurs more in people treated with conventional therapy than in people treated with laparoscopic adjustable gastric banding surgery.\n\nCANDIDATE_ABSTRACT:\nTITLE: Adjustable gastric banding and conventional therapy for type 2 diabetes: a randomized controlled trial.\nABSTRACT: CONTEXT Observational studies suggest that surgically induced loss of weight may be effective therapy for type 2 diabetes. OBJECTIVE To determine if surgically induced weight loss results in better glycemic control and less need for diabetes medications than conventional approaches to weight loss and diabetes control. DESIGN, SETTING, AND PARTICIPANTS Unblinded randomized controlled trial conducted from December 2002 through December 2006 at the University Obesity Research Center in Australia, with general community recruitment to established treatment programs. Participants were 60 obese patients (BMI >30 and <40) with recently diagnosed (<2 years) type 2 diabetes. INTERVENTIONS Conventional diabetes therapy with a focus on weight loss by lifestyle change vs laparoscopic adjustable gastric banding with conventional diabetes care. MAIN OUTCOME MEASURES Remission of type 2 diabetes (fasting glucose level <126 mg/dL [7.0 mmol/L] and glycated hemoglobin [HbA1c] value <6.2% while taking no glycemic therapy). Secondary measures included weight and components of the metabolic syndrome. Analysis was by intention-to-treat. RESULTS Of the 60 patients enrolled, 55 (92%) completed the 2-year follow-up. Remission of type 2 diabetes was achieved by 22 (73%) in the surgical group and 4 (13%) in the conventional-therapy group. Relative risk of remission for the surgical group was 5.5 (95% confidence interval, 2.2-14.0). Surgical and conventional-therapy groups lost a mean (SD) of 20.7% (8.6%) and 1.7% (5.2%) of weight, respectively, at 2 years (P < .001). Remission of type 2 diabetes was related to weight loss (R2 = 0.46, P < .001) and lower baseline HbA1c levels (combined R2 = 0.52, P < .001). There were no serious complications in either group. CONCLUSIONS Participants r [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Relative risk of remission for the surgical group was 5.5 (95% confidence interval, 2.2-14.0).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 341, "doc_id": "7098463", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Suboptimal nutrition is not predictive of chronic disease\n\nCANDIDATE_PASSAGE:\nGlobal, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015 BACKGROUND The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. METHODS We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors-the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1110", "doc_id": "13770184", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: A diminished ovarian reserve does not solely indicate infertility in an a priori non-infertile population.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\nABSTRACT: Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential. Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age. Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area. Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH. Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle). Conception was defined as a positive pregnancy test result. Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis. After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively). Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cy [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 39, "doc_id": "13497630", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: CR is associated with higher methylation age.\n\nCANDIDATE_ABSTRACT:\nTITLE: Caloric restriction delays age-related methylation drift\nABSTRACT: In mammals, caloric restriction consistently results in extended lifespan. Epigenetic information encoded by DNA methylation is tightly regulated, but shows a striking drift associated with age that includes both gains and losses of DNA methylation at various sites. Here, we report that epigenetic drift is conserved across species and the rate of drift correlates with lifespan when comparing mice, rhesus monkeys, and humans. Twenty-two to 30-year-old rhesus monkeys exposed to 30% caloric restriction since 7-14 years of age showed attenuation of age-related methylation drift compared to ad libitum-fed controls such that their blood methylation age appeared 7 years younger than their chronologic age. Even more pronounced effects were seen in 2.7-3.2-year-old mice exposed to 40% caloric restriction starting at 0.3 years of age. The effects of caloric restriction on DNA methylation were detectable across different tissues and correlated with gene expression. We propose that epigenetic drift is a determinant of lifespan in mammals. Caloric restriction has been shown to increase lifespan in mammals. Here, the authors provide evidence that age-related methylation drift correlates with lifespan and that caloric restriction in mice and rhesus monkeys results in attenuation of age-related methylation drift.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Twenty-two to 30-year-old rhesus monkeys exposed to 30% caloric restriction since 7-14 years of age showed attenuation of age-related methylation drift compared to ad libitum-fed controls such that their blood methylation age appeared 7 years younger than their chronologic age.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 212, "doc_id": "22038539", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Assembly of invadopodia is triggered by focal generation of phosphatidylinositol-3,4-biphosphate and the activation of the nonreceptor tyrosine kinase Src.\n\nCANDIDATE_PASSAGE:\nMolecular mechanisms of (-)-epicatechin and chlorogenic acid on the regulation of the apoptotic and survival/proliferation pathways in a human hepatoma cell line. Dietary polyphenols have been associated with reduced risk of chronic diseases, but the precise molecular mechanisms of protection remain unclear. This work was aimed at studying the effect of (-)-epicatechin (EC) and chlorogenic acid (CGA) on the regulation of apoptotic and survival/proliferation pathways in a human hepatoma cell line (HepG2). EC or CGA treatment for 18 h had a slight effect on cell viability and decreased reactive oxygen species formation, and EC alone promoted cell proliferation, whereas CGA increased glutathione levels. Phenols neither induced the caspase cascade for apoptosis nor affected expression levels of Bcl-xL or Bax. A sustained activation of the major survival signals AKT/PI-3-kinase and ERK was shown in EC-treated cells, rather than in CGA-exposed cells. These data suggest that EC and CGA have no effect on apoptosis and enhance the intrinsic cellular tolerance against oxidative insults either by activating survival/proliferation pathways or by increasing antioxidant potential in HepG2.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "133", "doc_id": "9197092", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: In transgenic mice harboring green florescent protein under the control of the Sox2 promoter, less than ten percent of the cells with green florescent colocalize with cell proliferation markers.\n\nCANDIDATE_ABSTRACT:\nTITLE: Cell Stem Cell Article In Vivo Fate Analysis Reveals the Multipotent and Self-Renewal Capacities of Sox2 + Neural Stem Cells in the Adult Hippocampus\nABSTRACT: To characterize the properties of adult neural stem cells (NSCs), we generated and analyzed Sox2-GFP transgenic mice. Sox2-GFP cells in the subgranular zone (SGZ) express markers specific for progenitors, but they represent two morphologically distinct populations that differ in proliferation levels. Lentivirus- and retrovirus-mediated fate-tracing studies showed that Sox2+ cells in the SGZ have potential to give rise to neurons and astrocytes, revealing their multipotency at the population as well as at a single-cell level. A subpopulation of Sox2+ cells gives rise to cells that retain Sox2, highlighting Sox2+ cells as a primary source for adult NSCs. In response to mitotic signals, increased proliferation of Sox2+ cells is coupled with the generation of Sox2+ NSCs as well as neuronal precursors. An asymmetric contribution of Sox2+ NSCs may play an important role in maintaining the constant size of the NSC pool and producing newly born neurons during adult neurogenesis.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 587, "doc_id": "16999023", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Addition of BMP4, activin A, CHIR99021, and SU504 to reprogramming fibroblasts generates, expands and maintains cardiovascular progenitor cells (CPCs)\n\nCANDIDATE_ABSTRACT:\nTITLE: Expandable Cardiovascular Progenitor Cells Reprogrammed from Fibroblasts.\nABSTRACT: Stem cell-based approaches to cardiac regeneration are increasingly viable strategies for treating heart failure. Generating abundant and functional autologous cells for transplantation in such a setting, however, remains a significant challenge. Here, we isolated a cell population with extensive proliferation capacity and restricted cardiovascular differentiation potentials during cardiac transdifferentiation of mouse fibroblasts. These induced expandable cardiovascular progenitor cells (ieCPCs) proliferated extensively for more than 18 passages in chemically defined conditions, with 10(5) starting fibroblasts robustly producing 10(16) ieCPCs. ieCPCs expressed cardiac signature genes and readily differentiated into functional cardiomyocytes (CMs), endothelial cells (ECs), and smooth muscle cells (SMCs) in vitro, even after long-term expansion. When transplanted into mouse hearts following myocardial infarction, ieCPCs spontaneously differentiated into CMs, ECs, and SMCs and improved cardiac function for up to 12 weeks after transplantation. Thus, ieCPCs are a powerful system to study cardiovascular specification and provide strategies for regenerative medicine in the heart.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 82, "doc_id": "3619372", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: CX3CR1 on the Th2 cells promotes airway inflammation.\n\nCANDIDATE_PASSAGE:\nCX3CR1 is required for airway inflammation by promoting T helper cell survival and maintenance in inflamed lung Allergic asthma is a T helper type 2 (T(H)2)-dominated disease of the lung. In people with asthma, a fraction of CD4(+) T cells express the CX3CL1 receptor, CX3CR1, and CX3CL1 expression is increased in airway smooth muscle, lung endothelium and epithelium upon allergen challenge. Here we found that untreated CX3CR1-deficient mice or wild-type (WT) mice treated with CX3CR1-blocking reagents show reduced lung disease upon allergen sensitization and challenge. Transfer of WT CD4(+) T cells into CX3CR1-deficient mice restored the cardinal features of asthma, and CX3CR1-blocking reagents prevented airway inflammation in CX3CR1-deficient recipients injected with WT T(H)2 cells. We found that CX3CR1 signaling promoted T(H)2 survival in the inflamed lungs, and injection of B cell leukemia/lymphoma-2 protein (BCl-2)-transduced CX3CR1-deficient T(H)2 cells into CX3CR1-deficient mice restored asthma. CX3CR1-induced survival was also observed for T(H)1 cells upon airway inflammation but not under homeostatic conditions or upon peripheral inflammation. Therefore, CX3CR1 and CX3CL1 may represent attractive therapeutic targets in asthma.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "218", "doc_id": "21366394", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The US health care system can save up to $750 million if 7% of patients waiting for kidney transplants participate in the optimized national kidney paired donation program.\n\nCANDIDATE_ABSTRACT:\nTITLE: Kidney paired donation and optimizing the use of live donor organs.\nABSTRACT: CONTEXT Blood type and crossmatch incompatibility will exclude at least one third of patients in need from receiving a live donor kidney transplant. Kidney paired donation (KPD) offers incompatible donor/recipient pairs the opportunity to match for compatible transplants. Despite its increasing popularity, very few transplants have resulted from KPD. OBJECTIVE To determine the potential impact of improved matching schemes on the number and quality of transplants achievable with KPD. DESIGN, SETTING, AND POPULATION We developed a model that simulates pools of incompatible donor/recipient pairs. We designed a mathematically verifiable optimized matching algorithm and compared it with the scheme currently used in some centers and regions. Simulated patients from the general community with characteristics drawn from distributions describing end-stage renal disease patients eligible for renal transplantation and their willing and eligible live donors. MAIN OUTCOME MEASURES Number of kidneys matched, HLA mismatch of matched kidneys, and number of grafts surviving 5 years after transplantation. RESULTS A national optimized matching algorithm would result in more transplants (47.7% vs 42.0%, P<.001), better HLA concordance (3.0 vs 4.5 mismatched antigens; P<.001), more grafts surviving at 5 years (34.9% vs 28.7%; P<.001), and a reduction in the number of pairs required to travel (2.9% vs 18.4%; P<.001) when compared with an extension of the currently used first-accept scheme to a national level. Furthermore, highly sensitized patients would benefit 6-fold from a national optimized scheme (2.3% vs 14.1% successfully matched; P<.001). Even if only 7% of patients awaiting kidney transplantation participated in an optimized national KPD program, the health care system c [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Even if only 7% of patients awaiting kidney transplantation participated in an optimized national KPD program, the health care system could save as much as $750 million.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1185, "doc_id": "16737210", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Hematopoietic Stem Cell purification reaches purity rate of up to 50%.\n\nCANDIDATE_PASSAGE:\nCell Stem Cell Review FoxO Transcription Factors and Stem Cell Homeostasis: Insights from the Hematopoietic System The forkhead O (FoxO) family of transcription factors participates in diverse physiologic processes, including induction of cell-cycle arrest, stress resistance, differentiation, apoptosis, and metabolism. Several recent studies indicate that FoxO-dependent signaling is required for long-term regenerative potential of the hematopoietic stem cell (HSC) compartment through regulation of HSC response to physiologic oxidative stress, quiescence, and survival. These observations link FoxO function in mammalian systems with the evolutionarily conserved role of FoxO in promotion of stress resistance and longevity in lower phylogenetic systems. Furthermore, these findings have implications for aging in higher organisms and in malignant stem cell biology, and suggest that FoxOs may play an important role in the maintenance and integrity of stem cell compartments in a broad spectrum of tissues.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "508", "doc_id": "16728949", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: In domesticated populations of Saccharomyces cerevisiae, whole chromosome aneuploidy is very uncommon.\n\nCANDIDATE_PASSAGE:\nDomestication and Divergence of Saccharomyces cerevisiae Beer Yeasts Whereas domestication of livestock, pets, and crops is well documented, it is still unclear to what extent microbes associated with the production of food have also undergone human selection and where the plethora of industrial strains originates from. Here, we present the genomes and phenomes of 157 industrial Saccharomyces cerevisiae yeasts. Our analyses reveal that today's industrial yeasts can be divided into five sublineages that are genetically and phenotypically separated from wild strains and originate from only a few ancestors through complex patterns of domestication and local divergence. Large-scale phenotyping and genome analysis further show strong industry-specific selection for stress tolerance, sugar utilization, and flavor production, while the sexual cycle and other phenotypes related to survival in nature show decay, particularly in beer yeasts. Together, these results shed light on the origins, evolutionary history, and phenotypic diversity of industrial yeasts and provide a resource for further selection of superior strains. PAPERCLIP.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "575", "doc_id": "10300888", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Normal expression of RUNX1 causes tumorsupressing effects.\n\nCANDIDATE_ABSTRACT:\nTITLE: Predicting mortality of patients hospitalized for acutely exacerbated chronic obstructive pulmonary disease.\nABSTRACT: PURPOSE To identify factors affecting the short-term prognosis of patients with acutely exacerbated chronic obstructive pulmonary disease (COPD). PATIENTS AND METHODS The 590 patients having COPD as primary disease who were hospitalized in the pneumology unit of a university hospital from 1981 to 1990 were studied. A standardized protocol for the treatment of acutely exacerbated COPD was adopted for all the patients. The patient records were retrospectively analyzed by two observers, and 23 clinical and laboratory variables defining the patient status on admission were collected. Age and arterial gas data were also taken into account, and the outcome mortality was recorded. Interobserver reproducibility was tested by computing the kappa coefficient and Spearman's rho for dichotomous and continuous variables, respectively. The relationship of clinical and laboratory factors to the outcome was assessed first by univariate analysis and then by a logistic regression analysis assessing the independent predictive role of variables previously shown to be univariately correlated with mortality. RESULTS The mortality rate was 14.4%. The logistic regression analysis identified four independent predictors of death: age (odds ratio [OR] 1.07; 95% confidence interval [CI] 1.04 to 1.11), alveolar-arterial oxygen gradient greater than 41 mm Hg (OR 2.33; 95% CI 1.39 to 3.90), ventricular arrhythmias (OR 1.91; 95% CI 1.10 to 3.31), and atrial fibrillation (OR 2.27; 95% CI 1.14 to 4.51). CONCLUSIONS Patients with acutely exacerbated COPD having a high risk of death can be identified at the time of admission. Variables reflecting heart dysfunction are important determinants of this risk. Among pulmonary function data, only alveolar-arterial oxygen gradient contributes to the p [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 858, "doc_id": "2032877", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: High levels of CRP reduces the risk of exacerbations in chronic obstructive pulmonary disease (COPD).\n\nCANDIDATE_ABSTRACT:\nTITLE: 2010 rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative.\nABSTRACT: OBJECTIVE The 1987 American College of Rheumatology (ACR; formerly the American Rheumatism Association) classification criteria for rheumatoid arthritis (RA) have been criticised for their lack of sensitivity in early disease. This work was undertaken to develop new classification criteria for RA. METHODS A joint working group from the ACR and the European League Against Rheumatism developed, in three phases, a new approach to classifying RA. The work focused on identifying, among patients newly presenting with undifferentiated inflammatory synovitis, factors that best discriminated between those who were and those who were not at high risk for persistent and/or erosive disease--this being the appropriate current paradigm underlying the disease construct 'RA'. RESULTS In the new criteria set, classification as 'definite RA' is based on the confirmed presence of synovitis in at least one joint, absence of an alternative diagnosis better explaining the synovitis, and achievement of a total score of 6 or greater (of a possible 10) from the individual scores in four domains: number and site of involved joints (range 0-5), serological abnormality (range 0-3), elevated acute-phase response (range 0-1) and symptom duration (two levels; range 0-1). CONCLUSION This new classification system redefines the current paradigm of RA by focusing on features at earlier stages of disease that are associated with persistent and/or erosive disease, rather than defining the disease by its late-stage features. This will refocus attention on the important need for earlier diagnosis and institution of effective disease-suppressing therapy to prevent or minimise the occurrence of the undesirable sequelae that currently comprise the paradigm underlying the disease construct 'RA'.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 516, "doc_id": "1191830", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Lice attenuated SIV vaccines induce a stronger antigen-specific T cell response in lymph node cells.\n\nCANDIDATE_PASSAGE:\nRoads to polyploidy: the megakaryocyte example. Polyploidy, recognized by multiple copies of the haploid chromosome number, has been described in plants, insects, and in mammalian cells such as, the platelet precursors, the megakaryocytes. Several of these cell types reach high ploidy via a different cell cycle. Megakaryocytes undergo an endomitotic cell cycle, which consists of an S phase interrupted by a gap, during which the cells enter mitosis but skip anaphase B and cytokinesis. Here, we review the mechanisms that lead to this cell cycle and to polyploidy in megakaryocytes, while also comparing them to those described for other systems in which high ploidy is achieved. Overall, polyploidy is associated with an orchestrated change in expression of several genes, of which, some may be a result of high ploidy and hence a determinant of a new cell physiology, while others are inducers of polyploidization. Future studies will aim to further explore these two groups of genes.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "694", "doc_id": "37297740", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Localization of PIN1 in the Arabidopsis embryo does not require VPS9a\n\nCANDIDATE_PASSAGE:\nPedestrian Detection via Periodic Motion Analysis We describe algorithms for detecting pedestrians in videos acquired by infrared (and color) sensors. Two approaches are proposed based on gait. The first employs computationally efficient periodicity measurements. Unlike other methods, it estimates a periodic motion frequency using two cascading hypothesis testing steps to filter out non-cyclic pixels so that it works well for both radial and lateral walking directions. The extraction of the period is efficient and robust with respect to sensor noise and cluttered background. In order to integrate shape and motion, we convert the cyclic pattern into a binary sequence by Maximal Principal Gait Angle (MPGA) fitting in the second method. It does not require alignment and continuously estimates the period using a Phase-locked Loop. Both methods are evaluated by experimental results that measure performance as a function of size, movement direction, frame rate and sequence length.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "700", "doc_id": "7261402", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Taxation of sugar-sweetened beverages reduced the incidence rate of type II diabetes in India.\n\nCANDIDATE_PASSAGE:\nRadiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. BACKGROUND Glioblastoma, the most common primary brain tumor in adults, is usually rapidly fatal. The current standard of care for newly diagnosed glioblastoma is surgical resection to the extent feasible, followed by adjuvant radiotherapy. In this trial we compared radiotherapy alone with radiotherapy plus temozolomide, given concomitantly with and after radiotherapy, in terms of efficacy and safety. METHODS Patients with newly diagnosed, histologically confirmed glioblastoma were randomly assigned to receive radiotherapy alone (fractionated focal irradiation in daily fractions of 2 Gy given 5 days per week for 6 weeks, for a total of 60 Gy) or radiotherapy plus continuous daily temozolomide (75 mg per square meter of body-surface area per day, 7 days per week from the first to the last day of radiotherapy), followed by six cycles of adjuvant temozolomide (150 to 200 mg per square meter for 5 days during each 28-day cycle). The primary end point was overall survival. RESULTS A total of 573 patients from 85 centers underwent randomization. The median age was 56 years, and 84 percent of patients had undergone debulking surgery. At a median follow-up of 28 months, the median survival was 14.6 months with radiotherapy plus temozolomide and 12.1 months with radiotherapy alone. The unadjusted hazard ratio for death in the radiotherapy-plus-temozolomide group was 0.63 (95 percent confidence interval, 0.52 to 0.75; P<0.001 by the log-rank test). The two-year survival rate was 26.5 percent with radiotherapy plus temozolomide and 10.4 percent with radiotherapy alone. Concomitant treatment with radiotherapy plus temozolomide resulted in grade 3 or 4 hematologic toxic effects in 7 percent of pati [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1145", "doc_id": "41340212", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does vaginal intraepithelial neoplasia have the same evolution as cervical intraepithelial neoplasia?\n\nABSTRACT:\nVaginal intraepithelial neoplasia is a little known disease which could be related to risk factors different from simple HPV infections. To ascertain wheter vaginal lesions have a natural history similar to cervical lesions.MATERIALS & A retrospective study to identify patients with vaginal lesions and synchronous cervical lesions through biopsy. The rate of mild cervical lesions (koilocytosis, warts, CIN I with and without koilocytosis) was compared with the rate of severe cervical lesions (CIN II and III, cervical carcinoma) in patients with mild vaginal lesions (warts and koilocytosis, and low-grade VAIN) and in patients with severe vaginal lesions (high-grade VAIN). Using koilocytosis as a marker, the rate of \"active\" cervical lesions was compared with the rate of \"non active\" cervical lesions in patients with \"active\" versus \"non active\" vaginal lesions. Finally, the rates of mild and severe cervical lesions were compared among each group of VAIN (low-grade, high-grade, with or without koilocytosis). In patients with mild vaginal lesions, mild cervical lesions were significantly more frequent than severe cervical lesions. In patients with \"active\" vaginal lesions the rate of \"active\" cervical lesions was significantly higher than \"non active\" cervical lesions. The differences in rates of mild cervical lesions and severe cervical lesions among patients with high-grade VAIN and low-grade VAIN (with and without koilocytosis) were not significant.", "output": "{\"label\": \"maybe\", \"rationale\": \"These data suggest that CIN and VAIN may have some common features in certain cases, i.e., if an HPV infection is proved.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 18714572, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does rugby headgear prevent concussion?\n\nABSTRACT:\nTo examine the attitudes of players and coaches to the use of protective headgear, particularly with respect to the prevention of concussion. A questionnaire designed to assess attitudes to headgear was administered to 63 players from four different Canadian teams, each representing a different level of play (high school, university, community club, national). In addition, coaches from all four levels were questioned about team policies and their personal opinions about the use of headgear to prevent concussion. Although the players tended to believe that the headgear could prevent concussion (62%), the coaches were less convinced (33%). Despite the players' belief that headgear offers protection against concussion, only a minority reported wearing headgear (27%) and few (24%) felt that its use should be made mandatory. Common reasons for not wearing headgear were \"its use is not mandatory\", \"it is uncomfortable\", and \"it costs too much\".", "output": "{\"label\": \"maybe\", \"rationale\": \"Although most players in the study believe that rugby headgear may prevent concussion, only a minority reported wearing it. Coaches tended to be less convinced than the players that rugby headgear can prevent concussion.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 11867487, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is restoration of CD4 T-cell responses to cytomegalovirus short-lived in severely immunodeficient HIV-infected patients responding to highly active antiretroviral therapy?\n\nABSTRACT:\nTo define the level of pathogen-specific immune reconstitution persisting over 3 to 5 years of highly active antiretroviral therapy (HAART) in HIV-infected patients who began therapy with CD4 T-cell counts below 50 cells/microL. Cytomegalovirus (CMV)-specific T-cell responses were analysed in adult HIV-1-infected patients with nadir CD4 T-cell counts below 50 cells/microL before HAART. CMV-specific CD4 T-cell responses were measured by interferon-gamma enzyme-linked immunospot assay (ELISpot assay), lymphoproliferation and interferon-gamma levels in cell culture supernatants. CD4 T-cell responses to CMV were low in untreated patients and remained low during the first year on HAART, but increased progressively to levels similar to those found in HIV-seronegative CMV-seropositive controls at 3 years. Responses then declined markedly and at 5 years were lower than controls. This could not be explained by changes in CD4 or CD8 T-cell counts or plasma HIV RNA levels. Interferon-gamma and interleukin-5 responses to a mitogen were maintained or elevated.", "output": "{\"label\": \"yes\", \"rationale\": \"CMV-specific CD4 T-cell responses were found to decline after 3-5 years on HAART and may provide inadequate long-term protection against CMV disease in patients who are severely immunodeficient prior to treatment.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 15544692, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Immune responses in immune cells are geographically segregated.\n\nCANDIDATE_PASSAGE:\nTCR stimulation with modified anti-CD3 mAb expands CD8+ T cell population and induces CD8+CD25+ Tregs. Modified anti-CD3 mAbs are emerging as a possible means of inducing immunologic tolerance in settings including transplantation and autoimmunity such as in type 1 diabetes. In a trial of a modified anti-CD3 mAb [hOKT3gamma1(Ala-Ala)] in patients with type 1 diabetes, we identified clinical responders by an increase in the number of peripheral blood CD8+ cells following treatment with the mAb. Here we show that the anti-CD3 mAb caused activation of CD8+ T cells that was similar in vitro and in vivo and induced regulatory CD8+CD25+ T cells. These cells inhibited the responses of CD4+ cells to the mAb itself and to antigen. The regulatory CD8+CD25+ cells were CTLA4 and Foxp3 and required contact for inhibition. Foxp3 was also induced on CD8+ T cells in patients during mAb treatment, which suggests a potential mechanism of the anti-CD3 mAb immune modulatory effects involving induction of a subset of regulatory CD8+ T cells.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "559", "doc_id": "24069089", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_ABSTRACT:\nTITLE: Human papillomavirus and Papanicolaou tests to screen for cervical cancer.\nABSTRACT: BACKGROUND Screening for cervical cancer based on testing for human papillomavirus (HPV) increases the sensitivity of detection of high-grade (grade 2 or 3) cervical intraepithelial neoplasia, but whether this gain represents overdiagnosis or protection against future high-grade cervical epithelial neoplasia or cervical cancer is unknown. METHODS In a population-based screening program in Sweden, 12,527 women 32 to 38 years of age were randomly assigned at a 1:1 ratio to have an HPV test plus a Papanicolaou (Pap) test (intervention group) or a Pap test alone (control group). Women with a positive HPV test and a normal Pap test result were offered a second HPV test at least 1 year later, and those who were found to be persistently infected with the same high-risk type of HPV were then offered colposcopy with cervical biopsy. A similar number of double-blinded Pap smears and colposcopies with biopsy were performed in randomly selected women in the control group. Comprehensive registry data were used to follow the women for a mean of 4.1 years. The relative rates of grade 2 or 3 cervical intraepithelial neoplasia or cancer detected at enrollment and at subsequent screening examinations were calculated. RESULTS At enrollment, the proportion of women in the intervention group who were found to have lesions of grade 2 or 3 cervical intraepithelial neoplasia or cancer was 51% greater (95% confidence interval [CI], 13 to 102) than the proportion of women in the control group who were found to have such lesions. At subsequent screening examinations, the proportion of women in the intervention group who were found to have grade 2 or 3 lesions or cancer was 42% less (95% CI, 4 to 64) and the proportion with grade 3 lesions or cancer was 47% less (95% CI, 2 to 71) than [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"BACKGROUND Screening for cervical cancer based on testing for human papillomavirus (HPV) increases the sensitivity of detection of high-grade (grade 2 or 3) cervical intraepithelial neoplasia, but whether this gain represents overdiagnosis or protection against future high-grade cervical epithelial neoplasia or cervical cancer is unknown.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 972, "doc_id": "46695481", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Myelin sheaths play a role in action potential propagation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Label-free in vivo imaging of myelinated axons in health and disease with spectral confocal reflectance microscopy\nABSTRACT: We report a newly developed technique for high-resolution in vivo imaging of myelinated axons in the brain, spinal cord and peripheral nerve that requires no fluorescent labeling. This method, based on spectral confocal reflectance microscopy (SCoRe), uses a conventional laser-scanning confocal system to generate images by merging the simultaneously reflected signals from multiple lasers of different wavelengths. Striking color patterns unique to individual myelinated fibers are generated that facilitate their tracing in dense axonal areas. These patterns highlight nodes of Ranvier and Schmidt-Lanterman incisures and can be used to detect various myelin pathologies. Using SCoRe we carried out chronic brain imaging up to 400 μm deep, capturing de novo myelination of mouse cortical axons in vivo. We also established the feasibility of imaging myelinated axons in the human cerebral cortex. SCoRe adds a powerful component to the evolving toolbox for imaging myelination in living animals and potentially in humans.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We report a newly developed technique for high-resolution in vivo imaging of myelinated axons in the brain, spinal cord and peripheral nerve that requires no fluorescent labeling.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 818, "doc_id": "17814815", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: IFIT1 speeds viral replication by allowing for the proliferation of mis-capped viral RNAs.\n\nCANDIDATE_PASSAGE:\nIdentification of p18 INK4c as a tumor suppressor gene in glioblastoma multiforme. Genomic alterations leading to aberrant activation of cyclin/cyclin-dependent kinase (cdk) complexes drive the pathogenesis of many common human tumor types. In the case of glioblastoma multiforme (GBM), these alterations are most commonly due to homozygous deletion of p16(INK4a) and less commonly due to genomic amplifications of individual genes encoding cyclins or cdks. Here, we describe deletion of the p18(INK4c) cdk inhibitor as a novel genetic alteration driving the pathogenesis of GBM. Deletions of p18(INK4c) often occurred in tumors also harboring homozygous deletions of p16(INK4a). Expression of p18(INK4c) was completely absent in 43% of GBM primary tumors studied by immunohistochemistry. Lentiviral reconstitution of p18(INK4c) expression at physiologic levels in p18(INK4c)-deficient but not p18(INK4c)-proficient GBM cells led to senescence-like G(1) cell cycle arrest. These studies identify p18(INK4c) as a GBM tumor suppressor gene, revealing an additional mechanism leading to aberrant activation of cyclin/cdk complexes in this terrible malignancy.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "545", "doc_id": "470625", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Mutations in RIM1 raise levels of IME1 RNA.\n\nCANDIDATE_ABSTRACT:\nTITLE: Molecular characterization of the yeast meiotic regulatory gene RIM1.\nABSTRACT: In the yeast Saccharomyces cerevisiae, genetic studies suggest that the RIM1 gene encodes a positive regulator of meiosis. rim1 mutations cause reduced expression of IME1, which is required for expression of many meiotic genes, and thus lead to a partial defect in meiosis and spore formation. We report the sequence of RIM1 and functional analysis of its coding region. The RIM1 gene product (RIM1) contains three regions similar to C2H2 zinc fingers. Serine substitutions for cysteine in each of the putative zinc fingers abolish RIM1 function. The carboxyl-terminus of RIM1 is enriched in acidic amino acids and is required for full RIM1 activity. RIM1 also contains two putative cAMP-dependent protein kinase (cAPK) phosphorylation sites. At one site, substitution of alanine for serine does not affect RIM1 activity; at the other site, this substitution impairs activity. This analysis of RIM1 suggests that the protein may function as a transcriptional activator. We have used the cloned RIM1 gene to create a complete rim1 deletion. This null allele, like previously isolated rim1 mutations, causes a partial meiotic defect. In addition to RIM1, maximum IME1 expression requires the MCK1 and IME4 gene products. Defects associated with rim1, mck1, and ime4 mutations in expression of a meiotic reporter gene (ime2-lacZ) and in sporulation are additive. These findings suggest that RIM1 acts independently of MCK1 and IME4 to stimulate IME1 expression.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"rim1 mutations cause reduced expression of IME1, which is required for expression of many meiotic genes, and thus lead to a partial defect in meiosis and spore formation.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 816, "doc_id": "8148304", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Hyperfibrinogenemia decreases rates of femoropopliteal bypass thrombosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Influence of smoking and plasma factors on patency of femoropopliteal vein grafts.\nABSTRACT: OBJECTIVE To determine the effects of smoking, plasma lipids, lipoproteins, apolipoproteins, and fibrinogen on the patency of saphenous vein femoropopliteal bypass grafts at one year. DESIGN Prospective study of patients with saphenous vein femoropopliteal bypass grafts entered into a multicentre trial. SETTING Surgical wards, outpatient clinics, and home visits coordinated by two tertiary referral centres in London and Birmingham. PATIENTS 157 Patients (mean age 66.6 (SD 8.2) years), 113 with patent grafts and 44 with occluded grafts one year after bypass. MAIN OUTCOME MEASURE Cumulative percentage patency at one year. RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts. Serum cholesterol concentrations were significantly higher in patients with grafts that remained patent one year after bypass (p less than 0.005). Analysis of the smoking markers indicated that a quarter of patients (40) were untruthful in their claims to have stopped smoking. Based on smoking markers, patency of grafts in smokers was significantly lower at one year by life table analysis than in non-smokers (63% v 84%, p less than 0.02). Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002). Surprisingly, increased plasma low density lipoprotein cholesterol concentration was significantly associated with improved patency at one year (85%) at values above the median compared w [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 532, "doc_id": "12991445", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: COPI coatmer is involved in lipid homeostasis.\n\nCANDIDATE_ABSTRACT:\nTITLE: PML induces compaction, TRF2 depletion and DNA damage signaling at telomeres and promotes their alternative lengthening.\nABSTRACT: The alternative lengthening of telomeres (ALT) mechanism allows cancer cells to escape senescence and apoptosis in the absence of active telomerase. A characteristic feature of this pathway is the assembly of ALT-associated promyelocytic leukemia (PML) nuclear bodies (APBs) at telomeres. Here, we dissected the role of APBs in a human ALT cell line by performing an RNA interference screen using an automated 3D fluorescence microscopy platform and advanced 3D image analysis. We identified 29 proteins that affected APB formation, which included proteins involved in telomere and chromatin organization, protein sumoylation and DNA repair. By integrating and extending these findings, we found that APB formation induced clustering of telomere repeats, telomere compaction and concomitant depletion of the shelterin protein TRF2 (also known as TERF2). These APB-dependent changes correlated with the induction of a DNA damage response at telomeres in APBs as evident by a strong enrichment of the phosphorylated form of the ataxia telangiectasia mutated (ATM) kinase. Accordingly, we propose that APBs promote telomere maintenance by inducing a DNA damage response in ALT-positive tumor cells through changing the telomeric chromatin state to trigger ATM phosphorylation.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 210, "doc_id": "213017", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Do emergency medical services professionals think they should participate in disease prevention?\n\nABSTRACT:\nThe primary objective of the study was to determine emergency medical services (EMS) professionals' opinions regarding participation in disease and injury prevention programs. A secondary objective was to determine the proportion of EMS professionals who had participated in disease prevention programs. As part of the National Registry of Emergency Medical Technicians' biennial reregistration process, EMS professionals reregistering in 2006 were asked to complete an optional survey regarding their opinions on and participation in disease and injury prevention. Demographic characteristics were also collected. Data were analyzed using descriptive statistics and 99% confidence intervals (CIs). The chi-square test was used to compare differences by responder demographics (alpha = 0.01). A 10% difference between groups was determined to be clinically significant. The survey was completed by 27,233 EMS professionals. Of these responders, 82.7% (99% CI: 82.1-83.3) felt that EMS professionals should participate in disease prevention, with those working 20 to 29 hours per week being the least likely to think they should participate (67.4%, p<0.001). About a third, 33.8% (99% CI: 33.1-34.6), of the respondents reported having provided prevention services, with those having a graduate degree (43.5%, p<0.001), those working in EMS for more than 21 years (44%, p<0.001), those working for the military (57%, p<0.001), those working 60 to 69 hours per week (41%, p<0.001), and those responding to zero emergency calls in a typical week (43%, p<0.001) being the most likely to report having provided prevention services. About half, 51.1% (99% CI: 50.4-51.9), of the respondents agreed that prevention services should be provided during emergency calls, and 7.7% (99% CI: 7.3-8.1) o [TRUNCATED]", "output": "{\"label\": \"maybe\", \"rationale\": \"The majority of EMS professionals thought that they should participate in disease and injury prevention programs. The respondents were mixed as to whether prevention services should be provided while on emergency calls, but those with experience providing these services were more likely to agree with providing them during emergency calls.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 19145527, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Ethanol stress increases the expression of IBP in bacteria.\n\nCANDIDATE_PASSAGE:\nSvpA, a novel surface virulence-associated protein required for intracellular survival of Listeria monocytogenes. A previously unknown protein, designated SvpA (surface virulence-associated protein) and implicated in the virulence of the intracellular pathogen Listeria monocytogenes, was identified. This 64 kDa protein, encoded by svpA, is both secreted in culture supernatants and surface-exposed, as shown by immunogold labelling of whole bacteria with an anti-SvpA antibody. Analysis of the peptide sequence revealed that SvpA contains a leader peptide, a predicted C-terminal transmembrane region and a positively charged tail resembling that of the surface protein ActA, suggesting that SvpA might partially reassociate with the bacterial surface by its C-terminal membrane anchor. An allelic mutant was constructed by disrupting svpA in the wild-type strain LO28. The virulence of this mutant was strongly attenuated in the mouse, with a 2 log decrease in the LD50 and restricted bacterial growth in organs as compared to the wild-type strain. This reduced virulence was not related either to a loss of adherence or to a lower expression of known virulence factors, which remained unaffected in the svpA mutant. It was caused by a restriction of intracellular growth of mutant bacteria. By following the intracellular behaviour of bacteria within bone-marrow-derived macrophages by confocal and electron microscopy studies, it was found that most svpA mutant bacteria remained confined within phagosomes, in contrast to wild-type bacteria which rapidly escaped to the cytoplasm. The regulation of svpA was independent of PrfA, the transcriptional activator of virulence genes in L. monocytogenes. In fact, SvpA was down-regulated by MecA, ClpC and ClpP, which are highly homologou [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "389", "doc_id": "35085326", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Increased microtubule acetylation worsens interference of axonal transport caused by LRRK2 Roc-COR domain mutations.\n\nCANDIDATE_PASSAGE:\nThe Ran GTPase regulates mitotic spindle assembly Ran is an abundant nuclear GTPase with a clear role in nuclear transport during interphase but with roles in mitotic regulation that are less well understood. The nucleotide-binding state of Ran is regulated by a GTPase activating protein, RanGAP1, and by a guanine nucleotide exchange factor, RCC1. Ran also interacts with a guanine nucleotide dissociation inhibitor, RanBP1. RanBP1 has a high affinity for GTP-bound Ran, and it acts as a cofactor for RanGAP1, increasing the rate of GAP-mediated GTP hydrolysis on Ran approximately tenfold. RanBP1 levels oscillate during the cell cycle [4], and increased concentrations of RanBP1 prolong mitosis in mammalian cells and in Xenopus egg extracts (our unpublished observations). We investigated how increased concentrations of RanBP1 disturb mitosis. We found that spindle assembly is dramatically disrupted when exogenous RanBP1 is added to M phase Xenopus egg extracts. We present evidence that the role of Ran in spindle assembly is independent of nuclear transport and is probably mediated through changes in microtubule dynamics.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "615", "doc_id": "14119470", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Certain immunomodulator-human dialyzable leukocyte extract (hDLE) peptides are recognized by toll-like receptors (TLRs) on macrophages and dendritic cells.\n\nCANDIDATE_PASSAGE:\nTLR activation triggers the rapid differentiation of monocytes into macrophages and dendritic cells Leprosy enables investigation of mechanisms by which the innate immune system contributes to host defense against infection, because in one form, the disease progresses, and in the other, the infection is limited. We report that Toll-like receptor (TLR) activation of human monocytes induces rapid differentiation into two distinct subsets: DC-SIGN+ CD16+ macrophages and CD1b+ DC-SIGN− dendritic cells. DC-SIGN+ phagocytic macrophages were expanded by TLR-mediated upregulation of interleukin (IL)-15 and IL-15 receptor. CD1b+ dendritic cells were expanded by TLR-mediated upregulation of granulocyte-macrophage colony-stimulating factor (GM-CSF) and its receptor, promoted T cell activation and secreted proinflammatory cytokines. Whereas DC-SIGN+ macrophages were detected in lesions and after TLR activation in all leprosy patients, CD1b+ dendritic cells were not detected in lesions or after TLR activation of peripheral monocytes in individuals with the progressive lepromatous form, except during reversal reactions in which bacilli were cleared by T helper type 1 (TH1) responses. In tuberculoid lepromatous lesions, DC-SIGN+ cells were positive for macrophage markers, but negative for dendritic cell markers. Thus, TLR-induced differentiation of monocytes into either macrophages or dendritic cells seems to crucially influence effective host defenses in human infectious disease.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "244", "doc_id": "21498497", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Induced hepatic stem cells possess the potential to differentiate into hepatocytic cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Reprogramming fibroblasts into bipotential hepatic stem cells by defined factors.\nABSTRACT: Recent studies have demonstrated direct reprogramming of fibroblasts into a range of somatic cell types, but to date stem or progenitor cells have only been reprogrammed for the blood and neuronal lineages. We previously reported generation of induced hepatocyte-like (iHep) cells by transduction of Gata4, Hnf1α, and Foxa3 in p19 Arf null mouse embryonic fibroblasts (MEFs). Here, we show that Hnf1β and Foxa3, liver organogenesis transcription factors, are sufficient to reprogram MEFs into induced hepatic stem cells (iHepSCs). iHepSCs can be stably expanded in vitro and possess the potential of bidirectional differentiation into both hepatocytic and cholangiocytic lineages. In the injured liver of fumarylacetoacetate hydrolase (Fah)-deficient mice, repopulating iHepSCs become hepatocyte-like cells. They also engraft as cholangiocytes into bile ducts of mice with DDC-induced bile ductular injury. Lineage conversion into bipotential expandable iHepSCs provides a strategy to enable efficient derivation of both hepatocytes and cholangiocytes for use in disease modeling and tissue engineering.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"iHepSCs can be stably expanded in vitro and possess the potential of bidirectional differentiation into both hepatocytic and cholangiocytic lineages.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 625, "doc_id": "20033112", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Combining phosphatidylinositide 3-kinase and MEK 1/2 inhibitors is effective at treating KRAS mutant tumors.\n\nCANDIDATE_PASSAGE:\nCancer-Associated Fibroblasts Neutralize the Anti-tumor Effect of CSF1 Receptor Blockade by Inducing PMN-MDSC Infiltration of Tumors. Tumor-associated macrophages (TAM) contribute to all aspects of tumor progression. Use of CSF1R inhibitors to target TAM is therapeutically appealing, but has had very limited anti-tumor effects. Here, we have identified the mechanism that limited the effect of CSF1R targeted therapy. We demonstrated that carcinoma-associated fibroblasts (CAF) are major sources of chemokines that recruit granulocytes to tumors. CSF1 produced by tumor cells caused HDAC2-mediated downregulation of granulocyte-specific chemokine expression in CAF, which limited migration of these cells to tumors. Treatment with CSF1R inhibitors disrupted this crosstalk and triggered a profound increase in granulocyte recruitment to tumors. Combining CSF1R inhibitor with a CXCR2 antagonist blocked granulocyte infiltration of tumors and showed strong anti-tumor effects.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "275", "doc_id": "3559136", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Human embryonic stem cells have the capacity to give rise to differentiated progeny representative of all three embryonic germ layers.\n\nCANDIDATE_ABSTRACT:\nTITLE: Establishment and in vitro differentiation of a new embryonic stem cell line from human blastocyst.\nABSTRACT: Embryonic stem cells have the ability to remain undifferentiated and proliferate indefinitely in vitro while maintaining the potential to differentiate into derivatives of all three embryonic germ layers. These cells have, therefore, potential for in vitro differentiation studies, gene function, and so on. The aim of this study was to produce a human embryonic stem cell line. An inner cell mass of a human blastocyst was separated and cultured on mouse embryonic fibroblasts in embryonic stem cell medium with related additives. The established line was evaluated by morphology; passaging; freezing and thawing; alkaline phosphatase; Oct-4 expression; anti-surface markers including Tra-1-60 and Tra-1-81; and karyotype and spontaneous differentiation. Differentiated cardiomyocytes and neurons were evaluated by transmission electron microscopy and immunocytochemistry. Here, we report the derivation of a new embryonic stem cell line (Royan H1) from a human blastocyst that remains undifferentiated in morphology during continuous passaging for more than 30 passages, maintains a normal XX karyotype, is viable after freezing and thawing, and expresses alkaline phosphatase, Oct-4, Tra-1-60, and Tra-1-81. These cells remain undifferentiated when grown on mouse embryonic fibroblast feeder layers in the presence or absence of recombinant human leukemia inhibitory factor. Royan H1 cells can differentiate in vitro in the absence of feeder cells and can produce embryoid bodies that can further differentiate into beating cardiomyocytes as well as neurons. These results define Royan H1 cells as a new human embryonic stem cell line.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Embryonic stem cells have the ability to remain undifferentiated and proliferate indefinitely in vitro while maintaining the potential to differentiate into derivatives of all three embryonic germ layers.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 531, "doc_id": "36651210", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Macropinocytosis contributes to a cell's supply of amino acids via the intracellular uptake of protein.\n\nCANDIDATE_PASSAGE:\nA direct role for IFN-gamma in regulation of Th1 cell development. IL-12 has been identified as a major cytokine influencing the differentiation of CD4 cells to a Th1 phenotype, whereas a role for IFN-gamma is controversial. We investigated the interrelationship between IL-12 and IFN-gamma in promoting Th1 responses using naive CD4 cells reactive with pigeon cytochrome c from TCR transgenics and memory CD4 cells derived by in vivo priming with KLH. Without exogenous rIL-12 or rIFN-gamma, primary and memory effectors induced by Ag or anti-CD3 and anti-CD28 secreted variable levels of IL-2 and IFN-gamma. The level of IFN-gamma secreted by effectors correlated with endogenous IFN-gamma produced in primary cultures, and anti-IFN-gamma largely inhibited the development of effectors producing IFN-gamma. With optimal TCR stimulation and costimulation, endogenous IFN-gamma, without IL-12, was sufficient to elicit Th1 cells via an autocrine mechanism, whereas with suboptimal stimulation, exogenous rIFN-gamma or rIL-12 was required for Th1 development. However, rIL-12 was more effective than rIFN-gamma, partially because rIL-12 greatly enhanced autocrine production of IFN-gamma, and optimal development of the Th1 phenotype was mediated by the synergistic actions of both cytokines. Thus, both IFN-gamma and IL-12 can independently regulate Th1 development, but because of IFN-gamma-mediated feedback, their relative contributions are determined by the conditions of T cell stimulation. The extent of differentiation to a Th1 phenotype may, therefore, depend on the availability of both APC-derived IL-12 and autocrine IFN-gamma consequent to the overall strength of T cell stimulation.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "744", "doc_id": "39539647", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does limb-salvage surgery offer patients better quality of life and functional capacity than amputation?\n\nABSTRACT:\nPatients with aggressive lower extremity musculoskeletal tumors may be candidates for either above-knee amputation or limb-salvage surgery. However, the subjective and objective benefits of limb-salvage surgery compared with amputation are not fully clear.QUESTIONS/ We therefore compared functional status and quality of life for patients treated with above-knee amputation versus limb-salvage surgery. We reviewed 20 of 51 patients aged 15 years and older treated with above-knee amputation or limb-salvage surgery for aggressive musculoskeletal tumors around the knee between 1994 and 2004 as a retrospective cohort study. At last followup we obtained the Physiological Cost Index, the Reintegration to Normal Living Index, SF-36, and the Toronto Extremity Salvage Score questionnaires. The minimum followup was 12 months (median, 56 months; range, 12-108 months). Compared with patients having above-knee amputation, patients undergoing limb-salvage surgery had superior Physiological Cost Index scores and Reintegration to Normal Living Index. The Toronto Extremity Salvage scores and SF-36 scores were similar in the two groups.", "output": "{\"label\": \"maybe\", \"rationale\": \"These data suggest that limb-salvage surgery offers better gait efficiency and return to normal living compared with above-knee amputation, but does not improve the patient's perception of quality of life.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 22302658, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Reduced responsiveness to interleukin-2 in regulatory T cells is associated with autoimmune diseases such as Type 1 Diabetes.\n\nCANDIDATE_PASSAGE:\nShared and distinct genetic variants in type 1 diabetes and celiac disease. BACKGROUND Two inflammatory disorders, type 1 diabetes and celiac disease, cosegregate in populations, suggesting a common genetic origin. Since both diseases are associated with the HLA class II genes on chromosome 6p21, we tested whether non-HLA loci are shared. METHODS We evaluated the association between type 1 diabetes and eight loci related to the risk of celiac disease by genotyping and statistical analyses of DNA samples from 8064 patients with type 1 diabetes, 9339 control subjects, and 2828 families providing 3064 parent-child trios (consisting of an affected child and both biologic parents). We also investigated 18 loci associated with type 1 diabetes in 2560 patients with celiac disease and 9339 control subjects. RESULTS Three celiac disease loci--RGS1 on chromosome 1q31, IL18RAP on chromosome 2q12, and TAGAP on chromosome 6q25--were associated with type 1 diabetes (P<1.00x10(-4)). The 32-bp insertion-deletion variant on chromosome 3p21 was newly identified as a type 1 diabetes locus (P=1.81x10(-8)) and was also associated with celiac disease, along with PTPN2 on chromosome 18p11 and CTLA4 on chromosome 2q33, bringing the total number of loci with evidence of a shared association to seven, including SH2B3 on chromosome 12q24. The effects of the IL18RAP and TAGAP alleles confer protection in type 1 diabetes and susceptibility in celiac disease. Loci with distinct effects in the two diseases included INS on chromosome 11p15, IL2RA on chromosome 10p15, and PTPN22 on chromosome 1p13 in type 1 diabetes and IL12A on 3q25 and LPP on 3q28 in celiac disease. CONCLUSIONS A genetic susceptibility to both type 1 diabetes and celiac disease shares common alleles. These data suggest th [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1028", "doc_id": "25571386", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Gpr124 increases BBB breakdown in mouse models of ischemic stroke.\n\nCANDIDATE_ABSTRACT:\nTITLE: Gpr124 is essential for blood–brain barrier integrity in central nervous system disease\nABSTRACT: Although blood–brain barrier (BBB) compromise is central to the etiology of diverse central nervous system (CNS) disorders, endothelial receptor proteins that control BBB function are poorly defined. The endothelial G-protein-coupled receptor (GPCR) Gpr124 has been reported to be required for normal forebrain angiogenesis and BBB function in mouse embryos, but the role of this receptor in adult animals is unknown. Here Gpr124 conditional knockout (CKO) in the endothelia of adult mice did not affect homeostatic BBB integrity, but resulted in BBB disruption and microvascular hemorrhage in mouse models of both ischemic stroke and glioblastoma, accompanied by reduced cerebrovascular canonical Wnt–β-catenin signaling. Constitutive activation of Wnt–β-catenin signaling fully corrected the BBB disruption and hemorrhage defects of Gpr124-CKO mice, with rescue of the endothelial gene tight junction, pericyte coverage and extracellular-matrix deficits. We thus identify Gpr124 as an endothelial GPCR specifically required for endothelial Wnt signaling and BBB integrity under pathological conditions in adult mice. This finding implicates Gpr124 as a potential therapeutic target for human CNS disorders characterized by BBB disruption.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Here Gpr124 conditional knockout (CKO) in the endothelia of adult mice did not affect homeostatic BBB integrity, but resulted in BBB disruption and microvascular hemorrhage in mouse models of both ischemic stroke and glioblastoma, accompanied by reduced cerebrovascular canonical Wnt–β-catenin signaling.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 479, "doc_id": "6325527", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The myocardial lineage develops from cardiac progenitors of mesodermal origin.\n\nCANDIDATE_ABSTRACT:\nTITLE: Children's estimates of food portion size: the development and evaluation of three portion size assessment tools for use with children.\nABSTRACT: A number of methods have been developed to assist subjects in providing an estimate of portion size but their application in improving portion size estimation by children has not been investigated systematically. The aim was to develop portion size assessment tools for use with children and to assess the accuracy of children's estimates of portion size using the tools. The tools were food photographs, food models and an interactive portion size assessment system (IPSAS). Children (n 201), aged 4-16 years, were supplied with known quantities of food to eat, in school. Food leftovers were weighed. Children estimated the amount of each food using each tool, 24 h after consuming the food. The age-specific portion sizes represented were based on portion sizes consumed by children in a national survey. Significant differences were found between the accuracy of estimates using the three tools. Children of all ages performed well using the IPSAS and food photographs. The accuracy and precision of estimates made using the food models were poor. For all tools, estimates of the amount of food served were more accurate than estimates of the amount consumed. Issues relating to reporting of foods left over which impact on estimates of the amounts of foods actually consumed require further study. The IPSAS has shown potential for assessment of dietary intake with children. Before practical application in assessment of dietary intake of children the tool would need to be expanded to cover a wider range of foods and to be validated in a 'real-life' situation.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1241, "doc_id": "2659805", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does pacifier use alter sleep and spontaneous arousal patterns in healthy term-born infants?\n\nABSTRACT:\nImpaired arousal from sleep has been implicated in sudden infant death syndrome (SIDS). Sleeping in the prone position is a major risk factor for SIDS. Epidemiological studies have shown that pacifier use decreases the risk of SIDS, even when infants sleep prone. We examined spontaneous arousability in infants slept prone and supine over the first 6 months of life and hypothesised that spontaneous arousals would be increased in pacifier users, particularly in the prone position. Healthy term infants (n = 30) were studied on three occasions over the first 6 months after birth. Spontaneous cortical arousals and subcortical activations were scored and converted into frequency per hour of sleep. There was no effect of pacifier use on total time spent sleeping or awake or the number of spontaneous awakenings at any age. There was also no effect of pacifier use on the frequency or duration of the total number of spontaneous arousals or on cortical arousals and subcortical activations.", "output": "{\"label\": \"no\", \"rationale\": \"Pacifier use did not alter infant spontaneous arousability at any of the three ages studied, in either the prone or supine sleeping position. Any preventative effect of pacifiers for SIDS may be through physiological mechanisms other than increased arousability.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 25169652, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: MafA ubiquitination decreases the recruitment of coavtivator P/CAF by MafA.\n\nCANDIDATE_PASSAGE:\nTie2/Angiopoietin-1 Signaling Regulates Hematopoietic Stem Cell Quiescence in the Bone Marrow Niche The quiescent state is thought to be an indispensable property for the maintenance of hematopoietic stem cells (HSCs). Interaction of HSCs with their particular microenvironments, known as the stem cell niches, is critical for adult hematopoiesis in the bone marrow (BM). Here, we demonstrate that HSCs expressing the receptor tyrosine kinase Tie2 are quiescent and antiapoptotic, and comprise a side-population (SP) of HSCs, which adhere to osteoblasts (OBs) in the BM niche. The interaction of Tie2 with its ligand Angiopoietin-1 (Ang-1) induced cobblestone formation of HSCs in vitro and maintained in vivo long-term repopulating activity of HSCs. Furthermore, Ang-1 enhanced the ability of HSCs to become quiescent and induced adhesion to bone, resulting in protection of the HSC compartment from myelosuppressive stress. These data suggest that the Tie2/Ang-1 signaling pathway plays a critical role in the maintenance of HSCs in a quiescent state in the BM niche.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "747", "doc_id": "17271462", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Combination nicotine replacement therapies with varenicline or bupropion are more effective after 12 weeks of reatment compared to varenicline monotherapy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Combination varenicline and bupropion SR for tobacco-dependence treatment in cigarette smokers: a randomized trial.\nABSTRACT: IMPORTANCE Combining pharmacotherapies for tobacco-dependence treatment may increase smoking abstinence. OBJECTIVE To determine efficacy and safety of varenicline and bupropion sustained-release (SR; combination therapy) compared with varenicline (monotherapy) in cigarette smokers. DESIGN, SETTING, AND PARTICIPANTS Randomized, blinded, placebo-controlled multicenter clinical trial with a 12-week treatment period and follow-up through week 52 conducted between October 2009 and April 2013 at 3 midwestern clinical research sites. Five hundred six adult (≥18 years) cigarette smokers were randomly assigned and 315 (62%) completed the study. INTERVENTIONS Twelve weeks of varenicline and bupropion SR or varenicline and placebo. MAIN OUTCOMES AND MEASURES Primary outcome was abstinence rates at week 12, defined as prolonged (no smoking from 2 weeks after the target quit date) abstinence and 7-day point-prevalence (no smoking past 7 days) abstinence. Secondary outcomes were prolonged and point-prevalence smoking abstinence rates at weeks 26 and 52. Outcomes were biochemically confirmed. RESULTS At 12 weeks, 53.0% of the combination therapy group achieved prolonged smoking abstinence and 56.2% achieved 7-day point-prevalence smoking abstinence compared with 43.2% and 48.6% in varenicline monotherapy (odds ratio [OR], 1.49; 95% CI, 1.05-2.12; P = .03 and OR, 1.36; 95% CI, 0.95-1.93; P = .09, respectively). At 26 weeks, 36.6% of the combination therapy group achieved prolonged and 38.2% achieved 7-day point-prevalence smoking abstinence compared with 27.6% and 31.9% in varenicline monotherapy (OR, 1.52; 95% CI, 1.04-2.22; P = .03 and OR, 1.32; 95% CI, 0.91-1.91; P = .14, respectively). At 52 weeks, 30.9% of the combination therapy group achieved prolonged and 36.6% achi [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"RESULTS At 12 weeks, 53.0% of the combination therapy group achieved prolonged smoking abstinence and 56.2% achieved 7-day point-prevalence smoking abstinence compared with 43.2% and 48.6% in varenicline monotherapy (odds ratio [OR], 1.49; 95% CI, 1.05-2.12; P = .03 and OR, 1.36; 95% CI, 0.95-1.93; P = .09, respectively).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 272, "doc_id": "11614737", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: PrimPol generates short DNA replication intermediates on the leading strand during DNA replication.\n\nCANDIDATE_PASSAGE:\nDNA replication is required To elicit cellular responses to psoralen-induced DNA interstrand cross-links. Following introduction of DNA interstrand cross-links (ICLs), mammalian cells display chromosome breakage or cell cycle delay with a 4N DNA content. To further understand the nature of the delay, previously described as a G(2)/M arrest, we developed a protocol to generate ICLs during specific intervals of the cell cycle. Synchronous populations of G(1), S, and G(2) cells were treated with photoactivated 4'-hydroxymethyl-4,5',8-trimethylpsoralen (HMT) and scored for normal passage into mitosis. In contrast to what was found for ionizing radiation, ICLs introduced during G(2) did not result in a G(2)/M arrest, mitotic arrest, or chromosome breakage. Rather, subsequent passage through S phase was required to trigger both chromosome breakage and arrest in the next cell cycle. Similarly, ICLs introduced during G(1) did not cause a G(1)/S arrest. We conclude that DNA replication is required to elicit the cellular responses of cell cycle arrest and genomic instability after psoralen-induced ICLs. In primary human fibroblasts, the 4N DNA content cell cycle arrest triggered by ICLs was long lasting but reversible. Kinetic analysis suggested that these cells could remove up to approximately 2,500 ICLs/genome at an average rate of 11 ICLs/genome/h.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "970", "doc_id": "9291596", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does irregularity distinguish limb tremor in cervical dystonia from essential tremor?\n\nABSTRACT:\nPatients with cervical dystonia (CD) often have limb tremor that is clinically indistinguishable from essential tremor (ET). Whether a common central mechanism underlies the tremor in these conditions is unknown. We addressed this issue by quantifying limb tremor in 19 patients with CD and 35 patients with ET. Postural, resting and kinetic tremors were quantified (amplitude, mean frequency and regularity) using a three-axis accelerometer. The amplitude of limb tremor in ET was significantly higher than in CD, but the mean frequency was not significantly different between the groups. The cycle-to-cycle variability of the frequency (ie the tremor irregularity), however, was significantly greater (approximately 50%) in CD. Analysis of covariance excluded the possibility that the increased irregularity was related to the smaller amplitude of tremor in CD (ANCOVA: p = 0.007, F = 5.31).", "output": "{\"label\": \"yes\", \"rationale\": \"We propose that tremor in CD arises from oscillators with different dynamic characteristics, producing a more irregular output, whereas the tremor in ET arises from oscillators with similar dynamic characteristics, producing a more regular output. We suggest that variability of tremor is an important parameter for distinguishing tremor mechanisms. It is possible that changes in membrane kinetics based on the pattern of ion channel expression underlie the differences in tremor in some diseases.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 17872981, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Patients in stable partnerships progress from HIV to death at the same rate as patients not in partnerships.\n\nCANDIDATE_ABSTRACT:\nTITLE: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\nABSTRACT: OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART). DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study). SETTING Seven outpatient clinics throughout Switzerland. PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years). MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound. RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion. When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership. In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without. Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression. CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 925, "doc_id": "17077004", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does antral localization worsen the efficacy of enteral stents in malignant digestive tumors?\n\nABSTRACT:\nMalignant gastric outlet obstruction can be treated by means of enteral stenting or surgical gastrojejunalanatomosis. We evaluated in a prospective and multicentre study the efficacy of the enteral stent on food intake, the quality of life impact, and the relationship between efficacy and determined clinical and technical parameters. Seventy one patients affected by symptoms arising from gastroduodenal obstruction due to malignant tumors, with criteria of irresecability, metastatic disease or very high surgical risk, were treated by means of self expanding metal stents. We used the GOOSS index to evaluate efficacy, and the Euro Qol-5D index to evaluate quality of life. Before stenting patients with GOOSS 0 and 1 were 68 (98.5%). After stenting patients with GOOSS 2 and 3 (semisolid and solid food) were 58 (84,1%) (P<.0001). The Euro Qol-5D index measured before and a month after stenting were 10.17 and 10.04 respectively (P=.6). The median survival was 91 days (9-552). The enteral stents for localised tumors in the duodenum and the gastrojejunalanastomosis were effective in 26 patients (70.2%) and 13 patients respectively (86.6%), while the enteral stents of tumors in the antrum were effective in only 5 patients (29.4%).", "output": "{\"label\": \"yes\", \"rationale\": \"The palliative treatment of malignant gastric outlet obstruction with a uncovered metal stent produces a significant improvement of oral food intake and maintains the overall quality of life index. The antral localization is associated with a lower efficacy of the procedure.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 21353341, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: GATA3 regulates cell cycle progression in bone marrow hematopoietic stem cells.\n\nCANDIDATE_PASSAGE:\nmiR-294/miR-302 promotes proliferation, suppresses G1-S restriction point, and inhibits ESC differentiation through separable mechanisms. The miR-294 and miR-302 microRNAs promote the abbreviated G1 phase of the embryonic stem cell (ESC) cell cycle and suppress differentiation induced by let-7. Here, we evaluated the role of the retinoblastoma (Rb) family proteins in these settings. Under normal growth conditions, miR-294 promoted the rapid G1-S transition independent of the Rb family. In contrast, miR-294 suppressed the further accumulation of cells in G1 in response to nutrient deprivation and cell-cell contact in an Rb-dependent fashion. We uncovered five additional miRNAs (miR-26a, miR-99b, miR-193, miR-199a-5p, and miR-218) that silenced ESC self-renewal in the absence of other miRNAs, all of which were antagonized by miR-294 and miR-302. Four of the six differentiation-inducing miRNAs induced an Rb-dependent G1 accumulation. However, all six still silenced self-renewal in the absence of the Rb proteins. These results show that the miR-294/miR-302 family acts through Rb-dependent and -independent pathways to regulate the G1 restriction point and the silencing of self-renewal, respectively.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "444", "doc_id": "28704738", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Exercise increases cancer mortality rates among Chinese citizens.\n\nCANDIDATE_ABSTRACT:\nTITLE: Combined Impact of Lifestyle-Related Factors on Total and Cause-Specific Mortality among Chinese Women: Prospective Cohort Study\nABSTRACT: BACKGROUND Although cigarette smoking, excessive alcohol drinking, obesity, and several other well-studied unhealthy lifestyle-related factors each have been linked to the risk of multiple chronic diseases and premature death, little is known about the combined impact on mortality outcomes, in particular among Chinese and other non-Western populations. The objective of this study was to quantify the overall impact of lifestyle-related factors beyond that of active cigarette smoking and alcohol consumption on all-cause and cause-specific mortality in Chinese women. METHODS AND FINDINGS We used data from the Shanghai Women's Health Study, an ongoing population-based prospective cohort study in China. Participants included 71,243 women aged 40 to 70 years enrolled during 1996-2000 who never smoked or drank alcohol regularly. A healthy lifestyle score was created on the basis of five lifestyle-related factors shown to be independently associated with mortality outcomes (normal weight, lower waist-hip ratio, daily exercise, never exposed to spouse's smoking, higher daily fruit and vegetable intake). The score ranged from zero (least healthy) to five (most healthy) points. During an average follow-up of 9 years, 2,860 deaths occurred, including 775 from cardiovascular disease (CVD) and 1,351 from cancer. Adjusted hazard ratios for mortality decreased progressively with an increasing number of healthy lifestyle factors. Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality. The inverse association between the healthy lifestyle score and mortality was seen consistently regardless of ch [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 396, "doc_id": "1456068", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Dscam1 acts as a hypervariable pattern-recognition receptor for the immune system.\n\nCANDIDATE_ABSTRACT:\nTITLE: AgDscam, a Hypervariable Immunoglobulin Domain-Containing Receptor of the Anopheles gambiae Innate Immune System \nABSTRACT: Activation of the insect innate immune system is dependent on a limited number of pattern recognition receptors (PRRs) capable of interacting with pathogen-associated molecular pattern. Here we report a novel role of an alternatively spliced hypervariable immunoglobulin domain-encoding gene, Dscam, in generating a broad range of PRRs implicated in immune defense in the malaria vector Anopheles gambiae. The mosquito Down syndrome cell adhesion molecule gene, AgDscam, has a complex genome organization with 101 exons that can produce over 31,000 potential alternative splice forms with different combinations of adhesive domains and interaction specificities. AgDscam responds to infection by producing pathogen challenge-specific splice form repertoires. Transient silencing of AgDscam compromises the mosquito's resistance to infections with bacteria and the malaria parasite Plasmodium. AgDscam is mediating phagocytosis of bacteria with which it can associate and defend against in a splice form–specific manner. AgDscam is a hypervariable PRR of the A. gambiae innate immune system.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"AgDscam responds to infection by producing pathogen challenge-specific splice form repertoires.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 356, "doc_id": "6144337", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Vitamin D is an important factor in the relationship between calcium and parathyroid hormone.\n\nCANDIDATE_ABSTRACT:\nTITLE: Relationship between serum parathyroid hormone levels, vitamin D sufficiency, and calcium intake.\nABSTRACT: CONTEXT Adequate vitamin D status for optimum bone health has received increased recognition in recent years; however, the ideal intake is not known. Serum 25-hydroxyvitamin D is the generally accepted indicator of vitamin D status, but no universal reference level has been reached. OBJECTIVE To investigate the relative importance of high calcium intake and serum 25-hydroxyvitamin D for calcium homeostasis, as determined by serum intact parathyroid hormone (PTH). DESIGN, SETTING, AND PARTICIPANTS Cross-sectional study of 2310 healthy Icelandic adults who were divided equally into 3 age groups (30-45 years, 50-65 years, or 70-85 years) and recruited from February 2001 to January 2003. They were administered a semi-quantitative food frequency questionnaire, which assessed vitamin D and calcium intake. Participants were further divided into groups according to calcium intake (<800 mg/d, 800-1200 mg/d, and >1200 mg/d) and serum 25-hydroxyvitamin D level (<10 ng/mL, 10-18 ng/mL, and >18 ng/mL). MAIN OUTCOME MEASURE Serum intact PTH as determined by calcium intake and vitamin D. RESULTS A total of 944 healthy participants completed all parts of the study. After adjusting for relevant factors, serum PTH was lowest in the group with a serum 25-hydroxyvitamin D level of more than 18 ng/mL but highest in the group with a serum 25-hydroxyvitamin D level of less than 10 ng/mL. At the low serum 25-hydroxyvitamin D level (<10 ng/mL), calcium intake of less than 800 mg/d vs more than 1200 mg/d was significantly associated with higher serum PTH (P = .04); and at a calcium intake of more than 1200 mg/d, there was a significant difference between the lowest and highest vitamin D groups (P = .04). CONCLUSIONS As long as vitamin D status is ensured, calcium intake levels of mor [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"After adjusting for relevant factors, serum PTH was lowest in the group with a serum 25-hydroxyvitamin D level of more than 18 ng/mL but highest in the group with a serum 25-hydroxyvitamin D level of less than 10 ng/mL. At the low serum 25-hydroxyvitamin D level (<10 ng/mL), calcium intake of less than 800 mg/d vs more than 1200 mg/d was significantly associated with higher serum PTH (P = .04); and at a calcium intake of more than 1200 mg/d, there was a significant difference between the lowest and highest vitamin D groups (P = .04).\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1371, "doc_id": "16256507", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Consumption of whole fruits increases the risk of type 2 diabetes.\n\nCANDIDATE_PASSAGE:\nSugar-sweetened beverages, weight gain, and incidence of type 2 diabetes in young and middle-aged women. CONTEXT Sugar-sweetened beverages like soft drinks and fruit punches contain large amounts of readily absorbable sugars and may contribute to weight gain and an increased risk of type 2 diabetes, but these relationships have been minimally addressed in adults. OBJECTIVE To examine the association between consumption of sugar-sweetened beverages and weight change and risk of type 2 diabetes in women. DESIGN, SETTING, AND PARTICIPANTS Prospective cohort analyses conducted from 1991 to 1999 among women in the Nurses' Health Study II. The diabetes analysis included 91,249 women free of diabetes and other major chronic diseases at baseline in 1991. The weight change analysis included 51,603 women for whom complete dietary information and body weight were ascertained in 1991, 1995, and 1999. We identified 741 incident cases of confirmed type 2 diabetes during 716,300 person-years of follow-up. MAIN OUTCOME MEASURES Weight gain and incidence of type 2 diabetes. RESULTS Those with stable consumption patterns had no difference in weight gain, but weight gain over a 4-year period was highest among women who increased their sugar-sweetened soft drink consumption from 1 or fewer drinks per week to 1 or more drinks per day (multivariate-adjusted means, 4.69 kg for 1991 to 1995 and 4.20 kg for 1995 to 1999) and was smallest among women who decreased their intake (1.34 and 0.15 kg for the 2 periods, respectively) after adjusting for lifestyle and dietary confounders. Increased consumption of fruit punch was also associated with greater weight gain compared with decreased consumption. After adjustment for potential confounders, women consuming 1 or more sugar-sweetened s [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "283", "doc_id": "9822397", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: HIF1A as a major vascular endothelial growth factor regulator: do its polymorphisms have an association with age-related macular degeneration?\n\nABSTRACT:\nTo investigate the association between age-related macular degeneration (AMD) and the polymorphisms of HIF1A, a major vascular epithelial growth factor regulator under hypoxic conditions. The associations of AMD and polymorphisms of genes CFH, SKIV2L and MYRIP were also studied. Prospective study. Eighty-seven AMD patients and 80 healthy subjects admitted to the Department of Ophthalmology at Pamukkale University Hospital, Denizli, Turkey, were included: 45 (52%) had wet type AMD, and 42 (48%) had dry type AMD. Polymorphisms rs1061170 (CFH), rs429608 (SKIV2L), rs2679798 (MYRIP) and both rs11549465 and rs11549467 (HIF1A) were investigated in DNA isolated from peripheral blood samples of the cases and controls by dye-termination DNA sequencing. Genotype distribution of rs1061170 (CFH), rs429608 (SKIV2L), rs2679798 (MYRIP) and both rs11549465 and rs11549467 (HIF1A) in AMD cases and healthy controls; association between genotypes and AMD subtypes. Given the significant difference between the mean age of case and control groups (72.13 ± 5.77 vs. 62.80 ± 5.22, respectively) (P = .000), subsequent analyses were adjusted for age. We found that having at least one C allele for polymorphism rs1061170 increases AMD risk independent of age (OR = 2.42, 95% confidence interval [CI], 1.22-4.81). The ancestral T allele for polymorphism rs1061170 has a protective effect for AMD (OR = 0.53, 95% CI, 0.34-0.83). No statistically significant difference for distributions of other single nucleotide polymorphisms (SNPs) emerged between patients and healthy subjects.", "output": "{\"label\": \"maybe\", \"rationale\": \"No associations appeared between HIF1A SNPs and AMD, which were studied here for the first time; however, polymorphism rs1061170 of the CFH gene is associated with AMD in our population.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 24995509, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Elevated cell-free mitochondrial DNA levels are associated with mortality.\n\nCANDIDATE_PASSAGE:\nLDL inhibits the mediation of cholesterol efflux from macrophage foam cells by apoA-I-containing lipoproteins. A putative mechanism for foam cell formation. Although the accumulation of cholesterol in macrophages appears to be an initial step in atherogenesis, low-density lipoprotein (LDL), a major risk factor for atherosclerosis, does not promote cholesterol accumulation in macrophages in its native form. On the other hand, apolipoprotein (apo) A-I-containing lipoprotein removes cholesterol from cholesterol-loaded macrophages (foam cells) and prevents cholesterol from accumulating in the cells. We examined the effect of LDL on cholesterol removal by two species of apoA-I-containing lipoproteins, one containing only apoA-I (LpA-I) and the other containing apoA-I and apoA-II (LpA-I/A-II). When foam cells were incubated with LpA-I or LpA-I/A-II, cellular cholesterol mass was reduced. In contrast, when LDL was added, the cholesterol-reducing capacities of these lipoproteins were dose-dependently inhibited by LDL. In the presence of LDL, LpA-I and LpA-I/A-II removed free cholesterol preferentially from LDL rather than from the plasma membrane of foam cells. In addition, a fair amount of cellular cholesterol was directly moved to LDL rather than to LpA-I or LpA-I/A-II. The cellular cholesterol that moved to LDL was completely compensated for by the cholesterol influx from LDL to foam cells. Thus, net cholesterol efflux (a combination of influx and efflux) from foam cells was inhibited by LDL. These results, taken together, indicate that LDL may accelerate foam cell formation by inhibiting cholesterol removal from the cells and that elevated levels of plasma LDL may become a risk factor for atherosclerosis by inhibiting the function of LpA-I and LpA-I/A-II at the [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "375", "doc_id": "9814332", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: There is a positive correlation between hip fractures and statin use.\n\nCANDIDATE_ABSTRACT:\nTITLE: HMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients.\nABSTRACT: CONTEXT Recent animal studies have found that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) lipid-lowering drugs (statins) substantially increase bone formation, but whether statin use in humans results in clinically meaningful bone formation or a reduction in the risk of osteoporotic fractures is not known. OBJECTIVE To determine whether the use of statins is associated with reduced hip fracture risk. DESIGN Case-control study. SETTING AND PATIENTS A total of 6110 New Jersey residents aged 65 years or older and enrolled in Medicare and either Medicaid or the Pharmacy Assistance for the Aged and Disabled program. Case patients (n=1222) underwent surgical repair of a hip fracture in 1994. Control patients (n=4888) were identified at a ratio of 4:1 and frequency-matched to case patients for age and sex. MAIN OUTCOME MEASURE Adjusted odds ratio (OR) of hip fracture by statin use in the 180 days and 3 years prior to the index date (the earliest date of admission for surgery), adjusted for demographic and clinical characteristics and health care utilization. RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus. No significant relationship was observed between use of nonstatin lipid-lowering agents and hip fracture risk. Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowe [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS These findings support an association between statin use by elderly patients and reduction in the risk of hip fracture.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1288, "doc_id": "4687948", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Nonsteroidal antinflammatory drugs show potential anticancer indications.\n\nCANDIDATE_PASSAGE:\nAutophagy and mTORC1 regulate the stochastic phase of somatic cell reprogramming We describe robust induction of autophagy during the reprogramming of mouse fibroblasts to induced pluripotent stem cells by four reprogramming factors (Sox2, Oct4, Klf4 and c-Myc), henceforth 4F. This process occurs independently of p53 activation, and is mediated by the synergistic downregulation of mechanistic target of rapamycin complex 1 (mTORC1) and the induction of autophagy-related genes. The 4F coordinately repress mTORC1, but bifurcate in their regulation of autophagy-related genes, with Klf4 and c-Myc inducing them but Sox2 and Oct4 inhibiting them. On one hand, inhibition of mTORC1 facilitates reprogramming by promoting cell reshaping (mitochondrial remodelling and cell size reduction). On the other hand, mTORC1 paradoxically impairs reprogramming by triggering autophagy. Autophagy does not participate in cell reshaping in reprogramming but instead degrades p62, whose accumulation in autophagy-deficient cells facilitates reprogramming. Our results thus reveal a complex signalling network involving mTORC1 inhibition and autophagy induction in the early phase of reprogramming, whose delicate balance ultimately determines reprogramming efficiency.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "857", "doc_id": "31882215", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: RUNX1 is downregulated or mutated in TLX1 T-ALL.\n\nCANDIDATE_ABSTRACT:\nTITLE: Reverse engineering of TLX oncogenic transcriptional networks identifies RUNX1 as tumor suppressor in T-ALL\nABSTRACT: The TLX1 and TLX3 transcription factor oncogenes have a key role in the pathogenesis of T cell acute lymphoblastic leukemia (T-ALL). Here we used reverse engineering of global transcriptional networks to decipher the oncogenic regulatory circuit controlled by TLX1 and TLX3. This systems biology analysis defined T cell leukemia homeobox 1 (TLX1) and TLX3 as master regulators of an oncogenic transcriptional circuit governing T-ALL. Notably, a network structure analysis of this hierarchical network identified RUNX1 as a key mediator of the T-ALL induced by TLX1 and TLX3 and predicted a tumor-suppressor role for RUNX1 in T cell transformation. Consistent with these results, we identified recurrent somatic loss-of-function mutations in RUNX1 in human T-ALL. Overall, these results place TLX1 and TLX3 at the top of an oncogenic transcriptional network controlling leukemia development, show the power of network analyses to identify key elements in the regulatory circuits governing human cancer and identify RUNX1 as a tumor-suppressor gene in T-ALL.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Overall, these results place TLX1 and TLX3 at the top of an oncogenic transcriptional network controlling leukemia development, show the power of network analyses to identify key elements in the regulatory circuits governing human cancer and identify RUNX1 as a tumor-suppressor gene in T-ALL.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1009, "doc_id": "1982286", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Primary cervical cancer screening with HPV detection has higher longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_PASSAGE:\nPhysician knowledge levels and barriers to coronary risk prevention in women: survey results from the Women and Heart Disease Physician Education Initiative. BACKGROUND Few studies have examined whether physician knowledge, attitudes, or practice patterns might contribute to gender disparities in the primary prevention of coronary heart disease (CHD), including among physicians caring for the largest number of reproductive-age women, obstetricians and gynecologists (OB/GYNs). We sought to identify barriers affecting the provision of recommended coronary risk factor therapies in women. METHODS We surveyed internists and OB/GYNs who attended Grand Rounds presentations developed for the New York State Women and Heart Disease Physician Education Initiative. This program was designed to improve screening and management of coronary risk factors in women. Attendees were asked to complete a 7-minute questionnaire. RESULTS The mean age of the 529 respondents was 40.3 years (standard deviation = 12.3), 75.1% were internists (n=378), and 42.7% (n=226) were women. Physicians correctly responded to 71.5% of the 13 questions assessing knowledge of coronary risk prevention (range, 4-13). Almost one third of internists and half of the OB/GYNs did not know that tobacco use was the leading cause of myocardial infarction in young women. For patients who smoked tobacco, only two thirds of internists and 55.4% of OB/GYNs reported suggesting a quit date (p=.007). After controlling for covariates, physicians who did not perceive time as a barrier were more likely to discuss smoking cessation (odds ratio=1.7 [1.1-2.7]). CONCLUSIONS Among the internists and OB/GYNs surveyed, time was perceived as a barrier to implementing risk prevention. These physicians also underestimated the imp [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "971", "doc_id": "6085365", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The availability of safe places to study is not effective at decreasing homelessness.\n\nCANDIDATE_PASSAGE:\nCollective trauma in northern Sri Lanka: a qualitative psychosocial-ecological study BACKGROUND Complex situations that follow war and natural disasters have a psychosocial impact on not only the individual but also on the family, community and society. Just as the mental health effects on the individual psyche can result in non pathological distress as well as a variety of psychiatric disorders; massive and widespread trauma and loss can impact on family and social processes causing changes at the family, community and societal levels. METHOD This qualitative, ecological study is a naturalistic, psychosocial ethnography in Northern Sri Lanka, while actively involved in psychosocial and community mental health programmes among the Tamil community. Participatory observation, key informant interviews and focus group discussion with community level relief and rehabilitation workers and government and non-governmental officials were used to gather data. The effects on the community of the chronic, man-made disaster, war, in Northern Sri Lanka were compared with the contexts found before the war and after the tsunami. RESULTS Fundamental changes in the functioning of the family and the community were observed. While the changes after the tsunami were not so prominent, the chronic war situation caused more fundamental social transformations. At the family level, the dynamics of single parent families, lack of trust among members, and changes in significant relationships, and child rearing practices were seen. Communities tended to be more dependent, passive, silent, without leadership, mistrustful, and suspicious. Additional adverse effects included the breakdown in traditional structures, institutions and familiar ways of life, and deterioration in social norms a [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1197", "doc_id": "15780826", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Long - range chromatin interactions regulate transcription.\n\nCANDIDATE_PASSAGE:\nDirect in vivo assessment of microcirculatory dysfunction in severe falciparum malaria. BACKGROUND This study sought to describe and quantify microcirculatory changes in the mucosal surfaces of patients with severe malaria, by direct in vivo observation using orthogonal polarization spectral (OPS) imaging. METHODS The microcirculation in the rectal mucosa of adult patients with severe malaria was assessed by use of OPS imaging, at admission and then daily. Comparison groups comprised patients with uncomplicated falciparum malaria, patients with bacterial sepsis, and healthy individuals. RESULTS Erythrocyte velocities were measured directly in 43 adult patients with severe falciparum malaria, of whom 20 died. Microcirculatory blood flow was markedly disturbed, with heterogeneous obstruction that was proportional to severity of disease. Blocked capillaries were found in 29 patients (67%) and were associated with concurrent hyperdynamic blood flow (erythrocyte velocity, >750 mm/s) in adjacent vessels in 27 patients (93%). The proportion of blocked capillaries correlated with the base deficit in plasma and with the concentration of lactate. Abnormalities disappeared when the patients recovered. In healthy individuals and in patients with uncomplicated malaria or sepsis, no stagnant erythrocytes were detected, and, in patients with sepsis, hyperdynamic blood flow was prominent. CONCLUSION Patients with severe falciparum malaria show extensive microvascular obstruction that is proportional to the severity of the disease. This finding underscores the prominent role that microvascular obstruction plays in the pathophysiology of severe malaria and illustrates the fundamental difference between the microvascular pathophysiology of malaria and that of bacterial sepsis.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "704", "doc_id": "17168045", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Mice are incapable of producing neutralizing antibodies in reponse to the Chikungunya virus (CHIKV) produced in mosquitos.\n\nCANDIDATE_PASSAGE:\nStimulation of CD25+CD4+ regulatory T cells through GITR breaks immunological self-tolerance CD25+CD4+ regulatory T cells in normal animals are engaged in the maintenance of immunological self-tolerance. We show here that glucocorticoid-induced tumor necrosis factor receptor family–related gene (GITR, also known as TNFRSF18)—a member of the tumor necrosis factor–nerve growth factor (TNF-NGF) receptor gene superfamily—is predominantly expressed on CD25+CD4+ T cells and on CD25+CD4+CD8− thymocytes in normal naïve mice. We found that stimulation of GITR abrogated CD25+CD4+ T cell–mediated suppression. In addition, removal of GITR-expressing T cells or administration of a monoclonal antibody to GITR produced organ-specific autoimmune disease in otherwise normal mice. Thus, GITR plays a key role in dominant immunological self-tolerance maintained by CD25+CD4+ regulatory T cells and could be a suitable molecular target for preventing or treating autoimmune disease.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "772", "doc_id": "21185923", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The relationship between a breast cancer patient's capacity to metabolize tamoxifen and treatment outcome is dependent on the patient's genetic make-up.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association between CYP2D6 polymorphisms and outcomes among women with early stage breast cancer treated with tamoxifen.\nABSTRACT: CONTEXT The growth inhibitory effect of tamoxifen, which is used for the treatment of hormone receptor-positive breast cancer, is mediated by its metabolites, 4-hydroxytamoxifen and endoxifen. The formation of active metabolites is catalyzed by the polymorphic cytochrome P450 2D6 (CYP2D6) enzyme. OBJECTIVE To determine whether CYP2D6 variation is associated with clinical outcomes in women receiving adjuvant tamoxifen. DESIGN, SETTING, AND PATIENTS Retrospective analysis of German and US cohorts of patients treated with adjuvant tamoxifen for early stage breast cancer. The 1325 patients had diagnoses between 1986 and 2005 of stage I through III breast cancer and were mainly postmenopausal (95.4%). Last follow-up was in December 2008; inclusion criteria were hormone receptor positivity, no metastatic disease at diagnosis, adjuvant tamoxifen therapy, and no chemotherapy. DNA from tumor tissue or blood was genotyped for CYP2D6 variants associated with reduced (*10, *41) or absent (*3, *4, *5) enzyme activity. Women were classified as having an extensive (n=609), heterozygous extensive/intermediate (n=637), or poor (n=79) CYP2D6 metabolism. MAIN OUTCOME MEASURES Time to recurrence, event-free survival, disease-free survival, and overall survival. RESULTS Median follow-up was 6.3 years. At 9 years of follow-up, the recurrence rates were 14.9% for extensive metabolizers, 20.9% for heterozygous extensive/intermediate metabolizers, and 29.0% for poor metabolizers, and all-cause mortality rates were 16.7%, 18.0%, and 22.8%, respectively. Compared with extensive metabolizers, there was a significantly increased risk of recurrence for heterozygous extensive/intermediate metabolizers (time to recurrence adjusted hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.04 [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Compared with extensive metabolizers, there was a significantly increased risk of recurrence for heterozygous extensive/intermediate metabolizers (time to recurrence adjusted hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.04-1.90) and for poor metabolizers (time to recurrence HR, 1.90; 95% CI, 1.10-3.28).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1259, "doc_id": "24341590", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cells undergoing methionine restriction may activate miRNAs.\n\nCANDIDATE_ABSTRACT:\nTITLE: microRNAs: A Safeguard against Turmoil?\nABSTRACT: Emerging data suggest that microRNAs (miRNAs) are instrumental in a variety of stress responses in addition to their more recognized role in development. Surprisingly, miRNAs, which normally suppress expression of target transcripts, may become activators of expression during stress. This might be partially explained by new interactions of miRNA/Argonaute complexes with RNA-binding proteins that relocate from different subcellular compartments during stress.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 238, "doc_id": "2251426", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: IFIT1 restricts viral replication by sequestrating mis-capped viral RNAs.\n\nCANDIDATE_PASSAGE:\nEB virus-encoded RNAs are recognized by RIG-I and activate signaling to induce type I IFN. Epstein-Barr virus (EBV)-encoded small RNAs (EBERs) are nonpolyadenylated, untranslated RNAs, exist most abundantly in latently EBV-infected cells, and are expected to show secondary structures with many short stem-loops. Retinoic acid-inducible gene I (RIG-I) is a cytosolic protein that detects viral double-stranded RNA (dsRNA) inside the cell and initiates signaling pathways leading to the induction of protective cellular genes, including type I interferons (IFNs). We investigated whether EBERs were recognized by RIG-I as dsRNA. Transfection of RIG-I plasmid induced IFNs and IFN-stimulated genes (ISGs) in EBV-positive Burkitt's lymphoma (BL) cells, but not in their EBV-negative counterparts or EBER-knockout EBV-infected BL cells. Transfection of EBER plasmid or in vitro-synthesized EBERs induced expression of type I IFNs and ISGs in RIG-I-expressing, EBV-negative BL cells, but not in RIG-I-minus counterparts. EBERs activated RIG-I's substrates, NF-kappaB and IFN regulatory factor 3, which were necessary for type I IFN activation. It was also shown that EBERs co-precipitated with RIG-I. These results indicate that EBERs are recognized by RIG-I and activate signaling to induce type I IFN in EBV-infected cells.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "544", "doc_id": "37727521", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Post-transcriptional handling of mitochondrial transcripts occurs in mitochondrial RNA granules.\n\nCANDIDATE_PASSAGE:\nThe mitochondrial RNA-binding protein GRSF1 localizes to RNA granules and is required for posttranscriptional mitochondrial gene expression. RNA-binding proteins are at the heart of posttranscriptional gene regulation, coordinating the processing, storage, and handling of cellular RNAs. We show here that GRSF1, previously implicated in the binding and selective translation of influenza mRNAs, is targeted to mitochondria where it forms granules that colocalize with foci of newly synthesized mtRNA next to mitochondrial nucleoids. GRSF1 preferentially binds RNAs transcribed from three contiguous genes on the light strand of mtDNA, the ND6 mRNA, and the long noncoding RNAs for cytb and ND5, each of which contains multiple consensus binding sequences. RNAi-mediated knockdown of GRSF1 leads to alterations in mitochondrial RNA stability, abnormal loading of mRNAs and lncRNAs on the mitochondrial ribosome, and impaired ribosome assembly. This results in a specific protein synthesis defect and a failure to assemble normal amounts of the oxidative phosphorylation complexes. These data implicate GRSF1 as a key regulator of posttranscriptional mitochondrial gene expression.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "962", "doc_id": "935538", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Foxp3 enables the expression of transcriptional regulators implicated in memory T cell development.\n\nCANDIDATE_ABSTRACT:\nTITLE: Extrathymic Generation of Regulatory T Cells in Placental Mammals Mitigates Maternal-Fetal Conflict\nABSTRACT: Regulatory T (Treg) cells, whose differentiation and function are controlled by X chromosome-encoded transcription factor Foxp3, are generated in the thymus (tTreg) and extrathymically (peripheral, pTreg), and their deficiency results in fatal autoimmunity. Here, we demonstrate that a Foxp3 enhancer, conserved noncoding sequence 1 (CNS1), essential for pTreg but dispensable for tTreg cell generation, is present only in placental mammals. CNS1 is largely composed of mammalian-wide interspersed repeats (MIR) that have undergone retrotransposition during early mammalian radiation. During pregnancy, pTreg cells specific to a model paternal alloantigen were generated in a CNS1-dependent manner and accumulated in the placenta. Furthermore, when mated with allogeneic, but not syngeneic, males, CNS1-deficient females showed increased fetal resorption accompanied by increased immune cell infiltration and defective remodeling of spiral arteries. Our results suggest that, during evolution, a CNS1-dependent mechanism of extrathymic differentiation of Treg cells emerged in placental animals to enforce maternal-fetal tolerance.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 434, "doc_id": "9500590", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does perspective-taking increase patient satisfaction in medical encounters?\n\nABSTRACT:\nTo assess whether perspective-taking, which researchers in other fields have shown to induce empathy, improves patient satisfaction in encounters between student-clinicians and standardized patients (SPs). In three studies, randomly assigned students (N = 608) received either a perspective-taking instruction or a neutral instruction prior to a clinical skills examination in 2006-2007. SP satisfaction was the main outcome in all three studies. Study 1 involved 245 third-year medical students from two universities. Studies 2 and 3 extended Study 1 to examine generalizability across student and SP subpopulations. Study 2 (105 physician assistant students, one university) explored the effect of perspective-taking on African American SPs' satisfaction. Study 3 (258 third-year medical students, two universities) examined the intervention's effect on students with high and low baseline perspective-taking tendencies. Intervention students outscored controls in patient satisfaction in all studies: Study 1: P = .01, standardized effect size = 0.16; Study 2: P = .001, standardized effect size = 0.31; Study 3: P = .009, standardized effect size = 0.13. In Study 2, perspective-taking improved African American SPs' satisfaction. In Study 3, intervention students with high baseline perspective-taking tendencies outscored controls (P = .0004, standardized effect size = 0.25), whereas those with low perspective-taking tendencies did not (P = .72, standardized effect size = 0.00).", "output": "{\"label\": \"maybe\", \"rationale\": \"Perspective-taking increased patient satisfaction in all three studies, across medical schools, clinical disciplines, and racially diverse students and SPs. Perspective-taking as a means for improving patient satisfaction deserves further exploration in clinical training and practice.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 20736672, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Primary cervical cytology screening with HPV detection has higher longitudinal sensitivity to detect severe cervical intraepithelial neoplasia than conventional cytology.\n\nCANDIDATE_PASSAGE:\nHTRF: A Technology Tailored for Drug Discovery –A Review of Theoretical Aspects and Recent Applications HTRF (Homogeneous Time Resolved Fluorescence) is the most frequently used generic assay technology to measure analytes in a homogenous format, which is the ideal platform used for drug target studies in high-throughput screening (HTS). This technology combines fluorescence resonance energy transfer technology (FRET) with time-resolved measurement (TR). In TR-FRET assays, a signal is generated through fluorescent resonance energy transfer between a donor and an acceptor molecule when in close proximity to each other. Buffer and media interference is dramatically reduced by dual-wavelength detection, and the final signal is proportional to the extent of product formation. The HTRF assay is usually sensitive and robust that can be miniaturized into the 384 and 1536-well plate formats. This assay technology has been applied to many antibody-based assays including GPCR signaling (cAMP and IP-One), kinases, cytokines and biomarkers, bioprocess (antibody and protein production), as well as the assays for protein-protein, proteinpeptide, and protein-DNA/RNA interactions. Since its introduction to the drug-screening world over ten years ago, researchers have used HTRF to expedite the study of GPCRs, kinases, new biomarkers, protein-protein interactions, and other targets of interest. HTRF has also been utilized as an alternative method for bioprocess monitoring. The first-generation HTRF technology, which uses Europium cryptate as a fluorescence donor to monitor reactions between biomolecules, was extended in 2008 through the introduction of a second-generation donor, Terbium cryptate (Tb), enhancing screening performance. Terbium cryptate possesses different photo [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "973", "doc_id": "159469", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Ethanol stress increases the expression of SRL in bacteria.\n\nCANDIDATE_PASSAGE:\nProtein S-nitrosylation: a physiological signal for neuronal nitric oxide Nitric oxide (NO) has been linked to numerous physiological and pathophysiological events that are not readily explained by the well established effects of NO on soluble guanylyl cyclase. Exogenous NO S-nitrosylates cysteine residues in proteins, but whether this is an important function of endogenous NO is unclear. Here, using a new proteomic approach, we identify a population of proteins that are endogenously S-nitrosylated, and demonstrate the loss of this modification in mice harbouring a genomic deletion of neuronal NO synthase (nNOS). Targets of NO include metabolic, structural and signalling proteins that may be effectors for neuronally generated NO. These findings establish protein S-nitrosylation as a physiological signalling mechanism for nNOS.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "391", "doc_id": "32985041", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: CX3CR1 on the Th2 cells suppresses airway inflammation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Inhibition of fatty acid oxidation modulates immunosuppressive functions of myeloid-derived suppressor cells and enhances cancer therapies\nABSTRACT: Myeloid-derived suppressor cells (MDSC) promote tumor growth by inhibiting T-cell immunity and promoting malignant cell proliferation and migration. The therapeutic potential of blocking MDSC in tumors has been limited by their heterogeneity, plasticity, and resistance to various chemotherapy agents. Recent studies have highlighted the role of energy metabolic pathways in the differentiation and function of immune cells; however, the metabolic characteristics regulating MDSC remain unclear. We aimed to determine the energy metabolic pathway(s) used by MDSC, establish its impact on their immunosuppressive function, and test whether its inhibition blocks MDSC and enhances antitumor therapies. Using several murine tumor models, we found that tumor-infiltrating MDSC (T-MDSC) increased fatty acid uptake and activated fatty acid oxidation (FAO). This was accompanied by an increased mitochondrial mass, upregulation of key FAO enzymes, and increased oxygen consumption rate. Pharmacologic inhibition of FAO blocked immune inhibitory pathways and functions in T-MDSC and decreased their production of inhibitory cytokines. FAO inhibition alone significantly delayed tumor growth in a T-cell-dependent manner and enhanced the antitumor effect of adoptive T-cell therapy. Furthermore, FAO inhibition combined with low-dose chemotherapy completely inhibited T-MDSC immunosuppressive effects and induced a significant antitumor effect. Interestingly, a similar increase in fatty acid uptake and expression of FAO-related enzymes was found in human MDSC in peripheral blood and tumors. These results support the possibility of testing FAO inhibition as a novel approach to block MDSC and enhance various cancer therapies.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 219, "doc_id": "2030623", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: r-protein chaperones are found in complexes with their r-protein binding partners.\n\nCANDIDATE_ABSTRACT:\nTITLE: Rational Extension of the Ribosome Biogenesis Pathway Using Network-Guided Genetics\nABSTRACT: Biogenesis of ribosomes is an essential cellular process conserved across all eukaryotes and is known to require >170 genes for the assembly, modification, and trafficking of ribosome components through multiple cellular compartments. Despite intensive study, this pathway likely involves many additional genes. Here, we employ network-guided genetics-an approach for associating candidate genes with biological processes that capitalizes on recent advances in functional genomic and proteomic studies-to computationally identify additional ribosomal biogenesis genes. We experimentally evaluated >100 candidate yeast genes in a battery of assays, confirming involvement of at least 15 new genes, including previously uncharacterized genes (YDL063C, YIL091C, YOR287C, YOR006C/TSR3, YOL022C/TSR4). We associate the new genes with specific aspects of ribosomal subunit maturation, ribosomal particle association, and ribosomal subunit nuclear export, and we identify genes specifically required for the processing of 5S, 7S, 20S, 27S, and 35S rRNAs. These results reveal new connections between ribosome biogenesis and mRNA splicing and add >10% new genes-most with human orthologs-to the biogenesis pathway, significantly extending our understanding of a universally conserved eukaryotic process.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1402, "doc_id": "8126244", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Ivermectin is used to treat onchocerciasis.\n\nCANDIDATE_PASSAGE:\n“Rapid-Impact Interventions”: How a Policy of Integrated Control for Africa's Neglected Tropical Diseases Could Benefit the Poor Over the past two decades there have been significant achievements in the control of a handful of important human tropical infections [1]. These achievements include the substantive reductions in the prevalence and incidence of the so-called neglected diseases such as lymphatic filariasis, onchocerciasis, guinea worm, leprosy, and trachoma (Box 1) [2]. Each of these neglected diseases is a poverty-promoting and often stigmatizing condition occurring primarily in rural areas of low-income countries (Box 2) [3]. They are ancient afflictions, described in the Bible and other ancient texts, which have burdened humanity for millennia [3]. But now, as a result of aggressive regional vertical interventions, there is a possibility that some neglected tropical infections could be eventually controlled to the point of elimination in some areas of endemicity [2–8]. In the case of guinea worm infection, disease eradication might also soon be possible [9]. Box 2. Common Features of the Neglected Tropical Diseases Ancient afflictions that have burdened humanity for centuries Poverty-promoting conditions Associated with stigma Rural areas of low-income countries and fragile states No commercial markets for products that target these diseases Interventions, when applied, have a history of success", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "660", "doc_id": "1215116", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Subcutaneous fat depots undergo extensive browning processes after cold exposure.\n\nCANDIDATE_PASSAGE:\nVegetarian diet improves insulin resistance and oxidative stress markers more than conventional diet in subjects with Type 2 diabetes AIMS The aim of this study was to compare the effects of calorie-restricted vegetarian and conventional diabetic diets alone and in combination with exercise on insulin resistance, visceral fat and oxidative stress markers in subjects with Type 2 diabetes. METHODS A 24-week, randomized, open, parallel design was used. Seventy-four patients with Type 2 diabetes were randomly assigned to either the experimental group (n = 37), which received a vegetarian diet, or the control group (n = 37), which received a conventional diabetic diet. Both diets were isocaloric, calorie restricted (-500 kcal/day). All meals during the study were provided. The second 12 weeks of the diet were combined with aerobic exercise. Participants were examined at baseline, 12 weeks and 24 weeks. Primary outcomes were: insulin sensitivity measured by hyperinsulinaemic isoglycaemic clamp; volume of visceral and subcutaneous fat measured by magnetic resonance imaging; and oxidative stress measured by thiobarbituric acid reactive substances. Analyses were by intention to treat. RESULTS Forty-three per cent of participants in the experimental group and 5% of participants in the control group reduced diabetes medication (P < 0.001). Body weight decreased more in the experimental group than in the control group [-6.2 kg (95% CI -6.6 to -5.3) vs. -3.2 kg (95% CI -3.7 to -2.5); interaction group × time P = 0.001]. An increase in insulin sensitivity was significantly greater in the experimental group than in the control group [30% (95% CI 24.5-39) vs. 20% (95% CI 14-25), P = 0.04]. A reduction in both visceral and subcutaneous fat was greater in the experimental gro [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1107", "doc_id": "5687200", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: In pediatric tissue, most T cells are naive T cell emigrants from the thymus.\n\nCANDIDATE_PASSAGE:\nEndosome-ER Contacts Control Actin Nucleation and Retromer Function through VAP-Dependent Regulation of PI4P VAP (VAPA and VAPB) is an evolutionarily conserved endoplasmic reticulum (ER)-anchored protein that helps generate tethers between the ER and other membranes through which lipids are exchanged across adjacent bilayers. Here, we report that by regulating PI4P levels on endosomes, VAP affects WASH-dependent actin nucleation on these organelles and the function of the retromer, a protein coat responsible for endosome-to-Golgi traffic. VAP is recruited to retromer budding sites on endosomes via an interaction with the retromer SNX2 subunit. Cells lacking VAP accumulate high levels of PI4P, actin comets, and trans-Golgi proteins on endosomes. Such defects are mimicked by downregulation of OSBP, a VAP interactor and PI4P transporter that participates in VAP-dependent ER-endosomes tethers. These results reveal a role of PI4P in retromer-/WASH-dependent budding from endosomes. Collectively, our data show how the ER can control budding dynamics and association with the cytoskeleton of another membrane by direct contacts leading to bilayer lipid modifications.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "580", "doc_id": "600437", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Incidence of heart failure decreased by 10% in women since 1979.\n\nCANDIDATE_ABSTRACT:\nTITLE: Beyond melanoma: inhibiting the PD-1/PD-L1 pathway in solid tumors.\nABSTRACT: Immune checkpoint inhibitors have been identified as breakthrough treatment in melanoma given its dramatic response to PD-1/PD-L1 blockade. This is likely to extend to many other cancers as hundreds of clinical trials are being conducted or proposed using this exciting modality of therapy in a variety of malignancies. While immune checkpoint inhibitors have been extensively studied in melanoma and more recently in lung cancer, little is known regarding immune checkpoint blockade in other cancers. This review will focus on the tumor immune microenvironment, the expression of PD-1/PD-L1 and the effect of immune modulation using PD-1 or PD-L1 inhibitors in patients with head and neck, prostate, urothelial, renal, breast, gastrointestinal and lung cancers.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 593, "doc_id": "1900152", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The PRR MDA5 has a central DExD/H RNA helices domain.\n\nCANDIDATE_PASSAGE:\nImmune signaling by RIG-I-like receptors. The RIG-I-like receptors (RLRs) RIG-I, MDA5, and LGP2 play a major role in pathogen sensing of RNA virus infection to initiate and modulate antiviral immunity. The RLRs detect viral RNA ligands or processed self RNA in the cytoplasm to trigger innate immunity and inflammation and to impart gene expression that serves to control infection. Importantly, RLRs cooperate in signaling crosstalk networks with Toll-like receptors and other factors to impart innate immunity and to modulate the adaptive immune response. RLR regulation occurs at a variety of levels ranging from autoregulation to ligand and cofactor interactions and posttranslational modifications. Abberant RLR signaling or dysregulation of RLR expression is now implicated in the development of autoimmune diseases. Understanding the processes of RLR signaling and response will provide insights to guide RLR-targeted therapeutics for antiviral and immune-modifying applications.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1179", "doc_id": "31272411", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Commelina yellow mottle virus' (ComYMV) genome consists of 2140 baise pairs.\n\nCANDIDATE_ABSTRACT:\nTITLE: Molecular Basis for Target RNA Recognition and Cleavage by Human RISC\nABSTRACT: The RNA-Induced Silencing Complex (RISC) is a ribonucleoprotein particle composed of a single-stranded short interfering RNA (siRNA) and an endonucleolytically active Argonaute protein, capable of cleaving mRNAs complementary to the siRNA. The mechanism by which RISC cleaves a target RNA is well understood, however it remains enigmatic how RISC finds its target RNA. Here, we show, both in vitro and in vivo, that the accessibility of the target site correlates directly with the efficiency of cleavage, demonstrating that RISC is unable to unfold structured RNA. In the course of target recognition, RISC transiently contacts single-stranded RNA nonspecifically and promotes siRNA-target RNA annealing. Furthermore, the 5' part of the siRNA within RISC creates a thermodynamic threshold that determines the stable association of RISC and the target RNA. We therefore provide mechanistic insights by revealing features of RISC and target RNAs that are crucial to achieve efficiency and specificity in RNA interference.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 278, "doc_id": "950306", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Birth-weight is positively associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Role of birthweight in the etiology of breast cancer.\nABSTRACT: Breast cancer may originate in utero. We reviewed the available evidence on the association between birthweight and the risk of breast cancer. To date, 26 research papers addressing this issue have been published. The majority of studies identified a positive link between birthweight and premenopausal, but not postmenopausal, breast cancer. The relative risk estimate for breast cancer comparing women with high birthweight to women with low birthweight combining all studies including both pre- and postmenopausal breast cancer was 1.23 (95% confidence interval 1.13-1.34). The mechanisms underlying this association likely include elevated levels of growth factors that may increase the number of susceptible stem cells in the mammary gland or initiate tumors through DNA mutations. Loss of imprinting (LOI) of growth hormone genes relevant for intrauterine growth, such as insulin-like growth factor 2 (IGF2), leads to abnormally high levels of these hormones evidenced by high birthweight. LOI of IGF2 has also been found in mammary tumor tissue. The role of environmental factors that stimulate such epigenetic regulation of gene expression remains to be elucidated.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The relative risk estimate for breast cancer comparing women with high birthweight to women with low birthweight combining all studies including both pre- and postmenopausal breast cancer was 1.23 (95% confidence interval 1.13-1.34).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 179, "doc_id": "27123743", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Vitamin D deficiency effects birth weight.\n\nCANDIDATE_PASSAGE:\nActivation of AMPKα2 in adipocytes is essential for nicotine-induced insulin resistance in vivo Cigarette smoking promotes body weight reduction in humans while paradoxically also promoting insulin resistance (IR) and hyperinsulinemia. However, the mechanisms behind these effects are unclear. Here we show that nicotine, a major constituent of cigarette smoke, selectively activates AMP-activated protein kinase α2 (AMPKα2) in adipocytes, which in turn phosphorylates MAP kinase phosphatase-1 (MKP1) at serine 334, initiating its proteasome-dependent degradation. The nicotine-dependent reduction of MKP1 induces the aberrant activation of both p38 mitogen-activated protein kinase and c-Jun N-terminal kinase, leading to increased phosphorylation of insulin receptor substrate 1 (IRS1) at serine 307. Phosphorylation of IRS1 leads to its degradation, protein kinase B inhibition, and the loss of insulin-mediated inhibition of lipolysis. Consequently, nicotine increases lipolysis, which results in body weight reduction, but this increase also elevates the levels of circulating free fatty acids and thus causes IR in insulin-sensitive tissues. These results establish AMPKα2 as an essential mediator of nicotine-induced whole-body IR in spite of reductions in adiposity.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1367", "doc_id": "32408470", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: In breast cancer, the loss of myoepithelial cells slows the transition of ductal carcinoma in situ to invasive carcinoma.\n\nCANDIDATE_ABSTRACT:\nTITLE: Regulation of in situ to invasive breast carcinoma transition.\nABSTRACT: The transition of ductal carcinoma in situ (DCIS) to invasive carcinoma is a poorly understood key event in breast tumor progression. Here, we analyzed the role of myoepithelial cells and fibroblasts in the progression of in situ carcinomas using a model of human DCIS and primary breast tumors. Progression to invasion was promoted by fibroblasts and inhibited by normal myoepithelial cells. Molecular profiles of isolated luminal epithelial and myoepithelial cells identified an intricate interaction network involving TGFbeta, Hedgehog, cell adhesion, and p63 required for myoepithelial cell differentiation, the elimination of which resulted in loss of myoepithelial cells and progression to invasion.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Molecular profiles of isolated luminal epithelial and myoepithelial cells identified an intricate interaction network involving TGFbeta, Hedgehog, cell adhesion, and p63 required for myoepithelial cell differentiation, the elimination of which resulted in loss of myoepithelial cells and progression to invasion.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 571, "doc_id": "20333864", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Students who perform poorly in the early years of medical school are at increased risk for professional misconduct later in their careers.\n\nCANDIDATE_ABSTRACT:\nTITLE: Risk factors at medical school for subsequent professional misconduct: multicentre retrospective case-control study\nABSTRACT: OBJECTIVE To determine whether there are risk factors in a doctor's time at medical school that are associated with subsequent professional misconduct. DESIGN Matched case-control study. Setting Records from medical schools and the General Medical Council (GMC). PARTICIPANTS 59 doctors who had graduated from any one of eight medical schools in the United Kingdom in 1958-97 and had a proved finding of serious professional misconduct in GMC proceedings in 1999-2004 (cases); 236 controls (four for each case) were selected by systematic sampling from matching graduation cohorts. Case-control status was revealed by the GMC after completion of data entry. MAIN OUTCOME MEASURE Odds ratios for being a \"case,\" with multivariable conditional logistic regression of potential risk factors including pre-admission characteristics and progress during the course. These data were obtained from anonymised copies of the students' progress files held by their original medical schools. RESULTS Univariate conditional logistic regression analysis found that cases were more likely to be men, to be of lower estimated social class, and to have had academic difficulties during their medical course, especially in the early years. Multivariable analysis showed that male sex (odds ratio 9.80, 95% confidence interval 2.43 to 39.44, P=0.001), lower social class (4.28, 1.52 to 12.09, P=0.006), and failure of early or preclinical examinations (5.47, 2.17 to 13.79, P<0.001) were independently associated with being a case. CONCLUSIONS This small study suggests that male sex, a lower socioeconomic background, and early academic difficulties at medical school could be risk factors for subsequent professional misconduct. The findings are preliminary and should be interpreted with caution. Most do [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"RESULTS Univariate conditional logistic regression analysis found that cases were more likely to be men, to be of lower estimated social class, and to have had academic difficulties during their medical course, especially in the early years.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1105, "doc_id": "6710713", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: 7-day-old adult Caenorhabditis elegans exhibit approximately 75% of the learning capacity seen in 1-day old adults.\n\nCANDIDATE_PASSAGE:\nDeletion of the developmentally essential gene ATR in adult mice leads to age-related phenotypes and stem cell loss. Developmental abnormalities, cancer, and premature aging each have been linked to defects in the DNA damage response (DDR). Mutations in the ATR checkpoint regulator cause developmental defects in mice (pregastrulation lethality) and humans (Seckel syndrome). Here we show that eliminating ATR in adult mice leads to defects in tissue homeostasis and the rapid appearance of age-related phenotypes, such as hair graying, alopecia, kyphosis, osteoporosis, thymic involution, fibrosis, and other abnormalities. Histological and genetic analyses indicate that ATR deletion causes acute cellular loss in tissues in which continuous cell proliferation is required for maintenance. Importantly, thymic involution, alopecia, and hair graying in ATR knockout mice were associated with dramatic reductions in tissue-specific stem and progenitor cells and exhaustion of tissue renewal and homeostatic capacity. In aggregate, these studies suggest that reduced regenerative capacity in adults via deletion of a developmentally essential DDR gene is sufficient to cause the premature appearance of age-related phenotypes.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "20", "doc_id": "40349336", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Having a main partner improves HIV outcomes.\n\nCANDIDATE_PASSAGE:\nImmune activation and HIV persistence: implications for curative approaches to HIV infection. Despite complete or near-complete suppression of human immunodeficiency virus (HIV) replication with combination antiretroviral therapy, both HIV and chronic inflammation/immune dysfunction persist indefinitely. Untangling the association between the virus and the host immune environment during therapy might lead to novel interventions aimed at either curing the infection or preventing the development of inflammation-associated end-organ disease. Chronic inflammation and immune dysfunction might lead to HIV persistence by causing virus production, generating new target cells, enabling infecting of activated and resting target cells, altering the migration patterns of susceptible target cells, increasing the proliferation of infected cells, and preventing normal HIV-specific clearance mechanisms from function. Chronic HIV production or replication might contribute to persistent inflammation and immune dysfunction. The rapidly evolving data on these issues strongly suggest that a vicious cycle might exist in which HIV persistence causes inflammation that in turn contributes to HIV persistence.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "495", "doc_id": "44562058", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Mathematical models predict that using Artemisinin-based combination therapy over nongametocytocidal drugs have a dramatic impact in reducing malaria transmission.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association of Blood Monocyte and Platelet Markers with Carotid Artery Characteristics: The Atherosclerosis Risk in Communities Carotid MRI Study\nABSTRACT: Background: Atherosclerosis is characterized by infiltration of inflammatory cells from circulating blood. Blood cell activation could play an important role in plaque formation. Methods: We analyzed the relationship between blood cellular markers and quantitative measures of carotid wall components in 1,546 participants from the ARIC (Atherosclerosis Risk in Communities) Carotid MRI Study. Carotid imaging was performed using a gadolinium contrast-enhanced MRI and cellular phenotyping by flow cytometry. Results: Monocyte Toll-like receptor (TLR)-2 is associated with larger plaques, while CD14, myeloperoxidase, and TLR-4 associate with smaller. Platelet CD40L is associated with smaller plaques and thinner caps, while P-selectin is associated with smaller core size. Conclusions: Blood cell activation is significantly associated with atherosclerotic changes of the carotid wall.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 759, "doc_id": "2587396", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Binding of p53 to enhancer regions (p53BERs) regulates the activity of p53 transcription and cell cycle arrest through the production of p53-dependent eRNAs.\n\nCANDIDATE_PASSAGE:\nAlphavbeta6-Fyn signaling promotes oral cancer progression. We have previously shown that the integrin beta6 is neo-expressed in invasive oral squamous cell carcinoma (SCC) and is correlated with oral tumor progression. However, the mechanism by which the integrin beta6 promotes oral tumor progression is not well understood. The purpose of the present study was to determine whether integrin beta6 signaling activates Fyn and thus promotes oral squamous cell carcinoma progression. We analyzed the integrin beta6 signaling complex and investigated the function of these signaling molecules in oral SCC cells. We found that, upon ligation of the integrin beta6 with fibronectin, beta6 complexed with Fyn and activated it. The activation of Fyn recruited and activated focal adhesion kinase to this complex. This complex was necessary to activate Shc and to couple beta6 signaling to the Raf-ERK/MAPK pathway. This pathway transcriptionally activated the matrix metalloproteinase-3 gene and promoted oral SCC cell proliferation and experimental metastasis in vivo. These findings indicate that integrin beta6 signaling activates Fyn and thus promotes oral cancer progression.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "177", "doc_id": "12650610", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Continued HHV-8 transmission among MSM in San Francisco may be explained by urogenital contact.\n\nCANDIDATE_PASSAGE:\nAverting Obesity and Type 2 Diabetes in India through Sugar-Sweetened Beverage Taxation: An Economic-Epidemiologic Modeling Study BACKGROUND Taxing sugar-sweetened beverages (SSBs) has been proposed in high-income countries to reduce obesity and type 2 diabetes. We sought to estimate the potential health effects of such a fiscal strategy in the middle-income country of India, where there is heterogeneity in SSB consumption, patterns of substitution between SSBs and other beverages after tax increases, and vast differences in chronic disease risk within the population. METHODS AND FINDINGS Using consumption and price variations data from a nationally representative survey of 100,855 Indian households, we first calculated how changes in SSB price alter per capita consumption of SSBs and substitution with other beverages. We then incorporated SSB sales trends, body mass index (BMI), and diabetes incidence data stratified by age, sex, income, and urban/rural residence into a validated microsimulation of caloric consumption, glycemic load, overweight/obesity prevalence, and type 2 diabetes incidence among Indian subpopulations facing a 20% SSB excise tax. The 20% SSB tax was anticipated to reduce overweight and obesity prevalence by 3.0% (95% CI 1.6%-5.9%) and type 2 diabetes incidence by 1.6% (95% CI 1.2%-1.9%) among various Indian subpopulations over the period 2014-2023, if SSB consumption continued to increase linearly in accordance with secular trends. However, acceleration in SSB consumption trends consistent with industry marketing models would be expected to increase the impact efficacy of taxation, averting 4.2% of prevalent overweight/obesity (95% CI 2.5-10.0%) and 2.5% (95% CI 1.0-2.8%) of incident type 2 diabetes from 2014-2023. Given current consumpt [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "285", "doc_id": "10071552", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: T regulatory cells (tTregs) lacking αvβ8 are more adept at suppressing pathogenic T-cell responses during active inflammation.\n\nCANDIDATE_ABSTRACT:\nTITLE: Integrin αvβ8-Mediated TGF-β Activation by Effector Regulatory T Cells Is Essential for Suppression of T-Cell-Mediated Inflammation\nABSTRACT: Regulatory T (Treg) cells play a pivotal role in suppressing self-harmful T cell responses, but how Treg cells mediate suppression to maintain immune homeostasis and limit responses during inflammation is unclear. Here we show that effector Treg cells express high amounts of the integrin αvβ8, which enables them to activate latent transforming growth factor-β (TGF-β). Treg-cell-specific deletion of integrin αvβ8 did not result in a spontaneous inflammatory phenotype, suggesting that this pathway is not important in Treg-cell-mediated maintenance of immune homeostasis. However, Treg cells lacking expression of integrin αvβ8 were unable to suppress pathogenic T cell responses during active inflammation. Thus, our results identify a mechanism by which Treg cells suppress exuberant immune responses, highlighting a key role for effector Treg-cell-mediated activation of latent TGF-β in suppression of self-harmful T cell responses during active inflammation.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"However, Treg cells lacking expression of integrin αvβ8 were unable to suppress pathogenic T cell responses during active inflammation.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1130, "doc_id": "17997584", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: TCR/CD3 microdomains are a required to induce the immunologic synapse to activate T cells.\n\nCANDIDATE_PASSAGE:\nRegulation of the small GTP-binding protein Rho by cell adhesion and the cytoskeleton. Soluble factors from serum such as lysophosphatidic acid (LPA) are thought to activate the small GTP-binding protein Rho based on their ability to induce actin stress fibers and focal adhesions in a Rho-dependent manner. Cell adhesion to extracellular matrices (ECM) has also been proposed to activate Rho, but this point has been controversial due to the difficulty of distinguishing changes in Rho activity from the structural contributions of ECM to the formation of focal adhesions. To address these questions, we established an assay for GTP-bound cellular Rho. Plating Swiss 3T3 cells on fibronectin-coated dishes elicited a transient inhibition of Rho, followed by a phase of Rho activation. The activation phase was greatly enhanced by serum. In serum-starved adherent cells, LPA induced transient Rho activation, whereas in suspended cells Rho activation was sustained. Furthermore, suspended cells showed higher Rho activity than adherent cells in the presence of serum. These data indicate the existence of an adhesion-dependent negative-feedback loop. We also observed that both cytochalasin D and colchicine trigger Rho activation despite their opposite effects on stress fibers and focal adhesions. Our results show that ECM, cytoskeletal structures and soluble factors all contribute to regulation of Rho activity.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1132", "doc_id": "28195565", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Cellular aging closely links to an older appearance.\n\nCANDIDATE_PASSAGE:\nPerceived age as clinically useful biomarker of ageing: cohort study. OBJECTIVE To determine whether perceived age correlates with survival and important age related phenotypes. DESIGN Follow-up study, with survival of twins determined up to January 2008, by which time 675 (37%) had died. SETTING Population based twin cohort in Denmark. PARTICIPANTS 20 nurses, 10 young men, and 11 older women (assessors); 1826 twins aged >or=70. MAIN OUTCOME MEASURES Assessors: perceived age of twins from photographs. Twins: physical and cognitive tests and molecular biomarker of ageing (leucocyte telomere length). RESULTS For all three groups of assessors, perceived age was significantly associated with survival, even after adjustment for chronological age, sex, and rearing environment. Perceived age was still significantly associated with survival after further adjustment for physical and cognitive functioning. The likelihood that the older looking twin of the pair died first increased with increasing discordance in perceived age within the twin pair-that is, the bigger the difference in perceived age within the pair, the more likely that the older looking twin died first. Twin analyses suggested that common genetic factors influence both perceived age and survival. Perceived age, controlled for chronological age and sex, also correlated significantly with physical and cognitive functioning as well as with leucocyte telomere length. CONCLUSION Perceived age-which is widely used by clinicians as a general indication of a patient's health-is a robust biomarker of ageing that predicts survival among those aged >or=70 and correlates with important functional and molecular ageing phenotypes.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "239", "doc_id": "14079881", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Dexamethasone decreases risk of postoperative bleeding.\n\nCANDIDATE_ABSTRACT:\nTITLE: Dexamethasone and risk of nausea and vomiting and postoperative bleeding after tonsillectomy in children: a randomized trial.\nABSTRACT: CONTEXT Dexamethasone is widely used to prevent postoperative nausea and vomiting (PONV) in pediatric tonsillectomy. OBJECTIVE To assess whether dexamethasone dose-dependently reduces the risk of PONV at 24 hours after tonsillectomy. DESIGN, SETTING, AND PATIENTS Randomized placebo-controlled trial conducted among 215 children undergoing elective tonsillectomy at a major public teaching hospital in Switzerland from February 2005 to December 2007. INTERVENTIONS Children were randomly assigned to receive dexamethasone (0.05, 0.15, or 0.5 mg/kg) or placebo intravenously after induction of anesthesia. Acetaminophen-codeine and ibuprofen were given as postoperative analgesia. Follow-up continued until the 10th postoperative day. MAIN OUTCOME MEASURES The primary end point was prevention of PONV at 24 hours; secondary end points were decrease in the need for ibuprofen at 24 hours and evaluation of adverse effects. RESULTS At 24 hours, 24 of 54 participants who received placebo (44%; 95% confidence interval [CI], 31%-59%) had experienced PONV compared with 20 of 53 (38%; 95% CI, 25%-52%), 13 of 54 (24%; 95% CI, 13%-38%), and 6 of 52 (12%; 95% CI, 4%-23%) who received dexamethasone at 0.05, 0.15, and 0.5 mg/kg, respectively (P<.001 for linear trend). Children who received dexamethasone received significantly less ibuprofen. There were 26 postoperative bleeding episodes in 22 children. Two of 53 (4%; 95% CI, 0.5%-13%) children who received placebo had bleeding compared with 6 of 53 (11%; 95% CI, 4%-23%), 2 of 51 (4%; 95% CI, 0.5%-13%), and 12 of 50 (24%; 95% CI, 13%-38%) who received dexamethasone at 0.05, 0.15, and 0.5 mg/kg, respectively (P = .003). Dexamethasone, 0.5 mg/kg, was associated with the highest bleeding risk (adjusted relative risk, 6.80; 95% CI, 1.77-1 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Dexamethasone, 0.5 mg/kg, was associated with the highest bleeding risk (adjusted relative risk, 6.80; 95% CI, 1.77-16.5).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 338, "doc_id": "23349986", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does limb-salvage surgery offer patients better quality of life and functional capacity than amputation?\n\nABSTRACT:\nPatients with aggressive lower extremity musculoskeletal tumors may be candidates for either above-knee amputation or limb-salvage surgery. However, the subjective and objective benefits of limb-salvage surgery compared with amputation are not fully clear.QUESTIONS/ We therefore compared functional status and quality of life for patients treated with above-knee amputation versus limb-salvage surgery. We reviewed 20 of 51 patients aged 15 years and older treated with above-knee amputation or limb-salvage surgery for aggressive musculoskeletal tumors around the knee between 1994 and 2004 as a retrospective cohort study. At last followup we obtained the Physiological Cost Index, the Reintegration to Normal Living Index, SF-36, and the Toronto Extremity Salvage Score questionnaires. The minimum followup was 12 months (median, 56 months; range, 12-108 months). Compared with patients having above-knee amputation, patients undergoing limb-salvage surgery had superior Physiological Cost Index scores and Reintegration to Normal Living Index. The Toronto Extremity Salvage scores and SF-36 scores were similar in the two groups.", "output": "{\"label\": \"maybe\", \"rationale\": \"These data suggest that limb-salvage surgery offers better gait efficiency and return to normal living compared with above-knee amputation, but does not improve the patient's perception of quality of life.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 22302658, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does severe exercise-induced ischemia identify high risk patients with normal left ventricular function and one- or two-vessel coronary artery disease?\n\nABSTRACT:\nThis study was conducted to determine whether severe exercise-induced ischemia identifies high risk patients with a normal left ventricular ejection fraction and one- or two-vessel coronary artery disease. Severe ischemia during exercise radionuclide angiography has been shown to identify high risk patients among certain other patient subsets. Four hundred twenty patients with left ventricular ejection fraction > or = 50% and one- or two-vessel disease underwent exercise radionuclide angiography within 3 months of coronary angiography. Patients were treated initially with revascularization (n = 140) or medical therapy (n = 280) at the discretion of their physicians. Patients treated with revascularization were more likely to have angina by history, a positive exercise electrocardiogram, a lower exercise ejection fraction, two-vessel disease and proximal left anterior descending coronary artery disease. Two hundred sixty-four of the 280 patients given medical therapy who had complete follow-up data formed the study group. Outcome was compared between patients with (n = 56) and without (n = 208) severe exercise-induced ischemia, defined by previously published criteria (work load < or = 600 kg-m/min, ST segment depression > or = 1 mm and decrease in ejection fraction with exercise). During follow-up, there were 30 initial cardiac events (12 cardiac deaths and 18 nonfatal myocardial infarctions). There was no difference in the 5-year event-free survival rate: 91% in patients with and 87% in patients without severe ischemia (p = 0.89). There was no association between event-free survival and severe ischemia (chi 2 = 1.41, p = 0.24). The study had approximately 80% power at alpha = 0.05 to detect a 25% decrease in event-free survival in the group with severe isch [TRUNCATED]", "output": "{\"label\": \"no\", \"rationale\": \"Severe exercise-induced ischemia fails to identify a high risk subgroup among patients with normal left ventricular function and one- or two-vessel disease who are treated initially with medical therapy.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 8277084, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Basophils counteract disease development in patients with systemic lupus erythematosus (SLE).\n\nCANDIDATE_ABSTRACT:\nTITLE: BASOPHILS AND THE T HELPER 2 ENVIRONMENT CAN PROMOTE THE DEVELOPMENT OF LUPUS NEPHRITIS\nABSTRACT: In systemic lupus erythematosus (SLE), self-reactive antibodies can target the kidney (lupus nephritis), leading to functional failure and possible mortality. We report that activation of basophils by autoreactive IgE causes their homing to lymph nodes, promoting T helper type 2 (T(H)2) cell differentiation and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in mice lacking the Src family protein tyrosine kinase Lyn (Lyn(-/-) mice). Individuals with SLE also have elevated serum IgE, self-reactive IgEs and activated basophils that express CD62 ligand (CD62L) and the major histocompatibility complex (MHC) class II molecule human leukocyte antigen-DR (HLA-DR), parameters that are associated with increased disease activity and active lupus nephritis. Basophils were also present in the lymph nodes and spleen of subjects with SLE. Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Thus, in Lyn(-/-) mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 171, "doc_id": "12670680", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Blocking the interaction between TDP-43 and respiratory complex I proteins ND3 and ND6 prevents TDP-43-induced neuronal loss.\n\nCANDIDATE_PASSAGE:\nThe Inhibition of TDP-43 Mitochondrial Localization Blocks Its Neuronal Toxicity Genetic mutations in TAR DNA-binding protein 43 (TARDBP, also known as TDP-43) cause amyotrophic lateral sclerosis (ALS), and an increase in the presence of TDP-43 (encoded by TARDBP) in the cytoplasm is a prominent histopathological feature of degenerating neurons in various neurodegenerative diseases. However, the molecular mechanisms by which TDP-43 contributes to ALS pathophysiology remain elusive. Here we have found that TDP-43 accumulates in the mitochondria of neurons in subjects with ALS or frontotemporal dementia (FTD). Disease-associated mutations increase TDP-43 mitochondrial localization. In mitochondria, wild-type (WT) and mutant TDP-43 preferentially bind mitochondria-transcribed messenger RNAs (mRNAs) encoding respiratory complex I subunits ND3 and ND6, impair their expression and specifically cause complex I disassembly. The suppression of TDP-43 mitochondrial localization abolishes WT and mutant TDP-43-induced mitochondrial dysfunction and neuronal loss, and improves phenotypes of transgenic mutant TDP-43 mice. Thus, our studies link TDP-43 toxicity directly to mitochondrial bioenergetics and propose the targeting of TDP-43 mitochondrial localization as a promising therapeutic approach for neurodegeneration.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "181", "doc_id": "16966326", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Hypoglycemia increases the risk of dementia.\n\nCANDIDATE_PASSAGE:\nThe Incidence and Repetition of Hospital-Treated Deliberate Self Harm: Findings from the World's First National Registry BACKGROUND Suicide is a significant public health issue with almost one million people dying by suicide each year worldwide. Deliberate self harm (DSH) is the single most important risk factor for suicide yet few countries have reliable data on DSH. We developed a national DSH registry in the Republic of Ireland to establish the incidence of hospital-treated DSH at national level and the spectrum and pattern of presentations with DSH and repetition. METHODS AND FINDINGS Between 2003 and 2009, the Irish National Registry of Deliberate Self Harm collected data on DSH presentations to all 40 hospital emergency departments in the country. Data were collected by trained data registration officers using standard methods of case ascertainment and definition. The Registry recorded 75,119 DSH presentations involving 48,206 individuals. The total incidence rate fell from 209 (95% CI: 205-213) per 100,000 in 2003 to 184 (95% CI: 180-189) per 100,000 in 2006 and increased again to 209 (95% CI: 204-213) per 100,000 in 2009. The most notable annual changes were successive 10% increases in the male rate in 2008 and 2009. There was significant variation by age with peak rates in women in the 15-19 year age group (620 (95% CI: 605-636) per 100,000), and in men in the 20-24 age group (427 (95% CI: 416-439) per 100,000). Repetition rates varied significantly by age, method of self harm and number of previous episodes. CONCLUSIONS Population-based data on hospital-treated DSH represent an important index of the burden of mental illness and suicide risk in the community. The increased DSH rate in Irish men in 2008 and 2009 coincided with the advent of the econ [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "539", "doc_id": "1102268", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Up-regulation of the p53 pathway and related molecular events speeds cancer progression.\n\nCANDIDATE_PASSAGE:\nNotch promotes survival of pre–T cells at the β-selection checkpoint by regulating cellular metabolism Notch signals are necessary for the functional outcomes of T cell receptor β-selection, including differentiation, proliferation and rescue from apoptosis. The mechanism underlying this requirement for T cell development is unknown. Here we show that Notch receptor and Delta-like 1 ligand interactions promoted the survival of CD4−CD8− pre–T cells through the maintenance of cell size, glucose uptake and metabolism. Furthermore, the trophic effects of Notch signaling were mediated by the pathway of phosphatidylinositol-3-OH kinase and the kinase Akt, such that expression of active Atk overcame the requirement for Notch in β-selection. Collectively, our results demonstrate involvement of Notch receptor–ligand interactions in the regulation of cellular metabolism, thus enabling the autonomous signaling capacity of the pre–T cell receptor complex.*Note: In the version of this article initially published online, in the fourth sentence of the abstract, the term \"Atk\" was a misspelling; this should be \"Akt. \" In the fourth sentence of the second paragraph of the introduction, the name of the second kinase mentioned, \"PI(3)K-dependent kinase 1,\" was incorrect; this should read \"phosphoinositide-dependent kinase 1. \" These errors have been corrected for the HTML and print versions of the article.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1345", "doc_id": "24387017", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Crossover hot spots are found within gene promoters in Saccharomyces cerevisiae.\n\nCANDIDATE_PASSAGE:\nLongitudinal changes in maternal corin and mid-regional proatrial natriuretic peptide in women at risk of pre-eclampsia Objectives Corin, an atrial natriuretic peptide-converting enzyme, has been found to promote trophoblast invasion and spiral artery remodeling. Reduced maternal plasma atrial natriuretic peptide (ANP) levels and elevated corin levels have been reported in pregnancies complicated by PE. The aim of this study was to investigate longitudinal changes in maternal plasma levels of corin and midregional proatrial natriuretic peptide (MR-PANP) in pregnancies that develop preeclampsia (PE) and gestational hypertension (GH). Methods Nested case control study drawn from a larger prospective longitudinal study in singleton pregnancies identified by screening at 11 + 0 − 13 + 6 weeks’ gestation as being at high risk for PE. Blood samples were taken every four weeks until delivery. Values were compared in pregnancies that developed preterm-PE (requiring delivery before 37 weeks), term-PE, GH, and those that remained normotensive. The distribution of maternal plasma corin and PANP were made Gaussian after log 10 transformation. Analysis of repeated measures with multilevel mixed-effects linear model (fixed effects and random effects) was performed. The multilevel model was compared to one-level model by the likelihood radio (LR) test. Results A total of 471 samples were analyzed from 122 women, including 85 that remained normotensive, 12 that developed GH, 13 term-PE and 12 preterm-PE. In the normotensive group, log10corin levels were associated with gestational age ( p p = 0.001). In the GH and term-PE groups, corin did not differ significantly from the normotensive group ( p = 0.64 and p = 0.16, respectively). Compared to the normotensive group, MR-PANP [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "293", "doc_id": "68317730", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: COPI coatmer is involved in lipid homeostasis.\n\nCANDIDATE_ABSTRACT:\nTITLE: COPI Complex Is a Regulator of Lipid Homeostasis\nABSTRACT: Lipid droplets are ubiquitous triglyceride and sterol ester storage organelles required for energy storage homeostasis and biosynthesis. Although little is known about lipid droplet formation and regulation, it is clear that members of the PAT (perilipin, adipocyte differentiation related protein, tail interacting protein of 47 kDa) protein family coat the droplet surface and mediate interactions with lipases that remobilize the stored lipids. We identified key Drosophila candidate genes for lipid droplet regulation by RNA interference (RNAi) screening with an image segmentation-based optical read-out system, and show that these regulatory functions are conserved in the mouse. Those include the vesicle-mediated Coat Protein Complex I (COPI) transport complex, which is required for limiting lipid storage. We found that COPI components regulate the PAT protein composition at the lipid droplet surface, and promote the association of adipocyte triglyceride lipase (ATGL) with the lipid droplet surface to mediate lipolysis. Two compounds known to inhibit COPI function, Exo1 and Brefeldin A, phenocopy COPI knockdowns. Furthermore, RNAi inhibition of ATGL and simultaneous drug treatment indicate that COPI and ATGL function in the same pathway. These data indicate that the COPI complex is an evolutionarily conserved regulator of lipid homeostasis, and highlight an interaction between vesicle transport systems and lipid droplets.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"These data indicate that the COPI complex is an evolutionarily conserved regulator of lipid homeostasis, and highlight an interaction between vesicle transport systems and lipid droplets.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 210, "doc_id": "13794374", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: TNFAIP3 is a glioblastoma tumor suppressor.\n\nCANDIDATE_ABSTRACT:\nTITLE: Targeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth\nABSTRACT: Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs). GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets. We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels. To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA). Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis. The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays. The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts. In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival. Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation. Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may funct [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may function as a tumor enhancer in glioma through promotion of GSC survival.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1135, "doc_id": "33370", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Egr3 regulates the homeostasis of B and T cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Transcription Factors Egr2 and Egr3 Are Essential for the Control of Inflammation and Antigen-Induced Proliferation of B and T Cells\nABSTRACT: Lymphocytes provide optimal responses against pathogens with minimal inflammatory pathology. However, the intrinsic mechanisms regulating these responses are unknown. Here, we report that deletion of both transcription factors Egr2 and Egr3 in lymphocytes resulted in a lethal autoimmune syndrome with excessive serum proinflammatory cytokines but also impaired antigen receptor-induced proliferation of B and T cells. Egr2- and Egr3-defective B and T cells had hyperactive signal transducer and activator of transcription-1 (STAT1) and STAT3 while antigen receptor-induced activation of transcription factor AP-1 was severely impaired. We discovered that Egr2 and/or Egr3 directly induced expression of suppressor of cytokine signaling-1 (SOCS1) and SOCS3, inhibitors of STAT1 and STAT3, and also blocked the function of Batf, an AP-1 inhibitor, in B and T cells. Thus, Egr2 and Egr3 regulate B and T cell function in adaptive immune responses and homeostasis by promoting antigen receptor signaling and controlling inflammation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Egr2- and Egr3-defective B and T cells had hyperactive signal transducer and activator of transcription-1 (STAT1) and STAT3 while antigen receptor-induced activation of transcription factor AP-1 was severely impaired.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 371, "doc_id": "1550937", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Aspirin inhibits the production of PGE2.\n\nCANDIDATE_PASSAGE:\nExcess risk of lymphomas, leukemia and myeloma in patients with rheumatoid arthritis The incidence of malignant neoplasms among 11 483 male and 34 618 female individuals with rheumatoid arthritis was studied using two separate nationwide data registers covering the whole Finnish population: the Social Insurance Institution9s Population Data Register, which includes information on medication for certain chronic diseases, and the Finnish Cancer Registry, with data on all cancer patients diagnosed in Finland. The follow-up comprised a total of 213 911 person years. The total incidence of all malignant neoplasms was higher in males and on the level expected in females. The expected number of cases of leukemia, lymphomas, Hodgkin9s disease and myeloma in both sexes was 59·6 as compared with the 130 cases observed. This difference is statistically highly significant (p", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "132", "doc_id": "70633421", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Natriuretic peptides protect against diabetes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mendelian Randomization Study of B-Type Natriuretic Peptide and Type 2 Diabetes: Evidence of Causal Association from Population Studies\nABSTRACT: BACKGROUND Genetic and epidemiological evidence suggests an inverse association between B-type natriuretic peptide (BNP) levels in blood and risk of type 2 diabetes (T2D), but the prospective association of BNP with T2D is uncertain, and it is unclear whether the association is confounded. METHODS AND FINDINGS We analysed the association between levels of the N-terminal fragment of pro-BNP (NT-pro-BNP) in blood and risk of incident T2D in a prospective case-cohort study and genotyped the variant rs198389 within the BNP locus in three T2D case-control studies. We combined our results with existing data in a meta-analysis of 11 case-control studies. Using a Mendelian randomization approach, we compared the observed association between rs198389 and T2D to that expected from the NT-pro-BNP level to T2D association and the NT-pro-BNP difference per C allele of rs198389. In participants of our case-cohort study who were free of T2D and cardiovascular disease at baseline, we observed a 21% (95% CI 3%-36%) decreased risk of incident T2D per one standard deviation (SD) higher log-transformed NT-pro-BNP levels in analysis adjusted for age, sex, body mass index, systolic blood pressure, smoking, family history of T2D, history of hypertension, and levels of triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. The association between rs198389 and T2D observed in case-control studies (odds ratio = 0.94 per C allele, 95% CI 0.91-0.97) was similar to that expected (0.96, 0.93-0.98) based on the pooled estimate for the log-NT-pro-BNP level to T2D association derived from a meta-analysis of our study and published data (hazard ratio = 0.82 per SD, 0.74-0.90) and the difference in NT-pro-BNP levels (0.22 SD, 0.15-0.29) per C allele of r [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In participants of our case-cohort study who were free of T2D and cardiovascular disease at baseline, we observed a 21% (95% CI 3%-36%) decreased risk of incident T2D per one standard deviation (SD) higher log-transformed NT-pro-BNP levels in analysis adjusted for age, sex, body mass index, systolic blood pressure, smoking, family history of T2D, history of hypertension, and levels of triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 841, "doc_id": "15663829", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Mutant mice lacking SVCT2 have severely reduced ascorbic acid levels in both brain and adrenals.\n\nCANDIDATE_PASSAGE:\nPredicting immunogenic tumour mutations by combining mass spectrometry and exome sequencing Human tumours typically harbour a remarkable number of somatic mutations. If presented on major histocompatibility complex class I molecules (MHCI), peptides containing these mutations could potentially be immunogenic as they should be recognized as ‘non-self’ neo-antigens by the adaptive immune system. Recent work has confirmed that mutant peptides can serve as T-cell epitopes. However, few mutant epitopes have been described because their discovery required the laborious screening of patient tumour-infiltrating lymphocytes for their ability to recognize antigen libraries constructed following tumour exome sequencing. We sought to simplify the discovery of immunogenic mutant peptides by characterizing their general properties. We developed an approach that combines whole-exome and transcriptome sequencing analysis with mass spectrometry to identify neo-epitopes in two widely used murine tumour models. Of the >1,300 amino acid changes identified, ∼13% were predicted to bind MHCI, a small fraction of which were confirmed by mass spectrometry. The peptides were then structurally modelled bound to MHCI. Mutations that were solvent-exposed and therefore accessible to T-cell antigen receptors were predicted to be immunogenic. Vaccination of mice confirmed the approach, with each predicted immunogenic peptide yielding therapeutically active T-cell responses. The predictions also enabled the generation of peptide–MHCI dextramers that could be used to monitor the kinetics and distribution of the anti-tumour T-cell response before and after vaccination. These findings indicate that a suitable prediction algorithm may provide an approach for the pharmacodynamic monitoring of T- [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "812", "doc_id": "4462777", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Sepsis related mortality has remained stable between 2009-2014.\n\nCANDIDATE_PASSAGE:\nIncidence and Trends of Sepsis in US Hospitals Using Clinical vs Claims Data, 2009-2014 Importance Estimates from claims-based analyses suggest that the incidence of sepsis is increasing and mortality rates from sepsis are decreasing. However, estimates from claims data may lack clinical fidelity and can be affected by changing diagnosis and coding practices over time. Objective To estimate the US national incidence of sepsis and trends using detailed clinical data from the electronic health record (EHR) systems of diverse hospitals. Design, Setting, and Population Retrospective cohort study of adult patients admitted to 409 academic, community, and federal hospitals from 2009-2014. Exposures Sepsis was identified using clinical indicators of presumed infection and concurrent acute organ dysfunction, adapting Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) criteria for objective and consistent EHR-based surveillance. Main Outcomes and Measures Sepsis incidence, outcomes, and trends from 2009-2014 were calculated using regression models and compared with claims-based estimates using International Classification of Diseases, Ninth Revision, Clinical Modification codes for severe sepsis or septic shock. Case-finding criteria were validated against Sepsis-3 criteria using medical record reviews. Results A total of 173 690 sepsis cases (mean age, 66.5 [SD, 15.5] y; 77 660 [42.4%] women) were identified using clinical criteria among 2 901 019 adults admitted to study hospitals in 2014 (6.0% incidence). Of these, 26 061 (15.0%) died in the hospital and 10 731 (6.2%) were discharged to hospice. From 2009-2014, sepsis incidence using clinical criteria was stable (+0.6% relative change/y [95% CI, −2.3% to 3.5%], P = .67) whereas incide [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1072", "doc_id": "4824840", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The recruitment of Wdr5 to its target loci depends on Kat8.\n\nCANDIDATE_ABSTRACT:\nTITLE: The histone acetyltransferase MOF is a key regulator of the embryonic stem cell core transcriptional network.\nABSTRACT: Pluripotent embryonic stem cells (ESCs) maintain self-renewal and the potential for rapid response to differentiation cues. Both ESC features are subject to epigenetic regulation. Here we show that the histone acetyltransferase Mof plays an essential role in the maintenance of ESC self-renewal and pluripotency. ESCs with Mof deletion lose characteristic morphology, alkaline phosphatase (AP) staining, and differentiation potential. They also have aberrant expression of the core transcription factors Nanog, Oct4, and Sox2. Importantly, the phenotypes of Mof null ESCs can be partially suppressed by Nanog overexpression, supporting the idea that Mof functions as an upstream regulator of Nanog in ESCs. Genome-wide ChIP-sequencing and transcriptome analyses further demonstrate that Mof is an integral component of the ESC core transcriptional network and that Mof primes genes for diverse developmental programs. Mof is also required for Wdr5 recruitment and H3K4 methylation at key regulatory loci, highlighting the complexity and interconnectivity of various chromatin regulators in ESCs.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Mof is also required for Wdr5 recruitment and H3K4 methylation at key regulatory loci, highlighting the complexity and interconnectivity of various chromatin regulators in ESCs.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1258, "doc_id": "12040627", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pro-inflammatory cytokines are up regulated during tumor development.\n\nCANDIDATE_ABSTRACT:\nTITLE: Paraneoplastic thrombocytosis: the secrets of tumor self-promotion.\nABSTRACT: Paraneoplastic thrombocytosis is associated with many solid tumors and often correlates with reduced survival. Recent studies suggest that a pathogenic feed back loop may be operative between platelets and tumor cells, with reciprocal interactions between tumor growth/metastasis and thrombocytosis/platelet activation. Specific molecular pathways have been identified in which tumors can stimulate platelet production and activation; activated platelets can, in turn, promote tumor growth and metastasis. Taken together, these findings provide exciting new potential targets for therapeutic intervention.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 977, "doc_id": "14075252", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Fz/PCP-dependent Pk localizes to the anterior membrane of notochord cells during zebrafish neuralation.\n\nCANDIDATE_PASSAGE:\nPlanar cell polarity signalling couples cell division and morphogenesis during neurulation Environmental and genetic aberrations lead to neural tube closure defects (NTDs) in 1 out of every 1,000 births. Mouse and frog models for these birth defects have indicated that Van Gogh-like 2 (Vangl2, also known as Strabismus) and other components of planar cell polarity (PCP) signalling might control neurulation by promoting the convergence of neural progenitors to the midline. Here we show a novel role for PCP signalling during neurulation in zebrafish. We demonstrate that non-canonical Wnt/PCP signalling polarizes neural progenitors along the anteroposterior axis. This polarity is transiently lost during cell division in the neural keel but is re-established as daughter cells reintegrate into the neuroepithelium. Loss of zebrafish Vangl2 (in trilobite mutants) abolishes the polarization of neural keel cells, disrupts re-intercalation of daughter cells into the neuroepithelium, and results in ectopic neural progenitor accumulations and NTDs. Remarkably, blocking cell division leads to rescue of trilobite neural tube morphogenesis despite persistent defects in convergence and extension. These results reveal a function for PCP signalling in coupling cell division and morphogenesis at neurulation and indicate a previously unrecognized mechanism that might underlie NTDs.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "440", "doc_id": "4423559", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Side effects associated with antidepressants do not represent a mortality risk to postmenopausal women.\n\nCANDIDATE_ABSTRACT:\nTITLE: Antidepressant use and risk of adverse outcomes in older people: population based cohort study\nABSTRACT: OBJECTIVES To investigate the association between antidepressant treatment and risk of several potential adverse outcomes in older people with depression and to examine risks by class of antidepressant, duration of use, and dose. DESIGN Cohort study of people aged 65 and over diagnosed as having depression. SETTING 570 general practices in the United Kingdom supplying data to the QResearch primary care database. PARTICIPANTS 60,746 patients diagnosed as having a new episode of depression between the ages of 65 and 100 years from 1 January 1996 to 31 December 2007 and followed up until 31 December 2008. MAIN OUTCOME MEASURES Hazard ratios associated with antidepressant use for all cause mortality, attempted suicide/self harm, myocardial infarction, stroke/transient ischaemic attack, falls, fractures, upper gastrointestinal bleeding, epilepsy/seizures, road traffic accidents, adverse drug reactions, and hyponatraemia, adjusted for a range of potential confounding variables. Hazard ratios were calculated for antidepressant class (tricyclic and related antidepressants, selective serotonin reuptake inhibitors, other antidepressants), dose, and duration of use and for commonly prescribed individual drugs. RESULTS 54,038 (89.0%) patients received at least one prescription for an antidepressant during follow-up. A total of 1,398,359 antidepressant prescriptions were issued: 764,659 (54.7%) for selective serotonin reuptake inhibitors, 442,192 (31.6%) for tricyclic antidepressants, 2203 (0.2%) for monoamine oxidase inhibitors, and 189,305 (13.5%) for the group of other antidepressants. The associations with the adverse outcomes differed significantly between the antidepressant classes for seven outcomes. Selective serotonin reuptake inhibitors were associated with the [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The group of other antidepressants was associated with the highest adjusted hazard ratios for all cause mortality (1.66, 1.56 to 1.77), attempted suicide/self harm (5.16, 3.90 to 6.83), stroke/transient ischaemic attack (1.37, 1.22 to 1.55), fracture (1.64, 1.46 to 1.84), and epilepsy/seizures (2.24, 1.60 to 3.15), compared with when antidepressants were not being used.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1081, "doc_id": "5691302", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Sepsis related mortality has risen from 2009 to 2014.\n\nCANDIDATE_PASSAGE:\nPharmacist participation on physician rounds and adverse drug events in the intensive care unit. CONTEXT Pharmacist review of medication orders in the intensive care unit (ICU) has been shown to prevent errors, and pharmacist consultation has reduced drug costs. However, whether pharmacist participation in the ICU at the time of drug prescribing reduces adverse events has not been studied. OBJECTIVE To measure the effect of pharmacist participation on medical rounds in the ICU on the rate of preventable adverse drug events (ADEs) caused by ordering errors. DESIGN Before-after comparison between phase 1 (baseline) and phase 2 (after intervention implemented) and phase 2 comparison with a control unit that did not receive the intervention. SETTING A medical ICU (study unit) and a coronary care unit (control unit) in a large urban teaching hospital. PATIENTS Seventy-five patients randomly selected from each of 3 groups: all admissions to the study unit from February 1, 1993, through July 31, 1993 (baseline) and all admissions to the study unit (postintervention) and control unit from October 1, 1994, through July 7, 1995. In addition, 50 patients were selected at random from the control unit during the baseline period. INTERVENTION A senior pharmacist made rounds with the ICU team and remained in the ICU for consultation in the morning, and was available on call throughout the day. MAIN OUTCOME MEASURES Preventable ADEs due to ordering (prescribing) errors and the number, type, and acceptance of interventions made by the pharmacist. Preventable ADEs were identified by review of medical records of the randomly selected patients during both preintervention and postintervention phases. Pharmacists recorded all recommendations, which were then analyzed by type and [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1073", "doc_id": "12258338", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Birth-weight is negatively associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Intrauterine environments and breast cancer risk: meta-analysis and systematic review\nABSTRACT: INTRODUCTION Various perinatal factors, including birth weight, birth order, maternal age, gestational age, twin status, and parental smoking, have been postulated to affect breast cancer risk in daughters by altering the hormonal environment of the developing fetal mammary glands. Despite ample biologic plausibility, epidemiologic studies to date have yielded conflicting results. We investigated the associations between perinatal factors and subsequent breast cancer risk through meta-analyses. METHODS We reviewed breast cancer studies published from January 1966 to February 2007 that included data on birth weight, birth order, maternal age, gestational age, twin status, and maternal or paternal smoking. Meta-analyses using random effect models were employed to summarize the results. RESULTS We found that heavier birth weights were associated with increased breast cancer risk, with studies involving five categories of birth weight identifying odds ratios (ORs) of 1.24 (95% confidence interval [CI] 1.04 to 1.48) for 4,000 g or more and 1.15 (95% CI 1.04 to 1.26) for 3,500 g to 3,999 g, relative to a birth weight of 2,500 to 2,599 g. These studies provided no support for a J-shaped relationship of birthweight to risk. Support for an association with birthweight was also derived from studies based on three birth weight categories (OR 1.15 [95% CI 1.01 to 1.31] for > or =4,000 g relative to <3,000 g) and two birth weight categories (OR 1.09 [95% CI 1.02 to 1.18] for > or =3,000 g relative to <3,000 g). Women born to older mothers and twins were also at some increased risk, but the results were heterogeneous across studies and publication years. Birth order, prematurity, and maternal smoking were unrelated to breast cancer risk. CONCLUSION Our findings provide so [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"RESULTS We found that heavier birth weights were associated with increased breast cancer risk, with studies involving five categories of birth weight identifying odds ratios (ORs) of 1.24 (95% confidence interval [CI] 1.04 to 1.48) for 4,000 g or more and 1.15 (95% CI 1.04 to 1.26) for 3,500 g to 3,999 g, relative to a birth weight of 2,500 to 2,599 g. These studies provided no support for a J-shaped relationship of birthweight to risk.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 178, "doc_id": "17450673", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Hypothalamic glutamate neurotransmission is unrelated to energy balance.\n\nCANDIDATE_PASSAGE:\nA distinctive DNA damage response in human hematopoietic stem cells reveals an apoptosis-independent role for p53 in self-renewal. Highly regenerative tissues such as blood must possess effective DNA damage responses (DDR) that balance long-term regeneration with protection from leukemogenesis. Hematopoietic stem cells (HSCs) sustain life-long blood production, yet their response to DNA damage remains largely unexplored. We report that human HSCs exhibit delayed DNA double-strand break rejoining, persistent gammaH2AX foci, and enhanced p53- and ASPP1-dependent apoptosis after gamma-radiation compared to progenitors. p53 inactivation or Bcl-2 overexpression reduced radiation-induced apoptosis and preserved in vivo repopulating HSC function. Despite similar protection from irradiation-induced apoptosis, only Bcl-2-overexpressing HSCs showed higher self-renewal capacity, establishing that intact p53 positively regulates self-renewal independently from apoptosis. The reduced self-renewal of HSCs with inactivated p53 was associated with increased spontaneous gammaH2AX foci in secondary transplants of HSCs. Our data reveal distinct physiological roles of p53 that together ensure optimal HSC function: apoptosis regulation and prevention of gammaH2AX foci accumulation upon HSC self-renewal.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "541", "doc_id": "10015292", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Treatment with a protein named FN impairs regenerative abilities of aged muscles.\n\nCANDIDATE_PASSAGE:\nActivation of proteinase-activated receptor 2 in human osteoarthritic cartilage upregulates catabolic and proinflammatory pathways capable of inducing cartilage degradation: a basic science study Proteinase-activated receptors (PARs) belong to a family of G protein-coupled receptors. PARs are activated by a serine-dependent cleavage generating a tethered activating ligand. PAR-2 was shown to be involved in inflammatory pathways. We investigated the in situ levels and modulation of PAR-2 in human normal and osteoarthritis (OA) cartilage/chondrocytes. Furthermore, we evaluated the role of PAR-2 on the synthesis of the major catabolic factors in OA cartilage, including metalloproteinase (MMP)-1 and MMP-13 and the inflammatory mediator cyclooxygenase 2 (COX-2), as well as the PAR-2-activated signalling pathways in OA chondrocytes. PAR-2 expression was determined using real-time reverse transcription-polymerase chain reaction and protein levels by immunohistochemistry in normal and OA cartilage. Protein modulation was investigated in OA cartilage explants treated with a specific PAR-2-activating peptide (PAR-2-AP), SLIGKV-NH2 (1 to 400 μM), interleukin 1 beta (IL-1β) (100 pg/mL), tumor necrosis factor-alpha (TNF-α) (5 ng/mL), transforming growth factor-beta-1 (TGF-β1) (10 ng/mL), or the signalling pathway inhibitors of p38 (SB202190), MEK1/2 (mitogen-activated protein kinase kinase) (PD98059), and nuclear factor-kappa B (NF-κB) (SN50), and PAR-2 levels were determined by immunohistochemistry. Signalling pathways were analyzed on OA chondrocytes by Western blot using specific phospho-antibodies against extracellular signal-regulated kinase 1/2 (Erk1/2), p38, JNK (c-jun N-terminal kinase), and NF-κB in the presence or absence of the PAR-2-AP and/or IL-1β. PAR-2-ind [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1323", "doc_id": "1044552", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Noninvasive positive pressure ventilation is not predictive of acute respiratory failure after solid organ transplantation.\n\nCANDIDATE_PASSAGE:\nHealth-related quality of life among children with acute lymphoblastic leukemia. BACKGROUND The objective was to quantify the health-related quality of life (HRQL) of children treated for acute lymphoblastic leukemia (ALL) and identify specific disabilities for remediation. PROCEDURE Two types of subjects were included: ALL patients 5 plus years old in a multi-center clinical trial and general population control groups. Patients were assessed during all four major phases of active treatment and approximately 2 years after treatment. Health status and HRQL were measured using HEALTH UTILITIES INDEX® (HUI®) Mark 2 (HUI2) and Mark 3 (HUI3). HRQL scores were used to calculate quality-adjusted life years (QALYs). Excess disability rates identified attributes for remediation. RESULTS HUI assessments (n = 749) were collected during the five phases. Mean HRQL increased from induction through the post-treatment phase (P < 0.001). There were no significant demographic or treatment effects on HRQL, except for type of asparaginase during continuation therapy (P = 0.005 for HUI2 and P = 0.007 for HUI3). Differences in mean HRQL scores between patients and controls were important (P < 0.001) during the active treatment phases but not during the post-treatment phase. Relative to controls, patients lost approximately 0.2 QALYs during active treatment. Disability was evident in mobility/ambulation, emotion, self-care and pain, and declined over time. CONCLUSIONS Patients with ALL experienced important but declining deficits in HRQL during active treatment phases: Equivalent to losing approximately 2 months of life in perfect health. HRQL within the 2-years post-treatment phase was similar to controls. The policy challenge is to develop new treatment protocols producing fewer [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "855", "doc_id": "42913391", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Patients with microcytosis and higher erythrocyte count are more vulnerable to severe malarial anaemia when infected with Plasmodium falciparum.\n\nCANDIDATE_ABSTRACT:\nTITLE: Increased Microerythrocyte Count in Homozygous α+-Thalassaemia Contributes to Protection against Severe Malarial Anaemia\nABSTRACT: BACKGROUND The heritable haemoglobinopathy alpha(+)-thalassaemia is caused by the reduced synthesis of alpha-globin chains that form part of normal adult haemoglobin (Hb). Individuals homozygous for alpha(+)-thalassaemia have microcytosis and an increased erythrocyte count. Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count. We tested the hypothesis that the erythrocyte indices associated with alpha(+)-thalassaemia homozygosity provide a haematological benefit during acute malaria. METHODS AND FINDINGS Data from children living on the north coast of Papua New Guinea who had participated in a case-control study of the protection afforded by alpha(+)-thalassaemia against severe malaria were reanalysed to assess the genotype-specific reduction in erythrocyte count and Hb levels associated with acute malarial disease. We observed a reduction in median erythrocyte count of approximately 1.5 x 10(12)/l in all children with acute falciparum malaria relative to values in community children (p < 0.001). We developed a simple mathematical model of the linear relationship between Hb concentration and erythrocyte count. This model predicted that children homozygous for alpha(+)-thalassaemia lose less Hb than children of normal genotype for a reduction in erythrocyte count of >1.1 x 10(12)/l as a result of the reduced mean cell Hb in homozygous alpha(+)-thalassaemia. In addition, children homozygous for alpha(+)-thalassaemia require a 10% greater reduction in erythrocyte count than children of normal genotype (p = 0.02) for Hb concentration to fall to 50 g/l, the cutoff for SMA. We estimated that the haematological profile in [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Alpha(+)-thalassaemia homozygosity confers considerable protection against severe malaria, including severe malarial anaemia (SMA) (Hb concentration < 50 g/l), but does not influence parasite count.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 928, "doc_id": "18174210", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: TNFAIP3 is a tumor suppressor in glioblastoma.\n\nCANDIDATE_ABSTRACT:\nTITLE: Targeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth\nABSTRACT: Glioblastomas are deadly cancers that display a functional cellular hierarchy maintained by self-renewing glioblastoma stem cells (GSCs). GSCs are regulated by molecular pathways distinct from the bulk tumor that may be useful therapeutic targets. We determined that A20 (TNFAIP3), a regulator of cell survival and the NF-kappaB pathway, is overexpressed in GSCs relative to non-stem glioblastoma cells at both the mRNA and protein levels. To determine the functional significance of A20 in GSCs, we targeted A20 expression with lentiviral-mediated delivery of short hairpin RNA (shRNA). Inhibiting A20 expression decreased GSC growth and survival through mechanisms associated with decreased cell-cycle progression and decreased phosphorylation of p65/RelA. Elevated levels of A20 in GSCs contributed to apoptotic resistance: GSCs were less susceptible to TNFalpha-induced cell death than matched non-stem glioma cells, but A20 knockdown sensitized GSCs to TNFalpha-mediated apoptosis. The decreased survival of GSCs upon A20 knockdown contributed to the reduced ability of these cells to self-renew in primary and secondary neurosphere formation assays. The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts. In silico analysis of a glioma patient genomic database indicates that A20 overexpression and amplification is inversely correlated with survival. Together these data indicate that A20 contributes to glioma maintenance through effects on the glioma stem cell subpopulation. Although inactivating mutations in A20 in lymphoma suggest A20 can act as a tumor suppressor, similar point mutations have not been identified through glioma genomic sequencing: in fact, our data suggest A20 may funct [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The tumorigenic potential of GSCs was decreased with A20 targeting, resulting in increased survival of mice bearing human glioma xenografts.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1137, "doc_id": "33370", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Pro-inflammatory cytokines are up repressed during tumor development.\n\nCANDIDATE_PASSAGE:\nAssessing the cost effectiveness of using prognostic biomarkers with decision models: case study in prioritising patients waiting for coronary artery surgery OBJECTIVE To determine the effectiveness and cost effectiveness of using information from circulating biomarkers to inform the prioritisation process of patients with stable angina awaiting coronary artery bypass graft surgery. DESIGN Decision analytical model comparing four prioritisation strategies without biomarkers (no formal prioritisation, two urgency scores, and a risk score) and three strategies based on a risk score using biomarkers: a routinely assessed biomarker (estimated glomerular filtration rate), a novel biomarker (C reactive protein), or both. The order in which to perform coronary artery bypass grafting in a cohort of patients was determined by each prioritisation strategy, and mean lifetime costs and quality adjusted life years (QALYs) were compared. DATA SOURCES Swedish Coronary Angiography and Angioplasty Registry (9935 patients with stable angina awaiting coronary artery bypass grafting and then followed up for cardiovascular events after the procedure for 3.8 years), and meta-analyses of prognostic effects (relative risks) of biomarkers. RESULTS The observed risk of cardiovascular events while on the waiting list for coronary artery bypass grafting was 3 per 10,000 patients per day within the first 90 days (184 events in 9935 patients). Using a cost effectiveness threshold of pound20,000- pound30,000 (euro22,000-euro33,000; $32,000-$48,000) per additional QALY, a prioritisation strategy using a risk score with estimated glomerular filtration rate was the most cost effective strategy (cost per additional QALY was < pound410 compared with the Ontario urgency score). The impact on po [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "978", "doc_id": "13625993", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: PKG-la does not have a large impact on expression of spinal long term potentiation in PGK-la knockout mice.\n\nCANDIDATE_ABSTRACT:\nTITLE: Systems metabolic engineering of Escherichia coli for L-threonine production\nABSTRACT: Amino-acid producers have traditionally been developed by repeated random mutagenesis owing to the difficulty in rationally engineering the complex and highly regulated metabolic network. Here, we report the development of the genetically defined L-threonine overproducing Escherichia coli strain by systems metabolic engineering. Feedback inhibitions of aspartokinase I and III (encoded by thrA and lysC, respectively) and transcriptional attenuation regulations (located in thrL) were removed. Pathways for Thr degradation were removed by deleting tdh and mutating ilvA. The metA and lysA genes were deleted to make more precursors available for Thr biosynthesis. Further target genes to be engineered were identified by transcriptome profiling combined with in silico flux response analysis, and their expression levels were manipulated accordingly. The final engineered E. coli strain was able to produce Thr with a high yield of 0.393 g per gram of glucose, and 82.4 g/l Thr by fed-batch culture. The systems metabolic engineering strategy reported here may be broadly employed for developing genetically defined organisms for the efficient production of various bioproducts.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 910, "doc_id": "1818578", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: CHEK2 is not associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Linkage Disequilibrium Mapping of CHEK2: Common Variation and Breast Cancer Risk \nABSTRACT: Background Checkpoint kinase 2 (CHEK2) averts cancer development by promoting cell cycle arrest and activating DNA repair in genetically damaged cells. Previous investigation has established a role for the CHEK2 gene in breast cancer aetiology, but studies have largely been limited to the rare 1100delC mutation. Whether common polymorphisms in this gene influence breast cancer risk remains unknown. In this study, we aimed to assess the importance of common CHEK2 variants on population risk for breast cancer by capturing the majority of diversity in the gene using haplotype tagging single nucleotide polymorphisms (tagSNPs). Methods and Findings We analyzed 14 common SNPs spanning 52 kilobases (kb) of the CHEK2 gene in 92 Swedish women. Coverage evaluation indicated that these typed SNPs would efficiently convey association signal also from untyped SNPs in the same region. Six of the 14 SNPs predicted well both the haplotypic and single SNP variations within CHEK2. We genotyped these six tagSNPs in 1,577 postmenopausal breast cancer cases and 1,513 population controls, but found no convincing association between any common CHEK2 haplotype and breast cancer risk. The 1100delC mutation was rare in our Swedish population—0.7% in cases and 0.4% in controls— with a corresponding odds ratio for carriers versus noncarriers of 2.26 (95% confidence interval, 0.99–5.15). Estimates of the population frequency and the odds ratio of 1100delC indicate that our sample is representative of a Northern European population.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We genotyped these six tagSNPs in 1,577 postmenopausal breast cancer cases and 1,513 population controls, but found no convincing association between any common CHEK2 haplotype and breast cancer risk.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 208, "doc_id": "13519661", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Increased flux of microbial products provokes immune responses.\n\nCANDIDATE_PASSAGE:\nLiver-resident macrophage necroptosis orchestrates type 1 microbicidal inflammation and type-2-mediated tissue repair during bacterial infection. Kupffer cells, the phagocytes of fetal origin that line the liver sinusoids, are key contributors of host defense against enteroinvasive bacteria. Here, we found that infection by Listeria monocytogenes induced the early necroptotic death of Kupffer cells, which was followed by monocyte recruitment and an anti-bacterial type 1 inflammatory response. Kupffer cell death also triggered a type 2 response that involved the hepatocyte-derived alarmin interleukin-33 (IL-33) and basophil-derived interleukin-4 (IL-4). This led to the alternative activation of the monocyte-derived macrophages recruited to the liver, which thereby replaced ablated Kupffer cells and restored liver homeostasis. Kupffer cell death is therefore a key signal orchestrating type 1 microbicidal inflammation and type-2-mediated liver repair upon infection. This indicates that beyond the classical dichotomy of type 1 and type 2 responses, these responses can develop sequentially in the context of a bacterial infection and act interdependently, orchestrating liver immune responses and return to homeostasis, respectively.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "609", "doc_id": "5511240", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is tacrolimus ointment for the treatment of atopic dermatitis associated with an increase in cutaneous infections?\n\nABSTRACT:\nThe purpose of this study was to evaluate the risk of cutaneous infection in patients with atopic dermatitis treated with tacrolimus ointment. Data for 1554 patients with atopic dermatitis, treated with tacrolimus ointment in 5 clinical trials, were analyzed. In 3 controlled studies, the 12-week adjusted incidence of all cutaneous infections in patients treated with the vehicle, 0.03%, and 0.1% tacrolimus ointment, respectively, was 18.0%, 24.8%, and 17.7% for adult patients, and 20.9%, 19.6%, and 23.6% for pediatric patients. The incidence of any individual cutaneous infection was not significantly higher in the tacrolimus group than in the vehicle group, with the exception of folliculitis in adults. In two open-label studies, there was no evidence of an increased risk of cutaneous infections with long-term use of 0.1% tacrolimus ointment (up to 1 year), based on the incidence of adverse events, incidence by cumulative length of exposure, or hazard rates.", "output": "{\"label\": \"no\", \"rationale\": \"Treatment with tacrolimus ointment (0.03% or 0.1%) does not increase the risk of cutaneous bacterial, viral, or fungal infections in patients with atopic dermatitis.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 12271302, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: TRAP+ osteoclasts regulate mature osteoblast maintenance.\n\nCANDIDATE_ABSTRACT:\nTITLE: Biochemical Properties of Highly Neuroinvasive Prion Strains\nABSTRACT: Infectious prions propagate from peripheral entry sites into the central nervous system (CNS), where they cause progressive neurodegeneration that ultimately leads to death. Yet the pathogenesis of prion disease can vary dramatically depending on the strain, or conformational variant of the aberrantly folded and aggregated protein, PrP(Sc). Although most prion strains invade the CNS, some prion strains cannot gain entry and do not cause clinical signs of disease. The conformational basis for this remarkable variation in the pathogenesis among strains is unclear. Using mouse-adapted prion strains, here we show that highly neuroinvasive prion strains primarily form diffuse aggregates in brain and are noncongophilic, conformationally unstable in denaturing conditions, and lead to rapidly lethal disease. These neuroinvasive strains efficiently generate PrP(Sc) over short incubation periods. In contrast, the weakly neuroinvasive prion strains form large fibrillary plaques and are stable, congophilic, and inefficiently generate PrP(Sc) over long incubation periods. Overall, these results indicate that the most neuroinvasive prion strains are also the least stable, and support the concept that the efficient replication and unstable nature of the most rapidly converting prions may be a feature linked to their efficient spread into the CNS.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1138, "doc_id": "1292369", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Epigenetic modulating agents (EMAs) modulate antitumor immune response in a cancer model system.\n\nCANDIDATE_ABSTRACT:\nTITLE: Epigenetic therapy activates type I interferon signaling in murine ovarian cancer to reduce immunosuppression and tumor burden.\nABSTRACT: Ovarian cancer is the most lethal of all gynecological cancers, and there is an urgent unmet need to develop new therapies. Epithelial ovarian cancer (EOC) is characterized by an immune suppressive microenvironment, and response of ovarian cancers to immune therapies has thus far been disappointing. We now find, in a mouse model of EOC, that clinically relevant doses of DNA methyltransferase and histone deacetylase inhibitors (DNMTi and HDACi, respectively) reduce the immune suppressive microenvironment through type I IFN signaling and improve response to immune checkpoint therapy. These data indicate that the type I IFN response is required for effective in vivo antitumorigenic actions of the DNMTi 5-azacytidine (AZA). Through type I IFN signaling, AZA increases the numbers of CD45+ immune cells and the percentage of active CD8+ T and natural killer (NK) cells in the tumor microenvironment, while reducing tumor burden and extending survival. AZA also increases viral defense gene expression in both tumor and immune cells, and reduces the percentage of macrophages and myeloid-derived suppressor cells in the tumor microenvironment. The addition of an HDACi to AZA enhances the modulation of the immune microenvironment, specifically increasing T and NK cell activation and reducing macrophages over AZA treatment alone, while further increasing the survival of the mice. Finally, a triple combination of DNMTi/HDACi plus the immune checkpoint inhibitor α-PD-1 provides the best antitumor effect and longest overall survival, and may be an attractive candidate for future clinical trials in ovarian cancer.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 385, "doc_id": "9767444", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The relationship between a breast cancer patient's capacity to metabolize tamoxifen and treatment outcome is independent of the patient's genetic make-up.\n\nCANDIDATE_PASSAGE:\nAdult T-cell leukemia/lymphoma in London: clinical experience of 21 cases. Adult T-cell leukemia/lymphoma (ATLL) is uncommon in the United Kingdom and has so far been restricted to people of Afro-Caribbean extraction. Between 1981 and 1995, 21 cases presented to 2 inner London teaching hospitals where 17% of the population are of Afro-Caribbean origin. Clinical presentations were similar to those of the disease in HTLV-I-endemic areas. Major responses (CR + PR) were obtained in 10/16 assessable patients (63%) treated with combination chemotherapy. However, median survival was only 5.5 months. Disease progression and opportunistic infection were the major causes of treatment failure and death. Three patients (14%) relapsed in the central nervous system (CNS). Our cases confirm the profound immunosuppression in ATLL. The poor prognosis of acute and lymphoma types of ATLL highlight the need for new approaches to treatment such as zidovudine and alpha-interferon, incorporating prophylaxis against CNS disease and opportunistic infections.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1260", "doc_id": "28738741", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_PASSAGE:\nThe First Myriapod Genome Sequence Reveals Conservative Arthropod Gene Content and Genome Organisation in the Centipede Strigamia maritima Myriapods (e.g., centipedes and millipedes) display a simple homonomous body plan relative to other arthropods. All members of the class are terrestrial, but they attained terrestriality independently of insects. Myriapoda is the only arthropod class not represented by a sequenced genome. We present an analysis of the genome of the centipede Strigamia maritima. It retains a compact genome that has undergone less gene loss and shuffling than previously sequenced arthropods, and many orthologues of genes conserved from the bilaterian ancestor that have been lost in insects. Our analysis locates many genes in conserved macro-synteny contexts, and many small-scale examples of gene clustering. We describe several examples where S. maritima shows different solutions from insects to similar problems. The insect olfactory receptor gene family is absent from S. maritima, and olfaction in air is likely effected by expansion of other receptor gene families. For some genes S. maritima has evolved paralogues to generate coding sequence diversity, where insects use alternate splicing. This is most striking for the Dscam gene, which in Drosophila generates more than 100,000 alternate splice forms, but in S. maritima is encoded by over 100 paralogues. We see an intriguing linkage between the absence of any known photosensory proteins in a blind organism and the additional absence of canonical circadian clock genes. The phylogenetic position of myriapods allows us to identify where in arthropod phylogeny several particular molecular mechanisms and traits emerged. For example, we conclude that juvenile hormone signalling evolved with the e [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "972", "doc_id": "1332250", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Dscam1 acts as a hypervariable pattern-recognition receptor for the immune system.\n\nCANDIDATE_ABSTRACT:\nTITLE: RNA is favourable for analysing EGFR mutations in malignant pleural effusion of lung cancer.\nABSTRACT: Malignant pleural effusion (MPE) is a useful specimen allowing for the evaluation of EGFR status in nonsmall cell lung cancer (NSCLC). However, direct sequencing of genomic DNA from MPE samples was found not to be sensitive for EGFR mutation detection. To test whether EGFR analysis from RNA is less prone to interference from nontumour cells that have no or lower EGFR expression, we compared three methods (sequencing from cell-derived RNA versus sequencing and mass-spectrometric analysis from genomic DNA), in parallel, for EGFR mutation detection from MPE samples in 150 lung adenocarcinoma patients receiving first-line tyrosine kinase inhibitors (TKIs). Among these MPE samples, EGFR mutations were much more frequently identified by sequencing using RNA than by sequencing and mass-spectrometric analysis from genomic DNA (for all mutations, 67.3 versus 44.7 and 46.7%; for L858R or exon 19 deletions, 61.3 versus 41.3 and 46.7%, respectively). The better mutation detection yield of sequencing from RNA was coupled with the superior prediction of clinical efficacy of first-line TKIs. In patients with acquired resistance, EGFR sequencing from RNA provided satisfactory detection of T790M (54.2%). These results demonstrated that EGFR sequencing using RNA as template greatly improves sensitivity for EGFR mutation detection from samples of MPE, highlighting RNA as the favourable source for analysing EGFR mutations from heterogeneous MPE specimens in NSCLC.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 356, "doc_id": "711256", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Sympathetic nerve activity is reduced throughout normal pregnancy.\n\nCANDIDATE_ABSTRACT:\nTITLE: Regulation of sympathetic nerve activity during the cold pressor test in normotensive pregnant and nonpregnant women.\nABSTRACT: Baseline neurovascular transduction is reduced in normotensive pregnancy; however, little is known about changes to neurovascular transduction during periods of heightened sympathetic activation. We tested the hypothesis that, despite an exacerbated muscle sympathetic nerve activity (microneurography) response to cold pressor stimulation, the blunting of neurovascular transduction in normotensive pregnant women would result in similar changes in vascular resistance and mean arterial pressure (Finometer) relative to nonpregnant controls. Baseline neurovascular transduction was reduced in pregnant women relative to controls when expressed as the quotient of both total resistance and mean arterial pressure and sympathetic burst frequency (0.32±0.07 versus 0.58±0.16 mm Hg/L/min/bursts/min, P<0.001 and 2.4±0.7 versus 3.6±0.8 mm Hg/bursts/min, P=0.001). Sympathetic activation was greater across all 3 minutes of cold pressor stimulation in the pregnant women relative to the nonpregnant controls. Peak sympathoexcitation was also greater in pregnant than in nonpregnant women, whether expressed as sympathetic burst frequency (+17±13 versus +7±8 bursts/min, P=0.049), burst incidence (+17±9 versus +6±11 bursts/100 hb, P=0.03), or total activity (+950±660 versus +363±414 arbitrary units, P=0.04). However, neurovascular transduction during peak cold pressor-induced sympathoexcitation remained blunted in pregnant women (0.25±0.11 versus 0.45±0.08 mm Hg/L/min/bursts/min, P<0.001 and 1.9±1.0 versus 3.2±0.9 mm Hg/bursts/min, P=0.006). Therefore, mean arterial pressure (93±21 versus 99±6 mm Hg, P=0.4) and total peripheral resistance (12±3 versus 14±3 mm Hg/L/min) were not different between pregnant and nonpregnant women during peak sympathoexcitation. These data indicate that [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Sympathetic activation was greater across all 3 minutes of cold pressor stimulation in the pregnant women relative to the nonpregnant controls.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1120, "doc_id": "13907928", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Post-transcriptional handling of mitochondrial transcripts occurs in mitochondrial RNA granules.\n\nCANDIDATE_ABSTRACT:\nTITLE: Control of glutamate clearance and synaptic efficacy by glial coverage of neurons.\nABSTRACT: Analysis of excitatory synaptic transmission in the rat hypothalamic supraoptic nucleus revealed that glutamate clearance and, as a consequence, glutamate concentration and diffusion in the extracellular space, is associated with the degree of astrocytic coverage of its neurons. Reduction in glutamate clearance, whether induced pharmacologically or associated with a relative decrease of glial coverage in the vicinity of synapses, affected transmitter release through modulation of presynaptic metabotropic glutamate receptors. Astrocytic wrapping of neurons, therefore, contributes to the regulation of synaptic efficacy in the central nervous system.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 962, "doc_id": "306311", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Tonic signaling from the scFv induces constitutive stimulation.\n\nCANDIDATE_PASSAGE:\nCNTF reverses obesity-induced insulin resistance by activating skeletal muscle AMPK Ciliary neurotrophic factor (CNTF) induces weight loss and improves glucose tolerance in humans and rodents. CNTF is thought to act centrally by inducing hypothalamic neurogenesis to modulate food intake and peripherally by altering hepatic gene expression, in a manner similar to that of leptin. Here, we show that CNTF signals through the CNTFRα–IL-6R–gp130β receptor complex to increase fatty-acid oxidation and reduce insulin resistance in skeletal muscle by activating AMP-activated protein kinase (AMPK), independent of signaling through the brain. Thus, our findings further show that the antiobesogenic effects of CNTF in the periphery result from direct effects on skeletal muscle, and that these peripheral effects are not suppressed by diet-induced or genetic models of obesity, an essential requirement for the therapeutic treatment of obesity-related diseases.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1307", "doc_id": "5108807", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Rapid up-regulation and higher basal expression of interferon-induced genes increase survival of granule cell neurons that are infected by West Nile virus.\n\nCANDIDATE_PASSAGE:\nDifferential innate immune response programs in neuronal subtypes determine susceptibility to infection in the brain by positive stranded RNA viruses Although susceptibility of neurons in the brain to microbial infection is a major determinant of clinical outcome, little is known about the molecular factors governing this vulnerability. Here we show that two types of neurons from distinct brain regions showed differential permissivity to replication of several positive-stranded RNA viruses. Granule cell neurons of the cerebellum and cortical neurons from the cerebral cortex have unique innate immune programs that confer differential susceptibility to viral infection ex vivo and in vivo. By transducing cortical neurons with genes that were expressed more highly in granule cell neurons, we identified three interferon-stimulated genes (ISGs; Ifi27, Irg1 and Rsad2 (also known as Viperin)) that mediated the antiviral effects against different neurotropic viruses. Moreover, we found that the epigenetic state and microRNA (miRNA)-mediated regulation of ISGs correlates with enhanced antiviral response in granule cell neurons. Thus, neurons from evolutionarily distinct brain regions have unique innate immune signatures, which probably contribute to their relative permissiveness to infection.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1020", "doc_id": "9433958", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: A deficiency of vitamin B6 decreases blood levels of homocysteine.\n\nCANDIDATE_PASSAGE:\nFGF regulates TGF-β signaling and endothelial-to-mesenchymal transition via control of let-7 miRNA expression. Maintenance of normal endothelial function is critical to various aspects of blood vessel function, but its regulation is poorly understood. In this study, we show that disruption of baseline fibroblast growth factor (FGF) signaling to the endothelium leads to a dramatic reduction in let-7 miRNA levels that, in turn, increases expression of transforming growth factor (TGF)-β ligands and receptors and activation of TGF-β signaling, leading to endothelial-to-mesenchymal transition (Endo-MT). We also find that Endo-MT is an important driver of neointima formation in a murine transplant arteriopathy model and in rejection of human transplant lesions. The decline in endothelial FGF signaling input is due to the appearance of an FGF resistance state that is characterized by inflammation-dependent reduction in expression and activation of key components of the FGF signaling cascade. These results establish FGF signaling as a critical factor in maintenance of endothelial homeostasis and point to an unexpected role of Endo-MT in vascular pathology.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "37", "doc_id": "11771811", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Lysine histone demethylase inhibitor JIB 04 is inactive against KDM5A.\n\nCANDIDATE_PASSAGE:\nHistone methyltransferase activity associated with a human multiprotein complex containing the Enhancer of Zeste protein. Enhancer of Zeste [E(z)] is a Polycomb-group transcriptional repressor and one of the founding members of the family of SET domain-containing proteins. Several SET-domain proteins possess intrinsic histone methyltransferase (HMT) activity. However, recombinant E(z) protein was found to be inactive in a HMT assay. Here we report the isolation of a multiprotein E(z) complex that contains extra sex combs, suppressor of zeste-12 [Su(z)12], and the histone binding proteins RbAp46/RbAp48. This complex, which we termed Polycomb repressive complex (PRC) 2, possesses HMT activity with specificity for Lys 9 (K9) and Lys 27 (K27) of histone H3. The HMT activity of PRC2 is dependent on an intact SET domain in the E(z) protein. We hypothesize that transcriptional repression by the E(z) protein involves methylation-dependent recruitment of PRC1. The presence of Su(z)12, a strong suppressor of position effect variegation, in PRC2 suggests that PRC2 may play a widespread role in heterochromatin-mediated silencing.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "730", "doc_id": "23195302", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Integrated care is successful at tackling multiple comorbidities.\n\nCANDIDATE_ABSTRACT:\nTITLE: Functional outcomes of multi-condition collaborative care and successful ageing: results of randomised trial\nABSTRACT: OBJECTIVE To evaluate the effectiveness of integrated care for chronic physical diseases and depression in reducing disability and improving quality of life. DESIGN A randomised controlled trial of multi-condition collaborative care for depression and poorly controlled diabetes and/or risk factors for coronary heart disease compared with usual care among middle aged and elderly people SETTING Fourteen primary care clinics in Seattle, Washington. PARTICIPANTS Patients with diabetes or coronary heart disease, or both, and blood pressure above 140/90 mm Hg, low density lipoprotein concentration >3.37 mmol/L, or glycated haemoglobin 8.5% or higher, and PHQ-9 depression scores of ≥ 10. INTERVENTION A 12 month intervention to improve depression, glycaemic control, blood pressure, and lipid control by integrating a \"treat to target\" programme for diabetes and risk factors for coronary heart disease with collaborative care for depression. The intervention combined self management support, monitoring of disease control, and pharmacotherapy to control depression, hyperglycaemia, hypertension, and hyperlipidaemia. MAIN OUTCOME MEASURES Social role disability (Sheehan disability scale), global quality of life rating, and World Health Organization disability assessment schedule (WHODAS-2) scales to measure disabilities in activities of daily living (mobility, self care, household maintenance). RESULTS Of 214 patients enrolled (106 intervention and 108 usual care), disability and quality of life measures were obtained for 97 intervention patients at six months (92%) and 92 at 12 months (87%), and for 96 usual care patients at six months (89%) and 92 at 12 months (85%). Improvements from baseline on the Sheehan disability scale (-0.9, 95% confidence interval -1.5 to -0.2; [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Improvements from baseline on the Sheehan disability scale (-0.9, 95% confidence interval -1.5 to -0.2; P = 0.006) and global quality of life rating (0.7, 0.2 to 1.2; P = 0.005) were significantly greater at six and 12 months in patients in the intervention group.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 648, "doc_id": "15041758", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Varenicline monotherapy is more effective after 26 weeks of treatment compared to combination nicotine replacement therapies with varenicline or bupropion.\n\nCANDIDATE_ABSTRACT:\nTITLE: The BLM helicase contributes to telomere maintenance through processing of late-replicating intermediate structures\nABSTRACT: Werner's syndrome (WS) and Bloom's syndrome (BS) are cancer predisposition disorders caused by loss of function of the RecQ helicases WRN or BLM, respectively. BS and WS are characterized by replication defects, hyperrecombination events and chromosomal aberrations, which are hallmarks of cancer. Inefficient replication of the G-rich telomeric strand contributes to chromosome aberrations in WS cells, demonstrating a link between WRN, telomeres and genomic stability. Herein, we provide evidence that BLM also contributes to chromosome-end maintenance. Telomere defects (TDs) are observed in BLM-deficient cells at an elevated frequency, which is similar to cells lacking a functional WRN helicase. Loss of both helicases exacerbates TDs and chromosome aberrations, indicating that BLM and WRN function independently in telomere maintenance. BLM localization, particularly its recruitment to telomeres, changes in response to replication dysfunction, such as in WRN-deficient cells or after aphidicolin treatment. Exposure to replication challenge causes an increase in decatenated deoxyribonucleic acid (DNA) structures and late-replicating intermediates (LRIs), which are visible as BLM-covered ultra-fine bridges (UFBs) in anaphase. A subset of UFBs originates from telomeric DNA and their frequency correlates with telomere replication defects. We propose that the BLM complex contributes to telomere maintenance through its activity in resolving LRIs.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1360, "doc_id": "2679511", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Alteration of origin firing causes changes in termination zones of Okazaki fragments.\n\nCANDIDATE_PASSAGE:\nMechanical regulation of cell function with geometrically modulated elastomeric substrates We report the establishment of a library of micromolded elastomeric micropost arrays to modulate substrate rigidity independently of effects on adhesive and other material surface properties. We demonstrated that micropost rigidity impacts cell morphology, focal adhesions, cytoskeletal contractility and stem cell differentiation. Furthermore, early changes in cytoskeletal contractility predicted later stem cell fate decisions in single cells.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "105", "doc_id": "17388232", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Genomic sequences involved in alternative splicing responsible for Hutchinson-Gilford progeria syndrome (HGPS) are abundant in the ''progerinonly'' allele of Lmna knock-in models.\n\nCANDIDATE_ABSTRACT:\nTITLE: Familial amyloidotic polyneuropathy: current and emerging treatment options for transthyretin-mediated amyloidosis\nABSTRACT: Transthyretin familial amyloid polyneuropathy (TTR-FAP) is a fatal clinical disorder characterized by extracellular deposition of abnormal fibrils derived from misfolded, normally soluble transthyretin (TTR) molecules. The disease is most commonly caused by a point mutation within the TTR gene inherited in an autosomal dominant fashion. Over 100 of such mutations have been identified, leading to destabilization of the physiological TTR tetramer. As a result, many monomers originate with a tendency for spontaneous conformational changes and self-aggregation. The main clinical feature of TTR-FAP is progressive sensorimotor and autonomic neuropathy. In the beginning, this polyneuropathy predominantly involves small unmyelinated nerve fibers with the result of dissociated sensory loss disproportionately affecting sensation of pain and temperature. Autonomic neuropathy typically accompanies sensory deficits early in the disease course. The symptoms include orthostatic hypotension, constipation alternating with diarrhea, erectile dysfunction, anhydrosis, and urinary retention or incontinence. Later, involvement of motor fibers causes rapidly progressive weakness and gait disturbances. In addition to the peripheral nervous system, the heart and the gut are frequently affected. Onset of symptoms is bimodal, with one peak at age 33 years (early onset) and another distinct peak in the sixth decade of life (late onset). The course of TTR-FAP is uniformly progressive and fatal. Death occurs an average of 10.8 years after the onset of symptoms in Portuguese patients, and 7.3 years in late-onset Japanese patients. Common causes include cachexia, cardiac failure, arrhythmia, and secondary infections. Liver transplantation is the standard therapy for patients who are in a c [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 466, "doc_id": "2496002", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does glucosamine modulate TNF-α-induced ICAM-1 expression and function through O-linked and N-linked glycosylation in human retinal pigment epithelial cells?\n\nABSTRACT:\nThe purpose of this article was to investigate the effects of glucosamine (GlcN) on the TNF-α-induced expression of intercellular adhesion molecule 1 (ICAM-1) and the function of ICAM-1 in ARPE-19 cells in vitro. We quantified protein levels of TNF-α-induced ICAM-1 in ARPE-19 cells with Western blotting. The effects of GlcN on O-linked glycosylation, and therefore on ICAM-1 expression, were compared after the addition of alloxan, an inhibitor of O-linked N-acetylglucosamine transferase (OGT), or O-(2-acetamido-2-deoxy-d-glucopyranosylidene)amino-N-phenylcarbamate (PUGNAc), an inhibitor of N-acetylglucosaminidase (O-GlcNAcase [OGA]), or after OGT gene overexpression. The effect of GlcN on the N-linked glycosylation of ICAM-1 was evaluated by the change in its molecular mass on Western blotting. The effect of O-linked glycosylation on the nuclear factor κB (NF-κB) signaling pathway was examined using an NF-κB reporter gene assay. The effect of GlcN on ICAM-1 adhesion activity was examined using an ICAM-1 adhesion assay. GlcN, PUGNAc, and OGT overexpression inhibited TNF-α-induced ICAM-1 expression and NF-κB activity in ARPE-19 cells. Alloxan increased ICAM-1 expression and NF-κB activity in TNF-α-induced ARPE-19 cells. GlcN and tunicamycin reduced the molecular mass of TNF-α-induced ICAM-1 in ARPE-19 cells. The proteasome inhibitor MG-132 suppressed the GlcN-induced reduction in the molecular mass of TNF-α-induced ICAM-1. GlcN also attenuated the adhesion activity of TNF-α-induced ICAM-1.", "output": "{\"label\": \"yes\", \"rationale\": \"GlcN inhibits ICAM-1 expression and functions by modulating the O-linked glycosylation of factors involved in NF-κB signaling and by reducing the N-linked glycosylation of TNF-α-induced ICAM-1 in ARPE-19 cells. These effects may contribute to the GlcN-mediated anti-inflammatory effects in the eye.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 22427561, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does low-dose induction chemotherapy with Baby-BOP in patients with metastatic germ-cell tumours compromise outcome : a single-centre experience?\n\nABSTRACT:\nIn some institutions advanced metastatic germ-cell tumour (GCT) is treated with low-dose induction chemotherapy in specific settings. There is a lack of published data supporting its use. The data presented here specifically address this issue for the first time. Twenty patients with metastatic GCT treated were with low-dose induction chemotherapy [Baby-BOP (bBOP)] between 1998 and 2009. We report the toxicity and outcome and compare it with a control group. bBOP was well tolerated with no treatment-related deaths and a lack of chemotherapy-related toxicity. It was associated with a significant fall in tumour markers (median HCG fell from 35 195 to 11 028 IU/l). The first subsequent cycle of standard chemotherapy was administered a median of 9.5 days after initial treatment and was not associated with excess toxicity. The 2-year overall survival of the poor-prognosis patients treated with bBOP was 79.0% [95% confidence interval (CI) 48% to 93%], which is not significantly different from the 2-year overall survival of 80% [95% CI 55% to 92%] of the poor-prognosis patients, who did not receive bBOP.", "output": "{\"label\": \"no\", \"rationale\": \"Low-dose induction chemotherapy can be given safely in selected individuals and does not adversely affect subsequent chemotherapy or outcome.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 20164149, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Diabetes remission occurs more in people treated with conventional therapy than in people treated with laparoscopic adjustable gastric banding surgery.\n\nCANDIDATE_ABSTRACT:\nTITLE: Adjustable gastric banding and conventional therapy for type 2 diabetes: a randomized controlled trial.\nABSTRACT: CONTEXT Observational studies suggest that surgically induced loss of weight may be effective therapy for type 2 diabetes. OBJECTIVE To determine if surgically induced weight loss results in better glycemic control and less need for diabetes medications than conventional approaches to weight loss and diabetes control. DESIGN, SETTING, AND PARTICIPANTS Unblinded randomized controlled trial conducted from December 2002 through December 2006 at the University Obesity Research Center in Australia, with general community recruitment to established treatment programs. Participants were 60 obese patients (BMI >30 and <40) with recently diagnosed (<2 years) type 2 diabetes. INTERVENTIONS Conventional diabetes therapy with a focus on weight loss by lifestyle change vs laparoscopic adjustable gastric banding with conventional diabetes care. MAIN OUTCOME MEASURES Remission of type 2 diabetes (fasting glucose level <126 mg/dL [7.0 mmol/L] and glycated hemoglobin [HbA1c] value <6.2% while taking no glycemic therapy). Secondary measures included weight and components of the metabolic syndrome. Analysis was by intention-to-treat. RESULTS Of the 60 patients enrolled, 55 (92%) completed the 2-year follow-up. Remission of type 2 diabetes was achieved by 22 (73%) in the surgical group and 4 (13%) in the conventional-therapy group. Relative risk of remission for the surgical group was 5.5 (95% confidence interval, 2.2-14.0). Surgical and conventional-therapy groups lost a mean (SD) of 20.7% (8.6%) and 1.7% (5.2%) of weight, respectively, at 2 years (P < .001). Remission of type 2 diabetes was related to weight loss (R2 = 0.46, P < .001) and lower baseline HbA1c levels (combined R2 = 0.52, P < .001). There were no serious complications in either group. CONCLUSIONS Participants r [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Remission of type 2 diabetes was achieved by 22 (73%) in the surgical group and 4 (13%) in the conventional-therapy group.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 341, "doc_id": "7098463", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Adult tissue-resident macrophages possess a self-renewing capacity.\n\nCANDIDATE_PASSAGE:\nOrigin and functions of tissue macrophages. Macrophages are distributed in tissues throughout the body and contribute to both homeostasis and disease. Recently, it has become evident that most adult tissue macrophages originate during embryonic development and not from circulating monocytes. Each tissue has its own composition of embryonically derived and adult-derived macrophages, but it is unclear whether macrophages of distinct origins are functionally interchangeable or have unique roles at steady state. This new understanding also prompts reconsideration of the function of circulating monocytes. Classical Ly6c(hi) monocytes patrol the extravascular space in resting organs, and Ly6c(lo) nonclassical monocytes patrol the vasculature. Inflammation triggers monocytes to differentiate into macrophages, but whether resident and newly recruited macrophages possess similar functions during inflammation is unclear. Here, we define the tools used for identifying the complex origin of tissue macrophages and discuss the relative contributions of tissue niche versus ontological origin to the regulation of macrophage functions during steady state and inflammation.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "88", "doc_id": "22406695", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Dexamethasone decreases risk of postoperative bleeding.\n\nCANDIDATE_ABSTRACT:\nTITLE: Dexamethasone and risk of nausea and vomiting and postoperative bleeding after tonsillectomy in children: a randomized trial.\nABSTRACT: CONTEXT Dexamethasone is widely used to prevent postoperative nausea and vomiting (PONV) in pediatric tonsillectomy. OBJECTIVE To assess whether dexamethasone dose-dependently reduces the risk of PONV at 24 hours after tonsillectomy. DESIGN, SETTING, AND PATIENTS Randomized placebo-controlled trial conducted among 215 children undergoing elective tonsillectomy at a major public teaching hospital in Switzerland from February 2005 to December 2007. INTERVENTIONS Children were randomly assigned to receive dexamethasone (0.05, 0.15, or 0.5 mg/kg) or placebo intravenously after induction of anesthesia. Acetaminophen-codeine and ibuprofen were given as postoperative analgesia. Follow-up continued until the 10th postoperative day. MAIN OUTCOME MEASURES The primary end point was prevention of PONV at 24 hours; secondary end points were decrease in the need for ibuprofen at 24 hours and evaluation of adverse effects. RESULTS At 24 hours, 24 of 54 participants who received placebo (44%; 95% confidence interval [CI], 31%-59%) had experienced PONV compared with 20 of 53 (38%; 95% CI, 25%-52%), 13 of 54 (24%; 95% CI, 13%-38%), and 6 of 52 (12%; 95% CI, 4%-23%) who received dexamethasone at 0.05, 0.15, and 0.5 mg/kg, respectively (P<.001 for linear trend). Children who received dexamethasone received significantly less ibuprofen. There were 26 postoperative bleeding episodes in 22 children. Two of 53 (4%; 95% CI, 0.5%-13%) children who received placebo had bleeding compared with 6 of 53 (11%; 95% CI, 4%-23%), 2 of 51 (4%; 95% CI, 0.5%-13%), and 12 of 50 (24%; 95% CI, 13%-38%) who received dexamethasone at 0.05, 0.15, and 0.5 mg/kg, respectively (P = .003). Dexamethasone, 0.5 mg/kg, was associated with the highest bleeding risk (adjusted relative risk, 6.80; 95% CI, 1.77-1 [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSION In this study of children undergoing tonsillectomy, dexamethasone decreased the risk of PONV dose dependently but was associated with an increased risk of postoperative bleeding.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 338, "doc_id": "23349986", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: YAP/TAZ is required in intestinal regeneration in mouse models of ulcerative colitis.\n\nCANDIDATE_PASSAGE:\nAn Antidepressant Decreases CSF Aβ Production in Healthy Individuals and in Transgenic AD Mice Serotonin signaling suppresses generation of amyloid-β (Aβ) in vitro and in animal models of Alzheimer’s disease (AD). We show that in an aged transgenic AD mouse model (APP/PS1 plaque-bearing mice), the antidepressant citalopram, a selective serotonin reuptake inhibitor, decreased Aβ in brain interstitial fluid in a dose-dependent manner. Growth of individual amyloid plaques was assessed in plaque-bearing mice that were chronically administered citalopram. Citalopram arrested the growth of preexisting plaques and reduced the appearance of new plaques by 78%. In healthy human volunteers, citalopram’s effects on Aβ production and Aβ concentrations in cerebrospinal fluid (CSF) were measured prospectively using stable isotope labeling kinetics, with CSF sampling during acute dosing of citalopram. Aβ production in CSF was slowed by 37% in the citalopram group compared to placebo. This change was associated with a 38% decrease in total CSF Aβ concentrations in the drug-treated group. The ability to safely decrease Aβ concentrations is potentially important as a preventive strategy for AD. This study demonstrates key target engagement for future AD prevention trials.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1381", "doc_id": "5260382", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Gene expression does not vary appreciably across genetically identical cells.\n\nCANDIDATE_PASSAGE:\nMemory and Modularity in Cell-Fate Decision Making Genetically identical cells sharing an environment can display markedly different phenotypes. It is often unclear how much of this variation derives from chance, external signals, or attempts by individual cells to exert autonomous phenotypic programs. By observing thousands of cells for hundreds of consecutive generations under constant conditions, we dissect the stochastic decision between a solitary, motile state and a chained, sessile state in Bacillus subtilis. We show that the motile state is 'memoryless', exhibiting no autonomous control over the time spent in the state. In contrast, the time spent as connected chains of cells is tightly controlled, enforcing coordination among related cells in the multicellular state. We show that the three-protein regulatory circuit governing the decision is modular, as initiation and maintenance of chaining are genetically separable functions. As stimulation of the same initiating pathway triggers biofilm formation, we argue that autonomous timing allows a trial commitment to multicellularity that external signals could extend.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "452", "doc_id": "464511", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: There is an inverse relationship between hip fractures and statin use.\n\nCANDIDATE_ABSTRACT:\nTITLE: HMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients.\nABSTRACT: CONTEXT Recent animal studies have found that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) lipid-lowering drugs (statins) substantially increase bone formation, but whether statin use in humans results in clinically meaningful bone formation or a reduction in the risk of osteoporotic fractures is not known. OBJECTIVE To determine whether the use of statins is associated with reduced hip fracture risk. DESIGN Case-control study. SETTING AND PATIENTS A total of 6110 New Jersey residents aged 65 years or older and enrolled in Medicare and either Medicaid or the Pharmacy Assistance for the Aged and Disabled program. Case patients (n=1222) underwent surgical repair of a hip fracture in 1994. Control patients (n=4888) were identified at a ratio of 4:1 and frequency-matched to case patients for age and sex. MAIN OUTCOME MEASURE Adjusted odds ratio (OR) of hip fracture by statin use in the 180 days and 3 years prior to the index date (the earliest date of admission for surgery), adjusted for demographic and clinical characteristics and health care utilization. RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus. No significant relationship was observed between use of nonstatin lipid-lowering agents and hip fracture risk. Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowe [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowering agents.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1290, "doc_id": "4687948", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The peak incidence of fractures occurs during pubertal growth spurt in early adolescents.\n\nCANDIDATE_ABSTRACT:\nTITLE: Activin/Nodal signalling in stem cells.\nABSTRACT: Activin/Nodal growth factors control a broad range of biological processes, including early cell fate decisions, organogenesis and adult tissue homeostasis. Here, we provide an overview of the mechanisms by which the Activin/Nodal signalling pathway governs stem cell function in these different stages of development. We describe recent findings that associate Activin/Nodal signalling to pathological conditions, focusing on cancer stem cells in tumorigenesis and its potential as a target for therapies. Moreover, we will discuss future directions and questions that currently remain unanswered on the role of Activin/Nodal signalling in stem cell self-renewal, differentiation and proliferation.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1248, "doc_id": "226488", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does inhibition of the p38 MAPK pathway ameliorate renal fibrosis in an NPHP2 mouse model?\n\nABSTRACT:\nNephronophthisis (NPHP), the most frequent genetic cause of end-stage kidney disease in children and young adults, is characterized by a variable number of renal cysts associated with cortical tubular atrophy and interstitial fibrosis. The p38 mitogen-activated protein kinase (MAPK) pathway is an important intracellular signaling pathway involved in the production of profibrotic mediators. The relationship between p38 MAPK and renal fibrosis in NPHP2 is unknown. We administered a selective p38 MAPK inhibitor, FR167653, in a NPHP2 mouse model (inv/inv, invΔC mice) from 3 to 6 weeks old, and the kidneys were examined at 6 weeks of age. Phosphorylation of p38 MAPK (p-p38 MAPK) protein levels, the degree of renal fibrosis, messenger RNA (mRNA) levels for extracellular matrix genes and mRNA levels for transforming growth factor in the kidneys were studied. Effect of an extracellular signal-regulated protein kinase (ERK) kinase (MEK) inhibitor on renal fibrosis was also evaluated. Expression of extracellular matrix genes and p-p38 MAPK were increased in the NPHP2 mouse model kidney. FR167653 successfully decreased p-p38 MAPK levels, the degree of fibrosis and extracellular matrix gene expressions. However, the FR167653 did not prevent cyst expansion, abnormal cell proliferation and acceleration of apoptosis and did not influence ERK activation. In contrast, MEK inhibition reduced both cyst expansion and fibrosis without affecting p38 MAPK activation.", "output": "{\"label\": \"yes\", \"rationale\": \"These results suggest that inhibition of p38 MAPK reduced renal fibrosis but not cyst expansion, cell proliferation and apoptosis in NPHP2 model mice. Our results suggest that p38 MAPK and ERK signaling pathways independently affect renal fibrosis in inv mutant mice.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 22076433, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Increased microtubule acetylation worsens interference of axonal transport caused by LRRK2 Roc-COR domain mutations.\n\nCANDIDATE_ABSTRACT:\nTITLE: Increasing microtubule acetylation rescues axonal transport and locomotor deficits caused by LRRK2 Roc-COR domain mutations\nABSTRACT: Leucine-rich repeat kinase 2 (LRRK2) mutations are the most common genetic cause of Parkinson's disease. LRRK2 is a multifunctional protein affecting many cellular processes and has been described to bind microtubules. Defective microtubule-based axonal transport is hypothesized to contribute to Parkinson's disease, but whether LRRK2 mutations affect this process to mediate pathogenesis is not known. Here we find that LRRK2 containing pathogenic Roc-COR domain mutations (R1441C, Y1699C) preferentially associates with deacetylated microtubules, and inhibits axonal transport in primary neurons and in Drosophila, causing locomotor deficits in vivo. In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport. In vivo knockdown of the deacetylases HDAC6 and Sirt2, or administration of TSA rescues both axonal transport and locomotor behavior. Thus, this study reveals a pathogenic mechanism and a potential intervention for Parkinson's disease.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In vivo knockdown of the deacetylases HDAC6 and Sirt2, or administration of TSA rescues both axonal transport and locomotor behavior.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 615, "doc_id": "9638032", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: A deficiency of vitamin B12 increases blood levels of homocysteine.\n\nCANDIDATE_PASSAGE:\nBiomarkers of endothelial dysfunction and risk of type 2 diabetes mellitus. CONTEXT Endothelial dysfunction occurs in diagnosed type 2 diabetes mellitus but may also precede development of diabetes. OBJECTIVE To determine whether elevated plasma levels of biomarkers reflecting endothelial dysfunction (E-selectin; intercellular adhesion molecule 1 [ICAM-1]; and vascular cell adhesion molecule 1 [VCAM-1]) predict development of type 2 diabetes in initially nondiabetic women. DESIGN AND SETTING Prospective, nested case-control study within the Nurses' Health Study, an ongoing US study initiated in 1976. PARTICIPANTS Of 121 700 women initially enrolled, 32 826 provided blood samples in 1989-1990; of those free of diabetes, cardiovascular disease, or cancer at baseline, 737 developed incident diabetes by 2000. Controls (n = 785) were selected according to matched age, fasting status, and race. MAIN OUTCOME MEASURE Risk of confirmed clinically diagnosed type 2 diabetes by baseline levels of E-selectin, ICAM-1, and VCAM-1. RESULTS Baseline median levels of the biomarkers were significantly higher among cases than among controls (E-selectin, 61.2 vs 45.4 ng/mL; ICAM-1, 264.9 vs 247.0 ng/mL; VCAM-1, 545.4 vs 526.0 ng/mL [all P values < or =.004]). Elevated E-selectin and ICAM-1 levels predicted incident diabetes in logistic regression models conditioned on matching criteria and adjusted for body mass index (BMI), family history of diabetes, smoking, diet score, alcohol intake, activity index, and postmenopausal hormone use. The adjusted relative risks for incident diabetes in the top quintile vs the bottom quintiles were 5.43 for E-selectin (95% confidence interval [CI], 3.47-8.50), 3.56 for ICAM-1 (95% CI, 2.28-5.58), and 1.12 for VCAM-1 (95% CI, 0.76-1.66). Adjustm [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "36", "doc_id": "6176498", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nCANDIDATE_ABSTRACT:\nTITLE: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\nABSTRACT: Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens. However, signals underlying mTEC development remain largely unclear. Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals. Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment. Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner. These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1181, "doc_id": "2734421", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Active caspase-11 participate in regulating phagosome-lysosome fusion.\n\nCANDIDATE_PASSAGE:\n6-phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumor growth by inhibiting LKB1-AMPK signaling The oxidative pentose phosphate pathway (PPP) contributes to tumour growth, but the precise contribution of 6-phosphogluconate dehydrogenase (6PGD), the third enzyme in this pathway, to tumorigenesis remains unclear. We found that suppression of 6PGD decreased lipogenesis and RNA biosynthesis and elevated ROS levels in cancer cells, attenuating cell proliferation and tumour growth. 6PGD-mediated production of ribulose-5-phosphate (Ru-5-P) inhibits AMPK activation by disrupting the active LKB1 complex, thereby activating acetyl-CoA carboxylase 1 and lipogenesis. Ru-5-P and NADPH are thought to be precursors in RNA biosynthesis and lipogenesis, respectively; thus, our findings provide an additional link between the oxidative PPP and lipogenesis through Ru-5-P-dependent inhibition of LKB1-AMPK signalling. Moreover, we identified and developed 6PGD inhibitors, physcion and its derivative S3, that effectively inhibited 6PGD, cancer cell proliferation and tumour growth in nude mice xenografts without obvious toxicity, suggesting that 6PGD could be an anticancer target.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "78", "doc_id": "1686997", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Combination nicotine replacement therapies with varenicline or bupropion are more effective after 12 weeks of reatment compared to varenicline monotherapy.\n\nCANDIDATE_PASSAGE:\nEfficacy of HPV DNA testing with cytology triage and/or repeat HPV DNA testing in primary cervical cancer screening. BACKGROUND Primary cervical screening with both human papillomavirus (HPV) DNA testing and cytological examination of cervical cells with a Pap test (cytology) has been evaluated in randomized clinical trials. Because the vast majority of women with positive cytology are also HPV DNA positive, screening strategies that use HPV DNA testing as the primary screening test may be more effective. METHODS We used the database from the intervention arm (n = 6,257 women) of a population-based randomized trial of double screening with cytology and HPV DNA testing to evaluate the efficacy of 11 possible cervical screening strategies that are based on HPV DNA testing alone, cytology alone, and HPV DNA testing combined with cytology among women aged 32-38 years. The main outcome measures were sensitivity for detection of cervical intraepithelial neoplasia grade 3 or worse (CIN3+) within 6 months of enrollment or at colposcopy for women with a persistent type-specific HPV infection and the number of screening tests and positive predictive value (PPV) for each screening strategy. All statistical tests were two-sided. RESULTS Compared with screening by cytology alone, double testing with cytology and for type-specific HPV persistence resulted in a 35% (95% confidence interval [CI] = 15% to 60%) increase in sensitivity to detect CIN3+, without a statistically significant reduction in the PPV (relative PPV = 0.76, 95% CI = 0.52 to 1.10), but with more than twice as many screening tests needed. Several strategies that incorporated screening for high-risk HPV subtypes were explored, but they resulted in reduced PPV compared with cytology. Compared with cytology, [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "272", "doc_id": "6561200", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Risk-adjusted mortality rates are similar in teaching and non-teaching hospitals.\n\nCANDIDATE_ABSTRACT:\nTITLE: Involvement of S-nitrosylation of actin in inhibition of neurotransmitter release by nitric oxide\nABSTRACT: BACKGROUND The role of the diffusible messenger nitric oxide (NO) in the regulation of pain transmission is still a debate of matter, pro-nociceptive and/or anti-nociceptive. S-Nitrosylation, the reversible post-translational modification of selective cysteine residues in proteins, has emerged as an important mechanism by which NO acts as a signaling molecule. The occurrence of S-nitrosylation in the spinal cord and its targets that may modulate pain transmission remain unclarified. The \"biotin-switch\" method and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry were employed for identifying S-nitrosylated proteins. RESULTS Here we show that actin was a major protein S-nitrosylated in the spinal cord by the NO donor, S-nitroso-N-acetyl-DL-penicillamine (SNAP). Interestingly, actin was S-nitrosylated, more in the S2 fraction than in the P2 fraction of the spinal homogenate. Treatment of PC12 cells with SNAP caused rapid S-nitrosylation of actin and inhibited dopamine release from the cells. Just like cytochalasin B, which depolymerizes actin, SNAP decreased the amount of filamentous actin cytoskeleton just beneath the membrane. The inhibition of dopamine release was not attenuated by inhibitors of soluble guanylyl cyclase and cGMP-dependent protein kinase. CONCLUSION The present study demonstrates that actin is a major S-nitrosylated protein in the spinal cord and suggests that NO directly regulates neurotransmitter release by S-nitrosylation in addition to the well-known phosphorylation by cGMP-dependent protein kinase.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1055, "doc_id": "2139357", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Nonsteroidal antinflammatory drugs show potential anticancer indications.\n\nCANDIDATE_PASSAGE:\nTraining toddlers seated on mobile robots to drive indoors amidst obstacles The goal of this research is to train children seated on mobile robots to purposefully and safely drive indoors. Our previous studies show that in about six weeks of training, infants can learn to drive directly to a goal using conventional joysticks. However, they are unable to acquire the advanced skill to avoid obstacles while driving. This limits mobility impaired children from exploring their home environment safely, which in turn impacts their cognitive and social developments in the important early years. In this paper, we describe results where toddlers are trained to drive a robot within an obstacle course. Using algorithms based on artificial potential fields to avoid obstacles, we create force field on the joystick that trains them to navigate while avoiding obstacles. In this ‘assist-as-needed’ approach, if the child steers the mobile robot outside a force tunnel centered around the desired direction, the driver experiences a bias force on the hand. The results suggest that force-feedback joystick results in faster learning than with a conventional joystick.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "857", "doc_id": "108886332", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The Snf1 complex regulates carbon and energy metabolism in baker's yeast (Saccharomyces cerevisiae).\n\nCANDIDATE_ABSTRACT:\nTITLE: Murine Dishevelled 3 Functions in Redundant Pathways with Dishevelled 1 and 2 in Normal Cardiac Outflow Tract, Cochlea, and Neural Tube Development\nABSTRACT: Dishevelled (Dvl) proteins are important signaling components of both the canonical beta-catenin/Wnt pathway, which controls cell proliferation and patterning, and the planar cell polarity (PCP) pathway, which coordinates cell polarity within a sheet of cells and also directs convergent extension cell (CE) movements that produce narrowing and elongation of the tissue. Three mammalian Dvl genes have been identified and the developmental roles of Dvl1 and Dvl2 were previously determined. Here, we identify the functions of Dvl3 in development and provide evidence of functional redundancy among the three murine Dvls. Dvl3(-/-) mice died perinatally with cardiac outflow tract abnormalities, including double outlet right ventricle and persistent truncus arteriosis. These mutants also displayed a misorientated stereocilia in the organ of Corti, a phenotype that was enhanced with the additional loss of a single allele of the PCP component Vangl2/Ltap (LtapLp/+). Although neurulation appeared normal in both Dvl3(-/-) and LtapLp/+ mutants, Dvl3(+/-);LtapLp/+ combined mutants displayed incomplete neural tube closure. Importantly, we show that many of the roles of Dvl3 are also shared by Dvl1 and Dvl2. More severe phenotypes were observed in Dvl3 mutants with the deficiency of another Dvl, and increasing Dvl dosage genetically with Dvl transgenes demonstrated the ability of Dvls to compensate for each other to enable normal development. Interestingly, global canonical Wnt signaling appeared largely unaffected in the double Dvl mutants, suggesting that low Dvl levels are sufficient for functional canonical Wnt signals. In summary, we demonstrate that Dvl3 is required for cardiac outflow tract development and describe its importance in the PCP pathway during neurulation a [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1182, "doc_id": "317204", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: 0-dimensional biomaterials lack inductive properties.\n\nCANDIDATE_PASSAGE:\nNew opportunities: the use of nanotechnologies to manipulate and track stem cells. Nanotechnologies are emerging platforms that could be useful in measuring, understanding, and manipulating stem cells. Examples include magnetic nanoparticles and quantum dots for stem cell labeling and in vivo tracking; nanoparticles, carbon nanotubes, and polyplexes for the intracellular delivery of genes/oligonucleotides and protein/peptides; and engineered nanometer-scale scaffolds for stem cell differentiation and transplantation. This review examines the use of nanotechnologies for stem cell tracking, differentiation, and transplantation. We further discuss their utility and the potential concerns regarding their cytotoxicity.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "0", "doc_id": "31715818", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Taking anti-depresents is associated with a decrease in the Aβ level in the brain of experimental animals.\n\nCANDIDATE_PASSAGE:\nNeurite sprouting and synapse deterioration in the aging Caenorhabditis elegans nervous system. Caenorhabditis elegans is a powerful model for analysis of the conserved mechanisms that modulate healthy aging. In the aging nematode nervous system, neuronal death and/or detectable loss of processes are not readily apparent, but because dendrite restructuring and loss of synaptic integrity are hypothesized to contribute to human brain decline and dysfunction, we combined fluorescence microscopy and electron microscopy (EM) to screen at high resolution for nervous system changes. We report two major components of morphological change in the aging C. elegans nervous system: (1) accumulation of novel outgrowths from specific neurons, and (2) physical decline in synaptic integrity. Novel outgrowth phenotypes, including branching from the main dendrite or new growth from somata, appear at a high frequency in some aging neurons, but not all. Mitochondria are often associated with age-associated branch sites. Lowered insulin signaling confers some maintenance of ALM and PLM neuron structural integrity into old age, and both DAF-16/FOXO and heat shock factor transcription factor HSF-1 exert neuroprotective functions. hsf-1 can act cell autonomously in this capacity. EM evaluation in synapse-rich regions reveals a striking decline in synaptic vesicle numbers and a diminution of presynaptic density size. Interestingly, old animals that maintain locomotory prowess exhibit less synaptic decline than same-age decrepit animals, suggesting that synaptic integrity correlates with locomotory healthspan. Our data reveal similarities between the aging C. elegans nervous system and mammalian brain, suggesting conserved neuronal responses to age. Dissection of neuronal aging mechan [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1142", "doc_id": "13072113", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: 1/2000 in UK have abnormal PrP positivity.\n\nCANDIDATE_ABSTRACT:\nTITLE: Prevalent abnormal prion protein in human appendixes after bovine spongiform encephalopathy epizootic: large scale survey\nABSTRACT: OBJECTIVES To carry out a further survey of archived appendix samples to understand better the differences between existing estimates of the prevalence of subclinical infection with prions after the bovine spongiform encephalopathy epizootic and to see whether a broader birth cohort was affected, and to understand better the implications for the management of blood and blood products and for the handling of surgical instruments. DESIGN Irreversibly unlinked and anonymised large scale survey of archived appendix samples. SETTING Archived appendix samples from the pathology departments of 41 UK hospitals participating in the earlier survey, and additional hospitals in regions with lower levels of participation in that survey. SAMPLE 32,441 archived appendix samples fixed in formalin and embedded in paraffin and tested for the presence of abnormal prion protein (PrP). RESULTS Of the 32,441 appendix samples 16 were positive for abnormal PrP, indicating an overall prevalence of 493 per million population (95% confidence interval 282 to 801 per million). The prevalence in those born in 1941-60 (733 per million, 269 to 1596 per million) did not differ significantly from those born between 1961 and 1985 (412 per million, 198 to 758 per million) and was similar in both sexes and across the three broad geographical areas sampled. Genetic testing of the positive specimens for the genotype at PRNP codon 129 revealed a high proportion that were valine homozygous compared with the frequency in the normal population, and in stark contrast with confirmed clinical cases of vCJD, all of which were methionine homozygous at PRNP codon 129. CONCLUSIONS This study corroborates previous studies and suggests a high prevalence of infection with abnormal PrP, indicating vCJD carrier [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"RESULTS Of the 32,441 appendix samples 16 were positive for abnormal PrP, indicating an overall prevalence of 493 per million population (95% confidence interval 282 to 801 per million).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 5, "doc_id": "13734012", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Cell autonomous sex determination in somatic cells does not occur in Galliformes.\n\nCANDIDATE_PASSAGE:\nPEP-FOLD: an updated de novo structure prediction server for both linear and disulfide bonded cyclic peptides In the context of the renewed interest of peptides as therapeutics, it is important to have an on-line resource for 3D structure prediction of peptides with well-defined structures in aqueous solution. We present an updated version of PEP-FOLD allowing the treatment of both linear and disulphide bonded cyclic peptides with 9-36 amino acids. The server makes possible to define disulphide bonds and any residue-residue proximity under the guidance of the biologists. Using a benchmark of 34 cyclic peptides with one, two and three disulphide bonds, the best PEP-FOLD models deviate by an average RMS of 2.75 Å from the full NMR structures. Using a benchmark of 37 linear peptides, PEP-FOLD locates lowest-energy conformations deviating by 3 Å RMS from the NMR rigid cores. The evolution of PEP-FOLD comes as a new on-line service to supersede the previous server. The server is available at: http://bioserv.rpbs.univ-paris-diderot.fr/PEP-FOLD.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "233", "doc_id": "6974477", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nCANDIDATE_ABSTRACT:\nTITLE: The tumor necrosis factor family receptors RANK and CD40 cooperatively establish the thymic medullary microenvironment and self-tolerance.\nABSTRACT: Medullary thymic epithelial cells (mTECs) establish T cell self-tolerance through the expression of autoimmune regulator (Aire) and peripheral tissue-specific self-antigens. However, signals underlying mTEC development remain largely unclear. Here, we demonstrate crucial regulation of mTEC development by receptor activator of NF-kappaB (RANK) and CD40 signals. Whereas only RANK signaling was essential for mTEC development during embryogenesis, in postnatal mice, cooperation between CD40 and RANK signals was required for mTEC development to successfully establish the medullary microenvironment. Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner. These results show that developmental-stage-dependent cooperation between RANK and CD40 promotes mTEC development, thereby establishing self-tolerance.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Ligation of RANK or CD40 on fetal thymic stroma in vitro induced mTEC development in a tumor necrosis factor-associated factor 6 (TRAF6)-, NF-kappaB inducing kinase (NIK)-, and IkappaB kinase beta (IKKbeta)-dependent manner.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1181, "doc_id": "2734421", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Crossover hot spots are found within gene promoters in Saccharomyces cerevisiae.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mapping Meiotic Single-Strand DNA Reveals a New Landscape of DNA Double-Strand Breaks in Saccharomyces cerevisiae\nABSTRACT: DNA double-strand breaks (DSBs), which are formed by the Spo11 protein, initiate meiotic recombination. Previous DSB-mapping studies have used rad50S or sae2Δ mutants, which are defective in break processing, to accumulate Spo11-linked DSBs, and report large (≥ 50 kb) “DSB-hot” regions that are separated by “DSB-cold” domains of similar size. Substantial recombination occurs in some DSB-cold regions, suggesting that DSB patterns are not normal in rad50S or sae2Δ mutants. We therefore developed a novel method to map genome-wide, single-strand DNA (ssDNA)–associated DSBs that accumulate in processing-capable, repair-defective dmc1Δ and dmc1Δ rad51Δ mutants. DSBs were observed at known hot spots, but also in most previously identified “DSB-cold” regions, including near centromeres and telomeres. Although approximately 40% of the genome is DSB-cold in rad50S mutants, analysis of meiotic ssDNA from dmc1Δ shows that most of these regions have substantial DSB activity. Southern blot assays of DSBs in selected regions in dmc1Δ, rad50S, and wild-type cells confirm these findings. Thus, DSBs are distributed much more uniformly than was previously believed. Comparisons of DSB signals in dmc1, dmc1 rad51, and dmc1 spo11 mutant strains identify Dmc1 as a critical strand-exchange activity genome-wide, and confirm previous conclusions that Spo11-induced lesions initiate all meiotic recombination.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 293, "doc_id": "10874408", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is fertility altered in young adults born small for gestational age?\n\nABSTRACT:\nThe intrauterine environment may have a lifelong impact on individuals' health. However, results on the relationship between birth size and gonadal function are conflicting, and it remains unknown whether reproductive function is altered in adults born small for gestational age (SGA). The aim of the present study was to compare the fertility of young adults from the general population, born either SGA or appropriate for gestational age (AGA). There were 579 adults born SGA (birthweight under the 10th percentile) who were compared with 703 subjects of the same age (age 29.4 +/- 4.1 years) born AGA (birthweight between 25th and 75th percentiles). They fulfilled a questionnaire focusing on the first attempt to give birth, to have a measure of the time to pregnancy and an estimation of the fecundability (the monthly pregnancy probability), two relevant indicators of fertility at the couple level. Ratios of fecundability between AGA and SGA subjects were adjusted for known fertility factors (age, smoking, reproductive history) and for socioeconomic status. Time to pregnancy was comparable in the two groups: 5.7 +/- 8.0 versus 6.6 +/- 10.5 months in AGA and SGA, respectively (P = 0.31), in women and 5.1 +/- 7 versus 6.0 +/- 9 months in AGA and SGA, respectively, in men (P = 0.53). The adjusted ratios of fecundability comparing SGA to AGA subjects were not significant: HR = 0.91 [0.68;1.21] (P = 0.5) in women and HR = 0.95 [0.67;1.74] (P = 0.82) in men.", "output": "{\"label\": \"no\", \"rationale\": \"When studied in young adults from the general population, fertility is not reduced in those born SGA.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 20659911, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Vaccinating the gastrointestinal tract induces protection of rectal and vaginal mucosa.\n\nCANDIDATE_ABSTRACT:\nTITLE: Large intestine-targeted nanoparticle-releasing oral vaccine to control genitorectal viral infection\nABSTRACT: Both rectal and vaginal mucosal surfaces serve as transmission routes for pathogenic microorganisms. Vaccination through large intestinal mucosa, previously proven protective for both of these mucosal sites in animal studies, can be achieved successfully by direct intracolorectal (i.c.r.) administration, but this route is clinically impractical. Oral vaccine delivery seems preferable but runs the risk of the vaccine's destruction in the upper gastrointestinal tract. Therefore, we designed a large intestine-targeted oral delivery with pH-dependent microparticles containing vaccine nanoparticles, which induced colorectal immunity in mice comparably to colorectal vaccination and protected against rectal and vaginal viral challenge. Conversely, vaccine targeted to the small intestine induced only small intestinal immunity and provided no rectal or vaginal protection, demonstrating functional compartmentalization within the gut mucosal immune system. Therefore, using this oral vaccine delivery system to target the large intestine, but not the small intestine, may represent a feasible new strategy for immune protection of rectal and vaginal mucosa.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Therefore, using this oral vaccine delivery system to target the large intestine, but not the small intestine, may represent a feasible new strategy for immune protection of rectal and vaginal mucosa.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1356, "doc_id": "13764090", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Amitriptyline is an effective treatment for chronic tension-type headaches.\n\nCANDIDATE_PASSAGE:\nMulberry leaves (Morus alba L.) ameliorate obesity-induced hepatic lipogenesis, fibrosis, and oxidative stress in high-fat diet-fed mice Obesity is associated with chronic diseases such as fatty liver, type 2 diabetes, cardiovascular disease, and severe metabolic syndrome. Obesity causes metabolic impairment including excessive lipid accumulation and fibrosis in the hepatic tissue as well as the increase in oxidative stress. In order to investigate the effect of mulberry leaf (Morus alba L.) extract (MLE) on obesity-induced oxidative stress, lipogenesis, and fibrosis in liver, MLE has been gavaged for 12 weeks in high-fat diet (HFD)-induced obese mice. MLE treatment significantly ameliorated LXRα-mediated lipogenesis and hepatic fibrosis markers such as α-smooth muscle actin, while MLE up-regulated lipolysis-associated markers such as lipoprotein lipase in the HFD-fed mice. Moreover, MLE normalized the activities of antioxidant enzymes including heme oxygenase-1 and glutathione peroxidase in accordance with protein levels of 4-hydroxynonenal in the HFD-fed mice. MLE has beneficial effects on obesity-related fatty liver disease by regulation of hepatic lipid metabolism, fibrosis, and antioxidant defense system. MLE supplementation might be a potential therapeutic approach for obesity-related disease including non-alcoholic fatty liver disease.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "108", "doc_id": "4680262", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Antimicrobial agents are more effective due to the pressure of antimicrobial usage.\n\nCANDIDATE_PASSAGE:\nResistance to antimicrobials in humans and animals. Overusing antibiotics is not the only cause and reducing use is not the only solution W arning signs of antimicrobial resistance, chinks in the antimicrobial armour, began to appear in the middle of the last century, and by the 1990s various reports had signalled the dangers of excessive or inappropriate use of antibiotics in clinical medicine and of the use of antibiotics in animal feed as growth promoters.1–3 Overuse of antimicrobials emerged as the main culprit, and reducing their use was seen as the answer. But it may not be that simple. The idea that reducing antibiotic use would redress the problem formed part of a positive response on the part of the United Kingdom government to the House of Lords report,1 including a public information campaign, surveillance of resistance along the food chain, targets with respect to hospital acquired infections, and setting up of an overarching advisory body on all aspects of antibiotic use. However, the concept of overuse has proved too simplistic, for, although the evidence of overprescribing as the …", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "122", "doc_id": "31460499", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: R2D2 stops miRNA production by increasing the selectivity of Dcr2 for long dsRNA.\n\nCANDIDATE_ABSTRACT:\nTITLE: Phosphate and R2D2 restrict the substrate specificity of Dicer-2, an ATP-driven ribonuclease.\nABSTRACT: Drosophila Dicer-2 generates small interfering RNAs (siRNAs) from long double-stranded RNA (dsRNA), whereas Dicer-1 produces microRNAs (miRNAs) from pre-miRNA. What makes the two Dicers specific for their biological substrates? We find that purified Dicer-2 can efficiently cleave pre-miRNA, but that inorganic phosphate and the Dicer-2 partner protein R2D2 inhibit pre-miRNA cleavage. Dicer-2 contains C-terminal RNase III domains that mediate RNA cleavage and an N-terminal helicase motif, whose function is unclear. We show that Dicer-2 is a dsRNA-stimulated ATPase that hydrolyzes ATP to ADP; ATP hydrolysis is required for Dicer-2 to process long dsRNA, but not pre-miRNA. Wild-type Dicer-2, but not a mutant defective in ATP hydrolysis, can generate siRNAs faster than it can dissociate from a long dsRNA substrate. We propose that the Dicer-2 helicase domain uses ATP to generate many siRNAs from a single molecule of dsRNA before dissociating from its substrate.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1001, "doc_id": "5702790", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Inhibiting focal adhesion formation increases the rate at which cells convert mechanical strain into inflammation and fibrosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Focal adhesion kinase links mechanical force to skin fibrosis via inflammatory signaling\nABSTRACT: Exuberant fibroproliferation is a common complication after injury for reasons that are not well understood. One key component of wound repair that is often overlooked is mechanical force, which regulates cell-matrix interactions through intracellular focal adhesion components, including focal adhesion kinase (FAK). Here we report that FAK is activated after cutaneous injury and that this process is potentiated by mechanical loading. Fibroblast-specific FAK knockout mice have substantially less inflammation and fibrosis than control mice in a model of hypertrophic scar formation. We show that FAK acts through extracellular-related kinase (ERK) to mechanically trigger the secretion of monocyte chemoattractant protein-1 (MCP-1, also known as CCL2), a potent chemokine that is linked to human fibrotic disorders. Similarly, MCP-1 knockout mice form minimal scars, indicating that inflammatory chemokine pathways are a major mechanism by which FAK mechanotransduction induces fibrosis. Small-molecule inhibition of FAK blocks these effects in human cells and reduces scar formation in vivo through attenuated MCP-1 signaling and inflammatory cell recruitment. These findings collectively indicate that physical force regulates fibrosis through inflammatory FAK–ERK–MCP-1 pathways and that molecular strategies targeting FAK can effectively uncouple mechanical force from pathologic scar formation.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Fibroblast-specific FAK knockout mice have substantially less inflammation and fibrosis than control mice in a model of hypertrophic scar formation.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 633, "doc_id": "5172048", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: AIRE is expressed in some skin tumors.\n\nCANDIDATE_PASSAGE:\n[New guidelines to evaluate the response to treatment in solid tumors]. Anticancer agents go through a process by which their antitumor activity, on the basis of the amount of tumor shrinkage they could generate, has been investigated. In the late 1970s, the International Union Against Cancer and the World Health Organization (WHO) introduced specific criteria for the codification of tumor response evaluation. In 1994, several organizations involved in clinical cancer research joined together to undertake the review of these response evaluation criteria on the basis of their experience and knowledge. After several years of intensive discussions, new guidelines are ready and will replace the previous WHO criteria. In parallel to this initiative, one of the participating groups developed a model by which response rates could be derived from unidimensional measurement of tumor lesions instead of the usual bidimensional approach. This new concept has been largely validated by the Response Evaluation Criteria in Solid Tumors (Recist) Group and integrated into the present guidelines. This special article provides some philosophic background to clarify the various purposes of response evaluation. It proposes a model by which a combined assessment of all existing lesions, characterized by target lesion (to be measured) and nontarget lesions, is used to extrapolate an overall response to treatment. Methods of assessing tumor lesions are better codified. All other aspects of response evaluation have been discussed, reviewed, and amended whenever suitable.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "50", "doc_id": "15541119", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Trans-acting factors, such as lncRNAs, influence mRNA translation.\n\nCANDIDATE_PASSAGE:\nLincRNA-p21 suppresses target mRNA translation. Mammalian long intergenic noncoding RNAs (lincRNAs) are best known for modulating transcription. Here we report a posttranscriptional function for lincRNA-p21 as a modulator of translation. Association of the RNA-binding protein HuR with lincRNA-p21 favored the recruitment of let-7/Ago2 to lincRNA-p21, leading to lower lincRNA-p21 stability. Under reduced HuR levels, lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and β-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1311", "doc_id": "13763195", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: BRCA 1 mutation carriers' risk of breast and ovarian cancer depends on where the mutation is located.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association of type and location of BRCA1 and BRCA2 mutations with risk of breast and ovarian cancer.\nABSTRACT: IMPORTANCE Limited information about the relationship between specific mutations in BRCA1 or BRCA2 (BRCA1/2) and cancer risk exists. OBJECTIVE To identify mutation-specific cancer risks for carriers of BRCA1/2. DESIGN, SETTING, AND PARTICIPANTS Observational study of women who were ascertained between 1937 and 2011 (median, 1999) and found to carry disease-associated BRCA1 or BRCA2 mutations. The international sample comprised 19,581 carriers of BRCA1 mutations and 11,900 carriers of BRCA2 mutations from 55 centers in 33 countries on 6 continents. We estimated hazard ratios for breast and ovarian cancer based on mutation type, function, and nucleotide position. We also estimated RHR, the ratio of breast vs ovarian cancer hazard ratios. A value of RHR greater than 1 indicated elevated breast cancer risk; a value of RHR less than 1 indicated elevated ovarian cancer risk. EXPOSURES Mutations of BRCA1 or BRCA2. MAIN OUTCOMES AND MEASURES Breast and ovarian cancer risks. RESULTS Among BRCA1 mutation carriers, 9052 women (46%) were diagnosed with breast cancer, 2317 (12%) with ovarian cancer, 1041 (5%) with breast and ovarian cancer, and 7171 (37%) without cancer. Among BRCA2 mutation carriers, 6180 women (52%) were diagnosed with breast cancer, 682 (6%) with ovarian cancer, 272 (2%) with breast and ovarian cancer, and 4766 (40%) without cancer. In BRCA1, we identified 3 breast cancer cluster regions (BCCRs) located at c.179 to c.505 (BCCR1; RHR = 1.46; 95% CI, 1.22-1.74; P = 2 × 10(-6)), c.4328 to c.4945 (BCCR2; RHR = 1.34; 95% CI, 1.01-1.78; P = .04), and c. 5261 to c.5563 (BCCR2', RHR = 1.38; 95% CI, 1.22-1.55; P = 6 × 10(-9)). We also identified an ovarian cancer cluster region (OCCR) from c.1380 to c.4062 (approximately exon 11) with RHR = 0.62 (95% CI, 0.56- [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS AND RELEVANCE Breast and ovarian cancer risks varied by type and location of BRCA1/2 mutations.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 159, "doc_id": "9394119", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Birth-weight is positively associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Intrauterine factors and risk of breast cancer: a systematic review and meta-analysis of current evidence.\nABSTRACT: BACKGROUND Emerging evidence suggests an association between female prenatal experience and her subsequent risk of developing breast cancer. Potential underlying mechanisms include variation in amounts of maternal endogenous sex hormones and growth hormones, germ-cell mutations, formation of cancer stem-cells, and other genetic or epigenetic events. We reviewed and summarised quantitatively the available data on intrauterine exposures and risk of breast cancer. METHODS We systematically searched for studies that assessed association between perinatal factors and risk of breast cancer. We reviewed separately each of the perinatal factors, including birthweight, birth length, parental age at delivery, gestational age, intrauterine exposure to diethylstilbestrol, twin membership, maternal pre-eclampsia or eclampsia, and other factors. FINDINGS We identified 57 studies published between Oct 1, 1980, and June 21, 2007. Increased risk of breast cancer was noted with increased birthweight (relative risk [RR] 1.15 [95% CI 1.09-1.21]), birth length (1.28 [1.11-1.48]), higher maternal age (1.13 [1.02-1.25]), and paternal age (1.12 [1.05-1.19]). Decreased risk of breast cancer was noted for maternal pre-eclampsia and eclampsia (0.48 [0.30-0.78]) and twin membership (0.93 [0.87-1.00]). No association was noted between risk of breast cancer and gestational age at birth (0.95 [0.71-1.26]) or maternal diethylstilbestrol treatment (1.40 [0.86-2.28]). INTERPRETATION The intrauterine environment contributes to the predisposition of women to breast cancer in adulthood. The in-utero mechanisms responsible for such predisposition need to be elucidated.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Increased risk of breast cancer was noted with increased birthweight (relative risk [RR] 1.15 [95% CI 1.09-1.21]), birth length (1.28 [1.11-1.48]), higher maternal age (1.13 [1.02-1.25]), and paternal age (1.12 [1.05-1.19]).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 179, "doc_id": "23557241", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Modifying the epigenome in the brain affects the normal human aging process by affecting certain genes related to neurogenesis.\n\nCANDIDATE_PASSAGE:\nEmerging functional cross-talk between the Keap1-Nrf2 system and mitochondria Nuclear factor erythroid-derived 2-related factor 2 (Nrf2) was originally identified as a positive regulator of drug detoxifying enzyme gene expression during exposure to environmental electrophiles. Currently, Nrf2 is known to regulate the expression of hundreds of cytoprotective genes to counteract endogenously or exogenously generated oxidative stress. Furthermore, when activated in human tumors by somatic mutations, Nrf2 confers growth advantages and chemoresistance by regulating genes involved in various processes such as the pentose phosphate pathway and nucleotide synthesis in addition to antioxidant proteins. Interestingly, increasing evidence shows that Nrf2 is associated with mitochondrial biogenesis during environmental stresses in certain tissues such as the heart. Furthermore, SKN-1, a functional homolog of Nrf2 in C. elegans, is activated by mitochondrial reactive oxygen species and extends life span by promoting mitochondrial homeostasis (i.e., mitohormesis). Similarly, Nrf2 activation was recently observed in the heart of surfeit locus protein 1 (Surf1) -/- mice in which cellular respiration was decreased due to cytochrome c oxidase defects. In this review, we critically examine the relationship between Nrf2 and mitochondria and argue that the Nrf2 stress pathway intimately communicates with mitochondria to maintain cellular homeostasis during oxidative stress.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "800", "doc_id": "6259170", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: IFIT1 restricts viral replication by sequestrating mis-capped viral RNAs.\n\nCANDIDATE_PASSAGE:\nNeutrophilic infiltration within the airway smooth muscle in patients with COPD. BACKGROUND COPD is an inflammatory disorder characterised by chronic airflow limitation, but the extent to which airway inflammation is related to functional abnormalities is still uncertain. The interaction between inflammatory cells and airway smooth muscle may have a crucial role. METHODS To investigate the microlocalisation of inflammatory cells within the airway smooth muscle in COPD, surgical specimens obtained from 26 subjects undergoing thoracotomy (eight smokers with COPD, 10 smokers with normal lung function, and eight non-smoking controls) were examined. Immunohistochemical analysis was used to quantify the number of neutrophils, macrophages, mast cells, CD4+ and CD8+ cells localised within the smooth muscle of peripheral airways. RESULTS Smokers with COPD had an increased number of neutrophils and CD8+ cells in the airway smooth muscle compared with non-smokers. Smokers with normal lung function also had a neutrophilic infiltration in the airway smooth muscle, but to a lesser extent. When all the subjects were analysed as one group, neutrophilic infiltration was inversely related to forced expiratory volume in 1 second (% predicted). CONCLUSIONS Microlocalisation of neutrophils and CD8+ cells in the airway smooth muscle in smokers with COPD suggests a possible role for these cells in the pathogenesis of smoking induced airflow limitation.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "544", "doc_id": "6417632", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Smc5/6 engagment drives the activation of SUMO E3 ligase Mms21 by ATP-dependent remolding.\n\nCANDIDATE_PASSAGE:\nATPase-Dependent Control of the Mms21 SUMO Ligase during DNA Repair Modification of proteins by SUMO is essential for the maintenance of genome integrity. During DNA replication, the Mms21-branch of the SUMO pathway counteracts recombination intermediates at damaged replication forks, thus facilitating sister chromatid disjunction. The Mms21 SUMO ligase docks to the arm region of the Smc5 protein in the Smc5/6 complex; together, they cooperate during recombinational DNA repair. Yet how the activity of the SUMO ligase is controlled remains unknown. Here we show that the SUMO ligase and the chromosome disjunction functions of Mms21 depend on its docking to an intact and active Smc5/6 complex, indicating that the Smc5/6-Mms21 complex operates as a large SUMO ligase in vivo. In spite of the physical distance separating the E3 and the nucleotide-binding domains in Smc5/6, Mms21-dependent sumoylation requires binding of ATP to Smc5, a step that is part of the ligase mechanism that assists Ubc9 function. The communication is enabled by the presence of a conserved disruption in the coiled coil domain of Smc5, pointing to potential conformational changes for SUMO ligase activation. In accordance, scanning force microscopy of the Smc5-Mms21 heterodimer shows that the molecule is physically remodeled in an ATP-dependent manner. Our results demonstrate that the ATP-binding activity of the Smc5/6 complex is coordinated with its SUMO ligase, through the coiled coil domain of Smc5 and the physical remodeling of the molecule, to promote sumoylation and chromosome disjunction during DNA repair.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1089", "doc_id": "17628888", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Diabetic patients with acute coronary syndrome experience increased short-term and long-term risk for bleeding events.\n\nCANDIDATE_PASSAGE:\nImpact of diabetes on long-term prognosis in patients with unstable angina and non-Q-wave myocardial infarction: results of the OASIS (Organization to Assess Strategies for Ischemic Syndromes) Registry. BACKGROUND Although unstable coronary artery disease is the most common reason for admission to a coronary care unit, the long-term prognosis of patients with this diagnosis is unknown. This is particularly true for patients with diabetes mellitus, who are known to have a high morbidity and mortality after an acute myocardial infarction. METHODS AND RESULTS Prospectively collected data from 6 different countries in the Organization to Assess Strategies for Ischemic Syndromes (OASIS) registry were analyzed to determine the 2-year prognosis of diabetic and nondiabetic patients who were hospitalized with unstable angina or non-Q-wave myocardial infarction. Overall, 1718 of 8013 registry patients (21%) had diabetes. Diabetic patients had a higher rate of coronary bypass surgery than nondiabetic patients (23% versus 20%, P:<0.001) but had similar rates of catheterization and angioplasty. Diabetes independently predicted mortality (relative risk [RR], 1.57; 95% CI, 1.38 to 1.81; P:<0.001), as well as cardiovascular death, new myocardial infarction, stroke, and new congestive heart failure. Moreover, compared with their nondiabetic counterparts, women had a significantly higher risk than men (RR, 1.98; 95% CI, 1.60 to 2.44; and RR, 1.28; 95% CI, 1.06 to 1.56, respectively). Interestingly, diabetic patients without prior cardiovascular disease had the same event rates for all outcomes as nondiabetic patients with previous vascular disease. CONCLUSIONS Hospitalization for unstable angina or non-Q-wave myocardial infarction predicts a high 2-year morbidity and mortalit [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "343", "doc_id": "5884524", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The innate immune response struggles to remove small numbers of parasites.\n\nCANDIDATE_ABSTRACT:\nTITLE: Partitioning regulatory mechanisms of within-host malaria dynamics using the effective propagation number.\nABSTRACT: Immune clearance and resource limitation (via red blood cell depletion) shape the peaks and troughs of malaria parasitemia, which in turn affect disease severity and transmission. Quantitatively partitioning the relative roles of these effects through time is challenging. Using data from rodent malaria, we estimated the effective propagation number, which reflects the relative importance of contrasting within-host control mechanisms through time and is sensitive to the inoculating parasite dose. Our analysis showed that the capacity of innate responses to restrict initial parasite growth saturates with parasite dose and that experimentally enhanced innate immunity can affect parasite density indirectly via resource depletion. Such a statistical approach offers a tool to improve targeting of drugs or vaccines for human therapy by revealing the dynamics and interactions of within-host regulatory mechanisms.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Our analysis showed that the capacity of innate responses to restrict initial parasite growth saturates with parasite dose and that experimentally enhanced innate immunity can affect parasite density indirectly via resource depletion.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1223, "doc_id": "5289038", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Rank Signaling Links the Development of Invariant γδ T Cell Progenitors and Aire+ Medullary Epithelium\nABSTRACT: The thymic medulla provides a specialized microenvironment for the negative selection of T cells, with the presence of autoimmune regulator (Aire)-expressing medullary thymic epithelial cells (mTECs) during the embryonic-neonatal period being both necessary and sufficient to establish long-lasting tolerance. Here we showed that emergence of the first cohorts of Aire(+) mTECs at this key developmental stage, prior to αβ T cell repertoire selection, was jointly directed by Rankl(+) lymphoid tissue inducer cells and invariant Vγ5(+) dendritic epidermal T cell (DETC) progenitors that are the first thymocytes to express the products of gene rearrangement. In turn, generation of Aire(+) mTECs then fostered Skint-1-dependent, but Aire-independent, DETC progenitor maturation and the emergence of an invariant DETC repertoire. Hence, our data attributed a functional importance to the temporal development of Vγ5(+) γδ T cells during thymus medulla formation for αβ T cell tolerance induction and demonstrated a Rank-mediated reciprocal link between DETC and Aire(+) mTEC maturation.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Hence, our data attributed a functional importance to the temporal development of Vγ5(+) γδ T cells during thymus medulla formation for αβ T cell tolerance induction and demonstrated a Rank-mediated reciprocal link between DETC and Aire(+) mTEC maturation.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1004, "doc_id": "301838", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Oxidative DNA damage activates STING signalling.\n\nCANDIDATE_ABSTRACT:\nTITLE: Atm-deficient mice exhibit increased sensitivity to dextran sulfate sodium-induced colitis characterized by elevated DNA damage and persistent immune activation.\nABSTRACT: The role of ataxia telangiectasia mutated (ATM), a DNA double-strand break recognition and response protein, in inflammation and inflammatory diseases is unclear. We have previously shown that high levels of systemic DNA damage are induced by intestinal inflammation in wild-type mice. To determine the effect of Atm deficiency in inflammation, we induced experimental colitis in Atm(-/-), Atm(+/-), and wild-type mice via dextran sulfate sodium (DSS) administration. Atm(-/-) mice had higher disease activity indices and rates of mortality compared with heterozygous and wild-type mice. Systemic DNA damage and immune response were characterized in peripheral blood throughout and after three cycles of treatment. Atm(-/-) mice showed increased sensitivity to levels of DNA strand breaks in peripheral leukocytes, as well as micronucleus formation in erythroblasts, compared with heterozygous and wild-type mice, especially during remission periods and after the end of treatment. Markers of reactive oxygen and nitrogen species-mediated damage, including 8-oxoguanine and nitrotyrosine, were present both in the distal colon and in peripheral leukocytes, with Atm(-/-) mice manifesting more 8-oxoguanine formation than wild-type mice. Atm(-/-) mice showed greater upregulation of inflammatory cytokines and significantly higher percentages of activated CD69+ and CD44+ T cells in the peripheral blood throughout treatment. ATM, therefore, may be a critical immunoregulatory factor dampening the deleterious effects of chronic DSS-induced inflammation, necessary for systemic genomic stability and homeostasis of the gut epithelial barrier.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 898, "doc_id": "5572127", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: RANK-RANKL pathway signalling has no known association with development of Aire-expressing medullary thymic epithelial cells.\n\nCANDIDATE_PASSAGE:\nA European perspective on population studies of dementia. The change in the world's age demographics and the predicted rise in the incidence of age-related diseases, including dementia, is a source of major public health concern. Major research effort in both the United States and Europe has been targeted toward understanding the pathogenesis and epidemiology of dementia. This article presents a general overview of the history of dementia research in Europe and how it compares with that in the United States. The review highlights the common issues which both U.S. and European researchers have identified and attempted to tackle. To maximize information gained from studies across the world, better harmonization of methodology is needed, as informed from current research practice.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1004", "doc_id": "45457778", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Vitamin D deficiency effects birth weight.\n\nCANDIDATE_PASSAGE:\nActivation of AMPKα2 in adipocytes is essential for nicotine-induced insulin resistance in vivo Cigarette smoking promotes body weight reduction in humans while paradoxically also promoting insulin resistance (IR) and hyperinsulinemia. However, the mechanisms behind these effects are unclear. Here we show that nicotine, a major constituent of cigarette smoke, selectively activates AMP-activated protein kinase α2 (AMPKα2) in adipocytes, which in turn phosphorylates MAP kinase phosphatase-1 (MKP1) at serine 334, initiating its proteasome-dependent degradation. The nicotine-dependent reduction of MKP1 induces the aberrant activation of both p38 mitogen-activated protein kinase and c-Jun N-terminal kinase, leading to increased phosphorylation of insulin receptor substrate 1 (IRS1) at serine 307. Phosphorylation of IRS1 leads to its degradation, protein kinase B inhibition, and the loss of insulin-mediated inhibition of lipolysis. Consequently, nicotine increases lipolysis, which results in body weight reduction, but this increase also elevates the levels of circulating free fatty acids and thus causes IR in insulin-sensitive tissues. These results establish AMPKα2 as an essential mediator of nicotine-induced whole-body IR in spite of reductions in adiposity.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1367", "doc_id": "32408470", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Gluten tolerance in adult patients with celiac disease 20 years after diagnosis?\n\nABSTRACT:\nCeliac disease (CD) is believed to be a permanent intolerance to gluten. A number of patients, however, discontinue the gluten-free diet (GFD) without developing symptoms or signs. The aim of our study was to investigate whether CD patients are capable of developing tolerance to gluten. All 77 adult patients from our hospital known to have biopsy-proven CD for more than 10 years were invited to participate. We investigated symptoms, gluten consumption, antibodies for CD and other autoimmunity, human leukocyte antigen (HLA)-typing, bone mineral density, and performed small bowel biopsies. Tolerance was defined as no immunological or histological signs of CD while consuming gluten. Sixty-six patients accepted participation, but after review of the diagnostic biopsies 53 were found to have true CD. Twenty-three percent of patients had a gluten-containing diet, 15% admitted gluten transgression and 62% followed the GFD. Patients on a GFD had significantly more osteoporosis. Normal small bowel mucosa was found in four of eight on gluten-containing diet and in four of four with gluten transgression. Two patients were considered to have developed tolerance to gluten. One of them was HLA-DQ2/DQ8 negative.", "output": "{\"label\": \"maybe\", \"rationale\": \"Development of tolerance to gluten seems possible in some patients with CD. Further follow-up will show whether this tolerance is permanent or only a long-term return to latency. This feature may be associated with genetic characteristics, especially with HLA genotypes that differ from DQ2 or DQ8.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 18403944, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Primary cervical cytology screening with HPV detection has higher longitudinal sensitivity to detect severe cervical intraepithelial neoplasia than conventional cytology.\n\nCANDIDATE_ABSTRACT:\nTITLE: Rate of cervical cancer, severe intraepithelial neoplasia, and adenocarcinoma in situ in primary HPV DNA screening with cytology triage: randomised study within organised screening programme.\nABSTRACT: OBJECTIVE To assess the performance and impact of primary human papillomavirus (HPV) DNA screening with cytology triage compared with conventional cytology on cervical cancer and severe pre-cancerous lesions. DESIGN Randomised trial. SETTING Population based screening programme for cervical cancer in southern Finland in 2003-5. PARTICIPANTS 58 076 women, aged 30-60, invited to the routine population based screening programme for cervical cancer. INTERVENTIONS Primary HPV DNA test (hybrid capture II) with cytology triage if the result was positive or conventional cytological screening (reference). MAIN OUTCOME MEASURES Rate of cervical cancer, cervical intraepithelial neoplasia (CIN) grade III, and adenocarcinoma in situ (as a composite outcome referred to as CIN III+) during 2003-7 through record linkage between files from the screening registry and the national cancer registry. RESULTS In the HPV and conventional arms there were 95 600 and 95 700 woman years of follow-up and 76 and 53 cases of CIN III+, respectively (of which six and eight were cervical cancers). The relative rate of CIN III+ in the HPV arm versus the conventional arm was 1.44 (95% confidence interval 1.01 to 2.05) among all women invited for screening and 1.77 (1.16 to 2.74) among those who attended. Among women with a normal or negative test result, the relative rate of subsequent CIN III+ was 0.28 (0.04 to 1.17). The rate of cervical cancer between arms was 0.75 (0.25 to 2.16) among women invited for screening and 1.98 (0.52 to 9.38) among those who attended. CONCLUSIONS When incorporated into a well established organised screening programme, primary HPV screening with cytology triage was more sensitive than conventional cytology in detecting CIN III+ lesions. The number of cases of cerv [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The relative rate of CIN III+ in the HPV arm versus the conventional arm was 1.44 (95% confidence interval 1.01 to 2.05) among all women invited for screening and 1.77 (1.16 to 2.74) among those who attended.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 973, "doc_id": "27446873", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does timing of initial surfactant treatment make a difference in rates of chronic lung disease or mortality in premature infants?\n\nABSTRACT:\nTo compare two treatment strategies in preterm infants with or at risk of respiratory distress syndrome: early surfactant administration (within one hour of birth) versus late surfactant administration, in a geographically defined population. The primary outcome was chronic lung disease (CLD) and mortality before/at 36 weeks. Secondary outcomes included: duration of mechanical ventilation and continuous positive airway pressure (CPAP), post-natal steroids for CLD and major neonatal morbidities. Premature infants born at 22-32 weeks' gestation between January 2006 and December 2009. Ten neonatal intensive care units (NICUs) in New South Wales (NSW) and Australian Capital Territory (ACT), Australia. Retrospective analysis of prospectively collected data from the regional NICU database in NSW and ACT. Of the 2170 infants who received surfactant, 1182 (54.5%) and 988 (45.5%) received early and late surfactant, respectively. The early surfactant group was less mature (27.1 ± 2.1 versus 29.4 ± 2.1 weeks) and had more CLD and mortality (40.2% versus 20.0%). The multivariable analysis showed early surfactant to be associated with less duration of ventilation, longer duration of CPAP and longer hospital stay but had little or no impact on CLD/mortality.", "output": "{\"label\": \"maybe\", \"rationale\": \"Early surfactant administration is associated with shorter duration of ventilation but does not appear to be significantly protective against CLD/mortality among premature infants. This may support the growing evidence for consideration of CPAP as an alternative to routine intubation and early surfactant administration. Further investigation from large randomized clinical trials is warranted to confirm these results.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 25394614, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Mice without IFN-γ or its receptor are highly susceptible to EAM induced with α-MyHC/CFA.\n\nCANDIDATE_ABSTRACT:\nTITLE: the Development of Autoimmune Myocarditis in Mice by an\nABSTRACT: BACKGROUND Interleukin (IL)-12 exerts a potent proinflammatory effect by stimulating T-helper (Th) 1 responses. This effect is believed to be mediated primarily through the activation of STAT4 and subsequent production of interferon (IFN)-gamma. Methods and Results- We examined the role of IL-12 receptor (IL-12R) signaling in the development of murine experimental autoimmune myocarditis (EAM) induced by cardiac myosin immunization. Both IL-12Rbeta1-deficient mice and STAT4-deficient mice were resistant to the induction of myocarditis. Treatment with exogenous IL-12 exacerbated disease. We questioned whether IFN-gamma is required for the disease-promoting activity of IL-12. On the contrary, we found that IFN-gamma suppresses EAM. Lack of IFN-gamma due to either depletion with an antibody or a genetic deficiency exacerbated myocarditis. Spleens from IFN-gamma-deficient mice immunized with cardiac myosin showed increased cellularity; greater numbers of CD3+, CD4+, CD8+, and IL-2-producing cells; and heightened ability to produce cytokines on stimulation in vitro. Treatment of mice with recombinant IFN-gamma suppressed the development of myocarditis. CONCLUSIONS IL-12/IL-12R/STAT4 signaling promotes the development of EAM. In contrast, IFN-gamma plays a protective role. The disease-limiting effects of IFN-gamma might be explained by its ability to control the expansion of activated T lymphocytes.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"In contrast, IFN-gamma plays a protective role.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 782, "doc_id": "8246922", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Lack of FGF21 in mice leads to reduced lifespan.\n\nCANDIDATE_ABSTRACT:\nTITLE: Neutrophils Suppress Intraluminal NK Cell-Mediated Tumor Cell Clearance and Enhance Extravasation of Disseminated Carcinoma Cells.\nABSTRACT: UNLABELLED Immune cells promote the initial metastatic dissemination of carcinoma cells from primary tumors. In contrast to their well-studied functions in the initial stages of metastasis, the specific roles of immunocytes in facilitating progression through the critical later steps of the invasion-metastasis cascade remain poorly understood. Here, we define novel functions of neutrophils in promoting intraluminal survival and extravasation at sites of metastatic dissemination. We show that CD11b(+)/Ly6G(+) neutrophils enhance metastasis formation via two distinct mechanisms. First, neutrophils inhibit natural killer cell function, which leads to a significant increase in the intraluminal survival time of tumor cells. Thereafter, neutrophils operate to facilitate extravasation of tumor cells through the secretion of IL1β and matrix metalloproteinases. These results identify neutrophils as key regulators of intraluminal survival and extravasation through their cross-talk with host cells and disseminating carcinoma cells. SIGNIFICANCE This study provides important insights into the systemic contributions of neutrophils to cancer metastasis by identifying how neutrophils facilitate intermediate steps of the invasion-metastasis cascade. We demonstrate that neutrophils suppress natural killer cell activity and increase extravasation of tumor cells. Cancer Discov; 6(6); 630-49. ©2016 AACR.This article is highlighted in the In This Issue feature, p. 561.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 682, "doc_id": "381602", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does the microRNA miR-139 suppress metastasis and progression of hepatocellular carcinoma by down-regulating Rho-kinase 2?\n\nABSTRACT:\nWe investigated mechanisms of hepatocellular carcinoma (HCC) metastasis and identified an antimetastatic microRNA (miRNA), miR-139, that is down-regulated in human HCC samples. Effects of stable and transient expression of miRNA-139 and its inhibitors were studied in the human HCC cell lines SMMC-7721 and BEL7402; cells were analyzed for migration and invasion. Liver samples from patients with metastatic HCC were analyzed for levels of miRNA-139; data were compared with survival data using the Kaplan-Meier method and compared between groups by the log-rank test. Tumor formation and metastasis from human HCC MHCC97L cells that did or did not express miR-139 were analyzed in mice. Down-regulation of miR-139 in HCC was associated significantly with poor prognosis of patients and features of metastatic tumors, including venous invasion, microsatellite formation, absence of tumor encapsulation, and reduced differentiation. miR-139 expression was reduced in metastatic HCC tumors compared with primary tumors. Overexpression of miR-139 in HCC cells significantly reduced cell migration and invasion in vitro and the incidence and severity of lung metastasis from orthotopic liver tumors in mice. miR-139 interacted with the 3' untranslated region of Rho-kinase 2 (ROCK2) and reduced its expression in HCC cells. Levels of miR-139 were correlated inversely with ROCK2 protein in human HCC samples. Overexpression of miR-139 did not inhibit HCC cell motility when ROCK2 was knocked down.", "output": "{\"label\": \"yes\", \"rationale\": \"The microRNA miR-139 interacts with ROCK2 and reduces its expression in HCC cells. Down-regulation of miR-139 increased the invasive abilities of HCC cells in vitro and HCC metastasis in vivo. Expression of miR-139 is reduced in human metastatic HCC samples and correlates with prognosis.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 20951699, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: PrimPol generates short DNA replication intermediates on the leading strand during DNA replication.\n\nCANDIDATE_ABSTRACT:\nTITLE: hPrimpol1/CCDC111 is a human DNA primase-polymerase required for the maintenance of genome integrity.\nABSTRACT: Prim-pol is a recently identified DNA primase-polymerase belonging to the archaeao-eukaryotic primase (AEP) superfamily. Here, we characterize a previously unrecognized prim-pol in human cells, which we designate hPrimpol1 (human primase-polymerase 1). hPrimpol1 possesses primase and DNA polymerase activities in vitro, interacts directly with RPA1 and is recruited to sites of DNA damage and stalled replication forks in an RPA1-dependent manner. Cells depleted of hPrimpol1 display increased spontaneous DNA damage and defects in the restart of stalled replication forks. Both RPA1 binding and the primase activity of hPrimpol1 are required for its cellular function during DNA replication. Our results indicate that hPrimpol1 is a novel factor involved in the response to DNA replication stress.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 970, "doc_id": "19356271", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Cost effectiveness evaluations based on cRCT data accurately reflect prices for patients in actual clinical practice.\n\nCANDIDATE_PASSAGE:\nHow nascent phagosomes mature to become phagolysosomes. Phagocytosis mediates the clearance of apoptotic bodies and also the elimination of microbial pathogens. The nascent phagocytic vacuole formed upon particle engulfment lacks microbicidal and degradative activity. These capabilities are acquired as the phagosome undergoes maturation; a progressive remodeling of its membrane and contents that culminates in the formation of phagolysosomes. Maturation entails orderly sequential fusion of the phagosomal vacuole with specialized endocytic and secretory compartments. Concomitantly, the phagosomal membrane undergoes both inward and outward vesiculation and tubulation followed by fission, thereby recycling components and maintaining its overall size. Here, we summarize what is known about the molecular machinery that governs this complex metamorphosis of phagosome maturation.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "290", "doc_id": "22190276", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Primary cervical cancer screening with HPV detection has higher longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_ABSTRACT:\nTITLE: Evidence regarding human papillomavirus testing in secondary prevention of cervical cancer.\nABSTRACT: More than ever, clinicians need regularly updated reviews given the continuously increasing amount of new information regarding innovative cervical cancer prevention methods. A summary is given from recent meta-analyses and systematic reviews on 3 possible clinical applications of human papillomavirus (HPV) testing: triage of women with equivocal or low-grade cytologic abnormalities; prediction of the therapeutic outcome after treatment of cervical intraepithelial neoplasia (CIN) lesions, and last not but not least, primary screening for cervical cancer and pre-cancer. Consistent evidence is available indicating that HPV-triage with the Hybrid Capture(®) 2 assay (Qiagen Gaithersburg, Inc., MD, USA [previously Digene Corp.] (HC2) is more accurate (higher sensitivity, similar specificity) than repeat cytology to triage women with equivocal Pap smear results. Several other tests show at least similar accuracy but mRNA testing with the APTIMA(®) (Gen-Probe Inc., San Diego, CA, USA) test is similarly sensitive but more specific compared to HC2. In triage of low-grade squamous intraepithelial lesions (LSIL), HC2 is more sensitive but its specificity is substantially lower compared to repeat cytology. The APTIMA(®) test is more specific than HC2 without showing a loss in sensitivity. Identification of DNA of HPV types 16 and/or 18, or RNA from the five most carcinogenic HPV types allow selecting women at highest risk for CIN3+ but the sensitivity and negative predictive value of these markers are lower than full-range high-risk HPV (hrHPV) testing. After conservative treatment of cervical pre-cancer, HPV testing picks up more quickly, with higher sensitivity and not lower specificity, residual or recurrent high-grade CIN than follow-up cytology. Primary screening f [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Primary screening for hrHPV generally detects more CIN2, CIN3 or cancer compared to cytology at cut-off atypical squamous cells of undetermined significance (ASC-US) or LSIL, but is less specific.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 971, "doc_id": "28617573", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Bcp1 is a chaperone for Rpl23.\n\nCANDIDATE_PASSAGE:\nHistone/protein deacetylase inhibitors increase suppressive functions of human FOXP3+ Tregs. Histone/protein deacetylases (HDACs) decrease histone and protein acetylation, typically leading to suppression of gene transcription and modulation of various protein functions. We found significant differences in expression of HDAC before and after stimulation of human T regulatory (Treg) and T effector cells, suggesting the potential for future selective targeting of Tregs with HDAC inhibitors (HDACi). Use of various HDACi small molecules enhanced, by up to 4.5-fold (average 2-fold), the suppressive functions of both freshly isolated and expanded human Tregs, consistent with our previous murine data. HDACi use increased Treg expression of CTLA-4, a key negative regulator of immune response, and we found a direct and significant correlation between CTLA-4 expression and Treg suppression. Hence, HDACi compounds are promising pharmacologic tools to increase Treg suppressive functions, and this action may potentially be of use in patients with autoimmunity or post-transplantation.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "173", "doc_id": "22968257", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Transplanted human glial progenitor cells are incapable of forming a neural network with host animals' neurons.\n\nCANDIDATE_ABSTRACT:\nTITLE: Forebrain engraftment by human glial progenitor cells enhances synaptic plasticity and learning in adult mice.\nABSTRACT: Human astrocytes are larger and more complex than those of infraprimate mammals, suggesting that their role in neural processing has expanded with evolution. To assess the cell-autonomous and species-selective properties of human glia, we engrafted human glial progenitor cells (GPCs) into neonatal immunodeficient mice. Upon maturation, the recipient brains exhibited large numbers and high proportions of both human glial progenitors and astrocytes. The engrafted human glia were gap-junction-coupled to host astroglia, yet retained the size and pleomorphism of hominid astroglia, and propagated Ca2+ signals 3-fold faster than their hosts. Long-term potentiation (LTP) was sharply enhanced in the human glial chimeric mice, as was their learning, as assessed by Barnes maze navigation, object-location memory, and both contextual and tone fear conditioning. Mice allografted with murine GPCs showed no enhancement of either LTP or learning. These findings indicate that human glia differentially enhance both activity-dependent plasticity and learning in mice.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Long-term potentiation (LTP) was sharply enhanced in the human glial chimeric mice, as was their learning, as assessed by Barnes maze navigation, object-location memory, and both contextual and tone fear conditioning.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1320, "doc_id": "16284655", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is peak concentration needed in therapeutic drug monitoring of vancomycin?\n\nABSTRACT:\nWe analyzed the pharmacokinetic-pharmacodynamic relationship of vancomycin to determine the drug exposure parameters that correlate with the efficacy and nephrotoxicity of vancomycin in patients with methicillin-resistant Staphylococcus aureus pneumonia and evaluated the need to use peak concentration in therapeutic drug monitoring (TDM). Serum drug concentrations of 31 hospitalized patients treated with vancomycin for methicillin-resistant S. aureus pneumonia were collected. Significant differences in trough concentration (Cmin)/minimum inhibitory concentration (MIC) and area under the serum concentration-time curve (AUC0-24)/MIC were observed between the response and non-response groups. Significant differences in Cmin and AUC0-24 were observed between the nephrotoxicity and non-nephrotoxicity groups. Receiver operating characteristic curves revealed high predictive values of Cmin/MIC and AUC0-24/MIC for efficacy and of Cmin and AUC0-24 for safety of vancomycin.", "output": "{\"label\": \"no\", \"rationale\": \"These results suggest little need to use peak concentration in vancomycin TDM because Cmin/MIC and Cmin are sufficient to predict the efficacy and safety of vancomycin.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 23147106, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Forkhead 0 (fox0) transcription factors are involved in cellular differentiation.\n\nCANDIDATE_PASSAGE:\nCell Stem Cell Review FoxO Transcription Factors and Stem Cell Homeostasis: Insights from the Hematopoietic System The forkhead O (FoxO) family of transcription factors participates in diverse physiologic processes, including induction of cell-cycle arrest, stress resistance, differentiation, apoptosis, and metabolism. Several recent studies indicate that FoxO-dependent signaling is required for long-term regenerative potential of the hematopoietic stem cell (HSC) compartment through regulation of HSC response to physiologic oxidative stress, quiescence, and survival. These observations link FoxO function in mammalian systems with the evolutionarily conserved role of FoxO in promotion of stress resistance and longevity in lower phylogenetic systems. Furthermore, these findings have implications for aging in higher organisms and in malignant stem cell biology, and suggest that FoxOs may play an important role in the maintenance and integrity of stem cell compartments in a broad spectrum of tissues.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "428", "doc_id": "16728949", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: A deficiency of vitamin B12 decreases blood levels of homocysteine.\n\nCANDIDATE_PASSAGE:\nNovel Risk Factors for Systemic Atherosclerosis: A Comparison of C-Reactive Protein, Fibrinogen, Homocysteine, Lipoprotein(a), and Standard Cholesterol Screening as Predictors of Peripheral Arterial Disease ContextSeveral novel risk factors for atherosclerosis have recently been proposed, but few comparative data exist to guide clinical use of these emerging biomarkers. ObjectiveTo compare the predictive value of 11 lipid and nonlipid biomarkers as risk factors for development of symptomatic peripheral arterial disease (PAD).Design, Setting, and ParticipantsNested case-control study using plasma samples collected at baseline from a prospective cohort of 14 916 initially healthy US male physicians aged 40 to 84 years, of whom 140 subsequently developed symptomatic PAD (cases); 140 age- and smoking status–matched men who remained free of vascular disease during an average 9-year follow-up period were randomly selected as controls. Main Outcome MeasureIncident PAD, as determined by baseline total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total cholesterol–HDL-C ratio, triglycerides, homocysteine, C-reactive protein (CRP), lipoprotein(a), fibrinogen, and apolipoproteins (apo) A-I and B-100.ResultsIn univariate analyses, plasma levels of total cholesterol (P<.001), LDL-C (P = .001), triglycerides (P = .001), apo B-100 (P = .001), fibrinogen (P = .02), CRP (P = .006), and the total cholesterol–HDL-C ratio (P<.001) were all significantly higher at baseline among men who subsequently developed PAD compared with those who did not, while levels of HDL-C (P = .009) and apo A-I (P = .05) were lower. Nonsignificant baseline elevations of lipoprotein(a) (P = .40) and homocysteine (P = .90) were observed. In mul [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "35", "doc_id": "72933407", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Enhanced early production of inflammatory chemokines improves viral control in the lung.\n\nCANDIDATE_PASSAGE:\nBCL-6 represses genes that function in lymphocyte differentiation, inflammation, and cell cycle control. BCL-6, a transcriptional repressor frequently translocated in lymphomas, regulates germinal center B cell differentiation and inflammation. DNA microarray screening identified genes repressed by BCL-6, including many lymphocyte activation genes, suggesting that BCL-6 modulates B cell receptor signals. BCL-6 repression of two chemokine genes, MIP-1alpha and IP-10, may also attenuate inflammatory responses. Blimp-1, another BCL-6 target, is important for plasmacytic differentiation. Since BCL-6 expression is silenced in plasma cells, repression of blimp-1 by BCL-6 may control plasmacytic differentiation. Indeed, inhibition of BCL-6 function initiated changes indicative of plasmacytic differentiation, including decreased expression of c-Myc and increased expression of the cell cycle inhibitor p27kip1. These data suggest that malignant transformation by BCL-6 involves inhibition of differentiation and enhanced proliferation.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "380", "doc_id": "16550075", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Pre-mRNAs associated with spliceosomal components are more stable than unassociated splicing substrates.\n\nCANDIDATE_ABSTRACT:\nTITLE: Linking Splicing to Pol II Transcription Stabilizes Pre-mRNAs and Influences Splicing Patterns\nABSTRACT: RNA processing is carried out in close proximity to the site of transcription, suggesting a regulatory link between transcription and pre-mRNA splicing. Using an in vitro transcription/splicing assay, we demonstrate that an association of RNA polymerase II (Pol II) transcription and pre-mRNA splicing is required for efficient gene expression. Pol II-synthesized RNAs containing functional splice sites are protected from nuclear degradation, presumably because the local concentration of the splicing machinery is sufficiently high to ensure its association over interactions with nucleases. Furthermore, the process of transcription influences alternative splicing of newly synthesized pre-mRNAs. Because other RNA polymerases do not provide similar protection from nucleases, and their RNA products display altered splicing patterns, the link between transcription and RNA processing is RNA Pol II-specific. We propose that the connection between transcription by Pol II and pre-mRNA splicing guarantees an extended half-life and proper processing of nascent pre-mRNAs.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We propose that the connection between transcription by Pol II and pre-mRNA splicing guarantees an extended half-life and proper processing of nascent pre-mRNAs.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 964, "doc_id": "4162857", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: taa1 tar1 tar2 triple mutants in Arabidopsis do not make root meristem during embryogenesis.\n\nCANDIDATE_ABSTRACT:\nTITLE: TAA1-Mediated Auxin Biosynthesis Is Essential for Hormone Crosstalk and Plant Development\nABSTRACT: Plants have evolved a tremendous ability to respond to environmental changes by adapting their growth and development. The interaction between hormonal and developmental signals is a critical mechanism in the generation of this enormous plasticity. A good example is the response to the hormone ethylene that depends on tissue type, developmental stage, and environmental conditions. By characterizing the Arabidopsis wei8 mutant, we have found that a small family of genes mediates tissue-specific responses to ethylene. Biochemical studies revealed that WEI8 encodes a long-anticipated tryptophan aminotransferase, TAA1, in the essential, yet genetically uncharacterized, indole-3-pyruvic acid (IPA) branch of the auxin biosynthetic pathway. Analysis of TAA1 and its paralogues revealed a link between local auxin production, tissue-specific ethylene effects, and organ development. Thus, the IPA route of auxin production is key to generating robust auxin gradients in response to environmental and developmental cues.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1405, "doc_id": "10504681", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: TMEM27 is a marker for beta cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Tmem27: a cleaved and shed plasma membrane protein that stimulates pancreatic beta cell proliferation.\nABSTRACT: The signals and molecular mechanisms that regulate the replication of terminally differentiated beta cells are unknown. Here, we report the identification and characterization of transmembrane protein 27 (Tmem27, collectrin) in pancreatic beta cells. Expression of Tmem27 is reduced in Tcf1(-/-) mice and is increased in islets of mouse models with hypertrophy of the endocrine pancreas. Tmem27 forms dimers and its extracellular domain is glycosylated, cleaved and shed from the plasma membrane of beta cells. This cleavage process is beta cell specific and does not occur in other cell types. Overexpression of full-length Tmem27, but not the truncated or soluble protein, leads to increased thymidine incorporation, whereas silencing of Tmem27 using RNAi results in a reduction of cell replication. Furthermore, transgenic mice with increased expression of Tmem27 in pancreatic beta cells exhibit increased beta cell mass. Our results identify a pancreatic beta cell transmembrane protein that regulates cell growth of pancreatic islets.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"This cleavage process is beta cell specific and does not occur in other cell types.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1133, "doc_id": "24142891", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: RUNX1 is downregulated or mutated in TLX1 T-ALL.\n\nCANDIDATE_PASSAGE:\nReverse engineering of TLX oncogenic transcriptional networks identifies RUNX1 as tumor suppressor in T-ALL The TLX1 and TLX3 transcription factor oncogenes have a key role in the pathogenesis of T cell acute lymphoblastic leukemia (T-ALL). Here we used reverse engineering of global transcriptional networks to decipher the oncogenic regulatory circuit controlled by TLX1 and TLX3. This systems biology analysis defined T cell leukemia homeobox 1 (TLX1) and TLX3 as master regulators of an oncogenic transcriptional circuit governing T-ALL. Notably, a network structure analysis of this hierarchical network identified RUNX1 as a key mediator of the T-ALL induced by TLX1 and TLX3 and predicted a tumor-suppressor role for RUNX1 in T cell transformation. Consistent with these results, we identified recurrent somatic loss-of-function mutations in RUNX1 in human T-ALL. Overall, these results place TLX1 and TLX3 at the top of an oncogenic transcriptional network controlling leukemia development, show the power of network analyses to identify key elements in the regulatory circuits governing human cancer and identify RUNX1 as a tumor-suppressor gene in T-ALL.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1009", "doc_id": "1982286", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Nonhypertensive people who are 55 years old have a 90% chance of developing hypertension during their lifetime.\n\nCANDIDATE_PASSAGE:\nResidual lifetime risk for developing hypertension in middle-aged women and men: The Framingham Heart Study. CONTEXT The long-term risk for developing hypertension is best described by the lifetime risk statistic. The lifetime risk for hypertension and trends in this risk over time are unknown. OBJECTIVES To estimate the residual lifetime risk for hypertension in older US adults and to evaluate temporal trends in this risk. DESIGN, SETTING, AND PARTICIPANTS Community-based prospective cohort study of 1298 participants from the Framingham Heart Study who were aged 55 to 65 years and free of hypertension at baseline (1976-1998). MAIN OUTCOME MEASURES Residual lifetime risk (lifetime cumulative incidence not adjusted for competing causes of mortality) for hypertension, defined as blood pressure of 140/90 mm Hg or greater or use of antihypertensive medications. RESULTS The residual lifetime risks for developing hypertension and stage 1 high blood pressure or higher (greater-than-or-equal to 140/90 mm Hg regardless of treatment) were 90% in both 55- and 65-year-old participants. The lifetime probability of receiving antihypertensive medication was 60%. The risk for hypertension remained unchanged for women, but it was approximately 60% higher for men in the contemporary 1976-1998 period compared with an earlier 1952-1975 period. In contrast, the residual lifetime risk for stage 2 high blood pressure or higher (greater-than-or-equal to 160/100 mm Hg regardless of treatment) was considerably lower in both sexes in the recent period (35%-57% in 1952-1975 vs 35%-44% in 1976-1998), likely due to a marked increase in treatment of individuals with substantially elevated blood pressure. CONCLUSION The residual lifetime risk for hypertension for middle-aged and elderly in [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "854", "doc_id": "12206390", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does route of delivery affect maternal and perinatal outcome in women with eclampsia?\n\nABSTRACT:\nThe route of delivery in eclampsia is controversial. We hypothesized that adverse maternal and perinatal outcomes may not be improved by early cesarean delivery. This was a randomized controlled exploratory trial carried out in a rural teaching institution. In all, 200 eclampsia cases, carrying ≥34 weeks, were allocated to either cesarean or vaginal delivery. Composite maternal and perinatal event rates (death and severe morbidity) were compared by intention-to-treat principle. Groups were comparable at baseline with respect to age and key clinical parameters. Maternal event rate was similar: 10.89% in the cesarean arm vs 7.07% for vaginal delivery (relative risk, 1.54; 95% confidence interval, 0.62-3.81). Although the neonatal event rate was less in cesarean delivery-9.90% vs 19.19% (relative risk, 0.52; 95% confidence interval, 0.25-1.05)-the difference was not significant statistically.", "output": "{\"label\": \"no\", \"rationale\": \"A policy of early cesarean delivery in eclampsia, carrying ≥34 weeks, is not associated with better outcomes.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 22521460, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Risedronate increases risk of vertebral and non-vertebral fractures.\n\nCANDIDATE_PASSAGE:\nCatch and release: how do kinetochores hook the right microtubules during mitosis? Sport fishermen keep tension on their lines to prevent hooked fish from releasing. A molecular version of this angler's trick, operating at kinetochores, ensures accuracy during mitosis: the mitotic spindle attaches randomly to chromosomes and then correctly bioriented attachments are stabilized due to the tension exerted on them by opposing microtubules. Incorrect attachments, which lack tension, are unstable and release quickly, allowing another chance for biorientation. Stabilization of molecular interactions by tension also occurs in other physiological contexts, such as cell adhesion, motility, hemostasis, and tissue morphogenesis. Here, we review models for the stabilization of kinetochore attachments with an eye toward emerging models for other force-activated systems. Although attention in the mitosis field has focused mainly on one kinase-based mechanism, multiple mechanisms may act together to stabilize properly bioriented kinetochores and some principles governing other tension-sensitive systems may also apply to kinetochores.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1050", "doc_id": "17805221", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: \"Would a man smell a rose then throw it away?\n\nABSTRACT:\nBreast cancer is the most common malignancy afflicting women, and the most common cancer overall in Jordan. A woman's decision to go for screening is influenced by her social support network. This study aims to explore Jordanian men's individual and contextual perspectives on women's breast cancer and their own role in the breast health of the females within their families. An explorative qualitative design was used to purposively recruit 24 married men aged 27 to 65 years (median 43 years) from four governorates in Jordan. Data in the form of interviews transcriptions was subjected to qualitative content analysis. Three themes were identified: a) Supporting one's wife; b) Marital needs and obligations; c) Constrained by a culture of destiny and shame. The first theme was built on men's feelings of responsibility for the family's health and well-being, their experiences of encouraging their wives to seek health care and their providing counselling and instrumental support. The second theme emerged from men's views about other men's rejection of a wife inflicted by breast cancer, their own perceptions of diminished femininity due to mastectomy and their own concerns about protecting the family from the hereditary risk of breast cancer. The third theme was seen in men's perception of breast cancer as an inevitable act of God that is far away from one's own family, in associating breast cancer with improper behaviour and in their readiness to face the culture of Eib (shame).", "output": "{\"label\": \"maybe\", \"rationale\": \"Jordanian men perceive themselves as having a vital role in supporting, guiding and encouraging their wives to follow breast cancer early detection recommendations. Breast health awareness campaigns could involve husbands to capitalize on family support.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 24160268, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Sepsis related mortality has risen from 2009 to 2014.\n\nCANDIDATE_ABSTRACT:\nTITLE: Incidence and Trends of Sepsis in US Hospitals Using Clinical vs Claims Data, 2009-2014\nABSTRACT: Importance Estimates from claims-based analyses suggest that the incidence of sepsis is increasing and mortality rates from sepsis are decreasing. However, estimates from claims data may lack clinical fidelity and can be affected by changing diagnosis and coding practices over time. Objective To estimate the US national incidence of sepsis and trends using detailed clinical data from the electronic health record (EHR) systems of diverse hospitals. Design, Setting, and Population Retrospective cohort study of adult patients admitted to 409 academic, community, and federal hospitals from 2009-2014. Exposures Sepsis was identified using clinical indicators of presumed infection and concurrent acute organ dysfunction, adapting Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) criteria for objective and consistent EHR-based surveillance. Main Outcomes and Measures Sepsis incidence, outcomes, and trends from 2009-2014 were calculated using regression models and compared with claims-based estimates using International Classification of Diseases, Ninth Revision, Clinical Modification codes for severe sepsis or septic shock. Case-finding criteria were validated against Sepsis-3 criteria using medical record reviews. Results A total of 173 690 sepsis cases (mean age, 66.5 [SD, 15.5] y; 77 660 [42.4%] women) were identified using clinical criteria among 2 901 019 adults admitted to study hospitals in 2014 (6.0% incidence). Of these, 26 061 (15.0%) died in the hospital and 10 731 (6.2%) were discharged to hospice. From 2009-2014, sepsis incidence using clinical criteria was stable (+0.6% relative change/y [95% CI, −2.3% to 3.5%], P = .67) whereas incidence per claims increased (+10.3%/y [95% CI, 7.2% to 13.3%], P < .001). In-hospital morta [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Conclusions and Relevance In clinical data from 409 hospitals, sepsis was present in 6% of adult hospitalizations, and in contrast to claims-based analyses, neither the incidence of sepsis nor the combined outcome of death or discharge to hospice changed significantly between 2009-2014.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1073, "doc_id": "4824840", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Weighed food records (WFR) result in poor completion since they're costly to run and impose high participant burden.\n\nCANDIDATE_PASSAGE:\nAccuracy of weighed dietary records in studies of diet and health. OBJECTIVE To provide an independent evaluation of seven day weighed dietary records, which are currently accepted as the most accurate technique for assessing habitual dietary intake in studies investigating the links between diet and health. DESIGN Subjects who had previously participated in the Northern Ireland diet and health study were reselected by stratified random sampling to represent the range of energy intakes in the study as assessed by the seven day weighed dietary record. SETTING Northern Ireland. SUBJECTS 31 Free living adults (16 men and 15 women). MAIN OUTCOME MEASURES Energy intake as measured by the seven day weighed dietary record and total energy expenditure estimated concurrently by the doubly labelled water technique. RESULTS Average recorded energy intakes were significantly lower than measured expenditure in the group overall (9.66 MJ/day v 12.15 MJ/day, 95% confidence interval 1.45 to 3.53 MJ/day). Among those in the upper third of energy intakes the mean (SE) ratio of intake to expenditure was close to 1.0, indicating accurate records (men 1.01 (0.11), women 0.96 (0.08]. In the middle and lower thirds the ratios for men were only 0.74 (0.05) and 0.70 (0.07) respectively and for women 0.89 (0.07) and 0.61 (0.07). CONCLUSIONS These results show a serious bias in reporting habitual energy intake. If substantiated they may have wide implications for the interpretation of many nutritional studies.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1375", "doc_id": "21993510", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Pioglitazone use is not associated with an increased risk of prostate cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Pioglitazone Use and Risk of Bladder Cancer and Other Common Cancers in Persons With Diabetes.\nABSTRACT: IMPORTANCE Studies suggest pioglitazone use may increase risk of cancers. OBJECTIVE To examine whether pioglitazone use for diabetes is associated with risk of bladder and 10 additional cancers. DESIGN, SETTING, AND PARTICIPANTS Cohort and nested case-control analyses among persons with diabetes. A bladder cancer cohort followed 193,099 persons aged 40 years or older in 1997-2002 until December 2012; 464 case patients and 464 matched controls were surveyed about additional confounders. A cohort analysis of 10 additional cancers included 236,507 persons aged 40 years or older in 1997-2005 and followed until June 2012. Cohorts were from Kaiser Permanente Northern California. EXPOSURES Ever use, duration, cumulative dose, and time since initiation of pioglitazone as time dependent. MAIN OUTCOMES AND MEASURES Incident cancer, including bladder, prostate, female breast, lung/bronchus, endometrial, colon, non-Hodgkin lymphoma, pancreas, kidney/renal pelvis, rectum, and melanoma. RESULTS Among 193,099 persons in the bladder cancer cohort, 34,181 (18%) received pioglitazone (median duration, 2.8 years; range, 0.2-13.2 years) and 1261 had incident bladder cancer. Crude incidences of bladder cancer in pioglitazone users and nonusers were 89.8 and 75.9 per 100,000 person-years, respectively. Ever use of pioglitazone was not associated with bladder cancer risk (adjusted hazard ratio [HR], 1.06; 95% CI, 0.89-1.26). Results were similar in case-control analyses (pioglitazone use: 19.6% among case patients and 17.5% among controls; adjusted odds ratio, 1.18; 95% CI, 0.78-1.80). In adjusted analyses, there was no association with 8 of the 10 additional cancers; ever use of pioglitazone was associated with increased risk of prostate cancer (HR, 1.13; 95% CI, 1.02-1.26) and p [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The increased prostate and pancreatic cancer risks associated with ever use of pioglitazone merit further investigation to assess whether they are causal or are due to chance, residual confounding, or reverse causality.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 952, "doc_id": "3355397", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Hypothalamic glutamate neurotransmission is unrelated to energy balance.\n\nCANDIDATE_PASSAGE:\nAtaxia, dementia, and hypogonadotropism caused by disordered ubiquitination. BACKGROUND The combination of ataxia and hypogonadism was first described more than a century ago, but its genetic basis has remained elusive. METHODS We performed whole-exome sequencing in a patient with ataxia and hypogonadotropic hypogonadism, followed by targeted sequencing of candidate genes in similarly affected patients. Neurologic and reproductive endocrine phenotypes were characterized in detail. The effects of sequence variants and the presence of an epistatic interaction were tested in a zebrafish model. RESULTS Digenic homozygous mutations in RNF216 and OTUD4, which encode a ubiquitin E3 ligase and a deubiquitinase, respectively, were found in three affected siblings in a consanguineous family. Additional screening identified compound heterozygous truncating mutations in RNF216 in an unrelated patient and single heterozygous deleterious mutations in four other patients. Knockdown of rnf216 or otud4 in zebrafish embryos induced defects in the eye, optic tectum, and cerebellum; combinatorial suppression of both genes exacerbated these phenotypes, which were rescued by nonmutant, but not mutant, human RNF216 or OTUD4 messenger RNA. All patients had progressive ataxia and dementia. Neuronal loss was observed in cerebellar pathways and the hippocampus; surviving hippocampal neurons contained ubiquitin-immunoreactive intranuclear inclusions. Defects were detected at the hypothalamic and pituitary levels of the reproductive endocrine axis. CONCLUSIONS The syndrome of hypogonadotropic hypogonadism, ataxia, and dementia can be caused by inactivating mutations in RNF216 or by the combination of mutations in RNF216 and OTUD4. These findings link disordered ubiquitination to neurode [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "541", "doc_id": "24725136", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Vaccinating the gastrointestinal tract induces protection of rectal and vaginal mucosa.\n\nCANDIDATE_PASSAGE:\n[Pharmacokinetics and biotransformation of the antimycotic drug ciclopiroxolamine in animals and man after topical and systemic administration]. 1. Following the dermal application of the carbon-14 labelled broad spectrum antimycotic 6-cyclohexyl-1-hydroxy-4-methyl-2(1H)-pyridone, 2-aminoethanol salt (ciclopiroxolamine, Hoe 296, Batrafen) in the form of a 1% aqueous cream to healthy human dorsal skin (penetration time: 6 h; occlusive dressing for 5 h), percutaneous absorption accounted on average for 1.3% of the dose applied. Excretion occurred via the kidney, with biological half-lives of 1.7 h. As can be seen from penetration studies of cadaverous skin, the horny layer contained the highest concentrations, with values of 2300-4500 microgram/cm3. The levels determined in the corium were still above the minimum inhibitory concentrations. These concentrations were already obtained at the first test stage (1.5 h after application) and did not change virtually at all over the longer penetration period. According to studies using histoautoradiography, ciclopirox can penetrate the skin via the epidermis and the hair follicles. When ciclopirox-14C-olamine aqueous cream was spread on the surface of fingernails, the radioactive-labelled compound penetrated right through the nail. The percutaneous absorption in dogs was higher, at 5-15% of the dose, than it was in humans. 2. After vaginal application (1 mg/kg) of ciclopirox-14C-olamine in the form of a 1% aqueous cream to bitches, between 42 and 97% of the dose (depending on the animal) was recovered in the urine and faeces, the remainder having penetrated into the tampon used to close the vagina. 3. Ciclopirox is excreted by dogs and man in the urine, primarily as a glucuronide. In humans another glucuronide with pr [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1356", "doc_id": "26461066", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_PASSAGE:\nInterlaboratory reproducibility and proficiency testing within the human papillomavirus cervical cancer screening program in Catalonia, Spain. In Catalonia, a screening protocol for cervical cancer, including human papillomavirus (HPV) DNA testing using the Digene Hybrid Capture 2 (HC2) assay, was implemented in 2006. In order to monitor interlaboratory reproducibility, a proficiency testing (PT) survey of the HPV samples was launched in 2008. The aim of this study was to explore the repeatability of the HC2 assay's performance. Participating laboratories provided 20 samples annually, 5 randomly chosen samples from each of the following relative light unit (RLU) intervals: <0.5, 0.5 to 0.99, 1 to 9.99, and ≥10. Kappa statistics were used to determine the agreement levels between the original and the PT readings. The nature and origin of the discrepant results were calculated by bootstrapping. A total of 946 specimens were retested. The kappa values were 0.91 for positive/negative categorical classification and 0.79 for the four RLU intervals studied. Sample retesting yielded systematically lower RLU values than the original test (P<0.005), independently of the time elapsed between the two determinations (median, 53 days), possibly due to freeze-thaw cycles. The probability for a sample to show clinically discrepant results upon retesting was a function of the RLU value; samples with RLU values in the 0.5 to 5 interval showed 10.80% probability to yield discrepant results (95% confidence interval [CI], 7.86 to 14.33) compared to 0.85% probability for samples outside this interval (95% CI, 0.17 to 1.69). Globally, the HC2 assay shows high interlaboratory concordance. We have identified differential confidence thresholds and suggested the guidelines for interla [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "972", "doc_id": "32177659", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Normal granulomas form in the absence of TNF in Zebrafish.\n\nCANDIDATE_PASSAGE:\nTumor necrosis factor signaling mediates resistance to mycobacteria by inhibiting bacterial growth and macrophage death. Tumor necrosis factor (TNF), a key effector in controlling tuberculosis, is thought to exert protection by directing formation of granulomas, organized aggregates of macrophages and other immune cells. Loss of TNF signaling causes progression of tuberculosis in humans, and the increased mortality of Mycobacterium tuberculosis-infected mice is associated with disorganized necrotic granulomas, although the precise roles of TNF signaling preceding this endpoint remain undefined. We monitored transparent Mycobacterium marinum-infected zebrafish live to conduct a stepwise dissection of how TNF signaling operates in mycobacterial pathogenesis. We found that loss of TNF signaling caused increased mortality even when only innate immunity was operant. In the absence of TNF, intracellular bacterial growth and granuloma formation were accelerated and was followed by necrotic death of overladen macrophages and granuloma breakdown. Thus, TNF is not required for tuberculous granuloma formation, but maintains granuloma integrity indirectly by restricting mycobacterial growth within macrophages and preventing their necrosis.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "860", "doc_id": "16066726", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Rapid up-regulation and higher basal expression of interferon-induced genes increase survival of granule cell neurons that are infected by West Nile virus.\n\nCANDIDATE_PASSAGE:\nThe Germ Cell Determinant Blimp1 Is Not Required for Derivation of Pluripotent Stem Cells Blimp1 (Prdm1), the key determinant of primordial germ cells (PGCs), plays a combinatorial role with Prdm14 during PGC specification from postimplantation epiblast cells. They together initiate epigenetic reprogramming in early germ cells toward an underlying pluripotent state, which is equivalent to embryonic stem cells (ESCs). Whereas Prdm14 alone can promote reprogramming and is important for the propagation of the pluripotent state, it is not known whether Blimp1 is similarly involved. By using a genetic approach, we demonstrate that Blimp1 is dispensable for the derivation and maintenance of ESCs and postimplantation epiblast stem cells (epiSCs). Notably, Blimp1 is also dispensable for reprogramming epiSCs to ESCs. Thus, although Blimp1 is obligatory for PGC specification, it is not required for the reversion of epiSCs to ESCs and for their maintenance thereafter. This study suggests that reprogramming, including that of somatic cells to ESCs, may not entail an obligatory route through a Blimp1-positive PGC-like state.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1020", "doc_id": "13910150", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Ivermectin is used to treat onchocerciasis.\n\nCANDIDATE_PASSAGE:\n“Rapid-Impact Interventions”: How a Policy of Integrated Control for Africa's Neglected Tropical Diseases Could Benefit the Poor Over the past two decades there have been significant achievements in the control of a handful of important human tropical infections [1]. These achievements include the substantive reductions in the prevalence and incidence of the so-called neglected diseases such as lymphatic filariasis, onchocerciasis, guinea worm, leprosy, and trachoma (Box 1) [2]. Each of these neglected diseases is a poverty-promoting and often stigmatizing condition occurring primarily in rural areas of low-income countries (Box 2) [3]. They are ancient afflictions, described in the Bible and other ancient texts, which have burdened humanity for millennia [3]. But now, as a result of aggressive regional vertical interventions, there is a possibility that some neglected tropical infections could be eventually controlled to the point of elimination in some areas of endemicity [2–8]. In the case of guinea worm infection, disease eradication might also soon be possible [9]. Box 2. Common Features of the Neglected Tropical Diseases Ancient afflictions that have burdened humanity for centuries Poverty-promoting conditions Associated with stigma Rural areas of low-income countries and fragile states No commercial markets for products that target these diseases Interventions, when applied, have a history of success", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "660", "doc_id": "1215116", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is hyperfibrinolysis diagnosed by rotational thromboelastometry ( ROTEM ) associated with higher mortality in patients with severe trauma?\n\nABSTRACT:\nWe investigated whether hyperfibrinolysis and its severity was associated with outcome of traumatized and nontraumatized patients. From April 2008 to April 2010, all emergency patients with hyperfibrinolysis were enrolled in this study. Hyperfibrinolysis patients were divided into traumatized (trauma hyperfibrinolysis group) and nontraumatized (nontrauma hyperfibrinolysis group). The trauma hyperfibrinolysis group was matched with 24 polytrauma patients without hyperfibrinolysis (matched trauma group). Data from rotational thromboelastometry measurements, blood gas analysis (metabolic state), laboratory analysis, injury severity score, and 30-day mortality were collected. Thirty-five patients with hyperfibrinolysis were identified (13 traumatized, 22 nontraumatized). Overall mortality for hyperfibrinolysis was 54%. Mortality in the trauma hyperfibrinolysis group (77%±12%) was significantly higher than in the nontrauma hyperfibrinolysis group (41%±10%; P=0.001, 95% CI 5%-67%) and the matched trauma group (33%±10%; P=0.009, 95% CI 13%-74%). Hyperfibrinolysis is significantly (P=0.017) associated with mortality in trauma patients. In the blood gas analysis representing the metabolic state, only pH (P=0.02) and potassium (P=0.01) were significantly lower in the trauma hyperfibrinolysis group compared to the nontrauma hyperfibrinolysis group.", "output": "{\"label\": \"yes\", \"rationale\": \"Mortality from hyperfibrinolysis is significantly higher in trauma compared with nontrauma patients, and hyperfibrinolysis is an independent factor predicting mortality in trauma patients. Rotational thromboelastometry provides real-time recognition of hyperfibrinolysis allowing early treatment.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 21918164, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The proliferative capacity of neural progenitors differs across species.\n\nCANDIDATE_ABSTRACT:\nTITLE: 2D and 3D Stem Cell Models of Primate Cortical Development Identify Species-Specific Differences in Progenitor Behavior Contributing to Brain Size.\nABSTRACT: Variation in cerebral cortex size and complexity is thought to contribute to differences in cognitive ability between humans and other animals. Here we compare cortical progenitor cell output in humans and three nonhuman primates using directed differentiation of pluripotent stem cells (PSCs) in adherent two-dimensional (2D) and organoid three-dimensional (3D) culture systems. Clonal lineage analysis showed that primate cortical progenitors proliferate for a protracted period of time, during which they generate early-born neurons, in contrast to rodents, where this expansion phase largely ceases before neurogenesis begins. The extent of this additional cortical progenitor expansion differs among primates, leading to differences in the number of neurons generated by each progenitor cell. We found that this mechanism for controlling cortical size is regulated cell autonomously in culture, suggesting that primate cerebral cortex size is regulated at least in part at the level of individual cortical progenitor cell clonal output.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The extent of this additional cortical progenitor expansion differs among primates, leading to differences in the number of neurons generated by each progenitor cell.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1254, "doc_id": "16939583", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Charcoal shows no benefit for acute paraquat poisoning.\n\nCANDIDATE_PASSAGE:\nSystematic review of controlled clinical trials of gastric lavage in acute organophosphorus pesticide poisoning. BACKGROUND Organophosphorus pesticide (OP) self-poisoning is a major problem in the developing rural world. There is little clinical trial data to guide therapy, hindering the identification of best therapy. Despite the recognition of adverse effects, gastric lavage is commonly done in Asia. We aimed to identify studies assessing its effectiveness. METHOD We systematically searched the literature for controlled clinical studies that assessed the effect of gastric lavage in OP pesticide self-poisoning. RESULTS All 56 studies identified were Chinese and reported benefit from the intervention studied, including multiple gastric lavages, use of norepinephrine or pralidoxime in the lavage fluid, concurrent treatment with naloxone or scopolamine, insertion of the gastric tube via a laparotomy incision, and lavage later than 12 h post-ingestion. However, only 23 were RCTs and none presented adequate methodology for their quality to be assessed. The patient population and study treatment protocol were not defined - large variation in case fatality in the control arm of the studies (from 4.5 to 93%) suggests marked variation between studies and likely between study arms. No study compared an intervention against a control group receiving no gastric lavage or provided any data to indicate whether a significant quantity of poison was removed. CONCLUSION Despite widespread use of multiple gastric lavages for OP pesticide poisoning across Asia, there is currently no high-quality evidence to support its clinical effectiveness. There is a need for studies to identify in which patients and for what duration gastric lavage is able to remove significant quantities [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "246", "doc_id": "8447873", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nCANDIDATE_ABSTRACT:\nTITLE: Rank Signaling Links the Development of Invariant γδ T Cell Progenitors and Aire+ Medullary Epithelium\nABSTRACT: The thymic medulla provides a specialized microenvironment for the negative selection of T cells, with the presence of autoimmune regulator (Aire)-expressing medullary thymic epithelial cells (mTECs) during the embryonic-neonatal period being both necessary and sufficient to establish long-lasting tolerance. Here we showed that emergence of the first cohorts of Aire(+) mTECs at this key developmental stage, prior to αβ T cell repertoire selection, was jointly directed by Rankl(+) lymphoid tissue inducer cells and invariant Vγ5(+) dendritic epidermal T cell (DETC) progenitors that are the first thymocytes to express the products of gene rearrangement. In turn, generation of Aire(+) mTECs then fostered Skint-1-dependent, but Aire-independent, DETC progenitor maturation and the emergence of an invariant DETC repertoire. Hence, our data attributed a functional importance to the temporal development of Vγ5(+) γδ T cells during thymus medulla formation for αβ T cell tolerance induction and demonstrated a Rank-mediated reciprocal link between DETC and Aire(+) mTEC maturation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Hence, our data attributed a functional importance to the temporal development of Vγ5(+) γδ T cells during thymus medulla formation for αβ T cell tolerance induction and demonstrated a Rank-mediated reciprocal link between DETC and Aire(+) mTEC maturation.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1181, "doc_id": "301838", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is transforming growth factor-beta receptor type 1 ( TGFBR1 ) associated with non-syndromic cleft lip with or without cleft palate in patients of Central European descent?\n\nABSTRACT:\nTransforming growth factor-beta (TGF-β) type 1 receptor (also known as activin receptor-like kinase 5, ALK5) is expressed in palatal tissue during embryogenesis. Experimental studies in transgenic mice with a genetic deletion of Alk5 showed that TGF-β type 1 receptor is required for upper lip and midline fusion of the hard and soft palate. In humans, association of TGF-β type 1 receptor gene (TGFBR1) and the development of non-syndromic cleft lip with or without cleft palate (NSCL/P) had been observed in a multiethnic sample of Chinese, Philippine, Indian and Turkish families. In order to re-evaluate the relevance of these findings, we carried out a family-based association study among 218 NSCL/P families of Central European descent. Genomic DNA was obtained from peripheral blood of 218 complete parent-offspring triads with NSCL/P. The sample comprised 14 patients with cleft lip only (CLO) and 204 patients with cleft lip and palate (CLP). Genotyping and transmission disequilibrium test (TDT) were performed on all 218 triads with a total of 17 tagging single-nucleotide polymorphisms (SNPs). We also performed testing for extended haplotypes and a log-linear model by Weinberg was used to screen parent-of-origin effects. Furthermore the use of estimates for the relative risks (RR) of Weinberg's model was obtained. TDT analysis revealed no significant transmission distortion, neither at the level of individual markers nor at the level of haplotypes. Similarly negative results were obtained when we restricted our analysis to the subgroup of patients with CLP (n=204). Relative risk calculations (RR) of the children's and mothers' genotypes obtained negative results, after correction of p-values for multiple testing. Likewise application of Weinberg's log-linear mod [TRUNCATED]", "output": "{\"label\": \"no\", \"rationale\": \"Despite the ample evidence supporting the role of TGF-β type 1 receptor as a critically important and widespread morphogenetic regulator of craniofacial development in murine models, our results do not support TGFBR1 as major risk factor for NSCL/P in patients of Central European descent.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 19586667, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Blocking the interaction between TDP-43 and respiratory complex I proteins ND3 and ND6 leads to increased TDP-43-induced neuronal loss.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Inhibition of TDP-43 Mitochondrial Localization Blocks Its Neuronal Toxicity\nABSTRACT: Genetic mutations in TAR DNA-binding protein 43 (TARDBP, also known as TDP-43) cause amyotrophic lateral sclerosis (ALS), and an increase in the presence of TDP-43 (encoded by TARDBP) in the cytoplasm is a prominent histopathological feature of degenerating neurons in various neurodegenerative diseases. However, the molecular mechanisms by which TDP-43 contributes to ALS pathophysiology remain elusive. Here we have found that TDP-43 accumulates in the mitochondria of neurons in subjects with ALS or frontotemporal dementia (FTD). Disease-associated mutations increase TDP-43 mitochondrial localization. In mitochondria, wild-type (WT) and mutant TDP-43 preferentially bind mitochondria-transcribed messenger RNAs (mRNAs) encoding respiratory complex I subunits ND3 and ND6, impair their expression and specifically cause complex I disassembly. The suppression of TDP-43 mitochondrial localization abolishes WT and mutant TDP-43-induced mitochondrial dysfunction and neuronal loss, and improves phenotypes of transgenic mutant TDP-43 mice. Thus, our studies link TDP-43 toxicity directly to mitochondrial bioenergetics and propose the targeting of TDP-43 mitochondrial localization as a promising therapeutic approach for neurodegeneration.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The suppression of TDP-43 mitochondrial localization abolishes WT and mutant TDP-43-induced mitochondrial dysfunction and neuronal loss, and improves phenotypes of transgenic mutant TDP-43 mice.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 180, "doc_id": "16966326", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The US health care system can save up to $5 billion if 7% of patients waiting for kidney transplants participate in the optimized national kidney paired donation program.\n\nCANDIDATE_ABSTRACT:\nTITLE: Kidney paired donation and optimizing the use of live donor organs.\nABSTRACT: CONTEXT Blood type and crossmatch incompatibility will exclude at least one third of patients in need from receiving a live donor kidney transplant. Kidney paired donation (KPD) offers incompatible donor/recipient pairs the opportunity to match for compatible transplants. Despite its increasing popularity, very few transplants have resulted from KPD. OBJECTIVE To determine the potential impact of improved matching schemes on the number and quality of transplants achievable with KPD. DESIGN, SETTING, AND POPULATION We developed a model that simulates pools of incompatible donor/recipient pairs. We designed a mathematically verifiable optimized matching algorithm and compared it with the scheme currently used in some centers and regions. Simulated patients from the general community with characteristics drawn from distributions describing end-stage renal disease patients eligible for renal transplantation and their willing and eligible live donors. MAIN OUTCOME MEASURES Number of kidneys matched, HLA mismatch of matched kidneys, and number of grafts surviving 5 years after transplantation. RESULTS A national optimized matching algorithm would result in more transplants (47.7% vs 42.0%, P<.001), better HLA concordance (3.0 vs 4.5 mismatched antigens; P<.001), more grafts surviving at 5 years (34.9% vs 28.7%; P<.001), and a reduction in the number of pairs required to travel (2.9% vs 18.4%; P<.001) when compared with an extension of the currently used first-accept scheme to a national level. Furthermore, highly sensitized patients would benefit 6-fold from a national optimized scheme (2.3% vs 14.1% successfully matched; P<.001). Even if only 7% of patients awaiting kidney transplantation participated in an optimized national KPD program, the health care system c [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Even if only 7% of patients awaiting kidney transplantation participated in an optimized national KPD program, the health care system could save as much as $750 million.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1184, "doc_id": "16737210", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: NAC inhibits the generation of angiotensin-converting enzyme.\n\nCANDIDATE_PASSAGE:\nAcetylcysteine for prevention of acute deterioration of renal function following elective coronary angiography and intervention: a randomized controlled trial. CONTEXT The antioxidant acetylcysteine prevents acute contrast nephrotoxicity in patients with impaired renal function who undergo computed tomography scanning. However, its role in coronary angiography is unclear. OBJECTIVE To determine whether oral acetylcysteine prevents acute deterioration in renal function in patients with moderate renal insufficiency who undergo elective coronary angiography. DESIGN AND SETTING Prospective, randomized, double-blind, placebo-controlled trial conducted from May 2000 to December 2001 at the Grantham Hospital at the University of Hong Kong. PARTICIPANTS Two hundred Chinese patients aged mean (SD) 68 (6.5) years with stable moderate renal insufficiency (creatinine clearance <60 mL/min [1.00 mL/s]) who were undergoing elective coronary angiography with or without intervention. INTERVENTION Participants were randomly assigned to receive oral acetylcysteine(600 mg twice per day; n = 102) or matching placebo tablets (n = 98) on the day before and the day of angiography. All patients received low-osmolality contrast agent. MAIN OUTCOME MEASURES Occurrence of more than a 25% increase in serum creatinine level within 48 hours after contrast administration; change in creatinine clearance and serum creatinine level. RESULTS Twelve control patients (12%) and 4 acetylcysteine patients (4%) developed a more than 25% increase in serum creatinine level within 48 hours after contrast administration (relative risk, 0.32; 95% confidence interval [CI], 0.10-0.96; P =.03). Serum creatinine was lower in the acetylcysteine group (1.22 mg/dL [107.8 micromol/L]; 95% CI, 1.11-1.33 mg/dL vs [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "828", "doc_id": "4678846", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Chronic aerobic exercise alters endothelial function, improving vasodilating mechanisms mediated by NO.\n\nCANDIDATE_PASSAGE:\nGlycolytic oligodendrocytes maintain myelin and long-term axonal integrity Oligodendrocytes, the myelin-forming glial cells of the central nervous system, maintain long-term axonal integrity. However, the underlying support mechanisms are not understood. Here we identify a metabolic component of axon–glia interactions by generating conditional Cox10 (protoheme IX farnesyltransferase) mutant mice, in which oligodendrocytes and Schwann cells fail to assemble stable mitochondrial cytochrome c oxidase (COX, also known as mitochondrial complex IV). In the peripheral nervous system, Cox10 conditional mutants exhibit severe neuropathy with dysmyelination, abnormal Remak bundles, muscle atrophy and paralysis. Notably, perturbing mitochondrial respiration did not cause glial cell death. In the adult central nervous system, we found no signs of demyelination, axonal degeneration or secondary inflammation. Unlike cultured oligodendrocytes, which are sensitive to COX inhibitors, post-myelination oligodendrocytes survive well in the absence of COX activity. More importantly, by in vivo magnetic resonance spectroscopy, brain lactate concentrations in mutants were increased compared with controls, but were detectable only in mice exposed to volatile anaesthetics. This indicates that aerobic glycolysis products derived from oligodendrocytes are rapidly metabolized within white matter tracts. Because myelinated axons can use lactate when energy-deprived, our findings suggest a model in which axon–glia metabolic coupling serves a physiological function.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "261", "doc_id": "2601324", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Adult tissue-resident macrophages stem from the embryonal yolk sac and fetal liver.\n\nCANDIDATE_PASSAGE:\nFate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis. Mononuclear phagocytes, including monocytes, macrophages, and dendritic cells, contribute to tissue integrity as well as to innate and adaptive immune defense. Emerging evidence for labor division indicates that manipulation of these cells could bear therapeutic potential. However, specific ontogenies of individual populations and the overall functional organization of this cellular network are not well defined. Here we report a fate-mapping study of the murine monocyte and macrophage compartment taking advantage of constitutive and conditional CX(3)CR1 promoter-driven Cre recombinase expression. We have demonstrated that major tissue-resident macrophage populations, including liver Kupffer cells and lung alveolar, splenic, and peritoneal macrophages, are established prior to birth and maintain themselves subsequently during adulthood independent of replenishment by blood monocytes. Furthermore, we have established that short-lived Ly6C(+) monocytes constitute obligatory steady-state precursors of blood-resident Ly6C(-) cells and that the abundance of Ly6C(+) blood monocytes dynamically controls the circulation lifespan of their progeny.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "89", "doc_id": "7521113", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: MFGE8 regulates fat absorption by binding to av-Beta3 and av-Beta5 integrins.\n\nCANDIDATE_ABSTRACT:\nTITLE: Mfge8 promotes obesity by mediating the uptake of dietary fats and serum fatty acids\nABSTRACT: Fatty acids are integral mediators of energy storage, membrane formation and cell signaling. The pathways that orchestrate uptake of fatty acids remain incompletely understood. Expression of the integrin ligand Mfge8 is increased in human obesity and in mice on a high-fat diet, but its role in obesity is unknown. We show here that Mfge8 promotes the absorption of dietary triglycerides and the cellular uptake of fatty acid and that Mfge8-deficient (Mfge8−/−) mice are protected from diet-induced obesity, steatohepatitis and insulin resistance. Mechanistically, we found that Mfge8 coordinates fatty acid uptake through αvβ3 integrin– and αvβ5 integrin–dependent phosphorylation of Akt by phosphatidylinositide-3 kinase and mTOR complex 2, leading to translocation of Cd36 and Fatp1 from cytoplasmic vesicles to the cell surface. Collectively, our results imply a role for Mfge8 in regulating the absorption and storage of dietary fats, as well as in the development of obesity and its complications.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Mechanistically, we found that Mfge8 coordinates fatty acid uptake through αvβ3 integrin– and αvβ5 integrin–dependent phosphorylation of Akt by phosphatidylinositide-3 kinase and mTOR complex 2, leading to translocation of Cd36 and Fatp1 from cytoplasmic vesicles to the cell surface.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 736, "doc_id": "5389095", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Hematopoietic Stem Cell purification reaches purity rates above 90%.\n\nCANDIDATE_PASSAGE:\nRoles of exosomes in cardioprotection. Exosomes are extracellular vesicles of endosomal origin which have emerged as key mediators of intercellular communication. All major cardiac cell types-including cardiomyocytes, endothelial cells, and fibroblasts-release exosomes that modulate cellular functions. Exosomes released from human cardiac progenitor cells (CPCs) are cardioprotective and improve cardiac function after myocardial infarction to an extent comparable with that achieved by their parent cells. Cardiac progenitor cell-derived exosomes are enriched in cardioprotective microRNAs, particularly miR-146a-3p. Circulating exosomes mediate remote ischaemic preconditioning. Moreover, they currently are being investigated as diagnostic markers. The discovery that cell-derived extracellular signalling organelles mediate the paracrine effects of stem cells suggests that cell-free strategies could supplant cell transplantation. This review discusses emerging roles of exosomes in cardiovascular physiology, with a focus on cardioprotective activities of CPC-derived exosomes.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "509", "doc_id": "4020950", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Having a main partner improves HIV outcomes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Stable partnership and progression to AIDS or death in HIV infected patients receiving highly active antiretroviral therapy: Swiss HIV cohort study.\nABSTRACT: OBJECTIVES To explore the association between a stable partnership and clinical outcome in HIV infected patients receiving highly active antiretroviral therapy (HAART). DESIGN Prospective cohort study of adults with HIV (Swiss HIV cohort study). SETTING Seven outpatient clinics throughout Switzerland. PARTICIPANTS The 3736 patients in the cohort who started HAART before 2002 (median age 36 years, 29% female, median follow up 3.6 years). MAIN OUTCOME MEASURES Time to AIDS or death (primary endpoint), death alone, increases in CD4 cell count of at least 50 and 100 above baseline, optimal viral suppression (a viral load below 400 copies/ml), and viral rebound. RESULTS During follow up 2985 (80%) participants reported a stable partnership on at least one occasion. When starting HAART, 52% (545/1042) of participants reported a stable partnership; after five years of follow up 46% (190/412) of participants reported a stable partnership. In an analysis stratified by previous antiretroviral therapy and clinical stage when starting HAART (US Centers for Disease Control and Prevention group A, B, or C), the adjusted hazard ratio for progression to AIDS or death was 0.79 (95% confidence interval 0.63 to 0.98) for participants with a stable partnership compared with those without. Adjusted hazards ratios for other endpoints were 0.59 (0.44 to 0.79) for progression to death, 1.15 (1.06 to 1.24) for an increase in CD4 cells of 100 counts/microl or more, and 1.06 (0.98 to 1.14) for optimal viral suppression. CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS A stable partnership is associated with a slower rate of progression to AIDS or death in HIV infected patients receiving HAART.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 495, "doc_id": "17077004", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: RAD52 is involved in break-induced DNA replication (BIR).\n\nCANDIDATE_ABSTRACT:\nTITLE: Human cancer cells utilize mitotic DNA synthesis to resist replication stress at telomeres regardless of their telomere maintenance mechanism\nABSTRACT: Telomeres resemble common fragile sites (CFSs) in that they are difficult-to-replicate and exhibit fragility in mitosis in response to DNA replication stress. At CFSs, this fragility is associated with a delay in the completion of DNA replication until early mitosis, whereupon cells are proposed to switch to a RAD52-dependent form of break-induced replication. Here, we show that this mitotic DNA synthesis (MiDAS) is also a feature of human telomeres. Telomeric MiDAS is not restricted to those telomeres displaying overt fragility, and is a feature of a wide range of cell lines irrespective of whether their telomeres are maintained by telomerase or by the alternative lengthening of telomeres (ALT) mechanism. MiDAS at telomeres requires RAD52, and is mechanistically similar to CFS-associated MiDAS, with the notable exception that telomeric MiDAS does not require the MUS81-EME1 endonuclease. We propose a model whereby replication stress initiates a RAD52-dependent form of break-induced replication that bypasses a requirement for MUS81-EME1 to complete DNA synthesis in mitosis.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"At CFSs, this fragility is associated with a delay in the completion of DNA replication until early mitosis, whereupon cells are proposed to switch to a RAD52-dependent form of break-induced replication.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1003, "doc_id": "4899981", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: MeCP2 influences the synaptic maturation of neurons.\n\nCANDIDATE_ABSTRACT:\nTITLE: Structural Homeostasis: Compensatory Adjustments of Dendritic Arbor Geometry in Response to Variations of Synaptic Input \nABSTRACT: As the nervous system develops, there is an inherent variability in the connections formed between differentiating neurons. Despite this variability, neural circuits form that are functional and remarkably robust. One way in which neurons deal with variability in their inputs is through compensatory, homeostatic changes in their electrical properties. Here, we show that neurons also make compensatory adjustments to their structure. We analysed the development of dendrites on an identified central neuron (aCC) in the late Drosophila embryo at the stage when it receives its first connections and first becomes electrically active. At the same time, we charted the distribution of presynaptic sites on the developing postsynaptic arbor. Genetic manipulations of the presynaptic partners demonstrate that the postsynaptic dendritic arbor adjusts its growth to compensate for changes in the activity and density of synaptic sites. Blocking the synthesis or evoked release of presynaptic neurotransmitter results in greater dendritic extension. Conversely, an increase in the density of presynaptic release sites induces a reduction in the extent of the dendritic arbor. These growth adjustments occur locally in the arbor and are the result of the promotion or inhibition of growth of neurites in the proximity of presynaptic sites. We provide evidence that suggest a role for the postsynaptic activity state of protein kinase A in mediating this structural adjustment, which modifies dendritic growth in response to synaptic activity. These findings suggest that the dendritic arbor, at least during early stages of connectivity, behaves as a homeostatic device that adjusts its size and geometry to the level and the distribution of input received. The growing arbor thus counterbalan [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 761, "doc_id": "10009203", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: A country's Vaccine Alliance (GAVI) eligibility is not indictivate of accelerated adoption of the Hub vaccine.\n\nCANDIDATE_PASSAGE:\nDelayed and Accelerated Aging Share Common Longevity Assurance Mechanisms Mutant dwarf and calorie-restricted mice benefit from healthy aging and unusually long lifespan. In contrast, mouse models for DNA repair-deficient progeroid syndromes age and die prematurely. To identify mechanisms that regulate mammalian longevity, we quantified the parallels between the genome-wide liver expression profiles of mice with those two extremes of lifespan. Contrary to expectation, we find significant, genome-wide expression associations between the progeroid and long-lived mice. Subsequent analysis of significantly over-represented biological processes revealed suppression of the endocrine and energy pathways with increased stress responses in both delayed and premature aging. To test the relevance of these processes in natural aging, we compared the transcriptomes of liver, lung, kidney, and spleen over the entire murine adult lifespan and subsequently confirmed these findings on an independent aging cohort. The majority of genes showed similar expression changes in all four organs, indicating a systemic transcriptional response with aging. This systemic response included the same biological processes that are triggered in progeroid and long-lived mice. However, on a genome-wide scale, transcriptomes of naturally aged mice showed a strong association to progeroid but not to long-lived mice. Thus, endocrine and metabolic changes are indicative of \"survival\" responses to genotoxic stress or starvation, whereas genome-wide associations in gene expression with natural aging are indicative of biological age, which may thus delineate pro- and anti-aging effects of treatments aimed at health-span extension.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "32", "doc_id": "2466614", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Long - range chromatin interactions regulate transcription.\n\nCANDIDATE_PASSAGE:\nEnhancer Evolution across 20 Mammalian Species The mammalian radiation has corresponded with rapid changes in noncoding regions of the genome, but we lack a comprehensive understanding of regulatory evolution in mammals. Here, we track the evolution of promoters and enhancers active in liver across 20 mammalian species from six diverse orders by profiling genomic enrichment of H3K27 acetylation and H3K4 trimethylation. We report that rapid evolution of enhancers is a universal feature of mammalian genomes. Most of the recently evolved enhancers arise from ancestral DNA exaptation, rather than lineage-specific expansions of repeat elements. In contrast, almost all liver promoters are partially or fully conserved across these species. Our data further reveal that recently evolved enhancers can be associated with genes under positive selection, demonstrating the power of this approach for annotating regulatory adaptations in genomic sequences. These results provide important insight into the functional genetics underpinning mammalian regulatory evolution.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "704", "doc_id": "14658685", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Mutant mice lacking SVCT2 have severely reduced ascorbic acid levels in both brain and adrenals.\n\nCANDIDATE_ABSTRACT:\nTITLE: Visualization of volatile substances in different organelles with an atmospheric-pressure mass microscope.\nABSTRACT: We have developed a mass microscope (mass spectrometry imager with spatial resolution higher than the naked eye) equipped with an atmospheric pressure ion-source chamber for laser desorption/ionization (AP-LDI) and a quadrupole ion trap time-of-flight (QIT-TOF) analyzer. The optical microscope combined with the mass spectrometer permitted us to precisely determine the relevant tissue region prior to performing imaging mass spectrometry (IMS). An ultraviolet laser tightly focused with a triplet lens was used to achieve high spatial resolution. An atmospheric pressure ion-source chamber enables us to analyze fresh samples with minimal loss of intrinsic water or volatile compounds. Mass-microscopic AP-LDI imaging of freshly cut ginger rhizome sections revealed that 6-gingerol ([M + K](+)at m/z 333.15, positive mode; [M - H](-) at m/z 293.17, negative mode) and the monoterpene ([M + K](+) at m/z 191.09), which are the compounds related to pungency and flavor, respectively, were localized in oil drop-containing organelles. AP-LDI-tandem MS/MS analyses were applied to compare authentic signals from freshly cut ginger directly with the standard reagent. Thus, our atmosphere-imaging mass spectrometer enabled us to monitor a quality of plants at the organelle level.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 812, "doc_id": "712320", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: B3-Galectin increases cell resistance to tyrosine kinase inhibitors (TKIs) by engaging the alternate KRAS-RalB signaling complex downstream of EGFR.\n\nCANDIDATE_PASSAGE:\nGuanylate binding protein 1 is a novel effector of EGFR-driven invasion in glioblastoma Although GBP1 (guanylate binding protein 1) was among the first interferon-inducible proteins identified, its function is still largely unknown. Epidermal growth factor receptor (EGFR) activation by amplification or mutation is one of the most frequent genetic lesions in a variety of human tumors. These include glioblastoma multiforme (GBM), which is characterized by independent but interrelated features of extensive invasion into normal brain parenchyma, rapid growth, necrosis, and angiogenesis. In this study, we show that EGFR activation promoted GBP1 expression in GBM cell lines through a signaling pathway involving Src and p38 mitogen-activated protein kinase. Moreover, we identified YY1 (Yin Yang 1) as the downstream transcriptional regulator regulating EGFR-driven GBP1 expression. GBP1 was required for EGFR-mediated MMP1 (matrix metalloproteinase 1) expression and glioma cell invasion in vitro. Although deregulation of GBP1 expression did not affect glioma cell proliferation, overexpression of GBP1 enhanced glioma cell invasion through MMP1 induction, which required its C-terminal helical domain and was independent of its GTPase activity. Reducing GBP1 levels by RNA interference in invasive GBM cells also markedly inhibited their ability to infiltrate the brain parenchyma of mice. GBP1 expression was high and positively correlated with EGFR expression in human GBM tumors and cell lines, particularly those of the neural subtype. Together, these findings establish GBP1 as a previously unknown link between EGFR activity and MMP1 expression and nominate it as a novel potential therapeutic target for inhibiting GBM invasion.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "154", "doc_id": "12685434", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Silencing of Bcl2 is important for the maintenance and progression of tumors.\n\nCANDIDATE_ABSTRACT:\nTITLE: Antiapoptotic BCL-2 is required for maintenance of a model leukemia.\nABSTRACT: Resistance to apoptosis, often achieved by the overexpression of antiapoptotic proteins, is common and perhaps required in the genesis of cancer. However, it remains uncertain whether apoptotic defects are essential for tumor maintenance. To test this, we generated mice expressing a conditional BCL-2 gene and constitutive c-myc that develop lymphoblastic leukemia. Eliminating BCL-2 yielded rapid loss of leukemic cells and significantly prolonged survival, formally validating BCL-2 as a rational target for cancer therapy. Loss of this single molecule resulted in cell death, despite or perhaps attributable to the presence of other oncogenic events. This suggests a generalizable model in which aberrations inherent to cancer generate tonic death signals that would otherwise kill the cell if not opposed by a requisite apoptotic defect(s).", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Eliminating BCL-2 yielded rapid loss of leukemic cells and significantly prolonged survival, formally validating BCL-2 as a rational target for cancer therapy.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1088, "doc_id": "37549932", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Birth-weight is positively associated with breast cancer.\n\nCANDIDATE_ABSTRACT:\nTITLE: Implementation of a Clinical Pharmacy Education Program in a Teaching Hospital: Resident Oriented Documentation and Intervention\nABSTRACT: The aim of this study was to provide a clinical pharmacy education program at Masih Daneshvari hospital, a University affiliated hospital, located in Tehran, Iran. For this purpose, the most common pharmacist involved interventions and aspects of potential fields for pharmacy students and residents education was firstly identified. Clinical pharmacy interventions and drug information forms were filled during the study period, from January 2006 till January 2007. Based on the results of this study, a total number of 772 interventions were conducted during the study year. Drug information had the highest rate of 22.30% among all interventions, followed by dose adjustment, and therapeutic reduction or addition. The mean number of medications per patient was 8.62 ± 7.54. In conclusion, it could be said that although in our country the challenge for the pharmacy as a profession is in its initial stages compared to the developed countries, the result of this study revealed a high demand for this service among health care providers.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 179, "doc_id": "2276126", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Do haplotypes of susceptibility to chronic periodontitis in the Interleukin 8 gene influence protein level in the gingival crevicular fluid?\n\nABSTRACT:\nPreviously, we identified that the ATC/TTC haplotype formed by polymorphisms in the Interleukin-(IL)8 gene conferred susceptibility to chronic periodontitis (CP). The aim of the study was to investigate whether the IL8 haplotype ATC/TTC was associated with the volume of gingival crevicular fluid (GCF), the concentration of interleukin IL-8 in the GCF, as well as periodontal conditions in patients with CP in comparison to controls without CP. Seventy-nine individuals (CP: n=41, controls: n=38) were grouped according to the presence (susceptible for CP) or absence (not susceptible for CP) of the IL8 ATC/TTC haplotype. After periodontal clinical evaluation, they were subdivided by the presence or absence of CP. GCF was collected from each patient and the IL-8 levels were determined by ELISA. The GCF volume of each subject was measured by means of a calibrated electronic device. Comparisons of means between carriers and non-carriers of the ATC/TTC haplotype were evaluated using the Mann-Whitney test. Linear regression and stepwise linear regression analysis were used to analyse the association of the GCF volume with potential covariates and their contribution for the phenotype. We did not find significant differences of both periodontal conditions and IL-8 concentration in the GCF of patients with the presence or absence of the IL8 ATC/TTC haplotype. However, the GCF volume was significantly higher amongst the patients affected by CP that are absent for the IL8 ATC/TTC haplotype. In addition, linear regression analysis showed a statistically significant association between GCF volume and CP, IL8 haplotype ATC/TTC and IL-8 concentration.", "output": "{\"label\": \"no\", \"rationale\": \"The IL8 haplotype of susceptibility to CP was neither associated with IL-8 cytokine levels nor with clinical periodontal parameters. Also, CP, IL8 haplotype and IL-8 concentration showed a positive association with the GCF volume levels in the studied patients.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 22877792, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: In rhesus macaques, daily subcutaneous injections of emtricitabine are ineffective at protecting against rectally transmitted simian-human immunodeficiency virus.\n\nCANDIDATE_PASSAGE:\nHuman Cytomegalovirus Latency-Associated Proteins Elicit Immune-Suppressive IL-10 Producing CD4+ T Cells Human cytomegalovirus (HCMV) is a widely prevalent human herpesvirus, which, after primary infection, persists in the host for life. In healthy individuals, the virus is well controlled by the HCMV-specific T cell response. A key feature of this persistence, in the face of a normally robust host immune response, is the establishment of viral latency. In contrast to lytic infection, which is characterised by extensive viral gene expression and virus production, long-term latency in cells of the myeloid lineage is characterised by highly restricted expression of viral genes, including UL138 and LUNA. Here we report that both UL138 and LUNA-specific T cells were detectable directly ex vivo in healthy HCMV seropositive subjects and that this response is principally CD4⁺ T cell mediated. These UL138-specific CD4⁺ T cells are able to mediate MHC class II restricted cytotoxicity and, importantly, show IFNγ effector function in the context of both lytic and latent infection. Furthermore, in contrast to CDCD4⁺ T cells specific to antigens expressed solely during lytic infection, both the UL138 and LUNA-specific CD4⁺ T cell responses included CD4⁺ T cells that secreted the immunosuppressive cytokine cIL-10. We also show that cIL-10 expressing CD4⁺ T-cells are directed against latently expressed US28 and UL111A. Taken together, our data show that latency-associated gene products of HCMV generate CD4⁺ T cell responses in vivo, which are able to elicit effector function in response to both lytic and latently infected cells. Importantly and in contrast to CD4⁺ T cell populations, which recognise antigens solely expressed during lytic infection, include a subset of cell [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "582", "doc_id": "10450300", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Localization of PIN1 in the roots of Arabidopsis requires VPS9a\n\nCANDIDATE_PASSAGE:\nIntegration of Smad and MAPK pathways: a link and a linker revisited. Cells develop by reading mixed signals. Nowhere is this clearer than in the highly dynamic processes that propel embryogenesis, when critical cell-fate decisions are made swiftly in response to well-orchestrated growthfactor combinations. Learning how diverse signaling pathways are integrated is therefore essential for understanding physiology. This requires the identification, in tangible molecular terms, of key nodes for pathway integration that operate in vivo. A report in this issue, on the integration of Smad and Ras/MAPK pathways during neural induction (Pera et al. 2003), provides timely insights into the relevance of one such node. Pera et al. (2003) report that FGF8 and IGF2—two growth factors that activate the Ras/MAPK pathway— favor neural differentiation and mesoderm dorsalization in Xenopus by inhibiting BMP (Bone Morphogenetic Protein) signaling. Mesoderm is formed from ectoderm in response to Nodal-related signals from the endoderm at the blastula stage and beyond (Fig. 1; for review, see De Robertis et al. 2000). BMP induces differentiation of ectoderm into epidermal cell fates at the expense of neural fates, and it ventralizes the mesoderm at the expense of dorsal fates (for review, see Weinstein and HemmatiBrivanlou 1999; De Robertis et al. 2000). Accordingly, neural differentiation and dorsal mesoderm formation are favored when BMP signaling is attenuated. Noggin, Chordin, Cerberus, and Follistatin, secreted by the Spemann organizer on the dorsal side at the gastrula stage, facilitate the formation of neural tissue by sequestering BMP (Weinstein and Hemmati-Brivanlou 1999; De Robertis et al. 2000). Experimentally blocking BMP signaling with a dominant-negative BMP recept [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "703", "doc_id": "39291138", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Interferon stimulated genes (ISGs) Irf1, Irg1, Ifi27, and Rsad2 inhibit West Nile virus replication in cortical neurons.\n\nCANDIDATE_PASSAGE:\nBRACHYURY and CDX2 Mediate BMP-Induced Differentiation of Human and Mouse Pluripotent Stem Cells into Embryonic and Extraembryonic Lineages BMP is thought to induce hESC differentiation toward multiple lineages including mesoderm and trophoblast. The BMP-induced trophoblast phenotype is a long-standing paradox in stem cell biology. Here we readdressed BMP function in hESCs and mouse epiblast-derived cells. We found that BMP4 cooperates with FGF2 (via ERK) to induce mesoderm and to inhibit endoderm differentiation. These conditions induced cells with high levels of BRACHYURY (BRA) that coexpressed CDX2. BRA was necessary for and preceded CDX2 expression; both genes were essential for expression not only of mesodermal genes but also of trophoblast-associated genes. Maximal expression of the latter was seen in the absence of FGF but these cells coexpressed mesodermal genes and moreover they differed in cell surface and epigenetic properties from placental trophoblast. We conclude that BMP induces human and mouse pluripotent stem cells primarily to form mesoderm, rather than trophoblast, acting through BRA and CDX2.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "652", "doc_id": "5633876", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Up-regulation of the p53 pathway and related molecular events speeds cancer progression.\n\nCANDIDATE_PASSAGE:\nSenescent Cells, Tumor Suppression, and Organismal Aging: Good Citizens, Bad Neighbors Cells from organisms with renewable tissues can permanently withdraw from the cell cycle in response to diverse stress, including dysfunctional telomeres, DNA damage, strong mitogenic signals, and disrupted chromatin. This response, termed cellular senescence, is controlled by the p53 and RB tumor suppressor proteins and constitutes a potent anticancer mechanism. Nonetheless, senescent cells acquire phenotypic changes that may contribute to aging and certain age-related diseases, including late-life cancer. Thus, the senescence response may be antagonistically pleiotropic, promoting early-life survival by curtailing the development of cancer but eventually limiting longevity as dysfunctional senescent cells accumulate.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1345", "doc_id": "9559146", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: ART substantially reduces infectiveness of HIV-positive people.\n\nCANDIDATE_PASSAGE:\nRibosomal DNA copy loss and repeat instability in ATRX-mutated cancers ATRX (alpha thalassemia/mental retardation X-linked) complexes with DAXX to deposit histone variant H3.3 into repetitive heterochromatin. Recent genome sequencing studies in cancers have revealed mutations in ATRX and their association with ALT (alternative lengthening of telomeres) activation. Here we report depletion of ATRX in mouse ES cells leads to selective loss in ribosomal RNA gene (rDNA) copy number. Supporting this, ATRX-mutated human ALT-positive tumors also show a substantially lower rDNA copy than ALT-negative tumors. Further investigation shows that the rDNA copy loss and repeat instability are caused by a disruption in H3.3 deposition and thus a failure in heterochromatin formation at rDNA repeats in the absence of ATRX. We also find that ATRX-depleted cells are reduced in ribosomal RNA transcription output and show increased sensitivity to RNA polymerase I (Pol I) transcription inhibitor CX5461. In addition, human ALT-positive cancer cell lines are also more sensitive to CX5461 treatment. Our study provides insights into the contribution of ATRX loss of function to tumorigenesis through the loss of rDNA stability and suggests the therapeutic potential of targeting Pol I transcription in ALT cancers.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "61", "doc_id": "4993011", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Replacement of OCT4 and SOX2 genes with GATA3 is not capable of reprogramming human cells.\n\nCANDIDATE_PASSAGE:\nA C-Type Lectin Collaborates with a CD45 Phosphatase Homolog to Facilitate West Nile Virus Infection of Mosquitoes West Nile virus (WNV) is the most common arthropod-borne flavivirus in the United States; however, the vector ligand(s) that participate in infection are not known. We now show that an Aedes aegypti C-type lectin, mosGCTL-1, is induced by WNV, interacts with WNV in a calcium-dependent manner, and facilitates infection in vivo and in vitro. A mosquito homolog of human CD45 in A. aegypti, designated mosPTP-1, recruits mosGCTL-1 to enable viral attachment to cells and to enhance viral entry. In vivo experiments show that mosGCTL-1 and mosPTP-1 function as part of the same pathway and are critical for WNV infection of mosquitoes. A similar phenomenon was also observed in Culex quinquefasciatus, a natural vector of WNV, further demonstrating that these genes participate in WNV infection. During the mosquito blood-feeding process, WNV infection was blocked in vivo with mosGCTL-1 antibodies. A molecular understanding of flaviviral-arthropod interactions may lead to strategies to control viral dissemination in nature.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1038", "doc_id": "12885341", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Metastatic colorectal cancer treated with a single agent fluoropyrimidines resulted in similar efficacy and better quality of life when compared with oxaliplatin-based chemotherapy in elderly patients.\n\nCANDIDATE_PASSAGE:\nDosimetry and risk estimates of radioiodine therapy for large, multinodular goiters. UNLABELLED In patients with a large, multinodular goiter (> 100 g), radiation absorbed doses in the thyroid, surrounding tissues and remainder of the body were estimated after therapeutic administration of 131I(3.7 MBq or 100 microCi/g of thyroid tissue retained at 24 hr). METHODS Thermoluminescent dosimeter (TLD) measurements were performed on 23 patients (12 euthyroid and 1I hyperthyroid; thyroid weight 222 +/- 72 g; 2.1 +/- 0.9 GBq 131I) on the skin over the thyroid, over the submandibular gland and over the parotid gland. Thyroid radioactivity measurements were done daily in 6 euthyroid and 6 hyperthyroid patients (thyroid weight 204 +/- 69 g; 1.9 +/- 0.9 GBq 131I). An iodine biokinetic model and the MIRD methodology were used to estimate absorbed doses in organs. Cancer risks were calculated using ICRP Publication 60. RESULTS Cumulated absorbed doses on the skin (TLD measurements) were 4.2 +/- 1.4 Gy (thyroid), 1.2 +/- 0.6 Gy (submandibular) and 0.4 +/- 0.2 Gy (parotid). All these values were significantly correlated with the amount of radioiodine retained in the thyroid at 24 hr (euthyroid versus hyperthyroid not significant). Absorbed doses in the thyroid of 94 +/- 25 Gy for euthyroid and 93 +/- 17 Gy for hyperthyroid patients were calculated (thyroid radioactivity measurements). Extrathyroidal absorbed doses (means of 12 patients) were 0.88 Gy in the urinary bladder, 0.57 Gy in the small intestine, 0.38 Gy in the stomach, and ranged from 0.05 to 0.30 Gy in other organs (euthyroid versus hyperthyroid not significant). A 1.6% life-time risk of development of cancer outside the thyroid gland was calculated. When applied to people of 65 yr and older the estimated risk is [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "771", "doc_id": "6751418", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Do women residents delay childbearing due to perceived career threats?\n\nABSTRACT:\nTo assess gender differences among residents regarding their plans to have children during residency and determine the most influential reasons for these differences. Using the Health Belief Model as a framework, the authors created an instrument to survey 424 residents from 11 residency programs at three academic medical institutions about their intentions to have children during residency. The authors developed a scale to assess the perceived career threats of having children during residency, evaluated its psychometric properties, and calculated the effect of the mediators. The response rate was 77% (328/424). Forty-one percent of men versus 27% of women planned to have children during residency (P = .01). The instrument measured four career threats-extended training, loss of fellowship positions, pregnancy complications, and interference with career plans-on a five-point Likert scale. The scale had a Cronbach alpha of 0.84 and an eigenvalue of 2.2. Compared with men, women had higher scores for each item and a higher mean score (2.9 versus 2.1, P = .001), signifying greater belief in the potential of pregnancy to threaten careers. After adjusting for age, institution, postgraduate year, and knowledge of parental leave policies, women were less likely to plan to have children during residency (odds ratio 0.46 [95% confidence interval 0.25-0.84]). In mediation analysis, threats to career explained 67% of the gender variance.", "output": "{\"label\": \"yes\", \"rationale\": \"Women residents intentionally postpone pregnancy because of perceived threats to their careers. Medical educators should be aware of these findings when counseling female trainees.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 20354380, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Gluten tolerance in adult patients with celiac disease 20 years after diagnosis?\n\nABSTRACT:\nCeliac disease (CD) is believed to be a permanent intolerance to gluten. A number of patients, however, discontinue the gluten-free diet (GFD) without developing symptoms or signs. The aim of our study was to investigate whether CD patients are capable of developing tolerance to gluten. All 77 adult patients from our hospital known to have biopsy-proven CD for more than 10 years were invited to participate. We investigated symptoms, gluten consumption, antibodies for CD and other autoimmunity, human leukocyte antigen (HLA)-typing, bone mineral density, and performed small bowel biopsies. Tolerance was defined as no immunological or histological signs of CD while consuming gluten. Sixty-six patients accepted participation, but after review of the diagnostic biopsies 53 were found to have true CD. Twenty-three percent of patients had a gluten-containing diet, 15% admitted gluten transgression and 62% followed the GFD. Patients on a GFD had significantly more osteoporosis. Normal small bowel mucosa was found in four of eight on gluten-containing diet and in four of four with gluten transgression. Two patients were considered to have developed tolerance to gluten. One of them was HLA-DQ2/DQ8 negative.", "output": "{\"label\": \"maybe\", \"rationale\": \"Development of tolerance to gluten seems possible in some patients with CD. Further follow-up will show whether this tolerance is permanent or only a long-term return to latency. This feature may be associated with genetic characteristics, especially with HLA genotypes that differ from DQ2 or DQ8.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 18403944, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does perspective-taking increase patient satisfaction in medical encounters?\n\nABSTRACT:\nTo assess whether perspective-taking, which researchers in other fields have shown to induce empathy, improves patient satisfaction in encounters between student-clinicians and standardized patients (SPs). In three studies, randomly assigned students (N = 608) received either a perspective-taking instruction or a neutral instruction prior to a clinical skills examination in 2006-2007. SP satisfaction was the main outcome in all three studies. Study 1 involved 245 third-year medical students from two universities. Studies 2 and 3 extended Study 1 to examine generalizability across student and SP subpopulations. Study 2 (105 physician assistant students, one university) explored the effect of perspective-taking on African American SPs' satisfaction. Study 3 (258 third-year medical students, two universities) examined the intervention's effect on students with high and low baseline perspective-taking tendencies. Intervention students outscored controls in patient satisfaction in all studies: Study 1: P = .01, standardized effect size = 0.16; Study 2: P = .001, standardized effect size = 0.31; Study 3: P = .009, standardized effect size = 0.13. In Study 2, perspective-taking improved African American SPs' satisfaction. In Study 3, intervention students with high baseline perspective-taking tendencies outscored controls (P = .0004, standardized effect size = 0.25), whereas those with low perspective-taking tendencies did not (P = .72, standardized effect size = 0.00).", "output": "{\"label\": \"maybe\", \"rationale\": \"Perspective-taking increased patient satisfaction in all three studies, across medical schools, clinical disciplines, and racially diverse students and SPs. Perspective-taking as a means for improving patient satisfaction deserves further exploration in clinical training and practice.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 20736672, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: In S. cerevisiae, the absence of RNA surveillance pathways causes sensitivity to high iron conditions.\n\nCANDIDATE_ABSTRACT:\nTITLE: Multiple RNA surveillance pathways limit aberrant expression of iron uptake mRNAs and prevent iron toxicity in S. cerevisiae.\nABSTRACT: Tight regulation of the expression of mRNAs encoding iron uptake proteins is essential to control iron homeostasis and avoid intracellular iron toxicity. We show that many mRNAs encoding iron uptake or iron mobilization proteins are expressed in iron-replete conditions in the absence of the S. cerevisiae RNase III ortholog Rnt1p or of the nuclear exosome component Rrp6p. Extended forms of these mRNAs accumulate in the absence of Rnt1p or of the 5'-->3' exonucleases Xrn1p and Rat1p, showing that multiple degradative pathways contribute to the surveillance of aberrant forms of these transcripts. RNase III-deficient cells are hypersensitive to high iron concentrations, suggesting that Rnt1p-mediated RNA surveillance is required to prevent iron toxicity. These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"These results show that RNA surveillance through multiple ribonucleolytic pathways plays a role in iron homeostasis in yeast to avoid the potentially toxic effects of the expression of the iron starvation response in iron-replete conditions.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 565, "doc_id": "16120395", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Nonsteroidal antinflammatory drugs show potential anticancer indications.\n\nCANDIDATE_PASSAGE:\nTraining toddlers seated on mobile robots to drive indoors amidst obstacles The goal of this research is to train children seated on mobile robots to purposefully and safely drive indoors. Our previous studies show that in about six weeks of training, infants can learn to drive directly to a goal using conventional joysticks. However, they are unable to acquire the advanced skill to avoid obstacles while driving. This limits mobility impaired children from exploring their home environment safely, which in turn impacts their cognitive and social developments in the important early years. In this paper, we describe results where toddlers are trained to drive a robot within an obstacle course. Using algorithms based on artificial potential fields to avoid obstacles, we create force field on the joystick that trains them to navigate while avoiding obstacles. In this ‘assist-as-needed’ approach, if the child steers the mobile robot outside a force tunnel centered around the desired direction, the driver experiences a bias force on the hand. The results suggest that force-feedback joystick results in faster learning than with a conventional joystick.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "857", "doc_id": "108886332", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Side effects associated with antidepressants do not represent a mortality risk to postmenopausal women.\n\nCANDIDATE_ABSTRACT:\nTITLE: Antidepressant use and risk of adverse outcomes in older people: population based cohort study\nABSTRACT: OBJECTIVES To investigate the association between antidepressant treatment and risk of several potential adverse outcomes in older people with depression and to examine risks by class of antidepressant, duration of use, and dose. DESIGN Cohort study of people aged 65 and over diagnosed as having depression. SETTING 570 general practices in the United Kingdom supplying data to the QResearch primary care database. PARTICIPANTS 60,746 patients diagnosed as having a new episode of depression between the ages of 65 and 100 years from 1 January 1996 to 31 December 2007 and followed up until 31 December 2008. MAIN OUTCOME MEASURES Hazard ratios associated with antidepressant use for all cause mortality, attempted suicide/self harm, myocardial infarction, stroke/transient ischaemic attack, falls, fractures, upper gastrointestinal bleeding, epilepsy/seizures, road traffic accidents, adverse drug reactions, and hyponatraemia, adjusted for a range of potential confounding variables. Hazard ratios were calculated for antidepressant class (tricyclic and related antidepressants, selective serotonin reuptake inhibitors, other antidepressants), dose, and duration of use and for commonly prescribed individual drugs. RESULTS 54,038 (89.0%) patients received at least one prescription for an antidepressant during follow-up. A total of 1,398,359 antidepressant prescriptions were issued: 764,659 (54.7%) for selective serotonin reuptake inhibitors, 442,192 (31.6%) for tricyclic antidepressants, 2203 (0.2%) for monoamine oxidase inhibitors, and 189,305 (13.5%) for the group of other antidepressants. The associations with the adverse outcomes differed significantly between the antidepressant classes for seven outcomes. Selective serotonin reuptake inhibitors were associated with the [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"The group of other antidepressants was associated with the highest adjusted hazard ratios for all cause mortality (1.66, 1.56 to 1.77), attempted suicide/self harm (5.16, 3.90 to 6.83), stroke/transient ischaemic attack (1.37, 1.22 to 1.55), fracture (1.64, 1.46 to 1.84), and epilepsy/seizures (2.24, 1.60 to 3.15), compared with when antidepressants were not being used.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1081, "doc_id": "5691302", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Piezo1 channels are sensors for cell migration in epithelial cells.\n\nCANDIDATE_PASSAGE:\nPiezo1 Is as a Novel Trefoil Factor Family 1 Binding Protein that Promotes Gastric Cancer Cell Mobility In Vitro Trefoil factor family 1 (TFF1) is a member of the TFF-domain peptide family involved in epithelial restitution and cell motility. Recently, we screened Piezo1 as a candidate TFF1-binding protein. We aimed to confirm Piezo1 as a novel TFF1 binding protein and to assess the role of this interaction in mediating gastric cancer cell mobility. This interaction was confirmed by co-immunoprecipitation and co-localisation of TFF1 and Piezo1 in GES-1 cells. We used stable RNA interference to knockdown Piezo1 protein expression and restored the expression of TFF1 in the gastric cancer cell lines SGC-7901 and BGC-823. Cell motility was evaluated using invasion assay and migration assay in vitro. The expression levels of the integrin subunits β1, β5, α1 as well as the expression of β-catenin and E-cadherin were detected by Western blot. We demonstrate that TFF1, but not TFF2 or TFF3, bind to and co-localize with Piezo1 in the cytoplasm in vitro. TFF1 interacts with the C-terminal portion of the Piezo1 protein. Wound healing and trans-well assays demonstrated that the restored expression of TFF1 promoted cell mobility in gastric cancer cells, and this effect was attenuated by the knockdown of Piezo1. Western blots demonstrated the decreased expression of integrin β1 in Piezo1-knockdown cells. Our data demonstrate that Piezo1 is a novel TFF1 binding protein that is important for TFF1-mediated cell migration and suggest that this interaction may be a therapeutic target in the invasion and metastasis of gastric cancer.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "951", "doc_id": "21414718", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Activator-inhibitor pairs are provided ventrally by Xrl-sizzled.\n\nCANDIDATE_PASSAGE:\nSurviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2016 Objective: To provide an update to “Surviving Sepsis Campaign Guidelines for Management of Sepsis and Septic Shock: 2012. ” Design: A consensus committee of 55 international experts representing 25 international organizations was convened. Nominal groups were assembled at key international meetings (for those committee members attending the conference). A formal conflict-of-interest (COI) policy was developed at the onset of the process and enforced throughout. A stand-alone meeting was held for all panel members in December 2015. Teleconferences and electronic-based discussion among subgroups and among the entire committee served as an integral part of the development. Methods: The panel consisted of five sections: hemodynamics, infection, adjunctive therapies, metabolic, and ventilation. Population, intervention, comparison, and outcomes (PICO) questions were reviewed and updated as needed, and evidence profiles were generated. Each subgroup generated a list of questions, searched for best available evidence, and then followed the principles of the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system to assess the quality of evidence from high to very low, and to formulate recommendations as strong or weak, or best practice statement when applicable. Results: The Surviving Sepsis Guideline panel provided 93 statements on early management and resuscitation of patients with sepsis or septic shock. Overall, 32 were strong recommendations, 39 were weak recommendations, and 18 were best-practice statements. No recommendation was provided for four questions. Conclusions: Substantial agreement exists among a large cohort of international [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "73", "doc_id": "52827184", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Increased lipolysis leads to higher P38 phosphorylation in adipose tissue.\n\nCANDIDATE_ABSTRACT:\nTITLE: Activation of AMPKα2 in adipocytes is essential for nicotine-induced insulin resistance in vivo\nABSTRACT: Cigarette smoking promotes body weight reduction in humans while paradoxically also promoting insulin resistance (IR) and hyperinsulinemia. However, the mechanisms behind these effects are unclear. Here we show that nicotine, a major constituent of cigarette smoke, selectively activates AMP-activated protein kinase α2 (AMPKα2) in adipocytes, which in turn phosphorylates MAP kinase phosphatase-1 (MKP1) at serine 334, initiating its proteasome-dependent degradation. The nicotine-dependent reduction of MKP1 induces the aberrant activation of both p38 mitogen-activated protein kinase and c-Jun N-terminal kinase, leading to increased phosphorylation of insulin receptor substrate 1 (IRS1) at serine 307. Phosphorylation of IRS1 leads to its degradation, protein kinase B inhibition, and the loss of insulin-mediated inhibition of lipolysis. Consequently, nicotine increases lipolysis, which results in body weight reduction, but this increase also elevates the levels of circulating free fatty acids and thus causes IR in insulin-sensitive tissues. These results establish AMPKα2 as an essential mediator of nicotine-induced whole-body IR in spite of reductions in adiposity.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 611, "doc_id": "32408470", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Fibroblast growth factor 21 protects against atherosclerosis by modulating adiponectin and SREBP2 levels.\n\nCANDIDATE_ABSTRACT:\nTITLE: The DNA Methylome of Human Peripheral Blood Mononuclear Cells\nABSTRACT: DNA methylation plays an important role in biological processes in human health and disease. Recent technological advances allow unbiased whole-genome DNA methylation (methylome) analysis to be carried out on human cells. Using whole-genome bisulfite sequencing at 24.7-fold coverage (12.3-fold per strand), we report a comprehensive (92.62%) methylome and analysis of the unique sequences in human peripheral blood mononuclear cells (PBMC) from the same Asian individual whose genome was deciphered in the YH project. PBMC constitute an important source for clinical blood tests world-wide. We found that 68.4% of CpG sites and <0.2% of non-CpG sites were methylated, demonstrating that non-CpG cytosine methylation is minor in human PBMC. Analysis of the PBMC methylome revealed a rich epigenomic landscape for 20 distinct genomic features, including regulatory, protein-coding, non-coding, RNA-coding, and repeat sequences. Integration of our methylome data with the YH genome sequence enabled a first comprehensive assessment of allele-specific methylation (ASM) between the two haploid methylomes of any individual and allowed the identification of 599 haploid differentially methylated regions (hDMRs) covering 287 genes. Of these, 76 genes had hDMRs within 2 kb of their transcriptional start sites of which >80% displayed allele-specific expression (ASE). These data demonstrate that ASM is a recurrent phenomenon and is highly correlated with ASE in human PBMCs. Together with recently reported similar studies, our study provides a comprehensive resource for future epigenomic research and confirms new sequencing technology as a paradigm for large-scale epigenomics studies.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 420, "doc_id": "18670", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The G34R/V mutation creates a hypomethylated phenotype at the H3K36 histone.\n\nCANDIDATE_PASSAGE:\nIntegrins promote cytokinesis through the RSK signaling axis. Cytokinesis is the final stage in cell division. Although integrins can regulate cytokinesis, the mechanisms involved are not fully understood. In this study, we demonstrate that integrin-regulated ERK (extracellular signal-related kinase) and RSK (p90 ribosomal S6 kinase) signaling promotes successful cytokinesis. Inhibiting the activation of ERK and RSK in CHO cells by a mutation in the integrin β1 cytoplasmic tail or with pharmacological inhibitors results in the accumulation of cells with midbodies and the formation of binucleated cells. Activation of ERK and RSK signaling by the expression of constitutively active RAF1 suppresses the mutant phenotype in a RSK-dependent manner. Constitutively active RSK2 also restores cytokinesis inhibited by the mutant integrin. Importantly, the regulatory role of the RSK pathway is not specific to CHO cells. MCF-10A human mammary epithelial cells and HPNE human pancreatic ductal epithelial cells exhibit a similar dependence on RSK for successful cytokinesis. In addition, depriving mitotic MCF10A cells of integrin-mediated adhesion by incubating them in suspension suppressed ERK and RSK activation and resulted in a failure of cytokinesis. Furthermore, inhibition of RSK or integrins within the 3D context of a developing salivary gland organ explant also leads to an accumulation of epithelial cells with midbodies, suggesting a similar defect in cytokinesis. Interestingly, neither ERK nor RSK regulates cytokinesis in human fibroblasts, suggesting cell-type specificity. Taken together, our results identify the integrin-RSK signaling axis as an important regulator of cytokinesis in epithelial cells. We propose that the proper interaction of cells with their microe [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1164", "doc_id": "5321708", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Hyperfibrinogenemia decreases rates of femoropopliteal bypass thrombosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Influence of smoking and plasma factors on patency of femoropopliteal vein grafts.\nABSTRACT: OBJECTIVE To determine the effects of smoking, plasma lipids, lipoproteins, apolipoproteins, and fibrinogen on the patency of saphenous vein femoropopliteal bypass grafts at one year. DESIGN Prospective study of patients with saphenous vein femoropopliteal bypass grafts entered into a multicentre trial. SETTING Surgical wards, outpatient clinics, and home visits coordinated by two tertiary referral centres in London and Birmingham. PATIENTS 157 Patients (mean age 66.6 (SD 8.2) years), 113 with patent grafts and 44 with occluded grafts one year after bypass. MAIN OUTCOME MEASURE Cumulative percentage patency at one year. RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts. Serum cholesterol concentrations were significantly higher in patients with grafts that remained patent one year after bypass (p less than 0.005). Analysis of the smoking markers indicated that a quarter of patients (40) were untruthful in their claims to have stopped smoking. Based on smoking markers, patency of grafts in smokers was significantly lower at one year by life table analysis than in non-smokers (63% v 84%, p less than 0.02). Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002). Surprisingly, increased plasma low density lipoprotein cholesterol concentration was significantly associated with improved patency at one year (85%) at values above the median compared w [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"A more forceful approach is needed to stop patients smoking; therapeutic measures to improve patency of vein grafts should focus on decreasing plasma fibrinogen concentration rather than serum cholesterol concentration.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 532, "doc_id": "12991445", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Reduced responsiveness to interleukin-2 in regulatory T cells is associated with autoimmune diseases such as Type 1 Diabetes.\n\nCANDIDATE_PASSAGE:\nAire deficiency promotes TRP-1-specific immune rejection of melanoma. The thymic transcription factor autoimmune regulator (Aire) prevents autoimmunity in part by promoting expression of tissue-specific self-antigens, which include many cancer antigens. For example, AIRE-deficient patients are predisposed to vitiligo, an autoimmune disease of melanocytes that is often triggered by efficacious immunotherapies against melanoma. Therefore, we hypothesized that Aire deficiency in mice may elevate immune responses to cancer and provide insights into how such responses might be triggered. In this study, we show that Aire deficiency decreases thymic expression of TRP-1 (TYRP1), which is a self-antigen in melanocytes and a cancer antigen in melanomas. Aire deficiency resulted in defective negative selection of TRP-1-specific T cells without affecting thymic numbers of regulatory T cells. Aire-deficient mice displayed elevated T-cell immune responses that were associated with suppression of melanoma outgrowth. Furthermore, transplantation of Aire-deficient thymic stroma was sufficient to confer more effective immune rejection of melanoma in an otherwise Aire wild-type host. Together, our work showed how Aire deficiency can enhance immune responses against melanoma and how manipulating TRP-1-specific T-cell negative selection may offer a logical strategy to enhance immune rejection of melanoma.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1028", "doc_id": "25738896", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Recognition of start codons depends on the translation initiation factor IF3.\n\nCANDIDATE_ABSTRACT:\nTITLE: Large-Scale Movements of IF3 and tRNA during Bacterial Translation Initiation\nABSTRACT: In bacterial translational initiation, three initiation factors (IFs 1-3) enable the selection of initiator tRNA and the start codon in the P site of the 30S ribosomal subunit. Here, we report 11 single-particle cryo-electron microscopy (cryoEM) reconstructions of the complex of bacterial 30S subunit with initiator tRNA, mRNA, and IFs 1-3, representing different steps along the initiation pathway. IF1 provides key anchoring points for IF2 and IF3, thereby enhancing their activities. IF2 positions a domain in an extended conformation appropriate for capturing the formylmethionyl moiety charged on tRNA. IF3 and tRNA undergo large conformational changes to facilitate the accommodation of the formylmethionyl-tRNA (fMet-tRNA(fMet)) into the P site for start codon recognition.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"IF3 and tRNA undergo large conformational changes to facilitate the accommodation of the formylmethionyl-tRNA (fMet-tRNA(fMet)) into the P site for start codon recognition.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1023, "doc_id": "16927286", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Antiretroviral therapy increases rates of tuberculosis across a broad range of CD4 strata.\n\nCANDIDATE_PASSAGE:\nComparison of allogeneic vs autologous bone marrow–derived mesenchymal stem cells delivered by transendocardial injection in patients with ischemic cardiomyopathy: the POSEIDON randomized trial. CONTEXT Mesenchymal stem cells (MSCs) are under evaluation as a therapy for ischemic cardiomyopathy (ICM). Both autologous and allogeneic MSC therapies are possible; however, their safety and efficacy have not been compared. OBJECTIVE To test whether allogeneic MSCs are as safe and effective as autologous MSCs in patients with left ventricular (LV) dysfunction due to ICM. DESIGN, SETTING, AND PATIENTS A phase 1/2 randomized comparison (POSEIDON study) in a US tertiary-care referral hospital of allogeneic and autologous MSCs in 30 patients with LV dysfunction due to ICM between April 2, 2010, and September 14, 2011, with 13-month follow-up. INTERVENTION Twenty million, 100 million, or 200 million cells (5 patients in each cell type per dose level) were delivered by transendocardial stem cell injection into 10 LV sites. MAIN OUTCOME MEASURES Thirty-day postcatheterization incidence of predefined treatment-emergent serious adverse events (SAEs). Efficacy assessments included 6-minute walk test, exercise peak VO2, Minnesota Living with Heart Failure Questionnaire (MLHFQ), New York Heart Association class, LV volumes, ejection fraction (EF), early enhancement defect (EED; infarct size), and sphericity index. RESULTS Within 30 days, 1 patient in each group (treatment-emergent SAE rate, 6.7%) was hospitalized for heart failure, less than the prespecified stopping event rate of 25%. The 1-year incidence of SAEs was 33.3% (n = 5) in the allogeneic group and 53.3% (n = 8) in the autologous group (P = .46). At 1 year, there were no ventricular arrhythmia SAEs observed among all [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "123", "doc_id": "40164383", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Ambulatory blood pressure monitoring is inaccurate at diagnosing hypertension.\n\nCANDIDATE_ABSTRACT:\nTITLE: Relative effectiveness of clinic and home blood pressure monitoring compared with ambulatory blood pressure monitoring in diagnosis of hypertension: systematic review\nABSTRACT: OBJECTIVE To determine the relative accuracy of clinic measurements and home blood pressure monitoring compared with ambulatory blood pressure monitoring as a reference standard for the diagnosis of hypertension. DESIGN Systematic review with meta-analysis with hierarchical summary receiver operating characteristic models. Methodological quality was appraised, including evidence of validation of blood pressure measurement equipment. DATA SOURCES Medline (from 1966), Embase (from 1980), Cochrane Database of Systematic Reviews, DARE, Medion, ARIF, and TRIP up to May 2010. Eligibility criteria for selecting studies Eligible studies examined diagnosis of hypertension in adults of all ages using home and/or clinic blood pressure measurement compared with those made using ambulatory monitoring that clearly defined thresholds to diagnose hypertension. RESULTS The 20 eligible studies used various thresholds for the diagnosis of hypertension, and only seven studies (clinic) and three studies (home) could be directly compared with ambulatory monitoring. Compared with ambulatory monitoring thresholds of 135/85 mm Hg, clinic measurements over 140/90 mm Hg had mean sensitivity and specificity of 74.6% (95% confidence interval 60.7% to 84.8%) and 74.6% (47.9% to 90.4%), respectively, whereas home measurements over 135/85 mm Hg had mean sensitivity and specificity of 85.7% (78.0% to 91.0%) and 62.4% (48.0% to 75.0%). CONCLUSIONS Neither clinic nor home measurement had sufficient sensitivity or specificity to be recommended as a single diagnostic test. If ambulatory monitoring is taken as the reference standard, then treatment decisions based on clinic or home blood pressure alone might result in substantial overdiagnosis. Ambulatory monitoring before the start of lifelong [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Compared with ambulatory monitoring thresholds of 135/85 mm Hg, clinic measurements over 140/90 mm Hg had mean sensitivity and specificity of 74.6% (95% confidence interval 60.7% to 84.8%) and 74.6% (47.9% to 90.4%), respectively, whereas home measurements over 135/85 mm Hg had mean sensitivity and specificity of 85.7% (78.0% to 91.0%) and 62.4% (48.0% to 75.0%).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 106, "doc_id": "25515907", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Normal expression of RUNX1 causes tumorsupressing effects.\n\nCANDIDATE_PASSAGE:\nFunctional inhibition of osteoblastic cells in an in vivo mouse model of myeloid leukemia. Pancytopenia is a major cause of morbidity in acute myeloid leukemia (AML), yet its cause is unclear. Normal osteoblastic cells have been shown to support hematopoiesis. To define the effects of leukemia on osteoblastic cells, we used an immunocompetent murine model of AML. Leukemic mice had inhibition of osteoblastic cells, with decreased serum levels of the bone formation marker osteocalcin. Osteoprogenitor cells and endosteal-lining osteopontin(+) cells were reduced, and osteocalcin mRNA in CD45(-) marrow cells was diminished. This resulted in severe loss of mineralized bone. Osteoclasts were only transiently increased without significant increases in bone resorption, and their inhibition only partially rescued leukemia-induced bone loss. In vitro data suggested that a leukemia-derived secreted factor inhibited osteoblastic cells. Because the chemokine CCL-3 was recently reported to inhibit osteoblastic function in myeloma, we tested its expression in our model and in AML patients. Consistent with its potential novel role in leukemic-dependent bone loss, CCL-3 mRNA was significantly increased in malignant marrow cells from leukemic mice and from samples from AML patients. Based on these results, we propose that therapeutic mitigation of leukemia-induced uncoupling of osteoblastic and osteoclastic cells may represent a novel approach to promote normal hematopoiesis in patients with myeloid neoplasms.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "858", "doc_id": "10795340", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The relationship between a breast cancer patient's capacity to metabolize tamoxifen and treatment outcome is independent of the patient's genetic make-up.\n\nCANDIDATE_ABSTRACT:\nTITLE: The DNA Methylome of Human Peripheral Blood Mononuclear Cells\nABSTRACT: DNA methylation plays an important role in biological processes in human health and disease. Recent technological advances allow unbiased whole-genome DNA methylation (methylome) analysis to be carried out on human cells. Using whole-genome bisulfite sequencing at 24.7-fold coverage (12.3-fold per strand), we report a comprehensive (92.62%) methylome and analysis of the unique sequences in human peripheral blood mononuclear cells (PBMC) from the same Asian individual whose genome was deciphered in the YH project. PBMC constitute an important source for clinical blood tests world-wide. We found that 68.4% of CpG sites and <0.2% of non-CpG sites were methylated, demonstrating that non-CpG cytosine methylation is minor in human PBMC. Analysis of the PBMC methylome revealed a rich epigenomic landscape for 20 distinct genomic features, including regulatory, protein-coding, non-coding, RNA-coding, and repeat sequences. Integration of our methylome data with the YH genome sequence enabled a first comprehensive assessment of allele-specific methylation (ASM) between the two haploid methylomes of any individual and allowed the identification of 599 haploid differentially methylated regions (hDMRs) covering 287 genes. Of these, 76 genes had hDMRs within 2 kb of their transcriptional start sites of which >80% displayed allele-specific expression (ASE). These data demonstrate that ASM is a recurrent phenomenon and is highly correlated with ASE in human PBMCs. Together with recently reported similar studies, our study provides a comprehensive resource for future epigenomic research and confirms new sequencing technology as a paradigm for large-scale epigenomics studies.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1260, "doc_id": "18670", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Energy balance requires hypothalamic glutamate neurotransmission.\n\nCANDIDATE_ABSTRACT:\nTITLE: Glutamate mediates the function of melanocortin receptor 4 on Sim1 neurons in body weight regulation.\nABSTRACT: The melanocortin receptor 4 (MC4R) is a well-established mediator of body weight homeostasis. However, the neurotransmitter(s) that mediate MC4R function remain largely unknown; as a result, little is known about the second-order neurons of the MC4R neural pathway. Single-minded 1 (Sim1)-expressing brain regions, which include the paraventricular nucleus of hypothalamus (PVH), represent key brain sites that mediate melanocortin action. We conditionally restored MC4R expression in Sim1 neurons in the background of Mc4r-null mice. The restoration dramatically reduced obesity in Mc4r-null mice. The anti-obesity effect was completely reversed by selective disruption of glutamate release from those same Sim1 neurons. The reversal was caused by lower energy expenditure and hyperphagia. Corroboratively, selective disruption of glutamate release from adult PVH neurons led to rapid obesity development via reduced energy expenditure and hyperphagia. Thus, this study establishes glutamate as the primary neurotransmitter that mediates MC4Rs on Sim1 neurons in body weight regulation.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Corroboratively, selective disruption of glutamate release from adult PVH neurons led to rapid obesity development via reduced energy expenditure and hyperphagia.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 378, "doc_id": "45154987", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Hematopoietic Stem Cell purification reaches purity rates above 90%.\n\nCANDIDATE_ABSTRACT:\nTITLE: Combined Single-Cell Functional and Gene Expression Analysis Resolves Heterogeneity within Stem Cell Populations\nABSTRACT: Heterogeneity within the self-renewal durability of adult hematopoietic stem cells (HSCs) challenges our understanding of the molecular framework underlying HSC function. Gene expression studies have been hampered by the presence of multiple HSC subtypes and contaminating non-HSCs in bulk HSC populations. To gain deeper insight into the gene expression program of murine HSCs, we combined single-cell functional assays with flow cytometric index sorting and single-cell gene expression assays. Through bioinformatic integration of these datasets, we designed an unbiased sorting strategy that separates non-HSCs away from HSCs, and single-cell transplantation experiments using the enriched population were combined with RNA-seq data to identify key molecules that associate with long-term durable self-renewal, producing a single-cell molecular dataset that is linked to functional stem cell activity. Finally, we demonstrated the broader applicability of this approach for linking key molecules with defined cellular functions in another stem cell system.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 509, "doc_id": "13980338", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Polymeal nutrition increases cardiovascular mortality.\n\nCANDIDATE_PASSAGE:\nThe Polymeal: a more natural, safer, and probably tastier (than the Polypill) strategy to reduce cardiovascular disease by more than 75%. OBJECTIVE Although the Polypill concept (proposed in 2003) is promising in terms of benefits for cardiovascular risk management, the potential costs and adverse effects are its main pitfalls. The objective of this study was to identify a tastier and safer alternative to the Polypill: the Polymeal. METHODS Data on the ingredients of the Polymeal were taken from the literature. The evidence based recipe included wine, fish, dark chocolate, fruits, vegetables, garlic, and almonds. Data from the Framingham heart study and the Framingham offspring study were used to build life tables to model the benefits of the Polymeal in the general population from age 50, assuming multiplicative correlations. RESULTS Combining the ingredients of the Polymeal would reduce cardiovascular disease events by 76%. For men, taking the Polymeal daily represented an increase in total life expectancy of 6.6 years, an increase in life expectancy free from cardiovascular disease of 9.0 years, and a decrease in life expectancy with cardiovascular disease of 2.4 years. The corresponding differences for women were 4.8, 8.1, and 3.3 years. CONCLUSION The Polymeal promises to be an effective, non-pharmacological, safe, cheap, and tasty alternative to reduce cardiovascular morbidity and increase life expectancy in the general population.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "959", "doc_id": "8780599", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Increased mobility of retrotransposons is assosciated with mutation and higher tumorigenesis rates.\n\nCANDIDATE_PASSAGE:\nA novel Ku70 function in colorectal homeostasis separate from nonhomologous end joining Ku70, a known nonhomologous end-joining (NHEJ) factor, also functions in tumor suppression, although this molecular mechanism remains uncharacterized. Previously, we showed that mice deficient for DNA ligase IV (Lig4), another key NHEJ factor, succumbed to aggressive lymphoma in the absence of tumor suppressor p53. However, the tumor phenotype is abrogated by the introduction of a hypomorphic mutant p53R172P, which impaired p53-mediated apoptosis but not cell-cycle arrest. However, Lig4−/−p53R172P mice succumbed to severe diabetes. To further elucidate the role of NHEJ and p53-mediated apoptosis in vivo, we bred Ku70−/− p53R172P mice. Unexpectedly, these mice were free of diabetes, although 80% of the mutant mice had abnormally enlarged colons with pronounced inflammation. Remarkably, most of these mutant mice progressed to dysplasia, adenoma and adenocarcinoma; this is in contrast to the Lig4−/−p53R172P phenotype, strongly suggesting an NHEJ-independent function of Ku70. Significantly, our analyses of Ku70−/−p53R172P colonic epithelial cells show nuclear stabilization of β-catenin accompanied by higher expression of cyclin D1 and c-Myc in affected colon sections than in control samples. This is not due to the p53 mutation, as Ku70−/− mice share this phenotype. Our results not only unravel a novel function of Ku70 essential for colon homeostasis, but also establish an excellent in vivo model in which to study how chronic inflammation and abnormal cellular proliferation underlie tumorigenesis and tumor progression in the colon.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "617", "doc_id": "26059876", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: PPAR-RXRs can be activated by PPAR ligands.\n\nCANDIDATE_PASSAGE:\nUnique response pathways are established by allosteric interactions among nuclear hormone receptors Heterodimerization is a common paradigm among eukaryotic transcription factors. The 9-cis retinoic acid receptor (RXR) serves as a common heterodimerization partner for several nuclear receptors, including the thyroid hormone receptor (T3R) and retinoic acid receptor (RAR). This raises the question as to whether these complexes possess dual hormonal responsiveness. We devised a strategy to examine the transcriptional properties of each receptor individually or when tethered to a heterodimeric partner. We find that the intrinsic binding properties of RXR are masked in T3R-RXR and RAR-RXR heterodimers. In contrast, RXR is active as a non-DNA-binding cofactor with the NGFI-B/Nurr1 orphan receptors. Heterodimerization of RXR with constitutively active NGFI-B/Nurr1 creates a novel hormone-dependent complex. These findings suggest that allosteric interactions among heterodimers create complexes with unique properties. We suggest that allostery is a critical feature underlying the generation of diversity in hormone response networks.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "914", "doc_id": "3203590", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: H.pylori-mediated gastric cancer occurs due to the accumulation of mutations in host epithelial cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Helicobacter pylori infection triggers aberrant expression of activation-induced cytidine deaminase in gastric epithelium\nABSTRACT: Infection with Helicobacter pylori (H. pylori) is a risk factor for the development of gastric cancer. Here we show that infection of gastric epithelial cells with 'cag' pathogenicity island (cagPAI)-positive H. pylori induced aberrant expression of activation-induced cytidine deaminase (AID), a member of the cytidine-deaminase family that acts as a DNA- and RNA-editing enzyme, via the IκB kinase–dependent nuclear factor-κB activation pathway. H. pylori–mediated upregulation of AID resulted in the accumulation of nucleotide alterations in the TP53 tumor suppressor gene in gastric cells in vitro. Our findings provide evidence that aberrant AID expression caused by H. pylori infection might be a mechanism of mutation accumulation in the gastric mucosa during H. pylori–associated gastric carcinogenesis.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"H. pylori–mediated upregulation of AID resulted in the accumulation of nucleotide alterations in the TP53 tumor suppressor gene in gastric cells in vitro.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 483, "doc_id": "22703082", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Tirasemtiv targets cardiac muscle.\n\nCANDIDATE_PASSAGE:\nRegulation of heterochromatic silencing and histone H3 lysine-9 methylation by RNAi. Eukaryotic heterochromatin is characterized by a high density of repeats and transposons, as well as by modified histones, and influences both gene expression and chromosome segregation. In the fission yeast Schizosaccharomyces pombe, we deleted the argonaute, dicer, and RNA-dependent RNA polymerase gene homologs, which encode part of the machinery responsible for RNA interference (RNAi). Deletion results in the aberrant accumulation of complementary transcripts from centromeric heterochromatic repeats. This is accompanied by transcriptional de-repression of transgenes integrated at the centromere, loss of histone H3 lysine-9 methylation, and impairment of centromere function. We propose that double-stranded RNA arising from centromeric repeats targets formation and maintenance of heterochromatin through RNAi.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1304", "doc_id": "2613813", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: BLM gene encodes RecQ-class DNA helicase.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Bloom's syndrome gene product is homologous to RecQ helicases\nABSTRACT: The Bloom's syndrome (BS) gene, BLM, plays an important role in the maintenance of genomic stability in somatic cells. A candidate for BLM was identified by direct selection of a cDNA derived from a 250 kb segment of the genome to which BLM had been assigned by somatic crossover point mapping. In this novel mapping method, cells were used from persons with BS that had undergone intragenic recombination within BLM. cDNA analysis of the candidate gene identified a 4437 bp cDNA that encodes a 1417 amino acid peptide with homology to the RecQ helicases, a subfamily of DExH box-containing DNA and RNA helicases. The presence of chain-terminating mutations in the candidate gene in persons with BS proved that it was BLM.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"cDNA analysis of the candidate gene identified a 4437 bp cDNA that encodes a 1417 amino acid peptide with homology to the RecQ helicases, a subfamily of DExH box-containing DNA and RNA helicases.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 157, "doc_id": "13439128", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Are elevated serum levels of interleukin 21 associated with disease severity in patients with psoriasis?\n\nABSTRACT:\nPsoriasis is an immune disorder involving numerous cytokines. Recent studies have shown that interleukin (IL)-21 plays an important role in a variety of inflammatory and autoimmune diseases. It is highly expressed in psoriatic plaques and promotes the proliferation of epidermis in mice. It seems that IL-21 plays an important role in the pathogenesis of psoriasis. However, whether or not it is elevated in the peripheral blood of patients with psoriasis and is associated with disease severity is unclear. Therefore, our study focuses on serum IL-21 levels and their correlation with disease severity. To detect serum IL-21 levels in patients with psoriasis and investigate the correlation between these and the Psoriasis Area and Severity Index (PASI) scores. Blood samples were collected from patients with plaque psoriasis and from healthy control subjects. Serum IL-21 levels were measured by enzyme-linked immunosorbent assay in 37 patients with psoriasis and 37 healthy controls. The PASI scores of patients with psoriasis and their correlation with serum IL-21 levels were evaluated. Serum IL-21 levels were higher in patients with psoriasis than in healthy controls (P < 0·01). Serum IL-21 levels were positively correlated with PASI scores in the patients with psoriasis (r = 0·471, P < 0·01).", "output": "{\"label\": \"yes\", \"rationale\": \"Serum IL-21 levels in patients with psoriasis are elevated and positively correlate with PASI scores. These results indicate that IL-21 may play an important role in the pathogenesis of psoriasis.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 22356196, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The DdrB protein from Deinococcus radiodurans is an alternative SSB.\n\nCANDIDATE_ABSTRACT:\nTITLE: The structure of DdrB from Deinococcus: a new fold for single-stranded DNA binding proteins\nABSTRACT: Deinococcus spp. are renowned for their amazing ability to recover rapidly from severe genomic fragmentation as a result of exposure to extreme levels of ionizing radiation or desiccation. Despite having been originally characterized over 50 years ago, the mechanism underlying this remarkable repair process is still poorly understood. Here, we report the 2.8 A structure of DdrB, a single-stranded DNA (ssDNA) binding protein unique to Deinococcus spp. that is crucial for recovery following DNA damage. DdrB forms a pentameric ring capable of binding single-stranded but not double-stranded DNA. Unexpectedly, the crystal structure reveals that DdrB comprises a novel fold that is structurally and topologically distinct from all other single-stranded binding (SSB) proteins characterized to date. The need for a unique ssDNA binding function in response to severe damage, suggests a distinct role for DdrB which may encompass not only standard SSB protein function in protection of ssDNA, but also more specialized roles in protein recruitment or DNA architecture maintenance. Possible mechanisms of DdrB action in damage recovery are discussed.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Unexpectedly, the crystal structure reveals that DdrB comprises a novel fold that is structurally and topologically distinct from all other single-stranded binding (SSB) proteins characterized to date.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1163, "doc_id": "15305881", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Peroxynitrite is required for induction of T cell tolerance.\n\nCANDIDATE_ABSTRACT:\nTITLE: The twin-arginine translocation (Tat) protein export pathway\nABSTRACT: The twin-arginine translocation (Tat) protein export system is present in the cytoplasmic membranes of most bacteria and archaea and has the highly unusual property of transporting fully folded proteins. The system must therefore provide a transmembrane pathway that is large enough to allow the passage of structured macromolecular substrates of different sizes but that maintains the impermeability of the membrane to ions. In the Gram-negative bacterium Escherichia coli, this complex task can be achieved by using only three small membrane proteins: TatA, TatB and TatC. In this Review, we summarize recent advances in our understanding of how this remarkable machine operates.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 935, "doc_id": "1320137", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Human embryonic stem cells give rise to cell types from the outer embryonic germ layer, but not the other two layers.\n\nCANDIDATE_ABSTRACT:\nTITLE: Characterization and culture of human embryonic stem cells\nABSTRACT: Objective To explore the in vitro maintenance and characterization of human embryonic stem cells(hESCs).Methods hESCs were cultured on feeder layer with ES culture medium,which consists of 20% Knockout Serum Replacement,Knockout DMEM and 10 ng/mL bFGF.Undifferentiated status of hESCs was identified by cell morphology,and the expressions of cell surface marker SSEA-1,SSEA-3 and TRA-1-60.G banding technique was employed for cell karyotype analysis. Pluropotency of cells were analyzed via in vitro embyoid body(EB) formation and in vivo terotoma formation. Results Most of cells showed undifferentiated properties in cell morphology and normal karyotype throughout extended culture periods. They maintained undifferentiated status with positive immunoreactivity to SSEA-3,SSEA-4 and TRA-1-60.in vitro EB formation and in vivo teratoma formation demonstrated the pluripotency of human ES cells. Conclusion The fundamental requirement to hESCs for research and clinical application were their undifferentiated status and pluropotency in culture. Our result demonstrated their potential for these purposes.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 530, "doc_id": "87610599", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Combination nicotine replacement therapies with varenicline or bupropion lead to significantly higher long-term abstinence rates at 52 weeks than varenicline monotherapy.\n\nCANDIDATE_PASSAGE:\nExcitotoxic brain injury in adult zebrafish stimulates neurogenesis and long-distance neuronal integration. Zebrafish maintain a greater capacity than mammals for central nervous system repair after injury. Understanding differences in regenerative responses between different vertebrate species may shed light on mechanisms to improve repair in humans. Quinolinic acid is an excitotoxin that has been used to induce brain injury in rodents for modeling Huntington's disease and stroke. When injected into the adult rodent striatum, this toxin stimulates subventricular zone neurogenesis and neuroblast migration to injury. However, most new neurons fail to survive and lesion repair is minimal. We used quinolinic acid to lesion the adult zebrafish telencephalon to study reparative processes. We also used conditional transgenic lineage mapping of adult radial glial stem cells to explore survival and integration of neurons generated after injury. Telencephalic lesioning with quinolinic acid, and to a lesser extent vehicle injection, produced cell death, microglial infiltration, increased cell proliferation, and enhanced neurogenesis in the injured hemisphere. Lesion repair was more complete with quinolinic acid injection than after vehicle injection. Fate mapping of her4-expressing radial glia showed injury-induced expansion of radial glial stem cells that gave rise to neurons which migrated to injury, survived at least 8 weeks and formed long-distance projections that crossed the anterior commissure and synapsed in the contralateral hemisphere. These findings suggest that quinolinic acid lesioning of the zebrafish brain stimulates adult neural stem cells to produce robust regeneration with long-distance integration of new neurons. This model should prove useful for e [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "274", "doc_id": "5395426", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does betulinic acid exert anti-hepatitis C virus activity via the suppression of NF-κB- and MAPK-ERK1/2-mediated COX-2 expression?\n\nABSTRACT:\nThis study was designed to evaluate the effect of betulinic acid (BA), extracted from Avicennia marina, on the replication of hepatitis C virus (HCV) and to investigate the mechanism of this BA-mediated anti-HCV activity. HCV replicon and infectious systems were used to evaluate the anti-HCV activity of BA. Exogenous COX-2 or knock-down of COX-2 expression was used to investigate the role of COX-2 in the anti-HCV activity of BA. The effects of BA on the phosphorylation of NF-κB and on kinases in the MAPK signalling pathway were determined. The anti-HCV activity of BA in combination with other HCV inhibitors was also determined to assess its use as an anti-HCV supplement. BA inhibited HCV replication in both Ava5 replicon cells and in a cell culture-derived infectious HCV particle system. Treatment with a combination of BA and IFN-α, the protease inhibitor telaprevir or the NS5B polymerase inhibitor sofosbuvir resulted in the synergistic suppression of HCV RNA replication. Exogenous overexpression of COX-2 gradually attenuated the inhibitory effect of BA on HCV replication, suggesting that BA reduces HCV replication by suppressing the expression of COX-2. In particular, BA down-regulated HCV-induced COX-2 expression by reducing the phosphorylation of NF-κB and ERK1/2 of the MAPK signalling pathway.", "output": "{\"label\": \"yes\", \"rationale\": \"BA inhibits HCV replication by suppressing the NF-κB- and ERK1/2-mediated COX-2 pathway and may serve as a promising compound for drug development or as a potential supplement for use in the treatment of HCV-infected patients.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 26102077, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Propriospinal interneurons that play a role in the plastic reorganization of spinal circuits are integral for recovery from spinal cord injury.\n\nCANDIDATE_PASSAGE:\nRecovery of supraspinal control of stepping via indirect propriospinal relay connections after spinal cord injury Spinal cord injuries (SCIs) in humans and experimental animals are often associated with varying degrees of spontaneous functional recovery during the first months after injury. Such recovery is widely attributed to axons spared from injury that descend from the brain and bypass incomplete lesions, but its mechanisms are uncertain. To investigate the neural basis of spontaneous recovery, we used kinematic, physiological and anatomical analyses to evaluate mice with various combinations of spatially and temporally separated lateral hemisections with or without the excitotoxic ablation of intrinsic spinal cord neurons. We show that propriospinal relay connections that bypass one or more injury sites are able to mediate spontaneous functional recovery and supraspinal control of stepping, even when there has been essentially total and irreversible interruption of long descending supraspinal pathways in mice. Our findings show that pronounced functional recovery can occur after severe SCI without the maintenance or regeneration of direct projections from the brain past the lesion and can be mediated by the reorganization of descending and propriospinal connections. Targeting interventions toward augmenting the remodeling of relay connections may provide new therapeutic strategies to bypass lesions and restore function after SCI and in other conditions such as stroke and multiple sclerosis.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "980", "doc_id": "20128547", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: 76-85% of people with severe mental disorder receive no treatment in low and middle income countries.\n\nCANDIDATE_PASSAGE:\nPrevalence, severity, and unmet need for treatment of mental disorders in the World Health Organization World Mental Health Surveys. CONTEXT Little is known about the extent or severity of untreated mental disorders, especially in less-developed countries. OBJECTIVE To estimate prevalence, severity, and treatment of Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) mental disorders in 14 countries (6 less developed, 8 developed) in the World Health Organization (WHO) World Mental Health (WMH) Survey Initiative. DESIGN, SETTING, AND PARTICIPANTS Face-to-face household surveys of 60 463 community adults conducted from 2001-2003 in 14 countries in the Americas, Europe, the Middle East, Africa, and Asia. MAIN OUTCOME MEASURES The DSM-IV disorders, severity, and treatment were assessed with the WMH version of the WHO Composite International Diagnostic Interview (WMH-CIDI), a fully structured, lay-administered psychiatric diagnostic interview. RESULTS The prevalence of having any WMH-CIDI/DSM-IV disorder in the prior year varied widely, from 4.3% in Shanghai to 26.4% in the United States, with an interquartile range (IQR) of 9.1%-16.9%. Between 33.1% (Colombia) and 80.9% (Nigeria) of 12-month cases were mild (IQR, 40.2%-53.3%). Serious disorders were associated with substantial role disability. Although disorder severity was correlated with probability of treatment in almost all countries, 35.5% to 50.3% of serious cases in developed countries and 76.3% to 85.4% in less-developed countries received no treatment in the 12 months before the interview. Due to the high prevalence of mild and subthreshold cases, the number of those who received treatment far exceeds the number of untreated serious cases in every country. CONCLUSIONS Realloc [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "22", "doc_id": "6490571", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Upon viral challenge, influenza-specific memory CD4+ T cells greatly diminish the early production of inflammatory chemokines in the lung.\n\nCANDIDATE_PASSAGE:\nPRRSV receptors and their roles in virus infection Porcine reproductive and respiratory syndrome virus (PRRSV) has a restricted cell tropism and prefers to invade well-differentiated cells of the monocyte/macrophage lineage, such as pulmonary alveolar macrophages and African green monkey kidney cell line MA-104 and its derivatives, such as Marc-145, Vero and CL-2621. PRRSV infection of the host cells actually is a receptor-mediated endocytosis and replication process. The presence and absence of the cellular receptors decide whether the cell lines are permissive or non-permissive to PRRSV infection. Several PRRSV non-permissive cell lines, such as BHK-21, PK-15 and CHO-K1, have been shown to become sensitive to the virus infection upon expression of the recombinant receptor proteins. Up to now, heparin sulfate, sialoadhesin, CD163, CD151 and vimentin have been identified as the important PRRSV receptors via their involvement in virus attachment, internalization or uncoating. Each receptor is characterized by the distribution in different cells, the function in virus different infection stages and the interaction model with the viral proteins or genes. Joint forces of the receptors recently attract attentions due to the specific function. PRRSV receptors have become the targets for designing the new anti-viral reagents or the recombinant cell lines used for isolating the viruses or developing more effective vaccines due to their more conserved sequences compared with the genetic variation of the virus. In this paper, the role of PRRSV receptors and the molecular mechanism of the interaction between the virus and the receptors are reviewed.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1347", "doc_id": "8005007", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does timing of initial surfactant treatment make a difference in rates of chronic lung disease or mortality in premature infants?\n\nABSTRACT:\nTo compare two treatment strategies in preterm infants with or at risk of respiratory distress syndrome: early surfactant administration (within one hour of birth) versus late surfactant administration, in a geographically defined population. The primary outcome was chronic lung disease (CLD) and mortality before/at 36 weeks. Secondary outcomes included: duration of mechanical ventilation and continuous positive airway pressure (CPAP), post-natal steroids for CLD and major neonatal morbidities. Premature infants born at 22-32 weeks' gestation between January 2006 and December 2009. Ten neonatal intensive care units (NICUs) in New South Wales (NSW) and Australian Capital Territory (ACT), Australia. Retrospective analysis of prospectively collected data from the regional NICU database in NSW and ACT. Of the 2170 infants who received surfactant, 1182 (54.5%) and 988 (45.5%) received early and late surfactant, respectively. The early surfactant group was less mature (27.1 ± 2.1 versus 29.4 ± 2.1 weeks) and had more CLD and mortality (40.2% versus 20.0%). The multivariable analysis showed early surfactant to be associated with less duration of ventilation, longer duration of CPAP and longer hospital stay but had little or no impact on CLD/mortality.", "output": "{\"label\": \"maybe\", \"rationale\": \"Early surfactant administration is associated with shorter duration of ventilation but does not appear to be significantly protective against CLD/mortality among premature infants. This may support the growing evidence for consideration of CPAP as an alternative to routine intubation and early surfactant administration. Further investigation from large randomized clinical trials is warranted to confirm these results.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 25394614, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Ribosome-inactivating protein-2 (RIP-2) interacts with the p75 NTR death domain\n\nCANDIDATE_ABSTRACT:\nTITLE: Gamma-Secretase Represents a Therapeutic Target for the Treatment of Invasive Glioma Mediated by the p75 Neurotrophin Receptor\nABSTRACT: The multifunctional signaling protein p75 neurotrophin receptor (p75(NTR)) is a central regulator and major contributor to the highly invasive nature of malignant gliomas. Here, we show that neurotrophin-dependent regulated intramembrane proteolysis (RIP) of p75(NTR) is required for p75(NTR)-mediated glioma invasion, and identify a previously unnamed process for targeted glioma therapy. Expression of cleavage-resistant chimeras of p75(NTR) or treatment of animals bearing p75(NTR)-positive intracranial tumors with clinically applicable gamma-secretase inhibitors resulted in dramatically decreased glioma invasion and prolonged survival. Importantly, proteolytic processing of p75(NTR) was observed in p75(NTR)-positive patient tumor specimens and brain tumor initiating cells. This work highlights the importance of p75(NTR) as a therapeutic target, suggesting that gamma-secretase inhibitors may have direct clinical application for the treatment of malignant glioma.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1047, "doc_id": "14706752", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Diabetes remission occurs less in people treated with conventional therapy than in people treated with laparoscopic adjustable gastric banding surgery.\n\nCANDIDATE_PASSAGE:\nAdjustable gastric banding and conventional therapy for type 2 diabetes: a randomized controlled trial. CONTEXT Observational studies suggest that surgically induced loss of weight may be effective therapy for type 2 diabetes. OBJECTIVE To determine if surgically induced weight loss results in better glycemic control and less need for diabetes medications than conventional approaches to weight loss and diabetes control. DESIGN, SETTING, AND PARTICIPANTS Unblinded randomized controlled trial conducted from December 2002 through December 2006 at the University Obesity Research Center in Australia, with general community recruitment to established treatment programs. Participants were 60 obese patients (BMI >30 and <40) with recently diagnosed (<2 years) type 2 diabetes. INTERVENTIONS Conventional diabetes therapy with a focus on weight loss by lifestyle change vs laparoscopic adjustable gastric banding with conventional diabetes care. MAIN OUTCOME MEASURES Remission of type 2 diabetes (fasting glucose level <126 mg/dL [7.0 mmol/L] and glycated hemoglobin [HbA1c] value <6.2% while taking no glycemic therapy). Secondary measures included weight and components of the metabolic syndrome. Analysis was by intention-to-treat. RESULTS Of the 60 patients enrolled, 55 (92%) completed the 2-year follow-up. Remission of type 2 diabetes was achieved by 22 (73%) in the surgical group and 4 (13%) in the conventional-therapy group. Relative risk of remission for the surgical group was 5.5 (95% confidence interval, 2.2-14.0). Surgical and conventional-therapy groups lost a mean (SD) of 20.7% (8.6%) and 1.7% (5.2%) of weight, respectively, at 2 years (P < .001). Remission of type 2 diabetes was related to weight loss (R2 = 0.46, P < .001) and lower baseline HbA1c levels (combin [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "340", "doc_id": "7098463", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Cost effectiveness evaluations based on cRCT data accurately reflect prices for patients in actual clinical practice.\n\nCANDIDATE_ABSTRACT:\nTITLE: A Comparison of Cost Effectiveness Using Data from Randomized Trials or Actual Clinical Practice: Selective Cox-2 Inhibitors as an Example\nABSTRACT: BACKGROUND Data on absolute risks of outcomes and patterns of drug use in cost-effectiveness analyses are often based on randomised clinical trials (RCTs). The objective of this study was to evaluate the external validity of published cost-effectiveness studies by comparing the data used in these studies (typically based on RCTs) to observational data from actual clinical practice. Selective Cox-2 inhibitors (coxibs) were used as an example. METHODS AND FINDINGS The UK General Practice Research Database (GPRD) was used to estimate the exposure characteristics and individual probabilities of upper gastrointestinal (GI) events during current exposure to nonsteroidal anti-inflammatory drugs (NSAIDs) or coxibs. A basic cost-effectiveness model was developed evaluating two alternative strategies: prescription of a conventional NSAID or coxib. Outcomes included upper GI events as recorded in GPRD and hospitalisation for upper GI events recorded in the national registry of hospitalisations (Hospital Episode Statistics) linked to GPRD. Prescription costs were based on the prescribed number of tables as recorded in GPRD and the 2006 cost data from the British National Formulary. The study population included over 1 million patients prescribed conventional NSAIDs or coxibs. Only a minority of patients used the drugs long-term and daily (34.5% of conventional NSAIDs and 44.2% of coxibs), whereas coxib RCTs required daily use for at least 6-9 months. The mean cost of preventing one upper GI event as recorded in GPRD was US$104k (ranging from US$64k with long-term daily use to US$182k with intermittent use) and US$298k for hospitalizations. The mean costs (for GPRD events) over calendar time were US$58k during 1990-1993 and US$174k during 2002-2005. Using RCT data rather [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS The published cost-effectiveness analyses of coxibs lacked external validity, did not represent patients in actual clinical practice, and should not have been used to inform prescribing policies.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 290, "doc_id": "15048300", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: HNF4A mutations are associated with macrosomia in infancy.\n\nCANDIDATE_PASSAGE:\nOccurrence of chromosome 9 and p53 alterations in multifocal dysplasia and carcinoma in situ of human urinary bladder To define the genetic changes of flat urothelial lesions, carcinoma in situ (CIS) and moderate dysplasias (DII) were investigated for alterations in the two chromosomal regions most frequently involved in bladder cancer. Overall, 33 CIS and 16 DII from 21 patients were used to microdissect urothelium. Dual color fluorescence in situ hybridization (FISH) using gene locus probes of 9q22 (FACC), 9p21 (CDK), 17p13 (p53), and related centromeric probes was applied on interphase nuclei. In parallel, preamplified DNA of these samples was used for loss of heterozygosity (LOH) analyses with eight microsatellite markers on chromosomes 9p, 9q and 17p, and for sequencing of exons 5-9 of p53. Data indicated nearly identical deletion frequencies for chromosomes 9 and 17 for CIS (chromosome 9, 86%; p53, 84%). DII showed a lower deletion rate in comparison with CIS (chromosome 9, 75%; p53, 53%). A very high correlation between the results of FISH and LOH analyses was found. p53 mutations were detected in 12 of 15 patients (CIS, 72%; DII, 67%). In three of 16 patients with multifocal tumors, oligoclonal lesions were identified by LOH analyses, a finding further supported by sequencing of p53, by which two different p53 deletions were detected in two cases. In conclusion, data from microdissected flat urothelial lesions indicate that chromosome 9 deletions cannot be regarded as indicators of papillary growth, because they are found frequently in both types of flat lesions of the urothelium: those associated with papillary tumors and those that are not. The similar distribution and lower amount of genetic changes in DII render DII a possible precursor lesion of CIS.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "490", "doc_id": "11861374", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Macrolides have no protective effect against myocardial infarction.\n\nCANDIDATE_PASSAGE:\nInfluence of cigarette smoking on inhaled corticosteroid treatment in mild asthma. BACKGROUND Although inhaled corticosteroids have an established role in the treatment of asthma, studies have tended to concentrate on non-smokers and little is known about the possible effect of cigarette smoking on the efficacy of treatment with inhaled steroids in asthma. A study was undertaken to investigate the effect of active cigarette smoking on responses to treatment with inhaled corticosteroids in patients with mild asthma. METHODS The effect of treatment with inhaled fluticasone propionate (1000 microg daily) or placebo for 3 weeks was studied in a double blind, prospective, randomised, placebo controlled study of 38 steroid naïve adult asthmatic patients (21 non-smokers). Efficacy was assessed using morning and evening peak expiratory flow (PEF) readings, spirometric parameters, bronchial hyperreactivity, and sputum eosinophil counts. Comparison was made between responses to treatment in non-smoking and smoking asthmatic patients. RESULTS There was a significantly greater increase in mean morning PEF in non-smokers than in smokers following inhaled fluticasone (27 l/min v -5 l/min). Non-smokers had a statistically significant increase in mean morning PEF (27 l/min), mean forced expiratory volume in 1 second (0.17 l), and geometric mean PC20 (2.6 doubling doses), and a significant decrease in the proportion of sputum eosinophils (-1.75%) after fluticasone compared with placebo. No significant changes were observed in the smoking asthmatic patients for any of these parameters. CONCLUSIONS Active cigarette smoking impairs the efficacy of short term inhaled corticosteroid treatment in mild asthma. This finding has important implications for the management of patients w [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "742", "doc_id": "20611846", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Blocking the interaction between TDP-43 and respiratory complex I proteins ND3 and ND6 leads to increased TDP-43-induced neuronal loss.\n\nCANDIDATE_PASSAGE:\nInteraction of Helicobacter pylori with gastric epithelial cells is mediated by the p53 protein family. BACKGROUND & AIMS Although the p53 tumor suppressor has been extensively studied, many critical questions remain unanswered about the biological functions of p53 homologs, p73 and p63. Accumulating evidence suggests that both p73 and p63 play important roles in regulation of apoptosis, cell differentiation, and therapeutic drug sensitivity. METHODS Gastric epithelial cells were cocultured with Helicobacter pylori, and the roles of p63 and p73 proteins were assessed by luciferase reporter, real-time polymerase chain reaction, immunoblotting, and cell survival assays. Short hairpin RNA and dominant-negative mutants were used to inhibit activity of p73 and p63 isoforms. Human and murine gastric tissues were analyzed by immunohistochemistry with p73 and p63 antibodies and modified Steiner's silver method. RESULTS Interaction of H pylori with gastric epithelial cells leads to robust up-regulation of p73 protein in vitro and in vivo in human gastritis specimens and H pylori-infected mice. The p73 increase resulted in up-regulation of pro-apoptotic genes, NOXA, PUMA, and FAS receptor in gastric epithelial cells. Down-regulation of p73 activity suppressed cell death and Fas receptor induced by H pylori. Bacterial virulence factors within the cag pathogenicity island, c-Abl tyrosine kinase, and interaction with p63 isoforms control the activity of p73. CONCLUSION Our findings implicate p73 in H pylori-induced apoptosis and more generally suggest that the p53 family may play a role in the epithelial cell response to H pylori infection.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "180", "doc_id": "29367554", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Mice without IFN-γ or its receptor are resistant to EAM induced with α-MyHC/CFA.\n\nCANDIDATE_PASSAGE:\nParathyroid hormone induces E4bp4 messenger ribonucleic acid expression primarily through cyclic adenosine 3',5'-monophosphate signaling in osteoblasts. PTH binding to its receptor activates protein kinase A (PKA), protein kinase C (PKC), and calcium signaling to induce transcription of primary response genes in osteoblasts. Adenovirus E4 promoter-binding protein/nuclear factor regulated by IL-3 (E4BP4/NFIL3), a transcriptional repressor, is a PTH-induced primary response gene in primary mouse osteoblasts (MOBs). Here we investigate the signaling pathway(s) that lead to PTH induction of E4bp4 mRNA expression. Ten and 100 nm PTH induced maximum E4bp4 expression in MOBs. Forskolin (FSK), an adenylate cyclase inducer, 8-bromo-cAMP, a cAMP analog, and phorbol myristate acetate, a PKC activator, increased E4bp4 mRNA levels, whereas ionomycin, a calcium ionophore, had no effect. Pretreatment of cells with 30 microm H89, a PKA inhibitor, strongly inhibited PTH- and FSK-induced E4bp4 expression. In contrast, overnight pretreatment with 1 microm phorbol myristate acetate to down-regulate PKC signaling did not alter PTH and FSK effects. Moreover, PTH (3-34) that does not activate cAMP signaling did not increase E4bp4 expression. Prostaglandin E(2), which signals through cAMP, increased E4bp4 mRNA at all doses, whereas prostaglandin F(2alpha) that primarily activates PKC and calcium signaling, induced E4bp4 only at high doses and fluprostenol that only activates PKC and calcium signaling, had no effect. Finally, 80 microg/kg PTH (1-34) ip injection induced E4bp4 mRNA expression at 1 h in mice. In contrast, 80 microg/kg PTH (3-34) had no effect. Our data suggest that PTH-induced E4bp4 mRNA expression is mediated primarily through cAMP-PKA signaling in vitro and in vivo. [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "783", "doc_id": "21199527", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Are anti-proline-glycine-proline or antielastin autoantibodies evident in chronic inflammatory lung disease?\n\nABSTRACT:\nIn patients with chronic inflammatory lung disease, pulmonary proteases can generate neoantigens from elastin and collagen with the potential to fuel autoreactive immune responses. Antielastin peptide antibodies have been implicated in the pathogenesis of tobacco-smoke-induced emphysema. Collagen-derived peptides may also play a role. To determine whether autoantibodies directed against elastin- and collagen-derived peptides are present in plasma from three groups of patients with chronic inflammatory lung disease compared with a nonsmoking healthy control group and to identify whether autoimmune responses to these peptides may be an important component of the disease process in these patients. A total of 124 patients or healthy control subjects were recruited for the study (Z-A1AT deficiency, n = 20; cystic fibrosis, n = 40; chronic obstructive pulmonary disease, n = 31; healthy control, n = 33). C-reactive protein, IL-32, and antinuclear antibodies were quantified. Antielastin and anti-N-acetylated-proline-glycine-proline autoantibodies were measured by reverse ELISA. All patients were deemed stable and noninfective on the basis of the absence of clinical or radiographic evidence of recent infection. There were no significant differences in the levels of autoantibodies or IL-32 in the patients groups compared with the healthy control subjects.", "output": "{\"label\": \"no\", \"rationale\": \"Antielastin or anti-N-acetylated proline-glycine-proline autoantibodies are not evident in chronic inflammatory lung disease.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 19762563, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Retinoic acid receptor-related orphan receptor gamma (RORγ) is a therapeutic target for castration-resistant prostate cancer (CRPC)\n\nCANDIDATE_ABSTRACT:\nTITLE: ROR-γ drives androgen receptor expression and represents a therapeutic target in castration-resistant prostate cancer\nABSTRACT: The androgen receptor (AR) is overexpressed and hyperactivated in human castration-resistant prostate cancer (CRPC). However, the determinants of AR overexpression in CRPC are poorly defined. Here we show that retinoic acid receptor-related orphan receptor γ (ROR-γ) is overexpressed and amplified in metastatic CRPC tumors, and that ROR-γ drives AR expression in the tumors. ROR-γ recruits nuclear receptor coactivator 1 and 3 (NCOA1 and NCOA3, also known as SRC-1 and SRC-3) to an AR-ROR response element (RORE) to stimulate AR gene transcription. ROR-γ antagonists suppress the expression of both AR and its variant AR-V7 in prostate cancer (PCa) cell lines and tumors. ROR-γ antagonists also markedly diminish genome-wide AR binding, H3K27ac abundance and expression of the AR target gene network. Finally, ROR-γ antagonists suppressed tumor growth in multiple AR-expressing, but not AR-negative, xenograft PCa models, and they effectively sensitized CRPC tumors to enzalutamide, without overt toxicity, in mice. Taken together, these results establish ROR-γ as a key player in CRPC by acting upstream of AR and as a potential therapeutic target for advanced PCa.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Finally, ROR-γ antagonists suppressed tumor growth in multiple AR-expressing, but not AR-negative, xenograft PCa models, and they effectively sensitized CRPC tumors to enzalutamide, without overt toxicity, in mice.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1043, "doc_id": "17671145", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Rapamycin decreases the concentration of triacylglycerols in fruit flies.\n\nCANDIDATE_PASSAGE:\nYoung adolescents' nutrition assessment on computer (YANA-C) Objective:To assess the relative validity and acceptability of the computerised 24-h recall ‘Young Adolescent's Nutrition Assessment on Computer (YANA-C)’.Design:Food and nutrient intakes assessed with YANA-C were compared with food records (study 1) and 24-h dietary recall interviews (study 2).Main outcome measures:Intakes of food groups (fruit, fruit juice, vegetables, potatoes, bread, cereals, milk, cheese, other milk products, soft drinks, diet soft drinks, sugar/sweets, pastry/cookies, savoury snacks, butter/sauces, eggs, fish, meat) and nutrients (energy, carbohydrates, protein, fat, fiber, calcium, vitamin C and iron).Subjects and setting:A total of 237 pupils (11–14 y) from two primary and four secondary schools (study 1: n=136; study 2: n=101) in Belgium-Flanders. Results:YANA-C proved to agree well with both standard methods in categorizing subjects in consumers and nonconsumers (κstudy 1=0.48–0.92; κstudy 2=0.38–0.90). Spearman's correlations for energy and nutrient intakes ranged between 0.44 and 0.79 for study 1 and between 0.44 and 0.86 for study 2. Nutrient and energy intakes were in general (excluding calcium) significantly higher in YANA-C in comparison with the food record, but not in comparison with the interview (only fiber). Statistics used to investigate whether YANA-C agreed with the other methods in ranking portions/amounts in consumers only were fair to moderate for most of the food groups (weighted κ study 1=0.11–0.55; study 2=0.04–0.73); amounts in consumers only, were significantly lower in YANA-C against both standards for cereals; amounts were significantly higher in YANA-C against the food record for milk, soft drinks, sugar/sweets and savoury snacks and against the i [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1014", "doc_id": "4857093", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: During non-homologous end joining, the ligation step is not as tolerant of disrepairs and other distortions when joining 5' of strand breaks as compared to 3' strand breaks.\n\nCANDIDATE_PASSAGE:\nFamilial risk of lymphoproliferative tumors in families of patients with chronic lymphocytic leukemia: results from the Swedish Family-Cancer Database. The importance of genetic factors in etiology of chronic lymphocytic leukemia (CLL) is suggested by family and population studies. However, the spectrum of malignancies sharing common genetic factors with CLL and the effects of sex and age on familial risk are unknown. We used the Swedish Family-Cancer Database to test for increased familial risks of CLL and other lymphoproliferative tumors. Cancer diagnoses from 1958 to 1998 were assessed in 14 336 first-degree relatives of 5918 CLL cases and in 28 876 first-degree relatives of 11 778 controls. Cancer risks in relatives of cases were compared with those in relatives of controls using marginal survival models. Relatives of cases were at significantly increased risk for CLL (relative risk [RR] = 7.52; 95% confidence interval [CI], 3.63-15.56), for non-Hodgkin lymphoma (RR = 1.45; 95% CI, 0.98-2.16), and for Hodgkin lymphoma (RR = 2.35; 95% CI, 1.08-5.08). CLL risks were similar in parents, siblings, and offspring of cases, in male and female relatives, and were not affected by the case's age at diagnosis. Anticipation was not significant when analyzed using life table methods. We conclude that the familial component of CLL is shared with other lymphoproliferative malignances, suggesting common genetic pathways. However, because clinically diagnosed CLL is uncommon, absolute excess risk to relatives is small.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "358", "doc_id": "1153655", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: 7-day-old adult Caenorhabditis elegans exhibit approximately 75% of the learning capacity seen in 1-day old adults.\n\nCANDIDATE_ABSTRACT:\nTITLE: Insulin Signaling and Dietary Restriction Differentially Influence the Decline of Learning and Memory with Age\nABSTRACT: Of all the age-related declines, memory loss is one of the most devastating. While conditions that increase longevity have been identified, the effects of these longevity-promoting factors on learning and memory are unknown. Here we show that the C. elegans Insulin/IGF-1 receptor mutant daf-2 improves memory performance early in adulthood and maintains learning ability better with age but, surprisingly, demonstrates no extension in long-term memory with age. By contrast, eat-2 mutants, a model of Dietary Restriction (DR), exhibit impaired long-term memory in young adulthood but maintain this level of memory longer with age. We find that crh-1, the C. elegans homolog of the CREB transcription factor, is required for long-term associative memory, but not for learning or short-term memory. The expression of crh-1 declines with age and differs in the longevity mutants, and CREB expression and activity correlate with memory performance. Our results suggest that specific longevity treatments have acute and long-term effects on cognitive functions that decline with age through their regulation of rate-limiting genes required for learning and memory.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 20, "doc_id": "3202143", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Deletion of αvβ8 does not result in a spontaneous inflammatory phenotype.\n\nCANDIDATE_PASSAGE:\nMapping of a gene for severe pediatric gastroesophageal reflux to chromosome 13q14. CONTEXT Gastroesophageal reflux (GER) has not previously been widely regarded as a hereditary disease. A few reports have suggested, however, that a genetic component may contribute to the incidence of GER, especially in its severe or chronic forms. OBJECTIVE To identify a genetic locus that cosegregates with a severe pediatric GER phenotype in families with multiple affected members. DESIGN A genome-wide scan of families affected by severe pediatric GER using polymorphic microsatellite markers spaced at an average of 8 centimorgans (cM), followed by haplotyping and by pairwise and multipoint linkage analyses. SETTING General US community, with research performed in a university tertiary care hospital. SUBJECTS Affected and unaffected family members from 5 families having multiple individuals affected by severe pediatric GER, identified through a patient support group. MAIN OUTCOME MEASURES Determination of inheritance patterns and linkage of a genetic locus with the severe pediatric GER phenotype by logarithm-of-odds (lod) score analysis, considering a lod score of 3 or greater as evidence of linkage. RESULTS In these families, severe pediatric GER followed an autosomal dominant hereditary pattern with high penetrance. A gene for severe pediatric GER was mapped to a 13-cM region on chromosome 13q between microsatellite markers D13S171 and D13S263. A maximum multifamily 2-point lod score of 5.58 and a maximum multifamily multipoint lod score of 7.15 were obtained for marker D13S1253 at map position 35 cM when presumptively affected persons were modeled as unknown (a maximum multipoint score of 4.88 was obtained when presumptively affected persons were modeled as unaffected). [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "327", "doc_id": "12428137", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: A deficiency of vitamin B12 increases blood levels of homocysteine.\n\nCANDIDATE_PASSAGE:\nLong-term effect of aspirin on cancer risk in carriers of hereditary colorectal cancer: an analysis from the CAPP2 randomised controlled trial BACKGROUND Observational studies report reduced colorectal cancer in regular aspirin consumers. Randomised controlled trials have shown reduced risk of adenomas but none have employed prevention of colorectal cancer as a primary endpoint. The CAPP2 trial aimed to investigate the antineoplastic effects of aspirin and a resistant starch in carriers of Lynch syndrome, the major form of hereditary colorectal cancer; we now report long-term follow-up of participants randomly assigned to aspirin or placebo. METHODS In the CAPP2 randomised trial, carriers of Lynch syndrome were randomly assigned in a two-by-two factorial design to 600 mg aspirin or aspirin placebo or 30 g resistant starch or starch placebo, for up to 4 years. Randomisation was in blocks of 16 with provision for optional single-agent randomisation and extended postintervention double-blind follow-up; participants and investigators were masked to treatment allocation. The primary endpoint was development of colorectal cancer. Analysis was by intention to treat and per protocol. This trial is registered, ISRCTN59521990. RESULTS 861 participants were randomly assigned to aspirin or aspirin placebo. At a mean follow-up of 55·7 months, 48 participants had developed 53 primary colorectal cancers (18 of 427 randomly assigned to aspirin, 30 of 434 to aspirin placebo). Intention-to-treat analysis of time to first colorectal cancer showed a hazard ratio (HR) of 0·63 (95% CI 0·35-1·13, p=0·12). Poisson regression taking account of multiple primary events gave an incidence rate ratio (IRR) of 0·56 (95% CI 0·32-0·99, p=0·05). For participants completing 2 years of interve [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "36", "doc_id": "15648443", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Ethanol stress increases the expression of PSP in bacteria.\n\nCANDIDATE_PASSAGE:\nMatrix Remodeling Promotes Pulmonary Hypertension through Feedback Mechanoactivation of the YAP/TAZ-miR-130/301 Circuit. Pulmonary hypertension (PH) is a deadly vascular disease with enigmatic molecular origins. We found that vascular extracellular matrix (ECM) remodeling and stiffening are early and pervasive processes that promote PH. In multiple pulmonary vascular cell types, such ECM stiffening induced the microRNA-130/301 family via activation of the co-transcription factors YAP and TAZ. MicroRNA-130/301 controlled a PPAR?-APOE-LRP8 axis, promoting collagen deposition and LOX-dependent remodeling and further upregulating YAP/TAZ via a mechanoactive feedback loop. In turn, ECM remodeling controlled pulmonary vascular cell crosstalk via such mechanotransduction, modulation of secreted vasoactive effectors, and regulation of associated microRNA pathways. In vivo, pharmacologic inhibition of microRNA-130/301, APOE, or LOX activity ameliorated ECM remodeling and PH. Thus, ECM remodeling, as controlled by the YAP/TAZ-miR-130/301 feedback circuit, is an early PH trigger and offers combinatorial therapeutic targets for this devastating disease.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "390", "doc_id": "1727042", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is sSRI/SNRI Use Associated with Increased Risk of Delayed Cerebral Ischemia After aSAH?\n\nABSTRACT:\nTo determine the effect of selective serotonin reuptake inhibitor (SSRI)/selective norepinephrine reuptake inhibitor (SNRI) use on the risk of symptomatic vasospasm and delayed cerebral ischemia (DCI) in patients hospitalized with aneurysmal subarachnoid hemorrhage (aSAH). Retrospective review of consecutive patients with aSAH at Mayo Clinic, Rochester from January 2001 to December 2013. The variables collected and analyzed included age, sex, SSRI/SNRI use, active smoking, transfusion, modified Fisher score, WFNS grade, and outcome at discharge. Multivariate logistic regression analysis was used to evaluate factors associated with DCI, symptomatic vasospasm, and poor outcome (modified Rankin score 3-6) within 1 year. 579 [females 363 (62.7%)] patients with a median age of 55 (IQR 47-65) years were admitted with aSAH during the study period. WFNS at nadir was IV-V in 240 (41.5%), and modified Fisher score was 3-4 in 434 (75.0%). 81 (13.9%) patients had been prescribed an SSRI or SNRI prior to admission and all continued to receive these medications during hospitalization. Symptomatic vasospasm was present in 154 (26.4%), radiological infarction in 172 (29.5%), and DCI in 250 (42.9%) patients. SSRI/SNRI use was not associated with the occurrence of DCI (p = 0.458), symptomatic vasospasm (p = 0.097), radiological infarction (p = 0.972), or poor functional outcome at 3 months (p = 0.376).", "output": "{\"label\": \"no\", \"rationale\": \"The use of SSRI/SNRI prior to and during hospitalization is not associated with DCI or functional outcome in patients with aSAH.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 26264066, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: High levels of copeptin decrease risk of diabetes.\n\nCANDIDATE_PASSAGE:\nLIN28B induces neuroblastoma and enhances MYCN levels via let-7 suppression LIN28B regulates developmental processes by modulating microRNAs (miRNAs) of the let-7 family. A role for LIN28B in cancer has been proposed but has not been established in vivo. Here, we report that LIN28B showed genomic aberrations and extensive overexpression in high-risk neuroblastoma compared to several other tumor entities and normal tissues. High LIN28B expression was an independent risk factor for adverse outcome in neuroblastoma. LIN28B signaled through repression of the let-7 miRNAs and consequently resulted in elevated MYCN protein expression in neuroblastoma cells. LIN28B–let-7–MYCN signaling blocked differentiation of normal neuroblasts and neuroblastoma cells. These findings were fully recapitulated in a mouse model in which LIN28B expression in the sympathetic adrenergic lineage induced development of neuroblastomas marked by low let-7 miRNA levels and high MYCN protein expression. Interference with this pathway might offer therapeutic perspectives.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "517", "doc_id": "12337611", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Many transmembrane receptors transmit signals by long-range conformational changes in the association of alpha-helices across the plasma membrane.\n\nCANDIDATE_PASSAGE:\nConsumption of added sugars from liquid but not solid sources predicts impaired glucose homeostasis and insulin resistance among youth at risk of obesity. Little is known about longitudinal associations between added sugar consumption (solid and liquid sources) and glucose-insulin homeostasis among youth. Caucasian children (8-10 y) with at least one obese biological parent were recruited in the QUébec Adipose and Lifestyle InvesTigation in Youth (QUALITY) cohort (n = 630) and followed-up 2 y later (n = 564). Added sugars were assessed by 3 24-h dietary recalls at baseline. Two-year changes were examined in multivariate linear regression models, adjusting for baseline level, age, sex, Tanner stage, energy intake, fat mass (dual-energy X-ray absorptiometry), and physical activity (7 d accelerometer). Added sugar intake in either liquid or solid sources was not related to changes in adiposity measures (fat mass, body mass index, or waist circumference). However, a higher consumption (10 g/d) of added sugars from liquid sources was associated with 0.04 mmol/L higher fasting glucose, 2.3 pmol/L higher fasting insulin, 0.1 unit higher homeostasis model assessment of insulin resistance (HOMA-IR), and 0.4 unit lower Matsuda-insulin sensitivity index (Matsuda-ISI) in all participants (P < 0.01). No associations were observed with consumption of added sugars from solid sources. Overweight/obese children at baseline had greater increases in adiposity indicators, fasting insulin, and HOMA-IR and decreases in Matsuda-ISI during those 2 y than normal-weight children. Consumption of added sugars from liquid or solid sources was not associated with changes in adiposity, but liquid added sugars were a risk factor for the development of impaired glucose homeostasis and insul [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "757", "doc_id": "11201004", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: PGE 2 suppresss intestinal tumor growth by altering the expression of tumor suppressing and DNA repair genes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Prostaglandin E2 promotes intestinal tumor growth via DNA methylation\nABSTRACT: Although aberrant DNA methylation is considered to be one of the key ways by which tumor-suppressor and DNA-repair genes are silenced during tumor initiation and progression, the mechanisms underlying DNA methylation alterations in cancer remain unclear. Here we show that prostaglandin E(2) (PGE(2)) silences certain tumor-suppressor and DNA-repair genes through DNA methylation to promote tumor growth. These findings uncover a previously unrecognized role for PGE(2) in the promotion of tumor progression.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 908, "doc_id": "6923961", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Ly6C hi monocytes have a lower inflammatory capacity than Ly6C lo monocytes.\n\nCANDIDATE_PASSAGE:\nAssociation of hypomethylation of LINE-1 repetitive element in blood leukocyte DNA with an increased risk of hepatocellular carcinoma Global DNA hypomethylation has been associated with increased risk for cancers of the colorectum, bladder, breast, head and neck, and testicular germ cells. The aim of this study was to examine whether global hypomethylation in blood leukocyte DNA is associated with the risk of hepatocellular carcinoma (HCC). A total of 315 HCC cases and 356 age-, sex- and HBsAg status-matched controls were included. Global methylation in blood leukocyte DNA was estimated by analyzing long interspersed element-1 (LINE-1) repeats using bisulfite-polymerase chain reaction (PCR) and pyrosequencing. We observed that the median methylation level in HCC cases (percentage of 5-methylcytosine (5mC)=77.7%) was significantly lower than that in controls (79.5% 5mC) (P=0.004, Wilcoxon rank-sum test). The odds ratios (ORs) of HCC for individuals in the third, second, and first (lowest) quartiles of LINE-1 methylation were 1.1 (95% confidence interval (CI) 0.7–1.8), 1.4 (95% CI 0.8–2.2), and 2.6 (95% CI 1.7–4.1) (P for trend <0.001), respectively, compared to individuals in the fourth (highest) quartile. A 1.9-fold (95% CI 1.4–2.6) increased risk of HCC was observed among individuals with LINE-1 methylation below the median compared to individuals with higher (>median) LINE-1 methylation. Our results demonstrate for the first time that individuals with global hypomethylation measured in LINE-1 repeats in blood leukocyte DNA have an increased risk for HCC. Our data provide the evidence that global hypomethylation detected in the easily obtainable DNA source of blood leukocytes may help identify individuals at risk of HCC.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "728", "doc_id": "23665162", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Cancers that initially benefit from epidermal growth factor receptor targeted therapies later become refractory through several mechanisms.\n\nCANDIDATE_PASSAGE:\nActivation of the estrogen receptor through phosphorylation by mitogen-activated protein kinase. The phosphorylation of the human estrogen receptor (ER) serine residue at position 118 is required for full activity of the ER activation function 1 (AF-1). This Ser118 is phosphorylated by mitogen-activated protein kinase (MAPK) in vitro and in cells treated with epidermal growth factor (EGF) and insulin-like growth factor (IGF) in vivo. Overexpression of MAPK kinase (MAPKK) or of the guanine nucleotide binding protein Ras, both of which activate MAPK, enhanced estrogen-induced and antiestrogen (tamoxifen)-induced transcriptional activity of wild-type ER, but not that of a mutant ER with an alanine in place of Ser118. Thus, the activity of the amino-terminal AF-1 of the ER is modulated by the phosphorylation of Ser118 through the Ras-MAPK cascade of the growth factor signaling pathways.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "227", "doc_id": "4662264", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: A diminished ovarian reserve is a very strong indicator of infertility, even in an a priori non-infertile population.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\nABSTRACT: Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential. Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age. Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area. Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH. Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle). Conception was defined as a positive pregnancy test result. Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis. After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively). Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cy [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not have a significantly different predicted probability of conceiving after 6 cycles of attempt (61%; 95% CI, 46%-74%) compared with women (n = 660) with normal values (62%; 95% CI, 58%-66%) or after 12 cycles of attempt (70% [95% CI, 54%-80%] vs 76% [95% CI, 72%-80%], respectively).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 40, "doc_id": "13497630", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Rapamycin decreases the concentration of triacylglycerols in fruit flies.\n\nCANDIDATE_PASSAGE:\nYoung adolescents' nutrition assessment on computer (YANA-C) Objective:To assess the relative validity and acceptability of the computerised 24-h recall ‘Young Adolescent's Nutrition Assessment on Computer (YANA-C)’.Design:Food and nutrient intakes assessed with YANA-C were compared with food records (study 1) and 24-h dietary recall interviews (study 2).Main outcome measures:Intakes of food groups (fruit, fruit juice, vegetables, potatoes, bread, cereals, milk, cheese, other milk products, soft drinks, diet soft drinks, sugar/sweets, pastry/cookies, savoury snacks, butter/sauces, eggs, fish, meat) and nutrients (energy, carbohydrates, protein, fat, fiber, calcium, vitamin C and iron).Subjects and setting:A total of 237 pupils (11–14 y) from two primary and four secondary schools (study 1: n=136; study 2: n=101) in Belgium-Flanders. Results:YANA-C proved to agree well with both standard methods in categorizing subjects in consumers and nonconsumers (κstudy 1=0.48–0.92; κstudy 2=0.38–0.90). Spearman's correlations for energy and nutrient intakes ranged between 0.44 and 0.79 for study 1 and between 0.44 and 0.86 for study 2. Nutrient and energy intakes were in general (excluding calcium) significantly higher in YANA-C in comparison with the food record, but not in comparison with the interview (only fiber). Statistics used to investigate whether YANA-C agreed with the other methods in ranking portions/amounts in consumers only were fair to moderate for most of the food groups (weighted κ study 1=0.11–0.55; study 2=0.04–0.73); amounts in consumers only, were significantly lower in YANA-C against both standards for cereals; amounts were significantly higher in YANA-C against the food record for milk, soft drinks, sugar/sweets and savoury snacks and against the i [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1014", "doc_id": "4857093", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: LSD1-positive promoters are associated with RNA polymerase II\n\nCANDIDATE_PASSAGE:\nHistone Methylation-Dependent Mechanisms Impose Ligand Dependency for Gene Activation by Nuclear Receptors Nuclear receptors undergo ligand-dependent conformational changes that are required for corepressor-coactivator exchange, but whether there is an actual requirement for specific epigenetic landmarks to impose ligand dependency for gene activation remains unknown. Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases (HMTs) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals. This strategy, based at least in part on an HMT-dependent inhibitory histone code, imposes a requirement for specific histone demethylases, including LSD1, to permit ligand- and signal-dependent activation of regulated gene expression. These events link an inhibitory methylation component of the histone code to a broadly used strategy that circumvents pathological constitutive gene induction by physiologically regulated transcription factors.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "679", "doc_id": "13639330", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Hyperfibrinogenemia increases rates of femoropopliteal bypass thrombosis.\n\nCANDIDATE_ABSTRACT:\nTITLE: Influence of smoking and plasma factors on patency of femoropopliteal vein grafts.\nABSTRACT: OBJECTIVE To determine the effects of smoking, plasma lipids, lipoproteins, apolipoproteins, and fibrinogen on the patency of saphenous vein femoropopliteal bypass grafts at one year. DESIGN Prospective study of patients with saphenous vein femoropopliteal bypass grafts entered into a multicentre trial. SETTING Surgical wards, outpatient clinics, and home visits coordinated by two tertiary referral centres in London and Birmingham. PATIENTS 157 Patients (mean age 66.6 (SD 8.2) years), 113 with patent grafts and 44 with occluded grafts one year after bypass. MAIN OUTCOME MEASURE Cumulative percentage patency at one year. RESULTS Markers for smoking (blood carboxyhaemoglobin concentration (p less than 0.05) and plasma thiocyanate concentration (p less than 0.01) and plasma concentrations of fibrinogen (p less than 0.001) and apolipoproteins AI (p less than 0.04) and (a) (p less than 0.05) were significantly higher in patients with occluded grafts. Serum cholesterol concentrations were significantly higher in patients with grafts that remained patent one year after bypass (p less than 0.005). Analysis of the smoking markers indicated that a quarter of patients (40) were untruthful in their claims to have stopped smoking. Based on smoking markers, patency of grafts in smokers was significantly lower at one year by life table analysis than in non-smokers (63% v 84%, p less than 0.02). Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002). Surprisingly, increased plasma low density lipoprotein cholesterol concentration was significantly associated with improved patency at one year (85%) at values above the median compared w [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Patency was significantly higher by life table analysis in patients with a plasma fibrinogen concentration below the median than in those with a concentration above (90% v 57%, p less than 0.0002).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 533, "doc_id": "12991445", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Forkhead 0 (fox0) transcription factors are involved in apoptosis.\n\nCANDIDATE_PASSAGE:\nCell Stem Cell Review FoxO Transcription Factors and Stem Cell Homeostasis: Insights from the Hematopoietic System The forkhead O (FoxO) family of transcription factors participates in diverse physiologic processes, including induction of cell-cycle arrest, stress resistance, differentiation, apoptosis, and metabolism. Several recent studies indicate that FoxO-dependent signaling is required for long-term regenerative potential of the hematopoietic stem cell (HSC) compartment through regulation of HSC response to physiologic oxidative stress, quiescence, and survival. These observations link FoxO function in mammalian systems with the evolutionarily conserved role of FoxO in promotion of stress resistance and longevity in lower phylogenetic systems. Furthermore, these findings have implications for aging in higher organisms and in malignant stem cell biology, and suggest that FoxOs may play an important role in the maintenance and integrity of stem cell compartments in a broad spectrum of tissues.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "426", "doc_id": "16728949", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Ultrasound guidance significantly reduces the number of traumatic procedures when attempting needle insertion.\n\nCANDIDATE_PASSAGE:\nUltrasound imaging for lumbar punctures and epidural catheterisations: systematic review and meta-analysis. OBJECTIVE To determine whether ultrasound imaging can reduce the risk of failed lumbar punctures or epidural catheterisations, when compared with standard palpation methods, and whether ultrasound imaging can reduce traumatic procedures, insertion attempts, and needle redirections. DESIGN Systematic review and meta-analysis of randomised controlled trials. DATA SOURCES Ovid Medline, Embase, and Cochrane Central Register of Controlled Trials up to May 2012, without restriction by language or publication status. REVIEW METHODS Randomised trials that compared ultrasound imaging with standard methods (no imaging) in the performance of a lumbar puncture or epidural catheterisation were identified. RESULTS 14 studies with a total of 1334 patients were included (674 patients assigned to the ultrasound group, 660 to the control group). Five studies evaluated lumbar punctures and nine evaluated epidural catheterisations. Six of 624 procedures conducted in the ultrasound group failed; 44 of 610 procedures in the control group failed. Ultrasound imaging reduced the risk of failed procedures (risk ratio 0.21 (95% confidence interval 0.10 to 0.43), P<0.001). Risk reduction was similar when subgroup analysis was performed for lumbar punctures (risk ratio 0.19 (0.07 to 0.56), P=0.002) or epidural catheterisations (0.23 (0.09 to 0.60), P=0.003). Ultrasound imaging also significantly reduced the risk of traumatic procedures (risk ratio 0.27 (0.11 to 0.67), P=0.005), the number of insertion attempts (mean difference -0.44 (-0.64 to -0.24), P<0.001), and the number of needle redirections (mean difference -1.00 (-1.24 to -0.75), P<0.001). CONCLUSIONS Ultrasound imaging ca [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1341", "doc_id": "15482274", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Cancers that initially benefit from epidermal growth factor receptor targeted therapies later become refractory through several mechanisms.\n\nCANDIDATE_ABSTRACT:\nTITLE: Primary cilia and coordination of receptor tyrosine kinase (RTK) signalling.\nABSTRACT: Primary cilia are microtubule-based sensory organelles that coordinate signalling pathways in cell-cycle control, migration, differentiation and other cellular processes critical during development and for tissue homeostasis. Accordingly, defects in assembly or function of primary cilia lead to a plethora of developmental disorders and pathological conditions now known as ciliopathies. In this review, we summarize the current status of the role of primary cilia in coordinating receptor tyrosine kinase (RTK) signalling pathways. Further, we present potential mechanisms of signalling crosstalk and networking in the primary cilium and discuss how defects in ciliary RTK signalling are linked to human diseases and disorders.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 227, "doc_id": "1917068", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Participating in six months of physical activity improves cognitive functioning.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effect of physical activity on cognitive function in older adults at risk for Alzheimer disease: a randomized trial.\nABSTRACT: CONTEXT Many observational studies have shown that physical activity reduces the risk of cognitive decline; however, evidence from randomized trials is lacking. OBJECTIVE To determine whether physical activity reduces the rate of cognitive decline among older adults at risk. DESIGN AND SETTING Randomized controlled trial of a 24-week physical activity intervention conducted between 2004 and 2007 in metropolitan Perth, Western Australia. Assessors of cognitive function were blinded to group membership. PARTICIPANTS We recruited volunteers who reported memory problems but did not meet criteria for dementia. Three hundred eleven individuals aged 50 years or older were screened for eligibility, 89 were not eligible, and 52 refused to participate. A total of 170 participants were randomized and 138 participants completed the 18-month assessment. INTERVENTION Participants were randomly allocated to an education and usual care group or to a 24-week home-based program of physical activity. MAIN OUTCOME MEASURE Change in Alzheimer Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) scores (possible range, 0-70) over 18 months. RESULTS In an intent-to-treat analysis, participants in the intervention group improved 0.26 points (95% confidence interval, -0.89 to 0.54) and those in the usual care group deteriorated 1.04 points (95% confidence interval, 0.32 to 1.82) on the ADAS-Cog at the end of the intervention. The absolute difference of the outcome measure between the intervention and control groups was -1.3 points (95% confidence interval,-2.38 to -0.22) at the end of the intervention. At 18 months, participants in the intervention group improved 0.73 points (95% confidence interval, -1.27 to 0.03) on the ADAS-Cog, and those in the usual care group improved 0.04 p [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"The absolute difference of the outcome measure between the intervention and control groups was -1.3 points (95% confidence interval,-2.38 to -0.22) at the end of the intervention.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 921, "doc_id": "1642727", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: GATA3 regulates cell cycle progression in bone marrow hematopoietic stem cells.\n\nCANDIDATE_PASSAGE:\nEngraftment of engineered ES cell–derived cardiomyocytes but not BM cells restores contractile function to the infarcted myocardium Cellular cardiomyoplasty is an attractive option for the treatment of severe heart failure. It is, however, still unclear and controversial which is the most promising cell source. Therefore, we investigated and examined the fate and functional impact of bone marrow (BM) cells and embryonic stem cell (ES cell)–derived cardiomyocytes after transplantation into the infarcted mouse heart. This proved particularly challenging for the ES cells, as their enrichment into cardiomyocytes and their long-term engraftment and tumorigenicity are still poorly understood. We generated transgenic ES cells expressing puromycin resistance and enhanced green fluorescent protein cassettes under control of a cardiac-specific promoter. Puromycin selection resulted in a highly purified (>99%) cardiomyocyte population, and the yield of cardiomyocytes increased 6–10-fold because of induction of proliferation on purification. Long-term engraftment (4–5 months) was observed when co-transplanting selected ES cell–derived cardiomyocytes and fibroblasts into the injured heart of syngeneic mice, and no teratoma formation was found (n = 60). Although transplantation of ES cell–derived cardiomyocytes improved heart function, BM cells had no positive effects. Furthermore, no contribution of BM cells to cardiac, endothelial, or smooth muscle neogenesis was detected. Hence, our results demonstrate that ES-based cell therapy is a promising approach for the treatment of impaired myocardial function and provides better results than BM-derived cells.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "444", "doc_id": "2559303", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is perforation of the appendix a risk factor for tubal infertility and ectopic pregnancy?\n\nABSTRACT:\nTo critically assess the evidence that appendiceal perforation is a risk factor for subsequent tubal infertility or ectopic pregnancy. Epidemiologic studies investigating the relationship between appendectomy and infertility or ectopic pregnancy were identified by searching the MEDLINE database from 1966 to 1997. Appropriate citations were also extracted from a manual search of the bibliographies of selected papers. Twenty-three articles were retrieved. Only 4 presented original data including comparisons to a nonexposed control group and they form the basis for this study. Because the raw data or specific techniques of data analysis were not always explicitly described, indices of risk for exposure were extracted from the data as presented and were analysed without attempting to convert them to a common measure. Articles were assessed according to the criteria of the Evidence-Based Medicine Working Group for evaluating articles on harm. Review of the literature yielded estimates of the risk of adverse fertility outcomes ranging from 1.6 (95% confidence interval [CI] 1.1 to 2.5) for ectopic pregnancy after an appendectomy to 4.8 (95% CI 1.5 to 14.9) for tubal infertility from perforation of the appendix. Recall bias, and poor adjustment for confounding variables in some reports, weakened the validity of the studies.", "output": "{\"label\": \"maybe\", \"rationale\": \"The methodologic weaknesses of the studies do not permit acceptance of increased risk of tubal pregnancy or infertility as a consequence of perforation of the appendix, so a causal relationship cannot be supported by the data currently available. Only a well-designed case-control study with unbiased ascertainment of exposure and adjustment for confounding variables will provide a definitive answer.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 10223070, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Increased microtubule acetylation exacerbates LRRK2 Roc-COR domain mutation induced locomotor deficits.\n\nCANDIDATE_ABSTRACT:\nTITLE: Increasing microtubule acetylation rescues axonal transport and locomotor deficits caused by LRRK2 Roc-COR domain mutations\nABSTRACT: Leucine-rich repeat kinase 2 (LRRK2) mutations are the most common genetic cause of Parkinson's disease. LRRK2 is a multifunctional protein affecting many cellular processes and has been described to bind microtubules. Defective microtubule-based axonal transport is hypothesized to contribute to Parkinson's disease, but whether LRRK2 mutations affect this process to mediate pathogenesis is not known. Here we find that LRRK2 containing pathogenic Roc-COR domain mutations (R1441C, Y1699C) preferentially associates with deacetylated microtubules, and inhibits axonal transport in primary neurons and in Drosophila, causing locomotor deficits in vivo. In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport. In vivo knockdown of the deacetylases HDAC6 and Sirt2, or administration of TSA rescues both axonal transport and locomotor behavior. Thus, this study reveals a pathogenic mechanism and a potential intervention for Parkinson's disease.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In vitro, increasing microtubule acetylation using deacetylase inhibitors or the tubulin acetylase αTAT1 prevents association of mutant LRRK2 with microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 612, "doc_id": "9638032", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: The locus rs647161 is associated with colorectal carcinoma.\n\nCANDIDATE_ABSTRACT:\nTITLE: Genome-wide association analyses in East Asians identify new susceptibility loci for colorectal cancer\nABSTRACT: To identify new genetic factors for colorectal cancer (CRC), we conducted a genome-wide association study in east Asians. By analyzing genome-wide data in 2,098 cases and 5,749 controls, we selected 64 promising SNPs for replication in an independent set of samples, including up to 5,358 cases and 5,922 controls. We identified four SNPs with association P values of 8.58 × 10(-7) to 3.77 × 10(-10) in the combined analysis of all east Asian samples. Three of the four were replicated in a study conducted in 26,060 individuals of European descent, with combined P values of 1.22 × 10(-10) for rs647161 (5q31.1), 6.64 × 10(-9) for rs2423279 (20p12.3) and 3.06 × 10(-8) for rs10774214 (12p13.32 near the CCND2 gene), derived from meta-analysis of data from both east Asian and European-ancestry populations. This study identified three new CRC susceptibility loci and provides additional insight into the genetics and biology of CRC.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Three of the four were replicated in a study conducted in 26,060 individuals of European descent, with combined P values of 1.22 × 10(-10) for rs647161 (5q31.1), 6.64 × 10(-9) for rs2423279 (20p12.3) and 3.06 × 10(-8) for rs10774214 (12p13.32 near the CCND2 gene), derived from meta-analysis of data from both east Asian and European-ancestry populations.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1225, "doc_id": "9650982", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Suboptimal nutrition is not predictive of chronic disease\n\nCANDIDATE_ABSTRACT:\nTITLE: Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015\nABSTRACT: BACKGROUND The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. METHODS We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors-the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. We characterised risk exposure in relation to a Socio-demographic Index (SDI). FINDINGS Between 1990 and 2015, global exposure to unsafe sanitation, household air pollution, childhood underweight, childhood stunting, and smoking [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"In 2015, the ten largest contributors to global DALYs among Level 3 risks were high systolic blood pressure (211·8 million [192·7 million to 231·1 million] global DALYs), smoking (148·6 million [134·2 million to 163·1 million]), high fasting plasma glucose (143·1 million [125·1 million to 163·5 million]), high BMI (120·1 million [83·8 million to 158·4 million]), childhood undernutrition (113·3 million [103·9 million to 123·4 million]), ambient particulate matter (103·1 million [90·8 million to 115·1 million]), high total cholesterol (88·7 million [74·6 million to 105·7 million]), household air pollution (85·6 million [66·7 million to 106·1 million]), alcohol use (85·0 million [77·2 million to 93·0 million]), and diets high in sodium (83·0 million [49·3 million to 127·5 million]).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1110, "doc_id": "13770184", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Smc5/6 engagment halts the activation of SUMO E3 ligase Mms21 by ATP-dependent remolding.\n\nCANDIDATE_PASSAGE:\nAnother Barrier to Regeneration in the CNS: Activated Macrophages Induce Extensive Retraction of Dystrophic Axons through Direct Physical Interactions Injured axons of the adult CNS undergo lengthy retraction from the initial site of axotomy after spinal cord injury. Macrophage infiltration correlates spatiotemporally with this deleterious phenomenon, but the direct involvement of these inflammatory cells has not been demonstrated. In the present study, we examined the role of macrophages in axonal retraction within the dorsal columns after spinal cord injury in vivo and found that retraction occurred between days 2 and 28 after lesion and that the ends of injured axons were associated with ED-1+ cells. Clodronate liposome-mediated depletion of infiltrating macrophages resulted in a significant reduction in axonal retraction; however, we saw no evidence of regeneration. We used time-lapse imaging of adult dorsal root ganglion neurons in an in vitro model of the glial scar to examine macrophage-axon interactions and observed that adhesive contacts and considerable physical interplay between macrophages and dystrophic axons led to extensive axonal retraction. The induction of retraction was dependent on both the growth state of the axon and the activation state of the macrophage. Only dystrophic adult axons were susceptible to macrophage \"attack. \" Unlike intrinsically active cell line macrophages, both primary macrophages and microglia required activation to induce axonal retraction. Contact with astrocytes had no deleterious effect on adult dystrophic axons, suggesting that the induction of extensive retraction was specific to phagocytic cells. Our data are the first to indicate a direct role of activated macrophages in axonal retraction by physical cell-cel [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1090", "doc_id": "16905344", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: MFGE8 regulates fat absorption by binding to av-Beta3 and av-Beta5 integrins.\n\nCANDIDATE_PASSAGE:\nPrognostic Value of Late Gadolinium Enhancement Cardiovascular Magnetic Resonance in Cardiac Amyloidosis BACKGROUND The prognosis and treatment of the 2 main types of cardiac amyloidosis, immunoglobulin light chain (AL) and transthyretin (ATTR) amyloidosis, are substantially influenced by cardiac involvement. Cardiovascular magnetic resonance with late gadolinium enhancement (LGE) is a reference standard for the diagnosis of cardiac amyloidosis, but its potential for stratifying risk is unknown. METHODS AND RESULTS Two hundred fifty prospectively recruited subjects, 122 patients with ATTR amyloid, 9 asymptomatic mutation carriers, and 119 patients with AL amyloidosis, underwent LGE cardiovascular magnetic resonance. Subjects were followed up for a mean of 24±13 months. LGE was performed with phase-sensitive inversion recovery (PSIR) and without (magnitude only). These were compared with extracellular volume measured with T1 mapping. PSIR was superior to magnitude-only inversion recovery LGE because PSIR always nulled the tissue (blood or myocardium) with the longest T1 (least gadolinium). LGE was classified into 3 patterns: none, subendocardial, and transmural, which were associated with increasing amyloid burden as defined by extracellular volume (P<0.0001), with transitions from none to subendocardial LGE at an extracellular volume of 0.40 to 0.43 (AL) and 0.39 to 0.40 (ATTR) and to transmural at 0.48 to 0.55 (AL) and 0.47 to 0.59 (ATTR). Sixty-seven patients (27%) died. Transmural LGE predicted death (hazard ratio, 5.4; 95% confidence interval, 2.1-13.7; P<0.0001) and remained independent after adjustment for N-terminal pro-brain natriuretic peptide, ejection fraction, stroke volume index, E/E', and left ventricular mass index (hazard ratio, 4.1; 95% conf [TRUNCATED]", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "736", "doc_id": "13768432", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Cold exposure reduces BAT recruitment.\n\nCANDIDATE_PASSAGE:\nDifferential distribution of IL28B.rs12979860 single-nucleotide polymorphism among Egyptian healthcare workers with and without a hepatitis C virus-specific cellular immune response The CC genotype of the interleukin (IL)-28B.rs12979860 gene has been associated with spontaneous hepatitis C virus (HCV) clearance and treatment response. The distribution and correlation of an IL28B.rs12979860 single-nucleotide polymorphism (SNP) with HCV-specific cell-mediated immune (CMI) responses among Egyptian healthcare workers (HCWs) is not known. We determined this relationship in 402 HCWs who serve a patient cohort with ~85 % HCV prevalence. We enrolled 402 HCWs in four groups: group 1 (n = 258), seronegative aviremic subjects; group 2 (n = 25), seronegative viremic subjects; group 3 (n = 41), subjects with spontaneously resolved HCV infection; and group 4 (n = 78), chronic HCV patients. All subjects were tested for an HCV-specific CMI response using an ex-vivo interferon-gamma (IFNγ) ELISpot assay with nine HCV genotype-4a overlapping 15-mer peptide pools corresponding to all of the HCV proteins. All subjects were tested for IL28B.rs12979860 SNP by real-time PCR. An HCV-specific CMI was demonstrated in ~27 % of the seronegative aviremic HCWs (group 1), suggesting clearance of infection after low-level exposure to HCV. The frequency of IL28B.rs12979860 C allele homozygosity in the four groups was 49 %, 48 %, 49 %, and 23 %, while that of the T allele was 14 %, 16 %, 12 and 19 %, respectively, suggesting differential distributions among subjects with different HCV status. As reported, IL28B.rs12979860 predicted the outcome of HCV infection (p < 0.05), but we did not find any relationship between the IL28B genotypes and the outcome of HCV-specific CMI responses in the fou [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "269", "doc_id": "991139", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: MICAL redox enzymes regulate actin dynamics in many cell types.\n\nCANDIDATE_PASSAGE:\nDynamics in the plasma membrane: how to combine fluidity and order. Cell membranes are fascinating supramolecular aggregates that not only form a barrier between compartments but also harbor many chemical reactions essential to the existence and functioning of a cell. Here, it is proposed to review the molecular dynamics and mosaic organization of the plasma membrane, which are thought to have important functional implications. We will first summarize the basic concepts of Brownian diffusion and lipid domain formation in model membranes and then track the development of ideas and tools in this field, outlining key results obtained on the dynamic processes at work in membrane structure and assembly. We will focus in particular on findings made using fluorescent labeling and imaging procedures to record these dynamic processes. We will also discuss a few examples showing the impact of lateral diffusion on cell signal transduction, and outline some future methodological challenges which must be met before we can answer some of the questions arising in this field of research.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "737", "doc_id": "6190603", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Excess gestational weight gain is associated with obesity-related pregnancy outcomes.\n\nCANDIDATE_ABSTRACT:\nTITLE: Effects of interventions in pregnancy on maternal weight and obstetric outcomes: meta-analysis of randomised evidence\nABSTRACT: OBJECTIVE To evaluate the effects of dietary and lifestyle interventions in pregnancy on maternal and fetal weight and to quantify the effects of these interventions on obstetric outcomes. DESIGN Systematic review and meta-analysis. DATA SOURCES Major databases from inception to January 2012 without language restrictions. STUDY SELECTION Randomised controlled trials that evaluated any dietary or lifestyle interventions with potential to influence maternal weight during pregnancy and outcomes of pregnancy. DATA SYNTHESIS Results summarised as relative risks for dichotomous data and mean differences for continuous data. RESULTS We identified 44 relevant randomised controlled trials (7278 women) evaluating three categories of interventions: diet, physical activity, and a mixed approach. Overall, there was 1.42 kg reduction (95% confidence interval 0.95 to 1.89 kg) in gestational weight gain with any intervention compared with control. With all interventions combined, there were no significant differences in birth weight (mean difference -50 g, -100 to 0 g) and the incidence of large for gestational age (relative risk 0.85, 0.66 to 1.09) or small for gestational age (1.00, 0.78 to 1.28) babies between the groups, though by itself physical activity was associated with reduced birth weight (mean difference -60 g, -120 to -10 g). Interventions were associated with a reduced the risk of pre-eclampsia (0.74, 0.60 to 0.92) and shoulder dystocia (0.39, 0.22 to 0.70), with no significant effect on other critically important outcomes. Dietary intervention resulted in the largest reduction in maternal gestational weight gain (3.84 kg, 2.45 to 5.22 kg), with improved pregnancy outcomes compared with other interventions. The overall evidence rating was low to very low for i [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS Dietary and lifestyle interventions in pregnancy can reduce maternal gestational weight gain and improve outcomes for both mother and baby.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 394, "doc_id": "11360768", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: A diminished ovarian reserve does not solely indicate infertility in an a priori non-infertile population.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\nABSTRACT: Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential. Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age. Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area. Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH. Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle). Conception was defined as a positive pregnancy test result. Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis. After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively). Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cy [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Inhibin B levels (n = 737) were not associated with the probability of conceiving in a given cycle (hazard ratio per 1-pg/mL increase, 0.999; 95% CI, 0.997-1.001).\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 39, "doc_id": "13497630", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Medications to treat obesity have unwanted side effects.\n\nCANDIDATE_ABSTRACT:\nTITLE: Myocardial muscarinic receptor upregulation and normal response to isoproterenol in denervated hearts by familial amyloid polyneuropathy.\nABSTRACT: BACKGROUND Patients with familial amyloid polyneuropathy, a rare hereditary form of amyloidosis, have progressive autonomic neuropathy. The disease usually does not induce heart failure but is associated with sudden death, conduction disturbances, and an increased risk of complications during anesthesia. Although cardiac sympathetic denervation has been clearly demonstrated, the postsynaptic status of the cardiac autonomic nervous system remains unelucidated. METHODS AND RESULTS Twenty-one patients were studied (age, 39+/-11 years; normal coronary arteries; left ventricular ejection fraction 68+/-9%). To evaluate the density and affinity constants of myocardial muscarinic receptors, PET with (11)C-MQNB (methylquinuclidinyl benzilate), a specific hydrophilic antagonist, was used. Cardiac beta-receptor functional efficiency was studied by the heart rate (HR) response to intravenous infusion of isoproterenol (5 minutes after 2 mg of atropine, 5, 10, and 15 ng/kg per minute during 5 minutes per step). The mean muscarinic receptor density was higher in patients than in control subjects (B'(max), 35.5+/-8.9 versus 26.1+/-6.7 pmol/mL, P=0.003), without change in receptor affinity. The increase in HR after injection of atropine as well as of MQNB was lower in patients compared with control subjects despite a similar basal HR (DeltaHR after atropine, 11+/-21% versus 62+/-17%; P<0.001), consistent with parasympathetic denervation. Incremental infusion of isoproterenol induced a similar increase in HR in patients and control subjects. CONCLUSIONS Cardiac autonomic denervation in familial amyloid polyneuropathy results in an upregulation of myocardial muscarinic receptors but without change in cardiac beta-receptor responsiveness to catecholamines.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 766, "doc_id": "1686881", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: RAD52 is involved in break-induced DNA replication (BIR).\n\nCANDIDATE_PASSAGE:\nQuantitative, genome-wide analysis of eukaryotic replication initiation and termination. Many fundamental aspects of DNA replication, such as the exact locations where DNA synthesis is initiated and terminated, how frequently origins are used, and how fork progression is influenced by transcription, are poorly understood. Via the deep sequencing of Okazaki fragments, we comprehensively document replication fork directionality throughout the S. cerevisiae genome, which permits the systematic analysis of initiation, origin efficiency, fork progression, and termination. We show that leading-strand initiation preferentially occurs within a nucleosome-free region at replication origins. Using a strain in which late origins can be induced to fire early, we show that replication termination is a largely passive phenomenon that does not rely on cis-acting sequences or replication fork pausing. The replication profile is predominantly determined by the kinetics of origin firing, allowing us to reconstruct chromosome-wide timing profiles from an asynchronous culture.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1003", "doc_id": "36606083", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is alcohol-related diseases and alcohol dependence syndrome associated with increased gout risk : A nationwide population-based cohort study?\n\nABSTRACT:\nAlcohol intake is strongly associated with hyperuricemia, which may cause gout. This study evaluated the risk of gout in patients with alcohol-related diseases and alcohol dependence syndrome. We used the Taiwan National Health Insurance Research Database (NHIRD) to conduct a nationwide population-based cohort study to assess the risk of gout and gout incidence in patients with alcohol-related diseases and alcohol dependence syndrome (as defined by the International Classification of Diseases, Ninth Revision). In the NHIRD records from 1998 to 2008, we identified 11,675 cases of alcohol-related diseases. The control group comprised 23,350 cases without alcohol-related diseases propensity score-matched (1 case: 2 controls) for age, age group, and sex. The results revealed that alcohol-related diseases were significantly associated with gout risk (adjusted hazard ratio 1.88; P<0.0001). Of the alcohol-related disease cases, 34.1% of the patients had alcohol dependence syndrome (males 34.8%; females 32.4%), and alcohol dependence was independently associated with gout occurrence (relative risk [RR] 2.01; P<0.0001). Severe alcohol-dependent patients (who were also the heavy benzodiazepines users), were associated with an increased risk of gout (RR 1.71 to 4.21, P≤0.0182).", "output": "{\"label\": \"yes\", \"rationale\": \"Physicians should be aware of the association between alcohol dependence syndrome and gout occurrence, and alcohol use assessment and measures to prevent alcohol dependence should be implemented in the integrative care for patients with gout.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 27238189, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Human T-lymphotropic virus type-I-associated myelopathy / tropical spastic paraparesis (HAM/TSP) patients produce Immunoglobulin G (IgG) antibodies which cross-react with an immunodominant epitope in Tax.\n\nCANDIDATE_PASSAGE:\nMicroarray analysis of pneumococcal gene expression during invasive disease. Streptococcus pneumoniae is a leading cause of invasive bacterial disease. This is the first study to examine the expression of S. pneumoniae genes in vivo by using whole-genome microarrays available from The Institute for Genomic Research. Total RNA was collected from pneumococci isolated from infected blood, infected cerebrospinal fluid, and bacteria attached to a pharyngeal epithelial cell line in vitro. Microarray analysis of pneumococcal genes expressed in these models identified body site-specific patterns of expression for virulence factors, transporters, transcription factors, translation-associated proteins, metabolism, and genes with unknown function. Contributions to virulence predicted for several unknown genes with enhanced expression in vivo were confirmed by insertion duplication mutagenesis and challenge of mice with the mutants. Finally, we cross-referenced our results with previous studies that used signature-tagged mutagenesis and differential fluorescence induction to identify genes that are potentially required by a broad range of pneumococcal strains for invasive disease.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "528", "doc_id": "39285547", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is the oocyte population renewed in transplanted or irradiated adult ovaries?\n\nABSTRACT:\nAccording to conventional theory, the oocyte population is not renewed in mammalian ovaries after birth. A new hypothesis proposes that oocytes are generated continuously from haematopoietic progenitor cells. There is, however, no evidence that they can ovulate, although they may partially restore fertility by organizing 'helper follicles'. The hypothesis that follicles can form de novo in adult ovaries has been tested in a transplant model. Ovaries from adult mice were transplanted under the kidney capsule or into the ovarian bursa of histocompatible, transgenic CAG::H2B-EGFP host animals. Some donors were sterilized before transplantation by X-irradiation to ensure 'empty niches' were available for repopulation. The phenotype of follicular oocytes at 2, 4 and 8 weeks post-transplantation was scored by epifluorescence. A total of 819 oocytes were examined in 30 ovarian grafts. None expressed green fluorescence, as would be predicted if they had formed de novo from germ cell progenitors in the systemic circulation of the host. Furthermore, small follicles eliminated by irradiation were not replaced in transplanted ovaries, and the few growing follicles present were apparently survivors of the original population.", "output": "{\"label\": \"no\", \"rationale\": \"No evidence was found to support the hypothesis that progenitor cells from extra-ovarian sources can repopulate the adult ovary. The findings are consistent with the conventional view that a limited number of oocytes are formed before birth and declines with age. The study did not, however, rule out the possibility that germline stem cells may reside in the adult ovary.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 18596027, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Binding of p53 to enhancer regions (p53BERs) regulates the activity of p53 transcription and cell cycle arrest through the production of p53-dependent eRNAs.\n\nCANDIDATE_PASSAGE:\nE2F-6: a novel member of the E2F family is an inhibitor of E2F-dependent transcription The E2F family of transcription factors are essential for the regulation of genes required for appropriate progression through the cell cycle. Five members of the E2F family have been previously reported, namely E2F1-5. All five are key elements in transcriptional regulation of essential genes, and they can be divided into two functional groups, those that induce S-phase progression when overexpressed in quiescent cells (E2Fs 1–3), and those that do not (E2Fs 4–5). Here, we describe the identification of a novel member of this family, which we refer to as E2F-6. E2F-6 shares significant homology with E2Fs 1–5, especially within the DNA binding, heterodimerization and marked box domains. Unlike E2Fs 1–5, E2F-6 lacks a transactivation and a pocket protein binding domain, hence, forms a unique third group within the E2F family. E2F-6 is a nuclear protein that can form heterodimers with the DP proteins (both DP-1 and DP-2) in vitro and in vivo. Our results show that the complex formed between E2F-6 and the DP proteins, possesses high DNA binding activity, displaying a preference for a TTTCCCGC E2F recognition site, which is slightly different to the E2F consensus site derived from the E2 promoter (TTTCGCGC). In contrast to the other members of the E2F family, ectopic expression of E2F-6 inhibits transcription from promoters possessing E2F recognition sites rather than activating transcription. In addition, overexpression of E2F-6 suppresses the transactivational effects of co-expression of E2F-1 and DP-1. The inhibitory effect of E2F-6 is dependent on its DNA binding activity and its ability to form heterodimers with the DPs. Interestingly, ectopic expression of E2F-6 leads to [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "177", "doc_id": "7688110", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does fas/Fas ligand regulation mediate cell death in human Ewing 's sarcoma cells treated with melatonin?\n\nABSTRACT:\nDespite recent advances in cancer therapy, the 5-year survival rate for Ewing's sarcoma is still very low, and new therapeutic approaches are necessary. It was found previously that melatonin induces cell death in the Ewing's sarcoma cell line, SK-N-MC, by activating the extrinsic apoptotic pathway. Melatonin actions were analysed by metabolic viability/survival cell assays, flow cytometry, quantitative PCR for mRNA expression, western blot for protein activation/expression and electrophoretic mobility shift assay for transcription factor activation. Melatonin increases the expression of Fas and its ligand Fas L, this increase being responsible for cell death induced by the indolamine. Melatonin also produces a transient increase in intracellular oxidants and activation of the redox-regulated transcription factor Nuclear factor-kappaB. Inhibition of such activation prevents cell death and Fas/Fas L upregulation. Cytotoxic effect and Fas/Fas L regulation occur in all Ewing's cell lines studied, and do not occur in the other tumour cell lines studied where melatonin does not induce cell death.", "output": "{\"label\": \"yes\", \"rationale\": \"Our data offers new insights in the study of alternative therapeutic strategies in the treatment of Ewing's sarcoma. Further attention deserves to be given to the differences in the cellular biology of sensitive tumours that could explain the cytotoxic effect of melatonin and the increase in the level of free radicals caused by this molecule, in particular cancer types.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 22382690, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Primary cervical cancer screening with HPV detection has higher longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_PASSAGE:\nEvaluation of human papillomavirus testing in primary screening for cervical abnormalities: comparison of sensitivity, specificity, and frequency of referral. CONTEXT Human papillomavirus (HPV) DNA testing of women having Papanicolaou (Pap) smears showing atypical squamous cells of undetermined significance (ASCUS) has clinical usefulness. Whether HPV DNA testing alone is useful in primary screening remains to be determined. OBJECTIVE To determine the accuracy of HPV DNA testing for detecting cervical intraepithelial neoplasia (CIN) grade 3 or cancer (the criterion standard). DESIGN, SETTING, AND PARTICIPANTS Between December 1997 and October 2000, 4075 women who attended Planned Parenthood clinics in Washington State were screened simultaneously using thin-layer Pap and HPV DNA testing by a polymerase chain reaction (PCR)-based method and by a liquid-based RNA-DNA hybridization capture with signal amplification assay (signal amplification). Women who were positive for high-risk HPV types, or had Pap results of ASCUS or higher, were considered to have positive screening test results and were referred for colposcopy and biopsy. Additionally, a random sample of women with negative screening test results was referred for colposcopy. Based on individual and combined thin-layer Pap, HPV PCR, and HPV signal amplification test results from the screening and the colposcopy visits, 7 colposcopy triage strategies were defined and evaluated. MAIN OUTCOME MEASURE Sensitivity and specificity for detecting cervical lesions graded CIN 3 or higher for each of the 7 triage strategies. RESULTS The estimated prevalence of CIN 3 or higher was 3.2%. The sensitivity (95% confidence interval) of thin-layer Pap (with a result of > or = ASCUS) for identifying women with CIN 3 or hig [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "971", "doc_id": "19140422", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Is decompressive surgery effective for spinal cord sarcoidosis accompanied with compressive cervical myelopathy?\n\nABSTRACT:\nA retrospective multicenter study of series of 12 patients with spinal cord sarcoidosis who underwent surgery. To evaluate the postoperative outcomes of patients with cervical spinal cord sarcoidosis accompanied with compressive myelopathy and effect of decompressive surgery on the prognosis of sarcoidosis. Sarcoidosis is a chronic, multisystem noncaseating granulomatous disease. It is difficult to differentiate spinal cord sarcoidosis from cervical compressive myelopathy. There are no studies regarding the coexistence of compressive cervical myelopathy with cervical spinal cord sarcoidosis and the effect of decompressive surgery. Nagoya Spine Group database included 1560 cases with cervical myelopathy treated with cervical laminectomy or laminoplasty from 2001 to 2005. A total of 12 patients (0.08% of cervical myelopathy) were identified spinal cord sarcoidosis treated with decompressive surgery. As a control subject, 8 patients with spinal cord sarcoidosis without compressive lesion who underwent high-dose steroid therapy without surgery were recruited. In the surgery group, enhancing lesions on magnetic resonance imaging (MRI) were mostly seen at C5-C6, coincident with the maximum compression level in all cases. Postoperative recovery rates in the surgery group at 1 week and 4 weeks were -7.4% and -1.1%, respectively. Only 5 cases had showed clinical improvement, and the condition of these 5 patients had worsened again at averaged 7.4 weeks after surgery. Postoperative oral steroid therapy was initiated at an average of 6.4 weeks and the average initial dose was 54.0 mg in the surgery group, while 51.3 mg in the nonsurgery group. The recovery rate of the Japanese Orthopedic Association score, which increased after steroid therapy, was better in the nonsur [TRUNCATED]", "output": "{\"label\": \"no\", \"rationale\": \"The effect of decompression for spinal cord sarcoidosis with compressive myelopathy was not evident. Early diagnosis for sarcoidosis from other organ and steroid therapy should be needed.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 20736887, "truncated": true, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Post-transcriptional handling of mitochondrial transcripts occurs in mitochondrial RNA granules.\n\nCANDIDATE_ABSTRACT:\nTITLE: GRSF1 Regulates RNA Processing in Mitochondrial RNA Granules\nABSTRACT: Various specialized domains have been described in the cytosol and the nucleus; however, little is known about compartmentalization within the mitochondrial matrix. GRSF1 (G-rich sequence factor 1) is an RNA binding protein that was previously reported to localize in the cytosol. We found that an isoform of GRSF1 accumulates in discrete foci in the mitochondrial matrix. These foci are composed of nascent mitochondrial RNA and also contain RNase P, an enzyme that participates in mitochondrial RNA processing. GRSF1 was found to interact with RNase P and to be required for processing of both classical and tRNA-less RNA precursors. In its absence, cleavage of primary RNA transcripts is abnormal, leading to decreased expression of mitochondrially encoded proteins and mitochondrial dysfunction. Our findings suggest that the foci containing GRSF1 and RNase P correspond to sites where primary RNA transcripts converge to be processed. We have termed these large ribonucleoprotein structures \"mitochondrial RNA granules. \"", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Our findings suggest that the foci containing GRSF1 and RNase P correspond to sites where primary RNA transcripts converge to be processed.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 962, "doc_id": "13931771", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Upregulation of mosGCTL-1 is induced upon infection with West Nile virus.\n\nCANDIDATE_ABSTRACT:\nTITLE: The DNA Methylome of Human Peripheral Blood Mononuclear Cells\nABSTRACT: DNA methylation plays an important role in biological processes in human health and disease. Recent technological advances allow unbiased whole-genome DNA methylation (methylome) analysis to be carried out on human cells. Using whole-genome bisulfite sequencing at 24.7-fold coverage (12.3-fold per strand), we report a comprehensive (92.62%) methylome and analysis of the unique sequences in human peripheral blood mononuclear cells (PBMC) from the same Asian individual whose genome was deciphered in the YH project. PBMC constitute an important source for clinical blood tests world-wide. We found that 68.4% of CpG sites and <0.2% of non-CpG sites were methylated, demonstrating that non-CpG cytosine methylation is minor in human PBMC. Analysis of the PBMC methylome revealed a rich epigenomic landscape for 20 distinct genomic features, including regulatory, protein-coding, non-coding, RNA-coding, and repeat sequences. Integration of our methylome data with the YH genome sequence enabled a first comprehensive assessment of allele-specific methylation (ASM) between the two haploid methylomes of any individual and allowed the identification of 599 haploid differentially methylated regions (hDMRs) covering 287 genes. Of these, 76 genes had hDMRs within 2 kb of their transcriptional start sites of which >80% displayed allele-specific expression (ASE). These data demonstrate that ASM is a recurrent phenomenon and is highly correlated with ASE in human PBMCs. Together with recently reported similar studies, our study provides a comprehensive resource for future epigenomic research and confirms new sequencing technology as a paradigm for large-scale epigenomics studies.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1352, "doc_id": "18670", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Assembly of invadopodia is triggered by focal generation of phosphatidylinositol-3,4-biphosphate and the activation of the nonreceptor tyrosine kinase Src.\n\nCANDIDATE_PASSAGE:\nPhosphorylation site mutations in heterochromatin protein 1 (HP1) reduce or eliminate silencing activity. HP1 is an essential heterochromatin-associated protein in Drosophila. HP1 has dosage-dependent effects on the silencing of euchromatic genes that are mislocalized to heterochromatin and is required for the normal expression of at least two heterochromatic genes. HP1 is multiply phosphorylated in vivo, and HP1 hyperphosphorylation is correlated with heterochromatin assembly during development. The purpose of this study was to test whether HP1 phosphorylation modifies biological activity and biochemical properties of HP1. To determine sites of HP1 phosphorylation in vivo and whether phosphorylation affects any biochemical properties of HP1, we expressed Drosophila HP1 in lepidopteran cultured cells using a recombinant baculovirus vector. Phosphopeptides were identified by matrix-assisted laser desorption ionization/time of flight mass spectroscopy; these peptides contain target sites for casein kinase II, protein tyrosine kinase, and PIM-1 kinase. Purified HP1 from bacterial (unphosphorylated) and lepidopteran (phosphorylated) cells has similar secondary structure. Phosphorylation has no effect on HP1 self-association but alters the DNA binding properties of HP1, suggesting that phosphorylation could differentially regulate HP1-dependent interactions. Serine-to-alanine and serine-to-glutamate substitutions at consensus protein kinase motifs resulted in reduction or loss of silencing activity of mutant HP1 in transgenic flies. These results suggest that dynamic phosphorylation/dephosphorylation regulates HP1 activity in heterochromatic silencing.", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "133", "doc_id": "8417211", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Infection of human T-cell lymphotropic virus type 1 is most frequent in individuals of African origin.\n\nCANDIDATE_ABSTRACT:\nTITLE: HTLV-I/II associated disease in England and Wales, 1993-7: retrospective review of serology requests.\nABSTRACT: Apart from HIV two exogenous retroviruses (human T cell leukaemia viruses type I (HTLV-I) and type II (HTLV-II)) infect humans. HTLV-I infection is endemic in Japan, the Caribbean, Africa, and Melanesia and is found among immigrants from these regions in Europe. HTLV-I infection is associated with a 1-5% lifetime risk of adult T cell leukaemia/lymphoma, 1 a 0.25% lifetime risk of HTLV-I associated myelopathy, 2 and other inflammatory conditions (uveitis, alveolitis, and arthritis).1 HTLV-II infection is endemic in some native American and African peoples and among injecting drug users and has been associated with neurological disease.1 Between 1986 and 1992, 100 cases of HTLV-I associated myelopathy and 44 cases of adult T cell leukaemia/lymphoma were diagnosed in the United Kingdom.3 Adult T cell leukaemia/lymphoma was first described in 1977 and patients with it have a mean life expectancy of only six months, so most of the 44 cases were probably incident cases. …", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 628, "doc_id": "24512064", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Obesity is determined solely by environmental factors.\n\nCANDIDATE_ABSTRACT:\nTITLE: Familial obesity and leanness.\nABSTRACT: Using the Princeton School District Family Study cohort, our specific aim was to estimate the prevalence of suspected familial ponderosity and leanness, to provide empirical risk estimates for the proportion of probands' first-degree relatives who were similarly affected, and to estimate the contributions of diseases, drugs and caloric intake to relative obesity and leanness. We studied 379 probands, 125 whites and 52 blacks from a random recall group, 147 whites and 55 blacks from a hyperlipidemic recall group. Suspected familial obesity and leanness were arbitrarily identified in those kindreds with at least two first-degree relatives in the same Quetelet index decile as the proband, top or bottom respectively. Suspected familial obesity was observed in 2.4 percent and 6 percent respectively of random and hyperlipidemic recall group whites. Suspected familial leanness was identified in 2.4 percent and 1.4 percent of random and hyperlipidemic recall whites and in 3.8 percent of randomly recalled blacks. Approximately twice as many as expected white first-degree relatives of top Quetelet index decile probands themselves had top decile Quetelet indices; approximately three times as many as expected first-degree relatives of bottom decile Quetelet index probands themselves had bottom decile Quetelet indices. Nineteen percent and 31 percent of top decile Quetelet index white probands from random and hyperlipidemic recall groups came from families where at least two other first-degree relatives were similarly obese; 18 percent and 20 percent of white random and hyperlipidemic recall group probands with bottom decile Quetelet indices had suspected familial leanness. Nearly all subjects with familial obesity or leanness had no overt metabolic or pharmacological ex [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Nearly all subjects with familial obesity or leanness had no overt metabolic or pharmacological explanations for their body habitus.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 873, "doc_id": "19307912", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The amount of publicly available DNA data doubles every 10 months.\n\nCANDIDATE_PASSAGE:\nThe EMBL nucleotide sequence database. The EMBL Nucleotide Sequence Database (http://www.ebi.ac.uk/embl. html ) constitutes Europe's primary nucleotide sequence resource. DNA and RNA sequences are directly submitted from researchers and genome sequencing groups and collected from the scientific literature and patent applications (Fig. 1). In collaboration with DDBJ and GenBank the database is produced, maintained and distributed at the European Bioinformatics Institute. Database releases are produced quarterly and are distributed on CD-ROM. EBI's network services allow access to the most up-to-date data collection via Internet and World Wide Web interface, providing database searching and sequence similarity facilities plus access to a large number of additional databases.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1190", "doc_id": "30655442", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Ribosome-inactivating protein-2 (RIP-2) interacts with the p75 NTR death domain\n\nCANDIDATE_PASSAGE:\nGamma-Secretase Represents a Therapeutic Target for the Treatment of Invasive Glioma Mediated by the p75 Neurotrophin Receptor The multifunctional signaling protein p75 neurotrophin receptor (p75(NTR)) is a central regulator and major contributor to the highly invasive nature of malignant gliomas. Here, we show that neurotrophin-dependent regulated intramembrane proteolysis (RIP) of p75(NTR) is required for p75(NTR)-mediated glioma invasion, and identify a previously unnamed process for targeted glioma therapy. Expression of cleavage-resistant chimeras of p75(NTR) or treatment of animals bearing p75(NTR)-positive intracranial tumors with clinically applicable gamma-secretase inhibitors resulted in dramatically decreased glioma invasion and prolonged survival. Importantly, proteolytic processing of p75(NTR) was observed in p75(NTR)-positive patient tumor specimens and brain tumor initiating cells. This work highlights the importance of p75(NTR) as a therapeutic target, suggesting that gamma-secretase inhibitors may have direct clinical application for the treatment of malignant glioma.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1047", "doc_id": "14706752", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: AMP-activated protein kinase (AMPK) activation increases inflammation-related fibrosis in the lungs.\n\nCANDIDATE_ABSTRACT:\nTITLE: Metformin reverses established lung fibrosis in a bleomycin model\nABSTRACT: Fibrosis is a pathological result of a dysfunctional repair response to tissue injury and occurs in a number of organs, including the lungs1. Cellular metabolism regulates tissue repair and remodelling responses to injury2-4. AMPK is a critical sensor of cellular bioenergetics and controls the switch from anabolic to catabolic metabolism5. However, the role of AMPK in fibrosis is not well understood. Here, we demonstrate that in humans with idiopathic pulmonary fibrosis (IPF) and in an experimental mouse model of lung fibrosis, AMPK activity is lower in fibrotic regions associated with metabolically active and apoptosis-resistant myofibroblasts. Pharmacological activation of AMPK in myofibroblasts from lungs of humans with IPF display lower fibrotic activity, along with enhanced mitochondrial biogenesis and normalization of sensitivity to apoptosis. In a bleomycin model of lung fibrosis in mice, metformin therapeutically accelerates the resolution of well-established fibrosis in an AMPK-dependent manner. These studies implicate deficient AMPK activation in non-resolving, pathologic fibrotic processes, and support a role for metformin (or other AMPK activators) to reverse established fibrosis by facilitating deactivation and apoptosis of myofibroblasts.", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"These studies implicate deficient AMPK activation in non-resolving, pathologic fibrotic processes, and support a role for metformin (or other AMPK activators) to reverse established fibrosis by facilitating deactivation and apoptosis of myofibroblasts.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 54, "doc_id": "49556906", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: There is a relation between Erythromycin use and hypertrophic pyloric stenosis.\n\nCANDIDATE_PASSAGE:\nCannabinoids in Clinical Practice Cannabis has a potential for clinical use often obscured by unreliable and purely anecdotal reports. The most important natural cannabinoid is the psychoactive tetrahydrocannabinol (Δ9-THC); others include cannabidiol (CBD) and cannabigerol (CBG). Not all the observed effects can be ascribed to THC, and the other constituents may also modulate its action; for example CBD reduces anxiety induced by THC. A standardised extract of the herb may be therefore be more beneficial in practice and clinical trial protocols have been drawn up to assess this. The mechanism of action is still not fully understood, although cannabinoid receptors have been cloned and natural ligands identified. Cannabis is frequently used by patients with multiple sclerosis (MS) for muscle spasm and pain, and in an experimental model of MS low doses of cannabinoids alleviated tremor. Most of the controlled studies have been carried out with THC rather than cannabis herb and so do not mimic the usual clincal situation. Small clinical studies have confirmed the usefulness of THC as an analgesic; CBD and CBG also have analgesic and antiinflammatory effects, indicating that there is scope for developing drugs which do not have the psychoactive properties ofTHC. Patients taking the synthetic derivative nabilone for neurogenic pain actually preferred cannabis herb and reported that it relieved not only pain but the associated depression and anxiety. Cannabinoids are effective in chemotherapy-induced emesis and nabilone has been licensed for this use for several years. Currently, the synthetic cannabinoid HU211 is undergoing trials as a protective agent after brain trauma. Anecdotal reports of cannabis use include case studies in migraine and Tourette’s syndrome, [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1289", "doc_id": "27024392", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: The one-child policy has created a hospitable environment for female infants.\n\nCANDIDATE_PASSAGE:\nOnce-a-day Concerta methylphenidate versus three-times-daily methylphenidate in laboratory and natural settings. OBJECTIVE Methylphenidate (MPH), the most commonly prescribed drug for attention-deficit/hyperactivity disorder (ADHD), has a short half-life, which necessitates multiple daily doses. The need for multiple doses produces problems with medication administration during school and after-school hours, and therefore with compliance. Previous long-acting stimulants and preparations have shown effects equivalent to twice-daily dosing of MPH. This study tests the efficacy and duration of action, in natural and laboratory settings, of an extended-release MPH preparation designed to last 12 hours and therefore be equivalent to 3-times-daily dosing. METHODS Sixty-eight children with ADHD, 6 to 12 years old, participated in a within-subject, double-blind comparison of placebo, immediate-release (IR) MPH 3 times a day (tid), and Concerta, a once-daily MPH formulation. Three dosing levels of medication were used: 5 mg IR MPH tid/18 mg Concerta once a day (qd); 10 mg IR MPH tid/36 mg Concerta qd; and 15 mg IR MPH tid/54 mg Concerta qd. All children were currently medicated with MPH at enrollment, and each child's dose level was based on that child's MPH dosing before the study. The doses of Concerta were selected to be comparable to the daily doses of MPH that each child received. To achieve the ascending rate of MPH delivery determined by initial investigations to provide the necessary continuous coverage, Concerta doses were 20% higher on a daily basis than a comparable tid regimen of IR MPH. Children received each medication condition for 7 days. The investigation was conducted in the context of a background clinical behavioral intervention in both the natura [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1246", "doc_id": "2475059", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: There is a positive correlation between hip fractures and statin use.\n\nCANDIDATE_ABSTRACT:\nTITLE: HMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients.\nABSTRACT: CONTEXT Recent animal studies have found that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) lipid-lowering drugs (statins) substantially increase bone formation, but whether statin use in humans results in clinically meaningful bone formation or a reduction in the risk of osteoporotic fractures is not known. OBJECTIVE To determine whether the use of statins is associated with reduced hip fracture risk. DESIGN Case-control study. SETTING AND PATIENTS A total of 6110 New Jersey residents aged 65 years or older and enrolled in Medicare and either Medicaid or the Pharmacy Assistance for the Aged and Disabled program. Case patients (n=1222) underwent surgical repair of a hip fracture in 1994. Control patients (n=4888) were identified at a ratio of 4:1 and frequency-matched to case patients for age and sex. MAIN OUTCOME MEASURE Adjusted odds ratio (OR) of hip fracture by statin use in the 180 days and 3 years prior to the index date (the earliest date of admission for surgery), adjusted for demographic and clinical characteristics and health care utilization. RESULTS Use of statins in either the prior 180 days (adjusted OR, 0.50; 95% confidence interval [CI], 0.33-0.76) or prior 3 years (adjusted OR, 0.57; 95% CI, 0.40-0.82) was associated with a significant reduction in the risk of hip fracture, even after controlling for variables such as race, insurance status, psychoactive medications, estrogen and thiazide use, ischemic heart disease, cancer, and diabetes mellitus. No significant relationship was observed between use of nonstatin lipid-lowering agents and hip fracture risk. Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowe [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Clear relationships were observed between the degree of reduction in hip fracture risk and the extent of statin use; there was no evidence of such relationships with nonstatin lipid-lowering agents.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1288, "doc_id": "4687948", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Foxk2 regulates autophagy genes in muscle cells and fibroblast cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Arginine depletion as a mechanism for the immune privilege of corneal allografts\nABSTRACT: The cornea is an immune privileged tissue. Since arginase has been found to modulate T-cell function by depleting arginine, we investigated the expression of arginase in the cornea and its possible role in immune privilege using a murine transplant model. We found that both the endothelium and epithelium of murine corneas express functional arginase I, capable of down-regulating T-cell proliferation in an in vitro culture system. The administration of the specific arginase inhibitor N-hydroxy-nor-L-Arg to recipient mice resulted in an accelerated rejection of allogeneic C57BL/6 (B6) corneal grafts. In contrast, in vivo blockade of arginase activity had no effect in altering the course of rejection of primary skin grafts that express little, if any, arginase. In addition, the inhibition of arginase did not alter systemic T-cell proliferation. These data show that arginase is functional in the cornea and contributes to the immune privilege of the eye, and that modulation of arginase contributes to graft survival.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 432, "doc_id": "2474731", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Suboptimal nutrition is a leading cause of premature death\n\nCANDIDATE_PASSAGE:\nGlobal, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015 BACKGROUND The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. METHODS We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors-the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. [TRUNCATED]", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1109", "doc_id": "13770184", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: British female students are bullied more than British male students.\n\nCANDIDATE_PASSAGE:\nMechanism of NO-mediated oxidative and nitrative DNA damage in hamsters infected with Opisthorchis viverrini: a model of inflammation-mediated carcinogenesis. Inflammation mediated by infection is an important factor causing carcinogenesis. Opisthorchis viverrini (OV) infection is a risk factor of cholangiocarcinoma (CHCA), probably through chronic inflammation. Formation of 8-nitroguanine and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), and expression of inducible nitric oxide synthase (iNOS) and heme oxygenase-1 (HO-1) were assessed in the liver of hamsters infected with OV. We newly produced specific anti-8-nitroguanine antibody without cross-reaction. Double immunofluorescence staining revealed that 8-oxodG and 8-nitroguanine were formed mainly in the same inflammatory cells and epithelium of bile ducts from day 7 and showed the strongest immunoreactivity on days 21 and 30, respectively. It is noteworthy that 8-oxodG and 8-nitroguanine still remained in epithelium of bile ducts on day 180, although amount of alanine aminotransferase activity returned to normal level. A time course of 8-nitroguanine was associated with iNOS expression. Furthermore, this study demonstrated that HO-1 expression and subsequent iron accumulation may be involved in enhancement of oxidative DNA damage in epithelium of small bile ducts. In conclusion, nitrative and oxidative DNA damage via iNOS expression in hamsters infected with OV may participate in CHCA carcinogenesis.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "186", "doc_id": "22059387", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Pioglitazone use is significantly associated with an increased risk of prostate cancer.\n\nCANDIDATE_PASSAGE:\nPlatelet glycoprotein IIb/IIIa inhibitors reduce mortality in diabetic patients with non-ST-segment-elevation acute coronary syndromes. BACKGROUND Diabetes mellitus is a major risk factor for adverse outcomes after acute coronary syndromes (ACS). Because this disease may be associated with increased platelet aggregation, we investigated whether diabetic patients with ACS derive particular benefit from platelet glycoprotein (GP) IIb/IIIa receptor inhibition. METHODS AND RESULTS We performed a meta-analysis of the diabetic populations enrolled in the 6 large-scale platelet GP IIb/IIIa inhibitor ACS trials: PRISM, PRISM-PLUS, PARAGON A, PARAGON B, PURSUIT, and GUSTO IV. Among 6458 diabetic patients, platelet GP IIb/IIIa inhibition was associated with a significant mortality reduction at 30 days, from 6.2% to 4.6% (OR 0.74; 95% CI 0.59 to 0.92; P=0.007). Conversely, 23 072 nondiabetic patients had no survival benefit (3.0% versus 3.0%). The interaction between platelet GP IIb/IIIa inhibition and diabetic status was statistically significant (P=0.036). Among 1279 diabetic patients undergoing percutaneous coronary intervention (PCI) during index hospitalization, the use of these agents was associated with a mortality reduction at 30 days from 4.0% to 1.2% (OR 0.30; 95% CI 0.14 to 0.69; P=0.002). CONCLUSIONS This meta-analysis, including the entire large-scale trial experience of intravenous platelet GP IIb/IIIa inhibitors for the medical management of non-ST-segment-elevation ACS, shows that these agents may significantly reduce mortality at 30 days in diabetic patients. Although not based on a randomized assessment, the survival benefit appears to be of greater magnitude in patients undergoing PCI. Therefore, the use of platelet GP IIb/IIIa inhibitors should be s [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "954", "doc_id": "7873737", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: PDPN promotes efficient motility along stromal surfaces by activating the C-type lectin receptor to rearrange the actin cytoskeleton in dendritic cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: Podoplanin-Rich Stromal Networks Induce Dendritic Cell Motility via Activation of the C-type Lectin Receptor CLEC-2\nABSTRACT: To initiate adaptive immunity, dendritic cells (DCs) move from parenchymal tissues to lymphoid organs by migrating along stromal scaffolds that display the glycoprotein podoplanin (PDPN). PDPN is expressed by lymphatic endothelial and fibroblastic reticular cells and promotes blood-lymph separation during development by activating the C-type lectin receptor, CLEC-2, on platelets. Here, we describe a role for CLEC-2 in the morphodynamic behavior and motility of DCs. CLEC-2 deficiency in DCs impaired their entry into lymphatics and trafficking to and within lymph nodes, thereby reducing T cell priming. CLEC-2 engagement of PDPN was necessary for DCs to spread and migrate along stromal surfaces and sufficient to induce membrane protrusions. CLEC-2 activation triggered cell spreading via downregulation of RhoA activity and myosin light-chain phosphorylation and triggered F-actin-rich protrusions via Vav signaling and Rac1 activation. Thus, activation of CLEC-2 by PDPN rearranges the actin cytoskeleton in DCs to promote efficient motility along stromal surfaces.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Thus, activation of CLEC-2 by PDPN rearranges the actin cytoskeleton in DCs to promote efficient motility along stromal surfaces.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 904, "doc_id": "7370282", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Integrated care is ineffective at tackling multiple comorbidities.\n\nCANDIDATE_ABSTRACT:\nTITLE: Functional outcomes of multi-condition collaborative care and successful ageing: results of randomised trial\nABSTRACT: OBJECTIVE To evaluate the effectiveness of integrated care for chronic physical diseases and depression in reducing disability and improving quality of life. DESIGN A randomised controlled trial of multi-condition collaborative care for depression and poorly controlled diabetes and/or risk factors for coronary heart disease compared with usual care among middle aged and elderly people SETTING Fourteen primary care clinics in Seattle, Washington. PARTICIPANTS Patients with diabetes or coronary heart disease, or both, and blood pressure above 140/90 mm Hg, low density lipoprotein concentration >3.37 mmol/L, or glycated haemoglobin 8.5% or higher, and PHQ-9 depression scores of ≥ 10. INTERVENTION A 12 month intervention to improve depression, glycaemic control, blood pressure, and lipid control by integrating a \"treat to target\" programme for diabetes and risk factors for coronary heart disease with collaborative care for depression. The intervention combined self management support, monitoring of disease control, and pharmacotherapy to control depression, hyperglycaemia, hypertension, and hyperlipidaemia. MAIN OUTCOME MEASURES Social role disability (Sheehan disability scale), global quality of life rating, and World Health Organization disability assessment schedule (WHODAS-2) scales to measure disabilities in activities of daily living (mobility, self care, household maintenance). RESULTS Of 214 patients enrolled (106 intervention and 108 usual care), disability and quality of life measures were obtained for 97 intervention patients at six months (92%) and 92 at 12 months (87%), and for 96 usual care patients at six months (89%) and 92 at 12 months (85%). Improvements from baseline on the Sheehan disability scale (-0.9, 95% confidence interval -1.5 to -0.2; [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"There was a trend toward greater improvement in disabilities in activities of daily living (-1.5, -3.3 to 0.4; P = 0.10).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 647, "doc_id": "15041758", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: The RANK-RANK-Ligand (RANKL) pathway is involved in the development of Aire-expressing medullary thymic epithelial cells (mTECs).\n\nCANDIDATE_PASSAGE:\nRank Signaling Links the Development of Invariant γδ T Cell Progenitors and Aire+ Medullary Epithelium The thymic medulla provides a specialized microenvironment for the negative selection of T cells, with the presence of autoimmune regulator (Aire)-expressing medullary thymic epithelial cells (mTECs) during the embryonic-neonatal period being both necessary and sufficient to establish long-lasting tolerance. Here we showed that emergence of the first cohorts of Aire(+) mTECs at this key developmental stage, prior to αβ T cell repertoire selection, was jointly directed by Rankl(+) lymphoid tissue inducer cells and invariant Vγ5(+) dendritic epidermal T cell (DETC) progenitors that are the first thymocytes to express the products of gene rearrangement. In turn, generation of Aire(+) mTECs then fostered Skint-1-dependent, but Aire-independent, DETC progenitor maturation and the emergence of an invariant DETC repertoire. Hence, our data attributed a functional importance to the temporal development of Vγ5(+) γδ T cells during thymus medulla formation for αβ T cell tolerance induction and demonstrated a Rank-mediated reciprocal link between DETC and Aire(+) mTEC maturation.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1181", "doc_id": "301838", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_ABSTRACT:\nTITLE: Efficacy of human papillomavirus testing for the detection of invasive cervical cancers and cervical intraepithelial neoplasia: a randomised controlled trial.\nABSTRACT: BACKGROUND Human papillomavirus (HPV) testing is known to be more sensitive, but less specific than cytology for detecting cervical intraepithelial neoplasia (CIN). We assessed the efficacy of cervical-cancer screening policies that are based on HPV testing. METHODS Between March, 2004, and December, 2004, in two separate recruitment phases, women aged 25-60 years were randomly assigned to conventional cytology or to HPV testing in combination with liquid-based cytology (first phase) or alone (second phase). Randomisation was done by computer in two screening centres and by sequential opening of numbered sealed envelopes in the remaining seven centres. During phase one, women who were HPV-positive and aged 35-60 years were referred to colposcopy, whereas women aged 25-34 years were referred to colposcopy only if cytology was also abnormal or HPV testing was persistently positive. During phase two, women in the HPV group were referred for colposcopy if the HPV test was positive. Two rounds of screening occurred in each phase, and all women had cytology testing only at the second round. The primary endpoint was the detection of grade 2 and 3 CIN, and of invasive cervical cancers during the first and second screening rounds. Analysis was done by intention to screen. This trial is registered, number ISRCTN81678807. FINDINGS In total for both phases, 47,001 women were randomly assigned to the cytology group and 47,369 to HPV testing. 33,851 women from the cytology group and 32,998 from the HPV-testing group had a second round of screening. We also retrieved the histological diagnoses from screening done elsewhere. The detection of invasive cervical cancers was similar for the two groups in the first round of screening (nine in the cytology group vs seven in the H [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Among women aged 35-60 years, at round one the relative detection (HPV vs cytology) was 2.00 (95% CI 1.44-2.77) for CIN2, 2.08 (1.47-2.95) for CIN3, and 2.03 (1.60-2.57) for CIN2 and 3 together.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 972, "doc_id": "27873158", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: RANK-RANKL pathway signalling is linked to development of Aire-expressing medullary thymic epithelial cells.\n\nCANDIDATE_PASSAGE:\nRANK signals from CD4+3− inducer cells regulate development of Aire-expressing epithelial cells in the thymic medulla Aire-expressing medullary thymic epithelial cells (mTECs) play a key role in preventing autoimmunity by expressing tissue-restricted antigens to help purge the emerging T cell receptor repertoire of self-reactive specificities. Here we demonstrate a novel role for a CD4+3− inducer cell population, previously linked to development of organized secondary lymphoid structures and maintenance of T cell memory in the functional regulation of Aire-mediated promiscuous gene expression in the thymus. CD4+3− cells are closely associated with mTECs in adult thymus, and in fetal thymus their appearance is temporally linked with the appearance of Aire+ mTECs. We show that RANKL signals from this cell promote the maturation of RANK-expressing CD80−Aire− mTEC progenitors into CD80+Aire+ mTECs, and that transplantation of RANK-deficient thymic stroma into immunodeficient hosts induces autoimmunity. Collectively, our data reveal cellular and molecular mechanisms leading to the generation of Aire+ mTECs and highlight a previously unrecognized role for CD4+3−RANKL+ inducer cells in intrathymic self-tolerance.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1005", "doc_id": "3952288", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The minor G allele of FOXO3 is related to less severe symptoms of Crohn's Disease.\n\nCANDIDATE_ABSTRACT:\nTITLE: Human SNP Links Differential Outcomes in Inflammatory and Infectious Disease to a FOXO3-Regulated Pathway\nABSTRACT: The clinical course and eventual outcome, or prognosis, of complex diseases varies enormously between affected individuals. This variability critically determines the impact a disease has on a patient's life but is very poorly understood. Here, we exploit existing genome-wide association study data to gain insight into the role of genetics in prognosis. We identify a noncoding polymorphism in FOXO3A (rs12212067: T > G) at which the minor (G) allele, despite not being associated with disease susceptibility, is associated with a milder course of Crohn's disease and rheumatoid arthritis and with increased risk of severe malaria. Minor allele carriage is shown to limit inflammatory responses in monocytes via a FOXO3-driven pathway, which through TGFβ1 reduces production of proinflammatory cytokines, including TNFα, and increases production of anti-inflammatory cytokines, including IL-10. Thus, we uncover a shared genetic contribution to prognosis in distinct diseases that operates via a FOXO3-driven pathway modulating inflammatory responses.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"We identify a noncoding polymorphism in FOXO3A (rs12212067: T > G) at which the minor (G) allele, despite not being associated with disease susceptibility, is associated with a milder course of Crohn's disease and rheumatoid arthritis and with increased risk of severe malaria.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1231, "doc_id": "13905670", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Upregulation of PD1 causes the downmodulation of Satb1.\n\nCANDIDATE_PASSAGE:\nNovel proteinaceous infectious particles cause scrapie. After infection and a prolonged incubation period, the scrapie agent causes a degenerative disease of the central nervous system in sheep and goats. Six lines of evidence including sensitivity to proteases demonstrate that this agent contains a protein that is required for infectivity. Although the scrapie agent is irreversibly inactivated by alkali, five procedures with more specificity for modifying nucleic acids failed to cause inactivation. The agent shows heterogeneity with respect to size, apparently a result of its hydrophobicity; the smallest form may have a molecular weight of 50,000 or less. Because the novel properties of the scrapie agent distinguish it from viruses, plasmids, and viroids, a new term \"prion\" is proposed to denote a small proteinaceous infectious particle which is resistant to inactivation by most procedures that modify nucleic acids. Knowledge of the scrapie agent structure may have significance for understanding the causes of several degenerative diseases.", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1349", "doc_id": "7447120", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: MafA ubiquitination increases the recruitment of coavtivator P/CAF by MafA.\n\nCANDIDATE_ABSTRACT:\nTITLE: GSK-3-mediated phosphorylation enhances Maf-transforming activity.\nABSTRACT: The Maf oncoproteins are b-Zip transcription factors of the AP-1 superfamily. They are involved in developmental, metabolic, and tumorigenic processes. Maf proteins are overexpressed in about 50% of human multiple myelomas. Here, we show that Maf-transforming activity is controlled by GSK-3-dependent phosphorylation and that phosphorylation by GSK-3 can increase the oncogenic activity of a protein. Using microarray analysis, we identify a gene-expression subprogram regulated by GSK-3-mediated Maf phosphorylation involved in extracellular matrix remodeling and relevant to cancer progression. We also demonstrate that GSK-3 triggers MafA sequential phosphorylation on residues S61, T57, T53, and S49, inducing its ubiquitination and degradation. Paradoxically, this phosphorylation increases MafA-transcriptional activity through the recruitment of the coactivator P/CAF. We further demonstrate that P/CAF protects MafA from ubiquitination and degradation, suggesting that, upon the release of the coactivator complex, MafA becomes polyubiquitinated and degraded to allow the response to terminate.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Paradoxically, this phosphorylation increases MafA-transcriptional activity through the recruitment of the coactivator P/CAF.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 748, "doc_id": "11291348", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Primary cervical cancer screening with HPV detection has lower longitudinal sensitivity than conventional cytology to detect cervical intraepithelial neoplasia grade 2.\n\nCANDIDATE_ABSTRACT:\nTITLE: Human papillomavirus testing for the detection of high-grade cervical intraepithelial neoplasia and cancer: final results of the POBASCAM randomised controlled trial.\nABSTRACT: BACKGROUND Human papillomavirus (HPV) testing is more sensitive for the detection of high-grade cervical lesions than is cytology, but detection of HPV by DNA screening in two screening rounds 5 years apart has not been assessed. The aim of this study was to assess whether HPV DNA testing in the first screen decreases detection of cervical intraepithelial neoplasia (CIN) grade 3 or worse, CIN grade 2 or worse, and cervical cancer in the second screening. METHODS In this randomised trial, women aged 29-56 years participating in the cervical screening programme in the Netherlands were randomly assigned to receive HPV DNA (GP5+/6+-PCR method) and cytology co-testing or cytology testing alone, from January, 1999, to September, 2002. Randomisation (in a 1:1 ratio) was done with computer-generated random numbers after the cervical specimen had been taken. At the second screening 5 years later, HPV DNA and cytology co-testing was done in both groups; researchers were masked to the patient's assignment. The primary endpoint was the number of CIN grade 3 or worse detected. Analysis was done by intention to screen. The trial is now finished and is registered, number ISRCTN20781131. FINDINGS 22,420 women were randomly assigned to the intervention group and 22 518 to the control group; 19 999 in the intervention group and 20,106 in the control group were eligible for analysis at the first screen. At the second screen, 19 579 women in the intervention group and 19,731 in the control group were eligible, of whom 16,750 and 16,743, respectively, attended the second screen. In the second round, CIN grade 3 or worse was less common in the intervention group than in the control group (88 of 19 579 in the intervention group vs 122 of 19,731 in the control group; relative risk [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Furthermore, significantly more cases of CIN grade 2 or worse were detected in the intervention group than in the control group (267 of 19 999 vs 215 of 20,106; 1·25, 1·05-1·50; p=0·015).\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 972, "doc_id": "9764256", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Is current better than energy as predictor of success for biphasic defibrillatory shocks in a porcine model of ventricular fibrillation?\n\nABSTRACT:\nThe evidence that monophasic defibrillation success is mainly determined by current is secure. However, modern defibrillators use biphasic waveforms. The aim of this study was to compare energy, peak voltage and peak current in predicting biphasic shock success in a porcine model of ventricular fibrillation (VF) where the impedance varies within a wide of ranges. In 14 domestic male pigs weighing between 27 and 38 kg, VF was electrically induced and untreated for 15 s. Animals were randomized to receive defibrillation attempts from one of two defibrillators with different impedance compensation methods. A grouped up-and-down defibrillation threshold testing protocol was used to maintain the average success rate in the neighborhood of 50%. After a recovery interval of 5 min, the testing sequence was repeated for a total of 60 test shocks for each animal. A high defibrillation success was observed when high peak current was delivered. The area under ROC curve for predicting shock success was 0.681 for peak current, 0.585 for peak voltage and 0.562 for energy. The odds ratio revealed that peak current was a better predictor (OR=1.321, p<0.001) for defibrillation outcome compared with energy (OR=0.979, p<0.001) and peak voltage (OR=1.000, p=0.69) when multivariable logistic regression was conducted.", "output": "{\"label\": \"yes\", \"rationale\": \"In this porcine model of VF within a wide range of transthoracic impedance, peak current was a better indicator for shock success than the currently used energy for biphasic defibrillatory shocks. This finding may encourage design of new current-based biphasic defibrillators.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 23032689, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does ultrasound imaging before puncture facilitate internal jugular vein cannulation?\n\nABSTRACT:\nTo investigate whether prepuncture ultrasound evaluation of vascular anatomy facilitates internal jugular vein cannulation compared with landmark-guided puncture. Prospective randomized study. Single community hospital. Adult patients undergoing general anesthesia (n = 240). The right internal jugular vein was cannulated using either anatomic landmarks or prepuncture ultrasound (3.75/7.5 MHz) guidance. In the landmark group, respiratory jugular venodilation was used as the primary landmark for locating the vein. Results of cannulation and the incidence of complications were compared. Patients were randomly assigned to the ultrasound or landmark group. Respiratory jugular venodilation was identified in 188 patients (78.3%), in whom results of cannulation did not differ between the 2 techniques with respect to the venous access rate (cannulated at the first attempt: 83.5% in the landmark v 85.7% in the ultrasound group), the success rate (cannulated within 3 attempts: 96.9% v 95.6%), and the incidence of arterial puncture (1.0% v 3.3%). In the remaining 52 respiratory jugular venodilation-unidentified patients, the access rate (30.4% v 86.2%, p<0.001) and the success rate (78.3 v 100%, p<0.05) were significantly better in the ultrasound group, and no arterial puncture was recorded in the ultrasound group, whereas the incidence was 13.0% in the landmark group. The results were similar regardless of the ultrasound frequency used.", "output": "{\"label\": \"maybe\", \"rationale\": \"Prepuncture ultrasound evaluation did not improve the result of right internal jugular vein cannulation compared with the respiratory jugular venodilation-guided approach. When the landmark was not observed, however, the prepuncture ultrasound guidance was helpful in facilitating the cannulation.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 12407608, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Side effects associated with antidepressants lower risk of myocardial infarction.\n\nCANDIDATE_PASSAGE:\nA specific amyloid-β protein assembly in the brain impairs memory Memory function often declines with age, and is believed to deteriorate initially because of changes in synaptic function rather than loss of neurons. Some individuals then go on to develop Alzheimer's disease with neurodegeneration. Here we use Tg2576 mice, which express a human amyloid-β precursor protein (APP) variant linked to Alzheimer's disease, to investigate the cause of memory decline in the absence of neurodegeneration or amyloid-β protein amyloidosis. Young Tg2576 mice (< 6 months old) have normal memory and lack neuropathology, middle-aged mice (6–14 months old) develop memory deficits without neuronal loss, and old mice (> 14 months old) form abundant neuritic plaques containing amyloid-β (refs 3–6). We found that memory deficits in middle-aged Tg2576 mice are caused by the extracellular accumulation of a 56-kDa soluble amyloid-β assembly, which we term Aβ*56 (Aβ star 56). Aβ*56 purified from the brains of impaired Tg2576 mice disrupts memory when administered to young rats. We propose that Aβ*56 impairs memory independently of plaques or neuronal loss, and may contribute to cognitive deficits associated with Alzheimer's disease.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1085", "doc_id": "4407385", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Energy balance requires hypothalamic glutamate neurotransmission.\n\nCANDIDATE_PASSAGE:\nSynaptic glutamate release by ventromedial hypothalamic neurons is part of the neurocircuitry that prevents hypoglycemia. The importance of neuropeptides in the hypothalamus has been experimentally established. Due to difficulties in assessing function in vivo, the roles of the fast-acting neurotransmitters glutamate and GABA are largely unknown. Synaptic vesicular transporters (VGLUTs for glutamate and VGAT for GABA) are required for vesicular uptake and, consequently, synaptic release of neurotransmitters. Ventromedial hypothalamic (VMH) neurons are predominantly glutamatergic and express VGLUT2. To evaluate the role of glutamate release from VMH neurons, we generated mice lacking VGLUT2 selectively in SF1 neurons (a major subset of VMH neurons). These mice have hypoglycemia during fasting secondary to impaired fasting-induced increases in the glucose-raising pancreatic hormone glucagon and impaired induction in liver of mRNAs encoding PGC-1alpha and the gluconeogenic enzymes PEPCK and G6Pase. Similarly, these mice have defective counterregulatory responses to insulin-induced hypoglycemia and 2-deoxyglucose (an antimetabolite). Thus, glutamate release from VMH neurons is an important component of the neurocircuitry that functions to prevent hypoglycemia.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "378", "doc_id": "11886686", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: Does body surface area predict plasma oxaliplatin and pharmacokinetic advantage in hyperthermic intraoperative intraperitoneal chemotherapy?\n\nABSTRACT:\nHyperthermic intraoperative intraperitoneal chemotherapy (HIPEC) is used to treat peritoneal surface-spreading malignancies to maximize local drug concentrations while minimizing systemic effects. The pharmacokinetic advantage of HIPEC is defined as the intraperitoneal to intravascular ratio of drug concentrations. We hypothesized that body surface area (BSA) would correlate with the pharmacokinetic advantage of HIPEC. Because oxaliplatin is administered in 5 % dextrose, we hypothesized that BSA would correlate with glycemia. We collected blood and peritoneal perfusate samples from ten patients undergoing HIPEC with a BSA-based dose of 250 mg/m(2) oxaliplatin, and measured drug concentrations by inductively coupled plasma mass spectrophotometry. We monitored blood glucose for 24 h postoperatively. Areas under concentration-time curves (AUC) were calculated by trapezoidal rule. Pharmacokinetic advantage was calculated by (AUC[peritoneal fluid]/AUC[plasma]). We used linear regression to test for statistical significance. Higher BSA was associated with lower plasma oxaliplatin AUC (p = 0.0075) and with a greater pharmacokinetic advantage (p = 0.0198) over the 60-minute duration of HIPEC. No statistically significant relationships were found between BSA and blood glucose AUC or peak blood glucose levels.", "output": "{\"label\": \"yes\", \"rationale\": \"Higher BSA is correlated with lower plasma drug levels and greater pharmacokinetic advantage in HIPEC, likely because of increased circulating blood volume with inadequate time for equilibration. Plasma glucose levels after oxaliplatin HIPEC were not clearly related to BSA.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 23456384, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: GATA3 regulates cell cycle progression in bone marrow hematopoietic stem cells.\n\nCANDIDATE_ABSTRACT:\nTITLE: GATA-3 regulates hematopoietic stem cell maintenance and cell-cycle entry.\nABSTRACT: Maintaining hematopoietic stem cell (HSC) quiescence is a critical property for the life-long generation of blood cells. Approximately 75% of cells in a highly enriched long-term repopulating HSC (LT-HSC) pool (Lin(-)Sca1(+)c-Kit(hi)CD150(+)CD48(-)) are quiescent, with only a small percentage of the LT-HSCs in cycle. Transcription factor GATA-3 is known to be vital for the development of T cells at multiple stages in the thymus and for Th2 differentiation in the peripheral organs. Although it is well documented that GATA-3 is expressed in HSCs, a role for GATA-3 in any prethymic progenitor cell has not been established. In the present study, we show that Gata3-null mutant mice generate fewer LT-HSCs and that fewer Gata3-null LT-HSCs are in cycle. Furthermore, Gata3 mutant hematopoietic progenitor cells fail to be recruited into an increased cycling state after 5-fluorouracil-induced myelosuppression. Therefore, GATA-3 is required for the maintenance of a normal number of LT-HSCs and for their entry into the cell cycle.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Furthermore, Gata3 mutant hematopoietic progenitor cells fail to be recruited into an increased cycling state after 5-fluorouracil-induced myelosuppression. Therefore, GATA-3 is required for the maintenance of a normal number of LT-HSCs and for their entry into the cell cycle.\\\".\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 444, "doc_id": "10165258", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Exercise reduces cancer mortality rates among Chinese citizens.\n\nCANDIDATE_ABSTRACT:\nTITLE: Combined Impact of Lifestyle-Related Factors on Total and Cause-Specific Mortality among Chinese Women: Prospective Cohort Study\nABSTRACT: BACKGROUND Although cigarette smoking, excessive alcohol drinking, obesity, and several other well-studied unhealthy lifestyle-related factors each have been linked to the risk of multiple chronic diseases and premature death, little is known about the combined impact on mortality outcomes, in particular among Chinese and other non-Western populations. The objective of this study was to quantify the overall impact of lifestyle-related factors beyond that of active cigarette smoking and alcohol consumption on all-cause and cause-specific mortality in Chinese women. METHODS AND FINDINGS We used data from the Shanghai Women's Health Study, an ongoing population-based prospective cohort study in China. Participants included 71,243 women aged 40 to 70 years enrolled during 1996-2000 who never smoked or drank alcohol regularly. A healthy lifestyle score was created on the basis of five lifestyle-related factors shown to be independently associated with mortality outcomes (normal weight, lower waist-hip ratio, daily exercise, never exposed to spouse's smoking, higher daily fruit and vegetable intake). The score ranged from zero (least healthy) to five (most healthy) points. During an average follow-up of 9 years, 2,860 deaths occurred, including 775 from cardiovascular disease (CVD) and 1,351 from cancer. Adjusted hazard ratios for mortality decreased progressively with an increasing number of healthy lifestyle factors. Compared to women with a score of zero, hazard ratios (95% confidence intervals) for women with four to five factors were 0.57 (0.44-0.74) for total mortality, 0.29 (0.16-0.54) for CVD mortality, and 0.76 (0.54-1.06) for cancer mortality. The inverse association between the healthy lifestyle score and mortality was seen consistently regardless of ch [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSIONS In this first study, to our knowledge, to quantify the combined impact of lifestyle-related factors on mortality outcomes in Chinese women, a healthier lifestyle pattern-including being of normal weight, lower central adiposity, participation in physical activity, nonexposure to spousal smoking, and higher fruit and vegetable intake-was associated with reductions in total and cause-specific mortality among lifetime nonsmoking and nondrinking women, supporting the importance of overall lifestyle modification in disease prevention.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 397, "doc_id": "1456068", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: 1/2000 in UK have abnormal PrP positivity.\n\nCANDIDATE_ABSTRACT:\nTITLE: Health-Related Quality of Life as Measured with EQ-5D among Populations with and without Specific Chronic Conditions: A Population-Based Survey in Shaanxi Province, China\nABSTRACT: INTRODUCTION The aim of this study was to examine health-related quality of life (HRQoL) as measured by EQ-5D and to investigate the influence of chronic conditions and other risk factors on HRQoL based on a distributed sample located in Shaanxi Province, China. METHODS A multi-stage stratified cluster sampling method was performed to select subjects. EQ-5D was employed to measure the HRQoL. The likelihood that individuals with selected chronic diseases would report any problem in the EQ-5D dimensions was calculated and tested relative to that of each of the two reference groups. Multivariable linear regression models were used to investigate factors associated with EQ VAS. RESULTS The most frequently reported problems involved pain/discomfort (8.8%) and anxiety/depression (7.6%). Nearly half of the respondents who reported problems in any of the five dimensions were chronic patients. Higher EQ VAS scores were associated with the male gender, higher level of education, employment, younger age, an urban area of residence, access to free medical service and higher levels of physical activity. Except for anemia, all the selected chronic diseases were indicative of a negative EQ VAS score. The three leading risk factors were cerebrovascular disease, cancer and mental disease. Increases in age, number of chronic conditions and frequency of physical activity were found to have a gradient effect. CONCLUSION The results of the present work add to the volume of knowledge regarding population health status in this area, apart from the known health status using mortality and morbidity data. Medical, policy, social and individual attention should be given to the management of chronic diseases and improvement of HRQoL. Longitudinal studies must be performed to monitor ch [TRUNCATED]", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 5, "doc_id": "463533", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Genomic sequences involved in alternative splicing responsible for Hutchinson-Gilford progeria syndrome (HGPS) are abundant in the ''progerinonly'' allele of Lmna knock-in models.\n\nCANDIDATE_PASSAGE:\nShort-term medical service trips: a systematic review of the evidence. Short-term medical service trips (MSTs) aim to address unmet health care needs of low- and middle-income countries. The lack of critically reviewed empirical evidence of activities and outcomes is a concern. Developing evidence-based recommendations for health care delivery requires systematic research review. I focused on MST publications with empirical results. Searches in May 2013 identified 67 studies published since 1993, only 6% of the published articles on the topic in the past 20 years. Nearly 80% reported on surgical trips. Although the MST field is growing, its medical literature lags behind, with nearly all of the scholarly publications lacking significant data collection. By incorporating data collection into service trips, groups can validate practices and provide information about areas needing improvement.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "466", "doc_id": "38180456", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Primary cervical cytology screening with HPV detection has higher longitudinal sensitivity to detect severe cervical intraepithelial neoplasia than conventional cytology.\n\nCANDIDATE_PASSAGE:\nPerformance of an abbreviated version of the Lubben Social Network Scale among three European community-dwelling older adult populations. PURPOSE There is a need for valid and reliable short scales that can be used to assess social networks and social supports and to screen for social isolation in older persons. DESIGN AND METHODS The present study is a cross-national and cross-cultural evaluation of the performance of an abbreviated version of the Lubben Social Network Scale (LSNS-6), which was used to screen for social isolation among community-dwelling older adult populations in three European countries. Based on the concept of lack of redundancy of social ties we defined clinical cut-points of the LSNS-6 for identifying persons deemed at risk for social isolation. RESULTS Among all three samples, the LSNS-6 and two subscales (Family and Friends) demonstrated high levels of internal consistency, stable factor structures, and high correlations with criterion variables. The proposed clinical cut-points showed good convergent validity, and classified 20% of the respondents in Hamburg, 11% of those in Solothurn (Switzerland), and 15% of those in London as at risk for social isolation. IMPLICATIONS We conclude that abbreviated scales such as the LSNS-6 should be considered for inclusion in practice protocols of gerontological practitioners. Screening older persons based on the LSNS-6 provides quantitative information on their family and friendship ties, and identifies persons at increased risk for social isolation who might benefit from in-depth assessment and targeted interventions.", "output": "{\"label\": 0, \"rationale\": \"The passage is irrelevant to the query intent.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "973", "doc_id": "12470783", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: A diminished ovarian reserve is a very strong indicator of infertility, even in an a priori non-infertile population.\n\nCANDIDATE_ABSTRACT:\nTITLE: Association Between Biomarkers of Ovarian Reserve and Infertility Among Older Women of Reproductive Age\nABSTRACT: Importance Despite lack of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers of reproductive potential. Objective To determine the associations between biomarkers of ovarian reserve and reproductive potential among women of late reproductive age. Design, Setting, and Participants Prospective time-to-pregnancy cohort study (2008 to date of last follow-up in March 2016) of women (N = 981) aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, recruited from the community in the Raleigh-Durham, North Carolina, area. Exposures Early-follicular-phase serum level of antimüllerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH. Main Outcomes and Measures The primary outcomes were the cumulative probability of conception by 6 and 12 cycles of attempt and relative fecundability (probability of conception in a given menstrual cycle). Conception was defined as a positive pregnancy test result. Results A total of 750 women (mean age, 33.3 [SD, 3.2] years; 77% white; 36% overweight or obese) provided a blood and urine sample and were included in the analysis. After adjusting for age, body mass index, race, current smoking status, and recent hormonal contraceptive use, women with low AMH values (<0.7 ng/mL [n = 84]) did not have a significantly different predicted probability of conceiving by 6 cycles of attempt (65%; 95% CI, 50%-75%) compared with women (n = 579) with normal values (62%; 95% CI, 57%-66%) or by 12 cycles of attempt (84% [95% CI, 70%-91%] vs 75% [95% CI, 70%-79%], respectively). Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a significantly different predicted probability of conceiving after 6 cy [TRUNCATED]", "output": "{\"label\": \"REFUTES\", \"rationale\": \"Evidence snippet: \\\"Conclusions and Relevance Among women aged 30 to 44 years without a history of infertility who had been trying to conceive for 3 months or less, biomarkers indicating diminished ovarian reserve compared with normal ovarian reserve were not associated with reduced fertility.\\\". The claim is refutes by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 40, "doc_id": "13497630", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: Migraine with aura is associated with ischemic stroke.\n\nCANDIDATE_ABSTRACT:\nTITLE: Migraine and cardiovascular disease: systematic review and meta-analysis.\nABSTRACT: OBJECTIVE To evaluate the association between migraine and cardiovascular disease, including stroke, myocardial infarction, and death due to cardiovascular disease. DESIGN Systematic review and meta-analysis. DATA SOURCES Electronic databases (PubMed, Embase, Cochrane Library) and reference lists of included studies and reviews published until January 2009. Selection criteria Case-control and cohort studies investigating the association between any migraine or specific migraine subtypes and cardiovascular disease. Review methods Two investigators independently assessed eligibility of identified studies in a two step approach. Disagreements were resolved by consensus. Studies were grouped according to a priori categories on migraine and cardiovascular disease. DATA EXTRACTION Two investigators extracted data. Pooled relative risks and 95% confidence intervals were calculated. RESULTS Studies were heterogeneous for participant characteristics and definition of cardiovascular disease. Nine studies investigated the association between any migraine and ischaemic stroke (pooled relative risk 1.73, 95% confidence interval 1.31 to 2.29). Additional analyses indicated a significantly higher risk among people who had migraine with aura (2.16, 1.53 to 3.03) compared with people who had migraine without aura (1.23, 0.90 to 1.69; meta-regression for aura status P=0.02). Furthermore, results suggested a greater risk among women (2.08, 1.13 to 3.84) compared with men (1.37, 0.89 to 2.11). Age less than 45 years, smoking, and oral contraceptive use further increased the risk. Eight studies investigated the association between migraine and myocardial infarction (1.12, 0.95 to 1.32) and five between migraine and death due to cardiovascular disease (1.03, 0.79 to 1.34). Only o [TRUNCATED]", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"CONCLUSION Migraine is associated with a twofold increased risk of ischaemic stroke, which is only apparent among people who have migraine with aura.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 791, "doc_id": "15984735", "truncated": true, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Statins increase blood cholesterol.\n\nCANDIDATE_PASSAGE:\nThe Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). IMPORTANCE Definitions of sepsis and septic shock were last revised in 2001. Considerable advances have since been made into the pathobiology (changes in organ function, morphology, cell biology, biochemistry, immunology, and circulation), management, and epidemiology of sepsis, suggesting the need for reexamination. OBJECTIVE To evaluate and, as needed, update definitions for sepsis and septic shock. PROCESS A task force (n = 19) with expertise in sepsis pathobiology, clinical trials, and epidemiology was convened by the Society of Critical Care Medicine and the European Society of Intensive Care Medicine. Definitions and clinical criteria were generated through meetings, Delphi processes, analysis of electronic health record databases, and voting, followed by circulation to international professional societies, requesting peer review and endorsement (by 31 societies listed in the Acknowledgment). KEY FINDINGS FROM EVIDENCE SYNTHESIS Limitations of previous definitions included an excessive focus on inflammation, the misleading model that sepsis follows a continuum through severe sepsis to shock, and inadequate specificity and sensitivity of the systemic inflammatory response syndrome (SIRS) criteria. Multiple definitions and terminologies are currently in use for sepsis, septic shock, and organ dysfunction, leading to discrepancies in reported incidence and observed mortality. The task force concluded the term severe sepsis was redundant. RECOMMENDATIONS Sepsis should be defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. For clinical operationalization, organ dysfunction can be represented by an increase in the Sequential [S [TRUNCATED]", "output": "{\"label\": 2, \"rationale\": \"The passage provides closely relevant background for the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1100", "doc_id": "5596332", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Decide SUPPORTS, REFUTES, or NEI using only the candidate abstract. Return JSON label and rationale.", "input": "CLAIM: The PRDM1 gene, when combined with the PRDM14 gene, plays an important role during primordial germ cell specification.\n\nCANDIDATE_ABSTRACT:\nTITLE: The Germ Cell Determinant Blimp1 Is Not Required for Derivation of Pluripotent Stem Cells\nABSTRACT: Blimp1 (Prdm1), the key determinant of primordial germ cells (PGCs), plays a combinatorial role with Prdm14 during PGC specification from postimplantation epiblast cells. They together initiate epigenetic reprogramming in early germ cells toward an underlying pluripotent state, which is equivalent to embryonic stem cells (ESCs). Whereas Prdm14 alone can promote reprogramming and is important for the propagation of the pluripotent state, it is not known whether Blimp1 is similarly involved. By using a genetic approach, we demonstrate that Blimp1 is dispensable for the derivation and maintenance of ESCs and postimplantation epiblast stem cells (epiSCs). Notably, Blimp1 is also dispensable for reprogramming epiSCs to ESCs. Thus, although Blimp1 is obligatory for PGC specification, it is not required for the reversion of epiSCs to ESCs and for their maintenance thereafter. This study suggests that reprogramming, including that of somatic cells to ESCs, may not entail an obligatory route through a Blimp1-positive PGC-like state.", "output": "{\"label\": \"SUPPORTS\", \"rationale\": \"Evidence snippet: \\\"Blimp1 (Prdm1), the key determinant of primordial germ cells (PGCs), plays a combinatorial role with Prdm14 during PGC specification from postimplantation epiblast cells.\\\". The claim is supports by this abstract.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 1177, "doc_id": "13910150", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Determine whether the abstract supports a yes/no/maybe answer. Return JSON label and rationale.", "input": "QUESTION: Does skeletal muscle oxygen saturation estimate mixed venous oxygen saturation in patients with severe left heart failure and additional severe sepsis or septic shock?\n\nABSTRACT:\nLow cardiac output states such as left heart failure are characterized by preserved oxygen extraction ratio, which is in contrast to severe sepsis. Near infrared spectroscopy (NIRS) allows noninvasive estimation of skeletal muscle tissue oxygenation (StO2). The aim of the study was to determine the relationship between StO2 and mixed venous oxygen saturation (SvO2) in patients with severe left heart failure with or without additional severe sepsis or septic shock. Sixty-five patients with severe left heart failure due to primary heart disease were divided into two groups: groups A (n = 24) and B (n = 41) included patients without and with additional severe sepsis/septic shock, respectively. Thenar muscle StO2 was measured using NIRS in the patients and in 15 healthy volunteers. StO2 was lower in group A than in group B and in healthy volunteers (58 +/- 13%, 90 +/- 7% and 84 +/- 4%, respectively; P < 0.001). StO2 was higher in group B than in healthy volunteers (P = 0.02). In group A StO2 correlated with SvO2 (r = 0.689, P = 0.002), although StO2 overestimated SvO2 (bias -2.3%, precision 4.6%). In group A changes in StO2 correlated with changes in SvO2 (r = 0.836, P < 0.001; DeltaSvO2 = 0.84 x DeltaStO2 - 0.67). In group B important differences between these variables were observed. Plasma lactate concentrations correlated negatively with StO2 values only in group A (r = -0.522, P = 0.009; lactate = -0.104 x StO2 + 10.25).", "output": "{\"label\": \"no\", \"rationale\": \"Skeletal muscle StO2 does not estimate SvO2 in patients with severe left heart failure and additional severe sepsis or septic shock. However, in patients with severe left heart failure without additional severe sepsis or septic shock, StO2 values could be used to provide rapid, noninvasive estimation of SvO2; furthermore, the trend in StO2 may be considered a surrogate for the trend in SvO2.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_artificial", "task_name": "qa", "pubid": 17227587, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: VgrG (Tssl) protein punctures membranes by forming a spike at the tip of the tube apparatus.\n\nCANDIDATE_PASSAGE:\nPAAR-repeat proteins sharpen and diversify the Type VI secretion system spike The bacterial type VI secretion system (T6SS) is a large multicomponent, dynamic macromolecular machine that has an important role in the ecology of many Gram-negative bacteria. T6SS is responsible for translocation of a wide range of toxic effector molecules, allowing predatory cells to kill both prokaryotic as well as eukaryotic prey cells. The T6SS organelle is functionally analogous to contractile tails of bacteriophages and is thought to attack cells by initially penetrating them with a trimeric protein complex called the VgrG spike. Neither the exact protein composition of the T6SS organelle nor the mechanisms of effector selection and delivery are known. Here we report that proteins from the PAAR (proline-alanine-alanine-arginine) repeat superfamily form a sharp conical extension on the VgrG spike, which is further involved in attaching effector domains to the spike. The crystal structures of two PAAR-repeat proteins bound to VgrG-like partners show that these proteins sharpen the tip of the T6SS spike complex. We demonstrate that PAAR proteins are essential for T6SS-mediated secretion and target cell killing by Vibrio cholerae and Acinetobacter baylyi. Our results indicate a new model of the T6SS organelle in which the VgrG-PAAR spike complex is decorated with multiple effectors that are delivered simultaneously into target cells in a single contraction-driven translocation event.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1366", "doc_id": "4406819", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Answer with yes, no, or maybe from the abstract, then provide a short rationale. Return JSON label and rationale.", "input": "QUESTION: 30-Day and 1-year mortality in emergency general surgery laparotomies: an area of concern and need for improvement?\n\nABSTRACT:\nEmergency surgery is associated with poorer outcomes and higher mortality with recent studies suggesting the 30-day mortality to be 14-15%. The aim of this study was to analyse the 30-day mortality, age-related 30-day mortality and 1-year mortality following emergency laparotomy. We hope this will encourage prospective data collection, improvement of care and initiate strategies to establish best practice in this area. This was a retrospective study of patients who underwent emergency laparotomy from June 2010 to May 2012. The primary end point of the study was 30-day mortality, age-related 30-day mortality and 1-year all-cause mortality. 477 laparotomies were performed in 446 patients. 57% were aged<70 and 43% aged>70 years. 30-day mortality was 12, 4% in those aged<70 years and 22% in those>70 years (p<0.001). 1-year mortality was 25, 15% in those aged under 70 years and 38% in those aged>70 years (p<0.001).", "output": "{\"label\": \"maybe\", \"rationale\": \"Emergency laparotomy carries a high rate of mortality, especially in those over the age of 70 years, and more needs to be done to improve outcomes, particularly in this group. This could involve increasing acute surgical care manpower, early recognition of patients requiring emergency surgery, development of clear management protocols for such patients or perhaps even considering centralisation of emergency surgical services to specialist centres with multidisciplinary teams involving emergency surgeons and care of the elderly physicians in hospital and related community outreach services for post-discharge care.\"}", "meta": {"source_dataset": "PubMedQA", "source_split": "pqa_labeled", "task_name": "qa", "pubid": 26037986, "truncated": false, "label_space": ["yes", "no", "maybe"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Assign relevance class 0,1,2,3 for query-passage matching and return JSON label and rationale.", "input": "QUERY: Adult tissue-resident macrophages stem from the embryonal yolk sac and fetal liver.\n\nCANDIDATE_PASSAGE:\nFate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis. Mononuclear phagocytes, including monocytes, macrophages, and dendritic cells, contribute to tissue integrity as well as to innate and adaptive immune defense. Emerging evidence for labor division indicates that manipulation of these cells could bear therapeutic potential. However, specific ontogenies of individual populations and the overall functional organization of this cellular network are not well defined. Here we report a fate-mapping study of the murine monocyte and macrophage compartment taking advantage of constitutive and conditional CX(3)CR1 promoter-driven Cre recombinase expression. We have demonstrated that major tissue-resident macrophage populations, including liver Kupffer cells and lung alveolar, splenic, and peritoneal macrophages, are established prior to birth and maintain themselves subsequently during adulthood independent of replenishment by blood monocytes. Furthermore, we have established that short-lived Ly6C(+) monocytes constitute obligatory steady-state precursors of blood-resident Ly6C(-) cells and that the abundance of Ly6C(+) blood monocytes dynamically controls the circulation lifespan of their progeny.", "output": "{\"label\": 3, \"rationale\": \"The passage directly answers or verifies the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "89", "doc_id": "7521113", "truncated": false, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}} {"task": "", "instruction": " Classify the claim against the candidate abstract. Return JSON with keys label and rationale.", "input": "CLAIM: Mutant mice lacking SVCT2 have severely reduced ascorbic acid levels in both brain and adrenals.\n\nCANDIDATE_ABSTRACT:\nTITLE: Identification of a Brainstem Circuit Controlling Feeding\nABSTRACT: Hunger, driven by negative energy balance, elicits the search for and consumption of food. While this response is in part mediated by neurons in the hypothalamus, the role of specific cell types in other brain regions is less well defined. Here, we show that neurons in the dorsal raphe nucleus, expressing vesicular transporters for GABA or glutamate (hereafter, DRNVgat and DRNVGLUT3 neurons), are reciprocally activated by changes in energy balance and that modulating their activity has opposite effects on feeding-DRNVgat neurons increase, whereas DRNVGLUT3 neurons suppress, food intake. Furthermore, modulation of these neurons in obese (ob/ob) mice suppresses food intake and body weight and normalizes locomotor activity. Finally, using molecular profiling, we identify druggable targets in these neurons and show that local infusion of agonists for specific receptors on these neurons has potent effects on feeding. These data establish the DRN as an important node controlling energy balance. PAPERCLIP.", "output": "{\"label\": \"NEI\", \"rationale\": \"The abstract does not contain direct evidence to support or refute the claim.\"}", "meta": {"source_dataset": "SciFact", "task_name": "verification", "claim_id": 812, "doc_id": "2225918", "truncated": false, "label_space": ["SUPPORTS", "REFUTES", "NEI"], "output_schema": {"label": "string", "rationale": "string"}}} {"task": "", "instruction": " Score candidate passage relevance on 0-3 and return JSON with label and rationale.", "input": "QUERY: Students who perform poorly in the early years of medical school are less likely to commit professional misconduct later in their careers.\n\nCANDIDATE_PASSAGE:\nCytochemistry and C-values: the less-well-known world of nuclear DNA amounts. BACKGROUND In the plant sciences there are two widely applied technologies for measuring nuclear DNA content: Feulgen absorbance cytophotometry and flow cytometry (FCM). While FCM is, with good reasons, increasingly popular among plant scientists, absorbance-cytophotometric techniques lose ground. This results in a narrowing of the methodological repertoire, which is neither desirable nor beneficial. Both approaches have their advantages, but static cytophotometry seems to pose more instrumental difficulties and material-based problems than FCM, so that Feulgen-based data in the literature are often less reliable than one would expect. SCOPE The purpose of this article is to present a selective overview of the field of nuclear DNA content measurement, and C-values in particular, with a focus on the technical difficulties imposed by the characteristics of the biological material and with some comments on the photometrical aspects of the work. For over 20 years it has been known that plant polyphenols cause problems in Feulgen DNA cytophotometry, since they act as major staining inhibitors leading to unreliable results. However, little information is available about the chemical classes of plant metabolites capable of DNA staining interference and the mechanisms of their inhibition. Plant slimes are another source of concern. CONCLUSIONS In FCM research to uncover the effects of secondary metabolites on measurement results has begun only recently. In particular, the analysis of intraspecific genome size variation demands a stringent methodology which accounts for inhibitors. FCM tests for inhibitory effects of endogenous metabolites should become obligatory. The use of dry seeds for [TRUNCATED]", "output": "{\"label\": 1, \"rationale\": \"The passage is loosely related but does not directly answer the query.\"}", "meta": {"source_dataset": "mteb/scifact", "task_name": "rerank", "query_id": "1106", "doc_id": "24552097", "truncated": true, "label_space": [0, 1, 2, 3], "output_schema": {"label": "integer", "rationale": "string"}}}