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Neurodegenerative disease

A neurodegenerative disease is caused by the progressive loss of neurons, in the process known as neurodegeneration. Neuronal damage may also ultimately result in their death. Neurodegenerative diseases include amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease, Alzheimer's disease, Huntington's disease, multiple system atrophy, tauopathies, and prion diseases. Neurodegeneration can be found in the brain at many different levels of neuronal circuitry, ranging from molecular to systemic. Because there is no known way to reverse the progressive degeneration of neurons, these diseases are considered to be incurable; however research has shown that the two major contributing factors to neurodegeneration are oxidative stress and inflammation. Biomedical research has revealed many similarities between these diseases at the subcellular level, including atypical protein assemblies (like proteinopathy) and induced cell death. These similarities suggest that therapeutic advances against one neurodegenerative disease might ameliorate other diseases as well.

Within neurodegenerative diseases, it is estimated that 55 million people worldwide had dementia in 2019, and that by 2050 this figure will increase to 139 million people.

Specific disorders
The consequences of neurodegeneration can vary widely depending on the specific region affected, ranging from issues related to movement to the development of dementia.

Alzheimer's disease

Alzheimer's disease (AD) is a chronic neurodegenerative disease that results in the loss of neurons and synapses in the cerebral cortex and certain subcortical structures, resulting in gross atrophy of the temporal lobe, parietal lobe, and parts of the frontal cortex and cingulate gyrus. It is the most common neurodegenerative disease. Even with billions of dollars being used to find a treatment for Alzheimer's disease, no effective treatments have been found. Within clinical trials stable and effective AD therapeutic strategies have a 99.5% failure rate. Reasons for this failure rate include inappropriate drug doses, invalid target and participant selection, and inadequate knowledge of pathophysiology of AD. Currently, diagnoses of Alzheimer's is subpar, and better methods need to be utilized for various aspects of clinical diagnoses. Alzheimer's has a 20% misdiagnosis rate.

AD pathology is primarily characterized by the presence of amyloid plaques and neurofibrillary tangles. Plaques are made up of small peptides, typically 39–43 amino acids in length, called amyloid beta (also written as A-beta or Aβ). Amyloid beta is a fragment from a larger protein called amyloid precursor protein (APP), a transmembrane protein that penetrates through the neuron's membrane. APP appears to play roles in normal neuron growth, survival and post-injury repair. APP is cleaved into smaller fragments by enzymes such as gamma secretase and beta secretase. One of these fragments gives rise to fibrils of amyloid beta which can self-assemble into the dense extracellular amyloid plaques.

Parkinson's disease
Parkinson's disease (PD) is the second most common neurodegenerative disorder. It typically manifests as bradykinesia, rigidity, resting tremor and posture instability. The crude prevalence rate of PD has been reported to range from 15 per 100,000 to 12,500 per 100,000, and the incidence of PD from 15 per 100,000 to 328 per 100,000, with the disease being less common in Asian countries.

PD is primarily characterized by death of dopaminergic neurons in the substantia nigra, a region of the midbrain. The cause of this selective cell death is unknown. Notably, alpha-synuclein-ubiquitin complexes and aggregates are observed to accumulate in Lewy bodies within affected neurons. It is thought that defects in protein transport machinery and regulation, such as RAB1, may play a role in this disease mechanism. Impaired axonal transport of alpha-synuclein may also lead to its accumulation in Lewy bodies. Experiments have revealed reduced transport rates of both wild-type and two familial Parkinson's disease-associated mutant alpha-synucleins through axons of cultured neurons. Membrane damage by alpha-synuclein could be another Parkinson's disease mechanism.

The main known risk factor is age. Mutations in genes such as α-synuclein (SNCA), leucine-rich repeat kinase 2 (LRRK2), glucocerebrosidase (GBA), and tau protein (MAPT) can also cause hereditary PD or increase PD risk. While PD is the second most common neurodegenerative disorder, problems with diagnoses still persist. Problems with the sense of smell is a widespread symptom of Parkinson's disease (PD), however, some neurologists question its efficacy. This assessment method is a source of controversy among medical professionals. The gut microbiome might play a role in the diagnosis of PD, and research suggests various ways that could revolutionize the future of PD treatment.

Huntington's disease
Huntington's disease (HD) is a rare autosomal dominant neurodegenerative disorder caused by mutations in the huntingtin gene (HTT). HD is characterized by loss of medium spiny neurons and astrogliosis. The first brain region to be substantially affected is the striatum, followed by degeneration of the frontal and temporal cortices. The striatum's subthalamic nuclei send control signals to the globus pallidus, which initiates and modulates motion. The weaker signals from subthalamic nuclei thus cause reduced initiation and modulation of movement, resulting in the characteristic movements of the disorder, notably chorea. Huntington's disease presents itself later in life even though the proteins that cause the disease works towards manifestation from their early stages in the humans affected by the proteins. Along with being a neurodegenerative disorder, HD has links to problems with neurodevelopment.

HD is caused by polyglutamine tract expansion in the huntingtin gene, resulting in the mutant huntingtin. Aggregates of mutant huntingtin form as inclusion bodies in neurons, and may be directly toxic. Additionally, they may damage molecular motors and microtubules to interfere with normal axonal transport, leading to impaired transport of important cargoes such as BDNF. Huntington's disease currently has no effective treatments that would modify the disease.

Multiple sclerosis
Multiple sclerosis (MS) is a chronic debilitating demyelinating disease of the central nervous system, caused by an autoimmune attack resulting in the progressive loss of myelin sheath on neuronal axons. The resultant decrease in the speed of signal transduction leads to a loss of functionality that includes both cognitive and motor impairment depending on the location of the lesion. The progression of MS occurs due to episodes of increasing inflammation, which is proposed to be due to the release of antigens such as myelin oligodendrocyte glycoprotein, myelin basic protein, and proteolipid protein, causing an autoimmune response. This sets off a cascade of signaling molecules that result in T cells, B cells, and macrophages to cross the blood-brain barrier and attack myelin on neuronal axons leading to inflammation. Further release of antigens drives subsequent degeneration causing increased inflammation. Multiple sclerosis presents itself as a spectrum based on the degree of inflammation, a majority of patients experience early relapsing and remitting episodes of neuronal deterioration following a period of recovery. Some of these individuals may transition to a more linear progression of the disease, while about 15% of others begin with a progressive course on the onset of multiple sclerosis. The inflammatory response contributes to the loss of the grey matter, and as a result current literature devotes itself to combatting the auto-inflammatory aspect of the disease. While there are several proposed causal links between EBV and the HLA-DRB1*15:01 allele to the onset of MS – they may contribute to the degree of autoimmune attack and the resultant inflammation – they do not determine the onset of MS.

Amyotrophic lateral sclerosis
Amyotrophic lateral sclerosis (ALS), commonly referred to Lou Gehrig's disease, is a rare neurodegenerative disorder characterized by the gradual loss of both upper motor neurons (UMNs) and lower motor neurons (LMNs). Although initial symptoms may vary, most patients develop skeletal muscle weakness that progresses to involve the entire body. The precise etiology of ALS remains unknown. In 1993, missense mutations in the gene encoding the antioxidant enzyme superoxide dismutase 1 (SOD1) were discovered in a subsets of patients with familial ALS. More recently, TAR DNA-binding protein 43 (TDP-43) and Fused in Sarcoma (FUS) protein aggregates have been implicated in some cases of the disease, and a mutation in chromosome 9 (C9orf72) is thought to be the most common known cause of sporadic ALS. Early diagnosis of ALS is harder than with other neurodegenerative diseases as there are no highly effective means of determining its early onset. Currently, there is research being done regarding the diagnosis of ALS through upper motor neuron tests. The Penn Upper Motor Neuron Score (PUMNS) consists of 28 criteria with a score range of 0–32. A higher score indicates a higher level of burden present on the upper motor neurons. The PUMNS has proven quite effective in determining the burden that exists on upper motor neurons in affected patients.

Independent research provided in vitro evidence that the primary cellular sites where SOD1 mutations act are located on astrocytes. Astrocytes then cause the toxic effects on the motor neurons. The specific mechanism of toxicity still needs to be investigated, but the findings are significant because they implicate cells other than neuron cells in neurodegeneration.

Batten disease
Batten disease is a rare and fatal recessive neurodegenerative disorder that begins in childhood. Batten disease is the common name for a group of lysosomal storage disorders known as neuronal ceroid lipofuscinoses (NCLs) – each caused by a specific gene mutation, of which there are thirteen. Since Batten disease is quite rare, its worldwide prevalence is about 1 in every 100,000 live births. In North America, NCL3 disease (juvenile NCL) typically manifests between the ages of 4 and 7. Batten disease is characterized by motor impairment, epilepsy, dementia, vision loss, and shortened lifespan. A loss of vision is common first sign of Batten disease. Loss of vision is typically preceded by cognitive and behavioral changes, seizures, and loss of the ability to walk. It is common for people to establish cardiac arrhythmias and difficulties eating food as the disease progresses. Batten disease diagnosis depends on a conflation of many criteria: clinical signs and symptoms, evaluations of the eye, electroencephalograms (EEG), and brain magnetic resonance imaging (MRI) results. The diagnosis provided by these results are corroborated by genetic and biochemical testing. No effective treatments were available to prevent the disease from being widespread before the past few years. In recent years, more models have been created to expedite the research process for methods to treat Batten disease.

Creutzfeldt–Jakob disease
Creutzfeldt–Jakob disease (CJD) is a prion disease that is characterized by rapidly progressive dementia. Misfolded proteins called prions aggregate in brain tissue leading to nerve cell death. Variant Creutzfeldt–Jakob disease (vCJD) is the infectious form that comes from the meat of a cow that was infected with bovine spongiform encephalopathy, also called mad cow disease.

Aging
The greatest risk factor for neurodegenerative diseases is aging. Mitochondrial DNA mutations as well as oxidative stress both contribute to aging. Many of these diseases are late-onset, meaning there is some factor that changes as a person ages for each disease. One constant factor is that in each disease, neurons gradually lose function as the disease progresses with age. It has been proposed that DNA damage accumulation provides the underlying causative link between aging and neurodegenerative disease. About 20–40% of healthy people between 60 and 78 years old experience discernable decrements in cognitive performance in several domains including working, spatial, and episodic memory, and processing speed.

Infections
A study using electronic health records indicates that 45 (with 22 of these being replicated with the UK Biobank) viral exposures can significantly elevate risks of neurodegenerative disease, including up to 15 years after infection.

Genetics
Many neurodegenerative diseases are caused by genetic mutations, most of which are located in completely unrelated genes. In many of the different diseases, the mutated gene has a common feature: a repeat of the CAG nucleotide triplet. CAG codes for the amino acid glutamine. A repeat of CAG results in a polyglutamine (polyQ) tract. Diseases associated with such mutations are known as trinucleotide repeat disorders.

Polyglutamine repeats typically cause dominant pathogenesis. Extra glutamine residues can acquire toxic properties through a variety of ways, including irregular protein folding and degradation pathways, altered subcellular localization, and abnormal interactions with other cellular proteins. PolyQ studies often use a variety of animal models because there is such a clearly defined trigger – repeat expansion. Extensive research has been done using the models of nematode (C. elegans), and fruit fly (Drosophila), mice, and non-human primates.

Nine inherited neurodegenerative diseases are caused by the expansion of the CAG trinucleotide and polyQ tract, including Huntington's disease and the spinocerebellar ataxias.

Epigenetics
The presence of epigenetic modifications for certain genes has been demonstrated in this type of pathology. An example is FKBP5 gene, which progressively increases its expression with age and has been related to Braak staging and increased tau pathology both in vitro and in mouse models of AD.

Protein misfolding
Several neurodegenerative diseases are classified as proteopathies as they are associated with the aggregation of misfolded proteins. Protein toxicity is one of the key mechanisms of many neurodegenrative diseases.
 * alpha-synuclein: can aggregate to form insoluble fibrils in pathological conditions characterized by Lewy bodies, such as Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. Alpha-synuclein is the primary structural component of Lewy body fibrils. In addition, an alpha-synuclein fragment, known as the non-Abeta component (NAC), is found in amyloid plaques in Alzheimer's disease.
 * tau: hyperphosphorylated tau protein is the main component of neurofibrillary tangles in Alzheimer's disease; tau fibrils are the main component of Pick bodies found in behavioral variant frontotemporal dementia.
 * amyloid beta: the major component of amyloid plaques in Alzheimer's disease.
 * prion: main component of prion diseases and transmissible spongiform encephalopathy.

Protein degradation pathways
Parkinson's disease and Huntington's disease are both late-onset and associated with the accumulation of intracellular toxic proteins. Diseases caused by the aggregation of proteins are known as proteopathies, and they are primarily caused by aggregates in the following structures:
 * cytosol, e.g. Parkinson's and Huntington's
 * nucleus, e.g. Spinocerebellar ataxia type 1 (SCA1)
 * endoplasmic reticulum (ER), (as seen with neuroserpin mutations that cause familial encephalopathy with neuroserpin inclusion bodies)
 * extracellularly excreted proteins, amyloid-beta in Alzheimer's disease

There are two main avenues eukaryotic cells use to remove troublesome proteins or organelles:
 * ubiquitin–proteasome: protein ubiquitin along with enzymes is key for the degradation of many proteins that cause proteopathies including polyQ expansions and alpha-synucleins. Research indicates proteasome enzymes may not be able to correctly cleave these irregular proteins, which could possibly result in a more toxic species. This is the primary route cells use to degrade proteins.
 * Decreased proteasome activity is consistent with models in which intracellular protein aggregates form. It is still unknown whether or not these aggregates are a cause or a result of neurodegeneration.
 * autophagy–lysosome pathways: a form of programmed cell death (PCD), this becomes the favorable route when a protein is aggregate-prone meaning it is a poor proteasome substrate. This can be split into two forms of autophagy: macroautophagy and chaperone-mediated autophagy (CMA).
 * macroautophagy is involved with nutrient recycling of macromolecules under conditions of starvation, certain apoptotic pathways, and if absent, leads to the formation of ubiquinated inclusions. Experiments in mice with neuronally confined macroautophagy-gene knockouts develop intraneuronal aggregates leading to neurodegeneration.
 * chaperone-mediated autophagy defects may also lead to neurodegeneration. Research has shown that mutant proteins bind to the CMA-pathway receptors on lysosomal membrane and in doing so block their own degradation as well as the degradation of other substrates.

Membrane damage
Damage to the membranes of organelles by monomeric or oligomeric proteins could also contribute to these diseases. Alpha-synuclein can damage membranes by inducing membrane curvature, and cause extensive tubulation and vesiculation when incubated with artificial phospholipid vesicles. [http://www.jbc.org/content/287/35/29301.long The tubes formed from these lipid vesicles consist of both micellar as well as bilayer tubes. Extensive induction of membrane curvature is deleterious to the cell and would eventually lead to cell death.] Apart from tubular structures, alpha-synuclein can also form lipoprotein nanoparticles similar to apolipoproteins.

Mitochondrial dysfunction
The most common form of cell death in neurodegeneration is through the intrinsic mitochondrial apoptotic pathway. This pathway controls the activation of caspase-9 by regulating the release of cytochrome c from the mitochondrial intermembrane space. Reactive oxygen species (ROS) are normal byproducts of mitochondrial respiratory chain activity. ROS concentration is mediated by mitochondrial antioxidants such as manganese superoxide dismutase (SOD2) and glutathione peroxidase. Over production of ROS (oxidative stress) is a central feature of all neurodegenerative disorders. In addition to the generation of ROS, mitochondria are also involved with life-sustaining functions including calcium homeostasis, PCD, mitochondrial fission and fusion, lipid concentration of the mitochondrial membranes, and the mitochondrial permeability transition. Mitochondrial disease leading to neurodegeneration is likely, at least on some level, to involve all of these functions.

There is strong evidence that mitochondrial dysfunction and oxidative stress play a causal role in neurodegenerative disease pathogenesis, including in four of the more well known diseases Alzheimer's, Parkinson's, Huntington's, and amyotrophic lateral sclerosis.

Neurons are particularly vulnerable to oxidative damage due to their strong metabolic activity associated with high transcription levels, high oxygen consumption, and weak antioxidant defense.

DNA damage
The brain metabolizes as much as a fifth of consumed oxygen, and reactive oxygen species produced by oxidative metabolism are a major source of DNA damage in the brain. Damage to a cell's DNA is particularly harmful because DNA is the blueprint for protein production and unlike other molecules it cannot simply be replaced by re-synthesis. The vulnerability of post-mitotic neurons to DNA damage (such as oxidative lesions or certain types of DNA strand breaks), coupled with a gradual decline in the activities of repair mechanisms, could lead to accumulation of DNA damage with age and contribute to brain aging and neurodegeneration. DNA single-strand breaks are common and are associated with the neurodegenerative disease ataxia-oculomotor apraxia. Increased oxidative DNA damage in the brain is associated with Alzheimer's disease and Parkinson's disease. Defective DNA repair has been linked to neurodegenerative disorders such as Alzheimer's disease, amyotrophic lateral sclerosis, ataxia telangiectasia, Cockayne syndrome, Parkinson's disease and xeroderma pigmentosum.

Axonal transport
Axonal swelling, and axonal spheroids have been observed in many different neurodegenerative diseases. This suggests that defective axons are not only present in diseased neurons, but also that they may cause certain pathological insult due to accumulation of organelles. Axonal transport can be disrupted by a variety of mechanisms including damage to: kinesin and cytoplasmic dynein, microtubules, cargoes, and mitochondria. When axonal transport is severely disrupted a degenerative pathway known as Wallerian-like degeneration is often triggered.

Programmed cell death
Programmed cell death (PCD) is death of a cell in any form, mediated by an intracellular program. This process can be activated in neurodegenerative diseases including Parkinson's disease, amytrophic lateral sclerosis, Alzheimer's disease and Huntington's disease. PCD observed in neurodegenerative diseases may be directly pathogenic; alternatively, PCD may occur in response to other injury or disease processes.

Apoptosis (type I)
Apoptosis is a form of programmed cell death in multicellular organisms. It is one of the main types of programmed cell death (PCD) and involves a series of biochemical events leading to a characteristic cell morphology and death.
 * Extrinsic apoptotic pathways: Occur when factors outside the cell activate cell surface death receptors (e.g., Fas) that result in the activation of caspases-8 or -10.
 * Intrinsic apoptotic pathways: Result from mitochondrial release of cytochrome c or endoplasmic reticulum malfunctions, each leading to the activation of caspase-9. The nucleus and Golgi apparatus are other organelles that have damage sensors, which can lead the cells down apoptotic pathways.

Caspases (cysteine-aspartic acid proteases) cleave at very specific amino acid residues. There are two types of caspases: initiators and effectors. Initiator caspases cleave inactive forms of effector caspases. This activates the effectors that in turn cleave other proteins resulting in apoptotic initiation.

Autophagic (type II)
Autophagy is a form of intracellular phagocytosis in which a cell actively consumes damaged organelles or misfolded proteins by encapsulating them into an autophagosome, which fuses with a lysosome to destroy the contents of the autophagosome. Because many neurodegenerative diseases show unusual protein aggregates, it is hypothesized that defects in autophagy could be a common mechanism of neurodegeneration.

Cytoplasmic (type III)
PCD can also occur via non-apoptotic processes, also known as Type III or cytoplasmic cell death. For example, type III PCD might be caused by trophotoxicity, or hyperactivation of trophic factor receptors. Cytotoxins that induce PCD can cause necrosis at low concentrations, or aponecrosis (combination of apoptosis and necrosis) at higher concentrations. It is still unclear exactly what combination of apoptosis, non-apoptosis, and necrosis causes different kinds of aponecrosis.

Transglutaminase
Transglutaminases are human enzymes ubiquitously present in the human body and in the brain in particular.

The main function of transglutaminases is bind proteins and peptides intra- and intermolecularly, by a type of covalent bonds termed isopeptide bonds, in a reaction termed transamidation or crosslinking.

Transglutaminase binding of these proteins and peptides make them clump together. The resulting structures are turned extremely resistant to chemical and mechanical disruption.

Most relevant human neurodegenerative diseases share the property of having abnormal structures made up of proteins and peptides.

Each of these neurodegenerative diseases have one (or several) specific main protein or peptide. In Alzheimer's disease, these are amyloid-beta and tau. In Parkinson's disease, it is alpha-synuclein. In Huntington's disease, it is huntingtin.

Transglutaminase substrates: Amyloid-beta, tau, alpha-synuclein and huntingtin have been proved to be substrates of transglutaminases in vitro or in vivo, that is, they can be bonded by trasglutaminases by covalent bonds to each other and potentially to any other transglutaminase substrate in the brain.

Transglutaminase augmented expression: It has been proved that in these neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, and Huntington's disease) the expression of the transglutaminase enzyme is increased.

Presence of isopeptide bonds in these structures: The presence of isopeptide bonds (the result of the transglutaminase reaction) have been detected in the abnormal structures that are characteristic of these neurodegenerative diseases.

Co-localization: Co-localization of transglutaminase mediated isopeptide bonds with these abnormal structures has been detected in the autopsy of brains of patients with these diseases.

Management
The process of neurodegeneration is not well understood, so the diseases that stem from it have, as yet, no cures.

Animal models in research
In the search for effective treatments (as opposed to palliative care), investigators employ animal models of disease to test potential therapeutic agents. Model organisms provide an inexpensive and relatively quick means to perform two main functions: target identification and target validation. Together, these help show the value of any specific therapeutic strategies and drugs when attempting to ameliorate disease severity. An example is the drug Dimebon by Medivation, Inc. In 2009 this drug was in phase III clinical trials for use in Alzheimer's disease, and also phase II clinical trials for use in Huntington's disease. In March 2010, the results of a clinical trial phase III were released; the investigational Alzheimer's disease drug Dimebon failed in the pivotal CONNECTION trial of patients with mild-to-moderate disease. With CONCERT, the remaining Pfizer and Medivation Phase III trial for Dimebon (latrepirdine) in Alzheimer's disease failed in 2012, effectively ending the development in this indication.

In another experiment using a rat model of Alzheimer's disease, it was demonstrated that systemic administration of hypothalamic proline-rich peptide (PRP)-1 offers neuroprotective effects and can prevent neurodegeneration in hippocampus amyloid-beta 25–35. This suggests that there could be therapeutic value to PRP-1.

Other avenues of investigation
Protein degradation offers therapeutic options both in preventing the synthesis and degradation of irregular proteins. There is also interest in upregulating autophagy to help clear protein aggregates implicated in neurodegeneration. Both of these options involve very complex pathways that we are only beginning to understand.

The goal of immunotherapy is to enhance aspects of the immune system. Both active and passive vaccinations have been proposed for Alzheimer's disease and other conditions; however, more research must be done to prove safety and efficacy in humans.

A current therapeutic target for the treatment of Alzheimer's disease is the protease β-secretase, which is involved in the amyloidogenic processing pathway that leads to the pathological accumulation of proteins in the brain. When the gene that encodes for amyloid precursor protein (APP) is spliced by α-secretase rather than β-secretase, the toxic protein β amyloid is not produced. Targeted inhibition of β-secretase can potentially prevent the neuronal death that is responsible for the symptoms of Alzheimer's disease.

Dr. Antonio Barbera, a former obstetrics and gynaecology doctor, is prescribing table tennis for patients who are suffering from a serious neurological disorder.

title: Neurodegenerative disease


text:
Talk:108th United States Congress

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title: Talk:108th United States Congress


text:
Wikipedia:WikiProject Spam/LinkReports/djarafat.net

Links

 * djarafat.net resolves to [//<IP_ADDRESS> <IP_ADDRESS>]
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Users

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text:
1952–53 William & Mary Indians men's basketball team

The 1952–53 William & Mary Indians men's basketball team represented the College of William & Mary in intercollegiate basketball during the 1952–53 NCAA men's basketball season. Under the first year of head coach Boydson Baird, the team finished the season 10–13 and 6–13 in the Southern Conference. This was the 48th season of the collegiate basketball program at William & Mary, whose nickname is now the Tribe. William & Mary played its home games at Blow Gymnasium.

The Indians finished in 12th place in the conference and failed to qualify for the Southern Conference men's basketball tournament, the first such occurrence since 1947.

Program notes

 * On February 14, 1953, Bill Chambers set the NCAA record for highest single game rebound total (51) in a game against Virginia,
 * Boydson Baird came to William & Mary after three seasons at Davidson, where he had a 24–53 record.
 * Bill Chambers was named to the second team all-Southern Conference for the second straight season.
 * Following the 1952–53 season, seven of William & Mary's Southern Conference co-members departed for the new Atlantic Coast Conference: Clemson, Duke, Maryland, North Carolina, North Carolina State, South Carolina, and Wake Forest.

Schedule
!colspan=9 style="background:#006400; color:#FFD700;"| Regular season

Source


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Myja longicornis

Myja longicornis is a species of sea slug, an aeolid nudibranch, a marine gastropod mollusc in the family Tergipedidae. It was thought to be a close relative of Tergipes but molecular phylogeny reveals it to be a paedomorphic facelinid.

Distribution
This species was described from Ambon Island, Maluku Islands, Indonesia. It is reported from the Philippines to Papua New Guinea. Specimens from Thailand may not be this species and were described as Myja cf. longicornis in a revision of the genus Myja.

Description
Myja longicornis is a small nudibranch which is similar in appearance to Tergipes tergipes, but with more cerata and red markings. The cerata have a remarkable resemblance to the polyps of the hydroid Pennaria disticha on which it feeds. It has an elongated body that can reach up to 10 mm. Its rhinophores are similar in size to oral tentacles and smooth. Oral tentacles and rhinophores are with scattered opaque white dots. Digestive gland in the cerata is light to dark greyish, digestive gland in upper part of cerata with reddish internal spot, apices with white spot, and central branches of digestive gland are visible through dorsal part of body. Anterior cerata with prominent reddish basal spot in some cerata distributed over its whole surface. Jaws broadly triangular with prominent anterior wings, masticatory borders smooth. Radula uniserial, very small compared to pharynx internal volume.

title: Myja longicornis


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User:Dorbranov/sandbox

POSITIVE THINKING

One bright spring morning, I drive to work and intrusion into traffic chaos. I can’t avoid an hour of waiting and delay on the job. Unaware of this, I have two choices. First, I can be angry, nervous, concerned (What the boss will say, will I be fined or be fired?), I can swear, madly honk. The result will be a sweaty person with a carved pine between the eyebrows, which has allowed this unfortunate moment to overcome, and not be moved from the place. Another possibility: if I can’t do anything, I reconcile with the situation, I thank God (everyone has their "God" they secretly pray) that I woke up this morning (unfortunately many are not), I have work (in this recession many don’t have it), I have car (many don’t even have a bicycle, or foot). How would the world be better, how people would be happier if they only knew that the key to their happiness and success lies in themselves? You don’t let bad thoughts prevail over your life, one accident attracts other, in all try to find something positive, because life is sometimes gray sometimes yellow. If I didn’t stuck in the traffic chaos, maybe I could cause a car accident, or pedestrian crash, so I’m happy that I stuck in traffic and had one hour of meditation. For someone, one and the same sky is semi-clear, for another sky is semi-cloudy. This first looming the sun behind the clouds, and second always expects a downpour. You create your color of the sky. You are responsible for your own happiness.

In this article, I also want to write about opinions we have about ourselves. People, who have a positive image of themselves, self-confidence and self-esteem, often have positive attitude towards life and other people. While, people who have negative opinion about themselves, hardly pass through life and they are in great danger of developing depression, which is called the modern disease. In today’s fast life, it’s essential that people have a realistic theory of themselves and world they live in, they must know their possibilities and limits. Only then, people can build their self-concept that will positively affect their lives. The man himself has to decide whether he is satisfied with himself and his lifestyle or not, whether to make changes in his life. In the toughest challenges, people must believe in themselves, thinking about positive results, because way of thinking creates winners. Deleting negative beliefs about oneself helps in making decision and solving business problems. Often, opinion about themselves is shaped by other’s opinions. Don’t allow others to tailor your life and vice versa. Give praise to everyone who deserves it. The greatest power lies in the mind. If you learn to control thought, you will learn to control your life. "Believe in yourself! Have faith in your abilities! Without a humble but reasonable confidence in your own powers you cannot be successful or happy. [Norman Vincent Peale]"

title: User:Dorbranov/sandbox


text:
Internet Technologies/Usenet

Usenet is a "network" of newsgroup servers (often run by ISPs) working together. Once connected to Usenet one can find everything from logical conversation to porn. One bad thing about Usenet is that it is often used to distribute warez, or illegal digital content like mp3s, Screeners, or cracked video games. In most cases Usenet is the first step in the life of warez. Unfortunately this has caused many newsgroup servers to block access to known warez newsgroups.

Usenet providers normally charge money for access but many ISPs have newsgroup servers running that their customers can access for free. So if you would like to check out Usenet first call your ISP and find out if they have a newsgroup server running.

title: Internet Technologies/Usenet


text:
haarikka

Noun

 * 1)  a type of large, usually wooden, drinking vessel resembling a large tankard with two straight handles, one for each hand

title: haarikka


text:
tegenspraak

Etymology
From.

Noun

 * 1) backtalk, lip
 * 2) contradiction logical inconsistency
 * 3) expression of an opposite opinion

title: tegenspraak


text:
List of teams and cyclists in the 1993 Vuelta a España

For the 1993 Vuelta a España, the field consisted of 169 riders; 114 finished the race.


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User:Jonascox

Jonas, check your discussion page. People do not generally leave messages or edit this page. It is considered your personal space like a personal desktop. Discussion page is like bulletin board. Mirwin 03:20, 12 February 2007 (UTC)

title: User:Jonascox


text:
Sutton Scarsdale

Sutton Scarsdale is a village in Derbyshire, England. It is in the North East Derbyshire district. It is very close to the M1 motorway. It is in the civil parish of Sutton cum Duckmanton.

The settlement is notable for a large, ruined former stately home called Sutton Scarsdale Hall. Near to the settlement are the villages of Heath, Temple Normanton and Arkwright Town. Scarsdale, New York is named after the village.

Early history
This manor was in the Domesday book in 1086. Under the title of “The lands of Roger de Poitou” it said: "In Sutton Scarsdale Stenulf had four carucates of land to the geld. Land for five ploughs. The lord has there one plough and six villans and one bordar with one plough, There is a mill rendering two shillings and eight acres of meadow. Woodland pasture half a league long and three furlongs broad. TRE worth forty shillings now twenty shillings."

Bess of Hardwick
Bess of Hardwick built a house, "Oldcotes" or "Owlcotes", where Arbella Stuart stayed in 1603, south of Sutton Scarsdale. The building was completely demolished.

title: Sutton Scarsdale


text:
rotolo

Etymology
From. As a roll, from, from +. As a unit of weight, from, variant of classical , ultimately from.

Noun

 * 1)  A kind of roll.
 * : a former Middle Eastern and North African unit of dry weight, usually between 1–5 pounds (.5–2.5 kg).

Etymology 1
From <, from.

Noun

 * 1) roll
 * 2) coil
 * 3) scroll
 * 4) a form of pasta in which a filling is rolled up in a sheet of pasta and poached

Etymology 2
From, variant of classical , ultimately from.

Noun

 * 1)  rottol

title: rotolo


text:
Hashiridasu Shunkan

Hashiridasu Shunkan (走り出す瞬間) is the first album by Japanese idol girl group Hiragana Keyakizaka46. It was released on 20 June 2018. The album reached the top position on the weekly Oricon Albums Chart. It also reached number one on the Billboard Japan Hot Albums Chart.

Track listing
All lyrics written by Yasushi Akimoto.

title: Hashiridasu Shunkan


text:
IB Music/Music History/Medieval Period

Back to IB Music History

Medieval Period 450 - 1450

Music of the Medieval Period was categorized into sacred and secular music. Sacred music was music that was used by the Roman Catholic Church and secular music was music that had no relation to the Church.

Gregorian Chant
Sacred music evolved from a form called the Gregorian chant. Gregorian chants were named after Pope Gregory I and they are the official pieces of the Catholic Church.

Characteristics of Gregorian chants

 * Melody - The melody of a Gregorian chant is very free-flowing. The chant moves up and down by steps and small leaps within a narrow range. Melodies are often melismatic- syllables are held out over multiple notes.
 * Harmony - Gregorian chants are monophonic in texture, so have no harmony. However, the use of drone (singing of the same note for an extended period of time usually in at least whole notes) was common.
 * Rhythm - Notes may be held for a duration of “short” or “long,” but no complex rhythms are used.
 * Form - Some Gregorian chants tend to be in ternary (ABA) form. A cantor begins the piece with an introductory solo, called an incipit. The choir then sings the piece and at the end the cantor concludes with his solo, which was often in a reduced dynamic level and featured a narrower range of pitches.
 * Timbre - Sung by all male choirs. However, sometimes they were written for women who were nuns of convents as a teaching device.
 * Texture - Gregorian chants are one of the few pieces of music that are entirely monophonic. There is only one melodic line in a Gregorian chant.
 * Context - Gregorian chants were used by the Church to aid prayers. Monks (and occasionally nuns in convents) would sing them. As well, as it was the official music of the Roman Catholic Church, all gregorian chants had only vocals as instrumentation was considered to be Pagan. This also caused all text to be written in Latin. All gregorian chant was passed down orally, as the use of sheet music was very uncommon. They were performed at the "office" and "mass" of religious ceremony.
 * Church Modes - These were the scales in which gregorian chants were sung. They were used in the middle ages until the Renaissance. Most folk music uses them, this can be seen in the example "What can we do with a drunken sailor." Church modes use 7 tones and the eighth tone duplicates the tonic an octave higher.

Significant Composers

 * Hildegard of Bingen - The first woman composer with a significant output of works.
 * Important works
 * O Successores
 * Most other composers are unknown since works were given to the Church.
 * Other works
 * Alleluia: Vidimus Stellam

Organum
The Gregorian chant began to evolve around 700. From 700 - 900, composers would write a line in parallel motion to the chant at a fixed interval of a fifth or a fourth above the original line. This technique evolved further from 900 - 1200. During this period, the upper line moved independently of the original chant. After 1100, upper lines even began gaining rhythmic independence.

A Gregorian chant to which additional lines were added is called organum. The original Gregorian chant on which the upper lines are based is called the cantus firmus. Between the lines they are intervals of fourths and fifths that move in contrary motion.

Two composers, Leonin and Perotin, were instrumental to the development of organum. Leonin was the director of music at the Notre Dame Cathedral and Perotin, his pupil, succeeded him. These two composers and their students are thus appropriately referred to as the School of Notre Dame.

Significant Composers

 * Leonin- He is the first known composer to use measured rhythm in his compositions.
 * Perotin- He is the first known composer to write three simultaneous, distinct lines.
 * Important works
 * Alleluia: Nativitas

Sacred music was primarily vocal. This was mostly due to the connection of instruments to pagan rituals. Nevertheless, instruments did become more important over the span of the Medieval Period. The most important instrument of sacred music in the Medieval Period is the organ. Early organs are not like modern organs; though they were loud, they were much more difficult to operate and required a great deal of physical strength.

Secular Music
Unlike sacred music, secular music had a more clearly defined beat and its texture was closer to homophony or polyphony. (It was not true homophony since chords were only implied). Like sacred music, the texture was primarily vocal, though it didn’t regard instruments with as much suspicion as the Church.

Troubadours & Trouvères
Much secular music during the Medieval Period was written by troubadours and troubavères. These were French nobles and they often wrote music to gain prestige.

Significant Composers

 * Guillaume IX, duke of Aquitaine
 * Chastelain di Couci
 * Beatriz de Dia (a woman troubadour)

Jongleurs
Jongleurs also composed and performed secular music. Jongleurs were wandering minstrels that would entertain towns with music, juggling, and drama. They had no civil rights but were important parts of society since they spread news from town to town. One form of music they played is the estampie. An estampie is a fast dance in triple meter.

Ars Nova
Around 1350, a new style of music called Ars Nova (New Art) emerged. Ars Nova includes both sacred and secular music, though secular music gained importance during this period.

Important characteristics of Ars Nova are:
 * Development of polyphony
 * Use of duple meter
 * Syncopation

Sacred Music
Ars Nova saw the appearance of a grand form for sacred music- the mass ordinary. The mass ordinary consists of five prayers set to music as five different movements. The prayers are:

 * Kyrie
 * Gloria
 * Credo
 * Sanctos
 * Agnus Dei

Secular Music
Because of diminishing influence of the Church, secular music became more prominent in the Ars Nova Period. Instruments were used more often, though the music was still primarily vocal. A new secular form of the Ars Nova period is the ballata. The ballata is a dance in the form of A BB AA. A ballata is also known as a falala for its use of this line throughout its pieces.

Significant Composers

 * Guillaume de Machaut
 * Important works
 * Notre Dame Mass - This is the first known polyphonic mass.
 * Francesco Landini
 * Important works
 * Ecco la Primavera - This is an example of an Ars Nova ballata.

Instruments of the Period

 * Organ
 * Pipe
 * Rebec
 * Psaltery
 * Fiddle
 * Lute
 * Sackbut
 * Shawm

Back to IB Music History

title: IB Music/Music History/Medieval Period


text:
List of Leicestershire County Cricket Club grounds

Leicestershire County Cricket Club is one of the 18 member clubs of the English County Championship, representing the historic county of Leicestershire. The club was established on 25 March 1879. It has since played first-class cricket from 1894, List A cricket from 1963 and Twenty20 cricket from 2003. Unlike most professional sports, in which a team usually has a single fixed home ground, county cricket clubs have traditionally used different grounds in various towns and cities within the county for home matches, although the use of minor "out grounds" has diminished since the 1980s. Leicestershire's first XI have played home matches at fifteen different grounds.

The club's debut home match in first-class cricket was played at Grace Road in Leicester. After the 1900 season, the club ceased using Grace Road, as it was felt that it was located too far from the centre of the city. Instead, Aylestone Road became the club's headquarters, and staged nearly 400 first-class matches between 1901 and the outbreak of the Second World War. Due to a combination of wartime damage and industrial development, however, the club was forced to discontinue using Aylestone Road after the war, and Grace Road once again became the club's main venue. In the years after the war, the county also utilised grounds in other towns including Hinckley, Melton Mowbray, Barwell and Loughborough.

In addition to the county's inaugural first-class match, Grace Road also played host to Leicestershire's first home games in the other formats of cricket. In 1964 it staged the county's first home List A game against Northamptonshire and in 2003 it was the venue for the county's first home game in Twenty20 cricket against Yorkshire. The ground has hosted the vast majority of the county's games, including every Twenty20 match since the introduction of that format. Since 1991, when the club played its last game at Leicester Road in Hinckley, the only venue other than Grace Road to host any of Leicestershire's matches is the Oakham School Ground, which is actually located in the adjacent county of Rutland. The school was used for five first-class matches from 2000–07 and nine List A games from 2001–08, followed by a further List A game in 2018 after an absence of ten years.

Grounds
''Below is a complete list of grounds used by Leicestershire County Cricket Club for first-class, List A and Twenty20 matches. Statistics are complete through to the end of the 2020 season. Only matches played by Leicestershire CCC at the grounds are recorded in the table. Matches abandoned without any play occurring are not included.''


text:
Talk:Scouts' Day

Rename to Scouts Day
I think this could be expanded into a general article called Scouts Day, since there are different observances of this event in various countries (such as the St George's Day event in the UK where Scouters re-affirm their promise). Horus Kol 10:30, 5 October 2006 (UTC)
 * Can we see your proposed changes to the article before the change is made? --evrik 14:20, 5 October 2006 (UTC)
 * Okay - I'm just genning up an example in my sandbox Horus Kol 16:04, 5 October 2006 (UTC)
 * proposal for "Scouts Day" article - Horus Kol 16:51, 5 October 2006 (UTC)

 * Moved the proposed text to this page. I think I'll nominate it for a DYK. --evrik 14:08, 6 October 2006 (UTC)

im a boy scout and i think this need more information on what goes on on this day--Nascar09 (talk) 03:31, 29 March 2009 (UTC)

External links modified
Hello fellow Wikipedians,

I have just added archive links to 2 one external links on Scouts' Day. Please take a moment to review my edit. If necessary, add after the link to keep me from modifying it. Alternatively, you can add to keep me off the page altogether. I made the following changes:
 * Added archive https://web.archive.org/20101225125318/http://scout.org/en/around_the_world/eurasia/information_events/events to http://scout.org/en/around_the_world/eurasia/information_events/events
 * Added archive https://web.archive.org/20090614052851/http://www.liberiabroadcastingsystem.com:80/news/article_2009_05_28_3756.html to http://liberiabroadcastingsystem.com/news/article_2009_05_28_3756.html

Cheers.—cyberbot II  Talk to my owner :Online 00:23, 17 February 2016 (UTC)

External links modified
Hello fellow Wikipedians,

I have just added archive links to 1 one external link on Scouts' Day. Please take a moment to review my edit. If necessary, add after the link to keep me from modifying it. Alternatively, you can add to keep me off the page altogether. I made the following changes:
 * Added archive https://web.archive.org/20101225125318/http://scout.org/en/around_the_world/eurasia/information_events/events to http://scout.org/en/around_the_world/eurasia/information_events/events

Cheers.—cyberbot II  Talk to my owner :Online 09:29, 21 March 2016 (UTC)

Dhenser paeen
Dhenser paeen is a village located in District Gujranwala It covers an area of 1200 acres It is very beautiful village located near Siranwali, Mianwali bangla And Wahndo A canal runs through it Among the famous people there AZEEM ULLAH WIRK is at the top Muhammad Sharif Virk (talk) 13:08, 15 February 2022 (UTC)

title: Talk:Scouts' Day


text:
Ohm (disambiguation)

Ohm (symbol Ω) is a unit of electrical resistance named after Georg Ohm.

Ohm or OHM may also refer to:

People

 * Georg Ohm (1789–1854), German physicist and namesake of the term ohm
 * Germán Ohm (born 1936), Mexican boxer
 * Jörg Ohm (1944–2020), former East German football player
 * Martin Ohm (1792–1872), German mathematician
 * Rebecca Ohm, United States Air Force officer and fighter pilot
 * Rune Ohm (born 1980), Danish handball player
 * Thorsten Ohm, CEO of VDM Publishing
 * Pawat Chittsawangdee, Thai actor, nicknamed Ohm
 * Thitiwat Ritprasert, Thai actor, nicknamed Ohm

Germany

 * Ohm (river), right tributary of the Lahn near Cölbe
 * Zwester Ohm, left tributary of the Lahn near Fronhausen

Outer space

 * 24750 Ohm, an outer main belt asteroid
 * Ohm (crater) on the Moon

Science and technology

 * Acoustic ohm, a unit of measurement of acoustic impedance
 * Ohm's law, law that relates electrical resistance, current, and voltage
 * OHM (Observe. Hack. Make.), a 2013 outdoor hacker conference
 * OpenHistoricalMap, a collaboratively edited historical atlas of the world

Music

 * OHM (band), a rock/jazz fusion music group
 * OHM: The Early Gurus of Electronic Music, 2000 album
 * Ohms (album), a 2020 album by Deftones
 * "Ohm", song by indie band Yo La Tengo from the album Fade
 * "Ohm", a song by metalcore band Northlane from the album Node

Fictional entities

 * Ohm (One Piece), a character in the Japanese manga and anime
 * Johnny Ohm, a Marvel Comics supervillain
 * Ohm, a character from the Air Gear manga
 * Ohm, a race of arthropodean creatures, also "Ohmu", from the film Nausicaä of the Valley of the Wind

Other uses in media

 * Organisatie Hindoe Media, a Dutch public broadcaster
 * Ohm Krüger, a 1941 German biographical film

Other uses

 * Alternative spelling for Om, a sacred sound and symbol of several Indian religions
 * Alternative spelling for the Korean name Um

title: Ohm (disambiguation)


text:
Cre recombinase

Cre recombinase is a tyrosine recombinase enzyme derived from the P1 bacteriophage. The enzyme uses a topoisomerase I-like mechanism to carry out site specific recombination events. The enzyme (38 kDa) is a member of the integrase family of site specific recombinase and it is known to catalyse the site specific recombination event between two DNA recognition sites (LoxP sites). This 34 base pair (bp) loxP recognition site consists of two 13 bp palindromic sequences which flank an 8bp spacer region. The products of Cre-mediated recombination at loxP sites are dependent upon the location and relative orientation of the loxP sites. Two separate DNA species both containing loxP sites can undergo fusion as the result of Cre mediated recombination. DNA sequences found between two loxP sites are said to be "floxed". In this case the products of Cre mediated recombination depends upon the orientation of the loxP sites. DNA found between two loxP sites oriented in the same direction will be excised as a circular loop of DNA whilst intervening DNA between two loxP sites that are opposingly orientated will be inverted. The enzyme requires no additional cofactors (such as ATP) or accessory proteins for its function.

The enzyme plays important roles in the life cycle of the P1 bacteriophage, such as cyclization of the linear genome and resolution of dimeric chromosomes that form after DNA replication.

Cre recombinase is a widely used tool in the field of molecular biology. The enzyme's unique and specific recombination system is exploited to manipulate genes and chromosomes in a huge range of research, such as gene knock out or knock in studies. The enzyme's ability to operate efficiently in a wide range of cellular environments (including mammals, plants, bacteria, and yeast) enables the Cre-Lox recombination system to be used in a vast number of organisms, making it a particularly useful tool in scientific research.

Discovery
Studies carried out in 1981 by Sternberg and Hamilton demonstrated that the bacteriophage 'P1' had a unique site specific recombination system. EcoRI fragments of the P1 bacteriophage genome were generated and cloned into lambda vectors. A 6.5kb EcoRI fragment (Fragment 7) was found to permit efficient recombination events. The mechanism of these recombination events was known to be unique as they occurred in the absence of bacterial RecA and RecBCD proteins. The components of this recombination system were elucidated using deletion mutagenesis studies. These studies showed that a P1 gene product and a recombination site were both required for efficient recombination events to occur. The P1 gene product was named Cre ( c auses re combination) and the recombination site was named loxP ( lo cus of crossing ( x ) over, P 1). The Cre protein was purified in 1983 and was found to be a 35,000 Da protein. No high energy cofactors such as ATP or accessory proteins are required for the recombinase activity of the purified protein. Early studies also demonstrated that Cre binds to non specific DNA sequences whilst having a 20 fold higher affinity for loxP sequences and results of early DNA footprinting studies also suggested that Cre molecules bind loxP sites as dimers.

Structure
Cre recombinase consists of 343 amino acids that form two distinct domains. The amino terminal domain encompasses residues 20–129 and this domain contains 5 alpha helical segments linked by a series of short loops. Helices A & E are involved in the formation of the recombinase tetramer with the C terminus region of helix E known to form contacts with the C terminal domain of adjacent subunits. Helices B & D form direct contacts with the major groove of the loxP DNA. These two helices are thought to make three direct contacts to DNA bases at the loxP site. The carboxy terminal domain of the enzyme consists of amino acids 132–341 and it harbours the active site of the enzyme. The overall structure of this domain shares a great deal of structural resemblance to the catalytic domain of other enzymes of the same family such as λ Integrase and HP1 Integrase. This domain is predominantly helical in structure with 9 distinct helices (F−N). The terminal helix (N) protrudes from the main body of the carboxy domain and this helix is reputed to play a role in mediating interactions with other subunits. Crystal structures demonstrate that this terminal N helix buries its hydrophobic surface into an acceptor pocket of an adjacent Cre subunit.

The effect of the two-domain structure is to form a C-shaped clamp that grasps the DNA from opposite sides.

Active site

The active site of the Cre enzyme consists of the conserved catalytic triad residues Arg 173, His 289, Arg 292 as well as the conserved nucleophilic residues Tyr 324 and Trp 315. Unlike some recombinase enzymes such as Flp recombinase, Cre does not form a shared active site between separate subunits and all the residues that contribute to the active site are found on a single subunit. Consequently, when two Cre molecules bind at a single loxP site two active sites are present. Cre mediated recombination requires the formation of a synapse in which two Cre-LoxP complexes associate to form what is known as the synapse tetramer in which 4 distinct active sites are present. Tyr 324 acts as a nucleophile to form a covalent 3’-phosphotyrosine linkage to the DNA substrate. The scissile phosphate (phosphate targeted for nucleophilic attack at the cleavage site) is coordinated by the side chains of the 3 amino acid residues of the catalytic triad (Arg 173, His 289 & Trp 315). The indole nitrogen of tryptophan 315 also forms a hydrogen bond to this scissile phosphate. (n.b A Histidine occupies this site in other tyrosine recombinase family members and performs the same function). This reaction cleaves the DNA and frees a 5’ hydroxyl group. This process occurs in the active site of two out of the four recombinase subunits present at the synapse tetramer. If the 5’ hydroxyl groups attack the 3’-phosphotyrosine linkage one pair of the DNA strands will exchange to form a Holliday junction intermediate.

Role in bacteriophage P1
Cre recombinase plays important roles in the life cycle of the P1 bacteriophage. Upon infection of a cell the Cre-loxP system is used to cause circularization of the P1 DNA. In addition to this Cre is also used to resolve dimeric lysogenic P1 DNA that forms during the cell division of the phage.

Use in research
Inducible Cre activation is achieved using CreER (estrogen receptor) variant, which is only activated after delivery of tamoxifen. This is done through the fusion of a mutated ligand binding domain of the estrogen receptor to the Cre recombinase, resulting in Cre becoming specifically activated by tamoxifen. In the absence of tamoxifen, CreER will result in the shuttling of the mutated recombinase into the cytoplasm. The protein will stay in this location in its inactivated state until tamoxifen is given. Once tamoxifen is introduced, it is metabolized into 4-hydroxytamoxifen, which then binds to the ER and results in the translocation of the CreER into the nucleus, where it is then able to cleave the lox sites. Importantly, sometimes fluorescent reporters can be activated in the absence of tamoxifen, due to leakage of a few Cre recombinase molecules into the nucleus which, in combination with very sensitive reporters, results in unintended cell labelling. CreER(T2) was developed to minimize tamoxifen-independent recombination and maximize tamoxifen-sensitivity.

Improvements
In recent years, Cre recombinase has been improved with conversion to preferred mammalian codons, the removal of reported cryptic splice sites, an altered stop codon, and reduced CpG content to reduce the risk of epigenetic silencing in mammals. A number of mutants with enhanced accuracy have also been identified.

title: Cre recombinase


text:
The Nesbitts Are Coming

The Nesbitts Are Coming is a British comedy television series which first aired on ITV in 1980.

Main cast

 * Clive Swift as Ernie Nesbitt
 * Maggie Jones as Mrs. Nesbitt
 * Deirdre Costello as Marlene Nesbitt
 * John Price as Len Nesbitt
 * Christian Rodska as Tom Nesbitt
 * Ken Jones as Detective Sergeant Arnold Nixon
 * Tony Melody as Station Sergeant Billy Machin
 * John Clive as PC Emlyn Harris
 * Patsy Rowlands as WPC Kitty Naylor
 * Arthur White as PC Crowther

title: The Nesbitts Are Coming


text:
Talk:Casey Neistat

Wiki Education Foundation-supported course assignment
This article is or was the subject of a Wiki Education Foundation-supported course assignment. Further details are available on the course page. Student editor(s): Samgrasman.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 18:42, 17 January 2022 (UTC)

Google collaboration?
I don't believe that Casey ever made a movie specifically for Google as it says in the article. Can someone verify? I think they are referring to this video that he (Casey) shot on Google Glass. Gingakei (talk) 20:33, 30 April 2015 (UTC)

Fines
Any information of how much he had to pay for fines and law suites? For example spray painting advertisement posters or printing fake $2 american dollar currency notes. — Preceding unsigned comment added by <IP_ADDRESS> (talk) 21:01, 19 January 2016 (UTC)

wow
what a fascinatingly detailed biography, complete with so many unverifiable sources! <IP_ADDRESS> (talk) 12:15, 19 May 2014 (UTC)

 * it's also interesting that this guy hasn't done anything. it's like a long list of mediocre facts. what is the big deal? — Preceding unsigned comment added by Ulanda5 (talk • contribs) 22:37, 17 July 2015 (UTC)

-- This is a massive vanity project for someone of very little interest to the general population. — Preceding unsigned comment added by <IP_ADDRESS> (talk • contribs)

Picture(s)?
This person needs more pictures for the info box or the article in general. Can anyone find or upload some to add to this article?Adog104 (talk) 21:21, 10 September 2015 (UTC)Adog104

 * I added a photo released under CC by Neistat to the infobox. I couldn't find any free photos online of him. Mrtea (talk) 22:17, 13 January 2016 (UTC)
 * Thank you buddy.  A dog 104  Talk to me 02:01, 14 January 2016 (UTC)
 * Not sure if I'm doing this right, (I'm new to this, if I'm doing it wrong, please instruct me how to do it correctly) but I found some good pictures for Casey, Can someone tell me how to correctly add them to the page?(Amoney93 (talk) 22:02, 29 March 2019 (UTC))

Merge proposal
I propose that Neistat Brothers be merged into Casey Neistat. I do not think this would be too difficult as the most of the information on the Neistat Brothers article is already covered in the Casey Neistat article. Also, very few pages link to the Neistat Brothers article.Sro23 (talk) 21:47, 16 March 2016 (UTC)

 * Does anyone concur? It would be a very easy merge and redirect. Sro23 (talk) 01:09, 24 April 2016 (UTC)

 * Support. Seems like most coverage is about Casey. NinjaRobotPirate (talk) 01:24, 24 April 2016 (UTC)
 * Comment: I suggest merging the content about Casey into this article, but keep Neistat Brothers for content about the HBO series. A quick Google search shows a lot of sources about the show. If Van Neistat meets notability criteria, let him have his own article. Mrtea (talk) 13:34, 25 April 2016 (UTC)
 * Comment: I agree with Mrtea. However, I would even go so far as to having 3 pages: one for the HBO series, one for Casey, and the last about all 3 brothers (youngest being dean, an accomplished actor and stuntman). Alternatively, we could keep it like it is and merge the Casey-centric stuff from the series page to his personal page, and then create a new page for Dean (he should meet the criteria, right? I'd say he's more worthy of his own page than Van is). But I think the first option makes more sense. FROZYO! (talk) 18:59, 27 April 2016 (UTC)
 * Comment: I believe that Casey Neistat's page should be kept as its own single page because his life is based around his youtube channel and his job. The Neistat brothers can be another page because they have a whole other history, and it can be used as links within Casey's biography. Sahilkarnani (talk) 12:25, 30 June 2016 (UTC)
 * Comment: I think that Mrtea has hit the nail on the head. "The Neistat Brothers" wiki page should be on the HBO series and should be re-created into being a stub about it at first then with further expansion. I am able to edit the "Neistat Brothers" wiki page and turn it into a proper TV show page, but first I have to re-watch the eight episodes and summarise them :) Nicnote (talk) 14:37, 10 July 2016 (UTC)
 * Comment: You must be kidding - Van Neistat directed all the Tom Sachs movies including "A space program" that premiered at SXSW 2015. He is much more private but not the least bit less important than Casey Neistat. The work that they did together should still be referenced under "The Neistat brothers", although I too agree that the page could equally well be about the TV show rather than the duo. — Preceding unsigned comment added by <IP_ADDRESS> (talk) 17:55, 8 August 2016 (UTC)
 * Your opinion has swayed me from supporting, I would feel bad if I was him and my work was under the work of my brother, I have watched the Bike Lanes and the iPod dirty secret, so Van deserves some credit right there Alexis Ivanov (talk) 02:11, 10 August 2016 (UTC)

 * Support Hello. I agree that the page should be merged here, at least the biographical stuff here. However, could you merge the biographical info here and then move the page as The Neistat Brothers? About a separate page, I think there should be a page for each of the brothers as well, not just a joined article. Thanks. sheldon.andre (talk) 01:27, 11 August 2016 (UTC)
 * Oppose I feel that the Neistat Brothers page has to do with a certain branding that involved another one individual other than Casey Neistat. It is like having an actor and a production company both should have their own pages to frame them in the right perspective --M. Hassan talk here 04:29, 11 August 2016 (UTC)
 * Oppose I think the Neistat Brothers page should be devoted solely to their HBO series. — Preceding unsigned comment added by DuckPike (talk • contribs) 16:11, 27 September 2016 (UTC)
 * Support per nom.  JTP ( talk • contribs) 15:30, 7 November 2016 (UTC)
 * Oppose These should be two separate articles. The Neistat Brothers is worthy of its own page, was a different body of work and a different period of time. Van and Casey Neistat have had separate careers for some time. The Neistat Brothers page shouldn't be merged with this page any more than it should with an article on Van Neistat (which should also exist). Marrante (talk) 22:51, 19 January 2017 (UTC)
 * Support: Seems like there's only enough information to really support a single article. – Matthew  - (talk) 20:46, 27 February 2017 (UTC)
 * Oppose Just make this article about the show on HBO, not about the brothers. AlessandroTiandelli333 (talk) 08:06, 4 March 2017 (UTC)
 * Oppose I don't think that is a very good idea. Not to be critical, but it is probably a good idea to have a seperate article for the TV show. — Preceding unsigned comment added by Onealjack123 (talk • contribs) 01:22, 8 April 2017 (UTC)
 * Oppose Yeah, it should have a seperate page for the TV show like DuckPike said. OblivionOfficial (talk) 22:12, 13 June 2017 (UTC)
 * Comment I agree with Mrtea wholeheartedly. Otterhead 07:05, 21 June 2017 (UTC)

Marketing
Article Smells like well curated marketingStarbwoy (talk) 23:59, 29 July 2016 (UTC)
 * - Feel free to fix it. Cyphoidbomb (talk) 00:06, 30 July 2016 (UTC)

iPod's Dirty Secret "viewcount"
According to this article, "Within six days the video was viewed a million times". The WaPo article that is linked to a few sentences later (original link dead, syndicated copy here at the the Spartanberg Herald-Journal) says "a month later, nearly a million Internet surfers (and counting) had come to know the Neistat Brothers". Where did a million in six days come from? The article only (vaguely) indicates that www.ipods-dirtysecret.com had less than a million visitors in a month.

It was a widespread viral video that I remember seeing myself, but there's absolutely no point in specifying a specific viewcount to a Quicktime video either shared through emails or embedded as a copied file on other video hosting sites.

Danwroy (talk) 20:08, 3 August 2016 (UTC)
 * , your point seems reasonable. Such specificity would need to be properly sourced anyway. Cyphoidbomb (talk) 20:23, 3 August 2016 (UTC)

Neistat family.
I think mentioning his grandmother the dancer Louise Cecile Grossman that has inspired him might be crucial in the early life section. I'm also surprised by the lack of mentioning of his parents Barry Neistat and Amy Neistat Alexis Ivanov (talk) 02:17, 10 August 2016 (UTC)

Well, that's why this page focuses on Casey mostly. sheldon.andre (talk) 01:14, 11 August 2016 (UTC)

 * Which is excellent, just mentioning them once or twice isn't bad Alexis Ivanov (talk) 14:18, 11 August 2016 (UTC)

 * I think more information about Casey's family and his upbringing can be found in his older YouTube videos. He explains a lot about his family and his hometown in the beginning of his vlog channel. I think these can be used as great primary sources. --Siddkumaran (talk) 04:17, 6 February 2019 (UTC)

Fan stuff
Should the Boosted section from this article be removed? Going over it, it just seems like something only a WP:FAN would know, and it would be as if adding information about "Neistat's drones" or "Neistat's iPhone's and iPad's" or "The collection of tech in Neistat's studio apartment".  Adog 104  Talk to me 19:48, 17 August 2016 (UTC)
 * Arguably the Boosted boards are featured (sometimes extensively) in every single 'episode' and are as such a main part of what he does. But then again it does smell of WP:PLUG for the company. Maybe it doesn't need to be so well featured on this wiki page? Or at least re-written be a bit more encyclopedic... Best, Nicnote (talk) 20:49, 18 August 2016 (UTC)
 * ; Meh, but edits like this is definitely Fan cruft (does anyone really care how much long-boards a person has?), which is trivial at best.  Adog 104  Talk to me 18:30, 19 August 2016 (UTC)
 * I have no problems with deleting the section or at least re-placing it with a one-liner in somewhere along the lines of "Neistat is seen frequently discussing/using Boosted boards in his vlogs", etc. Nicnote (talk) 20:36, 19 August 2016 (UTC)
 * as long as it's referenced I can respect that. In the mean time, if I have more time, I'll probably be doing some reference add-ons and re-writes of some parts of the article, any help is appreciated.  Adog 104  Talk to me 20:44, 19 August 2016 (UTC)

Video Logs
His filmography fails to mention his video logs which, despite its casual nature, has become an important part of his curriculum vitae. Is there a way to talk about them without having to treat each as a new "great work", since they aren't really that? — Preceding unsigned comment added by HacksawPC (talk • contribs) 07:34, 23 February 2017 (UTC)

Article style
I normally don't have much to do with writing articles about living persons but I feel that there are a few changes that need to be made here in terms of the style of the article. First off, I think the youtube infobox needs to be changed with a person infobox. Lots of this article isn't even about his youtube channel, and besides, he has done other work like his app company. His active years should also be looked at, in his filmography section it states his part in a film in 2008, plus, the article covers his career all the way back to 2001. So I would think his years active should be "2001–present" or possibly "2008–present". – Hatio93 (talk) 10:17, 2 January 2018 (UTC)
 * Why should we change the infobox from YouTube? That would mean we lose all that information. Emir of Wikipedia (talk) 12:03, 2 January 2018 (UTC)
 * Articles like Trisha Paytas use infobox person and still hold youtube information. What I am trying to stress here is the fact that his career doesn't fully revolve around youtube but also his filmography, entrepreneurship, and youtube achievements. Information would not – Hatio93 (talk) 12:33, 2 January 2018 (UTC)
 * In the case of Paytas the YouTube information is there, but it is embedded in the other infobox. I do accept that Neistat has a career outside of YouTube though. Emir of Wikipedia (talk) 12:48, 2 January 2018 (UTC)
 * Sorry, thats what I was trying to say, having an infobox person, but embedding the youtube infobox into it. I can see how I wasn't very clear on that one. Also, regarding his years active, I don't think it should be "2010–present" the article talks about his career starting in 2001 but his biggest break in his career was probably in 2008 when he produced The Pleasure of Being Robbed. Regarding the using an infobox person and embedding the youtube one, I will make those changes now. – Hatio93 (talk) 12:59, 2 January 2018 (UTC)

Thanks for changing the infobox. Regarding the years active it might just best to remove so no confusion occurs, what do you think? Emir of Wikipedia (talk) 13:17, 2 January 2018 (UTC)
 * Yeah, that could be a good idea, but I feel that it is important to be there. Im leaning towards the year 2008. – Hatio93 (talk) 13:32, 2 January 2018 (UTC)
 * I have looked into how other articles have displayed a persons active years. Basically, its the start of their career, in this case, Neistat started his career in 2001, so I have made those changes. – Hatio93 (talk) 07:30, 3 January 2018 (UTC)
 * WP:Other stuff exists is not a good enough argument unless based on consensus. Infobox person says Date range in years during which the subject was active in their principal occupation(s) and/or other activity for which they are notable. Use the format 1950–2000, or 1970–present if still active (note the use of an en dash, not hyphen). --Emir of Wikipedia (talk) 11:44, 3 January 2018 (UTC)
 * I would say that this is a given, it doesn't need a consensus. If we are looking at a notability POV then it would be clear that he gained that title in 2003 with his iPod's Dirty Secret film. I do think something better than "2001–present" needs to be thought up. – Hatio93 (talk) 11:54, 3 January 2018 (UTC)

I removed the following.
I removed the following "Beme the company in partnership with CNN are now working on a YouTube news channel featuring Casey Neistat as host called Beme News. The Channel is still in trial stages to further refine the quality of the content." The was no source for this, and the next paragraph goes into detail that Neistat and CNN are no longer working with each other. Paige Matheson (talk) 22:19, 26 January 2018 (UTC)

More information on collaboration with other YouTubers
I think a section should be added on his collaboration with other YouTubers. He is a big YouTuber, so more information on him empowering other creators on the platform is important. This information can be found throughout his vlog channel. --Siddkumaran (talk) 04:30, 6 February 2019 (UTC)

Punt
I took a punt at cleaning up the article today - will come back for more shortly assumping that people are happy with my edits. There's a lot of rubbish that is covering up some genuinely interesting narrative.Joe (talk) 20:43, 13 February 2019 (UTC)

"Filmography" question
Should Neistat's involvement in YouTube Rewind 2019 be included in a new title called "web" in the "Filmography" section of this article? I feel that full coverage of one's involvement in film should be a priority in this situation. It's only fair, since no one has disputed adding Justin Roiland's involvement in PewDiePie's Meme Review into the Justin Roiland article.

RayDeeUx (talk) 01:46, 28 February 2019 (UTC)

title: Talk:Casey Neistat


text:
Van Dwelling

Contents

 * /Introduction/
 * A History of Van Dwelling and Historical Van Dwellers
 * /Choosing a Vehicle/
 * /Vehicle Repair/
 * /Heating & Cooling/
 * /Parking/
 * /Police/
 * Security (Alarms, Guns, Locks, Strategies)
 * /Campgrounds/
 * /Cooking/
 * /Bathroom/
 * /Shower/
 * /Exercise/
 * /Laundry/
 * /Storage/
 * /Internet/
 * /Power Systems/
 * /Equipment Checklists/
 * /Dating/
 * /Children/
 * /Stories from the Road/
 * Show Us Your Rig: Pictures of Vans
 * /Conversion Diaries/ -- Want to let others know how you did it? Keep a diary of your conversion here!
 * /Meet the Van Dwellers/
 * /Source List/
 * /Bibliography/
 * /Contributors/

title: Van Dwelling


text:
EG Awards of 2009

The EG Awards of 2009 are the fourth Annual The Age EG (Entertainment Guide) Awards and took place at the Prince of Wales on Friday 20 November 2009.

Hall of Fame inductees
Painters and Dockers

 * The Painters and Dockers formed in 1982 for a one-off benefit gig to pay a friend's parking fines. They went on to develop a reputation for wild shows and the ability to play anywhere— from suburban trains for Rockin' the Rails gigs, a boat for Rockin' the Docks, a float at the Moomba Parade to the 20th floor of a building site and on a picket line. The original lineup last played more than 20 years ago, but felt that they never had proper closure on their career.

Award nominees and winners
Winners indicated below in boldface

title: EG Awards of 2009


text:
Political and historical methodology

Part of the Strategic Studies curriculum

Welcome to STST122 Political and Historical Methodology. The purpose of this short first year course is to give you an understanding of how we study politics and history.

To ask questions or begin a discussion about this course, do not hesitate to go to this course's talk page.

Etymology
Etymology is the study of a word. Why is it formed like that? What was the thinking behind the creation of this word? Where does this word come from?

The word 'history' in English comes from the Greek historia, which meant to inquire. However, if we look at the word in German, Geschichte, it means what happened. There is an obvious tension here. Is history an inquiry, or what happened?

The two are not mutually exclusive. Indeed, it is logical to assert that we cannot know 'what happened' if we have not first 'inquired' in to a given event.

Academic History
It was not until the 19th Century that history became an academic discipline. What made it 'academic' was a method, much like scientific method, to ensure that assertions are not made without evidence. Academic history requires you to have both an object of study and a method with which to discover information about that object. This gave history a methodology, which will be discussed in detail below.

Definitions of History
As academics began to look at history, they attempted to define it. Marc Bloch gave the world an excellent definition of history as science des homme dans le tem -literally the science of man in time. Science, from the Latin scientia, a preposition of scire - to know, means here that we use a definite method in order to discover and expand our knowledge about the exploits of man within the framework of time. This is good because it tells us how we can contribute to this endeavour. There is a method, it isn't restricted to a few individuals, and its focus is people in the time that they have inhabited the Earth. Anything before that is prehistory, and we generally leave that to Paleontologists and their ilk. Anything during that time frame but not to do with humans is not history in this academic sense. Remember that this is all arguable, that it is one person's definition of history. What do you think? Is Bloch too narrow in defining it to include only humans?

If that is a 'good' definition of history, let's look at a 'bad' one, and the reasons it is 'bad'. The twentieth century English historian Arthur Marwick provided us with a longer definition, which has a few problems with it if we dissect his statement in detail:

[History is] bodies of knowledge about the past produced by historians, together with everything that is involved in the production, communication of and the teaching about that knowledge

This definition states that history is done by 'historians'. Who is a historian? Well, it is someone who 'teaches' and 'communicates' the knowledge that they have 'produced', although how the historian produces that knowledge is open for discussion. This definition does not provide us with any hint about historical method. It also implies that history can only be undertaken by certified 'historians', people who have 'communicated' - published - their research. It also implies that real history is a profession, as it is inextricably linked with teaching.

So, by this definition, stop your Wikiversity history courses now! Unless you can get published and begin teaching, you arn't a historian and there is no point in trying to be one. If you would like to try, then you will have to come up with your own method first.

Lecture Two: Historical methodology
History has its own version of scientific method, and we have seen above how this came into being and why. So what is the method?

Object of Study
As discussed above, you must start with an object of study. This should be stated as either a title or a question - that is up to you. So, let's say that as part of a four year degree course in Strategic Studies at Wikiversity, we are conducting a study in to the media reporting of the 1982 Falklands War. The title of our study will be: Was Truth the First Casualty in the Falklands War?

Initial Hypothesis
Now that you have a question, begin your research with a hypothesis. What do you think the answer to your chosen question is? This can be based on what little you have read so far, or just on a gut feeling. It doesn't matter particularly, since we are going to research it and prove or disprove it later. It is just there initially to give you a focus in your investigation. For our study: Truth was the first casualty in the Falklands War.

Research using Sources
Now you must research the question, using a mixture of available sources. There are different types of sources, organised in to primary, secondary and tertiary categories. Click on the links for more information, but roughly, primary sources are original documents such as letters, speeches, government reports etc; secondary sources are articles, essays and books based on primary sources (what you would recognise as a history book in your local bookshop) and tertiary sources are a more peripheral type of source which compiles primary and secondary source material, such as an encyclopedia or a library catalogue.

Your research should include as wide a range of primary sources and existing literature as possible, while attempting to stay away from using tertiary sources since they relate more to the practice of scholarship than your scholarship itself.

Note down all the ideas and quotations that you take from your sources, documenting the page number, the title, author, publisher, year published and place published, since you will need to cite these details in your final report to prove to others that you are not plagiarising exisiting ideas.

While you are researching, do not forget your object of study! All your notes and personal thoughts should be geared towards answering your question.

Conclusion
You will come to a conclusion based on your research. This is crucial. From your interpretation of the research that you have done, what is the answer? This is why we have a scientific method - your conclusion comes from a logical interpretation of the available evidence, not on a whim or swiftly-arrived-at idea - it's why we sought to prove or prove wrong your original hypothesis rather than just accept it.

Lecture Three: Methodologies in Political Science
This lecture is yet to be written.

Lecture Four: Writing an Essay
An essay will follow the method above. It will have three main parts:
 * An introduction
 * With a thesis statement (what your argument is)

 * A Main Body
 * A Conclusion

Rather than including your preliminary hypothesis in the introduction if your research has proved it wrong, include the thesis - the argument you support and will outline that you have arrived at after extensive research.

An old mantra about essay writing goes:

Say what you're going to say, say it, say what you've said. Although this is not strictly true, do keep it in mind when reading below how to craft an essay.

The Introduction
This should answer three questions:
 * 1) What is the essay about?
 * 2) Why is this topic important?
 * 3) How is the essay structured?

This then leads to a THESIS STATEMENT: what are you arguing?

In practice, the introduction will contain a 'hook' (something which gets you started), definitions of key terms, your thesis statement and an outline of the essay.

The Main Body
This is an elaboration of your thesis statement. It is the proof - you explain the points which caused you to arrive at your thesis, and the evidence that you found to support this. This is where you cite the research you did - any disputable fact or point made originally by someone else (i.e. it isn't your intellectual property) should be referenced.

The main body will show that your thesis is valid by doing making a series of points:
 * Point One - explain, qualify, discuss or compare
 * Point Two - explain, qualify, discuss or compare
 * Point Three - explain, qualify, discuss or compare
 * etc

This takes up the bulk of your available word count.

Conclusion
Restate your argument and explain now, in the light of your points, why you arrived at this belief yourself. It is not a summary - it is where you explain to the reader how all the points you just made fit together to support your thesis.

Lecture Five: Citing Sources
The Wikiversity Policy on Citing Sources can be found here

CITE YOUR SOURCES! Whether you are writing an essay, a lesson for Wikiversity or an article for Wikipedia, you must show where you got your evidence and ideas from. Anything which was not originally said or thought up by you must be cited.

If you are using someone else's words, word for word, you must put this passage in 'single quotation marks' and reference it after the next punctuation point. If you take someone's idea but express it in your own words, you must again reference that after the next available punctuation point. It may be in your own words, but it isn't your own point.

Your sources should be cited as footnotes in the text, and again as simple entries in a bibliography at the end of the essay.

Below is a guide on how to reference common resources. They take the form of bibliographical entries. For footnotes, you should also append the relevant page number(s) onto the end of the information so that the person reading your work can look up the exact same sources as you used.

Cite books like this
Surname, Forename (Year Published) Title in Italics: Include all subheadings, Edition Name if you did not use the first edition (City published: Published)

eg: Knightley, Phillip (2003) The First Casualty: The War Correspondent as Hero and Myth-Maker from the Crimea to Iraq, Updated Edn (London: Andre Deutsch)

Cite journals like this
Surname, Forename 'Title of Article in Single Marks' Title of Journal in Italics Volume Number, Issue Number (Date), Pages the article runs from and to in the journal

eg: Mearscheimer, John 'A Strategic Misstep: The Maritime Strategy and Deterrence in Europe' International Security Vol. 11, No. 2 (Autumn, 1986), pp. 3-57

title: Political and historical methodology


text:
10 Minutes 38 Seconds in This Strange World

10 Minutes 38 Seconds in This Strange World (On Dakika Otuz Sekiz Saniye) is a 2019 novel by Turkish writer Elif Shafak and her eleventh overall. It is a one-woman story about a sex worker in Istanbul. It was released by Viking Press in 2019.

Summary
10 Minutes and 38 Seconds in This Strange World opens in 1990 with "Tequila Leila", who is a prostitute. The story has her five outcast friends, who don't share a worthy importance in an illiberal country. Leila enters the state of awareness in her last moments, after she has been murdered and left in a dumpster outside Istanbul. "While the Turkish sun rises above her and her friends asleep soundly nearby, she contemplates her mortal existence before eternal rest." In the last minutes she recalls her previous life; "the taste of spiced goat stew, sacrificed by her father to celebrate the long-awaited birth of a son; the sight of bubbling vats of lemon and sugar which the women use to wax their legs while the men attend mosque; the scent of cardamom coffee that Leila shares with a handsome student in the brothel where she works. Each memory, too, recalls the friends she made at each key moment in her life—friends who are now desperately trying to find her..."

Awards

 * Shortlisted for the 2019 Booker Prize.
 * The Blackwell's Book of the Year, 2019
 * Shortlisted for RSL Ondaatje Prize, 2020


text:
Circuit Theory/Systems of Linear Equations

Linear equations
a1,a2, etc. are called the coefficients of the equations and b is called the constant term. Variables in linear algebra are usually denoted by xn instead of x, y, z, etc. because real world problems can have millions of variables. Problems in this text will have no more than 5 or 6.

Terms that appear on the left side of a linear equation must have a power of exactly 1. Terms that appear on the right hand side must have a power of zero.

Examples

1. $$2x_1 - 5x_2 + x_3 = 9 \!$$ a linear equation

2. $$x_1 + 2x_2 + 2\sqrt{x_3} = 1 \!$$ NOT a linear equation because of the square root. A square root $$\sqrt{x_3}$$ is the same as $$x_3$$ to the power $$1/2$$ and not to the power 1.

3. $$-10x_1 + 2x_2 = 0 \!$$ a linear equation

4. $$x_1x_2 + 2x_3 = 0 \!$$ NOT a linear equation because $$x_1x_2 $$ is a term of power 2.

Systems of linear equations
Note that if the coefficient of a variable in a linear equation is zero, we could omit it. Therefore not every variable needs to be present in every equation. Below are two systems of linear equations:

1. $$\begin{matrix}2x_1&-2x_2&+x_3&=&1\\-3x_1&+2x_2&&=&3\\3x_1&+2x_2&+x_3&=&7\end{matrix}$$

2. $$\begin{matrix}2x_1&-2x_2&-x_3&+2x_4&=&0\\-3x_1&&+2x_3&&=&0\\3x_1&+2x_2&+x_3&-x_4&=&0\end{matrix}$$

The second system is called a homogeneous system as all the constant terms are zero.

Usually, a system of linear equations consists of two or more linear equations that have the same variables. Theoretically, we may treat a single linear equation as a system also.

Matrix formulation
Arrange the coefficients of a linear system in a m-by-n matrix (i.e. an array with m rows and n columns), we get

 * $$A=\left(\begin{matrix}

a_{11}&a_{12}&\cdots&a_{1n}\\ a_{21}&a_{22}&\cdots&a_{2n}\\ \cdots&\cdots&\cdots&\cdots\\ a_{m1}&a_{m2}&\cdots&a_{mn} \end{matrix}\right)$$

and let $$b=\left(\begin{matrix}b_1\\b_2\\\vdots\\b_n\end{matrix}\right)$$ and $$x=\left(\begin{matrix}x_1\\x_2\\\vdots\\x_n\end{matrix}\right)$$. The system of linear equations could be written as

 * $$Ax=b$$

This motivates the study of matrix theory. For further introduction, see Linear Algebra/Matrices.

Solutions of systems of linear equations
A solution of a system of linear equations is a set of numbers for each variable that makes every equation true. For example, a solution of the first system given is (0,1.5,4) because 2(0)-1.5(2)+1(4)=1, -3(0)+2(1.5)=3, and 3(0)+2(1.5)+4=7.

See Algebra/Solutions of systems of linear equations.

Applications
Solving systems of linear equations is essential in modern engineering. Physical systems of high complexity, which would require impossible formulas to describe, are approximated with high accuracy by solving a very large set of linear equations. By breaking the subject at hand into tiny, finite pieces, a solution can be obtained after a great deal of brute-force calculation. When such numerical analysis introduces errors into the calculation at hand, a sufficiently complex analysis often makes up for the simplifications often introduced in less numerical methods. Error can be avoided with smaller pieces or with more sophisticated algorithms. Specific methods include finite difference analysis, finite element analysis, and boundary layer analysis. Specific applications include computational fluid dynamics, heat transfer, fatigue analysis, strain analysis, and stress analysis.

Systems of linear equations are also used in statistical regression. A common algorithm for the least squares regression uses a matrix with n rows and m columns, where n represents the number of data points and m represents the number of base functions, or the number of coefficients sought. (A polynomial ax^3 + bx^2 + cx + d, for example, uses four base functions: x^3, x^2, x, and 1.) A good explanation of this algorithm may be found in Numerical Recipes: The Art of Scientific Computing.


text:
Wikipedia:Sockpuppet investigations/Wiki watchdog/Archive

02 July 2012

 * Suspected sockpuppets

 * User compare report Auto-generated every hour.

Multiple accounts used to contest a suggested deletion of a page, all created within a day or two, all expressing the same opinions on the same page and all using the same writing style. All of them also make the same misspellings and grammatical mistakes. Wiki watchdog, a new user, is also posing as a person of authority on Wikipedia, telling others that the matter can no longer be discussed. Thomas.W (talk) 19:46, 2 July 2012 (UTC)

 * I'm requesting checkuser to confirm socking with the other accounts and check for sleeper accounts. Thomas.W (talk) 20:48, 2 July 2012 (UTC)

Comments by other users

Clerk, CheckUser, and/or patrolling admin comments

 * - There are a few distinct editing characteristics that match cleanly. Dennis Brown -  2¢    ©  19:03, 5 July 2012 (UTC)

The following are ✅ matches to each other: This group is related to. Elockid  ( Talk ) 01:28, 6 July 2012 (UTC)
 * Accounts blocked, IP is on an autoblock. -- DQ  (ʞlɐʇ)  13:28, 6 July 2012 (UTC)


text:
Great Auclum National Speed Hill Climb

Great Auclum National Speed Hill Climb was a motorcar course close to Burghfield Common in the English county of Berkshire.

It was based in the grounds of a large country house, formerly owned by a family connected to Huntley and Palmer – the famous biscuit manufacturers at nearby Reading, Berkshire. The hill climb was organised by the Hants and Berks Motor Club as a National Speed Hill Climb. This was part of the RAC British Hill Climb Championship, and at 440 yd long it was the shortest of events in the Championship. The course travelled nearly as far downhill as it did up, with a finish almost level with the start. Motor Sport reported : "The ¼-mile course embraces two sharp corners, one banked, and a twisty section, so that a premium is set on initial acceleration and low-speed cornering."

Early days
Prior to World War Two at least one event took place at Burghfield, as the event was then known. In 1939 Motor Sport listed a forthcoming event: 27 May 1939, Sporting O.D.C. Speed event, Burghfield, which was cancelled. An event took place in June organised by the Frazer-Nash and Frazer-Nash B.M.W. C.C. and Sporting O.D.C. "The postponed speed hill-climb up the private drive of Neil Gardner's (sic ) house at Burghfield Common happened on 24 June, complete with adjacent funfair and Lord Nuffield to present the prizes." P.W. Neale set fastest time of the day in 27.0 secs "winning the 2-litre class from Fane's B.M.W."

Racing resumed in 1947 when: "Salvadori's monoposto Alfa-Romeo won its class in 25.2 sec., but couldn't be extended, and it was L.J.D. Bartlett's home-brewed Mercury Special which made f.t.d. in 23.5 sec." The following year Ken Wharton's Wharton Special "beautifully crisp and fearlessly handled, made f.t.d. in 23.34 sec., beating Stirling Moss (23.46 sec.), who drove absolutely superbly getting into third gear in his Cooper 500,..."

The end
The last event was held in 1974 and the site has now been re-developed for housing. However the course itself is still there as it was the rear drive to Great Auclum house, which has now been redeveloped. The track is in a poor state of repair and very overgrown.

Great Auclum Hill Climb past winners
Key: R = Course Record.

title: Great Auclum National Speed Hill Climb