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Recent studies have shown that obesity is associated with the severity of coronavirus disease (COVID-19). We reviewed clinical studies to clarify the obesity relationship with COVID-19 severity, comorbidities, and discussing possible mechanisms.
Materials and methods
The electronic databases, including Web of Science, PubMed, Scopus, and Google Scholar, were searched and all studies conducted on COVID-19 and obesity were reviewed. All studies were independently screened by reviewers based on their titles and abstracts.
Forty relevant articles were selected, and their full texts were reviewed. Obesity affects the respiratory and immune systems through various mechanisms. Cytokine and adipokine secretion from adipose tissue leads to a pro-inflammatory state in obese patients, predisposing them to thrombosis, incoordination of innate and adaptive immune responses, inadequate antibody response, and cytokine storm. Obese patients had a longer virus shedding. Obesity is associated with other comorbidities such as hypertension, cardiovascular diseases, diabetes mellitus, and vitamin D deficiency. Hospitalization, intensive care unit admission, mechanical ventilation, and even mortality in obese patients were higher than normal-weight patients. Obesity could alter the direction of severe COVID-19 symptoms to younger individuals. Reduced physical activity, unhealthy eating habits and, more stress and fear experienced during the COVID-19 pandemic may result in more weight gain and obesity.
Obesity should be considered as an independent risk factor for the severity of COVID-19. Paying more attention to preventing weight gain in obese patients with COVID-19 infection in early levels of disease is crucial during this pandemic.
In December 2019, coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 infection has been emerged in Wuhan, China, and has spread rapidly and caused a global health crisis. By November 15, 2020, 53,766,728 confirmed cases of COVID-19, including 1,308,975 deaths, were reported to the World Health Organization  globally. COVID-19 manifestations include a spectrum of illnesses, ranging from asymptomatic infection  to severe pneumonia, adult/acute respiratory distress syndrome (ARDS), and even death . This has caused medical researchers to identify risk factors related to the severity of COVID-19. Preexisting diseases such as hypertension (HTN), cardiovascular disease, diabetes, chronic respiratory disease, or cancer were identified as risk factors for developing severe COVID-19 [4,5,6]. However, recently, obesity was proposed as a significant independent risk factor for developing severe COVID-19 .
The obesity prevalence has recently increased in many developed and developing countries [8, 9], and has doubled in 73 countries since 1980 . It is estimated that obesity prevalence is about 12% (603.7 million) among adults and 5% among children (107.7 million) worldwide . This global increase in the prevalence of obesity shows the need for more assessment of this possible risk factor.
The effects of obesity on the respiratory system have been observed since long before. Avicenna , the famous Persian physician, recognized obesity as a medical disorder, and also in his book titled Canon of Medicine, referred to the respiratory problems of obese patients . Also, the association between obesity and worse prognosis in the respiratory virus infections was observed in the “Spanish” influenza pandemic of 1918 . Moreover, during the 2009 H1N1 pandemic, obesity was considered as an independent risk factor for severe disease or complications .
Surprisingly, level 1 evidence supports an obesity association with better prognosis in patients with ARDS . However, previous studies have broken this paradox in COVID-19 patients [16,17,18]. These results and experiments with other viral respiratory infections reinforce the necessity of further research on this possible risk factor. Therefore, the aims of the present study were to: (1) review clinical studies in order to clarify the association between obesity and the severity of COVID-19, comorbidities and (2) discuss possible mechanisms.
Materials and methods
Search strategy and data collection
All studies conducted on COVID-19 and obesity were searched and reviewed. For this purpose, the electronic databases, including Web of Science, PubMed, Scopus, and Google Scholar, were searched. The search algorithm included all possible combinations of keywords from the following: “Severe acute respiratory syndrome coronavirus 2,” “COVID-19,” “2019-nCoV,” “SARS-CoV-2,” “coronavirus,” “obesity,” “weight,” “obese,” “body mass index,” and “adipose tissue.” Also, references of relevant review and editorial articles were reviewed to increase the coverage of included articles and ensure literature saturation.
All studies were independently screened by authors based on their titles and abstracts. The full texts of articles, potentially suitable for the review, were obtained to determine the relevance based on the study inclusion/exclusion criteria. The total of studies focusing on clinical characteristics and complications for SARS-CoV-2 was eligible for inclusion. The total of applicable studies (including case report, case series, and editorial, cross-sectional and cohort studies) was identified. We screened all reference lists of relevant studies in order to identify any missing publications. Studies that met the following criteria were included in the meta-analysis : cohort studies;  body mass index (BMI) assessment ≥ 25 kg/m2 reported;  those indicating the odds ratio for the obesity risk ; age and gender were not kept as a bar for inclusion. The primary outcomes were the body weight, BMI, morbidities, and other outcomes. The data were extracted independently from the included studies by two authors based on a predefined data extraction sheet. The extracted data included (a) general information (author, type of study, and location), (b) participants (sample size, sex, and age), (c) outcomes (BMI, most common comorbidities, and mortality), and (d) main findings.
Any disagreements in the assessment of data were resolved by discussion between the two authors, and all potential discrepancies were resolved on consultation with a third reviewer. Forty relevant articles were selected, and their full texts were reviewed.
The meta-analysis was performed on outcomes with at least three studies conducted on their effects on obesity. All studies that evaluated the effect of the obesity on all outcomes, poor outcome, intensive care unit (ICU) admission, required IMV, and mortality were included in the meta-analysis. We used STATA Direct 3.1.22 to perform meta-analysis. A p value ≤ 0.05 was considered statistically significant. ORs were reported for the effect estimate, along with its 95% confidence intervals (CIs). Adjusted ORs (aORs) were pooled for meta-analysis of obesity and poor outcome, ICU admission, IMV, and mortality. Random-effects model was used for the data analysis, regardless of heterogeneity. The degree of heterogeneity was quantified using I2 statistics. I2 values of 25%, 50%, and 75% were considered to correspond to low, medium, and high levels of heterogeneity, respectively.
Description of the included studies
After searching PubMed, Scopus, Web of Science, and Google Scholar databases, all relevant studies were identified. Finally, 55 articles were included in the study, and the full texts of the articles were reviewed. The characteristics of the included clinical trials and reasons behind the exclusion are summarized in Table 1.
All cohort, cross-sectional, descriptive, and retrospective studies were included in the study. Most countries that have conducted the studies on COVID-19 and obesity are China, the United States, Italy, UK, and France.
Obesity and COVID-19 severity and outcomes
We learned from the H1N1 Influenza epidemic that obesity is associated with more hospitalization, comorbidities, mechanical ventilation, and death [19, 20]. An increasing body of evidence shows that obesity influences severity and outcomes of COVID-19 (Table 1). A recent report released by the Intensive Care National Audit & Research Centre has shown that 39.3% of 9949 critically ill COVID-19 patients were obese, higher than the prevalence of 31.8% in the British age- and sex-matched general population. Also, the hazard ratio in survival analysis increased slightly above 1, when BMI rose above 30 kg/m2 .
Other studies also had similar results. A study conducted on 4103 COVID-19 patients in New York considered BMI > 40 kg/m2 as the most significant predictor of hospitalization after age . Moreover, a study performed on 383 patients in China showed that obese patients had a 2.42-fold increased risk of severe pneumonia compared to normal-weight patients, even after adjusting for potential confounders . Furthermore, Hajifathalian et al.  in a study conducted on 770 COVID-19 patients in New York found that patients with obesity were more likely to present overt symptoms and have twofold increased risk of ICU admission or death compared to normal-weight patients. Also, one study from China established that 88.24% of COVID-19 non-survivors had a BMI > 25 kg/m2 .
Mechanical ventilation, in addition to ICU admission, is considered as one of the most important indicators of severe disease. A small study in Seattle showed that 85% of obese patients need the mechanical ventilation . Other studies confirmed the higher need for mechanical ventilation in obese patients. A study of 124 COVID-19 patients admitted in the ICU in a university hospital in Lille, France, reported a 7.36-fold need for intubation in patients with BMI > 35 (85.7% of them) compared to those with BMI < 25 kg/m2, independent of other comorbidities. Obesity (BMI ≥ 30) and severe obesity (BMI ≥ 35) were found in 47.6% and 28.2% of cases . However, the results of another study in Lyon, France, were different. This study reported a lower prevalence of obesity and mechanical ventilation as compared to the Lille study. These differences may occur due to lower obesity prevalence in the Lyon area and different treatment protocols. However, the mechanical ventilation requirement was higher in obese patients (BMI ≥ 35 kg/m2) compared to lean patients (81.8 vs. 41.9%) . Also, another study on 92 patients with COVID-19-associated pneumonia in Italy demonstrated that obesity is linked to a higher requirement of assisted ventilation (mechanical or noninvasive ventilation) and ICU admission, as two important indicators of disease severity, after adjusting for other variables. This study reported intensive or semi-intensive respiratory unit admission and mortality in 41.3 and 47.4% of obese patients. However, in this study, obese patients did not show significantly higher mortality rates .
Obesity and COVID-19 severity in age groups
Obesity could lead to severe COVID-19 both in young and old patients, but obesity in elderly individuals may be accompanied by more comorbidities, for example, obesity is associated with type-2 diabetes mellitus (T2DM) that is seen frequently in those aged 65 years . Relative fat mass increases and muscle mass decreases in older individuals, even in nonobese ones, especially in patients with respiratory and cardiac diseases . It was furthermore shown that risk of ICU admission in obese patients is higher than that in lean individuals across all age groups .
However, a study in New York showed that younger people with COVID-19 admitted to the ICU were obese . Similarly, another study in New York demonstrated that people with a BMI between 30 and 34 kg/m2 and >35 kg/m2 were 1.8 and 3.6 times more likely to be admitted to the ICU, respectively. . Moreover, in an Italian study, obese patients were ~9 years younger than normal-weight patients and needed more assisted ventilation and intensive or semi-intensive care . It is essential to note that obesity may increase the chance of severe COVID-19 disease in younger individuals, especially in populations with high obesity prevalence.
Virus shedding in obese patients
Adipose tissue, as a viral reservoir, could make the virus shedding longer in obese patients. This pattern was also seen in influenza infection. More specifically this disease in obese patients was more contagious due to more prolonged shedding of virus , a lower interferon level , and a positive relationship of obesity with the virus load in exhaled air . Viral shedding is also prolonged in obese patients due to impaired immune response, particularly reduced macrophage activation and impaired B- and T-cell responses .
Challenges in diagnosis and managing of obese patients
Many countries face a heavy burden of the COVID-19 pandemic on the health care system. Obesity and the heavy burden associated with COVID-19 have a two-sided relationship. Obese patients require more ICU beds , and due to the pandemic, many ICU beds are occupied. On the contrary, a high prevalence of obesity among a population could lead to the lack of ICU beds. Also, shortage of bariatric beds and the difficulty of positioning and transportation make more burden on nurses and other health care workers [7, 35].
Furthermore, appropriate requirements for obese patients are frequently scarce in many hospitals, e.g., computed tomography (CT) machines that are not able to accommodate obese patients’ weights. Besides these weight limits on CT machines, diagnosis based on pulmonary ultrasound is more difficult in obese patients, and these challenges make an early diagnosis more difficult in obese patients . Also, difficult intubation due to additional adipose tissue on the larynx and difficult insertion of catheters are other factors that make managing obese patients so challenging [35, 36].
How obesity affects COVID-19?
Effects of obesity on the respiratory system
There are many hypotheses about the mechanism of how obesity affects COVID-19 (Fig. 1). It is not surprising that obese patients have many respiratory complications if infected with SARS-CoV-2. Obesity could affect the respiratory system in various ways. Previous studies have confirmed that obesity is a risk factor for many respiratory system diseases like asthma, obstructive sleep apnea syndrome, acute lung injury, and ARDS . Frequently, there are alterations in the respiratory system and chest wall physiology of obese individuals due to fat deposits in the mediastinum and abdomen. Reduced chest wall elasticity, limited truncal expansion, low respiratory muscle strength, and limited diaphragm excursion predispose these individuals to lower respiratory system compliance with a decrease in expiratory reserve volume [10, 28, 38]. Obesity is associated with increased airway resistance, impaired gas exchange, positional gas trapping, and surfactant dysfunction [38, 39]. These functional and physiological changes predispose them to hypoventilation-associated pneumonia, pulmonary HTN, and cardiac stress .
Moreover, the impaired ventilation of the base of the lungs in obese patients could result in reduced oxygen saturation of the blood . Lower lung zones have higher perfusion due to gravity; however, these zones are not well-ventilated because obese individuals’ functional residual capacity is near their residual volume [41,42,43]. This ventilation–perfusion mismatch could lead to lower partial pressure of oxygen (PO2) . Furthermore, obese patients require more oxygen consumption to reach this lower PO2 ; thus, more oxygen requirement and hypoxia in obese patients could lead to the exacerbation of problems in oxygenation.
Effects of obesity on the immune system
Obesity could impair the immune system in various ways. From past experiences, we know that antibody response to influenza vaccine was reduced in obese individuals, and their infection risk was double than that of lean individuals [32, 45]. Moreover, in animal studies, the severity and duration of viral infection were increased in obese animals . Also, obesity is an independent risk factor for an immune-mediated disease like psoriasis .
A balance between cytokines is necessary for an appropriate immune response. However, a pro-inflammatory state in obese patients disrupts this essential balance. This state may be due to the inappropriate secretion of adipokines and cytokines like tumor necrosis factor, interleukin-6 (IL-6), and C-reactive protein by adipocytes in hypoxic conditions [47, 48]. A previous study has shown that IL-6 is an independent risk factor for developing severe COVID-19 , and adipose tissue is one of the primary sources of IL-6 secretion . The creation of an auto-regenerating inflammation loop in this pro-inflammatory state by recruitment of immune cells (macrophages, T cells, and B cells) impairs the immune system . In this status, a viral infection could simply start an impaired immune response, leading to a cytokine storm by overproduction of pro-inflammatory cytokines. The cytokine storm could lead to vascular hyperpermeability and multiorgan failure seen in severe cases of COVID-19 . In the human model, studies have shown that IL-6 is responsible for the activation of multiple cytokine pathways in this pro-inflammatory state .
Obesity could lead to the incoordination of innate and adaptive immune responses by disruption of lymphoid tissue integrity and alterations in leukocyte development and activity . In particular, the impairment of CD8+ memory T cells was seen in obese patients vaccinated for influenza and considered as the leading cause of their weak antibody response to the vaccine . A decrease in macrophage activation due to pro-inflammatory status was regarded as another cause of this inadequate response [34, 53]. Also, memory T-cell impairment could lead to more tissue damage during viral infection challenge . Furthermore, a study in Wuhan showed that patients with severe COVID-19 had less memory, and regulatory T cells .
Leptin is an adipose tissue-derived cytokine that signals the body to stop caloric consumption . Also, leptin plays an essential role in the maturation, development, and function of B lymphocytes . Leptin function in obese individuals is impaired. Surprisingly, leptin serum levels were very high in obese patients due to leptin resistance, like insulin resistance in T2DM , and this leptin resistance was associated with disease severity in H1N1 influenza .
The complement system is inappropriately activated in obese patients . This overreaction is one of the possible mechanisms of the impaired immune reaction to SARS-CoV-2. In a study conducted on SARS-CoV, C3 deficient mice had better respiratory function and a lower level of IL-6 .
Dipeptidyl peptidase-4 (DDP4)
Furthermore, a high level of DDP4 in obese patients is another possible mechanism of immune system impairment. DDP4 is a transmembrane enzyme in human adipose tissue and has an association with obesity-related T2DM . DDP4 inhibition led to GLP-1 increasing and improved insulin sensitivity in adipose tissue . Even in nonobese patients, DDP4 inhibition could suppress pro-inflammatory cytokines like IL-6 and IL-10 .
SARS-CoV-2 receptors in obese patients
Visceral adipose tissues like epicardial fat tissue and ectopic fat tissue in the alveolar space may play a significant role in severe disease by expressing a high level of angiotensin-converting enzyme 2 (ACE-2) receptors. SARS-CoV-2 has a high affinity to bind the ACE-2 receptors . This receptor is expressed in many organs and tissue, particularly lung tissue . However, adipose tissue has a higher level of ACE-2 expression than lung tissue . Obese patients have more adipose tissue than lean individuals, resulting in more ACE-2 receptors.
Obesity and other comorbidities
Obesity could accompany other COVID-19 severity risk factors like T2DM, cardiovascular disease, and kidney diseases  (Fig. 2). In diabetic and obese patients, insulin resistance due to excess fat could lead to inadequate metabolic response to immunologic challenge and more insulin requirement during COVID-19 severe infection .
Even in the absence of other comorbidities, HTN, dyslipidemia, and insulin resistance could increase the risk of cardiovascular events in obese patients infected with SARS-CoV-2 . Left ventricular (LV) hypertrophy due to HTN is the most common cardiac morphology change [64, 65]. In addition, the hyperactivity of the renin–angiotensin–aldosterone system in obese patients could affect myocardium by increasing levels of angiotensin II . Furthermore, obesity could lead to right ventricular dysfunction as an issue in COVID-19 patients due to higher circulating plasma volume . Also, LV diastolic dysfunction and heart failure are common in obese patients [64, 65, 67]. Moreover, the pro-inflammatory state in obese patients may increase the risk of thrombosis by creating an imbalance of procoagulant and anticoagulant factors, increasing thrombin generation, and enhancing platelet activation [68, 69]. Recently, in some patients with severe COVID-19 infection, a generalized thrombotic microvascular injury was observed in pulmonary and cutaneous biopsy and autopsy samples .
Vitamin D deficiency is another possible risk factor for developing severe COVID-19 . Vitamin D as an immunomodulator plays an essential role in decreasing the production of pro-inflammatory cytokines . About 40–80% of the obese population is vitamin D deficient  due to volumetric dilution, sequestration of vitamin D in adipose tissue, and negative feedback from 1,25-dihydroxy vitamin D . Also, in the ICU, obese patients with malnutrition have worse outcomes than those without malnutrition . Moreover, increasing the need for calorie consumption due to a severe acute inflammatory state in SARS-CoV-2 infection could provoke malnutrition .
Role of visceral and abdominal adipose tissue
Adipose tissues in each part of the body could play a role in the severity of COVID-19. For example, abdominal obesity is linked to the impaired ventilation, particularly in the supine state, by reducing diaphragmatic excursion . There are two layers of adipose tissue in the abdomen: visceral and subcutaneous. Abdominal visceral fat is associated with T2DM, HTN, and cardiovascular disease ; however, a similar prevalence of T2DM to the USA in China may relate to more visceral and ectopic adipose tissue instead of abdominal fat in patients of Asian descent .
Visceral adipose tissue, either abdominal or non-abdominal, is responsible for a pro-inflammatory state by abnormal adipokine and cytokine secretion [54, 77]. This state makes visceral adipose tissue capable of driving inflammation in organs (such as heart, liver, kidney, and lungs) and also leads to immune response impairment . Moreover, adipose tissue expresses a high level of ACE-2 receptors, and this may ease the local spreading of the virus in visceral intrathoracic (lungs), epicardial (heart), and peri-renal (kidney) adipose tissue . H5N1 viral tropism has been shown for adipose tissue . Also, adipose tissue is capable of more influenza virus shedding . Moreover, visceral adipose tissue is one of the main sources of IL-6 secretion, and higher levels of IL-6 are associated with more mortality in SARS-CoV-2 .
Epicardial adipose tissue is another visceral fat tissue associated with increased BMI. This fat tissue could decrease myocardial function, in addition to adipokines secretion. Also, a high level of ACE-2 receptors in epicardial fat tissue could increase the risk of myocarditis in obese COVID-19 patients .
How COVID-19 lead to more obesity?
Social distancing during COVID-19 pandemic in many countries leads to significant changes in the individuals’ lifestyle. Decreasing activity, changing eating habits, sleep disorders, stress, and experiencing fear are some significant changes in people’s lives that may result in weight gain and obesity. Reduced level of daily physical activity may be due to the lockdown and keeping schools, gym, and parks closed, teleworking, depression, and fear.
On the other hand, stress and anxiety in people experiencing bad news may result in weight gain . Stress could result in weight gain by cortisol release (activation of the hypothalamo-adrenal-pituitary axis)  and more fat and sweet food consumption (activation of reward centers in the brain) . Also, stress is associated with sleep disruption and lower physical activity, resulting in weight gain .
Changing the diet to canned food due to food insecurity and fresh food unavailability, eating high-caloric snacks or junk foods during other activities and eating food late at night are unhealthy eating habits during the COVID-19 lockdown [81, 83]. These eating habits have more carbohydrate, fat, and sodium, and also processed food could lead to more food consumption by addictive-like behaviors. Furthermore, inadequate sleep may alter the circadian rhythm of hormones and immune system efficacy .
Moreover, self-isolation and depression are frequent in obese individuals due to weight stigma . During the lockdown, there were lots of fat-shaming memes on social media , and this content could lead to more isolation. Depression or stigmatizing may lead to delay in referring to health care centers in obese patients .
Obesity and poor outcome
In 17 studies, meta-analysis demonstrated that obesity (BMI ≥ 30) was associated with poor outcome (OR: 1.297 [1.178–1.416], p < 0.001; I2: 0.0%, heterogeneity = 13.69) (Fig. 3A).
Obesity and ICU admission
In six studies, meta-analysis demonstrated that obesity (BMI ≥ 30) was not associated with ICU admission and obesity did not significantly increase the ICU admission (OR: 1.189 [0.955–1.424], I2: 0.0%, heterogeneity = 1.92) (Fig. 3B).
Obesity and IMV
In eight studies, meta-analysis suggested that in patients hospitalized with COVID-19, obesity (BMI ≥ 30) was associated with invasive mechanical ventilation (OR: 2.049 [1.420–2.678], I2: 75.3%, heterogeneity = 28.34) (Fig. 3C).
Obesity and mortality
Ten retrospective cohort studies reported the effect of obesity on the mortality. Meta-analysis demonstrated that obesity (BMI ≥ 30) was associated with mortality and obesity increased mortality (OR: 1.35 [1.241–1.459], I2: 76.6%, heterogeneity = 38.44) (Fig. 3D).
Recommendations on weight control in COVID-19 era
Because of obesity effects on COVID-19, weight gain prevention is highly recommended during the pandemic. Changing lifestyle has been found to play an important role in the prevention of weight gain. Increased physical activity and exercise at home or outdoors with social distancing are critical ways to prevent weight gain in normal-weight people and also lose weight in overweight or obese individuals. Exercise also could improve the metabolic and immunologic functions of the body . Creative methods to do exercise more at home and high activity games with children may lead to more activity despite limitations. Reduced high-caloric food consumption is another feasible way to prevent weight gain. Increased fresh food and decreased canned and junk food consumption are notable points that should be considered during the pandemic. Moreover, psychological support and treatment or medical interventions to control stress and avoid emotional eating, and also, sleep regulation could also be useful to reach this goal.
In addition to these recommendations, obese patients should consider a steady low-caloric diet and proven weight loss drugs (synthetic or herbal drugs under physician observation) to lose weight due to their increased risk of disease [88, 89]. Furthermore, obese patients who have diabetes should tightly control their glycemic status and adjust their medication and calorie consumption with these new circumstances. As a result, telemedicine could play a crucial role in the close monitoring of obese patients during COVID-19 pandemic.
Recommendations and conclusion
Obesity affects the respiratory and immune systems through various mechanisms. Cytokine and adipokine secretion from adipose tissue leads to a pro-inflammatory state in obese patients, and this predisposes them to thrombosis, incoordination of innate and adaptive immune responses, inadequate antibody responses, and cytokine storm. Also, viral shedding is more in obese patients. Obesity is associated with other comorbidities such as HTN, cardiovascular disease, diabetes mellitus, and vitamin D deficiency.
Hospitalization, ICU admission, mechanical ventilation, and even mortality in obese patients are higher than normal-weight people. It seems obesity could shift severe COVID-19 symptoms to younger individuals. Also, early diagnosis and management of obese patients are harder than those of lean individuals. Decreasing activity, changing eating habits and, more stress and fear experienced during the COVID-19 pandemic may result in more weight gain and obesity. More attention to weight gain prevention is necessary during this pandemic.
Obesity should be considered as an independent risk factor for developing severe COVID-19. We recommend that clinicians consider more serious treatments in the early stages of disease for obese patients.
Reviewing all relevant studies conducted on “Obesity and COVID-19” and various possible mechanisms were the strength of this study. However, we have some limitations such as full-text unavailability for some non-English studies and lack of cohort studies. Most of the studies were cross-sectional and retrospective and also some had small sample sizes; we recommend that prospective cohort studies be conducted on larger sample sizes.
World Health Organization. WHO Coronavirus Disease (COVID-19) Dashboard. https://covid19.who.int. Accessed Nov 2020.
Mizumoto K, Kagaya K, Zarebski A, Chowell G. Estimating the asymptomatic proportion of coronavirus disease 2019 (COVID-19) cases on board the Diamond Princess cruise ship, Yokohama, Japan, 2020. Eurosurveillance. 2020;25. https://doi.org/10.2807/1560-7917.ES.2020.25.10.2000180.
Wu Z, McGoogan JM. Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China: summary of a report of 72314 cases from the Chinese Center for Disease Control and Prevention. JAMA. 2020;323:1239–42.
Zhou F, Yu T, Du R, Fan G, Liu Y, Liu Z, et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet. 2020;395:1054–62.
Mahbube E, Moloud P, Mahnaz Pejman S, Bagher L, Ebrahimpur M, Payab M, et al. Coronavirus disease (COVID-19): 10 questions and discussion points for diabetes and COVID-19. Adv J Emerg Med. 2020;0:118–23.
Parhizkar Roudsari P, Alavi-Moghadam S, Payab M, Sayahpour FA, Aghayan HR, Goodarzi P. et al. Auxiliary role of mesenchymal stem cells as regenerative medicine soldiers to attenuate inflammatory processes of severe acute respiratory infections caused by COVID-19. Cell Tissue Bank. 2020;21:405–25. https://doi.org/10.1007/s10561-020-09842-3.
Ryan DH, Ravussin E, Heymsfield S. COVID 19 and the Patient with Obesity - The Editors Speak Out. Obesity (Silver Spring). 2020;28:847. https://doi.org/10.1002/oby.22808.
Collaboration NCDRF, Di Cesare M, Bentham J, Stevens GA, Zhou B, Danaei G, et al. Trends in adult body-mass index in 200 countries from 1975 to 2014: a pooled analysis of 1698 population-based measurement studies with 19·2 million participants. Lancet. 2016;387:1377–96.
Forouzanfar MH, Afshin A, Alexander LT, Anderson HR, Bhutta ZA, Biryukov S, et al. 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. Lancet. 2016;388:1659–724.
GBD 2015 Obesity Collaborators, Afshin A, Forouzanfar MH, Reitsma MB, Sur P, Estep K, et al. Health effects of overweight and obesity in 195 countries over 25 years. N Engl J Med. 2017;377:13–27. https://doi.org/10.1056/NEJMoa1614362.
Avicenna. Al-Qanun fil-Tib. Cairo: Cairo Government Press; 1877, p. 304.
Nathan B, Cowan GSM. A medieval medical view on obesity. Obes Surg. 1992;2:217–8.
Short KR, Kedzierska K, van de Sandt CE. Back to the future: lessons learned from the 1918 influenza pandemic. Front Cell Infect Microbiol. 2018;8:343.
Morgan OW, Bramley A, Fowlkes A, Freedman DS, Taylor TH, Gargiullo P, et al. Morbid obesity as a risk factor for hospitalization and death due to 2009 pandemic influenza A(H1N1) disease. PLoS ONE. 2010;5. https://doi.org/10.1371/journal.pone.0009694.
Ni Y-N, Luo J, Yu H, Wang Y-W, Hu Y-H, Liu D, et al. Can body mass index predict clinical outcomes for patients with acute lung injury/acute respiratory distress syndrome? A meta-analysis. Crit Care. 2017;21:36.
Petrilli C, Jones S, Yang J, Rajagopalan H, O’Donnell L, Chernyak Y, et al. Factors associated with hospitalization and critical illness among 4,103 patients with COVID-19 disease in New York City. BMJ. 2020;369. https://doi.org/10.1101/2020.04.08.20057794.
Simonnet A, Chetboun M, Poissy J, Raverdy V, Noulette J, Duhamel A, et al. High prevalence of obesity in severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) requiring invasive mechanical ventilation. Obesity. 2020;28:1195–9.
Lighter J, Phillips M, Hochman S, Sterling S, Johnson D, Francois F, et al. Obesity in patients younger than 60 years is a risk factor for COVID-19 hospital admission. Clin Infect Dis. 2020;71:896–7.
Thompson DL, Jungk J, Hancock E, Smelser C, Landen M, Nichols M, et al. Risk factors for 2009 pandemic influenza A (H1N1)-related hospitalization and death among racial/ethnic groups in New Mexico. Am J Public Health. 2011;101:1776–84.
Louie JK, Acosta M, Winter K, Jean C, Gavali S, Schechter R, et al. Factors associated with death or hospitalization due to pandemic 2009 influenza A(H1N1) infection in California. J Am Med Assoc. 2009;302:1896–902.
Intensive Care National Audit Research Centre. ICNARC report on COVID-19 in critical care 19 June 2020. London: Intensive Care National Audit & Research Centre; 2020.
Cai Q, Chen F, Wang T, Luo F, Liu X, Wu Q, et al. Obesity and COVID-19 severity in a designated hospital in Shenzhen, China. Diabetes Care. 2020;43:1392–8.
Hajifathalian K, Kumar S, Newberry C, Shah S, Fortune B, Krisko T, et al. Obesity is associated with worse outcomes in COVID-19: analysis of early data from New York City. Obesity. 2020;28:1606–12.
Liu J, Ouyang L, Fu P, Cao Y, Yang D, Han X, et al. Epidemiological, clinical, radiological characteristics and outcomes of medical staff with COVID-19 in Wuhan, China: a single-centered, retrospective case series analysis. SSRN Electron J. 2020. https://doi.org/10.2139/ssrn.3555247.
Stefan N, Birkenfeld AL, Schulze MB, Ludwig DS. Obesity and impaired metabolic health in patients with COVID-19. Nat Rev Endocrinol. 2020;16:341–2.
Caussy C, Wallet F, Laville M, Disse E. Obesity is associated with severe forms of COVID-19 [letter]. Obesity. 2020;28:1175.
Busetto L, Bettini S, Fabris R, Serra R, Dal Pra C, Maffei P, et al. Obesity and COVID-19: an Italian snapshot. Obesity. 2020;28:1600–5.
Puig-Domingo M, Marazuela M, Giustina A. COVID-19 and endocrine diseases. A statement from the European Society of Endocrinology. Endocrine. 2020;68:2–5.
Sattar N, McInnes IB, McMurray JJV. Obesity is a risk factor for severe COVID-19 infection: multiple potential mechanisms. Circulation. 2020;142:4–6.
Kass DA, Duggal P, Cingolani O. Obesity could shift severe COVID-19 disease to younger ages. Lancet. 2020;395:1544–5.
Maier HE, Lopez R, Sanchez N, Ng S, Gresh L, Ojeda S, et al. Obesity increases the duration of influenza a virus shedding in adults. J Infect Dis. 2018;218:1378–82.
Honce R, Karlsson EA, Wohlgemuth N, Estrada LD, Meliopoulos VA, Yao J, et al. Obesity-related microenvironment promotes emergence of virulent influenza virus strains. MBio. 2020;11. https://doi.org/10.1128/mBio.03341-19.
Yan J, Grantham M, Pantelic J, De Mesquita PJB, Albert B, Liu F, et al. Infectious virus in exhaled breath of symptomatic seasonal influenza cases from a college community. Proc Natl Acad Sci USA. 2018. https://doi.org/10.1073/pnas.1716561115.
Ahn SY, Sohn SH, Lee SY, Park HL, Park YW, Kim H, et al. The effect of lipopolysaccharide-induced obesity and its chronic inflammation on influenza virus-related pathology. Environ Toxicol Pharmacol. 2015;40:924–30.
Michalakis K, Ilias I. SARS-CoV-2 infection and obesity: common inflammatory and metabolic aspects. Diabetes Metab Syndr. 2020;14:469–71.
Muscogiuri G, Pugliese G, Barrea L, Savastano S, Colao A. Comentary: obesity: the “achilles heel” for COVID-19? Metab Exp. 2020;108. https://doi.org/10.1016/j.metabol.2020.154251.
Watanabe M, Risi R, Tuccinardi D, Baquero CJ, Manfrini S, Gnessi L. Obesity and SARS-CoV-2: a population to safeguard. Diabetes Metab Res Rev. 2020;36:e3325.
Murugan AT, Sharma G. Obesity and respiratory diseases. Chron Respir Dis. 2008;5:233–42.
Parameswaran K, Todd DC, Soth M. Altered respiratory physiology in obesity. Can Respir J. 2006;13:203–10.
Dixon AE, Peters U. The effect of obesity on lung function. Expert Rev Respir Med. 2018;12:755–67.
Jones RL, Nzekwu MMU. The effects of body mass index on lung volumes. Chest. 2006;130:827–33.
Ladosky W, Botelho MAM, Albuquerque JP. Chest mechanics in morbidly obese non-hypoventilated patients. Respir Med. 2001;95:281–6.
Collet F, Mallart A, Bervar JF, Bautin N, Matran R, Pattou F, et al. Physiologic correlates of dyspnea in patients with morbid obesity. Int J Obes. 2007;31:700–6.
Fleischmann E, Kurz A, Niedermayr M, Schebesta K, Kimberger O, Sessler DI, et al. Tissue oxygenation in obese and non-obese patients during laparoscopy. Obes Surg. 2005;15:813–9.
Green WD, Beck MA. Obesity impairs the adaptive immune response to influenza virus. Ann Am Thorac Soc. 2017;14:s406–9.
Budu-Aggrey A, Brumpton B, Tyrrell J, Watkins S, Modalsli EH, Celis-Morales C, et al. Evidence of a causal relationship between body mass index and psoriasis: a mendelian randomization study. PLoS Med. 2019;16:1002739.
Park HS, Park JY, Yu R. Relationship of obesity and visceral adiposity with serum concentrations of CRP, TNF-alpha and IL-6. Diabetes Res Clin Pract. 2005;69:29–35.
Vieira-Potter VJ. Inflammation and macrophage modulation in adipose tissues. Cell Microbiol. 2014;16:1484–92.
Ruan Q, Yang K, Wang W, Jiang L, Song J. Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China. Intensive Care Med. 2020;46:846–8.
Sindhu S, Thomas R, Shihab P, Sriraman D, Behbehani K, Ahmad R. Obesity is a positive modulator of IL-6R and IL-6 expression in the subcutaneous adipose tissue: significance for metabolic inflammation. PLoS ONE. 2015;10:e0133494.
Jose RJ, Manuel A. Does coronavirus disease 2019 disprove the obesity paradox in acute respiratory distress syndrome? [letter]. Obesity. 2020;28:1007.
Yiu HH, Graham AL, Stengel RF. Dynamics of a cytokine storm. PLoS ONE. 2012;7:e45027.
Karlsson EA, Sheridan PA, Beck MA. Diet-induced obesity in mice reduces the maintenance of influenza-specific CD8+ memory T cells. J Nutr. 2010;140:1691–7.
Ryan PMD, Caplice NM. Is adipose tissue a reservoir for viral spread, immune activation, and cytokine amplification in coronavirus disease 2019? Obesity. 2020;28:1191–4.
Zhang AJX, To KKW, Li C, Lau CCY, Poon VKM, Chan CCS, et al. Leptin mediates the pathogenesis of severe 2009 pandemic influenza A(H1N1) infection associated with cytokine dysregulation in mice with diet-induced obesity. J Infect Dis. 2013;207:1270–80.
Karkhaneh M, Qorbani M, Mohajeri-Tehrani MR, Hoseini S. Association of serum complement C3 with metabolic syndrome components in normal weight obese women. J Diabetes Metab Disord. 2017;16:49.
Gralinski LE, Sheahan TP, Morrison TE, Menachery VD, Jensen K, Leist SR, et al. Complement activation contributes to severe acute respiratory syndrome coronavirus pathogenesis. MBio. 2018;9:e01753–18.
Malavazos AE, Corsi Romanelli MM, Bandera F, Iacobellis G. Targeting the adipose tissue in COVID-19. Obesity. 2020;28:1178–9.
Iacobellis G. COVID-19 and diabetes: can DPP4 inhibition play a role? Diabetes Res Clin Pract. 2020;162:1–2.
Reinhold D, Brocke S. DPP4-directed therapeutic strategies for MERS-CoV. Lancet Infect Dis. 2014;14:100–1.
Zhou P, Yang XL, Wang XG, Hu B, Zhang L, Zhang W, et al. A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature. 2020;579:270–3.
Hamming I, Timens W, Bulthuis MLC, Lely AT, Navis GJ, van Goor H. Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis. J Pathol. 2004;203:631–7.
Jia X, Yin C, Lu S, Chen Y, Liu Q, Bai J, et al. Two things about COVID-19 might need attention. Preprints. 2020. https://doi.org/10.20944/preprints202002.0315.v1.
Alpert MA. Obesity cardiomyopathy: pathophysiology and evolution of the clinical syndrome. Am J Med Sci. 2001;321:225–36.
Alpert MA, Lavie CJ, Agrawal H, Aggarwal KB, Kumar SA. Obesity and heart failure: epidemiology, pathophysiology, clinical manifestations, and management. Transl Res. 2014;164:345–56.
Wong C, Marwick TH. Obesity cardiomyopathy: pathogenesis and pathophysiology. Nat Clin Pract Cardiovasc Med. 2007;4:436–43.
Pascual M, Pascual DA, Soria F, Vicente T, Hernández AM, Tébar FJ, et al. Effects of isolated obesity on systolic and diastolic left ventricular function. Heart. 2003;89:1152–6.
Blokhin IO, Lentz SR. Mechanisms of thrombosis in obesity. Curr Opin Hematol. 2013;20:437–44.
Korakas E, Ikonomidis I, Kousathana F, Balampanis K, Kountouri A, Raptis A, et al. Obesity and COVID-19: immune and metabolic derangement as a possible link to adverse clinical outcomes. Am J Physiol Endocrinol Metab. 2020;19:100250.
Magro C, Mulvey JJ, Berlin D, Nuovo G, Salvatore S, Harp J, et al. Complement associated microvascular injury and thrombosis in the pathogenesis of severe COVID-19 infection: a report of five cases. Transl Res. 2020;220:1–13.
Grant WB, Lahore H, McDonnell SL, Baggerly CA, French CB, Aliano JL, et al. Evidence that vitamin d supplementation could reduce risk of influenza and covid-19 infections and deaths. Nutrients. 2020;12:988.
Teymoori-Rad M, Shokri F, Salimi V, Marashi SM. The interplay between vitamin D and viral infections. Rev Med Virol. 2019;29:e2032.
Walsh JS, Bowles S, Evans AL. Vitamin D in obesity. Curr Opin Endocrinol Diabetes Obes. 2017;24:389–94.
Robinson MK, Mogensen KM, Casey JD, McKane CK, Moromizato T, Rawn JD, et al. The relationship among obesity, nutritional status, and mortality in the critically Ill. Crit Care Med. 2015;43:87–100.
Dietz W, Santos-Burgoa C. Obesity and its implications for COVID-19 mortality [letter]. Obesity. 2020;28:1005.
Ibrahim MM. Subcutaneous and visceral adipose tissue: structural and functional differences. Obes Rev. 2010;11:11–8.
Huttunen R, Syrjänen J. Obesity and the risk and outcome of infection. Int J Obes. 2013;37:333–40.
Gupte M, Thatcher SE, Boustany-Kari CM, Shoemaker R, Yiannikouris F, Zhang X, et al. Angiotensin converting enzyme 2 contributes to sex differences in the development of obesity hypertension in C57BL/6 mice. Arterioscler Thromb Vasc Biol. 2012;32:1392–9.
Zhao L. Obesity accompanying COVID-19: the role of epicardial fat. Obesity. 2020. https://doi.org/10.1002/oby.22867.
Rodríguez MÁ, Crespo I, Olmedillas H. Exercising in times of COVID-19: what do experts recommend doing within four walls? Rev Esp Cardiol. 2020;73:527–9.
Schulte EM, Avena NM, Gearhardt AN. Which foods may be addictive? The roles of processing, fat content, and glycemic load. PLoS ONE. 2015;10:e0117959.
Isasi CR, Parrinello CM, Jung MM, Carnethon MR, Birnbaum-Weitzman O, Espinoza RA, et al. Psychosocial stress is associated with obesity and diet quality in Hispanic/Latino adults. Ann Epidemiol. 2015;25:84–9.
Abbas AM, Fathy SK, Fawzy AT, Salem AS, Shawky MS. The mutual effects of COVID-19 and obesity. Obes Med. 2020. https://doi.org/10.1016/j.obmed.2020.100250.
Rubino F, Puhl RM, Cummings DE, Eckel RH, Ryan DH, Mechanick JI, et al. Joint international consensus statement for ending stigma of obesity. Nat Med. 2020;26:1–13.
Frühbeck G, Baker JL, Busetto L, Dicker D, Goossens GH, Halford JCG, et al. European association for the study of obesity position statement on the global COVID-19 pandemic. Obes Facts. 2020;2:292–6.
Alberga AS, Edache IY, Forhan M, Russell-Mayhew S. Weight bias and health care utilization: a scoping review. Prim Health Care Res Dev. 2019;20:e116.
Wong GCL, Narang V, Lu Y, Camous X, Nyunt MSZ, Carre C, et al. Hallmarks of improved immunological responses in the vaccination of more physically active elderly females. Exerc Immunol Rev. 2019;25:20–32.
Payab M, Hasani-Ranjbar S, Baeeri M, Rahimifard M, Arjmand B, Haghi-Aminjan H, et al. Development of a novel anti-obesity compound with inhibiting properties on the lipid accumulation in 3T3-L1 adipocytes. Iran Biomed J. 2020;24:155–63.
Payab M, Hasani-Ranjbar S, Shahbal N, Qorbani M, Aletaha A, Haghi-Aminjan H, et al. Effect of the herbal medicines in obesity and metabolic syndrome: a systematic review and meta-analysis of clinical trials. Phyther Res. 2020;34:526–45.
McMichael TM, Currie DW, Clark S, Pogosjans S, Kay M, Schwartz NG, et al. Epidemiology of Covid-19 in a Long-Term Care Facility in King County, Washington. N Engl J Med. 2020;382:2005–11.
Liu M, He P, Liu HG, Wang XJ, Li FJ, Chen S, et al. Clinical characteristics of 30 medical workers infected with new coronavirus pneumonia. Zhonghua Jie He He Hu Xi Za Zhi. 2020. https://doi.org/10.3760/cma.j.issn.1001-0939.2020.03.014.
Liu J, Ouyang L, Guo P, Sheng Wu H, Fu P, liang Chen Y, et al. Epidemiological, clinical characteristics and outcome of medical staff infected with COVID-19 in Wuhan, China: a retrospective case series analysis. medRxiv. 2020. https://www.medrxiv.org/content/10.1101/2020.03.09.20033118v1.
Yang W, Cao Q, Qin L, Wang X, Cheng Z, Pan A, et al. Clinical characteristics and imaging manifestations of the 2019 novel coronavirus disease (COVID-19): a multi-center study in Wenzhou city, Zhejiang, China. J Infect. 2020;80:388–93.
Richardson S, Hirsch JS, Narasimhan M, Crawford JM, McGinn T, Davidson KW, et al. Presenting characteristics, comorbidities, and outcomes among 5700 patients hospitalized with COVID-19 in the New York City Area. JAMA. 2020;23:2052–9.
Peng YD, Meng K, Guan HQ, Leng L, Zhu RR, Wang BY, et al. Clinical characteristics and outcomes of 112 cardiovascular disease patients infected by 2019-nCoV. Zhonghua Xin Xue Guan Bing Za Zhi. 2020;48:e004.
Huang M, Yang Y, Shang F, Zheng Y, Zhao W, Luo L, et al. Early and critical care in severe patients with COVID-19 in Jiangsu Province, China: a descriptive study. SSRN Electron J. 2020. https://doi.org/10.2139/ssrn.3546056.
Cai Q, Huang D, Ou P, Yu H, Zhu Z, Xia Z, et al. COVID-19 in a designated infectious diseases hospital outside Hubei Province, China. Allergy. 2020;75:1742–52.
Xu Y, Xu Z, Liu XX, Cai L, Zheng H, Huang Y, et al. Clinical findings in critical ill patients infected with SARS-Cov-2 in Guangdong Province, China: a multi-center, retrospective, observational study. medRxiv. 2020:2020.03.03.20030668. https://doi.org/10.1101/2020.03.03.20030668.
McMichael TM, Clark S, Pogosjans S, Kay M, Lewis J, Baer A, et al. COVID-19 in a long-term care facility—King County, Washington, February 27–March 9, 2020. MMWR Morb Mortal Wkly Rep. 2020;69:343–6.
Liao J, Fan S, Chen J, Wu J, Xu S, Guo Y, et al. Epidemiological and clinical characteristics of COVID-19 in adolescents and young adults. Innovation. 2020;1:100001.
Goyal P, Choi JJ, Pinheiro LC, Schenck EJ, Chen R, Jabri A, et al. Clinical characteristics of Covid-19 in New York City [letter]. N Engl J Med. 2020;382:2372–4.
Bhatraju PK, Ghassemieh BJ, Nichols M, Kim R, Jerome KR, Nalla AK, et al. Covid-19 in critically ill patients in the Seattle region—case series. N Engl J Med. 2020;21:2012–22.
Wu J, Li W, Shi X, Chen Z, Jiang B, Liu J, et al. Early antiviral treatment contributes to alleviate the severity and improve the prognosis of patients with novel coronavirus disease (COVID-19). J Intern Med. 2020;288:128–38.
Khorrami Z, Nili S, Sharifi H, Eybpoosh S, Shokoohi M. Association of cigarette smoking, obesity, and underlying medical conditions with COVID-19 hospitalization and mortality in Iran: A nationwide retrospective ecological study. Med J Islam Repub Iran. 2020;34:133. https://doi.org/10.34171/mjiri.34.133.
Yu T, Cai S, Zheng Z, Cai X, Liu Y, Yin S, et al. Association between clinical manifestations and prognosis in patients with COVID-19. Clin Ther. 2020;42:964–72.
Bruno G, Perelli S, Fabrizio C, Buccoliero GB. Short-term outcomes in individuals aged 75 or older with severe coronavirus disease (COVID-19): first observations from an infectious diseases unit in Southern Italy. J Infect. 2020;81:e86–8.
Wei YY, Wang RR, Zhang DW, Tu YH, Chen CS, Ji S, et al. Risk factors for severe COVID-19: evidence from 167 hospitalized patients in Anhui, China. J Infect. 2020;81:e89–92.
Chao JY, Derespina KR, Herold BC, Goldman DL, Aldrich M, Weingarten J, et al. Clinical characteristics and outcomes of hospitalized and critically ill children and adolescents with coronavirus disease 2019 at a Tertiary Care Medical Center in New York City. J Pediatr. 2020;223:14–9.
Chen Q, Zheng Z, Zhang C, Zhang X, Wu H, Wang J. et al. Clinical characteristics of 145 patients with corona virus disease 2019 (COVID-19) in Taizhou, Zhejiang, China. Infection. 2020;48:543–51.
Dreher M, Kersten A, Bickenbach J, Balfanz P, Hartmann B, Cornelissen C, et al. The characteristics of 50 hospitalized COVID-19 patients with and without ARDS. Dtsch Arztebl Int. 2020;117:271.
Palaiodimos L, Kokkinidis DG, Li W, Karamanis D, Ognibene J, Arora S, et al. Severe obesity, increasing age and male sex are independently associated with worse in-hospital outcomes, and higher in-hospital mortality, in a cohort of patients with COVID-19 in the Bronx, New York. Metabolism. 2020;108:154262.
de Lusignan S, Dorward J, Correa A, Jones N, Akinyemi O, Amirthalingam G, et al. Risk factors for SARS-CoV-2 among patients in the Oxford Royal College of General Practitioners Research and Surveillance Centre primary care network: a cross-sectional study. Lancet Infect Dis. 2020;20:1034–42.
Yu X, Sun X, Cui P, Pan H, Lin S, Han R, et al. Epidemiological and clinical characteristics of 333 confirmed cases with coronavirus disease 2019 in Shanghai, China. Transbound Emerg Dis. 2020;76:1697–707.
Kalligeros M, Shehadeh F, Mylona EK, Benitez G, Beckwith CG, Chan PA, et al. Association of obesity with disease severity among patients with coronavirus disease 2019. Obesity. 2020;28:1200–4.
Zheng KI, Gao F, Wang XB, Sun QF, Pan KH, Wang TY, et al. Obesity as a risk factor for greater severity of COVID-19 in patients with metabolic associated fatty liver disease [letter]. Metabolism. 2020;108:154244.
Palmieri L, Vanacore N, Donfrancesco C, Lo Noce C, Canevelli M, Punzo O, et al. Clinical characteristics of hospitalized individuals dying with COVID-19 by age group in Italy. JGerontol A Biol Sci Med Sci. 2020;75:1796–800.
Argenziano MG, Bruce SL, Slater CL, Tiao JR, Baldwin MR, Barr RG, et al. Characterization and clinical course of 1000 patients with coronavirus disease 2019 in New York: retrospective case series. BMJ. 2020;369:m1996.
Caussy C, Pattou F, Wallet F, Simon C, Chalopin S, Telliam C, et al. Prevalence of obesity among adult inpatients with COVID-19 in France. Lancet Diabetes Endocrinol. 2020;8:562–4.
Zachariah P, Johnson CL, Halabi KC, Ahn D, Sen AI, Fischer A, et al. Epidemiology, clinical features, and disease severity in patients with coronavirus disease 2019 (COVID-19) in a Children’s Hospital in New York City, New York. JAMA Pediatr. 2020;174:e202430.
Bello-Chavolla OY, Bahena-López JP, Antonio-Villa NE, Vargas-Vázquez A, González-Díaz A, Márquez-Salinas A, et al. Predicting mortality due to SARS-CoV-2: a mechanistic score relating obesity and diabetes to COVID-19 outcomes in Mexico. J Clin Endocrinol Metab. 2020;105:2752–61.
Yates T, Razieh C, Zaccardi F, Davies MJ, Khunti K. Obesity and risk of COVID-19: analysis of UK biobank [letter]. Prim Care Diabetes. 2020;14:566–7.
Buckner FS, McCulloch DJ, Atluri V, Blain M, McGuffin SA, Nalla AK, et al. Clinical features and outcomes of 105 hospitalized patients with COVID-19 in Seattle, Washington. Clin Infect Dis. 2020;71:2167–73.
Docherty AB, Harrison EM, Green CA, Hardwick HE, Pius R, Norman L, et al. Features of 20 133 UK patients in hospital with covid-19 using the ISARIC WHO Clinical Characterisation Protocol: prospective observational cohort study. BMJ. 2020;369:m1985.
Giacomelli A, Ridolfo AL, Milazzo L, Oreni L, Bernacchia D, Siano M, et al. 30-day mortality in patients hospitalized with COVID-19 during the first wave of the Italian epidemic: a prospective cohort study. Pharmacol Res. 2020;158:104931.
Hu L, Chen S, Fu Y, Gao Z, Long H, Ren H, et al. Risk factors associated with clinical outcomes in 323 coronavirus disease 2019 (COVID-19) hospitalized Patients in Wuhan, China. Clin Infect Dis. 2020;71:2089–98.
Hur K, Price CPE, Gray EL, Gulati RK, Maksimoski M, Racette SD, et al. Factors associated with intubation and prolonged intubation in hospitalized patients With COVID-19. Otolaryngol Head Neck Surg. 2020;163:170–8.
Intensive Care National Audit & Research Centre. ICNARC report on COVID-19 in critical care 04 April 20. London: Intensive Care National Audit & Research Centre; 2020.
Itelman E, Wasserstrum Y, Segev A, Avaky C, Negru L, Cohen D, et al. Clinical Characterization of 162 COVID-19 patients in Israel: Preliminary Report from a Large Tertiary Center. Isr Med Assoc J. 2020;22:271–4.
Klang E, Kassim G, Soffer S, Freeman R, Levin MA, Reich DL. Severe obesity as an independent risk factor for COVID-19 mortality in hospitalized patients younger than 50. Obesity. 2020;29:1595–9.
Louisiana Coronavirus COVID-19 | Department of Health | State of Louisiana. https://ldh.la.gov/coronavirus/. Accessed Apr 2020.
Lodigiani C, Iapichino G, Carenzo L, Cecconi M, Ferrazzi P, Sebastian T, et al. Venous and arterial thromboembolic complications in COVID-19 patients admitted to an academic hospital in Milan, Italy. Thromb Res. 2020;191:9–14.
Ong SWX, Young BE, Leo YS, Lye DC. Association of higher body mass index (BMI) with severe coronavirus disease 2019 (COVID-19) in younger patients. Clin Infect Dis. 2020;71:2300–2.
Hussain A, Mahawar K, Xia Z, Yang W, El-Hasani S. Obesity and mortality of COVID-19. Meta-analysis. Obes Res Clin Pract. 2020;14:295–300. https://doi.org/10.1016/j.orcp.2020.07.002.
Implementation of this study was sponsored by Tehran University of Medical Sciences (Endocrinology and Metabolism Research Center).
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Aghili, S.M.M., Ebrahimpur, M., Arjmand, B. et al. Obesity in COVID-19 era, implications for mechanisms, comorbidities, and prognosis: a review and meta-analysis. Int J Obes 45, 998–1016 (2021). https://doi.org/10.1038/s41366-021-00776-8
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Perceiving the unusual: Temporal properties of hierarchical motor representations for action perception
- Demiris Yiannis, Simmons Gavin
- Neural Networks SCI(E) SCOPUS
- International Neural Network Society
- Cited Count
Recent computational approaches to action imitation have advocated the use of hierarchical representations in the perception and imitation of demonstrated actions. Hierarchical representations present several advantages, with the main one being their ability to process information at multiple levels of detail. However, the nature of the hierarchies in these approaches has remained relatively unsophisticated, and their relation with biological evidence has not been investigated in detail, in particular with respect to the timing of movements. Following recent neuroscience work on the modulation of the premotor mirror neuron activity during the observation of unpredictable grasping movements, we present here an implementation of our HAMMER architecture using the minimum variance model for implementing reaching and grasping movements that have biologically plausible trajectories. Subsequently, we evaluate the performance of our model in matching the temporal dynamics of the modulation of cortical excitability during the passive observation of normal and unpredictable movements of human demonstrators.
1.Imitating with alice: Learning to imitate corresponding actions across dissimilar embodiments. IEEE Transactions on Systems, Man, and Cybernetics, Part A: Systems and Humans. Vol. 32. 482496(2002)
2.Learning motor skills by imitation: A biologically inspired robotic model. Cybernetics and Systems. Vol. 32. 155193(2000)
3.Demiris, J. (1999). Movement imitation mechanisms in robots and humans, PhD thesis, University of Edinburgh, Scotland, UK. .
4.Demiris, Y. (2002). Imitation, mirror neurons, and the learning of movement sequences. In Proceedings of the international conference on neural information processing (ICONIP-2002) (pp. 111–115). IEEE Press: New York. .
5.Imitation as a dual route process featuring predictive and learning components: A biologically-plausible computational model. Imitation in animals and artifacts. 327361(2002) Dautenhahn K. et al.
6.Distributed, prediction perception of actions: A biologically inspired architecture for imitation and learning. Connection Science. Vol. 15. 231243(2003)
7.Demiris, Y., & Khadhouri, B. (2006). Hierarchical, attentive multiple models for execution and recognition. Robotics and Autonomous Systems in press, doi:10.1016/j.robot.2006.02.003. .
8.Hierarchical organization and functional streams in the visual cortex. Trends in Neurosciences. Vol. 6. 370375(1983)
9.Modeling parietal–premotor interactions in primate control of grasping(1998) Fagg Andrew H et al. Neural NetworksNeuroscience cited 35 times
10.Mirror neurons responding to observation of actions made with tools in monkey ventral premotor cortex. Journal of Cognitive Neuroscience. Vol. 17. 212226(2005)

domain: literature


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The temperature seemed to drop 40 degrees when I heard Red Smith had died. The chill reminded me of another very cold day, one we spent together.
It was January 1976. Red was in Pittsburgh to cover the AFC championship game between the Steelers and the Oakland Raiders. I was in Pittsburgh to cover Red Smith.
I was in journalism school, writing my master's essay about the best sportswriter America ever had. "Well, Jane," he said, the first time I spoke to him, "I think it's a lousy idea. But if you want to do it, it's okay with me."
Red had given up his seat in the heated football press box to sit outside with me. He noted the temperature (16 degrees) and the unlined boots on my feet. We watched the second half inside on TV.
I was too inexperienced to know how extraordinary that was for a writer on deadline to do, how perfectly ordinary the kindness was for Red.
After the game, Red and the rest of the horde followed the Steelers to the winners' locker room. A lanky Pinkerton guard stood watch outside the Raiders' door. I ventured forward. "Ladies Day today?" I asked. This was in the day when ladies did not go into locker rooms.
"Got credentials?" he replied. A yellow tag dangled from my coat. It said: Red Smith, New York Times. "You're Red Smith?" he said. I nodded as modestly as I knew Red would. "Go right in."
John Madden, the coach, looked up, glaring at the Pinkerton. "Who the hell is she?" he said.
"Don't worry about her," the guard replied. "She's Red Smith."
It was the last time I was thrown out of a locker room.
A lot of writers wanted to be Red Smith, to be as good as he was. That was impossible. Knowing him was enough.
In the beginning, we would sit in the barn behind his house and talk about writing, why he put a comma here, broke a sentence there. He had no answers to my questions. "Once I was asking the old boxer, Willie Pep, where he got his moves," Red said. "And my friend, Bill Heinz, looked at me and said, 'You silly son-of-a-bitch, can you say where you learned to write?' "
But I knew he knew, so I sent him stories to edit, as did so many other young writers. And it never failed to amaze me that he found time for so many of us. He would mark up the stories (never in red pen, that was for editors), apologizing in the margins for the changes he had made. One came back with the word "swell" on it. That didn't begin to describe how I felt.
One night, he came to dinner. Billie Jean King, who was then my boss at womenSports Magazine, wanted to meet him. She came dressed in cashmere, dripping jewelry. Red came, as usual, in a pink shirt and a burgundy tie. I was expecting fireworks. They hardly spoke. Both were so shy.
When Red and his wife Phyllis, whom he always called "my bride," got up to leave, Billie Jean stood, too. Looking down at her hand-made boots, she said in a little girl voice, "It was an honor to meet you, Mr. Smith. I've admired you for a very long time."
Red was uncomfortable, as he usually was among gushing admirers. But he didn't squirm when he won the Pulitzer in 1976. "You get awful tired," he said, "scuffing your feet in the dust and saying, 'Aw, gee.' "
Billie Jean's magazine folded, and I became a free-lancer for awhile. One day at Yankee Stadium, I needed to get into the locker room. Women still were not allowed. Red, who called himself a boy reporter and thought girls had no business in there, said, "Don't worry, I'll do your leg work for you."
Twenty minutes later, he returned with five pages of notes. He never took any for himself. He always said just listen for the key words of a sentence, for the way people talk. Red wrote the way he talked. Just listening to him, and the voice he called the croak of an old crock, you learned about words, about decency, about modesty.
Their first day in the Philippines for the Thrilla in Manila, Dave Anderson, Red's colleague at the Times, found him wandering about the corridors of their hotel. Red was distraught and, opening the door to his palatial suite, he showed Anderson why. "He looks at me," Anderson said, a few years back, "and says, 'You know, Dave, I really hate this dean treatment.' "
One night during the World Series in October, the interview room at Yankee Stadium caught fire. This was enough to make Red rejoice. He did a lot of rejoicing. He was unambivalent about what he did and the people he did it with. That was why he was still there at 2 a.m., although he did not have to be, getting ready to catch a charter flight to Los Angeles with the other reporters. There's no dean treatment on a red-eye.
The last time we spoke, they were taking some pictures for the jacket of a new book, a collection of obituaries he had written about his friends. "A bunch of stiffs," he said.
"I'm awfully tired of writing obituaries for people I care about," he said a few years ago. "But I know what the alternative is and I don't care for that, either."
I don't care much for writing this. But I know what Red would say. It's fine, Jane, but it's too long.


Tenshi Seafood, a seafood processing company, was fined $40,000 in Richmond Provincial Court for trapping undersized crabs.
The Richmond seafood company pleaded guilty to the offence after being caught by fishery officers from the Department of Fisheries and Oceans Canada (DFO) in January 2023.
“The harvest of undersized crab is the largest threat to conservation of Dungeness crab stocks, which is a traditional food source for Indigenous communities and core to the livelihood of commercial crab harvesters,” DFO said in a statement.
“Dungeness crab is also a significant economic benefit to coastal communities; specifically, the recreational fishery industry and tourism.”
This is the second fine for Tenshi Seafood.
In 2020, Richmond Provincial Court Judge Bonnie Craig found the company guilty of violating Canada’s Fisheries Act and ordered them to pay a fine of $75,000 and to hand over a list of its customers from the past two years to the Department of Fisheries and Ocean (DFO).
The company was also ordered to publish a letter addressing all its customers of the offences the company was found guilty of.
Tenshi’s co-owner Dishi Liu was also ordered in 2020 to pay a fine of $25,000 and Thuong Nguyen, master of the commercial fishing vessel Dream Chaser, was fined $10,000 for obstructing a fishery officer.
To disrupt and prevent illegal activity, the DFO is asking the public for information on activities of this nature or any activities in contravention of the Fisheries Act and regulations.
Anyone with information can call DFO Pacific region’s toll-free violation reporting line at 1-800-465-4336, or email the details to email@example.com.
- with files from Valerie Leung


text:
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Ozone Pure Water’s extensive variety enables our team to offer residential, commercial, and even industrial ozone water treatment around Ellicott City, MD. Our water purification systems can accomodate any budget with units that range from whole house purification to specific point-of-use purification directly from the faucet. Our systems are simple to install and include all of the parts you need to begin enjoying your purified water now. Ozone Pure Water’s expansive selection, you can always find the equipment you’re looking for and have it quick.|Never worry about replacement equipment again with our extensive selection and quick shipping.}The Ozone Pure Water Ellicott City, MD ozone water treatment professionals can help you decide which part is best for your system by giving you product details like lifespan, performance, and makeup. The Ozone Pure Water purification professionals can advise you on any service or product you’re looking for, from replacement filters to new system installations.
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domain: chemistry


A second pedophille walked free from Preah Sihanouk Provincial Prison on Tuesday after receiving a royal pardon, its director said yesterday.
German national Alexander Watrin – who had been serving a seven-year sentence for sex crimes against four boys under the age of 15 – was freed on the same day as Russian pedophille Alexander Trofimov, prison director Pich Veasna said yesterday.
“He served nearly six years of his seven years sentence, so he also walked free from prison like Trofimov,” Pich Veasna told the Post. He said he did not know where either had gone and declined to comment when asked what effect their early release would have on their victims.
Both pedophilles had targeted children from impoverished families living in and around the coastal resort of Sihanoukville. Combined, they were convicted of sex crimes against 21 children, though child protection officers who investigated both men said it was likely the number of victims was higher.
Trofimov had been visited in prison by two girls who had accused him of sex crimes but later dropped the charges, said Seila Samleang, country director of NGO Action Pour Les Enfants. One was 12 and the other 13 at the time they filed police complaints against Trofimov, he said. APLE and about 10 other NGOs have contacted the interior ministry to ask that the two men be deported and are seeking to have them charged in their own countries. They have also contacted Interpol, as Trofimov faces numerous allegations of raping girls as young as 9 in Russia.
“Our first concern is that he may approach his former victims,” Seila Samleang said, adding that they were also concerned Trofimov and Watrin would seek new victims.
Opposition MP and social activist Mu Sochua said she felt sickened when she heard of Trofimov’s release.
“I was sick to my stomach. I felt totally, totally exhausted. We have a moral obligation to protect our children from such characters. We have a moral obligation to expel [the pair],” she said.
“For all of those working for social justice, this hurts our morale, but it does not alter our conscience. It is not too late for Cambodia,” she said, reiterating that the government had a “moral obligation” to deport the two convicted pedophilles. “Otherwise, they are saying money can buy anything here, even our children.”
Watrin had been sentenced to 10 years in prison in October 2006, but the Court of Appeal reduced this by three years in 2009. Sochua pointed to the reduced sentences both men had received as dangerous signals. “The groups that protect children do such a great job, and there are so many police officers who work so hard to help, but the courts are corrupt. Freedom can be bought,” she said.
Trofimov had been convicted of sex crimes against 17 underage girls while he was chairman of Koh Pous (Snake Island) Investment Company.
Interior ministry spokesman Khieu Sopheak said he could not comment because Trofimov had received a Royal Pardon, then hung up the phone.


text:
Katpadi Junction railway station
|Express train and passenger train station|
View of Platforms 3 & 4
|Location||Vellore - Chittoor High Road, katpadi , Vellore city , Tamil Nadu|
|Elevation||213 metres (699 ft)|
|Owned by||Indian Railways|
|Operated by||Southern Railway zone|
|Line(s)||Chennai Central-Bangalore City line|
Gudur-Katpadi Branch line
Villupuram-Katpadi Branch line
|Fare zone||Indian Railways|
The station is served by five platforms. Platforms 4 and 5 primarily serve trains bound from and to Vellore Cantonment, south Tamil Nadu, and Andhra Pradesh.
Platforms 1 to 3 primarily serve trains bound to Chennai, Bangalore, Howrah,New delhi,Mumbai,Kanyakumari,Coimbatore and Kerala.
Nearly 245 trains halts at this Junction. Major commuters to Katpadi Railway station are people who travel to Vellore Golden Temple, CMC Hospital and VIT University. On an average it serves approximately 18,000 passengers daily, with 11 originating trains and 67 passing.

domain: geography


text:
As Governor Newsom unveiled the May Revision, there was much attention given to the size of California’s $97.5 billion “surplus.”
But it’s important to note that the functional “surplus” is roughly half of that since many dollars are legally owed to education spending under Proposition 98 and to reserves and debt payments under Proposition 2. Still, $49 billion in discretionary revenues is a big deal and presents a significant opportunity for California to help those most in need.
It’s also important to note that California’s healthy revenue — during a period of illness and economic instability for many families — is a symptom of growing income and wealth inequality. Despite a tumultuous two years of COVID-19, California’s wealthy and corporations continue to thrive.
Yet, for many Californians working isn’t enough. A job doesn’t necessarily mean you can pay the rent or put food on the table. And the 2022-23 state budget is a once-in-a-lifetime opportunity for state leaders to come together and provide significant relief for Californians who are most struggling to make ends meet. Prioritizing the urgent needs of Californians with low incomes isn’t just a fiscally prudent step — it’s the morally right thing to do.
Here are five ways state leaders can help Californians right now
1. Provide Meaningful Cash Relief to Californians with Low Incomes
Helping Californians with low incomes — who we know are struggling to make ends meet — should be a top priority for policymakers. California has the tools to provide relief that is thoughtful, targeted, meaningful, and efficient. This means building on the success of the Golden State Stimulus and targeting relief by income — not car ownership, as proposed in the governor’s ill-advised vehicle-based rebates plan.
State leaders can also provide targeted relief by building on existing ways to help Californians with the lowest incomes. This can be accomplished by strengthening the California Earned Income Tax Credit (CalEITC), expanding the Young Child Tax Credit, and increasing critical CalWORKs grants that keep families out of deep poverty.
2. Ensure Public Supports Include Undocumented Californians
Our state’s public support must be inclusive to all Californians regardless of immigration status. State leaders can better support the health and well-being of Californians who are undocumented by expanding food assistance programs to include eligible Californians of all ages. This is a necessary step to truly dismantle racist and xenophobic barriers and address persistent gaps in aid.
And while the governor’s proposal would expand Medi-Cal eligibility to undocumented immigrants ages 26 to 49 starting in 2024, policymakers can take steps to move up the implementation to increase access to comprehensive health care for people amid the ongoing pandemic.
3. Support Unhoused Individuals & Seriously Invest in Affordable Housing
California’s homelessness and housing affordability crises need to be met with the same urgency families and individuals feel when they’re at risk of losing their home or can’t pay rent, and this budget presents an opportunity for policymakers to help Californians get care and secure a safe place to call home.
The governor’s CARE Court proposal fails to follow a “housing first” approach, a key flaw. State leaders should consider instead allocating the funds to existing housing and behavioral health supports. Policymakers should also use the state’s unprecedented resources to significantly boost investments in affordable housing.
The governor’s May Revision Explained
Join us on May 20 as our Budget Center experts explore what the governor’s budget proposals mean for Californians with low incomes who we know are most struggling to make ends meet.
4. Help California Workers Access Paid Family Leave & State Disability Insurance
Helping California workers actually use paid leave should be an obvious step for California leaders. Yet, the updated spending proposal does not include a plan to increase payment rates — keeping these benefits out of reach for many workers. This move would most harm workers with low wages who are disproportionately women, Black, and Latinx Californians.
Policymakers should increase paid family leave and state disability insurance payment rates to allow more Californians to take time away from work to care for a new child, a family member, or their health.
5. Manage the Gann Limit for Now — and Move Toward Reform or Repeal in 2024
The Gann Limit is a decades-old spending limit that significantly constrains California’s ability to use revenues that exceed the arbitrary spending cap. While there’s no question that policymakers can keep spending under the Gann Limit this year, this is not a sustainable way to govern.
Unless the Gann Limit is repealed or significantly reformed, the state will face spending cuts to essential services, and California and its people will be kept from building a better and more equitable future. State leaders and the electorate must work together to significantly reform or repeal the spending cap no later than 2024 in order to avoid untenable budget choices.
These are just some steps policymakers can take to more equitably structure the 2022-23 state budget to provide much-needed relief to Californians who are most struggling to make ends meet. To learn more about the progress and missed opportunities in the governor’s May Revision, see the Budget Center’s comprehensive First Look analysis.

domain: finance


text:
Sermon preached at St. John the Baptist, West Seattle, November 26, 2014. Available in audio under “Sermons” above.
Tomorrow, most of us, will sit down and give thanks.
That wonderful information online resource Wikipedia says his of Thanksgiving, In the United States, the modern Thanksgiving holiday tradition is commonly, but not universally, traced to a poorly documented 1621 celebration at Plymouth in present-day Massachusetts. The event that Americans commonly call the “First Thanksgiving” was celebrated by the Pilgrims, in that year after their first harvest in what we Europeans called the “New World”, which said a lot about their feeling and regard for those that had already been here for centuries.
That first Thanksgiving was celebrated because the Europeans wanted to give their thanks for what the Native Americans did to help them. It is said this feast lasted three days, and it was attended by 90 Native Americans(as accounted by attendee Edward Winslow) The New England colonists were accustomed to regularly celebrating “thanksgivings”-days of prayer thanking God for blessings such as military victory or the end of a drought. It was most often a “happy” time.
After our recently completed Diocesan convention, as a group was telling me how much they enjoyed it, and saying it was one of our best conventions, one person opined that we were just “too happy.” I am always taken aback by such remarks, because I often wonder if there can be such a thing, as being “too happy. ”
Of course, I am pretty sure I knew what she meant. We get together and are simply glad to get through our work, without taking up some of the more difficult issues before us, as if all is well with the world, when we all know it’s not. I truly get that.
I explained that I agreed with that but found parliamentary procedure, which is not biblical or given to us by Jesus, to be a most difficult way for us Christians to talk about the hard issues, that it seems to lead toward winners and losers, and often not to any real resolution. Of course, she got that.
That said, I think I am going to make her happy, now, if no one else, by perhaps not being so “happy.” Last year in my Christmas Eve Sermon I tried to be light, and fun. One man said, as he left the Cathedral, “I am disappointed in you, this is not a night to have too much fun.” I assured him that the first gift he would get for Christmas was the promise that I would not be preaching next year. And I can probably offer you the same even before I finish this one.
So, I get it, these days especially are always a balance. Most people would prefer not to even have a sermon, so my apologies to those of you in that camp out there. But for those that can at least tolerate one, on these days especially, we want lightness, joy, happiness, and you are probably not going to get a lot of that in this one.
While most of us plan now to sit down at table with friends and family, and gorge ourselves on a feast tomorrow, our world is hurting. While we take our break and fill ourselves, these problems will not cease.
It is really the case every year, but this year some things are really fresh. School shootings, very close to home, which have been devastating to the Tulalip tribe, to the people of Marysville, to the perceived innocence and safety of school and of childhood. Those families will grieve tomorrow.
The entire Ferguson issue, which is only a symptom of much larger ones for us, will be still swirling in the air while we feast.
We have a race problem in our country. Ferguson is any town and everywhere. All over, but especially in the Pacific Northwest, we live in an illusion that we have figured this all out. Racism is something that happens somewhere else, not here. In our very city we see it daily, if we care to look. Racial profiling, inequalities in our schools, the whole Jon Greenberg issue, a teacher at my son’s School, the Center School, who taught and challenged on this subject, a course that was highly acclaimed by students and faculty alike, not only ended by complaint of one white family who said it made them feel “uncomfortable”, but resulted in his being reassigned by the school district who would rather sweep it away, than confront it. The discomfort of the black person, or any person of color, on a daily basis quickly dismissed or forgotten.
We cannot blame the School system truly, since this was barely noticed by the citizenry here either, and I might add by very few people of faith. It is what we all would prefer to do.
It is easier and happier.
It was only after much soul-searching, and a lot of African-American mentors and people who truly loved me, by challenging me and hanging in there with me, that I was able to see that, being a white male in this country, and raised in the South no less, I am a racist.
I believe I am now in recovery. I call myself a recovering racist. Like an alcoholic, one has to admit they are sick before we can heal. This country, and many of the whites in it, have yet to reach that place, and until we do, our race problem will continue. Our church does not get to escape this neglect. It is just as prevalent in our system. Some of you are squirming and already composing your later email to me right now. None of this will cease during our feast tomorrow, because it never does for people of color in this society.
The immigration crisis, which is also related to race. It will not go on recess tomorrow. I will not soon forget the nun telling me on the Mexico border in Arizona, to think about the over 2000 Mexicans that had died in the desert attempting to cross the border that year, and asking us if we think the response would be any different if those same 2000 had been Irish? That will all be going on tomorrow. Some will die there tomorrow.
Soldiers will die in the wars we fight, some will come home. Some of those we will fail miserably at helping with the wounds they carry on our behalf.
Ebola taking untold lives “there,” while we seem to be able to cure it over here with the very healthcare so many people think they should earn, instead of have as a human right.
Isis, and gruesome senseless killings there.
Our world is hurting, and it will all go on while we feast.
Most suffering in all these battles will not get the luxury of Thanksgiving.
But I think we should be thankful, and I believe and wish all could be happy. If we look at this Gospel tonight, of the lepers, and think of it as one of those surveys you hear on commercials, we would surmise that, what Jesus was trying to tell us is, 9 out of 10 people forget to turn and be thankful, even when their lives have been saved. Truly, most of us take for granted how many times that has happened.
Sometimes we forget the source. It is so easy to become immediately absorbed in the “happy. ”
We should sit down tomorrow and be thankful. I will, as I said, but I am going to do something tomorrow a bit differently and I ask you to consider it to. Don’t just bow your heads to pray, but first look at the table, look at it as an iconic history of all that has brought us to this day.
Remember the people, many of whom are what we would call “illegal” who most likely painstakingly worked to get that food to your table. Remember that the land it came from was first inhabited by a different nation, there were people here, it was not a wilderness. There were nations here. I am bold enough to claim I am descended from those “illegal immigrants.”
Remember those who are grieving, for whatever reason, for the loss of loved ones who they had hoped would be there, for the loss of the feeling of belonging in this country even though they fought for it, for feeling even though they are at home, they have no home.
Pray for a better tomorrow, where all are happy, fill yourself with the bounty of food and love that will surround you, and then, get up from that table and put those prayers into practice. Perhaps you could ask everyone at your table to think of one thing they are not only thankful for in their lives, but what they intend to do to make others thankful, to give others something to live for, to make others happy? How will they heal the lepers this next year?
I guess that woman was right, there is such a thing as being too happy, if it blinds us completely to those who are thousands of miles from it or leaves us in the illusion that everyone lives this way.
That is the reality from whence thanksgiving comes, knowing that is not true, and so it is not an end, but a call, so that next year, our world, in whatever way you and I can affect it, is more, in a word, happy.

domain: sociology


text:
As a general rule do not feed your cat or dog from 7 the evening before the scheduled surgery. Your pet should be allowed access to water right up to surgery time.
Rabbits and other small herbivores should NOT be starved prior to surgery.
Your pet will always be checked in by a veterinarian on the morning of the scheduled surgery. Please discuss any concerns you have with the vet at this time. We feel this check up is vital so please bear with us and allow a little time in your schedule for it to happen.
Pre-operation Blood Testing
We offer pre-op blood testing and are very keen to do it. Obviously being aware of any trouble prior to an anaesthetic could be life-saving but in more mundane terms the earlier we discover any abnormalities the more we will be able to help in the long term. A pre-op blood test adds to your costs but could be invaluable. This is especially true in older animals but we have on occasions picked up illness even in youngsters at neutering age and it is gratifying to be able to help from such an early age.

domain: pet


text:
I reviewed Lolo’s Lowdown, Lauren’s blog with content dedicated to wrestling. There is a lot of passion in her blog and she has chosen a good tone in which she communicates to her audience with.
Without a doubt, the content within her blog posts reflect her passion about wrestling, and by reading through them, and it is her passion which motivates me to continue reading. However, the blog itself is visually lacking. Its cliche to say that one picture is worth a thousand words, but cliches are cliches for a reason, they’re overused, but true. Digital content, especially digital content which is so quickly absorbed and taken in, needs to be engaging with its audience, whether that is through interactions or visually. And that is one of the key aspects which I find the blog lacking in. This lack of visuals makes her blog seem bland. From a design perspective, there is nothing which retains my attention, nothing that visually makes me appeal and want to come back to the blog.
And this is also mainly due to a lack of digital presence. As a content creator, she is missing that key identifier which makes her online self transparent. As design students, we are taught about developing an ethos which communicates who you are and how you are, and this directly translates to blogs and maintaining an audience. Originality is risky, but with such a unique topic, it’s okay to be risky. This allows you to be visually explicit about who you are and creates an even more authentic experience for your audience.
Asides from this, I do like the blog structure and I find it very intuitive to use. There are subtle affordances to the blog’s design which allows the user to recognize interactions, such as underlining and adding hover effects over links. However, I would argue that these affordances are too subtle, and could be done more interestingly, which would help with the visual identity of her blog.
Another element of her blog I like is the structure of it. Posts are easy to find and filter between, which assists with navigational flow and minimizes user resistance.

domain: artistic


text:
Hey. I've noticed that when I tongue, especially on higher notes, I can hear a little 'ta' sound of my tongue as it's striking and leaving the reed. This is quite annoying, especially when I'm playing softly. Any tips?
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I do have a instructor, but unfortunately he is away overseas for 1 month.I was hoping that one of the experts would weigh in. I do have a question before I make suggestions, as I can not listen to the sound myself. Is there an instructor that you could work with? Helping you from afar is very challenging. There is nothing like a personal coach to make solid and fast improvement.
Thanks for the reply, after some testing with my friends, it turns out that what I'm hearing is insignificant to the ears of my audience.One thing to keep in mind is what you are hearing might not be audible to those who are listening. Things like breath noise, key noise and the like are very audible to you, but they are subject to the same inverse square law as is all noise - sound levels drop off rapidly over distance.
Of all of the clarinet, flute, saxophone and oboe music that I have listened to, even in recordings that were miked close and tight, I have never heard any of these noises that are so obvious to me when I am playing. Over the years, I've learned to just stop worrying.
None of this applies to bassoon playing, of course. The long "clapper-style" keys on the long joint and bell are noisy as hell, and key noise shows up on many recordings of the faggot variety. I have one of a bassoon quintet over in Germany, and they play a lot of very fast stuff (like Czardas, arranged for solo violin and the five bassoons playing a very clever Wagner-themed accompaniment). The key noise on that one sounds like a platoon of excellent touch typists, all working like mad on old Remington upright typewriters.
And, this brings me to a new problem. The latest version of the Selmer bass clarinet has one or two "clapper style" keys on the lower joint. Another potential noise source...shame on you, Selmer - what were you thinking?
This is a good exercise for me, I have been doing it at the start of practice everyday, and it works well on perfecting my articulation.I am primarily a saxophonist who doubles on clarinet who has the same challenge articulating notes in the high register to make them sound good. More often than not I will use a breath entrance on the note (I hate the word "attack"). Hopefully one of the advanced clarinetists on the forum will weigh in with some advice.
One of the techniques I use with beginning players to teach tonguing is to have them blow an airstream into the mouthpiece below the level that makes the reed vibrate and to touch the tip of the reed with the portion of the tongue just behind the tip. The tst, tst, tst, tst, sound that is made lets me know they have the placement and movement of the tongue correct and then I have them increase the air volume while doing the same tongue movement to produce a full tone.
You might try this exercise making the tst, tst, tst, sound as soft and light as possible to see if that helps. It is also important to remember that tonguing involves the tongue pulling away from the reed (like spitting a piece of lint off the tip of your tongue) rather than going up an hitting the reed. Hope this helps. I have a lot to learn about this aspect of clarinet paying myself.

domain: hobby


Aeilts, Maroons top rivals for regional crown
MAHOMET — The white stitching on the back of the maroon baseball hats Central players and coaches wear spells out one word.
With every at-bat, every defensive play and every pitch, the Maroons did just that Saturday afternoon.
Their reward? A nail-biting 2-1 victory against rival Centennial to win the Class 3A Mahomet-Seymour Regional championship game and give the program its first postseason hardware in 21 years.
“It’s just an awesome feeling,” said Alec Altmyer, Central’s pitcher who recorded the win. “I’ve never felt like this before. It’s incredible.”
Altmyer wasn’t on the mound for the final out but had to anxiously watch from the third-base dugout as Centennial mounted a seventh-inning rally.
The Chargers (21-15) put runners on first and second base with one out against Central reliever Phillip Swartz. Then Swartz induced a groundball from Centennial’s Jeff Lindgren, whose two-hopper found its way into third baseman Joe Aeilts’ glove.
Aeilts stepped on third and then threw across the diamond to first baseman Matt Brown. It wasn’t the prettiest throw Aeilts made all season — to say the least — but Brown did a superb job, crouching down to pluck the ball out of the dirt to secure the win and set off a spontaneous celebration around home plate by the Maroons (35-2).
“I was ready for the ball to come to me,” Aeilts said. “I envisioned it in my mind if it did. I knew I’d have to step on the bag and beat it out over to first. It wasn’t a great throw, but Matt made a great scoop for me.”
Yes, he did. For the second time this postseason.
“In the first regional game, Matt had another scoop for me on one that bounced,” Aeilts said, “so he really got a good feel for this field and came up big.”
Central’s infielders will now get to adapt to the turf field at Springfield Sacred Heart-Griffin at 4:30 p.m. Wednesday in a sectional semifinal game against the host Cyclones (34-3). Having the record the Maroons have at this juncture in the season, along with a regional championship, wasn’t exactly on the minds of area baseball fans a few months ago.
“It feels great,” Aeilts said. “All season, with all the accomplishments we’ve had, we’ve had this one circled. We were underestimated going into the season, so it’s great to prove some people wrong.”
Aeilts came through with his bat, too, on Saturday. The sophomore laced a one-out single into center field in the bottom of the third inning to score Jake Snider — who had a double, triple and was hit by a pitch in his three plate appearances against the Chargers — and stake Central to a 2-1 lead.
“I just knew I had to get the guy in any way I could,” Aeilts said. “I wasn’t trying to do too much. I was just trying to hit it hard if I got a good pitch. I got one and just hit it up the middle.”
It was a lead the Maroons never relinquished. The right-handed arms of Altmyer (9-2), who lasted five innings and only gave up three hits to go along with four strikeouts and two walks, and Swartz, who gave up one hit in two innings of relief to earn his third save of the season, stifled Centennial after the third inning. The Chargers finished with four hits, and Quin Nottingham (2 for 3, RBI) had half of them.
“Altmyer and Swartz are good pitchers,” Centennial coach Ryan Remole said. “They’ve been raised on the philosophy that good pitching beats good hitting. Their pitchers did a great job.”
So did Centennial’s Anthony Martin. The right-hander (5-4) scattered six hits and worked out of several jams to give the Chargers a chance at the end.
“Hats off to Centennial,” Central coach John Staab said. “I coached a number of those kids in junior high, so I know the type of kids they are. Anthony Martin battled and battled all day.”
The win was especially sweet for Staab. In his 13th season, Staab stood off to the side of home plate after the game while his players celebrated with the regional championship plaque, gathering his emotions. Four previous trips to regional championship games had produced empty results for Staab. Saturday’s victory was one he savored, even as he deflected credit toward his players.
“It doesn’t get any better than this,” Staab said. “These kids have battled all year, and they’ve bought in to what we’re trying to do mentally. It’s their regional. I was just a spectator. I’m so proud of them.”


text:
After early kickoff return TD, nothing doing for Huss
CHARLOTTE — Hunter Huss could only stay with Vance for one quarter.
After that the Cougars scored almost at will and cruised to a 53-7 non-conference win over the Huskies Friday night at Cougar Stadium.
But despite the lopsided loss, first-year Huss coach Jamar McKoy was optimistic.
“I think they learned they can play with any team tonight,” McKoy said of his young squad. “We played with them in the first quarter, but fell apart after that. Our defense was on the field for 43 plays in the first half and that’s too long.”
Huss fell behind early as Miles Corpening returned the opening kickoff 85 yards for a touchdown. The Huskies answered, though, as Hafees Adams took the Vance kick 89 yards to the house to knot the score at 7-7.
Vance put together a sustained drive on its first full possession, traveling 68 yards in 11 plays with quarterback Omar Baker tossing a 12-yard touchdown pass to Myles Dorn for the score. The Huskies were stopped twice and they stopped the Cougars once as the first quarter ended at 14-7, but it was all Vance from that point.
“Our offense has got to learn to get the ball into the end zone,” McKoy said. “We made too many mistakes. Once we got behind, I think we just gave up.”
Vance exploded offensively in the second quarter as Baker tossed a touchdown pass to Jonathan Ifedi, Donnavan Spencer scored on a 16-yard run, and Baker found the end zone on the ground from the one. Baker tossed touchdown passes of 34 and four yards to Dorn in the third quarter before his back-up, Laquell Thames came in and zipped a 38-yard score to Jonathan Ifedi.
“There’s a lot of opportunity to build character here,” McKoy said. “After the loss to Kings Mountain, every player was there the next morning at 8:30 and I think they will be there (Saturday) because they are eager to learn.”
McKoy is also being realistic about the adjustments his team is having to make.
“It takes time to learn a new system,” McKoy said. “We’ve put in a new offense and a new defense and that takes time. We’ll show them the pluses and try to let them see what execution will do. After that, it’s up to them.”
The Huskies netted very little on the ground, but had a solid air attach as quarterback Andrew Jordan completed 14 of 15 passes for 168 yards. Sophomore wide receiver Antwanez Barnett was his favorite target, hauling in six passes for 75 yards.
Hunter Huss is at home next week to host Bessemer City.

domain: sports