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https://en.wikipedia.org/wiki/Artificial%20bee%20colony%20algorithm | In computer science and operations research, the artificial bee colony algorithm (ABC) is an optimization algorithm based on the intelligent foraging behaviour of honey bee swarm, proposed by Derviş Karaboğa (Erciyes University) in 2005.
Algorithm
In the ABC model, the colony consists of three groups of bees: employed bees, onlookers and scouts. It is assumed that there is only one artificial employed bee for each food source. In other words, the number of employed bees in the colony is equal to the number of food sources around the hive. Employed bees go to their food source and come back to hive and dance on this area. The employed bee whose food source has been abandoned becomes a scout and starts to search for finding a new food source. Onlookers watch the dances of employed bees and choose food sources depending on dances. The main steps of the algorithm are given below:
Initial food sources are produced for all employed bees
REPEAT
Each employed bee goes to a food source in her memory and determines a closest source, then evaluates its nectar amount and dances in the hive
Each onlooker watches the dance of employed bees and chooses one of their sources depending on the dances, and then goes to that source. After choosing a neighbour around that, she evaluates its nectar amount.
Abandoned food sources are determined and are replaced with the new food sources discovered by scouts.
The best food source found so far is registered.
UNTIL (requirements are met)
In |
https://en.wikipedia.org/wiki/Tribe%C4%8D | Tribeč () is a crystalline mountain range in western Slovakia, in the Inner Western Carpathians located in the Nitra Region. It is surrounded by the Danubian Lowland, Pohronský Inovec, Vtáčnik Mountains and the Upper Nitra Basin. Beech trees are predominate in the area. The highest mountain is Veľký Tribeč at . The area belongs to the Ponitrie Protected Landscape Area.
Landscape
The Tribeč mountain range is in length and about in width, which places it as the 50th largest series of mountains in Slovakia. It is surrounded by Zlaté Moravce, Topoľčany, Partizánske and Nitra, giving it a rectangular shape. Tribeč is also part of a larger belt of core mountains; The Fatra-Tatra Area. In the east, it connects to Pohronský Inovec and Vtáčnik, and descends into the Hornonitrian basin.
Disappearances
Since the popular Slovak bestseller book Trhlina and its follow-up film adaptation with the same name (The Rift), Tribeč became associated with conspiracies. Some are calling it the Bermuda Triangle of Slovakia.
The history of these strange disappearances dates back to the 18th and 19th century, when the first known legend was written.
References
Mountain ranges of Slovakia
Mountain ranges of the Western Carpathians |
https://en.wikipedia.org/wiki/Allotropes%20of%20sulfur | The element sulfur exists as many allotropes. In number of allotropes, sulfur is second only to carbon. In addition to the allotropes, each allotrope often exists in polymorphs (different crystal structures of the same covalently bonded S molecules) delineated by Greek prefixes (α, β, etc.).
Furthermore, because elemental sulfur has been an item of commerce for centuries, its various forms are given traditional names. Early workers identified some forms that have later proved to be single or mixtures of allotropes. Some forms have been named for their appearance, e.g. "mother of pearl sulfur", or alternatively named for a chemist who was pre-eminent in identifying them, e.g. "Muthmann's sulfur I" or "Engel's sulfur".
The most commonly encountered form of sulfur is the orthorhombic polymorph of , which adopts a puckered ring – or "crown" – structure. Two other polymorphs are known, also with nearly identical molecular structures. In addition to , sulfur rings of 6, 7, 9–15, 18, and 20 atoms are known. At least five allotropes are uniquely formed at high pressures, two of which are metallic.
The number of sulfur allotropes reflects the relatively strong S−S bond of 265 kJ/mol. Furthermore, unlike most elements, the allotropes of sulfur can be manipulated in solutions of organic solvents and are analysed by HPLC.
Phase diagram
The pressure-temperature (P-T) phase diagram for sulfur is complex (see image). The region labeled I (a solid region), is α-sulfur.
High pressure s |
https://en.wikipedia.org/wiki/Margaret%20T.%20Fuller | Margaret "Minx" T. Fuller is an American developmental biologist known for her research on the male germ line and defining the role of the stem cell environment (the hub cells that establish the niche of particular cells) in specifying cell fate and differentiation.
Fuller is the Reed-Hodgson Professor of Human Biology at Stanford University, and former chair of the Stanford Department of Developmental Biology.
Biography
Fuller earned a B.A. in physics from Brandeis University in 1974, and a Ph.D. in microbiology from MIT in 1980, working with Jonathan King. She completed her postdoctoral work in developmental genetics at Indiana University, working with Elizabeth Raff and Thomas Kaufman, from 1980 to 1983, Fuller joined the University of Colorado faculty and then joined Stanford University in 1990, where she began working on spermatogenesis, doing genetic analysis of microtubule structure and function.
Fuller is married to fellow biologist Matthew P. Scott.
Key papers
Raff, E.C. and M. T. Fuller, et al., "Regulation of tubulin gene expression during embryogenesis in Drosophila melanogaster", Cell v.28, pp. 33–40 (1982).
Fuller, M.T. et al., "Genetic Analysis of Microtubule Structure: A b-tubulin Mutation Causes the Formation of Aberrant Microtubule in vivo and in vitro", Journal of Cell Biology, v.104, pp. 385–394 (1987).
Fuller, M.T. and P.G. Wilson, "Force and Counter Force in the Mitotic Spindle", Cell, v.71, pp. 547–550 (1992).
Fuller, M.T., "Riding the Polar W |
https://en.wikipedia.org/wiki/Cerebrospinal%20fluid%20rhinorrhoea | Cerebrospinal fluid rhinorrhoea (CSF rhinorrhoea) refers to the drainage of cerebrospinal fluid through the nose (rhinorrhoea). It is typically caused by a basilar skull fracture, which presents complications such as infection. It may be diagnosed using brain scans (prompted based on initial symptoms), and by testing to see if discharge from the nose is cerebrospinal fluid. Treatment may be conservative (as many cases resolve spontaneously), but usually involves neurosurgery.
Classification
CSF rhinorrhoea may be spontaneous, traumatic, or congenital.
Traumatic CSF rhinorrhoea is the most common type of CSF rhinorrhoea. It may be due to severe head injury, or from complications from neurosurgery.
Spontaneous CSF rhinorrhoea is the most common acquired defect in the skull base bones (anterior cranial fossa) causing spontaneous nasal liquorrhea. Defects are often localized in the sphenoid bone and the ethmoid bone.
sphenoid sinus (43%).
ethmoid bone (29%).
cribriform plate (29%).
Congenital CSF rhinorrhoea is the least common type of CSF rhinorrhoea. It may be caused by problems in the embryological development of bones of the skull.
Signs and symptoms
CSF rhinorrhoea involves drainage of cerebrospinal fluid through the nose. This appears as a clear, colourless liquid.
Aldroubi sign "The liquid in CSF rhinorrhea is thin and clear, and an affected person might notice a sweet or salty taste due to the increased glucose and electrolytes present in cerebrospinal fluid so |
https://en.wikipedia.org/wiki/Glyoxalase%20system | The glyoxalase system is a set of enzymes that carry out the detoxification of methylglyoxal and the other reactive aldehydes that are produced as a normal part of metabolism. This system has been studied in both bacteria and eukaryotes. This detoxification is accomplished by the sequential action of two thiol-dependent enzymes; firstly glyoxalase І, which catalyzes the isomerization of the spontaneously formed hemithioacetal adduct between glutathione and 2-oxoaldehydes (such as methylglyoxal) into S-2-hydroxyacylglutathione. Secondly, glyoxalase ІІ hydrolyses these thiolesters and in the case of methylglyoxal catabolism, produces D-lactate and GSH from S-D-lactoyl-glutathione.
This system shows many of the typical features of the enzymes that dispose of endogenous toxins. Firstly, in contrast to the amazing substrate range of many of the enzymes involved in xenobiotic metabolism, it shows a narrow substrate specificity. Secondly, intracellular thiols are required as part of its enzymatic mechanism and thirdly, the system acts to recycle reactive metabolites back to a form which may be useful to cellular metabolism.
Overview of Glyoxalase Pathway
Glyoxalase I (GLO1), glyoxalase II (GLO2), and reduced glutathione (GSH). In bacteria, there is an additional enzyme that functions if there is no GSH, it is called the third glyoxalase protein, glyoxalase 3 (GLO3). GLO3 has not been found in humans yet.
The pathway begins with methylglyoxal (MG), which is produced from non-enzy |
https://en.wikipedia.org/wiki/MT-TL1 | Mitochondrially encoded tRNA leucine 1 (UUA/G) also known as MT-TL1 is a transfer RNA which in humans is encoded by the mitochondrial MT-TL1 gene.
Structure
The MT-TL1 gene is located on the p arm of the mitochondrial DNA at position 12 and it spans 75 base pairs. The structure of a tRNA molecule is a distinctive folded structure which contains three hairpin loops and resembles a three-leafed clover.
Function
MT-TL1 is a small 75 nucleotide RNA (human mitochondrial map position 3230–3304) that transfers the amino acid leucine to a growing polypeptide chain at the ribosome site of protein synthesis during translation. Also, some studies showed that the MT-TL1 gene pathogenic variants could be attributed to the alterations of mTERF binding efficiency.
Clinical significance
Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes
Mutations in MT-TL1 can result in multiple mitochondrial deficiencies and associated disorders. It is associated with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS). MELAS is a rare mitochondrial disorder known to affect many parts of the body, especially the nervous system and the brain. Symptoms of MELAS include recurrent severe headaches, muscle weakness (myopathy), hearing loss, stroke-like episodes with a loss of consciousness, seizures, and other problems affecting the nervous system. A common mutation is A3243G. This mutation has been theorized to be associated with several other mitocho |
https://en.wikipedia.org/wiki/MT-TH | Mitochondrially encoded tRNA histidine, also known as MT-TH, is a transfer RNA which, in humans, is encoded by the mitochondrial MT-TH gene.
Structure
The MT-TH gene is located on the p arm of the mitochondrial DNA at position 12 and it spans 69 base pairs. The structure of a tRNA molecule is a distinctive folded structure which contains three hairpin loops and resembles a three-leafed clover.
Function
MT-TH is a small 69 nucleotide transfer RNA (human mitochondrial map position 12138–12206) that transfers the amino acid histidine to a growing polypeptide at the ribosomal site of protein synthesis during translation.
Clinical significance
Mutations in MT-TH can result in multiple mitochondrial deficiencies and associated disorders. MT-TH is associated with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS), cardiomyopathy, and the MELAS/MERRF overlap syndrome.
Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS)
A small number of people with symptoms of mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) have been found to have mutations in the MT-TH gene. MELAS is a rare mitochondrial disorder known to affect many parts of the body, especially the nervous system and the brain. Symptoms of MELAS include recurrent severe headaches, muscle weakness (myopathy), hearing loss, stroke-like episodes with a loss of consciousness, seizures, and other problems affecting the nervous syste |
https://en.wikipedia.org/wiki/MT-ND5 | MT-ND5 is a gene of the mitochondrial genome coding for the NADH-ubiquinone oxidoreductase chain 5 protein (ND5). The ND5 protein is a subunit of NADH dehydrogenase (ubiquinone), which is located in the mitochondrial inner membrane and is the largest of the five complexes of the electron transport chain. Variations in human MT-ND5 are associated with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) as well as some symptoms of Leigh's syndrome and Leber's hereditary optic neuropathy (LHON).
Structure
MT-ND5 is located in mitochondrial DNA from base pair 12,337 to 14,148. The MT-ND5 gene produces a 67 kDa protein composed of 603 amino acids. MT-ND5 is one of seven mitochondrial genes encoding subunits of the enzyme NADH dehydrogenase (ubiquinone), together with MT-ND1, MT-ND2, MT-ND3, MT-ND4, MT-ND4L, and MT-ND6. Also known as Complex I, this enzyme is the largest of the respiratory complexes. The structure is L-shaped with a long, hydrophobic transmembrane domain and a hydrophilic domain for the peripheral arm that includes all the known redox centres and the NADH binding site. MT-ND5 and the rest of the mitochondrially encoded subunits are the most hydrophobic of the subunits of Complex I and form the core of the transmembrane region.
Function
The MT-ND5 product is a subunit of the respiratory chain Complex I that is supposed to belong to the minimal assembly of core proteins required to catalyze NADH dehydrogenation and electron transfer |
https://en.wikipedia.org/wiki/MT-ND1 | MT-ND1 is a gene of the mitochondrial genome coding for the NADH-ubiquinone oxidoreductase chain 1 (ND1) protein. The ND1 protein is a subunit of NADH dehydrogenase, which is located in the mitochondrial inner membrane and is the largest of the five complexes of the electron transport chain. Variants of the human MT-ND1 gene are associated with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS), Leigh's syndrome (LS), Leber's hereditary optic neuropathy (LHON) and increases in adult BMI.
Structure
MT-ND1 is located in mitochondrial DNA from base pair 3,307 to 4,262. The MT-ND1 gene produces a 36 kDa protein composed of 318 amino acids. MT-ND1 is one of seven mitochondrial genes encoding subunits of the enzyme NADH dehydrogenase (ubiquinone), together with MT-ND2, MT-ND3, MT-ND4, MT-ND4L, MT-ND5, and MT-ND6. Also known as Complex I, this enzyme is the largest of the respiratory complexes. The structure is L-shaped with a long, hydrophobic transmembrane domain and a hydrophilic domain for the peripheral arm that includes all the known redox centres and the NADH binding site. The MT-ND1 product and the rest of the mitochondrially encoded subunits are the most hydrophobic of the subunits of Complex I and form the core of the transmembrane region.
Function
MT-ND1-encoded NADH-ubiquinone oxidoreductase chain 1 is a subunit of the respiratory chain Complex I that is supposed to belong to the minimal assembly of core proteins required to catalyze |
https://en.wikipedia.org/wiki/Proteinase%20K | In molecular biology, Proteinase K (, protease K, endopeptidase K, Tritirachium alkaline proteinase, Tritirachium album serine proteinase, Tritirachium album proteinase K) is a broad-spectrum serine protease. The enzyme was discovered in 1974 in extracts of the fungus Parengyodontium album (formerly Engyodontium album or Tritirachium album). Proteinase K is able to digest hair (keratin), hence, the name "Proteinase K". The predominant site of cleavage is the peptide bond adjacent to the carboxyl group of aliphatic and aromatic amino acids with blocked alpha amino groups. It is commonly used for its broad specificity. This enzyme belongs to Peptidase family S8 (subtilisin). The molecular weight of Proteinase K is 28,900 daltons (28.9 kDa).
Enzyme activity
Activated by calcium, the enzyme digests proteins preferentially after hydrophobic amino acids (aliphatic, aromatic and other hydrophobic amino acids). Although calcium ions do not affect the enzyme activity, they do contribute to its stability.
Proteins will be completely digested if the incubation time is long and the protease concentration high enough. Upon removal of the calcium ions, the stability of the enzyme is reduced, but the proteolytic activity remains. Proteinase K has two binding sites for Ca2+, which are located close to the active center, but are not directly involved in the catalytic mechanism. The residual activity is sufficient to digest proteins, which usually contaminate nucleic acid preparations. The |
https://en.wikipedia.org/wiki/Product%20inhibition | Product inhibition is a type of enzyme inhibition where the product of an enzyme reaction inhibits its production. Cells utilize product inhibition to regulate of metabolism as a form of negative feedback controlling metabolic pathways. Product inhibition is also an important topic in biotechnology, as overcoming this effect can increase the yield of a product, such as an antibiotic. Product inhibition can be Competitive, non-competitive or uncompetitive.
Mitigation of product inhibition
Reactor Design
One method to reduce product inhibition is the use of a membrane reactor. These bioreactors uses a membrane to separate products from the rest of the reactor, limiting their inhibition. If the product differs greatly in size from the cells producing it, and the substrate feeding the cells, then the reactor can utilize a semipermeable membrane allowing to products to exit the reactor while leaving the cells and substrate behind to continue reacting making more product. Other reactor systems use chemical potential to separate products from the reactor, such as solubility of different compounds allowing one to pass through the membrane. Electrokinetic bioreactor systems have been developed which use electrolysis, a process that uses electrical charge to remove the product from the bioreactor system.
External loop reactor uses current created by air bubbles flowing through the reactor to create a flow that brings the reactor contents through an external loop. A separating mem |
https://en.wikipedia.org/wiki/Bayes%20linear%20statistics | Bayes linear statistics is a subjectivist statistical methodology and framework. Traditional subjective Bayesian analysis is based upon fully specified probability distributions, which are very difficult to specify at the necessary level of detail. Bayes linear analysis attempts to solve this problem by developing theory and practise for using partially specified probability models. Bayes linear in its current form has been primarily developed by Michael Goldstein. Mathematically and philosophically it extends Bruno de Finetti's Operational Subjective approach to probability and statistics.
Motivation
Consider first a traditional Bayesian Analysis where you expect to shortly know D and you would like to know more about some other observable B. In the traditional Bayesian approach it is required that every possible outcome is enumerated i.e. every possible outcome is the cross product of the partition of a set of B and D. If represented on a computer where B requires n bits and D m bits then the number of states required is . The first step to such an analysis is to determine a person's subjective probabilities e.g. by asking about their betting behaviour for each of these outcomes. When we learn D conditional probabilities for B are determined by the application of Bayes' rule.
Practitioners of subjective Bayesian statistics routinely analyse datasets where the size of this set is large enough that subjective probabilities cannot be meaningfully determined for every |
https://en.wikipedia.org/wiki/Generalized%20Ozaki%20cost%20function | In economics the generalized-Ozaki cost is a general description of cost described by Shuichi Nakamura.
For output y, at date t and a vector of m input prices p, the generalized-Ozaki cost, c, is
Discussion
In econometrics it is often desirable to have a model of the cost of production of a given output with given inputs—or in common terms, what it will cost to produce some number of goods at prevailing prices, or given prevailing prices and a budget, how much can be made. Generally there are two parts to a cost function, the fixed and variable costs involved in production.
The marginal cost is the change in the cost of production for a single unit. Most cost functions then take the price of the inputs and adjust for different factors of production, typically, technology, economies of scale, and elasticities of inputs.
Traditional cost functions include Cobb–Douglas and the constant elasticity of substitution models. These are still used because for a wide variety of activities, effects such as varying ability to substitute materials does not change. For example, for people running a bake sale, the ability to substitute one kind of chocolate chip for another will not vary over the number of cookies they can bake. However, as economies of scale and changes in substitution become important models that handle these effects become more useful, such as the transcendental log cost function.
The traditional forms are economically homothetic. This means they can be expressed a |
https://en.wikipedia.org/wiki/Allovectin-7 | Allovectin-7 is a substance that is being studied as a gene therapy agent in the treatment of cancer, such as malignant melanoma. It is a plasmid/lipid complex containing the DNA sequences encoding HLA-B7 and ß2 microglobulin - two components of major histocompatibility complex (MHC, class I). It increases the ability of the immune system to recognize cancer cells and kill them.
In 1999, FDA granted Allovectin-7 orphan drug designation for the treatment of invasive and metastatic melanoma.
References
Allovectin-7 entry in the public domain NCI Dictionary of Cancer Terms
Experimental cancer drugs |
https://en.wikipedia.org/wiki/ALVAC-CEA%20vaccine | ALVAC-CEA vaccine is a cancer vaccine containing a canary pox virus (ALVAC) combined with the carcinoembryonic antigen (CEA) human gene.
A phase I trial in 118 patients showed safety in humans.
References
External links
ALVAC-CEA vaccine entry in the public domain NCI Dictionary of Cancer Terms
Cancer vaccines |
https://en.wikipedia.org/wiki/Personal%20genomics | Personal genomics or consumer genetics is the branch of genomics concerned with the sequencing, analysis and interpretation of the genome of an individual. The genotyping stage employs different techniques, including single-nucleotide polymorphism (SNP) analysis chips (typically 0.02% of the genome), or partial or full genome sequencing. Once the genotypes are known, the individual's variations can be compared with the published literature to determine likelihood of trait expression, ancestry inference and disease risk.
Automated high-throughput sequencers have increased the speed and reduced the cost of sequencing, making it possible to offer whole genome sequencing including interpretation to consumers since 2015 for less than $1,000. The emerging market of direct-to-consumer genome sequencing services has brought new questions about both the medical efficacy and the ethical dilemmas associated with widespread knowledge of individual genetic information.
In personalized medicine
Personalized medicine is a medical method that targets treatment structures and medicinal decisions based on a patient's predicted response or risk of disease. The National Cancer Institute or NCI, an arm of the National Institutes of Health, lists a patient's genes, proteins, and environment as the primary factors analyzed to prevent, diagnose, and treat disease through personalized medicine.
There are various subcategories of the concept of personalized medicine such as predictive medicine, pr |
https://en.wikipedia.org/wiki/Generalized%20Hebbian%20algorithm | The generalized Hebbian algorithm (GHA), also known in the literature as Sanger's rule, is a linear feedforward neural network model for unsupervised learning with applications primarily in principal components analysis. First defined in 1989, it is similar to Oja's rule in its formulation and stability, except it can be applied to networks with multiple outputs. The name originates because of the similarity between the algorithm and a hypothesis made by Donald Hebb about the way in which synaptic strengths in the brain are modified in response to experience, i.e., that changes are proportional to the correlation between the firing of pre- and post-synaptic neurons.
Theory
The GHA combines Oja's rule with the Gram-Schmidt process to produce a learning rule of the form
,
where defines the synaptic weight or connection strength between the th input and th output neurons, and are the input and output vectors, respectively, and is the learning rate parameter.
Derivation
In matrix form, Oja's rule can be written
,
and the Gram-Schmidt algorithm is
,
where is any matrix, in this case representing synaptic weights, is the autocorrelation matrix, simply the outer product of inputs, is the function that diagonalizes a matrix, and is the function that sets all matrix elements on or above the diagonal equal to 0. We can combine these equations to get our original rule in matrix form,
,
where the function sets all matrix elements above the diagonal equal to 0, and not |
https://en.wikipedia.org/wiki/Catabolysis | Catabolysis is a biological process in which the body breaks down fat and muscle tissue in order to stay alive. Catabolysis occurs only when there is no longer any source of protein, carbohydrate, or vitamin nourishment feeding all body systems; it is the most severe type of malnutrition.
Mechanism
Due to the normal metabolic rate of humans catabolysis becomes life-threatening only after 1–2 months from the cessation of nutrition going into the body. After this time, the damage to muscles and organs can be permanent and can also eventually cause death, if left untreated. Catabolysis is the last metabolic resort for the body to keep itself — particularly the nervous system—functional.
Protein stores, especially in muscle tissue, provide the amino acids needed for the process. Amino acids are released into the blood and converted in the liver to alpha keto acids. Alpha keto acids can then be converted to glucose to maintain proper blood sugar levels.
The situation can become dire when one begins to lose muscle mass; this is a sign that the fat has been expended and the body is now metabolizing the muscle tissue. This results in muscle atrophy, a loss of strength and, ultimately, a depletion of muscular tissue completely. Muscle weakness is not necessarily a symptom of catabolysis: the muscles will normally feel fatigued when they are not receiving enough energy or oxygen. Ultimately, catabolysis can progress to the point of no return when the body's machinery for protei |
https://en.wikipedia.org/wiki/Gerald%20Pearson | Gerald L. Pearson (March 31, 1905 – October 25, 1987) was a physicist whose work on silicon rectifiers at Bell Labs led to the invention of the solar cell. In 2008, he was inducted into the National Inventors Hall of Fame.
Biography
Pearson was born in Salem, Oregon. He took a bachelor's degree in mathematics and physics from Willamette University and a master's degree in physics from Stanford University. From 1929 he worked as a research physicist at Bell Labs and his early work on temperature-sensitive resistors led to 13 patents on thermistors. After World War II he was part of William Shockley's group, where his experimental results were essential in developing models of semiconductor behaviour. In 1946, acting on a suggestion by Shockley he put a voltage on a droplet of glycol borate (gu) placed across a P-N junction producing the first evidence of power amplification in the search for the transistor.
In 1954 his work on silicon rectifiers led to the first practical photovoltaic cell (solar cell), together with Daryl Chapin and Calvin Souther Fuller.
He took early retirement from Bell in 1960 to take up the position of professor of electrical engineering at Stanford setting up a research program on compound semiconductors.
Awards and honors
In 1964, Pearson received the Golden Plate Award of the American Academy of Achievement.
References
External links
Oral history interview transcript with Gerald Pearson on 23 August 1976, American Institute of Physics, Niel |
https://en.wikipedia.org/wiki/Grain%20boundary%20strengthening | In materials science, grain-boundary strengthening (or Hall–Petch strengthening) is a method of strengthening materials by changing their average crystallite (grain) size. It is based on the observation that grain boundaries are insurmountable borders for dislocations and that the number of dislocations within a grain has an effect on how stress builds up in the adjacent grain, which will eventually activate dislocation sources and thus enabling deformation in the neighbouring grain as well. By changing grain size, one can influence the number of dislocations piled up at the grain boundary and yield strength. For example, heat treatment after plastic deformation and changing the rate of solidification are ways to alter grain size.
Theory
In grain-boundary strengthening, the grain boundaries act as pinning points impeding further dislocation propagation. Since the lattice structure of adjacent grains differs in orientation, it requires more energy for a dislocation to change directions and move into the adjacent grain. The grain boundary is also much more disordered than inside the grain, which also prevents the dislocations from moving in a continuous slip plane. Impeding this dislocation movement will hinder the onset of plasticity and hence increase the yield strength of the material.
Under an applied stress, existing dislocations and dislocations generated by Frank–Read sources will move through a crystalline lattice until encountering a grain boundary, where the large a |
https://en.wikipedia.org/wiki/Signet%20ring%20cell%20carcinoma | Signet ring cell carcinoma (SRCC) is a rare form of highly malignant adenocarcinoma that produces mucin. It is an epithelial malignancy characterized by the histologic appearance of signet ring cells.
Primary SRCC tumors are most often found in the glandular cells of the stomach (SRCC originates in the stomach in 56 percent of patients), and less frequently in the breast, gallbladder, urinary bladder, and pancreas. SRCCs do not normally form in the lungs, though a few instances have been reported.
Among colorectal cancers, the prevalence of SRCC is less than one percent. Though incidence and mortality of gastric cancer has declined in many countries over the past 50 years, there has been an increase in occurrences of gastric SRCC-type cancers.
SRCC tumors grow in characteristic sheets, which makes diagnosis using standard imaging techniques, like CT and PET scans, less effective.
Causes
Some cases are inherited, and these cases are often caused by mutations in the CDH1 gene, which encodes the important cell–cell adhesion glycoprotein E-cadherin. Somatic mutations of the APC gene have also been implicated in the development of gastric SRCCs.
The role of other risk factors in gastric cancer such as salt-preserved food, smoking, auto-immune gastritis are not well studied in SRCC.
Mechanism of formation
SRCCs are dedifferentiated adenocarcinomas that lose the capability for cell–cell interaction.
Highly differentiated adenocarcinomas form SRCCs via a loss of adherens an |
https://en.wikipedia.org/wiki/National%20Health%20and%20Nutrition%20Examination%20Survey | The National Health and Nutrition Examination Survey (NHANES) is a survey research program conducted by the National Center for Health Statistics (NCHS) to assess the health and nutritional status of adults and children in the United States, and to track changes over time. The survey combines interviews, physical examinations and laboratory tests.
The NHANES interview includes demographic, socioeconomic, dietary, and health-related questions. The examination component consists of medical, dental, and physiological measurements, as well as laboratory tests administered by medical personnel.
The first NHANES was conducted in 1971, and in 1999 the surveys became an annual event; the first report on the topic was published in 2001.
NHANES findings are used to determine the prevalence of major diseases and risk factors for diseases. Information is used to assess nutritional status and its association with health promotion and disease prevention. NHANES findings are also the basis for national standards for such measurements as height, weight, and blood pressure. NHANES data are used in epidemiological studies and health sciences research (including biomarkers of aging), which help develop sound public health policy, direct and design health programs and services, expand health knowledge, extend healthspan and lifespan.
Follow-up studies using NHANES data were made possible by creating linked mortality files and files based on Medicare and Medicaid data.
See also
National Arc |
https://en.wikipedia.org/wiki/Floral%20Genome%20Project | The Floral Genome Project is a collaborative research cooperation primarily between Penn State University, University of Florida, and Cornell University. The initial funding came from a grant of $7.4 million from the National Science Foundation. The Floral Genome Project was initiated to bridge the genomic gap between the most broadly studied plant model systems. According to the website, the following are the aims of the project:
External links
Official Website
Genome projects
Botany
University of Florida
Cornell University |
https://en.wikipedia.org/wiki/Biological%20neuron%20model | Biological neuron models, also known as a spiking neuron models, are mathematical descriptions of neurons. In particular, these models describe how the voltage potential across the cell membrane changes over time. In an experimental setting, stimulating neurons with an electrical current generates an action potential (or spike), that propagates down the neuron's axon. This spike branches out to a large number of downstream neurons, where the signals terminate at synapses. As many as 85% of neurons in the neocortex, the outermost layer of the mammalian brain, consist of excitatory pyramidal neurons, and each pyramidal neuron receives tens of thousands of inputs from other neurons. Thus, spiking neurons are a major information processing unit of the nervous system.
One such example of a spiking neuron model may be a highly detailed mathematical model that includes spatial morphology. Another may be a conductance-based neuron model that views neurons as points and describes the membrane voltage dynamics as a function of transmembrane currents. A mathematically simpler "integrate-and-fire" model significantly simplifies the description of ion channel and membrane potential dynamics (initially studied by Lapique in 1907).
Introduction: Biological background, classification and aims of neuron models
Non-spiking cells, spiking cells, and their measurement
Not all the cells of the nervous system produce the type of spike that define the scope of the spiking neuron models. For ex |
https://en.wikipedia.org/wiki/Adenosine%20A2B%20receptor | {{DISPLAYTITLE:Adenosine A2B receptor}}
The adenosine A2B receptor, also known as ADORA2B, is a G-protein coupled adenosine receptor, and also denotes the human adenosine A2b receptor gene which encodes it.
Mechanism
This integral membrane protein stimulates adenylate cyclase activity in the presence of adenosine. This protein also interacts with netrin-1, which is involved in axon elongation.
Gene
The gene is located near the Smith-Magenis syndrome region on chromosome 17.
Ligands
Research into selective A2B ligands has lagged somewhat behind the development of ligands for the other three adenosine receptor subtypes, but a number of A2B-selective compounds have now been developed, and research into their potential therapeutic applications is ongoing.
Agonists
BAY 60-6583
NECA (N-ethylcarboxamidoadenosine)
(S)-PHPNECA - high affinity and efficacy at A2B, but poor selectivity over other adenosine receptor subtypes
LUF-5835
LUF-5845 - partial agonist
Antagonists and inverse agonists
Compound 38: antagonist, high affinity and good subtype selectivity
ISAM-R56A: non-xanthinic high affinity selective antagonist (Ki: 1.50 nM)
ISAM-140: non-xanthinic selective antagonist (Ki = 3.49 nM).
ISAM-R324A: Soluble and metabolically stable non-xanthinic selective antagonist (Ki = 6.10 nM).
ATL-801
CVT-6883
MRS-1706
MRS-1754
OSIP-339,391
PSB-603: xanthinic antagonist
PSB-0788: xanthinic antagonist
PSB-1115: xanthinic antagonist
PSB-1901: xanthinic antagonist with |
https://en.wikipedia.org/wiki/Brain-specific%20angiogenesis%20inhibitor%201 | Brain-specific angiogenesis inhibitor 1 is a protein that in humans is encoded by the BAI1 gene. It is a member of the adhesion-GPCR family of receptors.
Function
Angiogenesis is controlled by a local balance between stimulators and inhibitors of new vessel growth and is suppressed under normal physiologic conditions. Angiogenesis has been shown to be essential for growth and metastasis of solid tumors. In order to obtain blood supply for their growth, tumor cells are potently angiogenic and attract new vessels as results of increased secretion of inducers and decreased production of endogenous negative regulators. BAI1 contains at least one 'functional' p53-binding site within an intron, and its expression has been shown to be induced by wildtype p53. There are two other brain-specific angiogenesis inhibitor genes, designated BAI2 and BAI3 which along with BAI1 have similar tissue specificities and structures, however only BAI1 is transcriptionally regulated by p53. BAI1 is postulated to be a member of the secretin receptor family, an inhibitor of angiogenesis and a growth suppressor of glioblastomas.
Interactions
Brain-specific angiogenesis inhibitor 1 has been shown to interact with BAIAP3 and MAGI1.
Model organisms
Model organisms have been used in the study of BAI1 function. A conditional knockout mouse line called Bai1tm2a(EUCOMM)Wtsi was generated at the Wellcome Trust Sanger Institute. Male and female animals underwent a standardized phenotypic screen to dete |
https://en.wikipedia.org/wiki/Brain-specific%20angiogenesis%20inhibitor%202 | Brain-specific angiogenesis inhibitor 2 is a protein that in humans is encoded by the BAI2 gene. It is a member of the adhesion-GPCR family of receptors.
BAI1, a p53-target gene, encodes brain-specific angiogenesis inhibitor, a seven-span transmembrane protein and is thought to be a member of the secretin receptor family. Brain-specific angiogenesis proteins BAI2 and BAI3 are similar to BAI1 in structure, have similar tissue specificities and may also play a role in angiogenesis.
References
External links
Further reading
G protein-coupled receptors |
https://en.wikipedia.org/wiki/Brain-specific%20angiogenesis%20inhibitor%203 | Brain-specific angiogenesis inhibitor 3 is a protein that in humans is encoded by the BAI3 gene.
BAI1, a p53-target gene, encodes brain-specific angiogenesis inhibitor, a seven-span transmembrane protein and is thought to be a member of the secretin receptor family. Brain-specific angiogenesis proteins BAI2 and BAI3 are similar to BAI1 in structure, have similar tissue specificities and may also play a role in angiogenesis. The BAI3 receptor has also been found to regulate dendrite morphogenesis, arborization growth and branching in cultured neurons.
The adhesion GPCR BaI3 is an orphan receptor that has a long N-terminus consisting of one cub domain, five BaI Thrombospondin type 1 repeats, and one hormone binding domain. BaI3 is expressed in neural tissues of the central nervous system. BaI3 has been shown to have a high affinity for C1q proteins. C1q added to hippocampal neurons expressing BaI3 resulted in a decrease in the number of synapses.
References
Further reading
External links
G protein-coupled receptors |
https://en.wikipedia.org/wiki/CD97 | Cluster of differentiation 97 is a protein also known as BL-Ac[F2] encoded by the ADGRE5 gene. CD97 is a member of the adhesion G protein-coupled receptor (GPCR) family.
Adhesion GPCRs are characterized by an extended extracellular region often possessing N-terminal protein modules that is linked to a TM7 region via a domain known as the GPCR-Autoproteolysis INducing (GAIN) domain.
CD97 is widely expressed on, among others, hematopoietic stem and progenitor cells, immune cells, epithelial cells, muscle cells as well as their malignant counterparts.
In the case of CD97 the N-terminal domains consist of alternatively spliced epidermal growth factor (EGF)-like domains. Alternative splicing has been observed for this gene and three variants have been found. The N-terminal fragment of CD97 contains 3-5 EGF-like domains in human and 3-4 EGF-like domains in mice.
Ligands
Decay accelerating factor (DAF/CD55), a regulatory protein of the complement cascade, interacts with the first and second EGF-like domains of CD97; chondroitin sulfate B with the fourth EGF-like domain; α5β1 and αvβ3 integrins with an RGD downstream the EGF-like domains; and CD90 (Thy-1) with the GAIN domain. N-glycosylation of CD97 within the EGF domains is crucial for CD55 binding.
Signaling
Transgenic expression of a CD97 in mice enhanced levels of nonphosphorylated membrane-bound β-catenin and phosphorylated Akt. Furthermore, ectopic CD97 expression facilitated RhoA activation through binding of Gα12/13 a |
https://en.wikipedia.org/wiki/Cerebrospinal%20fluid%20diversion | Cerebrospinal fluid diversion is a procedure that is used to drain fluid from the brain and spinal cord. A shunt is placed in a ventricle of the brain and threaded under the skin to another part of the body, usually the abdomen. It is used to treat hydrocephalus and idiopathic intracranial hypertension.
References
Neurology procedures |
https://en.wikipedia.org/wiki/Richard%20Tecwyn%20Williams | Richard Tecwyn Williams FRS (20 February 1909 – 29 December 1979) was a Welsh biochemist who founded the systematic study of xenobiotic metabolism with the publication of his book Detoxication mechanisms in 1947. This seminal book built on his earlier work on the role of glucuronic acid in the metabolism of borneol.
Biography
Williams was born in Abertillery, Wales, the first of five children of Richard Williams, a coalminer, and Mary Ellen (née Jones), a teacher. He grew up speaking Welsh and English. His initial schooling was at Gelli Crug Junior School, from where he gained a scholarship to Abertillery County School. This was followed by University College, Cardiff where he studied chemistry and physiology, and was awarded a BSc in 1928.
An opportunity arose for Williams to undertake research with Dr John Pryde at the Physiology Institute, Cardiff, where he worked on elucidating the structure of glucuronic acid. This work formed part of his PhD thesis; he was awarded the degree in 1932. After postdoctoral research at Cardiff he was appointed Lecturer in Biochemistry at the University of Birmingham in 1934. Here, Williams further developed his ideas concerning the metabolism of foreign compounds. His 1938 paper on detoxication of phenol in the rabbit proved to be the first in a series, culminating in Part 77 twenty years later. He was awarded a DSc at Birmingham in 1939.
In 1942, Williams was appointed Senior Lecturer in Biochemistry in the University of Liverpool. He |
https://en.wikipedia.org/wiki/CMKLR1 | Chemokine like receptor 1 also known as ChemR23 (Chemerin Receptor 23) is a protein that in humans is encoded by the CMKLR1 gene. Chemokine receptor-like 1 is a G protein-coupled receptor for the chemoattractant adipokine chemerin and the omega-3 fatty acid eicosapentaenoic acid-derived specialized pro-resolving molecule, resolvin E1 (see Specialized proresolving mediators#EPA-derived resolvins (i.e. RvE)). The murine receptor that shares almost 80% homology with the human receptor, is called Dez.
Tissue distribution
CMKLR1 shows wide RNA expression profile but is notably high in plasmacytoid dendritic cells, macrophages, cardiomyocytes, adipocytes and endothelial cells.
Function
Activating CMKLR1 by an agonist mobilizes intracellular calcium and causes the activation of several other signaling cascades like the ERK1 and NF-κB. Initial studies of CMKLR1 suggested that it might have a role in the inflammatory pathways. Its cognate ligand, chemerin was found in joint aspirate from rheumatoid arthritis and absent in aspirate from degenerative arthritis. CMKLR1 expression by plasmacytoid dendritic cells and macrophages also helped foster this idea. In vitro chemotaxis assays showed it to be utilized in attracting these cells. As an adipokine receptor it has a role in adipogenesis and adipocyte maturation. It seems also to have a role in peripheral insulin resistance.
Also studies using the mouse zymosan model and chemerin peptides showed that these peptides suppressed and |
https://en.wikipedia.org/wiki/Corticotropin-releasing%20hormone%20receptor%202 | Corticotropin-releasing hormone receptor 2 (CRHR2) is a protein, also known by the IUPHAR-recommended name CRF2, that is encoded by the CRHR2 gene and occurs on the surfaces of some mammalian cells. CRF2 receptors are type 2 G protein-coupled receptors for corticotropin-releasing hormone (CRH) that are resident in the plasma membranes of hormone-sensitive cells. CRH, a peptide of 41 amino acids synthesized in the hypothalamus, is the principal neuroregulator of the hypothalamic-pituitary-adrenal axis, signaling via guanine nucleotide-binding proteins (G proteins) and downstream effectors such as adenylate cyclase. The CRF2 receptor is a multi-pass membrane protein with a transmembrane domain composed of seven helices arranged in a V-shape. CRF2 receptors are activated by two structurally similar peptides, urocortin II, and urocortin III, as well as CRH.
Properties
The human CRHR2 gene contains 12 exons. Three major functional isoforms, alpha (411 amino acids), beta (438 amino acids), and gamma (397 amino acids), encoded by transcripts with alternative first exons, differ only in the N-terminal sequence comprising the signal peptide and part of the extracellular domain (amino acids 18-108 of CRHR2 alpha); the unique N-terminal sequence of each isoform (34 amino acids in CRHR2 alpha; 61 amino acids in Hs CRHR2 beta; 20 amino acids in CRHR2 gamma) is followed by a sequence common to all isoforms (377 amino acids) comprising most of the multi-pass transmembrane domain followed |
https://en.wikipedia.org/wiki/Dopamine%20receptor%20D5 | {{DISPLAYTITLE:Dopamine receptor D5}}
Dopamine receptor D5, also known as D1BR, is a protein that in humans is encoded by the DRD5 gene. It belongs to the D1-like receptor family along with the D1 receptor subtype.
Function
D5 receptor is a subtype of the dopamine receptor that has a 10-fold higher affinity for dopamine than the D1 subtype. The D5 subtype is a G-protein coupled receptor, which promotes synthesis of cAMP by adenylyl cyclase via activation of Gαs/olf family of G proteins. Both D5 and D1 subtypes activate adenylyl cyclase. D1 receptors were shown to stimulate monophasic dose-dependent accumulation of cAMP in response to dopamine, and the D5 receptors were able to stimulate biphasic accumulation of cAMP under the same conditions, suggesting that D5 receptors may use a different system of secondary messengers than D1 receptors.
Activation of D5 receptors is shown to promote expression of brain-derived neurotrophic factor and increase phosphorylation of protein kinase B in rat and mice prefrontal cortex neurons.
In vitro, D5 receptors show high constitutive activity that is independent of binding any agonists.
Primary structure
D5 receptor is highly homologous to the D1 receptor. Their amino acid sequences are 49% to 80% identical. D5 receptor has a long C-terminus of 93 amino acids, accounting for 26% of the entire protein. In spite of the high degree of homology between D5 and D1 receptors, their c-terminus tails have little similarity.
Chromosomal loca |
https://en.wikipedia.org/wiki/GPR183 | G-protein coupled receptor 183 also known as Epstein-Barr virus-induced G-protein coupled receptor 2 (EBI2) is a protein (GPCR) expressed on the surface of some immune cells, namely B cells and T cells; in humans it is encoded by the GPR183 gene. Expression of EBI2 is one critical mediator of immune cell localization within lymph nodes, responsible in part for the coordination of B cell, T cell, and dendritic cell movement and interaction following antigen exposure. EBI2 is a receptor for oxysterols. The most potent activator is 7α,25-dihydroxycholesterol (7α,25-OHC), with other oxysterols exhibiting varying affinities for the receptor. Oxysterol gradients drive chemotaxis, attracting the EBI2-expressing cells to locations of high ligand concentration. The GPR183 gene was identified due to its upregulation during Epstein-Barr virus infection of the Burkitt's lymphoma cell line BL41, hence its name: EBI2.
Tissue distribution and function
B cells
EBI2 helps B cell homing to the outer follicular region within a lymph node. Approximately three hours following B cell exposure to plasma-soluble antigen, EBI2 is upregulated via the transcription factor BRRF1. More surface receptors binding the oxysterol ligand results in cellular migration up the gradient, to the outer follicular region. The reason for this early migration is still unknown; however, because soluble antigen enters lymph nodes via afferent lymphatic vasculature, near the outer region of the follicle, it is hypothes |
https://en.wikipedia.org/wiki/LPAR1 | Lysophosphatidic acid receptor 1 also known as LPA1 is a protein that in humans is encoded by the LPAR1 gene. LPA1 is a G protein-coupled receptor that binds the lipid signaling molecule lysophosphatidic acid (LPA).
Function
The integral membrane protein encoded by this gene is a lysophosphatidic acid (LPA) receptor from a group known as EDG receptors. These receptors are members of the G protein-coupled receptor superfamily. Utilized by LPA for cell signaling, EDG receptors mediate diverse biologic functions, including proliferation, platelet aggregation, smooth muscle contraction, inhibition of neuroblastoma cell differentiation, chemotaxis, and tumor cell invasion. Alternative splicing of this gene has been observed and two transcript variants have been described, each encoding identical proteins. An alternate translation start codon has been identified, which results in isoforms differing in the N-terminal extracellular tail. In addition, an alternate polyadenylation site has been reported.
Cancer
LPAR1 gene has been detected progressively overexpressed in Human papillomavirus-positive neoplastic keratinocytes derived from uterine cervical preneoplastic lesions at different levels of malignancy. For this reason, this gene is likely to be associated with tumorigenesis and may be a potential prognostic marker for uterine cervical preneoplastic lesions progression.
See also
Lysophospholipid receptor
References
Further reading
External links
G protein-coupled rec |
https://en.wikipedia.org/wiki/S1PR3 | Sphingosine-1-phosphate receptor 3 also known as S1PR3 is a human gene which encodes a G protein-coupled receptor which binds the lipid signaling molecule sphingosine 1-phosphate (S1P). Hence this receptor is also known as S1P3.
Function
This gene encodes a member of the EDG family of receptors, which are G protein-coupled receptors. This protein has been identified as a functional receptor for sphingosine 1-phosphate and likely contributes to the regulation of angiogenesis and vascular endothelial cell function.
See also
Lysophospholipid receptor
References
Further reading
External links
G protein-coupled receptors |
https://en.wikipedia.org/wiki/CELSR3 | Cadherin EGF LAG seven-pass G-type receptor 3 is a protein that in humans is encoded by the CELSR3 gene.
The protein encoded by this gene is a member of the flamingo subfamily, part of the cadherin superfamily. The flamingo subfamily consists of nonclassic-type cadherins; a subpopulation that does not interact with catenins. The flamingo cadherins are located at the plasma membrane and have nine cadherin domains, seven epidermal growth factor-like repeats and two laminin A G-type repeats in their ectodomain. They also have seven transmembrane domains, a characteristic unique to this subfamily. It is postulated that these proteins are receptors involved in contact-mediated communication, with cadherin domains acting as homophilic binding regions and the EGF-like domains involved in cell adhesion and receptor-ligand interactions. The specific function of this particular member has not been determined.
See also
Flamingo (protein)
References
Further reading
External links
Adhesion G protein-coupled receptors
G protein-coupled receptors |
https://en.wikipedia.org/wiki/CELSR2 | Cadherin EGF LAG seven-pass G-type receptor 2 is a protein that in humans is encoded by the CELSR2 gene.
The protein encoded by this gene is a member of the flamingo subfamily, part of the cadherin superfamily. The flamingo subfamily consists of nonclassic-type cadherins; a subpopulation that does not interact with catenins. The flamingo cadherins are located at the plasma membrane and have nine cadherin domains, seven epidermal growth factor-like repeats and two laminin A G-type repeats in their ectodomain. They also have seven transmembrane domains, a characteristic unique to this subfamily. It is postulated that these proteins are receptors involved in contact-mediated communication, with cadherin domains acting as homophilic binding regions and the EGF-like domains involved in cell adhesion and receptor-ligand interactions. The specific function of this particular member has not been determined.
See also
Flamingo (protein)
References
Further reading
External links
Adhesion G protein-coupled receptors
G protein-coupled receptors |
https://en.wikipedia.org/wiki/Formyl%20peptide%20receptor%203 | N-formyl peptide receptor 3 (FPR3) is a receptor protein that in humans is encoded by the FPR3 gene.
Nomenclature note
Confusingly, there are two nomenclatures for FPR receptors and their genes, the first one used, FPR, FPR1, and FPR2 and its replacement (which corresponds directly to these three respective receptors and their genes), FPR1, FPR2, and FPR3. The latter nomenclature is recommended by the International Union of Basic and Clinical Pharmacology and is used here. Other previously used names for FPR1 are NFPR, and FMLPR; for FPR2 are FPRH1, FPRL1, RFP, LXA4R, ALXR, FPR2/ALX, HM63, FMLPX, and FPR2A; and for FPR3 are FPRH2, FPRL2, and FMLPY.
FPR3 function
The overall function of FPR3 is quite unclear. Compared to FPR1 and FPR2, FPR3 is highly phosphorylated (a signal for receptor inactivation and internalization) and more localized to small intracellular vesicles. This suggests that FPR3 rapidly internalizes after binding its ligands and thereby may serve as a "decoy" receptor to reduce the binding of its ligands to FRP1 and FRP2 receptors.
Genes
Humans
The FPR3 gene was cloned and named based on the similarity of the amino acid sequence which it encodes to that encoded by the gene for FPR1 (see formyl peptide receptor 1 for details) The studies indicated that FPR3 is composed of 352 amino acids and its gene, similar to FPR1, has an intronless open reading frames which encodes a protein with the 7 transmembrane structure of G protein coupled receptors; FPR3 |
https://en.wikipedia.org/wiki/Frizzled-2 | Frizzled-2 (Fz-2) is a protein that in humans is encoded by the FZD2 gene.
Members of the 'frizzled' gene family encode 7-transmembrane domain proteins that are receptors for Wnt signaling proteins. The expression of the FZD2 gene appears to be developmentally regulated, with high levels of expression in fetal kidney and lung and in adult colon and ovary.
References
Further reading
External links
G protein-coupled receptors |
https://en.wikipedia.org/wiki/Galanin%20receptor%201 | Galanin receptor 1 (GAL1) is a G-protein coupled receptor encoded by the GALR1 gene.
Function
The neuropeptide galanin elicits a range of biological effects by interaction with specific G-protein-coupled receptors. Galanin receptors are seven-trans membrane proteins shown to activate a variety of intracellular second-messenger pathways. GALR1 inhibits adenylyl cyclase via a G protein of the GI/GO family. GALR1 is widely expressed in the brain and spinal cord, as well as in peripheral sites such as the small intestine and heart.
See also
Galanin receptor
References
Further reading
External links
G protein-coupled receptors
sr:Galaninski receptor 3 |
https://en.wikipedia.org/wiki/GPR1 | G protein-coupled receptor 1, also known as GPR1, is a protein that in humans is encoded by the GPR1 gene.
GPR1 is a member of the G protein-coupled receptor family of transmembrane receptors. It functions as a receptor for chemerin. Other receptors for chemerin include CMKLR1 and CCRL2.
References
Further reading
G protein-coupled receptors |
https://en.wikipedia.org/wiki/CCR10 | C-C chemokine receptor type 10 is a protein that in humans is encoded by the CCR10 gene.
Function
Chemokines are a group of small (approximately 8 to 14 kD), mostly basic, structurally related molecules that regulate cell trafficking of various types of leukocytes through interactions with a subset of 7-transmembrane, G protein-coupled receptors. Chemokines also play fundamental roles in the development, homeostasis, and function of the immune system, and they have effects on cells of the central nervous system as well as on endothelial cells involved in angiogenesis or angiostasis. Chemokines are divided into 2 major subfamilies, CXC and CC, based on the arrangement of the first 2 of the 4 conserved cysteine residues; the 2 cysteines are separated by a single amino acid in CXC chemokines and are adjacent in CC chemokines.
CCR10 is a chemokine receptor. Its ligands are CCL27 and CCL28. This receptor is normally expressed by melanocytes, plasma cells and skin-homing T cells. B16 melanoma cell transduction of CCR10 significantly increases the development of lymph node metastasis in mice after inoculation in the skin, suggesting a role for the receptor in directing metastasis. CCR10-CCL27 interactions are involved in T cell-mediated skin inflammation.
References
Further reading
External links
Chemokine receptors |
https://en.wikipedia.org/wiki/GPR4 | G-protein coupled receptor 4 is a protein that in humans is encoded by the GPR4 gene.
See also
Proton-sensing G protein-coupled receptors
References
Further reading
G protein-coupled receptors |
https://en.wikipedia.org/wiki/GPR6 | G protein-coupled receptor 6, also known as GPR6, is a protein which in humans is encoded by the GPR6 gene.
Function
GPR6 is a member of the G protein-coupled receptor family of transmembrane receptors. It has been reported that GPR6 is both constitutively active but in addition is further activated by sphingosine-1-phosphate.
GPR6 up-regulates cyclic AMP levels and promotes neurite outgrowth.
Ligand
Inverse Agonist
Cannabidiol
See also
Lysophospholipid receptor
References
Further reading
External links
G protein-coupled receptors |
https://en.wikipedia.org/wiki/Neuropeptides%20B/W%20receptor%201 | Neuropeptides B/W receptor 1, also known as NPBW1 and GPR7, is a human protein encoded by the NPBWR1 gene. As implied by its name, it and related gene NPBW2 (with which it shares 70% nucleotide identity) are transmembranes protein that bind Neuropeptide B (NPB) and Neuropeptide W (NPW), both proteins expressed strongly in parts of the brain that regulate stress and fear including the extended amygdala and stria terminalis. When originally discovered in 1995, these receptors had no known ligands ("orphan receptors") and were called GPR7 and GPR8, but at least three groups in the early 2000s independently identified their endogenous ligands, triggering the name change in 2005.
Structure
NPBW1 has seven transmembrane domains, which it unsurprisingly shares with NPBWR2, but also a family of somatostatin and opioid receptors, and like these proteins couple to Gi-class G proteins.
Functions
In rodent models, NPBWR1 is over-expressed in Schwann cells associated with neuropathic pain, suggesting it inhibits inflammatory pain responses. Mice without NPBW1 exhibited a stronger hostile reaction to intruders, suggesting NPBW1 has a role in stress responses. Early studies indicated that NPB and NPW had a complex effect on appetite, but generally led to anorexia. Similarly, male rats lacking NPBWR1 exhibited hyperphagia and adult-onset obesity, though why female rats are unaffected is unknown. Researchers speculated that activating these pathways might decrease obesity, and synthesized |
https://en.wikipedia.org/wiki/Neuropeptides%20B/W%20receptor%202 | Neuropeptides B/W receptor 2, also known as NPBW2, is a human protein encoded by the NPBWR2 gene.
The protein encoded by this gene is an integral membrane protein and G protein-coupled receptor. The encoded protein is similar in sequence to another G protein-coupled receptor (GPR7), and it is structurally similar to opioid and somatostatin receptors. This protein binds neuropeptides B and W. This gene is intronless and is expressed primarily in the frontal cortex of the brain.
See also
Neuropeptide B/W receptor
References
Further reading
External links
G protein-coupled receptors |
https://en.wikipedia.org/wiki/Continuous%20hyperthermic%20peritoneal%20perfusion | Continuous hyperthermic peritoneal perfusion (CHPP) is a procedure in which the abdominal cavity is bathed in warm fluid that contains anticancer drugs. It is a kind of hyperthermia therapy.
References
Oncothermia |
https://en.wikipedia.org/wiki/Madelung%20equations | In theoretical physics, the Madelung equations, or the equations of quantum hydrodynamics, are Erwin Madelung's equivalent alternative formulation of the Schrödinger equation, written in terms of hydrodynamical variables, similar to the Navier–Stokes equations of fluid dynamics. The derivation of the Madelung equations is similar to the de Broglie–Bohm formulation, which represents the Schrödinger equation as a quantum Hamilton–Jacobi equation.
Equations
The Madelung equations are quantum Euler equations:
where
is the flow velocity,
is the mass density,
is the Bohm quantum potential,
is the potential from the Schrödinger equation.
The circulation of the flow velocity field along any closed path obeys the auxiliary condition for all integers .
Derivation
The Madelung equations are derived by writing the wavefunction in polar form:
and substituting this form into the Schrödinger equation
The flow velocity is defined by
from which we also find that
where is the probability current of standard quantum mechanics.
The quantum force, which is the negative of the gradient of the quantum potential, can also be written in terms of the quantum pressure tensor:
where
The integral energy stored in the quantum pressure tensor is proportional to the Fisher information, which accounts for the quality of measurements. Thus, according to the Cramér–Rao bound, the Heisenberg uncertainty principle is equivalent to a standard inequality for the efficiency of measurements. T |
https://en.wikipedia.org/wiki/Keith%20Marzullo | Keith Marzullo is the inventor of Marzullo's algorithm, which is part of the basis of the Network Time Protocol and the Windows Time Service. On August 1, 2016 he became the Dean of the University of Maryland College of Information Studies after serving as the Director of the NITRD National Coordination Office. Prior to this he was a Professor in the Department of Computer Science and Engineering at University of California, San Diego. In 2011 he was inducted as a Fellow of the Association for Computing Machinery.
Research
RAMP (Reliable Adaptive Multipath Networks)
GriPhyN (Master-worker computation in a wide-area network)
MURI (Dependent failure models & Collaborative backup for withstanding network catastrophes)
Mobility (Fault-tolerance for mobile agents & personal computational grids)
Publications
1999
Walfredo Cirne and Keith Marzullo. The computational Co-op: Gathering clusters into a metacomputer. Proceedings 13th International Parallel Processing Symposium and 10th Symposium on Parallel and Distributed Processing (IPPS/SPDP 1999). IEEE Computer Society 1999, pp. 160–6. Los Alamitos, CA, USA.
Meng-Jang Lin and Keith Marzullo. Directional gossip: gossip in a wide area network. Dependable Computing - EDDC-3. Third European Dependable Computing Conference. Proceedings (Lecture Notes in Computer Science Vol.1667). Springer-Verlag. 1999, pp. 364–79. Berlin, Germany.
Chanathip Namprempre, Jeremy Sussman, and Keith Marzullo. Implementing causal logging using OrbixWeb in |
https://en.wikipedia.org/wiki/Lester%27s%20theorem | In Euclidean plane geometry, Lester's theorem states that in any scalene triangle, the two Fermat points, the nine-point center, and the circumcenter lie on the same circle.
The result is named after June Lester, who published it in 1997, and the circle through these points was called the Lester circle by Clark Kimberling.
Lester proved the result by using the properties of complex numbers; subsequent authors have given elementary proofs, proofs using vector arithmetic, and computerized proofs.
See also
Parry circle
van Lamoen circle
References
External links
Theorems about triangles and circles |
https://en.wikipedia.org/wiki/Nokomis%2C%20Saskatchewan | Nokomis is a town in the Canadian province of Saskatchewan.
Demographics
In the 2021 Census of Population conducted by Statistics Canada, Nokomis had a population of living in of its total private dwellings, a change of from its 2016 population of . With a land area of , it had a population density of in 2021.
History
1904: The area was opened to homesteading.
1906: Florence Mary Halstead established a post office on the Halstead farm and called it "Nokomis". After the Grand Trunk Pacific Railway was built, the town requested the post office be moved into town, accepting the condition of the post-mistress that the town be renamed "Nokomis". The post office was first located in Henry's Men's Clothing Store, and moved into its own building just north of the Times Office the next year.
1907: The town was named Junction City, with the hopes that it would become the largest city in western Canada
1907: The Canadian Bank of Commerce was constructed with K.W. Reikie as manager, and the Northern Crown Bank with R.S. Inkster as manager. Inkster's residence (Earl McDougall's house) was one of the first residences constructed. Others were homes of Norman Townsend and J.I. Jamieson. Ewart's hall opened above the Northern Crown Bank, and here the first schoolroom classes were held. Mabel Dobbyn, who later married K.W. Reikie of the Bank of Commerce, was the first teacher.
1908: Carloads of lumber, hardware and carpenters were arriving, and the Sash and Door Factory was kept busy |
https://en.wikipedia.org/wiki/Trademark%20classification | A trademark classification is a way the trademark examiners and applicants' trademark attorneys arrange documents, such as trademark and service mark applications, according to the description and scope of the types of goods or services to which the marks apply. The same trademark or service may be (or in many cases MUST be) classified in several classes, and some countries permit several classes to be registered in the same document. There are fees ordinarily associated with each classification, whether for initial application or later renewal.
An application filed for descriptions covering more than one class of goods or services may also be divided later (for a fee) into several different applications for synchronization with a phased roll-out of multiple classes of products. Because of international priority claim issues, classes may be deleted from an application but not added after the initial filing date. There are often disputes regarding the exact classification to apply in an application, partly because prior registrations may already occupy broad areas that overlap the products described by a later applicant. Many countries permit marks to cover an entire class without regard to specific descriptions of goods or services.
There is a general classification of marks into trademarks, service marks, certification marks and collective marks, each of which have slightly different rules. Within the broad categories of trademarks and service marks there are dozens of i |
https://en.wikipedia.org/wiki/PHB%20%28bicycle%29 | The PHB was a bicycle, power-assisted by an electric motor that gets its power from a hydrogen fuel cell. It was manufactured by Pearl (SPHPST.Co). A concept version was unveiled at the 9th China International Exhibition on Gas Technology, Equipment and Applications in 2007. The vehicle weighed approximately 32 kilograms and used a proton-exchange membrane fuel cell to generate about 200 Watts.
It was able to reach approximately 25 km/h, and the company stated that, on a full tank, it could be ridden a distance of 60 to 100 kilometres. The motor was a brushless motor. The bike was announced in 2007 to sell for approximately US$2500, but no hydrogen supply network was available.
See also
Hydrogen vehicle
Electric bicycle
References
External links
Valeswood ETD Ltd, UK
Motorized bicycles |
https://en.wikipedia.org/wiki/Imperial%2C%20Saskatchewan | Imperial is a town in the Canadian province of Saskatchewan. The town is located along Saskatchewan Highway 2.
Demographics
In the 2021 Census of Population conducted by Statistics Canada, Imperial had a population of living in of its total private dwellings, a change of from its 2016 population of . With a land area of , it had a population density of in 2021.
See also
List of communities in Saskatchewan
List of towns in Saskatchewan
Footnotes
External links
Towns in Saskatchewan
Big Arm No. 251, Saskatchewan
Division No. 11, Saskatchewan |
https://en.wikipedia.org/wiki/Antigen-presenting%20cell%20vaccine | An antigen-presenting cell vaccine, or an APC vaccine, is a vaccine made of antigens and antigen-presenting cells (APCs).
, the only APC vaccine approved by the American Food and Drug Administration is for prostatic acid phosphatase, a commonly over-expressed prostate cancer antigen.
References
External links
Antigen-presenting cell vaccine entry in the public domain NCI Dictionary of Cancer Terms
Vaccines |
https://en.wikipedia.org/wiki/Arrestin%20beta%202 | Beta-arrestin-2, also known as arrestin beta-2, is an intracellular protein that in humans is encoded by the ARRB2 gene.
Members of arrestin/beta-arrestin protein family are thought to participate in agonist-mediated desensitization of G protein-coupled receptors and cause specific dampening of cellular responses to stimuli such as hormones, neurotransmitters, or sensory signals, as well as having signalling roles in their own right. Arrestin beta 2, like arrestin beta 1, was shown to inhibit beta-adrenergic receptor function in vitro. It is expressed at high levels in the central nervous system and may play a role in the regulation of synaptic receptors. Besides the brain, a cDNA for arrestin beta 2 was isolated from thyroid gland, and thus it may also be involved in hormone-specific desensitization of TSH receptors. Multiple alternatively spliced transcript variants have been found for this gene, but the full-length nature of some variants has not been defined.
The protein may interact with the agonist DOI in 5-HT2A receptor signaling.
Arrestin beta 2 is crucial for the development of tolerance to morphine and other opioids.
Interactions
Arrestin beta 2 has been shown to interact with
AP2B1,
PSCD2,
Mdm2, and
RALGDS.
References
Further reading
External links
Genes
Human proteins |
https://en.wikipedia.org/wiki/Atrasentan | Atrasentan is an experimental drug that is being studied for the treatment of various types of cancer, including non-small cell lung cancer. It is also being investigated as a therapy for diabetic kidney disease.
Atrasentan failed a phase 3 trial for prostate cancer in patients unresponsive to hormone therapy. A second trial confirmed this finding.
It is an endothelin receptor antagonist selective for subtype A (ETA). While other drugs of this type (sitaxentan, ambrisentan) exploit the vasoconstrictive properties of endothelin and are mainly used for the treatment of pulmonary arterial hypertension, atrasentan blocks endothelin induced cell proliferation.
In April 2014, de Zeeuw et al. showed that 0.75 mg and 1.25 mg of atrasentan reduced urinary albumin by 35 and 38% respectively with modest side effects. Patients also had decreased home blood pressures (but no change in office readings) decrease total cholesterol and LDL. Patients in the 1.25 mg dose group had increased weight gain which was presumably due to increased edema and had to withdraw from the study more than the placebo or 0.75 mg dose group. Reductions in proteinuria have been associated with beneficial patient outcomes in diabetic kidney disease with other interventions but is not an accepted end-point by the FDA.
In 2013, SONAR trial was initiated to determine if atrasentan reduces kidney failure in diabetic kidney disease.
References
Endothelin receptor antagonists
Experimental cancer drugs
Benzodioxol |
https://en.wikipedia.org/wiki/Cytochrome%20b-245%2C%20alpha%20polypeptide | Cytochrome b-245 light chain is a protein that in humans is encoded by the CYBA gene involved in superoxide production and phagocytosis.
Cytochrome b-245 is composed of a light chain (alpha) and a heavy chain (beta). This gene encodes the light, alpha subunit, which has been proposed as a primary component of the microbicidal oxidase system of phagocytes. Mutations in this gene are associated with autosomal recessive chronic granulomatous disease (CGD), which is characterized by the failure of activated phagocytes to generate superoxide, which is important for the microbicidal activity of these cells.
Discovery
The p22phox protein (phox for phagocytic oxidase) was first identified in 1987 during the purification of the cytochrome b-245mv from human neutrophils. A few years before, this low-potential cytochrome b, also called cytochrome b558 (cytb) because of its spectral properties, was demonstrated as the major component of the microbicidal nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex in phagocytes. Cytb, the redox element of the NADPH oxidase complex, is a membrane heterodimer composed of two subunits: p22phox (also called the alpha or small subunit or the light chain of the cytb) and gp91phox (renamed NOX2 in the 2000s) or the beta or heavy chain or large subunit. By screening a cDNA library constructed from human promyelocytic leukemia cells, Parkos et al. isolated a cDNA corresponding to the light chain of cytb. The importance of the role of p2 |
https://en.wikipedia.org/wiki/Bispecific%20monoclonal%20antibody | A bispecific monoclonal antibody (BsMAb, BsAb) is an artificial protein that can simultaneously bind to two different types of antigen or two different epitopes on the same antigen. Naturally occurring antibodies typically only target one antigen. BsAbs can be manufactured in several structural formats. BsAbs can be designed to recruit and activate immune cells, to interfere with receptor signaling and inactivate signaling ligands, and to force association of protein complexes. BsAbs have been explored for cancer immunotherapy, drug delivery, and Alzeimer's disease.
Development history
The original concept of BsAbs was proposed by Nisonoff and his collaborators in the 1960s, including the first idea of antibody architecture and other findings. In 1975, the problem of producing pure antibodies was solved by the creation of hybridoma technology, and the new era of monoclonal antibodies (MoAbs) came. In 1983, Milstein and Cuello created hybrid-hybridoma (quadroma) technology. In 1988, the single-chain variable fragment (scFv) was invented by the Huston team to minimize the refolding problems, which contains the incorrect domain pairing or aggregation of two-chain species. In 1996, the BsAbs became more developed when the knobs-into-holes technology emerged.
Structural types and manufacturing methods
There are many formats of BsAbs, but the two main categories are IgG-like and non-IgG-like. The main types of manufacturing methods are quadromas, chemical conjugation, and gene |
https://en.wikipedia.org/wiki/Endothelin%20receptor%20type%20B | Endothelin receptor type B, (ET-B) is a protein that in humans is encoded by the EDNRB gene.
Function
Endothelin receptor type B is a G protein-coupled receptor which activates a phosphatidylinositol-calcium second messenger system. Its ligand, endothelin, consists of a family of three potent vasoactive peptides: ET1, ET2, and ET3. A splice variant, named SVR, has been described; the sequence of the ETB-SVR receptor is identical to ETRB except for the intracellular C-terminal domain. While both splice variants bind ET1, they exhibit different responses upon binding which suggests that they may be functionally distinct.
Regulation
In melanocytic cells the EDNRB gene is regulated by the microphthalmia-associated transcription factor. Mutations in either gene are links to Waardenburg syndrome.
Clinical significance
The multigenic disorder, Hirschsprung disease type 2, is due to mutation in endothelin receptor type B gene.
Animals
In horses, a mutation in the middle of the EDNRB gene, Ile118Lys, when homozygous, causes Lethal White Syndrome. In this mutation, a mismatch in the DNA replication causes lysine to be made instead of isoleucine. The resulting EDNRB protein is unable to fulfill its role in the development of the embryo, limiting the migration of the melanocyte and enteric neuron precursors. A single copy of the EDNRB mutation, the heterozygous state, produces an identifiable and completely benign spotted coat color called frame overo.
Interactions
Endo |
https://en.wikipedia.org/wiki/EXC%20code | EXC is a condensed matter physics many-body theory software package implementing the Bethe–Salpeter equation in frequency-reciprocal space and on a plane wave basis set. Its purpose is to calculate, ab initio, dielectric and optical properties, like absorption, reflectivity, refraction index, electron and X-ray energy loss, for a large variety of systems, ranging from bulk systems, surfaces, to clusters or atoms. It is distributed under the GNU/GPL license.
See also
ABINIT
DP code
YAMBO code
PWscf
Quantum chemistry computer programs
References
Physics software
Computational chemistry software |
https://en.wikipedia.org/wiki/Homotrimer | A homotrimer is a protein which is composed of three identical units of polypeptide.
Examples
Hemagglutinin (influenza)
Spike protein (coronavirus)
See also
Protein trimer
References
Peptides |
https://en.wikipedia.org/wiki/Endothelin%20A%20receptor | Endothelin receptor type A, also known as ETA, is a human G protein-coupled receptor.
Interactions
Endothelin receptor type A has been shown to interact with HDAC7A and HTATIP.
See also
Endothelin receptor
References
External links
Further reading
G protein-coupled receptors |
https://en.wikipedia.org/wiki/EPH%20receptor%20B2 | Ephrin type-B receptor 2 is a protein that in humans is encoded by the EPHB2 gene.
Function
Ephrin receptors and their ligands, the ephrins, mediate numerous developmental processes, particularly in the nervous system. Based on their structures and sequence relationships, ephrins are divided into the ephrin-A (EFNA) class, which are anchored to the membrane by a glycosylphosphatidylinositol linkage, and the ephrin-B (EFNB) class, which are transmembrane proteins. The Eph family of receptors are divided into 2 groups based on the similarity of their extracellular domain sequences and their affinities for binding ephrin-A and ephrin-B ligands. Ephrin receptors make up the largest subgroup of the receptor tyrosine kinase (RTK) family. The protein encoded by this gene is a receptor for ephrin-B family members.
Animal studies
EphB2 is part of the NMDA signaling pathway and restoring expression rescues cognitive function in an animal model of Alzheimer's disease.
A recessive EphB2 gene is responsible for the crested-feather mutation in pigeons.
Interactions
EPH receptor B2 has been shown to interact with:
Abl gene
RAS p21 protein activator 1
Src
References
Tyrosine kinase receptors |
https://en.wikipedia.org/wiki/ID1 | DNA-binding protein inhibitor ID-1 is a protein that in humans is encoded by the ID1 gene.
Function
The protein encoded by this gene is a helix-loop-helix (HLH) protein that can form heterodimers with members of the basic HLH family of transcription factors. The encoded protein has no DNA binding activity and therefore can inhibit the DNA binding and transcriptional activation ability of basic HLH proteins with which it interacts. This protein may play a role in cell growth, senescence, and differentiation. Two transcript variants encoding different isoforms have been found for this gene.
Interactions
ID1 has been shown to interact weakly with MyoD but very tightly with ubiquitously expressed E proteins. E proteins heterodimerize with tissue restricted bHLH proteins such as Myod, NeuroD, etc. to form active transcription complexes so by sequestering E proteins, Id proteins can inhibit tissue restricted gene expression in multiple cell lineages using the same biochemical mechanism. Other interacting partners include CASK.
Clinical significance
ID1 can be used to mark endothelial progenitor cells which are critical to tumor growth and angiogenesis. Targeting ID1 results in decreased tumor growth. ID1 has been shown to be targeted by cannabidiol in certain gliomas and breast cancers.
See also
Inhibitor of DNA-binding protein
References
Further reading
External links
Transcription factors
Aging-related genes |
https://en.wikipedia.org/wiki/Brostallicin | Brostallicin is a chemical compound being studied in the treatment of cancer. It is an alkylating agent that binds DNA.
References
Experimental cancer drugs
Pyrroles
Organobromides
Halogen-containing natural products
Guanidine alkaloids
Alkene derivatives
Carboxamides |
https://en.wikipedia.org/wiki/MYH9 | Myosin-9 also known as myosin, heavy chain 9, non-muscle or non-muscle myosin heavy chain IIa (NMMHC-IIA) is a protein which in humans is encoded by the MYH9 gene.
Non-muscle myosin IIA (NM IIA) is expressed in most cells and tissues where it participates in a variety of processes requiring contractile force, such as cytokinesis, cell migration, polarization and adhesion, maintenance of cell shape, and signal transduction. Myosin IIs are motor proteins that are part of a superfamily composed of more than 30 classes. Class II myosins include muscle and non-muscle myosins that are organized as hexameric molecules consisting of two heavy chains (230 kDa), two regulatory light chains (20 KDa) controlling the myosin activity, and two essential light chains (17 kDa), which stabilize the heavy chain structure.
Gene and protein structure
MYH9 is a large gene spanning more than 106 kilo base pairs on chromosome 22q12.3. It is composed of 41 exons with the first ATG of the open reading frame localized in exon 2 and the stop codon in exon 41. It encodes non-muscle myosin heavy chain IIA (NMHC IIA), a protein of 1,960 amino acids. Consistent with its wide expression in cells and tissues, the promoter region of MYH9 is typical of housekeeping genes having no TATA box but high GC content, with multiple GC boxes. MYH9 is a well-conserved gene through evolution. The mouse ortholog (Myh9) is localized in a syntenic region on chromosome 15 and has the same genomic organization as that of th |
https://en.wikipedia.org/wiki/NAD%28P%29H%20dehydrogenase%20%28quinone%201%29 | NAD(P)H dehydrogenase [quinone] 1 is an enzyme that in humans is encoded by the NQO1 gene. This protein-coding gene is a member of the NAD(P)H dehydrogenase (quinone) family and encodes a 2-electron reductase (enzyme). This FAD-binding protein forms homodimers and performs two-electron reduction of quinones to hydroquinones and of other redox dyes. It has a preference for short-chain acceptor quinones, such as ubiquinone, benzoquinone, juglone and duroquinone. This gene has an important paralog NQO2. This protein is located in the cytosol.
NQO1 enzyme expression can be induced by dioxin and inhibited by dicoumarol.
Function
This gene is a member of the NAD(P)H dehydrogenase (quinone) family and encodes a cytoplasmic 2-electron reductase. This FAD-binding protein forms homodimers and reduces quinones to hydroquinones. This enzyme facilitates the two electron reduction of quinone to hydroquinone. NQO1-mediated two electron reduction of quinone to hydroquinone thereby indirectly prevents the one electron reduction of quinone to the semiquinone free radical.
The ubiquitin-independent p53 degradation pathway is regulated by NQO1. NQO1 stabilizes p53, protecting it from degradation. Individuals with decreased NQO1 expression/activity have reduced p53 stability, which may lead to resistance to drugs such as chemotherapeutics.
Detoxification
Quinonoid compounds generate reactive oxygen species (ROS) via redox cycling mechanisms and arylating nucleophiles. NQO1 removes quinone |
https://en.wikipedia.org/wiki/Treosulfan | Treosulfan, sold under the brand name Trecondi, is a medication given to people before they have a bone marrow transplant from a donor known as allogeneic hematopoietic stem cell transplantation. It is used as a 'conditioning' treatment to clear the bone marrow and make room for the transplanted bone marrow cells, which can then produce healthy blood cells. It is used together with another medicine called fludarabine in adults and children from one month of age with blood cancers as well as in adults with other severe disorders requiring a bone marrow transplant.
It belongs to the family of drugs called alkylating agents. In the body, treosulfan is converted into other compounds called epoxides which kill cells, especially cells that develop rapidly such as bone marrow cells, by attaching to their DNA while they are dividing.
The most common side effects in adults and children are infections, nausea (feeling sick), stomatitis (inflammation of the lining of the mouth), vomiting, diarrhoea and abdominal pain (belly ache). Tiredness, febrile neutropenia (low white blood cell counts with fever) and high blood levels of bilirubin (a breakdown product of red blood cells) are also seen in more than 1 in 10 adults, and rash also affects more than 1 in 10 children.
Medical Uses
Treosulfan in combination with fludarabine is indicated as part of conditioning treatment prior to allogeneic haematopoietic stem cell transplantation (alloHSCT) in adults with malignant and non malignant di |
https://en.wikipedia.org/wiki/Matrix%20Gla%20protein | Matrix Gla protein (MGP) is member of a family of vitamin K2 dependent, Gla-containing proteins. MGP has a high affinity binding to calcium ions, similar to other Gla-containing proteins. The protein acts as an inhibitor of vascular mineralization and plays a role in bone organization.
MGP is found in a number of body tissues in mammals, birds, and fish. Its mRNA is present in bone, cartilage, heart, and kidney.
It is present in bone together with the related vitamin K2-dependent protein osteocalcin. In bone, its production is increased by vitamin D.
Genetics
The MGP was linked to the short arm of chromosome 12 in 1990. Its mRNA sequence length is 585 bases long in humans.
Physiology
MGP and osteocalcin are both calcium-binding proteins that may participate in the organisation of bone tissue. Both have glutamate residues that are post-translationally carboxylated by the enzyme gamma-glutamyl carboxylase in a reaction that requires Vitamin K hydroquinone.
Role in disease
Abnormalities in the MGP gene have been linked with Keutel syndrome, a rare condition characterised by abnormal calcium deposition in cartilage, peripheral stenosis of the pulmonary artery, and midfacial hypoplasia.
Mice that lack MGP develop to term but die within two months as a result of arterial calcification which leads to blood-vessel rupture.
References
External links
Extracellular matrix proteins
Genes on human chromosome 12
Glycoproteins |
https://en.wikipedia.org/wiki/RIMPUFF | RIMPUFF is a local-scale puff diffusion model developed by Risø DTU National Laboratory for Sustainable Energy, Denmark. It is an emergency response model to help emergency management organisations deal with chemical, biological and radiological releases to the atmosphere.
RIMPUFF is in operational use in several European national emergency centres for preparedness and prediction of nuclear accidental releases (RODOS, EURANOS, ARGOS), chemical gas releases (ARGOS), and for airborne Foot-and Mouth Disease virus spread
Description
RIMPUFF builds from parameterized formulas for puff diffusion, wet and dry deposition, and gamma dose radiation. Its range of application covers distances up to ~1000 km from the point of release.
RIMPUFF calculates the instantaneous atmospheric dispersion taking into account the local wind variability and the local turbulence levels. The puff sizes represent instantaneous relative diffusion (no averaging) and is calculated from similarity scaling theory.
Puff diffusion is parameterized for travel times in the range from a few seconds and up to ~1 day.
Wet and dry deposition is also calculated as a function of local rain intensity and turbulence levels.
See also
List of atmospheric dispersion models
UK Atmospheric Dispersion Modelling Liaison Committee
UK Dispersion Modelling Bureau
Further reading
For those who are unfamiliar with air pollution dispersion modelling and would like to learn more about the subject, it is suggested that either |
https://en.wikipedia.org/wiki/Beery | Beery is a surname. Notable people with the surname include:
Adaline Hohf Beery (1859–1929), American author, newspaper editor, songbook compiler, hymnwriter
Dan Beery (born 1975), American competition rower, Olympic champion and world champion
Janet Beery, American mathematician and historian of mathematics
Noah Beery (1882–1946), American actor
Noah Beery Jr. (1913–1994), American actor
Wallace Beery (1885–1949), American actor |
https://en.wikipedia.org/wiki/Angiotensin%20II%20receptor%20type%202 | Angiotensin II receptor type 2, also known as the AT2 receptor is a protein that in humans is encoded by the AGTR2 gene.
Function
Angiotensin II is a potent pressor hormone and a primary regulator of aldosterone secretion. It is an important effector controlling blood pressure and volume in the cardiovascular system. It acts through at least two types of receptors termed AT1 and AT2. AGTR2 belongs to a family 1 of G protein-coupled receptors. It is an integral membrane protein. It plays a role in the central nervous system and cardiovascular functions that are mediated by the renin–angiotensin system. This receptor mediates programmed cell death (apoptosis). In adults, it is highly expressed in myometrium with lower levels in adrenal gland and fallopian tube. It is highly expressed in fetal kidney and intestine. The human AGTR2 gene is composed of three exons and spans at least 5 kb. Exons 1 and 2 encode for 5' untranslated mRNA sequence and exon 3 harbors the entire uninterrupted open reading frame.
Stimulation of AT2 by the selective agonist CGP 42112A increases mucosal nitric oxide production.
Model organisms
Model organisms have been used in the study of AGTR2 function. A conditional knockout mouse line, called Agtr2tm1a(EUCOMM)Wtsi was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists — at the Wellcome Trust Sanger Instit |
https://en.wikipedia.org/wiki/Autologous%20tumor%20cell | An autologous tumor cell is a cancer cell from an individual's own tumor.
References
Autologous tumor cell entry in the public domain NCI Dictionary of Cancer Terms
Oncology |
https://en.wikipedia.org/wiki/Brain-specific%20angiogenesis%20inhibitor | Brain-specific angiogenesis inhibitors are G-protein coupled receptors belonging to the class B secretin subfamily. Members include:
Brain-specific angiogenesis inhibitor 1
Brain-specific angiogenesis inhibitor 2
Brain-specific angiogenesis inhibitor 3
References
External links
Angiogenesis
G protein-coupled receptors |
https://en.wikipedia.org/wiki/OPN1SW | Blue-sensitive opsin is a protein that in humans is encoded by the OPN1SW gene.
See also
Opsin
References
Further reading
G protein-coupled receptors
Color vision |
https://en.wikipedia.org/wiki/Clumping%20factor%20A | Clumping factor A, or ClfA, is a virulence factor from Staphylococcus aureus (S. aureus) that binds to fibrinogen.
ClfA also has been shown to bind to complement regulator I protein.
It is responsible for the clumping of blood plasma observed when adding S. aureus to human plasma. Clumping factor can be detected by the slide test.
See also
Tefibazumab
Coagulase
References
Staphylococcaceae
Bacterial proteins
Virulence factors |
https://en.wikipedia.org/wiki/Extravasation |
Extravasation is the leakage of a fluid out of its contained space into the surrounding area, especially blood or blood cells from vessels. In the case of inflammation, it refers to the movement of white blood cells through the capillary wall, into the surrounding tissues. This is known as (leukocyte extravasation, also called diapedesis). In the case of cancer metastasis, it refers to cancer cells exiting the capillaries and entering other tissues, where secondary tumors may form. The term is commonly used in a medical context.
More specifically, extravasation can refer to:
Extravasation (intravenous)
Extravasation of infusates
Extravasation of irrigation fluid
Extravasation of urine
Leukocyte extravasation
Angiopellosis (non-leukocyte cell extravastion)
Extravasation of irrigation fluid
Extravasation of irrigation fluid is the unintended migration of irrigation fluid (e.g. saline) introduced into a human body. This may occur in a number of types of endoscopic surgery, such as minimally invasive orthopedic surgery, i.e. arthroscopy, TURP (trans-urethral resection of the prostate) and TCRE (trans-cervical resection of the endometrium).
In arthroscopy, fluid under pressure is used to inflate and distend a joint and make a working surgical space. Arthroscopy is typically performed on shoulder and knee joints; however, hip arthroscopy is becoming more popular. Arthroscopy is done by making surgical portals or puncture wounds into the joint. A surgical instrument calle |
https://en.wikipedia.org/wiki/Here%20Comes%20Santa%20Claus | "Here Comes Santa Claus (Right Down Santa Claus Lane)" is a popular Christmas song written and originally performed by Gene Autry, with music composed by Oakley Haldeman. Autry's original recording (in which he pronounces Santa Claus as "Santy Claus") was a top-10 hit on the pop and country charts; the song would go on to be covered many times in the subsequent decades.
History
Autry got the idea for the song after riding his horse in the 1946 Santa Claus Lane Parade (now the Hollywood Christmas Parade) in Los Angeles, during which crowds of spectators chanted, "Here comes Santa Claus". This inspired him to write a song that Haldeman set to music. Autry's lyrics combined two veins of the Christmas tradition, the mythology of Santa Claus and the Christian origin of the holiday (most explicitly in its mention of the nativity promise of "peace on Earth" to those who "follow the light"). A demo recording was made by singer/guitarist Johnny Bond, whose recording made use of ice cubes to mimic the sound of jingling sleigh bells. This inspired the use of real sleigh bells in Autry's own recording of the song.
Autry first recorded the song on August 28, 1947; released as a single by Columbia Records, It became a No. 5 country and No. 9 pop hit. Autry performed the song in his 1949 movie The Cowboy and the Indians. He re-recorded it again in 1953 for Columbia, and once more in 1957 for his own Challenge Records label, which released it on more than one album that year.
Other artis |
https://en.wikipedia.org/wiki/Marshall%2C%20Saskatchewan | Marshall is a town in Saskatchewan, Canada 19 km (12 miles) from Lloydminster on the Yellowhead Highway (Highway 16).
Demographics
In the 2021 Census of Population conducted by Statistics Canada, Marshall had a population of living in of its total private dwellings, a change of from its 2016 population of . With a land area of , it had a population density of in 2021.
Notable people
Braden Holtby - NHL goaltender
See also
List of communities in Saskatchewan
List of towns in Saskatchewan
References
Wilton No. 472, Saskatchewan
Towns in Saskatchewan
Division No. 17, Saskatchewan |
https://en.wikipedia.org/wiki/VPU | VPU may refer to:
Technology
Vector processing unit, a special processor architecture with features of pipelining for vector processing
Versatile Processor Unit, an Intel AI accelerator for inference, computer vision and deep learning
Video processing unit and visual processing unit, related to graphics processing units
Vision processing unit, a class of processor intended for accelerating machine vision tasks
Other uses
Viral protein U (Vpu), a regulatory protein found in HIV-1
Vancouver Police Union, a trade union in Canada
See also |
https://en.wikipedia.org/wiki/Trans-regulatory%20element | Trans-regulatory elements (TRE) are DNA sequences encoding upstream regulators (ie. trans-acting factors), which may modify or regulate the expression of distant genes. Trans-acting factors interact with cis-regulatory elements to regulate gene expression. TRE mediates expression profiles of a large number of genes via trans-acting factors. While TRE mutations affect gene expression, it is also one of the main driving factors for evolutionary divergence in gene expression.
Trans vs cis elements
Trans-regulatory elements work through an intermolecular interaction between two different molecules and so are said to be "acting in trans". For example (1) a transcribed and translated transcription factor protein derived from the trans-regulatory element; and a (2) DNA regulatory element that is adjacent to the regulated gene. This is in contrast to cis-regulatory elements that work through an intramolecular interaction between different parts of the same molecule: (1) a gene; and (2) an adjacent regulatory element for that gene in the same DNA molecule. Additionally, each trans-regulatory element affects a large number of genes on both alleles, while cis-regulatory element is allele specific and only controls genes nearby.
Exonic and promoter sequences of the genes are significantly more conserved than the genes in cis- and trans- regulatory elements. Hence, they have higher resistance to genetic divergence, yet retains its susceptibility to mutations in upstream regulators. Th |
https://en.wikipedia.org/wiki/CCR4 | C-C chemokine receptor type 4 is a protein that in humans is encoded by the CCR4 gene. CCR4 has also recently been designated CD194 (cluster of differentiation 194).
The protein encoded by this gene belongs to the G protein-coupled receptor family. It is a receptor for the following CC chemokines:
CCL2 (MCP-1)
CCL4 (MIP-1)
CCL5 (RANTES)
CCL17 (TARC)
CCL22 (Macrophage-derived chemokine)
Chemokines are a group of small structurally related proteins that regulate cell trafficking of various types of leukocytes. The chemokines also play fundamental roles in the development, homeostasis, and function of the immune system, and they have effects on cells of the central nervous system as well as on endothelial cells involved in angiogenesis or angiostasis.
CCR4 is a cell-surface protein and should not be confused with the unrelated carbon catabolite repression-negative on TATA-less (CCR4-Not), a nuclear protein complex that regulates gene expression.
Clinical significance
CCR4 is often expressed on leukemic cells in cutaneous T-cell lymphoma (CTCL).
As a drug target
Mogamulizumab is a humanised monoclonal antibody targeted at CCR4 and is an investigational drug for CTCL.
References
External links
Chemokine receptors
Clusters of differentiation |
https://en.wikipedia.org/wiki/CCR3%20%28gene%29 | C-C chemokine receptor type 3 is a protein that in humans is encoded by the CCR3 gene.
CCR3 has also recently been designated CD193 (cluster of differentiation 193).
Function
The protein encoded by this gene is a receptor for C-C type chemokines. It belongs to family 1 of the G protein-coupled receptors. This receptor binds and responds to a variety of chemokines, including eotaxin (CCL11), eotaxin-3 (CCL26), MCP-3 (CCL7), MCP-4 (CCL13), and RANTES (CCL5). It is highly expressed in eosinophils and basophils, and is also detected in TH1 and TH2 cells, as well as in airway epithelial cells. This receptor may contribute to the accumulation and activation of eosinophils and other inflammatory cells in the allergic airway, and possibly at sites of parasitic infection. It is also known to be an entry co-receptor for HIV-1, enabling viral infection in cells that also express CD4, the receptor of HIV-1. This gene and seven other chemokine receptor genes form a chemokine receptor gene cluster on the chromosomal region 3p21. Alternatively spliced transcript variants encoding the same protein have been described.
See also
Cluster of differentiation
Interactions
CCR3 (gene) has been shown to interact with CCL5.
References
Further reading
External links
Chemokine receptors
Clusters of differentiation |
https://en.wikipedia.org/wiki/CCR8%20%28gene%29 | Chemokine (C-C motif) receptor 8, also known as CCR8, is a protein which in humans is encoded by the CCR8 gene. CCR8 has also recently been designated CDw198 (cluster of differentiation w198).
Function
This gene encodes a member of the beta chemokine receptor family, which is predicted to be a seven transmembrane protein similar to G protein-coupled receptors. Chemokines and their receptors are important for the migration of various cell types into the inflammatory sites. This receptor protein preferentially expresses in the thymus. The ligand of the CCR8 is CCL1. CCL8 also functions as a CCR8 agonist.
Studies of this receptor and its ligands suggested its role in regulation of monocyte chemotaxis and thymic cell apoptosis. More specifically, this receptor may contribute to the proper positioning of activated T cells within the antigenic challenge sites and specialized areas of lymphoid tissues. This gene is located at the chemokine receptor gene cluster region.
See also
CC chemokine receptors
References
External links
Further reading
Chemokine receptors
Clusters of differentiation |
https://en.wikipedia.org/wiki/GPR12 | Probable G-protein coupled receptor 12 is a protein that in humans is encoded by the GPR12 gene.
The gene product of GPR12 is an orphan receptor, meaning that its endogenous ligand is currently unknown. Gene disruption of GPR12 in mice results in dyslipidemia and obesity.
Ligands
Inverse agonists
Cannabidiol
References
Further reading
G protein-coupled receptors |
https://en.wikipedia.org/wiki/GPR15 | G protein-coupled receptor 15 is a protein that in humans is encoded by the GPR15 gene.
GPR15 is a class A orphan G protein-coupled receptor (heterotrimeric guanine nucleotide-binding protein, GPCR). The GPR15 gene is localized at chromosome 3q11.2-q13.1. It is found in epithelial cells, synovial macrophages, endothelial cells and lymphocytes especially T cells.
From the mRNA sequence a 40.8 kD molecular weight of GPR15 is proposed. In an epithelial tumour cell line (HT-29), however, a 36 kD band, composed of GPR15 and galactosyl ceramide, was detected. Protein expression in lymphocytes is strongly associated with hypomethylation of its gene.
Tissue distribution
High gene expression was described for colonic mucosa, small bowel mucosa, liver and spleen. Moderate gene expression was found in blood, lymph node, thymus, testis and prostate. In peripheral blood, GPR15 is mainly found on T cells, especially on CD4+ T helper cells, and less prominent on B cells.
By immunohistochemistry GPR15 is found specifically in glandular cells of the stomach, α-cells of islet of Langerhans in pancreas, surface epithelium of small intestine and colon, hepatocytes in liver, tubular epithelium of the kidney and in diverse tumour tissues such as glioblastoma, melanoma, small cell lung carcinoma or colon carcinoma.
Function
The overall physiological role remains elusive. It seems to play a role in homing of single T cell types to the colon. In human, GPR15 controls together with α4β7-int |
https://en.wikipedia.org/wiki/GPR17 | Uracil nucleotide/cysteinyl leukotriene receptor is a G protein-coupled receptor that in humans is encoded by the GPR17 gene located on chromosome 2 at position q21. The actual activating ligands for and some functions of this receptor are disputed.
History
Initially discovered in 1998 as an Orphan receptor, i.e. a receptor whose activating ligand(s) and function were unknown, GPR17 was "deorphanized" in a study that reported it to be a receptor for LTC4, LTD4, and uracil nucleotides. In consequence, GPR17 attracted attention as a potential mediator of reactions caused by LTC4 and LTD4 viz., asthma, rhinitis, and urticarial triggered by allergens, nonsteroidal anti-inflammatory drugs, and exercise (see Aspirin-induced asthma). Subsequent reports, however, have varied in results: studies focusing on the allergen and non-allergen reactions find that GPR17-bearing cells do not respond to LTC4, LTD4, and uracil nucleotides while studies focusing on nerve tissue find that certain types of GPR17-bearing oligodendrocytes do indeed respond to them. In 2013 and 2014 reports, the International Union of Basic and Clinical Pharmacology took no position on which of these are true ligands for GPR17. GPR17 is a constitutively active receptor, i.e. a receptor that has baseline activity which is independent of, although potentially increased by, its ligands.
Biochemistry
GPR17 has a structure which is intermediate between the cysteinyl leukotriene receptor group (i.e. cysteinyl leukotriene |
https://en.wikipedia.org/wiki/NAGly%20receptor | N-Arachidonyl glycine receptor (NAGly receptor), also known as G protein-coupled receptor 18 (GPR18), is a protein that in humans is encoded by the GPR18 gene. Along with the other previously "orphan" receptors GPR55 and GPR119, GPR18 has been found to be a receptor for endogenous lipid neurotransmitters, several of which also bind to cannabinoid receptors. It has been found to be involved in the regulation of intraocular pressure.
Research supports the hypothesis that GPR18 is the abnormal cannabidiol receptor and N-arachidonoyl glycine, the endogenous lipid metabolite of anandamide, initiates directed microglial migration in the CNS through activation of GPR18, though recent evidence demonstrates that NAGly was not shown to be a GPR18 agonist in rat sympathetic neurons.
Resolvin D2 (RvD2), a member of the specialized proresolving mediators (SPM) class of polyunsaturated fatty acid metabolites, is an activating ligand for GPR18; RvD2 and its activation of GPR18 contribute to the resolution of inflammatory responses as well as inflammation-based and other diseases in animal models and are proposed to do so in humans. Furthermore, RvD2 is a metabolite of the omega-3 fatty acid, docosahexaenoic acid (DHA); the metabolism of DHA to RvD2 and RvD2's activation of GPR18 is proposed to one among many other mechanisms for the anti-inflammatory and other beneficial effects attributed to omega-3 fatty acid-rich diets
Ligands
Agonists
Ligands found to bind to GPR18 as agonists includ |
https://en.wikipedia.org/wiki/GPR19 | Probable G-protein coupled receptor 19 is a protein that in humans is encoded by the GPR19 gene. GPR19 has been proposed as the receptor for the peptide hormone adropin.
References
Further reading
G protein-coupled receptors |
https://en.wikipedia.org/wiki/GPR20 | Probable G-protein coupled receptor 20 is a protein that in humans is encoded by the GPR20 gene.
References
Further reading
G protein-coupled receptors |
https://en.wikipedia.org/wiki/GPR21 | Probable G-protein coupled receptor 21 is a protein that in humans is encoded by the GPR21 gene.
References
Further reading
G protein-coupled receptors |
https://en.wikipedia.org/wiki/GPR22 | Probable G-protein coupled receptor 22 is a protein that in humans is encoded by the GPR22 gene.
References
Further reading
G protein-coupled receptors |
https://en.wikipedia.org/wiki/LPAR4 | Lysophosphatidic acid receptor 4 also known as LPA4 is a protein that in humans is encoded by the LPAR4 gene. LPA4 is a G protein-coupled receptor that binds the lipid signaling molecule lysophosphatidic acid (LPA).
See also
Lysophospholipid receptor
P2Y receptor
References
Further reading
G protein-coupled receptors |
https://en.wikipedia.org/wiki/GPR25 | Probable G-protein coupled receptor 25 is a protein that in humans is encoded by the GPR25 gene.
References
Further reading
G protein-coupled receptors |
https://en.wikipedia.org/wiki/GPR26 | Probable G-protein coupled receptor 26 is a protein that in humans is encoded by the GPR26 gene. GPR26 expression is found to peak perinatally, when the visual system is first challenged, and contains a 53 kb LD-block enriched for association with introgressed Neanderthal-derived SNPs. Additionally, it is known to form oligomeric structures with the 5-HT1a receptor.
References
Further reading
G protein-coupled receptors |
https://en.wikipedia.org/wiki/GPR27 | Probable G-protein coupled receptor 27 is a protein that in humans is encoded by the GPR27 gene.
See also
SREB
References
G protein-coupled receptors |
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