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4,243,396 | https://en.wikipedia.org/wiki/Russula%20ochroleuca | Russula ochroleuca is a member of the genus Russula. A group that have become known as brittlegills. It has been commonly known as the common yellow russula for some years, and latterly the ochre brittlegill. It is widespread, and common in mixed woodland.
Taxonomy
Russula ochroleuca was first noted and named as a species of Agaricus by the pioneering South African mycologist Christian Hendrik Persoon in 1801.
Description
The cap is dull yellow and wide, initially convex, later flat, or slightly depressed. The cap margin becomes furrowed when mature, and it is two-thirds peeling. The gills are white to greyish white, and are adnexed. The stipe is long, wide, cylindrical, white or later greyish. The taste is mild to moderately hot.
It could be confused with the similar-looking and much better tasting Russula claroflava.
Distribution and habitat
Russula ochroleuca grows in deciduous and coniferous forest, where it (at least in Northwestern Europe) is very common. In the USA it is fairly common under conifers; birch, and aspen in the Northern States.
Edibility
Although considered edible, it is not known as particularly tasty. It is mild to moderately hot.
See also
List of Russula species
References
"Danske storsvampe. Basidiesvampe" [a key to Danish basidiomycetes] J.H. Petersen and J. Vesterholt eds. Gyldendal. Viborg, Denmark, 1990.
ochroleuca
Fungi described in 1801
Fungi of Europe
Taxa named by Christiaan Hendrik Persoon
Fungus species | Russula ochroleuca | [
"Biology"
] | 347 | [
"Fungi",
"Fungus species"
] |
4,243,413 | https://en.wikipedia.org/wiki/NGC%203766 | NGC 3766 (also known as Caldwell 97) is an open star cluster in the southern constellation Centaurus. It is located in the vast star-forming region known as the Carina molecular cloud, and was discovered by Nicolas Louis de Lacaille during his astrometric survey in 1751–1752. At a distance of about 1745 pc, the cluster subtends a diameter of about 12 minutes of arc.
There are 137 listed stars, but many are likely non-members, with only 36 having accurate photometric data. It has a total apparent magnitude of 5.3 and integrated spectral type of B1.7. NGC 3766 is relatively young, with an estimated age of log (7.160) or 14.4 million years, and is approaching us at 14.8 km/s. This cluster contains eleven Be stars, two red supergiants and four Ap stars.
36 examples of an unusual type of variable star were discovered in the cluster. These fast-rotating pulsating B-type stars vary by only a few hundredths of a magnitude with periods less than half a day. They are main sequence stars, hotter than δ Scuti variables and cooler than slowly pulsating B stars.
See also
New General Catalogue
References
External links
NGC 3766 at SEDS
WEBDA Data on NGC 3766 by Lynga
Open clusters
3766
Centaurus
097b | NGC 3766 | [
"Astronomy"
] | 280 | [
"Centaurus",
"Constellations"
] |
4,243,416 | https://en.wikipedia.org/wiki/NGC%206231 | NGC 6231 (also known as Caldwell 76 or the Baby Scorpion Cluster) is an open cluster in the southern sky located half a degrees north of Zeta Scorpii. NGC 6231 is part of a swath of young, bluish stars in the constellation Scorpius known as the Scorpius OB1 association. The star Zeta1 (HR 6262) is a member of this association, while its brighter apparent partner, Zeta2 (HR 6271), is only 150 ly from Earth and so is not a member.
This cluster is estimated to be about 2–7 million years old, and is approaching the Solar System at 22 km/s. The cluster and association lie in the neighboring Sagittarius Arm of the Milky Way. Zeta1 Scorpii (spectral type O8 and magnitude 4.71.) is the brightest star in the association, and one of the most radiant stars known in the galaxy. NGC 6231 was used to measure the binary fraction of B-type stars: 52 ± 8%, indicating that B-type stars are commonly found in binary systems, but not as commonly as in O-type stars.
NGC 6231 also includes three Wolf-Rayet stars: HD 151932, HD 152270, and HD 152408.
Discovery
The cluster was discovered by Giovanni Batista Hodierna before 1654. Hodierna listed it as Luminosae in his catalogue of deep sky observations. This catalogue was included in his book De Admirandis Coeli Characteribuse published in 1654 at Palermo. It was independently observed by other astronomers after Hodierna, including Edmond Halley (1678), Jean-Philippe de Cheseaux (1745–46), and Abbe Lacaille (1751–52).
Common names
The cluster forms the head of the False Comet, a wider collection of stars from Scorpius OB1 running northward from Zeta Scorpii and NGC 6231 roughly halfway toward Mu Scorpii. The tail is formed by two clusters, Collinder 316 and Trumpler 24. Trumpler 24 is surrounded by the emission nebula IC 4628, also known as the Prawn Nebula, where the tail appears to fan out.
The cluster is also sometimes known as The Northern Jewel Box, due to its similar appearance to the NGC 4755, the Jewel Box cluster, which is further south in the sky.
Chinese astronomy
The English astronomer Ian Ridpath has identified NGC 6231 with the Chinese constellation of Shengong (). Other sources, however, identify this constellation with Zeta Scorpii.
Gallery
See also
New General Catalogue
Notes
External links
SEDS
NGC 6231 at DOCdb (Deep Sky Observer's Companion)
Open clusters
6231
076b
Scorpius | NGC 6231 | [
"Astronomy"
] | 574 | [
"Scorpius",
"Constellations"
] |
4,243,417 | https://en.wikipedia.org/wiki/NGC%204833 |
NGC 4833 (also known as Caldwell 105) is a globular cluster discovered by Abbe Lacaille during his 1751-1752 journey to South Africa, and catalogued in 1755. It was subsequently observed and catalogued by James Dunlop and Sir John Herschel whose instruments could resolve it into individual stars.
The globular cluster is situated in the very southerly constellation Musca at a distance of 21,200 light years from Earth. It is partially obscured by a dusty region of the galactic plane. After corrections for the reddening by dust, evidence was obtained that it is in the order of 2 billion years older than globular clusters M5 or M92.
See also
New General Catalogue
References
CCD Photometry of the Globular Cluster NGC 4833 and Extinction Near the Galactic Plane, Melbourne et al., 25 September 2000, Astrophysical Journal
External links
Basic information and data
Photographed by the Antilhue amateur astronomical observatory
CCD Photometry of the Globular Cluster NGC 4833 and Extinction Near the Galactic Plane
Position relative to nearby cluster NGC 4372
Globular clusters
4833
Musca
105b | NGC 4833 | [
"Astronomy"
] | 232 | [
"Musca",
"Constellations"
] |
4,243,425 | https://en.wikipedia.org/wiki/Suillus%20luteus | Suillus luteus is a bolete fungus, and the type species of the genus Suillus. A common fungus native all across Eurasia from Ireland to Korea, it has been introduced widely elsewhere, including North and South America, southern Africa, Australia and New Zealand. Commonly referred to as slippery jack or sticky bun in English-speaking countries, its names refer to the brown cap, which is characteristically slimy in wet conditions. The fungus, initially described as Boletus luteus ("yellow mushroom") by Carl Linnaeus in 1753, is now classified in a different fungus family as well as genus. Suillus luteus (literally "yellow pig", from its greasy look in rain) is edible, though not as highly regarded as other bolete mushrooms. It is commonly prepared and eaten in soups, stews or fried dishes. The slime coating, however, may cause indigestion if not removed before eating. It is often sold as a dried mushroom.
The fungus grows in coniferous forests in its native range, and pine plantations in countries where it has become naturalized. It forms symbiotic ectomycorrhizal associations with living trees by enveloping the tree's underground roots with sheaths of fungal tissue. The fungus produces spore-bearing fruit bodies, often in large numbers, above ground in summer and autumn.
The fruit body cap often has a distinctive conical shape before flattening with age, reaching up to in diameter. Like other boletes, it has tubes extending downward from the underside of the cap, rather than gills; spores escape at maturity through the tube openings, or pores. The pore surface is yellow, and covered by a membranous partial veil when young. The pale stipe, or stem, measures up to 10 cm (4 in) tall and thick and bears small dots near the top. Unlike most other boletes, it bears a distinctive membranous ring that is tinged brown to violet on the underside.
Taxonomy and naming
The slippery jack was one of the many species first described in 1753 by the "father of taxonomy" Carl Linnaeus, who, in the second volume of his Species Plantarum, gave it the name Boletus luteus. The specific epithet is the Latin adjective lūtěus, meaning "yellow". The fungus was reclassified as (and became the type species of) the genus Suillus by French naturalist Henri François Anne de Roussel in 1796. Suillus is an ancient term for fungi, and is derived from swine. In addition to the British Mycological Society approved name "slippery jack", other common names for this bolete include "pine boletus" and "sticky bun"—the latter referring to its resemblance to the pastry.
German naturalist August Batsch described Boletus volvatus (the specific epithet derived from the Latin volva, meaning "sheath", "covering" or "womb") alongside B. luteus in his 1783 work Elenchus Fungorum. Batsch placed both of these species, along with B. bovinus and the now obsolete names Boletus mutabilis and B. canus, in a grouping of similar boletes he called "subordo Suilli". Boletus volvatus is now considered a synonym of Suillus luteus. Several authors have placed the slippery jack in other genera: Finnish mycologist Petter Karsten classified it as Cricunopus luteus in 1881—the genus Cricinopus defined by yellow adnate tubes; Lucien Quélet classified it as Viscipellis luteus in 1886, and Ixocomus luteus in 1888; and Paul Christoph Hennings placed it in the section Cricinopus of the genus Boletopsis in 1900.
In works published before 1987, the slippery jack was written fully as , as the description by Linnaeus had been name sanctioned in 1821 by the "father of mycology", Swedish naturalist Elias Magnus Fries. The starting date for all the mycota had been set by general agreement as 1 January 1821, the date of Fries's work. Furthermore, as Roussel's description of Suillus predated this as well, the authority for the genus was assigned to British botanist Samuel Frederick Gray in the first volume of his 1821 work A Natural Arrangement of British Plants. The 1987 edition of the International Code of Botanical Nomenclature changed the rules on the starting date and primary work for names of fungi, and names can now be considered valid as far back as 1 May 1753, the date of publication of Linnaeus's work. In 1986, a collection of fruit bodies from Sweden was designated as the neotype of Suillus luteus.
In their 1964 monograph on North American Suillus species, Alexander H. Smith and Harry Delbert Thiers classified S. luteus in the series Suilli of the sectionSuillus in genus Suillus. This group is characterized by the presence of either a ring on the stipe, a partial veil adhering to the cap margin, or a "false veil" not attached to the stipe but initially covering the tube cavity. Species closely related to Suillus luteus include S. pseudobrevipes (a sister species), S. brevipes and S. weaverae (formerly Fuscoboletinus weaverae). A genetic study of nucleotide DNA reinforced the species' monophyly and low genetic divergence, with material of S. luteus from the United Kingdom, Austria, Germany and North America forming a clade, in contrast with some other species, such as S. granulatus, which were shown to be polyphyletic.
Chemical analysis of pigments and chromogens showed that Suillus was more closely related to Gomphidius and Rhizopogon than to other boletes, and hence Suillus luteus and its allies were transferred from the Boletaceae to the newly circumscribed family Suillaceae in 1997. Molecular studies have reinforced how distantly related these fungi are from Boletus edulis and its allies.
Description
The cap is chestnut, rusty, olive brown, or dark brown in color and generally 4–10 cm (rarely to 20 cm) in diameter at maturity. The cap has a distinctive conical shape, later flattening out. It is slimy to the touch, bare, smooth, and glossy even when dry, and the cuticle is easily peeled off. The tiny, circular pores of the tubes are initially yellow but turn olive to dark yellow with maturity. Like the skin of the cap, they can be readily peeled away from the flesh.
Tubes comprising the hymenophore on the underside of the cap are deep, with an attachment to the stipe ranging from adnate to somewhat decurrent. The pores are tiny, numbering 3 per mm in young specimens and 1–2 per mm in maturity. The stipe is tall and wide. It is pale yellow and more or less cylindrical but may bear a swollen base. A membranous partial veil initially links the stipe with the edge of the cap. When it ruptures, it forms a membranous, hanging ring. The top side of the ring is whitish, while the underside is characteristically dark brown to violet. This species is one of the few members of the genus Suillus that have such a ring. Above the ring, the stipe features glandular dots—minute clumps of pigmented cells. Below the ring, the stipe is dingy white, sometimes streaked with brownish slime. In humid conditions, the ring has a gelatinous texture. The white flesh of the entire fungus does not discolour when damaged, and is soft—particularly in mature specimens. It has a "pleasant" taste and lacks any distinctive odour.
The spore print is ochre or clay coloured, the elongated elliptical spores measuring 7–10 by 3–3.5 μm. Basidia (spore-producing cells) are four spored, with dimensions of 14–18 by 4–5 μm. Cystidia are present on both the tube faces (pleurocystidia) and edges (cheilocystidia), either scattered or, more rarely, as bundles. They measure 20–35 by 5–7 μm and have a narrow club shape. Clamp connections are not present in the hyphae of S. luteus.
Similar species
Good field characteristics for Suillus luteus include the slimy brown cap, glandular dots on the upper stipe, and prominent purplish ring. A frequent lookalike is Suillus granulatus, which is another common, widely distributed and edible species occurring in the same habitat. Suillus granulatus is yellow fleshed and exudes latex droplets when young, but most conspicuously bears neither a partial veil nor a ring. Other than that, Suillus luteus is unlikely to be confused with other mushrooms, especially if its preferred habitat under pine trees and the whitish partial veil are considered. In Europe, the related Suillus grevillei is found under larch and has a yellow cap, while immature fruit bodies of Gomphidius glutinosus may look comparable from above but have gills rather than pores underneath. In North America, Suillus borealis and S. pseudobrevipes also have partial veils, but lack the distinctive ring of S. luteus. S. cothurnatus forms a band-like ring on the stipe that tends to be brownish rather than purplish.
In some specimens of S. luteus, the partial veil separates from the stipe (rather than the cap margin), leaving cottony patches of veil hanging from the cap margin. In this state, fruit bodies can be confused with those of S. albidipes. Unlike S. luteus, however, S. albidipes does not have glandular dots on its stipe.
Distribution and habitat
Suillus luteus can be found all over the Northern Hemisphere. Native to Eurasia, it is widespread across the British Isles. To the east it has been recorded from Pakistan, where it was found along canals in Dashkin in the district of Astore, and as far east as South Korea. It has also been widely introduced elsewhere by way of pine plantations around the globe. It is very commonly found in Monterey pine (Pinus radiata) plantations, despite the tree being native to California and hence not in the fungus' native range. In North America it is found in the northeastern, northwestern, and southwestern United States. According to Ernst Both, it was Charles Horton Peck who first suggested in 1887 that the fungus was introduced to the state of New York on Pinus sylvestris. DNA studies show that the North American populations differ little genetically from European populations, supporting the idea that the fungus arrived to North America relatively recently as a result of human activity. Suillus luteus is found in coastal and mountainous pine forests and exhibits a tolerance of the northern latitudes. Southern Hemisphere locales where the slippery jack grow with plantation pines include South America, Africa, Australia, and New Zealand. In southwestern Australia, the bolete is limited to areas of greater than 1000 mm (40 in) annual rainfall. It has been recorded as far north as the Darling Downs and southern Queensland, and occasionally in Tasmania. The fungus fruits in spring, summer and fairly prolifically in autumn, following periods of wet weather. Mushrooms can appear in large troops or fairy rings.
In Ecuador, Pinus radiata plantations were planted extensively around Cotopaxi National Park, and Suillus luteus boletes appear in abundance year-round. A 1985 field study estimated production to be 3000–6000 mushrooms per hectare—up to (dry weight) of mushrooms hectare per year. This continuous production contrasts with the bolete's seasonal appearance elsewhere. The fungus is not found in adjacent areas of native vegetation. The fruiting is so bountiful that the harvest of slippery jacks has become the main reason that pine plantations are established or maintained in parts of Ecuador.
In southern Brazil, it has been recorded in plantations of slash pine (P. elliottii) in the municipalities of Pelotas, Nova Petrópolis and Canela in Rio Grande do Sul, and Colombo in Paraná. It is particularly common in plantations in Patagonia. Suillus luteus is the commonest bolete encountered in the Falkland Islands, where it is found in windbreaks and gardens.
In South Africa, Suillus luteus has been occasionally recorded under pines in Bloemfontein, Johannesburg and Royal Natal National Park.
Ecology
Suillus luteus is a pioneer species that typically establishes itself in the early stages of forest succession. The fungus forms mycorrhizal associations with various species of pine, including Scots pine (P. sylvestris), black pine (P. nigra), and Macedonian pine (P. peuce) in Europe, and red pine (P. resinosa) and white pine (P. strobus) in North America. An in vitro experiment demonstrated that the species could form an ectomycorrhizal association with Aleppo pine (P. halepensis), a key species used in reforestation in the Mediterranean. A study of the ectomycorrhizal fungi associated with a lodgepole pine (P. contorta) invasion front near Coyhaique, Chile, showed that many invasive trees were supported by S. luteus as the sole mycorrhizal partner.
The ectomycorrhizae formed between the fungus and host plant can be influenced by soil microorganisms present in the mycorrhizosphere. For example, soil bacteria from the genera Paenibacillus and Burkholderia alter the branching structure of the root, whereas Bacillus species increase root growth and mycorrhizal colonization. The fungus does not require a specific soil but seems to prefer acidic and nutrient-deficient soil. Suillus luteus produces hydroxamic acid-based siderophores, which are compounds that can chelate iron and extract it from the soil in nutrient-poor conditions. Ignacio Chapela and colleagues analysed the carbon uptake of S. luteus in Ecuador, concluding pine plantations accompanied by S. luteus deplete carbon stored in the soil and raising concerns that these might not be a remedy for rising carbon dioxide levels in the atmosphere.
The fungus has been shown to provide a protective effect against heavy metal toxicity when associated with the host Pinus sylvestris, preventing copper accumulation in the needles, and protecting seedlings against cadmium toxicity. Owing to its frequent rate of sexual reproduction and the resulting extensive gene flow within populations, the fungus can rapidly evolve a trait to tolerate otherwise toxic levels of heavy metals in the environment. The genetic basis of this adaptation—intriguing to researchers investigating the bioremediation potential of metal-adapted plants and their fungal associates—are contained in the genome sequence of S. luteus, published in 2015.
Suillus luteus fruit bodies are sometimes infested with larvae, though not nearly as often as S. granulatus or B. edulis. Damage from maggots is much more common in warmer months, and rare late in the season with cooler weather. In a Finnish study, researchers found that 70–95% of fruit bodies collected from typical forest habitats were infested with larvae; the most common species were the flies Mycetophila fungorum, Pegomya deprimata, and Pegohylemyia silvatica. In contrast, other studies have shown that fruit bodies collected from pine plantations are relatively free of larvae. The fungus produces microscopic crystals of oxalic acid at the surface of its hyphae, a feature that is thought to help deter grazing by the springtail species Folsomia candida.
Edibility
Suillus luteus is an edible mushroom, but the slime/pileipellis must be removed. Although some authors regard it as one of low quality, and generally inferior to co-occurring species such as Boletus pinophilus, the species is considered a delicacy in Slavic cultures (known as maslyata in Russian or maslyuky in Ukrainian or maślaki in Polish, deriving from words meaning "buttery"). It was highly regarded in Calabria, even more than Boletus edulis, until the 1940s when increased interest in the latter species eclipsed the former. Mushrooms conforming to Suillus luteus are exported from Chile to Italy, and, since the 1970s, the United States. As of 2002, harvesters in Chile were paid on average US$0.5 per kilogram of fruit bodies.
In Burundi, Suillus luteus mushrooms are sold to Europeans as cepes in Bujumbura but not generally eaten by the Barundi. Based on samples collected from Chile, the boletes contain (as a percentage of dry weight) 20% protein, 57% carbohydrates, 6% fat, and 6% ash. Pinus radiata plantations in southeastern Australia have become tourist attractions as people flock to them in autumn to pick slippery jacks and saffron milk-caps (Lactarius deliciosus); Belanglo State Forest in particular has attracted large numbers of Polish foragers.
Slippery jacks do not keep for long after picking,. Zeitmar considers them unsuitable for drying, as their water content is too high. They are suited for frying, or cooking in stews and soups, either alone or with other mushroom species. Puréeing the mushroom is not recommended, however: "We once made the mistake of running it through a blender to make a soup. The result was a substance recommending itself for use when hanging wallpaper." S. luteus and other Suillus species may cause allergic reactions in some people or digestive problems that appear to result from consuming the slimy skin. The fungus is better cooked before eating, and some authors recommend discarding the glutinous cuticle and tubes before cooking. Moreover, the skin can spoil other fungi with which slippery jacks are collected.
Inexpensive powdered S. luteus fruit bodies are sometimes added to the more expensive B. edulis mushroom soup powder, a fraudulent practice that is difficult to detect by microscope because the tissues are no longer intact. This adulteration can be determined chemically, however, by testing for increased levels of the sugar alcohols arabitol and mannitol. The practice can also be determined with a DNA-based method that is sensitive enough to detect the addition of 1–2% of S. luteus to B. edulis powder.
See also
List of North American boletes
References
External links
Suillus luteus at MykoWeb
luteus
Edible fungi
Fungi of Europe
Fungi described in 1753
Fungi of Africa
Fungi of Asia
Fungi of Central America
Fungi of New Zealand
Fungi of the United States
Fungi found in fairy rings
Taxa named by Carl Linnaeus
Fungus species | Suillus luteus | [
"Biology"
] | 3,957 | [
"Fungi",
"Fungus species"
] |
4,243,440 | https://en.wikipedia.org/wiki/Russula%20virescens | Russula virescens is a basidiomycete mushroom of the genus Russula, and is commonly known as the green-cracking russula, the quilted green russula, or the green brittlegill. It can be recognized by its distinctive pale green cap that measures up to in diameter, the surface of which is covered with darker green angular patches. It has crowded white gills, and a firm, white stipe that is up to tall and thick. Considered to be one of the best edible mushrooms of the genus Russula, it is especially popular in Spain and China. With a taste that is described variously as mild, nutty, fruity, or sweet, it is cooked by grilling, frying, sautéeing, or eaten raw. Mushrooms are rich in carbohydrates and proteins, with a low fat content.
The species was described as new to science in 1774 by Jacob Christian Schaeffer. Its distribution encompasses Asia, North Africa, Europe, and Central America. Its presence in North America has not been clarified, due to confusion with the similar species Russula parvovirescens and R. crustosa. R. virescens fruits singly or scattered on the ground in both deciduous and mixed forests, forming mycorrhizal associations with broadleaf trees such as oak, European beech, and aspen. In Asia, it associates with several species of tropical lowland rainforest trees of the family Dipterocarpaceae. R. virescens has a ribonuclease enzyme with a biochemistry unique among edible mushrooms. It also has biologically active polysaccharides, and a laccase enzyme that can break down several dyes used in the laboratory and in the textile industry.
Taxonomy
Russula virescens was first described by German polymath Jacob Christian Schaeffer in 1774 as Agaricus virescens. The species was subsequently transferred to the genus Russula by Elias Fries in 1836. According to the nomenclatural authority MycoBank, Russula furcata var. aeruginosa (published by Christian Hendrik Persoon in 1796) and Agaricus caseosus (published by Karl Friedrich Wilhelm Wallroth in 1883) are synonyms of Russula virescens. The variety albidocitrina, defined by Claude Casimir Gillet in 1876, is no longer considered to have independent taxonomic significance. According to Rolf Singer's 1986 classification of Russula, R. virescens is the type species of subsection Virescentinae in section Rigidae, a grouping of mushrooms characterized by a cap surface that breaks into patches of bran-like (furfuraceous) particles. In a molecular phylogenetic analysis of European Russula, R. virescens formed a clade with R. mustelina; these two species were sister to a clade containing R. amoenicolor and R. violeipes.
The specific epithet virescens is Latin for "becoming green". The characteristic pattern of the cap surface has earned the species common names such as the green-cracking russula, the quilted green russula, and the green brittlegill. In the mid-Atlantic United States, it is also known locally as the moldy russula.
Description
Described by mushroom enthusiast Antonio Carluccio as "not exactly nice to look at", the cap is at first dome or barrel-shaped, becoming convex and flattened with age with a diameter of up to . The cap center is often depressed. The cuticle of the cap is green, most profoundly in the center, with patches of the same color dispersed radially around the center in an areolate pattern. The color of the cuticle is often of variable shade, ranging from gray to verdigris to grass-green. The extent of the patching of the cuticle is also variable, giving specimens with limited patches a resemblance to other green-capped species of Russula, such as R. aeruginea. The green patches of the cap lie on a white to pale green background. The cap, while frequently round, may also exhibit irregular lobes and cracks. The cap cuticle is thin, and can be readily peeled off the surface to a distance of about halfway towards the cap center.
The gills are white to cream colored, and fairly crowded together; they are mostly free from attachment to the stipe. Gills are interconnected at their bases by veins. The stipe is cylindrical, white, and of variable height, up to tall and wide; it is roughly the same thickness at both the top and the base. The top portion of the stipe may be farinose—covered with a white, mealy powder. It may turn slightly brown with age, or when it is injured or bruised from handling. Like other mushrooms in the Russulales, the flesh is brittle, owing to the sphaerocyst cytoarchitecture—cylindrical cells that contrast with the typical fibrous, filamentous hyphae present in other orders of the basidiomycota.
The spores of R. virescens are elliptical or ellipsoid with warts, translucent (hyaline), and produce a white, pale or pale yellow spore print; the spore dimensions are 6–9 by 5–7 μm. A partial reticulum (net-like pattern of ridges) interconnects the warts. The spore-bearing cells, the basidia, are club-shaped and have dimensions of 24–33 by 6–7.5 μm; they are colorless, and each hold from two to four spores. The pleurocystidia (cystidia on the gill face) are 40–85 by 6–8 μm and end abruptly in a sharp point.
Similar species
Russula parvovirescens, found in the eastern United States, can be distinguished from R. virescens by its smaller stature, with caps measuring wide and stipe up to long by thick. Compared to R. virescens, it tends to be more bluish-green, the patches on its cap are larger, and it has a lined cap margin. Microscopically, the terminal cells in the cap cuticle of R. parvovirescens are more swollen than those of R. virescens, which has tapered and elongated terminal cells. Another green-capped Russula is R. aeruginea, but this species may be distinguished from R. virescens by its smaller size and smooth cap. Other green russulas with a smooth cap include R. heterophylla and R. cyanoxantha var. peltereaui. Russula crustosa, like R. virescens, also has an areolate cap, but the cap becomes sticky (viscid) when moist, and its color is more variable, as it may be reddish, yellowish, or brown. Also, the spore print of R. crustosa is a darker yellow than R. virescens. R. redolens has a cap that is "drab-green to blue-green", but unlike R. virescens, is smooth. R. redolens has an unpleasant taste and smells of parsley.
Edibility
Russula virescens is an edible mushroom considered to be one of the best of the genus Russula, and is popular in Europe, particularly in Spain. In an 1875 work on the uses of fungi, English mycologist Mordecai Cubitt Cooke remarked about the mushroom that "the peasants about Milan are in the habit of putting [it] over wood embers to toast, and eating [it] afterwards with a little salt." The mushroom is often sold as a dried product in Asia; in China, it can be found in roadside markets, and used in traditional herbal medicines. Its smell is not distinctive, but its taste has been described as mild, nutty, fruity, or even sweet. Old specimens may smell of herrings. Drying the mushrooms enhances the nutty flavor. Mushrooms can be sautéed (the green color disappears with cooking), and young specimens that are prepared this way have a potato taste that pairs well with shallots. They are also fried or grilled, or used raw in salads. Young specimens are pale and can be hard to identify, but the characteristic pattern of older fruit bodies makes them hard to confuse with other species. When collecting R. virescens for consumption, caution is of vital importance to avoid confusion with the dangerously poisonous Amanita phalloides (better known as the death cap), a mushroom that can be most easily identified by its volva and ring.
The nutritional components of R. virescens mushrooms have been characterized. Fresh mushrooms contain about 92.5% moisture. A sample of dried mushroom (100 g dw) has 365 kcal (1527 kilojoules). Carbohydrates make up the bulk of the fruit bodies, comprising 62% of the dry weight; 11.1% of the carbohydrates are sugars, the large majority of which (10.9%) is mannitol. The total lipid, or crude fat, content makes up 1.85% of the dry matter of the mushroom. The proportion of fatty acids (expressed as a percentage of total fatty acids) are 28.78% saturated, 41.51% monounsaturated, and 29.71% polyunsaturated. The most prevalent fatty acids include: palmitic acid, 17.3% of total fatty acids; stearic acid, 7.16%; oleic acid, 40.27%; and linoleic acid, 29.18%. Several bioactive compounds are present in the mushroom. One hundred grams (dry weight) contains 49.3 micrograms (μg) of tocopherols (20.0 μg alpha, 21.3 μg beta, and 8.0 μg gamma) and 0.19 milligrams (mg) of the carotenoid pigment lycopene. There are 4.46 g of organic acids per 100 g of dry mushrooms, including oxalic acid (0.78 g), malic acid (2.71 g), citric acid (0.55 g), and fumaric acid (0.23 g). Mushrooms have 22.6 mg/100 g dw of the phenolic compound 4-hydroxybenzoic acid, and 15.8 mg/100 g dw of cinnamic acid.
Habitat and distribution
Russula virescens can be found fruiting on soil in both deciduous forests and mixed forests, forming ectomycorrhizal symbiotic relationships with a variety of trees, including oaks (Quercus), European beech (Fagus sylvatica), and aspen (Populus tremula). Preliminary investigations suggest that the fungus also associates with at least ten species of Dipterocarpaceae, an important tree family prevalent in the tropical lowland forests of Southeast Asia. Fruit bodies may appear singly or in groups, reappear in the same spots year after year, and are not common. In Europe, fruiting occurs mainly during the months of summer to early autumn. A Mexican study of the seasonal occurrence of several common mushroom species in subtropical forests in Xalapa showed that the fruiting period of R. virescens occurred in April, before the onset of the rainy season.
The distribution of R. virescens in North America is subject to debate, where a number of similar species such as R. parvovirescens and R. crustosa are also recognized. One author even suggests that R. virescens "is strictly a European species", citing Buyck and collaborators (2006), who say "the virescens-crustosa group is much more complex than suspected and embraces at least a dozen taxa in the eastern US". As in Europe, Russula virescens has a widespread distribution in Asia, having been recorded from India, Malaysia, Korea, the Philippines, Nepal, China, Thailand, and Vietnam. It is also found in North Africa and Central America.
Chemistry
Russula virescens has a limited capacity to bioaccumulate the micronutrients iron, copper, and zinc from the soil. The concentration of these trace metals is slightly higher in the caps than the stipes. A meal of fresh mushroom caps would supply 16% of the recommended daily allowance (RDA) of copper for an adult male or female (ages 19–50); 16% or 7.3% of the RDA of iron for an adult male or female, respectively; and 16–22% of the adult RDA of zinc. The mushroom is a poor bioaccumulator of the toxic heavy metals arsenic, cadmium, lead, mercury, and nickel.
Biologically active mushroom polysaccharides have been a frequent research topic in recent decades due to their possible stimulatory effect on innate and cell-mediated immune responses, antitumor activities, and other activities. Immunostimulatory activity, antioxidant activity, cholesterol-lowering, and blood sugar-lowering effects have been detected in extracts of R. virescens fruit bodies, which are attributed to polysaccharides. A water-insoluble beta-glucan, RVS3-II, has been isolated from the fruit bodies. Sulfated derivatives of this compound have antitumor activities against sarcoma tumor cell lines. RVP, a water-soluble polysaccharide present in the mushroom, is made largely of galactomannan subunits and has antioxidant activity.
Ribonucleases (or RNases) are enzymes that catalyze the hydrolysis of ribonucleic acid (RNA), and collectively they play a critical role in many biological processes. A RNase from R. virescens was shown to be biochemically unique amongst seven edible mushroom species in several ways: it has a co-specificity towards cleaving RNA at poly A and poly C, compared to the monospecific RNases of the others; it can be adsorbed on chromatography columns containing DEAE–cellulose as the adsorbent; it has a pH optimum of 4.5, lower than all other species; and, it has a "distinctly different" N-terminal amino acid sequence. The mushroom contains a unique laccase enzyme that can break down several dyes used in the laboratory and in the textile industry, such as bromothymol blue, eriochrome black T, malachite green, and reactive brilliant blue. Laccases are being used increasingly in the textile industry as environmental biocatalysts for the treatment of dye wastewater.
See also
List of Russula species
References
External links
virescens
Edible fungi
Fungi described in 1774
Fungi of Africa
Fungi of Asia
Fungi of Central America
Fungi of Europe
Fungi of North America
Fungus species | Russula virescens | [
"Biology"
] | 3,107 | [
"Fungi",
"Fungus species"
] |
4,243,493 | https://en.wikipedia.org/wiki/Benjamin%20Jesty | Benjamin Jesty (c. 1736 – 16 April 1816) was a farmer at Yetminster and Worth Matravers in Dorset, England, notable for his early experiments in inducing immunity against smallpox using cowpox.
The notion that those people infected with cowpox, a relatively mild disease, were subsequently protected against smallpox was not an uncommon observation with country folk in the late 18th century, but Jesty was one of the first to intentionally administer the less virulent virus. He was one of the six English, Danish and German people who reportedly administered cowpox to artificially induce immunity against smallpox from 1770 to 1791; only Jobst Bose of Göttingen, Germany with his 1769 inoculations pre-dated Jesty's work.
Unlike Edward Jenner, a medical doctor who is given broad credit for developing the smallpox vaccine in 1796, Jesty did not publicise his findings made some twenty years earlier in 1774.
Early life
Jesty was born in Yetminster, Dorset, and baptized there on 19 August 1736, the youngest of at least four sons of Robert Jesty, who was a butcher. Little else is known of his early life. In March 1770 he married Elizabeth Notley (1740–1824) in Longburton, four miles north-east of Yetminster. The couple lived at Upbury Farm, next to Yetminster church, and the couple had four sons and three daughters.
Jesty and smallpox
During the eighteenth century smallpox was widespread throughout England, with frequent epidemics. It was known in the dairy-farming areas in the south-west of the country that the milkmaids and other workers who contracted cowpox from handling cows' udders, were afterwards immune to smallpox. Such people were able to nurse smallpox victims without fear of contracting the disease themselves. This folk-knowledge gradually became more widely disseminated amongst the medical community: in 1765 a Dr Fewster (possibly John Fewster) of Thornbury, Gloucestershire presented a paper to the Medical Society of London entitled "Cow pox and its ability to prevent smallpox", and Dr. Rolph, another Gloucestershire physician, stated that all experienced physicians of the time were aware of this.
Jesty and two of his female servants, Ann Notley and Mary Reade, had been infected with cowpox. When an epidemic of smallpox came to Yetminster in 1774, Jesty decided to try to give his wife Elizabeth and two eldest sons immunity by infecting them with cowpox. He took his family to a cow at a farm in nearby Chetnole that had the disease, and using a darning needle, transferred pustular material from the cow by scratching their arms. The boys had mild local reactions and quickly recovered but his wife's arm became very inflamed and for a time her condition gave cause for concern, although she too recovered fully in time.
Jesty's experiment was met with hostility by his neighbours. He was labelled inhuman, and was "hooted at, reviled and pelted whenever he attended markets in the neighbourhood'". The introduction of an animal disease into a human body was thought disgusting and some even "feared their metamorphosis into horned beasts". But the treatment's efficacy was several times demonstrated in the years which followed, when Jesty's two elder sons, exposed to smallpox, failed to catch the disease.
Interest in the prophylactic powers of cowpox virus grew and in May 1796, over 20 years after Jesty had made his inoculations, Edward Jenner began his series of vaccination experiments. In about 1797 Jesty and his family moved from Yetminster, when Jesty took up the tenancy of Downshay Manor Farm in Worth Matravers near the Dorset coast. Here he came to the attention of Dr. Andrew Bell, rector of nearby Swanage who (possibly encouraged by Jesty's efforts) vaccinated over 200 of his parishioners in 1806.
Recognition and final years
In June 1802 Jenner was given a reward of £10,000 from the House of Commons for discovering and promoting vaccination, and another award of £20,000 followed in 1807. Before this first amount had been awarded, George Pearson, founder of the Original Vaccine Pock Institution, had brought evidence before the House of Commons of Jesty's work in 1774, work which pre-dated Jenner's by 22 years. Unfortunately, Jesty's well-documented case was weakened by his failure to petition in person, and Pearson's inclusion of other claimants whose evidence could not be validated, so no reward was forthcoming.
Unaware of George Pearson's previous petitions to the Pitt Government about the Dorset farmer, the Reverend Dr. Andrew Bell, rector of Swanage near where Jesty later resided, prepared a paper dated 1 August 1803, proposing Jesty as the first vaccinator, and sent copies to the Original Vaccine Pock Institute and the member of parliament, George Rose. Bell wrote to the Institution again in 1804, having learned of Pearson's involvement.
In 1805, at Pearson's instigation and the institution's invitation, Jesty gave his evidence before 12 medical officers of the institution at its base on the corner of Broadwick Street and Poland Street in Soho. Robert, Jesty's oldest son (by then 28 years old) also made the trip to London and agreed to be inoculated with smallpox again to prove that he still had immunity. After Jesty had been cross-examined, he was presented with a long testimonial and pair of gold mounted lancets. The verbal evidence of their examination was published in the Edinburgh Medical and Surgical Journal.
Report from the Original Vaccine Pock Institute, 1805 "That he was led to undertake this novel practice in 1774 to counteract the small-pox, at that time prevalent at Yetminster, where he then resided, from knowing the common opinion of the country ever since he was a boy (now 60 years ago) that persons who had gone through the cowpock naturally, ie by taking it from cows, were insusceptible of the small-pox; by himself being incapable of taking the small-pox, having gone through the cow-pock many years before; from knowing many individuals, who, after the cowpock, could not have the small-pox excited; from believing that the cow-pock was an affection free from danger; and from his opinion that, by the cow-pock inoculation, he should avoid ingrafting various diseases of the human constitution, such as "the Evil (scrofula), madnes, lues (syphilis), and many bad humours," as he called them."
For the event, Jesty's family had tried to persuade him to dress in a more up-to-date fashion, but he refused saying that "he did not see why he should dress better in London than in the country". Immediately after his interrogation, Jesty was taken round to the studio of the portrait painter Michael William Sharp in nearby Great Marlborough Street. Jesty proved an impatient sitter, and so Mrs Sharp played the piano to try to soothe him as Sharp painted. After a chequered history, the portrait is now owned by the Wellcome Trust and is on loan to the Dorset Museum in Dorchester.
On Sunday 15 July 1806, Bell preached the same sermon twice in honour of Jesty, "whose discovery of the efficacy of the cowpock against smallpox is so often forgotten by those who have heard of Dr Jenner".
Jesty died in Worth Matravers on 16 April 1816 and was buried in a prominent position in the parish churchyard. His widow, Elizabeth, died on 8 January 1824 and was buried alongside him. Both headstones are listed structures, primarily due to their historic interest. The full text on Jesty's headstone reads:
(Sacred) To the Memory OF Benj.in. Jesty (of Downshay) who departed this Life, April 16th 1816 aged 79 Years. He was born at Yetminster in this County, and was an upright honest Man: particularly noted for having been the first Person (known) that Introduced the Cow Pox by Inoculation, and who from his great strength of mind made the Experiment from the (Cow) on his Wife and two Sons in the Year 1774.
References
Further reading
Patrick J Pead, 2003, "Benjamin Jesty: new light in the dawn of vaccination" The Lancet Volume 362, Issue 9401, 20 December 2003, pages 2104–2109 (online at )
Patrick J Pead, 2006, "Benjamin Jesty: the first vaccinator revealed" The Lancet Volume 368, Issue 9554, 23 December 2006, page 2202
Pead, Patrick J. (2016). Benjamin Jesty – grandfather of vaccination. Chichester: Timefile Books.
External links
Dorset Page – First Recorded Small Pox Vaccination
The Jesty Family Tree – Jolyon Jesty
Oxford Dictionary of Biography
Jesty's portrait at the Wellcome Trust
Images of England page on Jesty's famhouse in Yetminster
1730s births
1816 deaths
People from Yetminster
Smallpox vaccines
Vaccinologists
18th-century English farmers | Benjamin Jesty | [
"Biology"
] | 1,909 | [
"Vaccination",
"Vaccinologists"
] |
4,243,637 | https://en.wikipedia.org/wiki/Talaromycosis | Talaromycosis is a fungal infection that presents with painless skin lesions of the face and neck, as well as an associated fever, anaemia, and enlargement of the lymph glands and liver.
It is caused by the fungus Talaromyces marneffei, which is found in soil and decomposing organic matter. The infection is thought to be contracted by inhaling the fungus from the environment, though the environmental source of the organism is not known. People already suffering from a weakened immune system due to conditions such as HIV/AIDS, cancer, organ transplant, long-term steroid use, old age, malnutrition or autoimmune disease are typically the ones to contract this infection. It generally does not affect healthy people and does not spread from person to person. Diagnosis is usually made by identification of the fungus from clinical specimens, either by microscopy or culture. Biopsies of skin lesions, lymph nodes, and bone marrow demonstrate the presence of organisms on histopathology. Medical imaging may reveal shadows in the lungs. The disease can look similar to tuberculosis and histoplasmosis.
Talaromycosis may be prevented in people at high risk, using the antifungal medication itraconazole, and is treatable with amphotericin B followed by itraconazole or voriconazole. The disease is fatal in 75% of those not given treatment.
Talaromycosis is endemic exclusively to southeast Asia (including southern China and eastern India), and particularly in young farmers. The exact number of people in the world affected is not known. Men are affected more than women. The first natural human case of talaromycosis was reported in 1973 in an American minister with Hodgkin's disease who lived in Southeast Asia.
Signs and symptoms
There may be no symptoms, or talaromycosis may present with small painless skin lesions. The head and neck are most often affected. Other features include: fever, general discomfort, weight loss, cough, difficulty breathing, diarrhoea, abdominal pain, swelling of the spleen (splenomegaly), liver swelling (hepatomegaly), swollen lymph nodes (lymphadenopathy), and anemia. There may be no symptoms.
In those without HIV infection, the lungs, liver, and mouth are usually affected, with systemic infection rarely occurring. The skin lesions are also often smooth. The disease tends to present differently in those with HIV infection; they are more likely to experience widespread infection. Their skin lesions however, are usually dented in the centre and can appear similar to molluscum contagiosum.
Cause
Talaromycosis is usually caused by T. marneffei, however, other species of the Talaromyces genus are also known to cause the disease in rare cases.
Risk factors
Talaromycosis rarely affects healthy people and generally occurs in people who are already sick and unable to fight infection such as HIV/AIDS, cancer, organ transplant, long-term steroid use, old age, malnutrition or autoimmune disease.
Mechanism
The infection is thought to be acquired through breathing in the organism from the environment. However, the exact source of infection is not known. The infection is not spread person-to-person. In Thailand, talaromycosis is more common during the rainy season; rain may promote the proliferation of the fungus in the environment.
Diagnosis
There is no accurate fast serological test. Diagnosis relies on identifying Talaromyces marneffei in cultures from clinical specimens such as sputum, blood, skin scrapings, lymph node, and bone marrow, by which time the disease is in the late-stage. Fungi in blood are found in half of case.
Non-specific laboratory findings may show evidence of the fungus invading tissue, such as low platelets due to bone marrow infiltration, and elevated transaminases due to liver involvement.
Biopsies of skin lesions, lymph nodes, and bone marrow demonstrate the presence of organisms on histopathology. Intracellular and extracellular forms are oval and have a characteristic transverse septum. In culture, colonies are powdery green and produce red pigment; however, cultures are negative in a significant number of cases.
Medical imaging may reveal shadows in the lungs.
Differential diagnosis
The disease can look similar to tuberculosis and histoplasmosis
Treatment
Talaromycosis may be prevented in people at high risk, using the antifungal medication itraconazole, and is treatable with amphotericin B followed by itraconazole or voriconazole.
Outcomes
With treatment, less than 25% of those affected die. Without treatment, more than 75% will die.
Epidemiology
The exact number of people in the world affected is not known. Once considered rare, its occurrence increased due to HIV/AIDS to become the third most common opportunistic infection (after extrapulmonary tuberculosis and cryptococcosis) in HIV-positive individuals within the endemic area of Southeast Asia. While incidence in those with HIV began to decrease due to antiretroviral treatment, the number of cases in those without HIV began to rise in some endemic areas since the mid-1990s, likely due to improved diagnosis and an increase in other conditions that reduce immunity. The disease has been found to be more common in young farmers. Men are affected more than women.
History
T. marneffei was first isolated from a bamboo rat in Vietnam in 1956. Three years later, it was described by Gabriel Segretain as a new species with disease potential. The first natural human case of talaromycosis was reported in 1973 in an American minister with Hodgkin's disease who lived in Southeast Asia.
Research
An antigen assay has been developed to detect a key virulence factor Mp1p that has been shown to have a high specificity for Talaromyces marneffei.
References
External links
Animal fungal diseases
Fungal diseases | Talaromycosis | [
"Biology"
] | 1,251 | [
"Fungi",
"Fungal diseases"
] |
4,244,086 | https://en.wikipedia.org/wiki/Open%20Graphics%20Project | The Open Graphics Project (OGP) was founded with the goal to design an open-source hardware / open architecture and standard for graphics cards, primarily targeting free software / open-source operating systems. The project created a reprogrammable development and prototyping board and had aimed to eventually produce a full-featured and competitive end-user graphics card.
OGD1
The project's first product was a PCI graphics card dubbed OGD1, which used a field-programmable gate array (FPGA) chip. Although the card did not have the same level of performance or functionality as graphics cards on the market at the time, it was intended to be useful as a tool for prototyping the project's first application-specific integrated circuit (ASIC) board, as well as for other professionals needing programmable graphics cards or FPGA-based prototyping boards. It was also hoped that this prototype would attract enough interest to gain some profit and attract investors for the next card, since it was expected to cost around US$2,000,000 to start the production of a specialized ASIC design. PCI Express and/or Mini-PCI variations were planned to follow. The OGD1 began shipping in September 2010, some six years after the project began and 3 years after the appearance of the first prototypes.
Full specifications will be published and open-source device drivers will be released. All RTL will be released. Source code to the device drivers and BIOS will be released under the MIT and BSD licenses. The RTL (in Verilog) used for the FPGA and the RTL used for the ASIC are planned to be released under the GNU General Public License (GPL).
It has 256 MiB of DDR RAM, is passively cooled, and follows the DDC, EDID, DPMS and VBE VESA standards. TV-out is also planned.
Versioning schema
Versioning schema for OGD1 will go like this:
{Root Number} – {Video Memory}{Video Output Interfaces}{Special Options e.g.: A1 OGA firmware installed}
OGD1 components
Main components of OGD1 graphics card (shown on the picture)
A) DVI transmitter pair A
B) DVI transmitter pair B
C) 330MHz triple 10-bit DAC (behind)
D) TV chip
E) 2x4 256 megabit DDR SDRAM (front, behind)
F) Xilinx 3S4000 FPGA (main chip)
G) Lattice XP10 FPGA (host interface)
H) SPI PROM 1 Mibit
J) SPI PROM 16 Mibit
K) 3x 500 MHz DACs (optional)
L) 64-bit PCI-X edge connector
M) DVI-I connector A and connector B
N) S-Video connector
O) 100-pin expansion bus connector
Divisions/terms related to OGP
Open Graphics Project (OGP)The group of people developing OGA, its written documentation, and its products.
Open Graphics Architecture (OGA)The trade name for open graphics architectures specified by the Open Graphics Project.
Open Graphics Development (OGD)The initial FPGA-based experimentation board used as a test platform for TRV ASICs.
Traversal Technology (TRV)The commercial name for the first ASIC products, based on the Open Graphics Architecture.
Open Graphics Card (OGC)Graphics cards based on TRV chips.
Open Hardware Foundation (OHF)A non-profit corporation whose charter is to promote the design and production of open-source and open-documentation hardware.
Current status
The OGP project failed to gain the necessary funding to produce an ASIC version of its card. The project appears to have been discontinued in 2011.
See also
Graphics hardware and FOSS
Open-source hardware
Open system (computing)
RISC-V
References
External links
The official Open Graphics wiki archived at the Wayback Machine June 9, 2010
Project VGA – another free graphics core project, aiming at cheaper hardware
Manticore – an older FPGA-based free graphics core implementation. As of 2009-05-04 no source is available.
The master thesis "An FPGA-based 3D Graphics System" illustrates very well the design decisions to make, while developing a FPGA-based 3D graphics core.
The master thesis "A performance-driven SoC architecture for video synthesis" gives a more complete and hands-on approach of some aspects.
Graphics hardware
Information technology projects
Open hardware electronic devices
Open-source hardware
Graphics cards | Open Graphics Project | [
"Technology",
"Engineering"
] | 943 | [
"Information technology",
"Information technology projects"
] |
4,244,144 | https://en.wikipedia.org/wiki/Handel-C | Handel-C is a high-level hardware description language aimed at low-level hardware and is most commonly used in programming FPGAs. Handel-C is to hardware design what the first high-level programming languages were to programming CPUs. It is a turing-complete rich subset of the C programming language, with an emphasis on parallel computing.
Unlike many other hardware design languages (HDL) that target a specific computer architecture Handel-C can be compiled to a number of HDLs and then synthesised to the corresponding hardware. This frees developers to concentrate on the programming task at hand rather than the idiosyncrasies of a specific design language and architecture.
Additional features
Handel-C's subset of C includes all common C language features necessary to describe complex algorithms. Like many embedded C compilers, floating point data types were omitted. Floating point arithmetic is supported through external libraries that are very efficient.
Parallel programs
In order to facilitate a way to describe parallel behavior some of the communicating sequential processes (CSP) keywords are used, along with the general file structure of the Occam programming language.
For example:
par {
++c;
a = d + e;
b = d + e;
}
Channels
Channels provide a mechanism for message passing between parallel threads. Channels can be defined as asynchronous or synchronous (with or without an inferred storage element respectively). A thread writing to a synchronous channel will be immediately blocked until the corresponding listening thread is ready to receive the message. Likewise the receiving thread will block on a read statement until the sending thread executes the next send. Thus they may be used as a means of synchronizing threads.
par {
chan int a; // declare a synchronous channel
int x;
// begin sending thread
seq (i = 0; i < 10; i++) {
a ! i; // send the values 0 to 9 sequentially into the channel
}
// begin receiving thread
seq (j = 0; j < 10; j++) {
a ? x; // perform a sequence of 10 reads from the channel into variable x
delay; // introduce a delay of 1 clock cycle between successive reads
// this has the effect of blocking the sending thread between writes
}
}
Asynchronous channels provide a specified amount of storage for data passing through them in the form of a FIFO. Whilst this FIFO neither full nor empty, both sending and receiving threads may proceed without being blocked. However, when the FIFO is empty, the receiving thread will block at the next read. When it is full, the sending thread will block at the next send. A channel with actors in differing clock domains is automatically asynchronous due to the need for at least one element of storage to mitigate metastability.
A thread may simultaneously wait on multiple channels, synchronous or asynchronous, acting upon the first one available given a specified order of priority or optionally executing an alternate path if none is ready.
Scope and variable sharing
The scope of declarations are limited to the code blocks ({ ... }) in which they were declared, the scope is hierarchical in nature as declarations are in scope within sub blocks.
For example:
int a;
void main(void)
{
int b;
/* "a" and "b" are within scope */
{
int c;
/* "a", "b" and "c" are within scope */
}
{
int d;
/* "a", "b" and "d" are within scope */
}
}
Extensions to the C language
In addition to the effects the standard semantics of C have on the timing of the program, the following keywords are reserved for describing the practicalities of the FPGA environment or for the language elements sourced from Occam:
Scheduling
In Handel-C, assignment and the delay command take one cycle. All other operations are "free". This allows programmers to manually schedule tasks and create effective pipelines. By arranging loops in parallel with the correct delays, pipelines can massively increase data throughput, at the expense of increased hardware resource use.
History
The historical roots of Handel-C are in a series of Oxford University Computing Laboratory hardware description languages developed by the hardware compilation group. Handel HDL evolved into Handel-C around early 1996. The technology developed at Oxford was spun off to mature as a cornerstone product for Embedded Solutions Limited (ESL) in 1996. ESL was renamed Celoxica in September 2000.
Handel-C was adopted by many University Hardware Research groups after its release by ESL, as a result was able to establish itself as a hardware design tool of choice within the academic community, especially in the United Kingdom.
In early 2008, Celoxica's ESL business was acquired by Agility, which developed and sold, among other products, ESL tools supporting Handel-C.
In early 2009, Agility ceased operations after failing to obtain further capital investments or credit
In January 2009, Mentor Graphics acquired Agility's C synthesis assets.
Other subset C HDL's that developed around the same time are Transmogrifier C in 1994 at University of Toronto (now the FpgaC open source project) and Streams-C at Los Alamos National Laboratory (now licensed to Impulse Accelerated Technologies under the name Impulse C)
See also
High- and low-level
C to HDL
References
External links
Handel-C language resources at Mentor Graphics
Oxford Handel-C
C programming language family
Hardware description languages
Electronic design automation | Handel-C | [
"Engineering"
] | 1,151 | [
"Electronic engineering",
"Hardware description languages"
] |
4,244,168 | https://en.wikipedia.org/wiki/ODMRP | In wireless networking, On-Demand Multicast Routing Protocol is a protocol for routing multicast and unicast traffic throughout Ad hoc wireless mesh networks.
ODMRP creates routes on demand, rather than proactively creating routes as OLSR does. This suffers from a route acquisition delay, although it helps reduce network traffic in general. To help reduce the problem of this delay, some implementations send the first data packet along with the route discovery packet.
Because some links may be asymmetric, the path from one node to another is not necessarily the same as the reverse path of these nodes.
See also
AODV
List of ad hoc routing protocols
Mesh Networks
External links
IETF Draft The latest draft specification published by the IETF
Original publication The first paper presenting ODMRP.
Wireless networking
Routing
Routing algorithms
Ad hoc routing protocols | ODMRP | [
"Technology",
"Engineering"
] | 167 | [
"Computing stubs",
"Wireless networking",
"Computer networks engineering",
"Computer network stubs"
] |
4,244,250 | https://en.wikipedia.org/wiki/Joel%20Spencer | Joel Spencer (born April 20, 1946) is an American mathematician. He is a combinatorialist who has worked on probabilistic methods in combinatorics and on Ramsey theory. He received his doctorate from Harvard University in 1970, under the supervision of Andrew Gleason. He is currently () a professor at the Courant Institute of Mathematical Sciences of New York University. Spencer's work was heavily influenced by Paul Erdős, with whom he coauthored many papers (giving him an Erdős number of 1).
In 1963, while studying at the Massachusetts Institute of Technology, Spencer became a Putnam Fellow. In 1984, Spencer received a Lester R. Ford Award. He was an Erdős Lecturer at Hebrew University of Jerusalem in 2001. In 2012, he became a fellow of the American Mathematical Society.
He was elected as a fellow of the Society for Industrial and Applied Mathematics in 2017, "for contributions to discrete mathematics and theory of computing, particularly random graphs and networks, Ramsey theory, logic, and randomized algorithms". In 2021, he received the Leroy P. Steele Prize for Mathematical Exposition with his coauthor Noga Alon for their book The Probabilistic Method.
Selected publications
Probabilistic methods in combinatorics, with Paul Erdős, New York: Academic Press, 1974.
Ramsey theory, with Bruce L. Rothschild and Ronald L. Graham, New York: Wiley, 1980; 2nd ed., 1990.
Ten lectures on the probabilistic method, Philadelphia: Society for Industrial and Applied Mathematics, 1987; 2nd ed., 1994.
The strange logic of random graphs, Berlin: Springer-Verlag, 2001.
The probabilistic method, with Noga Alon, New York: Wiley, 1992; 2nd ed., 2000; 3rd ed., 2008.
Deterministic random walks on regular trees, American Mathematical Society, New York, 2008.
Asymptopia, with Laura Florescu, American Mathematical Society, 2014.
See also
Packing in a hypergraph
References
External links
Joel Spencer's Website
1946 births
20th-century American mathematicians
21st-century American mathematicians
Living people
Harvard University alumni
Courant Institute of Mathematical Sciences faculty
Graph theorists
Putnam Fellows
Fellows of the American Mathematical Society
Fellows of the Society for Industrial and Applied Mathematics | Joel Spencer | [
"Mathematics"
] | 467 | [
"Mathematical relations",
"Graph theory",
"Graph theorists"
] |
4,244,391 | https://en.wikipedia.org/wiki/Playout | In broadcasting, channel playout is the generation of the source signal of a radio or television channel produced by a broadcaster, coupled with the transmission of this signal for primary distribution or direct-to-audience distribution via any network. Such radio or television distribution networks include terrestrial broadcasting (analogue or digital radio), cable networks, satellites (either for primary distribution intended for cable television headends or for direct reception, DTH / DBS), Internet Protocol television, OTT Video, point-to-point transport over managed networks or the public Internet, etc.
The television channel playout happens in master control room (MCR) in a playout area, which can be either situated in the central apparatus room or in purposely built playout centres, which can be owned by a broadcaster or run by an independent specialist company that has been contracted to handle the playout for a number of channels from different broadcasters.
Some of the larger playout centres in Europe, Southeast Asia and the United States handle well in excess of 50 radio and television "feeds". Feeds will often consist of several different versions of a core service, often different language versions or with separately scheduled content, such as local opt outs for news or promotions.
Playout systems
Centralcasting is multi-channel playout that generally uses broadcast automation systems with broadcast programming applications. These systems generally work in a similar way, controlling video servers, video tape recorder (VTR) devices, Flexicarts, audio mixing consoles, vision mixers and video routers, and other devices using a serial communications 9-Pin Protocol (RS-232 or RS-422). This provides deterministic control, enabling frame accurate playback, Instant replay or video switching. Many systems consist of a front end operator interface on a separate platform to the controllers – e.g. a Windows GUI will present a friendly easy to use method of editing a playlist, but actual control would be done on a platform with a real-time operating system such that any large-scale playlist amendments do not cause delays to device control.
Most broadcast automation systems will have a series of common device drivers built in, for example Sony VTR control (aka Sony Serial), Louth Video Disk Control Protocol (VDCP, a proprietary communications protocol), General Purpose Interface (GPI), PlayBox Technology Channel in a Box, or Grass Valley Group M21 Master Control. This ensures that a broadcast automation system bought "off the shelf" will at least be able to ingest and playout content, although may not be able to take advantage of more efficient methods of control. Most server, and especially most digital on-screen graphic and character generator (CG) manufacturers will have a specific device driver for their device, with increasing degrees of complexity, and different automation companies will include these drivers to enhance their product or to fit a customer's need.
This is the "traditional" method of playout automation, where there are multiple devices. Some modern automation systems use a unified playout method, where the broadcast server fulfills the functions of multiple devices as a self-contained system, like the PlayBox Technology channel-in-a-box.
Playout devices
Playout will usually involve an airchain of devices which begin with content, typically stored on video servers, and ultimately an output, either as an asynchronous serial interface (ASI), IP or serial digital interface (SDI) for on pass to a distribution company.
The devices in the chain depend on the service required under the contract with the Channel. Typically a standard television channel would require a Master Control, Video switcher, and/or a Video router to allow switching of live sources. This video switcher may include other functions such as keying (graphics) (also known as Down Stream Keyers), Audio Overs for mixing in voice overs (VO) or announcements, and facilitate transitions between events, such as a fade through black or crossfade (also known as mix).
Other devices include:
Graphics inserters – At least one Graphics inserter, or one with several layers. This allows for Station identification/Logo/Digital on-screen graphic (Dog or Bug) insertion, and can also be used for end credits sequences, coming next graphics or programme information straps
Subtitling inserters – This can be either closed or open – i.e. in vision as a graphic for all to see, or closed either as an MPEG stream item, Closed Captioning or World System Teletext.
Audio servers – An audio playout system would provide scheduled voiceovers
Aspect Ratio Converters – These alter the picture shape or send an embedded signal to allow the material format to be displayed correctly on a particular feed (e.g. Widescreen on a standard non-widescreen Analogue terrestrial feed)
Some of these more advanced devices require information from the playlist, and so do not tend to use an RS422/232 driver, but a complex XML based system which allows for more complex metadata to be passed, e.g. a "Now" or "Next" Graphic can be created from a template using text information from the playlist.
Channel-in-a-box concept
With the "softwarization" of the various functions required to generate the channel signal in a playout system, the possibility to gather all of them into a single piece of equipment became possible. Such all-in-one video playout servers are known as channel-in-a-box systems.
Playout Centers
Playout is one of the basic infrastructure of a playout center. Mostly called as channel in a box server, but basically composed of playout servers with integrated graphics and IP or ASI output. Aim of playout centers is mostly to serve customers a simple file based television facility. Up-link and TV Channel in a box servers simply provide the facility.
Scheduling
The playout system execute a scheduled and time-accurate playlist of content to generate a linear radio or television signal (or "feed"). Within that playlist, there is the content that goes "on-air": live or recorded shows/programs, ad breaks, auto-promo clips, etc.
Workflow
A common workflow is for the broadcast automation system to have a recording schedule to ingest material from a satellite or line feed source and then time-shift that material based on a playlist or schedule.
The playout schedule will have been created in the customer's broadcast programming scheduling system and exported into a format suitable to be used in the Playout system. There is a move to SMPTE-22, known as Broadcast Exchange Format (BXF) to try to standardise the messaging involved in this interaction.
The resulting playlist is "loaded" into the appropriate channel of the broadcast automation system in advance of the transmission time. Various processes will take place to ensure the content is available on the correct servers for playout at the right time, typically this involves advance requests to move material from deep storage such as Tape Archives or FTP Clusters to Broadcast Video servers, often using FTP.
On playing out the material, the audio and video signals are usually transported from the playout area to the network via a studio/transmitter link (STL), which may be fibre backlink, microwave or satellite uplink.
Playout is often referred to as Presentation or Transmission (TX), and is under control of an automatic transmission system.
See also
Broadcast
References
Broadcast engineering
Television terminology
it:Emissione | Playout | [
"Engineering"
] | 1,525 | [
"Broadcast engineering",
"Electronic engineering"
] |
4,244,871 | https://en.wikipedia.org/wiki/Andrew%20M.%20Gleason | Andrew Mattei Gleason (19212008) was an American mathematician who made fundamental contributions to widely varied areas of mathematics, including the solution of Hilbert's fifth problem, and was a leader in reform and innovation in teaching at all levels.<ref
name="mactutor"></ref> Gleason's theorem in quantum logic and the Greenwood–Gleason graph, an important example in Ramsey theory, are named for him.
As a young World War II naval officer, Gleason broke German and Japanese military codes. After the war he spent his entire academic career at Harvard University, from which he retired in 1992. His numerous academic and scholarly leadership posts included chairmanship of the Harvard Mathematics Department and the Harvard Society of Fellows, and presidency of the American Mathematical Society. He continued to advise the United States government on cryptographic security, and the Commonwealth of Massachusetts on education for children, almost until the end of his life.
Gleason won the Newcomb Cleveland Prize in 1952 and the Gung–Hu Distinguished Service Award of the American Mathematical Society in 1996. He was a member of the National Academy of Sciences and of the American Philosophical Society, and held the Hollis Chair of Mathematics and Natural Philosophy at Harvard.
He was fond of saying that proofs "really aren't there to convince you that something is truethey're there to show you why it is true." The Notices of the American Mathematical Society called him "one of the quiet giants of twentieth-century mathematics, the consummate professor dedicated to scholarship, teaching, and service in equal measure."
Biography
Gleason was born on November 4, 1921, in Fresno, California, the youngest of three children;
his father Henry Gleason was a botanist and a member of the Mayflower Society, and his mother was the daughter of Swiss-American winemaker Andrew Mattei.
His older brother Henry Jr. became a linguist.
He grew up in Bronxville, New York, where his father was the curator of the New York Botanical Garden.<ref
name="mmp">
.
</ref>
After briefly attending Berkeley High School (Berkeley, California)
he graduated from Roosevelt High School in Yonkers, winning a scholarship to Yale University.
Though Gleason's mathematics education had gone only so far as some self-taught calculus, Yale mathematician William Raymond Longley urged him to try a course in mechanics normally intended for juniors.
One month later he enrolled in a differential equations course ("mostly full of seniors") as well. When Einar Hille temporarily replaced the regular instructor, Gleason found Hille's style "unbelievably different ... He had a view of mathematics that was just vastly different ... That was a very important experience for me. So after that I took a lot of courses from Hille" including, in his sophomore year, graduate-level real analysis. "Starting with that course with Hille, I began to have some sense of what mathematics is about."
While at Yale he competed three times (1940, 1941 and 1942) in the recently founded William Lowell Putnam Mathematical Competition, always placing among the top five entrants in the country (making him the second three-time Putnam Fellow).
After the Japanese attacked Pearl Harbor during his senior year, Gleason applied for a commission in the US Navy,<ref
name="secret-life">.
</ref>
and on graduation
joined the team working to break Japanese naval codes.
(Others on this team included his future collaborator Robert E. Greenwood and Yale professor Marshall Hall Jr.)
He also collaborated with British researchers attacking the German Enigma cipher;
Alan Turing, who spent substantial time with Gleason while visiting Washington, called him "the brilliant young Yale graduate mathematician" in a report of his visit.
In 1946, at the recommendation of Navy colleague Donald Howard Menzel, Gleason was appointed a Junior Fellow at Harvard.
An early goal of the Junior Fellows program was to allow young scholars showing extraordinary promise to sidestep the lengthy PhD process; four years later Harvard appointed Gleason an assistant professor of mathematics,
though he was almost immediately recalled to Washington for cryptographic work related to the Korean War.
He returned to Harvard in the fall of 1952, and soon after published the most important of his results on Hilbert's fifth problem (see below).
Harvard awarded him tenure the following year.
In January 1959 he married Jean Berko
whom he had met at a party featuring the music of Tom Lehrer.<ref
name="lww">.
</ref>
Berko, a psycholinguist, worked for many years at Boston University.
They had three daughters.
In 1969 Gleason took the Hollis Chair of Mathematics and Natural Philosophy. Established in 1727, this is the oldest scientific endowed professorship in the US.
He retired from Harvard in 1992 but remained active in service to Harvard (as chair of the Society of Fellows, for example)
and to mathematics: in particular, promoting the Harvard Calculus Reform Project and working with the Massachusetts Board of Education.
He died on October 17, 2008 from complications following surgery.
Teaching and education reform
Gleason said he "always enjoyed helping other people with math"a colleague said he "regarded teaching mathematicslike doing mathematicsas both important and also genuinely fun."
At fourteen, during his brief attendance at Berkeley High School, he found himself not only bored with first-semester geometry, but also helping other students with their homeworkincluding those taking the second half of the course, which he soon began auditing.<ref
name="amsx">.
</ref>
At Harvard he "regularly taught at every level", including administratively burdensome multisection courses.
One class presented Gleason with a framed print of Picasso's Mother and Child in recognition of his care for them.
In 1964 he created "the first of the 'bridge' courses now ubiquitous for math majors, only twenty years before its time." Such a course is designed to teach new students, accustomed to rote learning of mathematics in secondary school, how to reason abstractly and construct mathematical proofs. That effort led to publication of his Fundamentals of Abstract Analysis, of which one reviewer wrote:
But Gleason's "talent for exposition" did not always imply that the reader would be enlightened without effort of his own. Even in a wartime memo on the urgently important decryption of the German Enigma cipher, Gleason and his colleagues wrote:
His notes and exercises on probability and statistics, drawn up for his lectures to code-breaking colleagues during the war (see below) remained in use in National Security Agency training for several decades; they were published openly in 1985.
In a 1964 Science article, Gleason wrote of an apparent paradox arising in attempts to explain mathematics to nonmathematicians:
Gleason was the first chairman of the advisory committee of the School Mathematics Study Group, which helped define the New Math of the 1960sambitious changes in American elementary and high school mathematics teaching emphasizing understanding of concepts over rote algorithms. Gleason was "always interested in how people learn"; as part of the New Math effort he spent most mornings over several months with second-graders. Some years later he gave a talk in which he described his goal as having been:
In 1986 he helped found the Calculus Consortium, which has published a successful and influential series of "calculus reform" textbooks for college and high school, on precalculus, calculus, and other areas. His "credo for this program as for all of his teaching was that the ideas should be based in equal parts of geometry for visualization of the concepts, computation for grounding in the real world, and algebraic manipulation for power." However, the program faced heavy criticism from the mathematics community for its omission of topics such as the mean value theorem, and for its perceived lack of mathematical rigor.
Cryptanalysis work
During World War II Gleason was part of OP-20-G, the U.S. Navy's signals intelligence and cryptanalysis group.
One task of this group, in collaboration with British cryptographers at Bletchley Park such as Alan Turing, was to penetrate German Enigma machine communications networks. The British had great success with two of these networks, but the third, used for German-Japanese naval coordination, remained unbroken because of a faulty assumption that it employed a simplified version of Enigma. After OP-20-G's Marshall Hall observed that certain metadata in Berlin-to-Tokyo transmissions used letter sets disjoint from those used in Tokyo-to-Berlin metadata, Gleason hypothesized that the corresponding unencrypted letters sets were A-M (in one direction) and N-Z (in the other), then devised novel statistical tests by which he confirmed this hypothesis. The result was routine decryption of this third network by 1944. (This work also involved deeper related to permutation groups and the graph isomorphism problem.)
OP-20-G then turned to the Japanese navy's "Coral" cipher. A key tool for the attack on Coral was the "Gleason crutch", a form of Chernoff bound on tail distributions of sums of independent random variables. Gleason's classified work on this bound predated Chernoff's work by a decade.
Toward the end of the war he concentrated on documenting the work of OP-20-G and developing systems for training new cryptographers.
In 1950 Gleason returned to active duty for the Korean War, serving as a Lieutenant Commander in the Nebraska Avenue Complex (which much later became the home of the DHS Cyber Security Division). His cryptographic work from this period remains classified, but it is known that he recruited mathematicians and taught them cryptanalysis.
He served on the advisory boards for the National Security Agency and the Institute for Defense Analyses, and he continued to recruit, and to advise the military on cryptanalysis, almost to the end of his life.
Mathematics research
Gleason made fundamental contributions to widely varied areas of mathematics, including the theory of Lie groups, quantum mechanics,<ref
name="ag-qm">.
</ref>
and combinatorics.
According to Freeman Dyson's famous classification of mathematicians as being either birds or frogs,
Gleason was a frog: he worked as a problem solver rather than a visionary formulating grand theories.<ref
name=50years>.</ref>
Hilbert's fifth problem
In 1900 David Hilbert posed 23 problems he felt would be central to next century of mathematics research. Hilbert's fifth problem concerns the characterization of Lie groups by their actions on topological spaces: to what extent does their topology provide information sufficient to determine their geometry?
The "restricted" version of Hilbert's fifth problem (solved by Gleason) asks, more specifically, whether every locally Euclidean topological group is a Lie group. That is, if a group G has the structure of a topological manifold, can that structure be strengthened to a real analytic structure, so that within any neighborhood of an element of G, the group law is defined by a convergent power series, and so that overlapping neighborhoods have compatible power series definitions? Prior to Gleason's work, special cases of the problem had been solved by L. E. J. Brouwer, John von Neumann, Lev Pontryagin, and Garrett Birkhoff, among others.<ref
name="illman">.
</ref>
Gleason's interest in the fifth problem began in the late 1940s, sparked by a course he took from George Mackey.
In 1949 he published a paper introducing the "no small subgroups" property of Lie groups (the existence of a neighborhood of the identity within which no nontrivial subgroup exists) that would eventually be crucial to its solution.
His 1952 paper on the subject, together with a paper published concurrently by Deane Montgomery and Leo Zippin, solves affirmatively the restricted version of Hilbert's fifth problem, showing that indeed every locally Euclidean group is a Lie group. Gleason's contribution was to prove that this is true when G has the no small subgroups property; Montgomery and Zippin showed every locally Euclidean group has this property. As Gleason told the story, the key insight of his proof was to apply the fact that monotonic functions are differentiable almost everywhere. On finding the solution, he took a week of leave to write it up, and it was printed in the Annals of Mathematics alongside the paper of Montgomery and Zippin; another paper a year later by Hidehiko Yamabe removed some technical side conditions from Gleason's proof.
The "unrestricted" version of Hilbert's fifth problem, closer to Hilbert's original formulation, considers both a locally Euclidean group G and another manifold M on which G has a continuous action. Hilbert asked whether, in this case, M and the action of G could be given a real analytic structure. It was quickly realized that the answer was negative, after which attention centered on the restricted problem. However, with some additional smoothness assumptions on G and M, it might yet be possible to prove the existence of a real analytic structure on the group action. The Hilbert–Smith conjecture, still unsolved, encapsulates the remaining difficulties of this case.
Quantum mechanics
The Born rule states that an observable property of a quantum system is defined by a Hermitian operator on a separable Hilbert space, that the only observable values of the property are the eigenvalues of the operator, and that the probability of the system being observed in a particular eigenvalue is the square of the absolute value of the complex number obtained by projecting the state vector (a point in the Hilbert space) onto the corresponding eigenvector.
George Mackey had asked whether Born's rule is a necessary consequence of a particular set of axioms for quantum mechanics, and more specifically whether every measure on the lattice of projections of a Hilbert space can be defined by a positive operator with unit trace. Though Richard Kadison proved this was false for two-dimensional Hilbert spaces, Gleason's theorem (published 1957) shows it to be true for higher dimensions.
Gleason's theorem implies the nonexistence of certain types of hidden variable theories for quantum mechanics, strengthening a previous argument of John von Neumann. Von Neumann had claimed to show that hidden variable theories were impossible, but (as Grete Hermann pointed out) his demonstration made an assumption that quantum systems obeyed a form of additivity of expectation for noncommuting operators that might not hold a priori. In 1966, John Stewart Bell showed that Gleason's theorem could be used to remove this extra assumption from von Neumann's argument.
Ramsey theory
The Ramsey number R(k,l) is the smallest number r such that every graph with at least r vertices contains either a k-vertex clique or an l-vertex independent set. Ramsey numbers require enormous effort to compute; when max(k,l) ≥ 3 only finitely many of them are known precisely, and an exact computation of R(6,6) is believed to be out of reach. In 1953, the calculation of R(3,3) was given as a question in the Putnam Competition. In 1955, motivated by this problem, Gleason and his co-author Robert E. Greenwood made significant progress in the computation of Ramsey numbers with their proof that R(3,4) = 9, R(3,5) = 14, and R(4,4) = 18. Since then, only five more of these values have been found. In the same 1955 paper, Greenwood and Gleason also computed the multicolor Ramsey number R(3,3,3): the smallest number r such that, if a complete graph on r vertices has its edges colored with three colors, then it necessarily contains a monochromatic triangle. As they showed, R(3,3,3) = 17; this remains the only nontrivial multicolor Ramsey number whose exact value is known. As part of their proof, they used an algebraic construction to show that a 16-vertex complete graph can be decomposed into three disjoint copies of a triangle-free 5-regular graph with 16 vertices and 40 edges<ref
name="spencer-dm">.
</ref>
(sometimes called the Greenwood–Gleason graph).
Ronald Graham writes that the paper by Greenwood and Gleason "is now recognized as a classic in the development of Ramsey theory". In the late 1960s, Gleason became the doctoral advisor of Joel Spencer, who also became known for his contributions to Ramsey theory.<ref
name="mathgenealogy">
</ref>
Coding theory
Gleason published few contributions to coding theory, but they were influential ones, and included "many of the seminal ideas and early results" in algebraic coding theory. During the 1950s and 1960s, he attended monthly meetings on coding theory with Vera Pless and others at the Air Force Cambridge Research Laboratory. Pless, who had previously worked in abstract algebra but became one of the world's leading experts in coding theory during this time, writes that "these monthly meetings were what I
lived for." She frequently posed her mathematical problems to Gleason and was often rewarded with a quick and insightful response.
The Gleason–Prange theorem is named after Gleason's work with AFCRL researcher Eugene Prange; it was originally published in a 1964 AFCRL research report by H. F. Mattson Jr. and E. F. Assmus Jr.
It concerns the quadratic residue code of order n, extended by adding a single parity check bit. This "remarkable theorem" shows that this code is highly symmetric, having the projective linear group PSL2(n) as a subgroup of its symmetries.
Gleason is the namesake of the Gleason polynomials, a system of polynomials that generate the weight enumerators of linear codes. These polynomials take a particularly simple form for self-dual codes: in this case there are just two of them, the two bivariate polynomials x2 + y2 and x8 + 14x2y2 + y8. Gleason's student Jessie MacWilliams continued Gleason's work in this area, proving a relationship between the weight enumerators of codes and their duals that has become known as the MacWilliams identity.
In this area, he also did pioneering work in experimental mathematics, performing computer experiments in 1960. This work studied the average distance to a codeword, for a code related to the Berlekamp switching game.
Other areas
Gleason founded the theory of Dirichlet algebras,
and made other contributions including work on
finite geometry and on
the enumerative combinatorics of permutations.
(In 1959 he wrote that his research "sidelines" included "an intense interest in combinatorial problems.")
As well, he was not above publishing research in more elementary mathematics, such as the derivation of the set of polygons that can be constructed with compass, straightedge, and an angle trisector.
Awards and honors
In 1952 Gleason was awarded the American Association for the Advancement of Science's Newcomb Cleveland Prize
for his work on Hilbert's fifth problem.
He was elected to the National Academy of Sciences and the American Philosophical Society, was a Fellow of the American Academy of Arts and Sciences,
and belonged to the Société Mathématique de France.
In 1981 and 1982 he was president of the American Mathematical Society,
and at various times held numerous other posts in professional and scholarly organizations,
including chairmanship of the Harvard Department of Mathematics.
In 1986 he chaired the organizing committee for the International Congress of Mathematicians in Berkeley, California, and was president of the Congress.
In 1996 the Harvard Society of Fellows held a special symposium honoring Gleason on his retirement after seven years as its chairman;
that same year, the Mathematics Association of America awarded him the Yueh-Gin Gung and Dr. Charles Y. Hu Distinguished Service to Mathematics Award.
A past president of the Association wrote:
After his death a 32-page collection of essays in the Notices of the American Mathematical Society recalled "the life and work of [this] eminent American mathematician",
calling him "one of the quiet giants of twentieth-century mathematics, the consummate professor dedicated to scholarship, teaching, and service in equal measure."
Selected publications
Research papers
.
.
.
.
.
.
Books
. Corrected reprint, Boston: Jones and Bartlett, 1991, .
.
. Unclassified reprint of a book originally published in 1957 by the National Security Agency, Office of Research and Development, Mathematical Research Division.
. Since its original publications this book has been extended to many different editions and variations with additional co-authors.
Film
. 63 minutes, black & white. Produced by Richard G. Long and directed by Allan Hinderstein.
See also
Bell's critique of von Neumann's proof
Pierpont prime, a class of prime numbers conjectured by Gleason to be infinite
Notes
References
External links
1921 births
2008 deaths
20th-century American mathematicians
21st-century American mathematicians
American cryptographers
American mathematical analysts
Coding theorists
Graph theorists
American quantum physicists
Harvard University Department of Mathematics faculty
Putnam Fellows
Yale University alumni
Presidents of the American Mathematical Society
Hollis Chair of Mathematics and Natural Philosophy
Fellows of the American Academy of Arts and Sciences
Members of the United States National Academy of Sciences
People from Fresno, California
American topologists
Mathematicians from California
United States Navy personnel of World War II | Andrew M. Gleason | [
"Mathematics"
] | 4,466 | [
"Mathematical relations",
"Graph theory",
"Graph theorists"
] |
4,245,290 | https://en.wikipedia.org/wiki/Danubit | Danubit was an industrial plastic explosive produced by the Slovak company .
It had been used for many decades intended primarily as a rock blasting explosive for surface and underground mass mining of mineral raw materials. Underwater blasting applications were possible as well.
The producer of Danubit, Istrochem, is a chemical company founded in 1847 by Alfred Nobel in Bratislava, Slovakia. The production of explosives ceased, when part of the company was acquired by the Czech company Explosia a.s., the producer of Semtex in 2009.
Characteristics
See also
Dynamite
External links
Istrochem (producer)
Explosives | Danubit | [
"Chemistry"
] | 125 | [
"Explosives",
"Explosions"
] |
4,245,349 | https://en.wikipedia.org/wiki/Overpotential | In electrochemistry, overpotential is the potential difference (voltage) between a half-reaction's thermodynamically determined reduction potential and the potential at which the redox event is experimentally observed. The term is directly related to a cell's voltage efficiency. In an electrolytic cell the existence of overpotential implies that the cell requires more energy than thermodynamically expected to drive a reaction. In a galvanic cell the existence of overpotential means less energy is recovered than thermodynamics predicts. In each case the extra/missing energy is lost as heat. The quantity of overpotential is specific to each cell design and varies across cells and operational conditions, even for the same reaction. Overpotential is experimentally determined by measuring the potential at which a given current density (typically small) is achieved.
Thermodynamics
The four possible polarities of overpotentials are listed below.
An electrolytic cell's anode is more positive, using more energy than thermodynamics require.
An electrolytic cell's cathode is more negative, using more energy than thermodynamics require.
A galvanic cell's anode is less negative, supplying less energy than thermodynamically possible.
A galvanic cell's cathode is less positive, supplying less energy than thermodynamically possible.
The overpotential increases with growing current density (or rate), as described by the Tafel equation. An electrochemical reaction is a combination of two half-cells and multiple elementary steps. Each step is associated with multiple forms of overpotential. The overall overpotential is the summation of many individual losses.
Voltage efficiency describes the fraction of energy lost through overpotential. For an electrolytic cell this is the ratio of a cell's thermodynamic potential divided by the cell's experimental potential converted to a percentile. For a galvanic cell it is the ratio of a cell's experimental potential divided by the cell's thermodynamic potential converted to a percentile. Voltage efficiency should not be confused with Faraday efficiency. Both terms refer to a mode through which electrochemical systems can lose energy. Energy can be expressed as the product of potential, current and time (joule = volt × Ampere × second). Losses in the potential term through overpotentials are described by voltage efficiency. Losses in the current term through misdirected electrons are described by Faraday efficiency.
Varieties
Overpotential can be divided into many different subcategories that are not all well defined. For example, "polarization overpotential" can refer to the electrode polarization and the hysteresis found in forward and reverse peaks of cyclic voltammetry. A likely reason for the lack of strict definitions is that it is difficult to determine how much of a measured overpotential is derived from a specific source. Overpotentials can be grouped into three categories: activation, concentration, and resistance.
Activation overpotential
The activation overpotential is the potential difference above the equilibrium value required to produce a current that depends on the activation energy of the redox event. While ambiguous, "activation overpotential" often refers exclusively to the activation energy necessary to transfer an electron from an electrode to an anolyte. This sort of overpotential can also be called "electron transfer overpotential" and is a component of "polarization overpotential", a phenomenon observed in cyclic voltammetry and partially described by the Cottrell equation.
Reaction overpotential
Reaction overpotential is an activation overpotential that specifically relates to chemical reactions that precede electron transfer. Reaction overpotential can be reduced or eliminated with the use of electrocatalysts. The electrochemical reaction rate and related current density is dictated by the kinetics of the electrocatalyst and substrate concentration.
The platinum electrode common to much of electrochemistry is electrocatalytically involved in many reactions. For example, hydrogen is oxidized and protons are reduced readily at the platinum surface of a standard hydrogen electrode in aqueous solution, in a Hydrogen Evolution Reaction. Substituting an electrocatalytically inert glassy carbon electrode for the platinum electrode produces irreversible reduction and oxidation peaks with large overpotentials.
Concentration overpotential
Concentration overpotential spans a variety of phenomena that involve the depletion of charge-carriers at the electrode surface. Bubble overpotential is a specific form of concentration overpotential in which the concentration of charge-carriers is depleted by the formation of a physical bubble. The "diffusion overpotential" can refer to a concentration overpotential created by slow diffusion rates as well as "polarization overpotential", whose overpotential is derived mostly from activation overpotential but whose peak current is limited by diffusion of analyte.
The potential difference is caused by differences in the concentration of charge-carriers between bulk solution and the electrode surface. It occurs when electrochemical reaction is sufficiently rapid to lower the surface concentration of the charge-carriers below that of bulk solution. The rate of reaction is then dependent on the ability of the charge-carriers to reach the electrode surface.
Bubble overpotential
Bubble overpotential is a specific form of concentration overpotential and is due to the evolution of gas at either the anode or cathode. This reduces the effective area for current and increases the local current density. An example is the electrolysis of an aqueous sodium chloride solution—although oxygen should be produced at the anode based on its potential, bubble overpotential causes chlorine to be produced instead, which allows the easy industrial production of chlorine and sodium hydroxide by electrolysis.
Resistance overpotential
Resistance overpotentials are those tied to a cell design. These include "junction overpotentials" that occur at electrode surfaces and interfaces like electrolyte membranes. They can also include aspects of electrolyte diffusion, surface polarization (capacitance) and other sources of counter electromotive forces.
See also
Electrolysis
Electrosynthesis
References
Electrochemical concepts
Electrochemical potentials | Overpotential | [
"Chemistry"
] | 1,285 | [
"Electrochemistry",
"Electrochemical concepts",
"Electrochemical potentials"
] |
4,245,815 | https://en.wikipedia.org/wiki/Mosaic%20gold | Mosaic gold or bronze powder refers to tin(IV) sulfide as used as a pigment in bronzing and gilding wood and metal work. It is obtained as a yellow scaly crystalline powder. The alchemists referred to it as aurum musivum, or aurum mosaicum. The term mosaic gold has also been used to refer to ormolu and to cut shapes of gold leaf, some darkened for contrast, arranged as a mosaic. The term bronze powder may also refer to powdered bronze alloy.
A recipe for mosaic gold is already provided in the 3th century A.D. treatise Baopuzi, composed by the Chinese alchemist Ge Hong. The earliest sources for its preparation in Europe, under the name porporina or purpurina, are the late 13th-century North Italian Liber colorum secundum Magistrum Bernardum and Cennino Cennini's Libro dell'arte from the 1420s. Instructions became more widespread and varied thereafter, the around 1500 recipe collection Liber illuministarum from Tegernsee Abbey in Bavaria alone offering six different methods for its preparation. Alchemists prepared it by combining mercury, tin, sal ammoniac, and sublimated sulfur (fleur de soufre), grinding, mixing, then setting them for three hours in a sand heat. The dirty sublimate being taken off, aurum mosaicum was found at the bottom of the matrass.
In the past it was used for medical purposes in most chronic and nervous ailments, and particularly convulsions of children; however, it is no longer recommended for any medical uses.
See also
List of inorganic pigments
References
Inorganic pigments
Visual arts materials
Alchemical substances
Tin(IV) compounds
Powders
Sulfides | Mosaic gold | [
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4,245,884 | https://en.wikipedia.org/wiki/List%20of%20spreadsheet%20software | The following is a list of spreadsheets.
Free and open-source software
Cloud and on-line spreadsheets
Collabora Online Calc — Enterprise-ready LibreOffice.
EtherCalc (successor to SocialCalc, which is based on wikiCalc)
LibreOffice Online Calc
ONLYOFFICE - Community Server Edition
Sheetster – "Community Edition" is available under the AGPL
Simple Spreadsheet
Tiki Wiki CMS Groupware includes a spreadsheet since 2004 and migrated to jQuery.sheet in 2010.
Spreadsheets that are parts of suites
Apache OpenOffice Calc — for MS Windows, Linux and the Apple Macintosh. Started as StarOffice, later as OpenOffice.org. It has not received a major update since 2014 and security fixes have not been prompt.
Collabora Online Calc — Enterprise-ready LibreOffice, included with Online, Mobile and Desktop apps
Gnumeric — for Linux. Started as the GNOME desktop spreadsheet. Reasonably lightweight but has very advanced features.
KSpread — following the fork of the Calligra Suite from KOffice in mid-2010, superseded by KCells in KOffice and Sheets in the Calligra Suite.
LibreOffice Calc — developed for MS Windows, Linux, BSD and Apple Macintosh (Mac) operating systems by The Document Foundation. The Document Foundation was formed in mid-2010 by several large organisations such as Google, Red Hat, Canonical (Ubuntu) and Novell along with the OpenOffice.org community (developed by Sun) and various OpenOffice.org forks, notably Go-oo. Go-oo had been the "OpenOffice" used in Ubuntu and elsewhere. Started as StarOffice in the late 1990s, it became OpenOffice under Sun and then LibreOffice in mid-2010. The Document Foundation works with external organisations such as the Apache Foundation to help drive all three products forward.
Siag — for Linux, OpenBSD and Apple Mac OS X. A simple old spreadsheet, part of Siag Office.
Sheets — for MS Windows, Linux, FreeBSD, Apple Mac OS X and Haiku. Part of the extensive Calligra Suite. Possibly still mainly for Linux, but ports have been developed for other operating systems.
Standalone spreadsheets
sc
GNU Oleo
Pyspread
Proprietary software
Online spreadsheets
Airtable – a spreadsheet-database hybrid, with the features of a database but applied to a spreadsheet.
Coda
EditGrid – access, collaborate and share spreadsheets online, with API support; discontinued since 2014
Google Sheets – as part of Google Workspace
iRows – closed since 31 December 2006
JotSpot Tracker – acquired by Google Inc.
Smartsheet – Online spreadsheet for project management, interactive Gantt, file sharing, integrated with Google Apps
Sourcetable – AI spreadsheet that generates formulas, charts, SQL, and analyzes data.
ThinkFree Online Calc – as part of the ThinkFree Office online office suite, using Java
Quadratic - A source available online spreadsheet for technical users, supporting Python, SQL, and Formulas.
Zoho Sheet Spreadsheet on the cloud that allows real-time collaboration and more, for free
Spreadsheets that are parts of suites
Ability Office Spreadsheet – for MS Windows.
Apple iWork Numbers, included with Apple's iWork '08 suite exclusively for Mac OS X v10.4 or higher.
AppleWorks – for MS Windows and Macintosh. This is a further development of the historical Claris Works Office suite.
WordPerfect Office Quattro Pro – for MS Windows. Was one of the big three spreadsheets (the others being Lotus 123 and Excel).
EasyOffice EasySpreadsheet – for MS Windows. No longer freeware, this suite aims to be more user friendly than competitors.
Framework – for MS Windows. Historical office suite still available and supported. It includes a spreadsheet.
Google Sheets – as part of Google Workspace suite, supporting both offline and online editing.
IBM Lotus Symphony – freeware for MS Windows, Apple Mac OS X and Linux.
Kingsoft Office Spreadsheets 2012 – For MS Windows. Both free and paid versions are available. It can handle Microsoft Excel .xls and .xlsx files, and also produce other file formats such as .et, .txt, .csv, .pdf, and .dbf. It supports multiple tabs, VBA macro and PDF converting.
Lotus SmartSuite Lotus 123 – for MS Windows. In its MS-DOS (character cell) version, widely considered to be responsible for the explosion of popularity of spreadsheets during the 80s and early 90s.
Microsoft Office Excel – for MS Windows and Apple Macintosh. The proprietary spreadsheet leader.
Microsoft Works Spreadsheet – for MS Windows (previously MS-DOS and Apple Macintosh). Only allows one sheet at a time.
PlanMaker – for MS Windows, Linux, MS Windows Mobile and CE; part of SoftMaker Office
Quattro Pro – Originally introduced as a stand-alone DOS and Microsoft Windows application, it eventually became part of WordPerfect Office in 1994.
StarOffice Calc – Cross-platform. StarOffice was originally developed by the German company Star Division which was purchased by Sun in 1998. The code was made open source and became OpenOffice.org. Sun continues developing the commercial version which periodically integrates the open source code with their own and third party code to make new low price versions.
WPS Office
Stand alone spreadsheets
As-Easy-As – from Trius, Inc.; unsupported; last MS-DOS and Windows versions available with free full license key.
Multi-dimensional spreadsheets
Javelin
Lotus Improv
Quantrix Financial Modeler
Spreadsheets on different paradigms
DADiSP – Combines the numerical capability of MATLAB with a spreadsheet like interface.
Javelin
Lotus Improv
Resolver One – a business application development tool that represents spreadsheets as IronPython programs, created and executed in real time and allowing the spreadsheet flow to be fully programmed
Spreadsheet 2000
Spreadsheet-related developmental software
ExtenXLS – Java Spreadsheet Toolkit.
Historical
In chronologial order, year launched, product, launched for which machine/OS.
1979, VisiCalc for Apple II with 32K RAM, the first widely used normal spreadsheet with A1 notation etc.
1980, SuperCalc for CP/M-80 operating system, included with early Osborne computers.
1982, ZX81 Memocalc, for low cost ~$100 personal computer with 16K RAM expansion, launched by Memotech in April 1982.
1982, Multiplan for CP/M operating system, later becoming Microsoft Excel, launched Aug 1982.
1983, Lotus 1-2-3 for MS-DOS, the first killer application for the IBM PC, it took the market from Visicalc in the early 1980s.
1983, Dynacalc for OS-9 a Unix-like operating system, similar to VisiCalc.
1984, Lotus Symphony for MS-DOS, the follow-on to Lotus 1-2-3
1985, Boeing Calc for MVS and MS-DOS, written by subsidiary of aviation manufacturer Boeing.
1985, StarOffice for MS-DOS, later becoming OpenOffice.org then currently LibreOffice and Collabora Online.
1985, 20/20, for MS-DOS, competitor to 1-2-3 with database integration, real-time data updating, multiplatform.
1986, VP Planner for MS-DOS, similar in look and feel to Lotus 1-2-3, but included 5 level multi-dimensional database
1987, PlanPerfect for MS-DOS, distributed by WordPerfect Corporation.
1988, Wingz for Classic Mac OS operating system, a multi dimensional Spreadsheet from Informix.
1989, Quattro Pro for MS-DOS by Borland. The Windows version, introduced several years later was included in the PerfectOffice 3.0 suite.
1991, 3D-Calc for Atari ST operating system, multi-dimensional spreadsheet
1991, Lotus Improv for NeXTSTEP, a novel design that went beyond A1 notation.
See also
Comparison of spreadsheet software
Logical spreadsheet
References
Spreadsheets | List of spreadsheet software | [
"Mathematics",
"Technology"
] | 1,737 | [
"Computing-related lists",
"Spreadsheet software",
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4,246,088 | https://en.wikipedia.org/wiki/West%20Virginia%20Broadband | West Virginia Broadband is a Wireless community network located in Braxton County, West Virginia operated by local volunteers and coordinated by the Gilmer-Braxton Research Zone. The effort gained recent attention by a National Public Radio story and MuniWireless and SmartMobs bloggers detailing how modified off-the-shelf Wi-Fi adapters were used to connect 7 communities with wireless internet for a total cost of little more than 4000 US dollars. The research group now coordinates wireless technology training throughout the United States.
References
Wireless network organizations
Community networks
Braxton County, West Virginia | West Virginia Broadband | [
"Technology"
] | 115 | [
"Wireless networking",
"Wireless network organizations"
] |
4,246,442 | https://en.wikipedia.org/wiki/Roundabout%20PlayPump | The Roundabout PlayPump is a system that uses the energy created by children playing to operate a water pump. It is manufactured by the South African company Roundabout Outdoor. It operates in a similar way to a windmill-driven water pump.
The PlayPump received heavy publicity and funding when first introduced, but has since been criticized for being too expensive, too complex to maintain or repair in low-resource settings, too reliant on child labor, and overall less effective than traditional handpumps. WaterAid, one of the biggest water charities in the world, opposes the PlayPump for these reasons.
Design
The PlayPump water system is a playground merry-go-round attached to a water pump. The spinning motion pumps underground water into a 2,500-liter tank raised seven meters above ground. The water in the tank is easily dispensed by a tap valve. According to the manufacturer the pump can raise up to 1400 liters of water per hour from a depth of 40 meters. Excess water is diverted below ground again.
The storage tank has a four-sided advertising panel. Two sides are used to advertise products, thereby providing money for maintenance of the pump, and the other two sides are devoted to public health messages about topics like HIV/AIDS prevention.
History
The PlayPump was invented in South Africa by Ronnie Stuiver, a borehole driller and engineer, who exhibited it at an agricultural fair in 1989. Trevor Field, an agricultural executive, saw the device at the fair and licensed it from Stuiver. Field installed the first two systems in KwaZulu-Natal province in South Africa in 1994, and began receiving media attention in 1999, when Nelson Mandela attended the opening of a school which had a PlayPump. In 2000, PlayPump received the World Bank Development Marketplace Award, and it became internationally prominent following a 2005 PBS Frontline report in 2005. At a 2006 Clinton Global Initiative ceremony, donors pledged $16.4 million to install more PlayPumps.
By 2008, 1,000 PlayPumps had been installed, and Field set a goal of installing 4,000 by 2010. However, in 2009 PlayPumps International turned its inventory of uninstalled PlayPumps over to Water For People, and stopped installing new PlayPumps in order to focus on maintenance of existing ones.
Effectiveness
The Guardian calculated in 2009 that children would have to "play" for 27 hours every day to meet PlayPumps' stated targets of providing 2,500 people per pump with their daily water needs.
In June 2010, PBS's Frontline/World aired an update about the failure of PlayPumps, particularly in Mozambique. Many older women, who were not consulted prior to the installation of the PlayPumps, found operating them to be difficult, especially when there were few children around. PlayPumps were also breaking down, with no way for villagers to make the expensive necessary repairs. A comprehensive report about these failures was released by UNICEF in 2007.
See also
Empower Playgrounds
Blood: Water Mission
Water privatisation in South Africa
Water scarcity in Africa
References
External links
Roundabout Water Solutions
One Water — official One Water site
"Why pumping water is child's play" (2005-04-25) - BBC News article
"The Play Pump: Turning water into child's play" (2004-10-24) - article with streaming video
African Well Fund
Human power
Water supply
Pumps | Roundabout PlayPump | [
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"Engineering",
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"Physical quantities",
"Turbomachinery",
"Physical systems",
"Power (physics)",
"Hydraulics",
"Human power",
"Environmental engineering",
"Water supply"
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4,246,605 | https://en.wikipedia.org/wiki/Antenna%20rotator | An antenna rotator (or antenna rotor) is a device used to change the orientation, within the horizontal plane, of a directional antenna. Most antenna rotators have two parts, the rotator unit and the controller. The controller is normally placed near the equipment which the antenna is connected to, while the rotator is mounted on the antenna mast directly below the antenna.
Rotators are commonly used in amateur radio and military communications installations. They are also used with TV and FM antennas, where stations are available from multiple directions, as the cost of a rotator is often significantly less than that of installing a second antenna to receive stations from multiple directions.
Rotators are manufactured for different sizes of antennas and installations. For example, a consumer TV antenna rotator has enough torque to turn a TV/FM or small ham antenna. These units typically cost around US$70 .
Heavy-duty ham rotators are designed to turn extremely large, heavy, high frequency (shortwave) beam antennas, and cost hundreds or possibly thousands of dollars.
In the center of the reference picture, the accompanying image includes an AzEl installation rotator, so named for its controlling of both the azimuth and the elevation components of the direction of an antenna system or array. Such antenna configurations are used in, for example, amateur radio satellite or moon-bounce communications.
An open hardware AzEl rotator system is provided by the SatNOGS Groundstation project.
The Alliance Manufacturing Co. of Alliance, Ohio, and the Astatic Corporation of Conneaut, Ohio, manufactured popular radio and TV booster and rotary antenna systems. These products were heavily advertised for radio use in newspapers starting in the early 1940s, and for use with commercial television sets from 1949 into the 1960s. Cinécraft Productions, a pioneer in early TV advertising, produced six commercials for the Astatic Booster TV in 1949 and 112 for the Alliance Tenna-Rotor, Tenna-Scope, and Casca-Matic Booster between 1949 and 1955.
Manufacturers of consumer TV antenna rotators
Past
Before the era of cable TV and the rise of satellite TV, many homes had outdoor antennas designed to capture over-the-air television signals. The rotator market was served by a number of manufacturers including
Alinco Electronics, Inc.
Alliance Manufacturing Co., Inc., Alliance, Ohio
American Phenolic Corporation
Astatic Corporation. Conneaut, Ohio
Channel Master
Cornell-Dubilier Corporation, South Plainfield, New Jersey
Gemini Industries, Inc., Passaic, New Jersey
Hy-Gain
Kenpro
Lance Industries, Sylmar, California
Leader Electronics, Inc., Cleveland, Ohio
Nippon Antenna
Philco
Philips
Pro Brand International, Inc. (Eagle Aspen brand)
Radio Merchandise Sales, Inc.
Radio Shack
RCA
Sears, Roebuck and Co.
Stolle
The Radiart Corp., Cleveland, Ohio
Zenith
Current
Although the cord-cutting movement has increased interest in receiving free over-the-air television signals, as of December 2021 consumer options are limited.
VOXX Accessories Corporation of Carmel, Indiana, a wholly-owned subsidiary of VOXX International, using the RCA trademark, offers a remote-controlled antenna rotator, the model VH226E.
Channel Master's stock of model CM-9521HD is depleted, and it is unclear whether more units will be manufactured.
Yaesu Musen sells a range of rotators aimed at the Amateur and FM (VHF) broadcast listener markets. Amateur products include an Azimuth-Elevation product.
References
External links
Alliance Tenna-Rotor Series 1-17 television commercials produced by Cinécraft Productions, Inc.
Yaesu Rotators
Antennas
Rotation | Antenna rotator | [
"Physics",
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] | 744 | [
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"Telecommunications engineering",
"Antennas",
"Classical mechanics",
"Rotation",
"Motion (physics)"
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4,246,753 | https://en.wikipedia.org/wiki/Liz%20McIntyre%20%28writer%29 | Liz McIntyre is a consumer privacy expert and founder of CAMCAT - Citizens Against Marking, Chipping and Tracking, an organization that works to prevent forced human tracking technologies like implantable microchips. She and co-author Katherine Albrecht wrote the RFID privacy book Spychips: How Major Corporations and Government Plan to Track your Every Move. At one time, McIntyre was the Communications Director for CASPIAN (Consumers Against Supermarket Privacy Invasion and Numbering), an organization that advocated free-market, consumer-based solutions to the problem of retail privacy invasion.
She and Katherine Albrecht, founder and director of CASPIAN, made the term "spychips" synonymous with RFID, and started the anti-RFID website http://www.spychips.com.
McIntyre continues to write and speak out on privacy issues and works as a privacy consultant.
Publications
Books
McIntyre co-authored the book Spychips: How Major Corporations and Government Plan to Track Your Every Move with Katherine Albrecht. The book, winner of the 2006 Lysander Spooner Award for advancing the literature of liberty, lays out the privacy and civil liberties implications of RFID. Not surprisingly, RFID industry representatives have criticized the work, claiming it exaggerates some RFID privacy threats. McIntyre and Albrecht have rebutted such criticisms.
McIntyre and Albrecht's second book The Spychips Threat: Why Christians Should Resist RFID and Electronic Surveillance explores how RFID could bring about a world that resembles the one described in Revelation—a world in which people cannot buy or sell without a number.
The book includes a disclaimer that it explores the connection without calling RFID the "Mark of the Beast," but McIntyre says it hasn't kept some from reading far more into her beliefs.
At the Spychips website, McIntyre states the following: "Could a technology like RFID enslave us? Theoretically, yes. Is the RFID implant the prophesied method of controlling humans and forcing beast worship? I don't think so. Could I be wrong? Yes. I don't believe anyone here on earth knows definitively what the future holds and exactly how events will unfold."
She adds, "There are many smart people--people much smarter than myself--Christians and non-Christians--who hold very strong contradictory beliefs on most matters of religion. I take this as a clue that I should remain humble and reverent when it comes to the mysteries of the universe. It's one thing to explore possibilities and keep a watchful eye. It's quite another to claim a hotline to God and infer that others have an inferior connection to the Almighty."
The authors use public documents and the words and deeds of the industry to support their arguments.
Articles
Position Paper on the Use of RFID in Consumer Products. Co-authored with Katherine Albrecht and Beth Givens. November 14, 2003.
"RFID: The Big Brother Bar Code" (Co-authored with Katherine Albrecht) ALEC Policy Forum, Winter 2004, Volume 6, Number 3, pp. 49–54.
Position Paper on the Use of RFID in Schools. Co-authored with Katherine Albrecht. August 21, 2012. https://web.archive.org/web/20170317015829/http://www.spychips.com/school/RFIDSchoolPositionPaper.pdf
How and Why to Keep the NSA Out of Your Private Stuff ? Even If You've "Got Nothing to Hide" IEEE Technology and Society Magazine, November 27, 2014 https://ieeexplore.ieee.org/document/6969183/
Protect Yourself from RFID: Fend off frightening tracking tech. Co-authored with Katherine Albrecht. IEEE Consumer Electronics Magazine, April 13, 2015. https://ieeexplore.ieee.org/document/7084753/
When Baby Monitors Go Bad. Co-authored with Katherine Albrecht. IEEE Technology and Society Magazine, September 16, 2015. https://ieeexplore.ieee.org/stamp/stamp.jsp?arnumber=7270426
RFID: Helpful New Technology or Threat to Privacy and Civil Liberties? Co-authored with Katina Michael and Katherine Albrecht. IEEE Potentials, September 4, 2015 https://ieeexplore.ieee.org/abstract/document/7243414/?reload=true
See also
Microchip implants (human)
References
External links
SpyChips Website
Official CASPIAN Website
American investigative journalists
Year of birth missing (living people)
Living people
Radio-frequency identification | Liz McIntyre (writer) | [
"Engineering"
] | 948 | [
"Radio-frequency identification",
"Radio electronics"
] |
4,247,261 | https://en.wikipedia.org/wiki/Oren%20Patashnik | Oren Patashnik (born 1954) is an American computer scientist. He co-created BibTeX, and co-authored Concrete Mathematics: A Foundation for Computer Science.
While working at Bell Labs in 1980, Patashnik proved that Qubic can always be won by the first player. Using 1500 hours of computer time, Patashnik's proof is an early example of a computer-assisted proof.
In 1985, Patashnik created the bibliography-system, BibTeX, in collaboration with Leslie Lamport, the creator of LaTeX. LaTeX is a system and programming language for formatting documents, which is especially designed for mathematical documents. BibTeX is a widely used bibliography-formatting tool for LaTeX.
Patashnik assisted Ronald Graham and Donald Knuth in writing the 1988 textbook Concrete Mathematics: A Foundation for Computer Science.
Patashnik became a doctoral student of Andrew Yao at Stanford University, where he completed his Ph.D. in 1990.
References
1954 births
Living people
American computer scientists
Jewish American scientists
Yale University alumni
Timothy Dwight College alumni
Stanford University alumni
BibTeX | Oren Patashnik | [
"Technology"
] | 225 | [
"Computing stubs",
"Computer specialist stubs"
] |
4,247,395 | https://en.wikipedia.org/wiki/CD%20publishing | CD publishing is the use of CD duplication systems to create a large number of unique discs. For instance, storing a unique serial number on each copy of a software application disc would be considered CD publishing.
The term CD publishing is believed to have been coined by the Rimage Corporation as part of a marketing program which referred to CD-R discs as "digital paper." Automated disc production and printing systems, such as those made by Rimage, can be shared on a computer network much like an office printer to facilitate the creation of unique discs. This is the root of both the digital paper and CD publishing terms.
The extension into CD publishing is a distinct advantage of CD duplication systems over traditional CD replication - where large quantities of identical discs must be made.
External links
Understanding CD-R & CD-RW: Duplication, Replication, and Publishing @ the Optical Storage Technology Association
Computer storage media
Optical disc authoring | CD publishing | [
"Technology"
] | 187 | [
"Multimedia",
"Optical disc authoring"
] |
4,247,871 | https://en.wikipedia.org/wiki/Astros%20II | Astros II (Artillery SaTuration ROcket System) is a self-propelled multiple rocket launcher produced in Brazil by the Avibras company. It features modular design and employs rockets with calibers ranging from 127 to 450 mm (5–17.72 inches). It was developed on the basis of a Tectran VBT-2028 6×6 all-terrain vehicle for enhanced mobility based on Mercedes-Benz 2028 truck chassis while later versions use Tatra 815-7 chassis.
Overview
A full Astros system includes 1 wheeled 4×4 Battalion level Command Vehicle (AV-VCC), which commands 3 batteries, and a series of 4x4 and 6×6 wheeled vehicles. Each battery consists of:
1 wheeled 4×4 Battery-level Command vehicle (AV-PCC)
1 wheeled 6×6 Radar Fire Control vehicle (AV-UCF)
6 wheeled 6×6 Universal Multiple Rocket Launchers vehicle (AV-LMU)
3 wheeled 6×6 Ammunition Resupply vehicles (AV-RMD)
1 wheeled 6×6 Field repair/workshop vehicle (AV-OFVE)
1 wheeled 4×4 Mobile Weather Station vehicle (AV-MET).
In the older version of the system, the fire control vehicle were listed as optional vehicle in a battery. The command vehicles and weather stations are recent additions, designed to improve overall system performance on newer versions. All vehicles are transportable in a C-130 Hercules. The launcher is capable of firing rockets of different calibers armed with a range of warheads.
Each rocket resupply truck carries up to two complete reloads.
Service history
The Astros II artillery system entered service with the Brazilian Army in the early 1990s. The system is battle proven, having been used in action by the Iraqi Army in the Gulf Wars.
In the 1980s, Avibrás sold an estimated 66 Astros II artillery systems to Iraq. Iraq also built the Sajeel-60 which is a license-built version of the Brazilian SS-60. Sixty Astros II were sold to Saudi Arabia and an unspecified number sold to Bahrain and Qatar. Total sales of the Astros II between 1982 and 1987 reached US$1 billion. This fact made the Astros II multiple rocket launcher the most profitable weapon produced by Avibrás.
In the 1980s and early 1990s, Avibrás manufactured almost exclusively rockets and multiple-launch rocket systems (MLRS), such as the Astros II, in addition to developing antitank and antiship missiles. At its peak, Avibrás employed 6,000 people; later it would be reduced to 900 people in the early 1990s as the arms industry demand fell. Even so, in the first Gulf War in 1991, the Astros II was successfully used by Saudi Arabia against Iraq. Years earlier, the Astros II system had helped Angola to defeat the UNITA.
New generation
The next step is an ambitious program, the Astros 2020 (Mk6), based on a 6×6 wheeled chassis. Being a new concept, it will require an estimated investment of R$1.2 billion, of which about US$210 million will be invested solely in development. It will be integrated with the cruise missile AVMT-300 with 300-km range during the stage of testing and certification. It is said that the venture will, for example, enable the Army to integrate the Astros with defense anti-aircraft guns, paving the way for the utilization of common platforms, trucks, parts of electronic sensors and command vehicles. The new MK6 system will use Tatra Trucks’ T815-790R39 6×6 and T815-7A0R59 4×4 trucks instead of the original Mercedes-Benz 2028A 6x6 truck. ASTROS 2020 offers several basic improvements including an improved armored cabin, modern digital communications and navigation systems, and a new tracking radar that replaces the AV-UCF's Contraves Fieldguard system. The new tracking radar used by MK6 AV-UCF was later revealed to be the Fieldguard 3 Military Measurement System from Rheinmetall Air Defence. The Astros 2020 will also be equipped with a 180 mm GPS-guided rocket called the SS-AV-40G with a range of and SS-150 newly developed rockets with a claimed maximum range of 150 km. Four of them are carried. 36 Astros 2020 systems are to be acquired.
Rocket variants
SS-09TS – fires 70 mm rockets – Loads 40
SS-30 – fires 127 mm rockets – Loads 32
SS-40 – fires 180 mm rockets – Loads 16
SS-40G – fires 180 mm rockets – Loads 16 (GPS Guided)
SS-60 – fires 300 mm rockets – Loads 4
SS-80 – fires 300 mm rockets – Loads 4
SS-80G – fires 300 mm rockets – Loads 4 (GPS Guided)
SS-150 – fires 450 mm rockets – Loads 4 (GPS Guided)
MANSUP – fires 330 mm anti-ship missile – Loads 1–4
AV-TM 300 – fires 450 mm cruise missile – Loads 2
FOG MPM – fiber optics guided multi-purpose missile – anti-tank, anti-fortification and anti-helicopter missile
FOG MLM – fiber optics guided multi-purpose missile
Specifications
Range in indirect fire mode (first figure is minimum range):
SS-09TS: 4–10 km
SS-30: 9–30 km
SS-40: 15–40 km
SS-40G: 15–40 km
SS-60: 20–60 km
SS-80: 22–90 km
SS-80G: 22–90 km
SS-150: 29–150 km
MANSUP: 70–200 km
AV-TM 300: 30–300 km
FOG MPM: 5–60 km
Armour: classified. Probably light composite to give protection against small-arms fire.
Armament: one battery of 2, 4, 16 or 32 rocket-launcher tubes
Performance:
fording 1.1 m
vertical obstacle 1 m
trench 2.29 m
Ammunition Type: High explosive (HE) with multiple warhead
Operators
Brazilian Army: 20 Astros II Mk3M, 18 Astros II Mk6.
Brazilian Marine Corps: 6 Astros II Mk6.
Indonesian Army: 63 Astros II Mk6 (first batch of 36 ordered in 2012 and second batch of 27 delivered in 2020).
: 66 Astros II. (also built under license as the Sajil-60). Only with rockets of shorter range SS-40 and SS-60.
Malaysian Army: 36 units of Astros II.
Saudi Arabia: 76 Astros II.
Potential operators
: Spain is currently evaluating K239 Chunmoo, Astros II and PULS systems, but the decision regarding a potential order of one of these systems has not been made.
: On December 4, 2022, the Brazilian media reported a Ukrainian interest in the ASTROS system, to equip the Army in the Russo-Ukrainian War efforts. The sale was blocked by the Bolsonaro administration. A diplomatic effort by the United States to persuade the president-elect of Brazil, Luiz Inácio Lula da Silva, to unblock the deal was reported on the 5th of December 2022.
See also
HIMARS
BM-21
RM-70
T-122 Sakarya
9A52-4 Tornado
Fajr-5
TOROS
Falaq-2
Pinaka multi-barrel rocket launcher
References
External links
Astros II Artillery Saturation Rocket System, Brazil
FAS Military Analysis Network
Wheeled self-propelled rocket launchers
Multiple rocket launchers of Brazil
Modular rocket launchers
Military vehicles introduced in the 1980s | Astros II | [
"Engineering"
] | 1,528 | [
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"Modular rocket launchers"
] |
4,248,265 | https://en.wikipedia.org/wiki/Zimm%E2%80%93Bragg%20model | In statistical mechanics, the Zimm–Bragg model is a helix-coil transition model that describes helix-coil transitions of macromolecules, usually polymer chains. Most models provide a reasonable approximation of the fractional helicity of a given polypeptide; the Zimm–Bragg model differs by incorporating the ease of propagation (self-replication) with respect to nucleation. It is named for co-discoverers Bruno H. Zimm and J. K. Bragg.
Helix-coil transition models
Helix-coil transition models assume that polypeptides are linear chains composed of interconnected segments. Further, models group these sections into two broad categories: coils, random conglomerations of disparate unbound pieces, are represented by the letter 'C', and helices, ordered states where the chain has assumed a structure stabilized by hydrogen bonding, are represented by the letter 'H'.
Thus, it is possible to loosely represent a macromolecule as a string such as CCCCHCCHCHHHHHCHCCC and so forth. The number of coils and helices factors into the calculation of fractional helicity, , defined as
where
is the average helicity and
is the number of helix or coil units.
Zimm–Bragg
The Zimm–Bragg model takes the cooperativity of each segment into consideration when calculating fractional helicity. The probability of any given monomer being a helix or coil is affected by which the previous monomer is; that is, whether the new site is a nucleation or propagation.
By convention, a coil unit ('C') is always of statistical weight 1. Addition of a helix state ('H') to a previously coiled state (nucleation) is assigned a statistical weight , where is the nucleation parameter and is the equilibrium constant
Adding a helix state to a site that is already a helix (propagation) has a statistical weight of . For most proteins,
which makes the propagation of a helix more favorable than nucleation of a helix from coil state.
From these parameters, it is possible to compute the fractional helicity . The average helicity is given by
where is the partition function given by the sum of the probabilities of each site on the polypeptide. The fractional helicity is thus given by the equation
Statistical mechanics
The Zimm–Bragg model is equivalent to a one-dimensional Ising model and has no long-range interactions, i.e., interactions between residues well separated along the backbone; therefore, by the famous argument of Rudolf Peierls, it cannot undergo a phase transition.
The statistical mechanics of the Zimm–Bragg model may be solved exactly using the transfer-matrix method. The two parameters of the Zimm–Bragg model are σ, the statistical weight for nucleating a helix and s, the statistical weight for propagating a helix. These parameters may depend on the residue j; for example, a proline residue may easily nucleate a helix but not propagate one; a leucine residue may nucleate and propagate a helix easily; whereas glycine may disfavor both the nucleation and propagation of a helix. Since only nearest-neighbour interactions are considered in the Zimm–Bragg model, the full partition function for a chain of N residues can be written as follows
where the 2x2 transfer matrix Wj of the jth residue equals the matrix of statistical weights for the state transitions
The row-column entry in the transfer matrix equals the statistical weight for making a transition from state row in residue j − 1 to state column in residue j. The two states here are helix (the first) and coil (the second). Thus, the upper left entry s is the statistical weight for transitioning from helix to helix, whereas the lower left entry σs is that for transitioning from coil to helix.
See also
Alpha helix
Lifson–Roig model
Random coil
Statistical mechanics
References
Polymer physics
Protein structure
Statistical mechanics
Thermodynamic models | Zimm–Bragg model | [
"Physics",
"Chemistry",
"Materials_science"
] | 846 | [
"Polymer physics",
"Thermodynamic models",
"Thermodynamics",
"Polymer chemistry",
"Structural biology",
"Statistical mechanics",
"Protein structure"
] |
4,248,332 | https://en.wikipedia.org/wiki/Biopharmaceutics%20Classification%20System | The Biopharmaceutics Classification System (BCS) is a system to differentiate drugs on the basis of their solubility and permeability.
This system restricts the prediction using the parameters solubility and intestinal permeability. The solubility classification is based on a United States Pharmacopoeia (USP) aperture. The intestinal permeability classification is based on a comparison to the intravenous injection. All those factors are highly important because 85% of the most sold drugs in the United States and Europe are orally administered.
Classes
According to the Biopharmaceutics Classification System (BCS) drug substances are classified to four classes upon their solubility and permeability:
Class I – high permeability, high solubility
Example: metoprolol, paracetamol
Those compounds are well absorbed and their absorption rate is usually higher than excretion.
Class II – high permeability, low solubility
Example: glibenclamide, bicalutamide, ezetimibe, aceclofenac
The bioavailability of those products is limited by their solvation rate. A correlation between the in vivo bioavailability and the in vitro solvation can be found.
Class III – low permeability, high solubility
Example: cimetidine
The absorption is limited by the permeation rate but the drug is solvated very fast. If the formulation does not change the permeability or gastro-intestinal duration time, then class I criteria can be applied.
Class IV – low permeability, low solubility
Example: bifonazole
Those compounds have a poor bioavailability. Usually they are not well absorbed over the intestinal mucosa and a high variability is expected.
Definitions
The drugs are classified in BCS on the basis of solubility and permeability.
Solubility class boundaries are based on the highest dose strength of an immediate release product. A drug is considered highly soluble when the highest dose strength is soluble in 250 ml or less of aqueous media over the pH range of 1 to 6.8. The volume estimate of 250 ml is derived from typical bioequivalence study protocols that prescribe administration of a drug product to fasting human volunteers with a glass of water.
Permeability class boundaries are based indirectly on the extent of absorption of a drug substance in humans and directly on the measurement of rates of mass transfer across human intestinal membrane. Alternatively non-human systems capable of predicting drug absorption in humans can be used (such as in-vitro culture methods). A drug substance is considered highly permeable when the extent of absorption in humans is determined to be 85% or more of the administered dose based on a mass-balance determination or in comparison to an intravenous dose.
See also
ADME
Partition coefficient
Bioavailability
Drug metabolism
First pass effect
Polar surface area
IVIVC
References
Further reading
External links
BCS guidance of the U.S. Food and Drug Administration
Pharmacological classification systems
Pharmacy in the United States | Biopharmaceutics Classification System | [
"Chemistry"
] | 642 | [
"Pharmacological classification systems",
"Pharmacology"
] |
4,248,491 | https://en.wikipedia.org/wiki/Gauche%20effect | In the study of conformational isomerism, the gauche effect is an atypical situation where a gauche conformation (groups separated by a torsion angle of approximately 60°) is more stable than the anti conformation (180°).
There are both steric and electronic effects that affect the relative stability of conformers. Ordinarily, steric effects predominate to place large substituents far from each other. However, this is not the case for certain substituents, typically those that are highly electronegative. Instead, there is an electronic preference for these groups to be gauche. Typically studied examples include 1,2-difluoroethane (H2FCCFH2), ethylene glycol, and vicinal-difluoroalkyl structures.
There are two main explanations for the gauche effect: hyperconjugation and bent bonds. In the hyperconjugation model, the donation of electron density from the C−H σ bonding orbital to the C−F σ* antibonding orbital is considered the source of stabilization in the gauche isomer. Due to the greater electronegativity of fluorine, the C−H σ orbital is a better electron donor than the C−F σ orbital, while the C−F σ* orbital is a better electron acceptor than the C−H σ* orbital. Only the gauche conformation allows good overlap between the better donor and the better acceptor.
Key in the bent bond explanation of the gauche effect in difluoroethane is the increased p orbital character of both C−F bonds due to the large electronegativity of fluorine. As a result, electron density builds up above and below to the left and right of the central C−C bond. The resulting reduced orbital overlap can be partially compensated when a gauche conformation is assumed, forming a bent bond. Of these two models, hyperconjugation is generally considered the principal cause behind the gauche effect in difluoroethane.
The molecular geometry of both rotamers can be obtained experimentally by high-resolution infrared spectroscopy augmented with in silico work. In accordance with the model described above, the carbon–carbon bond length is higher for the anti-rotamer (151.4 pm vs. 150 pm). The steric repulsion between the fluorine atoms in the gauche rotamer causes increased CCF bond angles (by 3.2°) and increased FCCF dihedral angles (from the default 60° to 71°).
In the related compound 1,2-difluoro-1,2-diphenylethane, the threo isomer is found (by X-ray diffraction and from NMR coupling constants) to have an anti conformation between the two phenyl groups and the two fluorine groups and a gauche conformation is found for both groups for the erythro isomer. According to in silico results, this conformation is more stable by 0.21 kcal/mol (880 J/mol).
A gauche effect has also been reported for a molecule featuring an all-syn array of four consecutive fluoro substituents. The reaction to install the fourth one is stereoselective:
The gauche effect is also seen in 1,2-dimethoxyethane and some vicinal-dinitroalkyl compounds.
The alkene cis effect is an analogous atypical stabilizing of certain alkenes.
External influences
The gauche effect is very sensitive to solvent effects, due to the large difference in polarity between the two conformers. For example, 2,3-dinitro-2,3-dimethylbutane, which in the solid state exists only in the gauche conformation, prefers the gauche conformer in benzene solution by a ratio of 79:21, but in carbon tetrachloride, it prefers the anti conformer by a ratio of 58:42. Another case is trans-1,2 difluorocyclohexane, which has a larger preference for the di-equatorial conformer, rather than the anti-diaxial conformer, in more polar solvents.
See also
Anomeric effect
References
Stereochemistry | Gauche effect | [
"Physics",
"Chemistry"
] | 913 | [
"Spacetime",
"Stereochemistry",
"Space",
"nan"
] |
4,248,526 | https://en.wikipedia.org/wiki/Computational%20aeroacoustics | Computational aeroacoustics is a branch of aeroacoustics that aims to analyze the generation of noise by turbulent flows through numerical methods.
History
The origin of computational aeroacoustics can only very likely be dated back to the middle of the 1980s, with a publication of Hardin and Lamkin who claimed, that "[...] the field of computational fluid mechanics has been advancing rapidly in the past few years and now offers the hope that "computational aeroacoustics," where noise is computed directly from a first principles determination of continuous velocity and vorticity fields, might be possible, [...]"
Later in a publication 1986 the same authors introduced the abbreviation CAA. The term was initially used for a low Mach number approach (Expansion of the acoustic perturbation field about an incompressible flow) as it is described under EIF. Later in the beginning 1990s the growing CAA community picked up the term and extensively used it for any kind of numerical method describing the noise radiation from an aeroacoustic source or the propagation of sound waves in an inhomogeneous flow field. Such numerical methods can be far field integration methods (e.g. FW-H) as well as direct numerical methods optimized for the solutions (e.g.) of a mathematical model describing the aerodynamic noise generation and/or propagation. With the rapid development of the computational resources this field has undergone spectacular progress during the last three decades.
Methods
Direct numerical simulation (DNS) approach to CAA
The compressible Navier-Stokes equation describes both the flow field, and the aerodynamically generated acoustic field. Thus both may be solved for directly. This requires very high numerical resolution due to the large differences in the length scale present between the acoustic variables and the flow variables. It is computationally very demanding and unsuitable for any commercial use.
Hybrid approach
In this approach the computational domain is split into different regions, such that the governing acoustic or flow field can be solved with different equations and numerical techniques. This would involve using two different numerical solvers, first a dedicated Computational fluid dynamics (CFD) tool and secondly an acoustic solver. The flow field is then used to calculate the acoustical sources. Both steady state (RANS, SNGR (Stochastic Noise Generation and Radiation), ...) and transient (DNS, LES, DES, URANS, ...) fluid field solutions can be used. These acoustical sources are provided to the second solver which calculates the acoustical propagation. Acoustic propagation can be calculated using one of the following methods:
Integral methods
Lighthill's analogy
Kirchhoff integral
FW-H
LEE
Pseudospectral
EIF
APE
Integral methods
There are multiple methods, which are based on a known solution of the acoustic wave equation to compute the acoustic far field of a sound source. Because a general solution for wave propagation in the free space can be written as an integral over all sources, these solutions are summarized as integral methods. The acoustic sources have to be known from some different source (e.g. a Finite Element simulation of a moving mechanical system or a fluid dynamic CFD simulation of the sources in a moving medium). The integral is taken over all sources at the retarded time (source time), which is the time at that the source is sent out the signal, which arrives now at a given observer position. Common to all integral methods is, that they cannot account for changes in the speed of sound or the average flow speed between source and observer position as they use a theoretical solution of the wave equation. When applying Lighthill's theory to the Navier Stokes equations of Fluid mechanics, one obtains volumetric sources, whereas the other two analogies provide the far field information based on a surface integral. Acoustic analogies can be very efficient and fast, as the known solution of the wave equation is used. One far away observer takes as long as one very close observer. Common for the application of all analogies is the integration over a large number of contributions, which can lead to additional numerical problems (addition/subtraction of many large numbers with result close to zero.) Furthermore, when applying an integral method, usually the source domain is limited somehow. While in theory the sources outside have to be zero, the application can not always fulfill this condition. Especially in connection with CFD simulations, this leads to large cut-off errors. By damping the source gradually to zero at the exit of the domain or adding some additional terms to correct this end-effect, these cut-off errors can be minimized.
Lighthill's analogy
Also called 'Acoustic Analogy'. To obtain Lighthill's aeroacoustic analogy the governing Navier-Stokes equations are rearranged. The left hand side is a wave operator, which is applied to the density perturbation or pressure perturbation respectively. The right hand side is identified as the acoustic sources in a fluid flow, then. As Lighthill's analogy follows directly from the Navier-Stokes equations without simplification, all sources are present. Some of the sources are then identified as turbulent or laminar noise. The far-field sound pressure is then given in terms of a volume integral over the domain containing the sound source. The source term always includes physical sources and such sources, which describe the propagation in an inhomogeneous medium.
The wave operator of Lighthill's analogy is limited to constant flow conditions outside the source zone. No variation of density, speed of sound and Mach number is allowed. Different mean flow conditions are identified as strong sources with opposite sign by the analogy, once an acoustic wave passes it. Part of the acoustic wave is removed by one source and a new wave is radiated to fix the different wave speed. This often leads very large volumes with strong sources. Several modifications to Lighthill's original theory have been proposed to account for the sound-flow interaction or other effects. To improve Lighthill's analogy different quantities inside the wave operator as well as different wave operators are considered by following analogies. All of them obtain modified source terms, which sometimes allow a more clear sight on the "real" sources. The acoustic analogies of Lilley, Pierce, Howe and Möhring are only some examples for aeroacoustic analogies based on Lighthill's ideas. All acoustic analogies require a volume integration over a source term.
The major difficulty with the acoustic analogy, however, is that the sound source is not compact in supersonic flow. Errors could be encountered in calculating the sound field, unless the computational domain could be extended in the downstream direction beyond the location where the sound source has completely decayed. Furthermore, an accurate account of the retarded time-effect requires keeping a long record of the time-history of the converged solutions of the sound source, which again represents a storage problem. For realistic problems, the required storage can reach the order of 1 terabyte of data.
Kirchhoff integral
Kirchhoff and Helmholtz showed, that the radiation of sound from a limited source region can be described by enclosing this source region by a control surface - the so-called Kirchhoff surface. Then the sound field inside or outside the surface, where no sources are allowed and the wave operator on the left hand side applies, can be produced as a superposition of monopoles and dipoles on the surface. The theory follows directly from the wave equation. The source strength of monopoles and dipoles on the surface can be calculated if the normal velocity (for monopoles) and the pressure (for dipoles) on the surface are known respectively. A modification of the method allows even to calculate the pressure on the surface based on the normal velocity only. The normal velocity could be given by a FE-simulation of a moving structure for instance. However, the modification to avoid the acoustic pressure on the surface to be known leads to problems, when considering an enclosed volume at its resonant frequencies, which is a major issue of the implementations of their method. The Kirchhoff integral method finds for instance application in Boundary element methods (BEM). A non-zero flow velocity is accounted by considering a moving frame of reference with the outer flow speed, in which the acoustic wave propagation takes place. Repetitive applications of the method can account for obstacles. First the sound field on the surface of the obstacle is calculated and then the obstacle is introduced by adding sources on its surface to cancel the normal velocity on the surface of the obstacle. Variations of the average flow field (speed of sound, density and velocity) can be taken into account by a similar method (e.g. dual reciprocity BEM).
FW-H
The integration method of Ffowcs Williams and Hawkings is based on Lighthill's acoustic analogy. However, by some mathematical modifications under the assumption of a limited source region, which is enclosed by a control surface (FW-H surface), the volume integral is avoided. Surface integrals over monopole and dipole sources remain. Different from the Kirchhoff method, these sources follow directly from the Navier-Stokes equations through Lighthill's analogy. Sources outside the FW-H surface can be accounted by an additional volume integral over quadrupole sources following from the Lighthill Tensor. However, when considering the same assumptions as Kirchhoffs linear theory, the FW-H method equals the Kirchhoff method.
Linearized Euler Equations
Considering small disturbances superimposed on a uniform mean flow of density , pressure and velocity on x-axis , the Euler equations for a two dimensional model is presented as:
,
where
where , , and are the acoustic field variables, the ratio of specific heats , for air at 20 °C , and the source term on the right-side represents distributed unsteady sources.
The application of LEE can be found in engine noise studies.
For high Mach number flows in compressible regimes, the acoustic propagation may be influenced by non-linearities and the LEE may no longer be the appropriate mathematical model.
Pseudospectral
A Fourier pseudospectral time-domain method can be applied to wave propagation problems pertinent to computational aeroacoustics. The original algorithm of the Fourier pseudo spectral time domain method works for periodical problems without the interaction with physical boundaries. A slip wall boundary condition, combined with buffer zone technique to solve some non-periodical aeroacoustic problems has been proposed. Compared to other computational methods, pseudospectral method is preferred for its high-order accuracy.
EIF
Expansion about Incompressible Flow
APE
Acoustic Perturbation Equations
Refer to the paper "Acoustic Perturbation Equations Based on Flow Decomposition via Source Filtering" by R.Ewert and W.Schroder.
See also
Aeroacoustics
Acoustic theory
References
Sources
Lighthill, M. J., "A General Introduction to Aeroacoustics and Atmospheric Sounds", ICASE Report 92-52, NASA Langley Research Centre, Hampton, VA, 1992
External links
Examples in Aeroacoustics from NASA
Computational Aeroacoustics at the Ecole Centrale de Lyon
Computational Aeroacoustics at the University of Leuven
Computational Aeroacoustics at Technische Universität Berlin
A CAA lecture script of Technische Universität Berlin
Computational fluid dynamics
Acoustics
Aerodynamics
Mechanics
Computational fields of study | Computational aeroacoustics | [
"Physics",
"Chemistry",
"Technology",
"Engineering"
] | 2,332 | [
"Computational fields of study",
"Computational fluid dynamics",
"Classical mechanics",
"Acoustics",
"Computational physics",
"Aerodynamics",
"Mechanics",
"Computing and society",
"Mechanical engineering",
"Aerospace engineering",
"Fluid dynamics"
] |
4,248,537 | https://en.wikipedia.org/wiki/Mumbai%20Refinery%20%28HPCL%29 | The HPCL Mumbai refinery is one of the most complex refineries in the country, is constructed on an area of 321 acres. This versatile refinery which is the first of India's modern refineries, symbolizes the country's industrial strength and progress in the oil industry. Mumbai Refinery has grown over the years as the main hub of petroleum products. The refinery has reached to present level through several upgradation and restructuring processes.
History
The Mumbai Refinery was commissioned by Esso Standard in 1954, with an installed capacity of 1.25 million tonnes per year. The lube refinery, Lube India Ltd, was commissioned in 1969 with a capacity of 165 million tonnes per year of Lube Oil Base Stock (LOBS) production.
Crude processing capacity increased to 3.5 million tonnes per year during 1969. In 1974, the Government of India took over Esso and Lube India by the Esso (Acquisition of Undertakings in India) Act 1974 and formed HPCL.
Expansion of the fuels block was carried out by installing new 2 million tonnes per year crude units in 1985. A second expansion of Lube Refinery took place to increase the capacity of the refinery to 335 million tonnes per year, so far the largest in India. The installed capacity of the refinery was later enhanced to 6.5 million tonnes per year.
The current installed capacity of the refinery is 9.5 million tonnes per year.
References
Buildings and structures in Mumbai
Oil refineries in India
1954 establishments in Bombay State
Economy of Mumbai
Energy in Maharashtra
Hindustan Petroleum
Hindustan Petroleum buildings and structures | Mumbai Refinery (HPCL) | [
"Chemistry"
] | 318 | [
"Petroleum",
"Petroleum stubs"
] |
4,248,773 | https://en.wikipedia.org/wiki/Cypress%20PSoC | PSoC (programmable system on a chip) is a family of microcontroller integrated circuits by Cypress Semiconductor. These chips include a CPU core and mixed-signal arrays of configurable integrated analog and digital peripherals.
History
In 2002, Cypress began shipping commercial quantities of the PSoC 1. To promote the PSoC, Cypress sponsored a "PSoC Design Challenge" in Circuit Cellar magazine in 2002 and 2004.
In April 2013, Cypress released the fourth generation, PSoC 4. The PSoC 4 features a 32-bit ARM Cortex-M0 CPU, with programmable analog blocks (operational amplifiers and comparators), programmable digital blocks (PLD-based UDBs), programmable routing and flexible GPIO (route any function to any pin), a serial communication block (for SPI, UART, I²C), a timer/counter/PWM block and more.
PSoC is used in devices as simple as Sonicare toothbrushes and Adidas sneakers, and as complex as the TiVo set-top box. One PSoC implements capacitive sensing for the touch-sensitive scroll wheel on the Apple iPod click wheel.
In 2014, Cypress extended the PSoC 4 family by integrating a Bluetooth Low Energy radio along with a PSoC 4 Cortex-M0-based SoC in a single, monolithic die.
In 2016, Cypress released PSoC 4 S-Series, featuring ARM Cortex-M0+ CPU.
Overview
A PSoC integrated circuit is composed of a core, configurable analog and digital blocks, and programmable routing and interconnect. The configurable blocks in a PSoC are the biggest difference from other microcontrollers.
PSoC has three separate memory spaces: paged SRAM for data, Flash memory for instructions and fixed data, and I/O registers for controlling and accessing the configurable logic blocks and functions. The device is created using SONOS technology.
PSoC resembles an ASIC: blocks can be assigned a wide range of functions and interconnected on-chip. Unlike an ASIC, there is no special manufacturing process required to create the custom configuration – only startup code that is created by Cypress' PSoC Designer (for PSoC 1) or PSoC Creator (for PSoC 3 / 4 / 5) IDE.
PSoC resembles an FPGA in that at power up it must be configured, but this configuration occurs by loading instructions from the built-in Flash memory.
PSoC most closely resembles a microcontroller combined with a PLD and programmable analog. Code is executed to interact with the user-specified peripheral functions (called "Components"), using automatically generated APIs and interrupt routines. PSoC Designer or PSoC Creator generate the startup configuration code. Both integrate APIs that initialize the user selected components upon the users needs in a Visual-Studio-like GUI.
Configurable analog and digital blocks
Using configurable analog and digital blocks, designers can create and change mixed-signal embedded applications. The digital blocks are state machines that are configured using the blocks registers. There are two types of digital blocks, Digital Building Blocks (DBBxx) and Digital Communication Blocks (DCBxx). Only the communication blocks can contain serial I/O user modules, such as SPI, UART, etc.
Each digital block is considered an 8-bit resource that designers can configure using pre-built digital functions or user modules (UM), or, by combining blocks, turn them into 16-, 24-, or 32-bit resources. Concatenating UMs together is how 16-bit PWMs and timers are created.
There are two types of analog blocks. The continuous time (CT) blocks are composed of an op-amp circuit and designated as ACBxx where xx is 00–03. The other type is the switch cap (SC) blocks, which allow complex analog signal flows and are designated by ASCxy where x is the row and y is the column of the analog block. Designers can modify and personalize each module to any design.
Programmable routing and interconnect
PSoC mixed-signal arrays' flexible routing allows designers to route signals to and from I/O pins more freely than with many competing microcontrollers. Global buses allow for signal multiplexing and for performing logic operations. Cypress suggests that this allows designers to configure a design and make improvements more easily and faster and with fewer PCB redesigns than a digital logic gate approach or competing microcontrollers with more fixed function pins.
Series
There are five different families of devices, each based around a different microcontroller core:
PSoC 1 – CY8C2xxxx series – M8C core.
PSoC 3 – CY8C3xxxx series – 8051 core.
PSoC 4 – CY8C4xxxx series – ARM Cortex-M0 core.
PSoC 5/5LP – CY8C5xxxx series – ARM Cortex-M3 core.
PSoC 6 – CY8C6xxxx series – ARM Cortex-M4 core with an added ARM Cortex-M0+ core (in some models).
Bluetooth Low Energy
Starting in 2014, Cypress began offering PSoC 4 BLE devices with integrated Bluetooth Low Energy (Bluetooth Smart). This can be used to create connected products leveraging the analog and digital blocks. Users can add and configure the BLE module directly in PSoC creator. Cypress also provides a complete Bluetooth Low Energy stack licensed from Mindtree with both Peripheral and Central functionality. The PSoC 6 series includes versions with BLE including Bluetooth 5 features including extended range or higher speed.
Summary
Development tools
PSoC Designer
This is the first generation software IDE to design and debug and program the PSoC 1 devices. It introduced unique features including a library of pre-characterized analog and digital peripherals in a drag-and-drop design environment which could then be customized to specific design needs by leveraging the dynamically generated API libraries of code.
PSoC Creator
PSoC Creator is the second generation software IDE to design debug and program the PSoC 3 / 4 / 5 devices. The development IDE is combined with an easy-to-use graphical design editor to form a powerful hardware/software co-design environment. PSoC Creator consists of two basic building blocks. The program allows the user to select, configure and connect existing circuits on the chip and the components which are the equivalent of peripherals on MCUs. What makes PSoC intriguing is the possibility of creating its own application-specific peripherals in hardware. Cypress publishes component packs several times a year. PSoC users get new peripherals for their existing hardware without being charged or having to buy new hardware. PSoC Creator also allows much freedom in the assignment of peripherals to I/O pins.
Cortex-M
Generic ARM development tools for PSoC 4 and PSoC 5.
Documentation
PSoC 4 / 5
The amount of documentation for all ARM chips is daunting, especially for newcomers. The documentation for microcontrollers from past decades would easily be inclusive in a single document, but as chips have evolved so has the documentation grown. The total documentation is especially hard to grasp for all ARM chips since it consists of documents from the IC manufacturer (Cypress Semiconductor) and documents from CPU core vendor (ARM Holdings).
A typical top-down documentation tree is: manufacturer website, manufacturer marketing slides, manufacturer datasheet for the exact physical chip, manufacturer detailed reference manual that describes common peripherals and aspects of a physical chip family, ARM core generic user guide, ARM core technical reference manual, ARM architecture reference manual that describes the instruction set(s).
PSoC 4 / 5 documentation tree (top to bottom)
PSoC website.
PSoC marketing slides.
PSoC datasheet.
PSoC reference manuals.
ARM core website.
ARM core generic user guide.
ARM core technical reference manual.
ARM architecture reference manual.
Cypress Semiconductor has additional documents, such as: evaluation board user manuals, application notes, getting started guides, software library documents, errata, and more. See External Links section for links to official PSoC and ARM documents.
See also
ARM architecture, List of ARM microprocessor cores, ARM Cortex-M
Embedded systems
Field-programmable analog array
Interrupt, Interrupt handler, Comparison of real-time operating systems
JTAG
Microcontroller, (List of common microcontrollers)
Reconfigurable computing
Single-board microcontroller
References
Further reading
External links
PSoC Official Documents
PSoC Designer software for PSoC 1 family
PSoC Creator software for PSoC 3 / 4 / 5LP families
PSoC Programmer software for PSoC 1 / 3 / 4 / 5LP families
ARM Official Documents for PSoC 4 / 5
Other
IoT Expert PSoC Tutorials
Psoc-chile El primer web site en Español sobre Microcontroladore Psoc
Integrated circuits
System on a chip | Cypress PSoC | [
"Technology",
"Engineering"
] | 1,865 | [
"Computer engineering",
"Integrated circuits"
] |
4,249,038 | https://en.wikipedia.org/wiki/M%C3%B8ller%20scattering | Møller scattering is the name given to electron-electron scattering in quantum field theory, named after the Danish physicist Christian Møller. The electron interaction that is idealized in Møller scattering forms the theoretical basis of many familiar phenomena such as the repulsion of electrons in the helium atom. While formerly many particle colliders were designed specifically for electron-electron collisions, more recently electron-positron colliders have become more common. Nevertheless, Møller scattering remains a paradigmatic process within the theory of particle interactions.
We can express this process in the usual notation, often used in particle physics:
In quantum electrodynamics, there are two tree-level Feynman diagrams describing the process: a t-channel diagram in which the electrons exchange a photon and a similar u-channel diagram. Crossing symmetry, one of the tricks often used to evaluate Feynman diagrams, in this case implies that Møller scattering should have the same cross section as Bhabha scattering (electron-positron scattering).
In the electroweak theory the process is instead described by four tree-level diagrams: the two from QED and an identical pair in which a Z boson is exchanged instead of a photon. The weak force is purely left-handed, but the weak and electromagnetic forces mix into the particles we observe. The photon is symmetric by construction, but the Z boson prefers left-handed particles to right-handed particles. Thus the cross sections for left-handed electrons and right-handed differ. The difference was first noticed by the Russian physicist Yakov Zel'dovich in 1959, but at the time he believed the parity violating asymmetry (a few hundred parts per billion) was too small to be observed. This parity violating asymmetry can be measured by firing a polarized beam of electrons through an unpolarized electron target (liquid hydrogen, for instance), as was done by an experiment at the Stanford Linear Accelerator Center, SLAC-E158. The asymmetry in Møller scattering is
where me is the electron mass, E the energy of the incoming electron (in the reference frame of the other electron), is Fermi's constant, is the fine structure constant, is the scattering angle in the center of mass frame, and is the weak mixing angle, also known as the Weinberg angle.
QED computation
The Møller scattering can be calculated from the QED point-of-view, at the tree-level, with the help of the two diagrams shown on this page. These two diagrams are contributing at leading order from the QED point-of-view. If we are taking in account the weak force, which is unified with the electromagnetic force at high energy, then we have to add two tree-level diagram for the exchange of a boson. Here we will focus our attention on a strict tree-level QED computation of the cross section, which is rather instructive but maybe not the most accurate description from a physical point-of-view.
Before the derivation, we write the 4-momenta as (and for incoming electrons, and for outgoing electrons, and ):
The Mandelstam variables are:
These Mandelstam variables satisfy the identity: .
According to the two diagrams on this page, the matrix element of t-channel is
the matrix element of u-channel is
So the sum is
Therefore,
To calculate the unpolarized cross section, we average over initial spins and sum over final spins, with the factor 1/4 (1/2 for each incoming electron):
where we have used the relation . We would next calculate the traces.
The first term in the braces is
Here , and we have used the -matrix identity
and that trace of any product of an odd number of is zero.
Similarly, the second term is
Using the -matrix identities
and the identity of Mandelstam variables: , we get the third term
Therefore,
Substitute in the momentums we have set here, which are
Finally we get the unpolarized cross section
with and .
In the nonrelativistic limit, ,
In the ultrarelativistic limit, ,
References
External links
SLAC E158: Measuring the Electron's WEAK Charge
Quantum electrodynamics
Scattering theory | Møller scattering | [
"Chemistry"
] | 882 | [
"Scattering",
"Scattering theory"
] |
14,720,989 | https://en.wikipedia.org/wiki/Outer%20membrane%20protein%20OpcA | Outer membrane adhesin OpcA protein family consists of several Neisseria species specific outer membrane proteins. Neisseria meningitidis causes meningococcal meningitis and sepsis. Opc (formerly called 5C) is one of the major outer membrane proteins and has been shown to play an important role in meningococcal adhesion and invasion of epithelial and endothelial cells, mediating attachment to host cells by binding proteoglycan cell-surface receptors.
OpcA forms a 10-stranded beta-barrel with five highly mobile extracellular loops that protrude above the surface of the membrane. These extracellular loops combine to form a crevice in the external surface that is lined by positively charged residues, which is predicted to be a binding site for proteoglycan polysaccharides involved in pathogenesis. Conformational changes in the extracellular loops modulate the surface of OpcA, which could affect the proteoglycan binding site. These conformational changes could also lead to pore opening.
References
Protein domains
Protein families
Outer membrane proteins | Outer membrane protein OpcA | [
"Biology"
] | 231 | [
"Protein families",
"Protein domains",
"Protein classification"
] |
14,721,292 | https://en.wikipedia.org/wiki/Outer%20membrane%20protein%20G | Outer membrane protein G (OmpG) is a porin, a channel proteins in the outer membrane of Gram-negative bacteria.
Escherichia coli OmpG forms a 14-stranded beta-barrel and in contrast to most porins, appears to function as a monomer. The central pore of OmpG is wider than other E. coli porins and it is speculated that it may form a non-specific channel for the transport of larger oligosaccharides.
References
Protein domains
Protein families
Outer membrane proteins | Outer membrane protein G | [
"Biology"
] | 108 | [
"Protein families",
"Protein domains",
"Protein classification"
] |
14,721,436 | https://en.wikipedia.org/wiki/Geography%20of%20chess | Chess, a strategy board game, is played all over the world. The international governing body of chess is FIDE, established in 1924. Most national chess federations are now members of FIDE; several supranational chess organizations are also affiliated with FIDE.
National level: Current FIDE members
The table below lists the member federations of FIDE and their national championship. The number of grandmasters and players registered for each federation in the FIDE database, as of January 2024, are also indicated.
{| class="sortable wikitable"
! Country !! Zone !! National federation !! #GM !! #FIDE !! National championship
|-
| || 3.4 || Afghan National Chess Federation || 0 || 452 || Afghan Chess Championship
|-
| || 1.5a || || 1 || 972 || Albanian Chess Championship
|-
| || 4.1 || || 3 || 6,376 || Algerian Chess Championship
|-
| || 1.10 || || 3 || 175 || Andorran Chess Championship
|-
| || 4.5 || || 0 || 1,889 || Angolan Chess Championship
|-
| || 2.3.5 || Antigua and Barbuda Chess Federation || 0 || 52 || –
|-
| || 2.5 || Argentine Chess Federation|| 23 || 14,121 || Argentine Chess Championship
|-
| || 1.5b || Armenian Chess Federation|| 40 || 2,356 || Armenian Chess Championship
|-
| || 2.3.5 || Federashon di Ajedrez di Aruba || 0 || 182 || –
|-
| || 3.6 || Australian Chess Federation|| 10 || 7,276 || Australian Chess Championship
|-
| || 1.2a || Österreichischer Schachbund|| 11 || 9,553 || Austrian Chess Championship
|-
| || 1.8 || Azerbaijan Chess Federation|| 30 || 7,219 || Azerbaijani Chess Championship
|-
| || 2.3.5 || Bahamas Chess Federation|| 0 || 202 || Bahamian Chess Championship
|-
| || 3.1 || Bahrain Mind Sports Association || 0 || 791 || Bahraini Chess Championship
|-
| || 3.2 || Bangladesh Chess Federation|| 5 || 9,637 || Bangladeshi Chess Championship
|-
| || 2.3.5 || Barbados Chess Federation|| 0 || 688 || Barbadian Chess Championship
|-
| || 1.8 || Belarus Chess Federation|| 15 || 3,119 || Belarusian Chess Championship
|-
| || 1.1b || || 9 || 8,893 || Belgian Chess Championship
|-
| || 2.3.2 || Belize Chess Federation|| 0 || 9 || Belize National Chess Championship
|-
| || 2.3.5 || Bermuda Chess Association|| 0 || 193 || –
|-
| || 3.2 || Bhutan Chess Federation || 0 || 133 || Bhutan National Premier Chess Championship
|-
| || 2.4 || Federación Boliviana de Ajedrez|| 1 || 5,454 || Bolivian Chess Championship
|-
| || 1.2b || Sahovski Savez Bosne i Hercegovine|| 7 || 3,881 || Bosnia and Herzegovina Chess Championship
|-
| || 4.5 || Botswana Chess Federation || 0 || 2,888 || Botswana Chess Championship
|-
| || 2.4 || Confed. Brasileira de Xadrez|| 15 || 26,903 || Brazilian Chess Championship
|-
| || 2.3.5 || British Virgin Islands Chess Federation || 0 || 10 || –
|-
| || 3.3 || Brunei Chess Federation|| 0 || 366 || Brunei Chess Championship
|-
| || 1.4 || Bulgarian Chess Federation|| 35 || 6,120 || Bulgarian Chess Championship
|-
| || 4.2 || Comité National Burkinabé des Échecs || 0 || 46 || Burkinabé Chess Championship
|-
| || 4.3 || || 0 || 82 || Burundian Chess Championship
|-
| || 3.3 || Cambodian Chess Federation || 0 || 20 || Cambodian Chess Championship
|-
| || 4.3 || || 0 || 196 || Cameroonian Chess Championship
|-
| || 2.2 || Chess Federation of Canada|| 14 || 6,051 || Canadian Chess Championship
|-
| || 4.2 || || 0 || 270 || Cape Verdean Chess Championship
|-
| || 2.3.5 || Cayman Islands Chess Federation|| 0 || 68 || -
|-
| || 4.3 || Chess Federation of Central African Republic || 0 || 100 || Central African Chess Championship
|-
| || 4.3 || Chad Chess Federation|| 0 || 17 || -
|-
| || 2.5 || Fed. Deportiva Nacional De Ajedrez || 6 || 7,422 || Chilean Chess Championship
|-
| || 3.5 || Chinese Chess Association|| 51 || 5,024 || Chinese Chess Championship
|-
| || 3.3 || Chinese Taipei Chess Association|| 1 || 521 || Taiwanese Chess Championship
|-
| || 2.3.4 || Fed. Colombiana de Ajedrez|| 11 || 13,176 || Colombian Chess Championship
|-
| || 4.4 || || 0 || 44 || Comorian Chess Championship
|-
| || 4.3 || || 0 || 97 || Congolese Chess Championship
|-
| || 2.3.2 || Federacion Central de Ajedrez|| 1 || 6,264 || Costa Rican Chess Championship
|-
| || 1.2b || Hrvatski šahovski savez|| 30 || 11,726 || Croatian Chess Championship
|-
| || 2.3.3 || Fed. Cubana de Ajedrez || 26 || 3,518 || Cuban Chess Championship
|-
| || 1.10 || Cyprus Chess Federation|| 0 || 1,296 || Cypriot Chess Championship
|-
| || 1.4 || Šachový svaz České republiky|| 33 || 16,984 || Czech Chess Championship
|-
| || 1.3 || Dansk Skak Union|| 16 || 8,092 || Danish Chess Championship
|-
| || 4.4 || Djiboutian Chess Federation || 0 || 130 || Djiboutian Chess Championship
|-
| || 2.3.5 || Dominica Chess Federation|| 0 || 37 || -
|-
| || 2.3.5 || Federación Dominicana de Ajedrez|| 1 || 3,470 || Dominican Chess Championship
|-
| || 2.4 || Fed. Ecuatoriana de Ajedrez|| 1 || 5,560 || Ecuadorian Chess Championship
|-
| || 4.1 || Egyptian Chess Federation || 6 || 16,217 || Egyptian Chess Championship
|-
| || 2.3.2 || Federación Salvadoreña de Ajedrez|| 0 || 1,072 || Salvadoran Chess Championship
|-
| || 1.1a || English Chess Federation|| 40 || 13,885 || British Chess Championship
|-
| || 4.3 || Asociación Nacional de Ajedrez de Guinea Ecuatorial|| 0 || 65 || -
|-
| || 4.4 || Eritrea Chess Federation || 0 || 171 || Eritrean Chess Championship
|-
| || 1.7 || Eesti Maleliit|| 6 || 2,685 || Estonian Chess Championship
|-
| || 4.5 || Eswatini National Chess Federation || 0 || 288 || Swazi Chess Championship
|-
| || 4.4 || Ethiopian Chess Federation|| 0 || 1,071 || Ethiopian Chess Championship
|-
| || 1.10 || Talvsamband Føroya|| 1 || 532 || Faroese Chess Championship
|-
| || 3.6 || Fiji Chess Federation|| 0 || 435 || Fijian Chess Championship
|-
| || 1.3 || Suomen Keskusshakkiliitto|| 4 || 2,154 || Finnish Chess Championship
|-
| || 1.1b || French Chess Federation|| 55 || 98,861 || French Chess Championship
|-
| || 4.3 || Fédération Gabonaise des Échecs || 0 || 123 || Gabonese Chess Championship
|-
| || 4.2 || Gambia Chess Federation || 0 || 75 || Gambian Chess Championship
|-
| || 1.5b || Chess Federation of Georgia || 31 || 4,542 || Georgian Chess Championship
|-
| || 1.2a || Deutscher Schachbund|| 97 || 47,579 || German Chess Championship
|-
| || 4.2 || || 0 || 358 || Ghanaian Chess Championship
|-
| || 1.5a || Elliniki Skakistiki Omospondia|| 17 || 28,134 || Greek Chess Championship
|-
| || 2.3.5 || Grenada Chess Federation|| 0 || 21 || -
|-
| || 3.6 || Guam Chess Federation || 0 || 432 || –
|-
| || 2.3.2 || Fed. Nac. de Ajedrez de Guatemala || 0 || 764 || Guatemalan Chess Championship
|-
| || 1.10 || Guernsey Chess Federation|| 0 || 41 || Guernsey Chess Championship
|-
| || 2.3.5 || Guyana Chess Federation || 0 || 302 || Guyanese Chess Championship
|-
| || 2.3.5 || Haitian Chess Federation || 0 || 252 || Haitian Chess Championship
|-
| || 2.3.2 || Federación Nacional de Ajedrez de Honduras|| 0 || 1,318 || Honduran Chess Championship
|-
| || 3.3 || Hong Kong Chess Federation || 0 || 1,654 || Hong Kong Chess Championship
|-
| || 1.4 || Magyar Sakkszövetség|| 52 || 12,532 || Hungarian Chess Championship
|-
| || 1.3 || Skáksamband Íslands|| 15 || 3,021 || Icelandic Chess Championship
|-
| || 3.7 || All India Chess Federation|| 83 || 134,560 || Indian Chess Championship
|-
| || 3.3 || Persatuan Catur Seluruh Indonesia|| 4 || 3,364 || Indonesian Chess Championship
|-
| || 3.1 || Chess Fed. of Islamic Rep. of Iran|| 15 || 63,462 || Iranian Chess Championship
|-
| || 3.1 || Iraqi Chess Federation || 0 || 3,705 || Iraqi Chess Championship
|-
| || 1.1a || Irish Chess Union|| 1 || 2,971 || Irish Chess Championship
|-
| || 1.2b || Israel Chess Federation|| 49 || 7,538 || Israeli Chess Championship
|-
| || 1.1c || Federazione Scacchistica Italiana|| 18 || 32,862 || Italian Chess Championship
|-
| || 4.2 || || 0 || 556 || Ivorian Chess Championship
|-
| || 2.3.5 || Jamaica Chess Federation|| 0 || 1,073 || Jamaican Chess Championship
|-
| || 3.3 || || 0 || 609 || Japanese Chess Championship
|-
| || 1.10 || Jersey Chess Federation|| 0 || 223 || Jersey Chess Championship
|-
| || 3.1 || Royal Jordanian Chess Federation|| 1 || 2,908 || Jordanian Chess Championship
|-
| || 3.4 || Kazakhstan Chess Federation|| 18 || 13,681 || Kazakhstani Chess Championship
|-
| || 4.4 || || 0 || 4,797 || Kenyan Chess Championship
|-
| || 1.2b || Kosovo Chess Federation|| 0 || 875 || Kosovan Chess Championship
|-
| || 3.1 || Kuwait Chess Federation || 0 || 834 || Kuwaiti Chess Championship
|-
| || 3.4 || Chess Federation of the Kyrgyz Republic || 0 || 4,782 || Kyrgyzstani Chess Championship
|-
| || 3.3 || Lao Chess Federation || 0 || 202 || Laotian Chess Championship
|-
| || 1.7 || Latvijas Šaha Federācija
| 10 || 4,537 || Latvian Chess Championship
|-
| || 3.1 || Federation Libanaise des Echecs|| 0 || 2,480 || Lebanese Chess Championship
|-
| || 4.5 || Chess Federation of Lesotho || 0 || 434 || Lesotho Chess Championship
|-
| || 4.2 || Liberia Chess Federation || 0 || 328 || Liberian Chess Championship
|-
| || 4.1 || General Libyan Chess Federation || 0 || 1,881 || Libyan Chess Championship
|-
| || 1.10 || Liechtensteiner Schachverband || 0 || 45 || Liechtenstein Chess Championship
|-
| || 1.7 || Lietuvos šachmatų federacija|| 11 || 6,341 || Lithuanian Chess Championship
|-
| || 1.10 || Federation Luxembourgeoise des Echecs|| 0 || 875 || Luxembourg Chess Championship
|-
| || 3.3 || Grupo de Xadrez de Macau || 0 || 86 || –
|-
| || 4.4 || || 0 || 953 || Malagasy Chess Championship
|-
| || 4.5 || Chess Association of Malawi || 0 || 1,009 || Malawian Chess Championship
|-
| || 3.3 || Malaysian Chess Federation|| 0 || 15,533 || Malaysian Chess Championship
|-
| || 3.2 || Maldives Chess Federation || 0 || 573 || Maldivian Chess Championship
|-
| || 4.2 || || 0 || 135 || Malian Chess Championship
|-
| || 1.10 || Il-Federazzjoni Maltija tac-Cess|| 0 || 142 || Maltese Chess Championship
|-
| || 4.1 || || 0 || 839 || Mauritanian Chess Championship
|-
| || 4.4 || || 0 || 69 || Mauritian Chess Championship
|-
| || 2.3.1 || Fed. Nac. de Ajedrez de Mexico AC|| 5 || 14,128 || Mexican Chess Championship
|-
| || 1.8 || Federația de Șah a Republicii Moldova|| 7 || 1,524 || Moldovan Chess Championship
|-
| || 1.10 || || 3 || 303 || Monaco Chess Championship
|-
| || 3.3 || Mongolian Chess Federation|| 8 || 2,663 || Mongolian Chess Championship
|-
| || 1.5a || Montenegro Chess Federation|| 11 || 1,377 || Montenegrin Chess Championship
|-
| || 4.1 || Fed. Royale Marocaine des Echecs|| 1 || 4,879 || Moroccan Chess Championship
|-
| || 4.5 || || 0 || 634 || Mozambican Chess Championship
|-
| || 3.3 || Myanmar Chess Federation|| 0 || 2,354 || Myanmar Chess Championship
|-
| || 4.5 || Namibia Chess Federation|| 0 || 1,206 || Namibian Chess Championship
|-
| || 3.6 || Nauru Chess Federation || 0 || 69 || Nauruan Chess Championship
|-
| || 3.2 || Nepal Chess Association|| 0 || 4,986 || Nepalese Chess Championship
|-
| || 1.1b || Koninklijke Nederlandse Schaakbond|| 43 || 10,479 || Dutch Chess Championship
|-
| || 2.3.5 || Curaçao Chess Federation || 0 || 276 || Netherlands Antilles Chess Championship
|-
| || 3.6 || New Zealand Chess Federation|| 1 || 2,547 || New Zealand Chess Championship
|-
| || 2.3.2 || Federacion Nicaragüense de Ajedrez || 0 || 1,255 || Nicaraguan Chess Championship
|-
| || 4.2 || Niger Chess Federation|| 0 || 69 || -
|-
| || 4.2 || Nigeria Chess Federation|| 0 || 3,878 || Nigerian Chess Championship
|-
| || 1.2b || Chess Federation of Macedonia|| 10 || 1,749 || Macedonian Chess Championship
|-
| || 1.3 || Norges Sjakkforbund|| 18 || 8,552 || Norwegian Chess Championship
|-
| || 3.1 || Oman Chess Committee|| 0 || 2,595 || Omani Chess Championship
|-
| || 3.2 || Chess Federation of Pakistan || 0 || 2,963 || Pakistani Chess Championship
|-
| || 3.6 || Palau Chess Federation|| 0 || 267 || Palauan Chess Championship
|-
| || 3.1 || Palestine Chess Federation || 0 || 2,410 || Palestinian Chess Championship
|-
| || 2.3.2 || Fed. de Ajedrez de Panama|| 0 || 2,786 || Panamanian Chess Championship
|-
| || 3.6 || Papua New Guinea Chess Federation || 0 || 22 || Papua New Guinean Chess Championship
|-
| || 2.5 || Federacion Paraguaya de Ajedrez|| 5 || 1,724 || Paraguayan Chess Championship
|-
| || 2.4 || Federacion Peruana de Ajedrez|| 10 || 13,178 || Peruvian Chess Championship
|-
| || 3.3 || National Chess Federation of the Philippines|| 13 || 11,996 || Philippine Chess Championship
|-
| || 1.4 || Polish Chess Federation|| 50 || 43,572 || Polish Chess Championship
|-
| || 1.1c || Federação Portuguesa de Xadrez|| 4 || 8,047 || Portuguese Chess Championship
|-
| || 2.3.5 || Fed. de Ajedrez de Puerto Rico|| 0 || 1,316 || Puerto Rican Chess Championship
|-
| || 3.1 || Qatar Chess Association|| 3 || 186 || Qatari Chess Championship
|-
| || 1.4 || Federația Română de Șah|| 26 || 13,041 || Romanian Chess Championship
|-
| || 3.8 || Chess Federation of Russia|| 185 || 120,128 || Russian Chess Championship
|-
| || 4.4 || || 0 || 192 || Rwandan Chess Championship
|-
| || 2.3.5 || Saint Kitts and Nevis Chess Federation|| 0 || 12 || -
|-
| || 2.3.5 || Saint Lucia Chess Federation|| 0 || 70 || -
|-
| || 2.3.5 || Saint Vincent and the Grenadines Chess Federation|| 0 || 21 || -
|-
| || 1.10 || Federazione Sammarinese degli Scacchi|| 0 || 54 || Sammarinese Chess Championship
|-
| || 4.3 || || 0 || 170 || São Tomé and Príncipe Chess Championship
|-
| || 3.1 || Saudi Chess Association|| 0 || 3,516 || Saudi Arabian Chess Championship
|-
| || 1.1a || Chess Scotland|| 6 || 1,468 || Scottish Chess Championship
|-
| || 4.2 || || 1 || 194 || Senegalese Chess Championship
|-
| || 1.5a || Chess Federation of Serbia || 53 || 12,767 || Serbian Chess Championship
|-
| || 4.4 || Seychelles Chess Federation || 0 || 79 || Seychelles Chess Championship
|-
| || 4.2 || Sierra Leone Chess Federation || 0 || 79 || Sierra Leonean Chess Championship
|-
| || 3.3 || Singapore Chess Federation|| 5 || 5,618 || Singaporean Chess Championship
|-
| || 1.4 || Slovenský šachový zväz|| 14 || 9,528 || Slovak Chess Championship
|-
| || 1.2a || Šahovska Zveza Slovenije|| 14 || 7,053 || Slovenian Chess Championship
|-
| || 3.6 || Solomon Islands Chess Federation || 0 || 122 || Solomon Island Chess Championship
|-
| || 4.4 || Somali Chess Federation || 0 || 146 || Somali Chess Championship
|-
| || 4.5 || Chess South Africa|| 1 || 8,599 || South African Chess Championship
|-
| || 3.3 || Korea Chess Federation|| 1 || 2,416 || South Korean Chess Championship
|-
| || 4.4 || South Sudan Chess Federation || 0 || 502 || South Sudanese Chess Championship
|-
| || 1.1c || Federacion Espanola de Ajedrez|| 59 || 74,610 || Spanish Chess Championship
|-
| || 3.2 || Chess Federation of Sri Lanka || 0 || 21,776 || Sri Lankan Chess Championship
|-
| || 4.4 || Sudan Chess Federation || 0 || 1,664 || Sudanese Chess Championship
|-
| || 2.3.5 || De Surinaamse Schaakbond|| 0 || 637 || Surinamese Chess Championship
|-
| || 1.3 || Sveriges Schackförbund|| 25 || 8,537 || Swedish Chess Championship
|-
| || 1.2a || Schweizerischer Schachbund|| 11 || 5,854 || Swiss Chess Championship
|-
| || 3.1 || Syrian Arab Chess Federation || 0 || 1,531 || Syrian Chess Championship
|-
| || 3.4 || Federazijai Shakhmati Tajikistan || 1 || 409 || Tajikistani Chess Championship
|-
| || 4.4 || Tanzania Chess Association || 0 || 242 || Tanzanian Chess Championship
|-
| || 3.3 || Thailand Chess Association|| 0 || 2,087 || Thai Chess Championship
|-
| || 3.3 || Federação Xadrez de Timor-Leste || 0 || 594 || Timorese Chess Championship
|-
| || 4.2 || || 0 || 546 || Togolese Chess Championship
|-
| || 2.3.5 || Trinidad and Tobago Chess Association|| 0 || 1,326 || Trinidad and Tobago Chess Championship
|-
| || 4.1 || || 3 || 4,933 || Tunisian Chess Championship
|-
| || 1.5a || Turkish Chess Federation|| 14 || 49,282 || Turkish Chess Championship
|-
| || 3.4 || Turkmenistan Chess Federation || 7 || 1,347 || Turkmen Chess Championship
|-
| || 4.4 || Uganda Chess Federation || 0 || 3,870 || Ugandan Chess Championship
|-
| || 1.9 || Ukrainian Chess Federation|| 88 || 18,518 || Ukrainian Chess Championship
|-
| || 3.1 || UAE Chess Federation|| 2 || 3,244 || Emirati Chess Championship
|-
| || 2.1 || United States Chess Federation|| 106 || 25,204 || U.S. Chess Championship U.S. Women's Chess Championship
|-
| || 2.3.5 || US Virgin Islands Chess Federation|| 0 || 73 || –
|-
| || 2.5 || Federación Uruguaya de Ajedrez|| 3 || 2,453 || Uruguayan Chess Championship
|-
| || 3.4 || Chess Federation of Uzbekistan|| 17 || 3,304 || Uzbekistani Chess Championship
|-
| || 2.3.5 || Fed. Venezolana de Ajedrez|| 1 || 11,363 || Venezuelan Chess Championship
|-
| || 3.3 || Vietnam Chess Federation|| 13 || 6,065 || Vietnamese Chess Championship
|-
| || 1.1a || Welsh Chess Union|| 0 || 830 || Welsh Chess Championship
|-
| || 3.1 || Yemen Chess Association || 0 || 656 || Yemeni Chess Championship
|-
| || 4.5 || Chess Federation of Zambia || 1 || 2,932 || Zambian Chess Championship
|-
| || 4.5 || Zimbabwe Chess Federation|| 0 || 1,863 || Zimbabwean Chess Championship
|}
In addition, the Isle of Man Chess Association (since 2020) and the Chess League of New Caledonia (Ligue d'Echecs de Nouvelle-Calédonie, since 2023) are affiliated organizations.
Former FIDE members
The list below includes nations that no longer exist as well as national federations that are currently not members of FIDE.
{| class="sortable wikitable"
! Country !! National federation !! National championship
|-
| || || Czechoslovak Chess Championship
|-
| || USSR Chess Federation || USSR Chess Championship
|-
| || || Yugoslav Chess Championship
|-
|}
Supranational level
{| class="sortable wikitable"
! Countries (zone) !! Federation !! Official Website !! Championships
|-
| Europe (1) || European Chess Union (ECU) || || Individual, Youth, Junior, Senior and Team
|-
| America (2) || Confederation of Chess for America (CCA) || || Pan American Chess Championship
|-
| Asia (3) || Asian Chess Federation (ACF) || || Asian Chess Championship, Asian Senior Chess Championship
|-
| Africa (4) || African Chess Confederation (ACC) || || African Chess Championship
|-
| Arab world || Arab Chess Federation (ACF) || || Arab Chess Championship
|-
| ASEAN || ASEAN Chess Confederation || || –
|-
| Commonwealth of Nations || Commonwealth Chess Association (CCA) || || Commonwealth Chess Championship
|-
| European microstates || – || – || European Small Nations Chess Championship
|-
| Francophone countries || International Chess Federation of French-speaking countries (AIDEF) || || AIDEF Chess Championship
|-
| Ibero-America || Iberoamerican Chess Federation (FIBDA) || || Iberoamerican Chess Championship
|-
| Mediterranean countries || Mediterranean Chess Association || || Mediterranean Chess Championship
|-
| Nordic countries || Nordic Chess Federation || || Nordic Chess Championship
|-
| Oceania (3.6) || Oceania Chess Confederation (OCC) || || Oceania Chess Championship
|-
| South America || - || - || South American Chess Championship
|}
References
Chess organizations
Geography
Chess-related lists
Human geography | Geography of chess | [
"Environmental_science"
] | 6,308 | [
"Environmental social science",
"Human geography"
] |
14,721,784 | https://en.wikipedia.org/wiki/Coupon%20collector%27s%20problem | In probability theory, the coupon collector's problem refers to mathematical analysis of "collect all coupons and win" contests. It asks the following question: if each box of a given product (e.g., breakfast cereals) contains a coupon, and there are n different types of coupons, what is the probability that more than t boxes need to be bought to collect all n coupons? An alternative statement is: given n coupons, how many coupons do you expect you need to draw with replacement before having drawn each coupon at least once? The mathematical analysis of the problem reveals that the expected number of trials needed grows as . For example, when n = 50 it takes about 225 trials on average to collect all 50 coupons.
Solution
Via generating functions
By definition of Stirling numbers of the second kind, the probability that exactly T draws are needed isBy manipulating the generating function of the Stirling numbers, we can explicitly calculate all moments of T:In general, the k-th moment is , where is the derivative operator .
For example, the 0th moment isand the 1st moment is , which can be explicitly evaluated to , etc.
Calculating the expectation
Let time T be the number of draws needed to collect all n coupons, and let ti be the time to collect the i-th coupon after i − 1 coupons have been collected. Then . Think of T and ti as random variables. Observe that the probability of collecting a coupon is . Therefore, has geometric distribution with expectation . By the linearity of expectations we have:
Here Hn is the n-th harmonic number. Using the asymptotics of the harmonic numbers, we obtain:
where is the Euler–Mascheroni constant.
Using the Markov inequality to bound the desired probability:
The above can be modified slightly to handle the case when we've already collected some of the coupons. Let k be the number of coupons already collected, then:
And when then we get the original result.
Calculating the variance
Using the independence of random variables ti, we obtain:
since (see Basel problem).
Bound the desired probability using the Chebyshev inequality:
Tail estimates
A stronger tail estimate for the upper tail be obtained as follows. Let denote the event that the -th coupon was not picked in the first trials. Then
Thus, for , we have . Via a union bound over the coupons, we obtain
Extensions and generalizations
Pierre-Simon Laplace, but also Paul Erdős and Alfréd Rényi, proved the limit theorem for the distribution of T. This result is a further extension of previous bounds. A proof is found in.
which is a Gumbel distribution. A simple proof by martingales is in the next section.
Donald J. Newman and Lawrence Shepp gave a generalization of the coupon collector's problem when m copies of each coupon need to be collected. Let Tm be the first time m copies of each coupon are collected. They showed that the expectation in this case satisfies:
Here m is fixed. When m = 1 we get the earlier formula for the expectation.
Common generalization, also due to Erdős and Rényi:
In the general case of a nonuniform probability distribution, according to Philippe Flajolet et al.
This is equal to
where m denotes the number of coupons to be collected and PJ denotes the probability of getting any coupon in the set of coupons J.
See also
McDonald's Monopoly – an example of the coupon collector's problem that further increases the challenge by making some coupons of the set rarer
Watterson estimator
Birthday problem
Notes
References
.
.
.
.
.
.
.
External links
"Coupon Collector Problem" by Ed Pegg, Jr., the Wolfram Demonstrations Project. Mathematica package.
How Many Singles, Doubles, Triples, Etc., Should The Coupon Collector Expect?, a short note by Doron Zeilberger.
Articles containing proofs
Gambling mathematics
Probability theorems
Probability problems | Coupon collector's problem | [
"Mathematics"
] | 826 | [
"Theorems in probability theory",
"Probability problems",
"Mathematical problems",
"Articles containing proofs",
"Mathematical theorems"
] |
14,721,851 | https://en.wikipedia.org/wiki/Germanium%20iodides | Germanium iodides are inorganic compound with the formula GeIx. Two such compounds exist: germanium(II) iodide, , and germanium(IV) iodide .
Germanium(II) iodide is an orange-yellow crystalline solid which decomposes on melting. Its specific density is 5.37 and it can be sublimed at 240 °C in a vacuum. It can be prepared by reducing germanium(IV) iodide with aqueous hypophosphorous acid in the presence of hydroiodic acid. It is oxidised by a solution of potassium iodide in hydrochloric acid to germanium(IV) iodide. It reacts with acetylene at 140 °C to form an analogue of cyclohexa-1,4-diene in which the methylene groups, , are replaced with diiodogermylene groups, .
Germanium(IV) iodide is an orange-red crystalline solid with melting point 144 °C and boiling point 440 °C (with decomposition). Its specific density is 4.32. It is soluble in non-polar solvents like carbon disulfide, chloroform or benzene, but hydrolyses readily.
Mixed anion compound germanide iodides are also known.
References
Germanium compounds
Iodides
Metal halides | Germanium iodides | [
"Chemistry"
] | 283 | [
"Inorganic compounds",
"Metal halides",
"Salts"
] |
14,721,984 | https://en.wikipedia.org/wiki/Polymerase%20chain%20reaction%20inhibitors | PCR inhibitors are any factor which prevent the amplification of nucleic acids through the polymerase chain reaction (PCR). PCR inhibition is the most common cause of amplification failure when sufficient copies of DNA are present. PCR inhibitors usually affect PCR through interaction with DNA or interference with the DNA polymerase. Inhibitors can escape removal during the DNA purification procedure by binding directly to single or double-stranded DNA. Alternatively, by reducing the availability of cofactors (such as Mg2+) or otherwise interfering with their interaction with the DNA polymerase, PCR is inhibited.
In a multiplex PCR reaction, it is possible for the different sequences to suffer from different inhibition effects to different extents, leading to disparity in their relative amplifications.
Types of inhibitors
Inhibitors may be present in the original sample, such as blood, fabrics, tissues and soil but may also be added as a result of the sample processing and DNA extraction techniques used. Excess salts including KCl and NaCl, ionic detergents such as sodium deocycholate, sarkosyl and SDS, ethanol, isopropanol and phenol among others, all contribute via various inhibitory mechanisms, to the reduction of PCR efficiency.
Quantifying extent of inhibition
In order to try to assess the extent of inhibition that occurs in a reaction, a control can be performed by adding a known amount of a template to the investigated reaction mixture (based on the sample under analysis). By comparing the amplification of this template in the mixture to the amplification observed in a separate experiment in which the same template is used in the absence of inhibitors, the extent of inhibition in the investigated reaction mixture can be inferred. Of course, if any part of the inhibition occurring in the sample-derived reaction mixture is sequence-specific, then this method will yield an underestimate of the inhibition as it applies to the investigate sequence(s).
Preventing PCR inhibition
Sample collection
The method of sample acquisition can be refined to avoid unnecessary collection of inhibitors. For example, in forensics, swab-transfer of blood on fabric or saliva on food, may prevent or reduce contamination with inhibitors present in the fabric or food.
DNA purification
Techniques exist and kits are commercially available to enable extraction of DNA to the exclusion of some inhibitors.
PCR reaction components
As well as methods for the removal of inhibitors from samples before PCR, some DNA polymerases offer varying resistance to different inhibitors and increasing the concentration of the chosen DNA polymerase also confers some resistance to polymerase-targeted inhibitors.
For PCR based on blood samples, the addition of bovine serum albumin reduces the effect of some inhibitors on PCR.
See also
PCR optimization
References
DNA
Polymerase chain reaction | Polymerase chain reaction inhibitors | [
"Chemistry",
"Biology"
] | 568 | [
"Biochemistry methods",
"Genetics techniques",
"Polymerase chain reaction"
] |
14,722,151 | https://en.wikipedia.org/wiki/Z%284430%29 | Z(4430) is a mesonic resonance discovered by the Belle experiment. It has a mass of . The resonant nature of the peak has been confirmed by the LHCb experiment with a significance of at least 13.9 σ. The particle is charged and is thought to have a quark content of , making it a tetraquark candidate. It has the spin-parity quantum numbers JP = 1+.
The particle joins the X(3872), Zc(3900) and Y(4140) as exotic hadron candidates observed by multiple experiments, although it is the first to be confirmed as a resonance.
See also
XYZ particle
References
External links
Major harvest of four-leaf clover
Mesons
2014 in science
Subatomic particles with spin 1 | Z(4430) | [
"Physics"
] | 163 | [
"Particle physics stubs",
"Particle physics"
] |
14,722,565 | https://en.wikipedia.org/wiki/APAF1 | Apoptotic protease activating factor 1, also known as APAF1, is a human homolog of C. elegans CED-4 gene.
Function
The protein was identified in the laboratory of Xiaodong Wang as an activator of caspase-3 in the presence of cytochromeC and dATP. This gene encodes a cytoplasmic protein that forms one of the central hubs in the apoptosis regulatory network. This protein contains (from the N terminal) a caspase recruitment domain (CARD), an ATPase domain (NB-ARC), few short helical domains and then several copies of the WD40 repeat domain. Upon binding cytochrome c and dATP, this protein forms an oligomeric apoptosome. The apoptosome binds and cleaves Procaspase-9 protein, releasing its mature, activated form. The precise mechanism for this reaction is still debated though work published by Guy Salvesen suggests that the apoptosome may induce caspase-9 dimerization and subsequent autocatalysis. Activated caspase-9 stimulates the subsequent caspase cascade that commits the cell to apoptosis.
Alternative splicing results in several transcript variants encoding different isoforms.
Structure
APAF1 contains a CARD domain with a Greek key motif composed of six helices, a Rossman fold nucleotide binding domains, a short helical motif and a winged-helix domain.
Interactions
APAF1 has been shown to interact with:
APIP,
BCL2-like 1
Caspase-9,
HSPA4, and
NLRP1.
References
Further reading
Programmed cell death
Apoptosis | APAF1 | [
"Chemistry",
"Biology"
] | 357 | [
"Senescence",
"Programmed cell death",
"Apoptosis",
"Signal transduction"
] |
14,722,571 | https://en.wikipedia.org/wiki/Analog%20sequencer | An analog sequencer is a music sequencer constructed from analog (analogue) electronics, invented in the first half of the 20th century.
Raymond Scott designed and constructed some of the first electro-mechanical music sequencers in the 1940s. The first electronic sequencer was invented by Raymond Scott, using thyratrons and relays. Incidentally in 1951, computer music was started from the music sequencing, and later its applicable fields were expanded into the music composition and sound generation. However, the RCA Mark II Sound Synthesizer in 1957 was still indirectly controlled via punch-tape system similar to piano rolls, a kind of mechanical sequencer.
Also, in earlier electronic music, artists used sound-on-film technology to generate sound waves as well as control sequences of notes.
At its most basic, an analog sequencer consists of a bank of potentiometers and a "clock" (pulse generator) connected to a sequencer, which steps through these potentiometers one at a time and then cycles back to the beginning. The output from the above is fed (as a control voltage and gate pulse) to a synthesizer. By "tuning" the potentiometers, a short repetitive rhythmic motif or riff can be set up.
The most commonly used analog sequencer was the Moog 960, which was a module of the Moog modular synthesizer. It consisted of three parallel banks of eight potentiometers: the three banks could either steer three different Voltage-controlled oscillators (VCOs) to allow three-note chords in the sequence, or (for example) one row could steer pitch while the second row is patched through to the filter cutoff or VCA volume, and a third steers filter cutoff for a white noise generator (thus creating an extremely primitive electronic drum track).
Under each of the eight steps, a switch offered three options: play this step, skip this step, or loop back to the beginning. To avoid the monotony of endlessly repeated sequences, pioneering electronic musicians like Chris Franke of Tangerine Dream and Michael Hoenig would manipulate these switches in real time during performance, adding and dropping notes and beats from a sequence. Also, the "pitch" row can be patched to two or more oscillators tuned to intervals, and the oscillators mixed in and out one at a time.
Good examples of all these techniques can be heard on the Phaedra, Rubycon, Ricochet, and Encore albums of Tangerine Dream, as well as on Departure from the Northern Wasteland by Michael Hoenig.
By synchronizing two sequencers, and manipulating them individually, swirling polyrhythmic phasing patterns (as introduced in minimalist music by Steve Reich) can be set up. The title track of the Michael Hoenig album (mentioned above) is an excellent example.
An additional module (Moog 962) allowed "daisy-chaining" the three rows to form one longer 24-step sequence. In addition, a switch on the 960 itself let the third (bottom) row be used for note lengths.
The output voltage of the sequencer can be added to the output voltage of a keyboard controller, and the latter used to transpose the sequence on the fly. Klaus Schulze was particularly fond of this technique, which lays the musical foundation for tracks like "Bayreuth Return" from Timewind, "Floating" from Moondawn, and any rhythmic piece from Klaus Schulze's "analog" years. Vangelis and Jean-Michel Jarre likewise availed themselves of this technique.
Apart from a temperature-controlled environment after warmup, pitch stability could be problematic. On the famous opening of Phaedra, the sequencer had drifted out of tune, and one can clearly hear Chris Franke retuning the sequence by ear in real time.
In addition to the 1027 module, which is a conventional 3x10 step sequencer, the ARP 2500 was often equipped with the 1050 Mix-Sequencer module. Unlike contemporary sequencers that only generated voltages, the 1050 could also sequence audio signals. This allowed each step of the sequence to come from a completely different sound source. The 8 positions could run in sequence or be split into two independent four-step sequencers. It's easily identified by its vertical column of 8 square white buttons that light up to indicate the active step(s).
Analog sequencers, have in some respects, been replaced by digital devices and software implementations. However, there is a continued interest by modular analog synthesists, who appreciate the real time control offered by the analog sequencer as evidenced by the 'Oberkorn' machine by Analog Solutions, amongst others.
Various analog sequencers
See also
Music sequencer
Modular synthesizer
Notes
External links
Silicon sequences, a video clip demonstrating realtime sequence(r) manipulation
Images and specifications of Moog 960 clone
Synthesiser modules
Music sequencers | Analog sequencer | [
"Engineering"
] | 1,009 | [
"Music sequencers",
"Automation"
] |
14,722,619 | https://en.wikipedia.org/wiki/Activating%20transcription%20factor%202 | Activating transcription factor 2, also known as ATF2, is a protein that, in humans, is encoded by the ATF2 gene.
Function
This gene encodes a transcription factor that is a member of the leucine zipper family of DNA-binding proteins. This protein binds to the cAMP-responsive element (CRE), an octameric palindrome. The protein forms a homodimer or heterodimer with c-Jun. The protein is also a histone acetyltransferase (HAT) that specifically acetylates histones H2B and H4 in vitro; thus, it may represent a class of sequence-specific factors that activate transcription by direct effects on chromatin components. Additional transcript variants have been identified but their biological validity has not been determined.
The gene atf2 is located at human chromosome 2q32. The protein ATF-2 has 505 amino acids. Studies in mice indicate a role for ATF-2 in the development of nervous system and the skeleton. ATF-2 is normally activated in response to signals that converge on stress-activated protein kinases p38 and JNK. ATF-2 phosphorylation in response to treatment of cells with tumor promoter phorbol ester has been demonstrated.
Several studies implicate abnormal activation of ATF-2 in growth and progression of mammalian skin tumors. ATF-2 may mediate oncogenesis caused by mutant Ras protein and regulate maintenance of the aggressive cancer phenotype of some types of epithelial cells.
ATF2 has also been shown to be phosphorylated at its C-terminal (serine 472 and 480 in mouse; serine 490 and 498 in human) by ATM upon double-stranded breaks. Mice with mutations of these two serines are sensitive to irradiation and easier to tumorigenesis under p53 knockout background.
Interactions
Activating transcription factor 2 has been shown to interact with
C-jun,
Casein kinase 2, alpha 1,
CREB binding protein,
CSNK2A2,
JDP2,
MAPK14,
MAPK8,
Mothers against decapentaplegic homolog 3
NCOA6,
RUVBL2,
UBE2I.
See also
Activating transcription factor
References
External links
Further reading
External links
PDBe-KB provides an overview of all the structure information available in the PDB for Human Cyclic AMP-dependent transcription factor ATF-2
Transcription factors
Moonlighting proteins | Activating transcription factor 2 | [
"Chemistry",
"Biology"
] | 513 | [
"Induced stem cells",
"Gene expression",
"Transcription factors",
"Signal transduction"
] |
14,722,667 | https://en.wikipedia.org/wiki/GRIN1 | Glutamate [NMDA] receptor subunit zeta-1 is a protein that in humans is encoded by the GRIN1 gene.
The protein encoded by this gene is a critical subunit of N-methyl-D-aspartate receptors, members of the glutamate receptor channel superfamily which are heteromeric protein complexes with multiple subunits arranged to form a ligand-gated ion channel. These subunits play a key role in the plasticity of synapses, which is believed to underlie memory and learning. The gene consists of 21 exons and is alternatively spliced, producing transcript variants differing in the C-terminus. The sequence of exon 5 is identical in vertebrates, with exon 5 splicing demonstrated in human, mouse and rat. Cell-specific factors are thought to control expression of different isoforms, possibly contributing to the functional diversity of the subunits.
See also
NMDA receptor
References
Further reading
Ionotropic glutamate receptors
Ion channels | GRIN1 | [
"Chemistry"
] | 205 | [
"Neurochemistry",
"Ion channels"
] |
14,722,972 | https://en.wikipedia.org/wiki/Colony%20stimulating%20factor%201%20receptor | Colony stimulating factor 1 receptor (CSF1R), also known as macrophage colony-stimulating factor receptor (M-CSFR), and CD115 (Cluster of Differentiation 115), is a cell-surface protein encoded by the human CSF1R gene (known also as c-FMS). CSF1R is a receptor that can be activated by two ligands: colony stimulating factor 1 (CSF-1) and interleukin-34 (IL-34). CSF1R is highly expressed in myeloid cells, and CSF1R signaling is necessary for the survival, proliferation, and differentiation of many myeloid cell types in vivo and in vitro. CSF1R signaling is involved in many diseases and is targeted in therapies for cancer, neurodegeneration, and inflammatory bone diseases.
Gene
In the human genome, the CSF1R gene is located on chromosome 5 (5q32), and in mice the Csf1r gene is located on chromosome 18 (18D). CSF1R is 60.002 kilobases (kbs) in length. Hematopoietic stem cells express CSF1R at low levels, but CSF1R is highly expressed in more differentiated myeloid cell types such as monocytes, macrophages, osteoclasts, myeloid dendritic cells, microglia, and Paneth cells. CSF1R expression is controlled by two alternative promoters that are active in specific tissue types. Exon 1 of CSF1R is specifically transcribed in trophoblastic cells whereas exon 2 is specifically transcribed in macrophages. Activation of CSF1R transcription is regulated by several transcription factors including Ets and PU.1. Macrophage expression of the CSF1R gene is regulated by the promoter upstream of exon 2 and another highly conserved region termed the fms intronic regulatory element (FIRE). The FIRE is a 250-bp region in intron 2 that regulates transcript elongation during transcription of CSF1R in macrophages. Specific deletion of FIRE prevents differentiation of only specific macrophage types such as brain microglia and macrophages in the skin, kidney, heart, and peritoneum whereas deletion of the entire mouse Csf1r gene widely prevents macrophage differentiation, causing profound developmental defects. Additionally, the first intron of the CSF1R gene contains a transcriptionally inactive ribosomal protein L7 processed pseudogene, oriented in the opposite direction to the CSF1R gene.
Protein
CSF1R, the protein encoded by the CSF1R gene is a tyrosine kinase transmembrane receptor and member of the CSF1/PDGF receptor family of tyrosine-protein kinases. CSF1R has 972 amino acids, is predicted to have a molecular weight of 107.984 kilodaltons, and is composed of an extracellular and a cytoplasmic domain. The extracellular domain has 3 N-terminal immunoglobulin (Ig) domains (D1-D3) which bind ligand, 2 Ig domains (D4-D5) which stabilize the ligand, a linker region, and a single-pass transmembrane helix. The cytoplasmic domain has a juxtamembrane domain and tyrosine kinase domain that is interrupted by a kinase insert domain. At rest, the juxtamembrane domain of CSF1R enters an autoinhibitory position to prevent signaling of the CSF1R cytosolic domain. Upon binding of ligand to extracellular Ig domains, CSF1R dimerizes noncovalently and autophosphorylates several tyrosine residues. This first wave of CSF1R tyrosine phosphorylation creates phosphotyrosine-binding domains to which effector proteins can bind and initiate various cellular responses. Many proteins become tyrosine phosphorylated in response to CSF1R signaling (Table 1) including p85, Cbl, and Gab3 which are important for survival, differentiation, chemotaxis, and actin cytoskeleton of myeloid cells. The first wave of tyrosine phosphorylation also leads to the covalent dimerization of CSF1R via disulfide bonds. Covalent CSF1R dimerization is important for a series of modifications to CSF1R itself including a second wave of tyrosine phosphorylation, serine phosphorylation, ubiquitination, and eventually endocytosis which terminates signaling by trafficking the ligand-CSF1R complex to the lysosome for degradation. Colony stimulating factor 1 (CSF-1) and interleukin-34 (IL-34) are both CSF1R ligands. Both ligands regulate myeloid cell survival, proliferation, and differentiation, but CSF-1 and IL-34 differ in their structure, distribution in the body, and the specific cellular signaling cascades triggered upon binding to CSF1R.
Function
Osteoclasts
Osteoclast are multi-nucleated cells that absorb and remove bone which is critical for growth of new bones and maintenance of bone strength. Osteoclasts are critical for the bone remodeling cycle which is achieved by the building of bone by osteoblasts, reabsorption by osteoclasts, and remodeling by osteoblasts. Osteoclasts precursor cells and mature osteoclast require stimulation of CSF1R for survival. Blockage of CSF1R signaling prevents osteoclast precursor cells from proliferating, maturing, and fusing into multi-nucleated cells. Stimulation of CSF1R promotes osteoclastogenesis (differentiation of monocytes into osteoclasts). CSF1R signaling in osteoclasts precursors promotes survival by upregulation of the Bcl-X(L) protein, an inhibitor of pro-apoptotic caspase-9. CSF1R signaling in mature osteoclasts promotes survival by stimulating mTOR/S6 kinase and the Na/HCO3 co-transporter, NBCn1. CSF1R signaling also directly regulates osteoclast function. Osteoclasts migrate along the bone surface, then adhere to the bone to degrade and reabsorb the bone matrix. CSF1R signaling positively regulates this behavior, increasing osteoclast chemotaxis and bone reabsorption.
Monocytes and macrophages
Monocytes and macrophages are mononuclear phagocytes. Monocytes circulate in the blood and are capable of differentiating into macrophages or dendritic cells, and macrophages are terminally differentiated tissue-resident cells. CSF1R signaling is necessary for differentiation of microglia and Langerhans cells which are derived from yolk sac progenitor cells with high expression of CSF1R. CSF1R signaling is only partially required for other tissue macrophages, and it is not necessary for monocytopoiesis (production of monocytes and macrophages) from hematopoietic stem cells. Macrophages of thymus and lymph nodes are almost completely independent of CSF1R signaling. In macrophages whose survival is fully or partially dependent on CSF1R signaling, CSF1R promotes survival by activating PI3K. CSF1R signaling also regulates macrophage function. One function of CSF1R signaling is to promote tissue protection and healing following damage. Damage to the kidney causes upregulation of CSF-1 and CSF1R in tubular epithelial cells. This promotes proliferation and survival of injured tubular epithelial cells and promotes anti-inflammatory phenotypes in resident macrophage to promote kidney healing. Lastly, activation of CSF1R is a strong chemokinetic signal, inducing macrophage polarization and chemotaxis towards the source of CSF1R ligand. This macrophage response requires rapid morphological changes which is achieved by remodeling of the actin cytoskeleton via the Src/ Pyk2 and PI3K signaling pathways.
Microglia
Microglia are the tissue-resident phagocytes of the central nervous system. CSF1R signaling promotes migration of primitive microglia precursor cells from the embryonic yolk sac to the developing brain prior to formation of the blood-brain-barrier. In perinatal development, microglia are instrumental in synaptic pruning, a process in which microglia phagocytose weak and inactive synapses via binding of microglial complement receptor 3 (CR3) (complex of CD11b and CD18) to synapse-bound iC3b. Csf1r loss-of-function inhibits synaptic pruning and leads to excessive non-functional synapses in the brain. In adulthood, CSF1R is required for the proliferation and survival of microglia. Inhibition of CSF1R signaling in adulthood causes near-complete (>99%) depletion (death) of brain microglia, however reversal of CSF1R inhibition stimulates remaining microglia to proliferate and repopulate microglia-free niches in the brain. Production of CSF1R ligands CSF-1 and IL-34 is increased in the brain following injury or viral infection, which directs microglia to proliferate and execute immune responses.
Neural progenitor cells
CSF1R signaling has been found to play important roles in non-myeloid cells such as neural progenitor cells, multipotent cells that are able to self-renew or terminally differentiate into neurons, astrocytes and oligodendrocytes. Mice with Csf1r loss-of-function have a significantly more neural progenitor cells in generative zones and fewer matured neurons in forebrain laminae due to failure of progenitor cell maturation and radial migration. These phenotypes were also seen in animals with Csf1r conditional knock-out specifically in neural progenitor cells, suggesting that CSF1R signaling by neural progenitor cells is important for maturation of certain neurons. Studies using cultured neural progenitor cells also show that CSF1R signaling stimulates neural progenitor cells maturation.
Germline cells
CSF1R is expressed in oocytes, the trophoblast, and fertilized embryos prior to implantation in the uterus. Studies using early mouse embryos in vitro have shown that activation of CSF1R stimulates formation of the blastocyst cavity and enhances the number of trophoblast cells. Csf1r loss-of-function mice exhibit several reproductive system abnormalities in the estrous cycle and ovulation rates as well as reduced antral follicles and ovarian macrophages. It is not clear whether ovulation dysfunction in Csf1r loss-of-function mice is due to loss of the protective effects of ovarian macrophages or loss of CSF1R signaling in oocytes themselves.
Clinical significance
Bone disease
Bone remodeling is regulated by mutual cross-regulation between osteoclasts and osteoblasts. As a result, the dysfunction of CSF1R signaling directly affects the reabsorption (osteoclasts) and indirectly affects bone deposition (osteoblasts). In inflammatory arthritis conditions such as rheumatoid arthritis, psoriatic arthritis, and Crohn's disease, proinflammatory cytokine TNF-α is secreted by synovial macrophages which stimulates stromal cells and osteoblasts to produce CSF-1. Increased CSF-1 promotes proliferation of osteoclasts and osteoclast precursors and increases osteoclast bone reabsorption. This pathogenic increase in osteoclast activity causes abnormal bone loss or osteolysis. In animal models of rheumatoid arthritis, administration of CSF-1 increases the severity of disease whereas Csf1r loss-of-function reduces inflammation and joint erosion. In a rare bone disease called Gorham‐Stout disease, elevated production of CSF-1 by lymphatic endothelial cells similarly produces excessive osteoclastogenesis and osteolysis. Additionally, postmenopausal loss of estrogen has also been found to impact CSF1R signaling and cause osteoporosis. Estrogen deficiency causes osteoporosis by upregulating production of TNF-α by activated T cells. As in inflammatory arthritis, TNF-α stimulates stromal cells to produce CSF-1 which increases CSF1R signaling in osteoclasts.
Cancer
Tumor-associated macrophages (TAMs) react to early stage cancers with anti-inflammatory immune responses that support tumor survival at the expense of healthy tissue. Tumor infiltration by CSF1R-expressing TAMs yields a negative prognosis and is correlated with poor survival rates for individuals with lymphoma and solid tumors. The tumor microenvironment often produces high levels of CSF-1, creating a positive feedback loop in which the tumor stimulates survival of TAMs and TAMs promote tumor survival and growth. Thus, CSF1R signaling in TAMs is associated tumor survival, angiogenesis, therapy resistance, and metastasis. Production of CSF-1 by brain tumors called glioblastomas causes microglia (brain-resident macrophages) to exhibit immunosuppressive, tumor-permissive phenotypes. CSF1R inhibition in mouse glioblastoma models is beneficial and improves survival by inhibiting tumor-promoting functions of microglia. Mouse models of breast cancer also show that Csf1r loss-of-function delays TAM infiltration and metastasis. Because anti-cancer macrophages and microglia rely on GM-CSF and IFN-γ signaling instead CSF-1, inhibition of CSF1R signaling has been posited as a therapeutic target in cancer to preferentially deplete tumor-permissive TAMs. Additionally, mutations in CSF1R gene itself are associated with certain cancers such as chronic myelomonocytic leukemia and type M4 acute myeloblastic leukemia.
Neurological disorders
Adult-onset leukoencephalopathy
Because of the importance of the CSF1R gene in myeloid cell survival, maturation, and function, loss-of-function in both inherited copies of the CSF1R gene causes postnatal mortality. Heterozygous mutations in the CSF1R gene prevent downstream CSF1R signaling and cause an autosomal dominant neurodegenerative disease called adult-onset leukoencephalopathy, which is characterized by dementia, executive dysfunction, and seizures. Partial loss of CSF1R in adult-onset leukoencephalopathy causes microglia to exhibit morphological and functional deficits (impaired cytokine production and phagocytosis) which is associated with axonal damage, demyelination, and neuronal loss. Signaling by a DAP12-TREM2 complex in microglia is downstream of CSF1R signaling and is needed for microglia phagocytosis of cellular debris and maintenance of brain homeostasis. TREM2 deficiency in cultured myeloid cells prevents stimulation of proliferation by treatment with CSF-1. Similarities between Nasu-Hakola disease (caused by mutations in either DAP12 or TREM2) and adult-onset leukoencephalopathy suggest partial loss of microglia CSF1R signaling promotes neurodegeneration. Defects in neurogenesis and neuronal survival are also seen in adult-onset leukoencephalopathy due to impaired CSF1R signaling in neural progenitor cells.
Other brain diseases and disorders
CSF1R signaling is involved in several diseases and disorders of the central nervous system. Research using animal models of epilepsy (kainic acid-induced seizures) suggests that CSF1 signaling during seizures protects neurons by activating neuronal CREB signaling. CSF1R agonism during seizures increases neuronal survival whereas neuron-specific Csf1r loss-of-function worsens kainic acid excitotoxicity, suggesting CSF1R signaling in neurons directly protects against seizure-related neuronal damage. Although CSF1R signaling is beneficial in certain contexts, it is detrimental in diseases where microglia drive tissue damage. In Charcot-Marie-Tooth disease type 1, CSF-1 secretion from endoneurial cells stimulates proliferation and activation of macrophages and microglia that cause demyelination. Likewise in multiple sclerosis, CSF1R signaling supports the survival of inflammatory microglia which promote demyelination. CSF1R inhibition prophylactically reduces demyelination in the experimental autoimmune encephalomyelitis animal model. The role of CSF1R signaling in Alzheimer's disease is more complicated because microglia both protect and damage the brain in response to Alzheimer's disease pathology. CSF-1 stimulates primary cultured human microglia to phagocytose toxic Aβ1–42 peptides. Microglia also initiate TREM2-dependent immune responses to amyloid plaques which protects neurons. However, Alzheimer's disease microglia also excessively secrete inflammatory cytokines and prune synapses promoting synapse loss, neuronal death, and cognitive impairment. Both CSF1R stimulation and inhibition improves cognitive function in Alzheimer's disease models. Thus, microglia seem to have both protective and neurotoxic functions during Alzheimer's disease neurodegeneration. Similar findings have been reported in lesion studies of the mouse brain, which showed that inhibition of CSF1R after lesioning improves recovery but inhibition during lesioning worsens recovery. CSF1R-targeting therapies for neurological disorders may impact both detrimental and beneficial microglia functions.
Therapeutics
Because TAM CSF1R signaling is tumor-permissive and can cause tumor treatment-resistance, CSF1R signaling is a promising therapeutic target in the treatment of cancer. Several studies have investigated the efficacy of CSF1R inhibitor as a monotherapy and as a combination therapy in refractory and metastatic cancers. Several small molecule inhibitors and monoclonal antibodies targeting CSF1R are in clinical development for cancer therapy (Table 2). Pexidartinib (PLX3397) is a small molecule inhibitor tyrosine of CSFR (as well as cKIT, FLT3, and VEGFR) with the most clinical development so far. Several completed and concurrent clinical trials have tested the efficacy and safety of Pexidartinib as a monotherapy for c-kit-mutated melanoma, prostate cancer, glioblastoma, classical Hodgkin lymphoma, neurofibroma, sarcoma, and leukemias. In 2019, Pexidartinib was FDA-approved for treatment of diffuse-type tenosynovial giant cell tumors, a non-malignant tumor that develops from synovial tissue lining the joints.
Safety of CSF1R inhibition
The safety of CSF1R inhibitors has been extensively characterized in clinical trials for the different small molecules and monoclonal antibodies in Table 2. In some studies, CSF1R inhibitors were not found to have dose-limiting toxicity while other studies did observe toxicity at high doses and have defined a maximum tolerated dose. Across multiple studies, the most frequent adverse effects included fatigue, elevated liver enzymes (creatine kinase, lactate dehydrogenase, aspartate aminotransferase, alanine transaminase), edema, nausea, lacrimation, and reduced appetite, but no signs of liver toxicity were found. There are some differences in the side effects of monoclonal antibody compared to small molecule CSF1R inhibitors. Edema was more common with monoclonal antibody treatment compared to small molecules, suggesting that immune response to monoclonal antibodies may drive some side effects. Additionally, some small molecule inhibitors are not specific for CSF1R, and off-target effects could explain observed side effects. For example, Pexidartinib treatment was found to change hair color, presumably by its impact on KIT kinase. Overall, CSF1R inhibitors have favorable safety profiles with limited toxicity.
Controversy
CSF1R inhibitors such as PLX5622 are widely used to study the role of microglia in mouse preclinical models of Alzheimer's disease, stroke, traumatic brain injury, and aging. PLX5622 is typically used for microglia research because PLX5622 has higher brain bioavailability and CSF1R-specificity compared to other CSF1R inhibitors such as PLX3397. In 2020, researchers David Hume (University of Queensland) and Kim Green (UCI) published a letter in the academic journal PNAS defending the use small molecule CSF1R inhibitors to study microglia in brain disease. This letter was in response to a primary research paper published in PNAS by lead correspondent Eleftherios Paschalis (HMS) and others which provided evidence that microglia research using PLX5622 is confounded by CSF1R inhibition in peripheral macrophages. Paschalis and colleagues published a subsequent letter in PNAS defending the findings of their published research.
Interactions
Colony stimulating factor 1 receptor has been shown to interact with:
Cbl gene,
FYN,
Grb2,
Suppressor of cytokine signaling 1, This receptor is also linked with the cells of MPS.
See also
Cluster of differentiation
Mouse models of breast cancer metastasis
Pimicotinib
References
Further reading
External links
Clusters of differentiation
Immunoglobulin superfamily cytokine receptors
Tyrosine kinase receptors | Colony stimulating factor 1 receptor | [
"Chemistry"
] | 4,689 | [
"Tyrosine kinase receptors",
"Signal transduction"
] |
14,722,987 | https://en.wikipedia.org/wiki/DNA%20damage-inducible%20transcript%203 | DNA damage-inducible transcript 3, also known as C/EBP homologous protein (CHOP), is a pro-apoptotic transcription factor that is encoded by the DDIT3 gene. It is a member of the CCAAT/enhancer-binding protein (C/EBP) family of DNA-binding transcription factors. The protein functions as a dominant-negative inhibitor by forming heterodimers with other C/EBP members, preventing their DNA binding activity. The protein is implicated in adipogenesis and erythropoiesis and has an important role in the cell's stress response.
Structure
C/EBP proteins are known to have a conserved C-terminal structure, basic leucine zipper domain(bZIP), that is necessary for the formation of DNA-binding capable homodimers or heterodimers with other proteins or members of the C/EBP protein family. CHOP is a relatively small (29kDa) protein that differs from most C/EBP proteins in several amino acid substitutions, which impacts its DNA-binding ability.
Regulation and function
Due to a variety of upstream and downstream regulatory interactions, CHOP plays an important role in ER stress-induced apoptosis caused by a variety of stimuli such as pathogenic microbial or viral infections, amino acid starvation, mitochondrial stress, neurological diseases, and neoplastic diseases.
Under normal physiological conditions, CHOP is ubiquitously present at very low levels. However, under overwhelming ER stress conditions, the expression of CHOP rises sharply along with the activation of apoptotic pathways in a wide variety of cells. Those processes are mainly regulated by three factors: protein kinase RNA-like endoplasmic reticulum kinase (PERK), activating transcription factor 6 (ATF6), and inositol requiring protein 1 (IRE1α)
Upstream regulatory pathways
During ER stress, CHOP is mainly induced via activation of the integrated stress response pathways through the subsequent downstream phosphorylation of a translation initiation factor, eukaryotic initiation factor 2α (eIF2α), and induction of a transcription factor, activation transcription factor 4 (ATF4), which converges on the promoters of target genes, including CHOP.
Integrated stress response, and thus CHOP expression, can be induced by
amino acid starvation through general control non-derepressible-2 (GCN2)
viral infection through the vertebrate-specific kinases - double-stranded RNA-activated protein kinase (PKR)
iron deficiency through heme-regulated inhibitor kinase (HRI)
stress from the accumulation of unfolded or misfolded proteins in the ER activates the integrated stress response through protein kinase RNA-like endoplasmic reticulum kinase (PERK).
Under ER stress, activated transmembrane protein ATF6 translocates to the nucleus and interacts with ATF/cAMP response elements and ER stress-response elements, binding the promoters and inducing transcription of several genes involved in unfolded protein response (including CHOP, XBP1 and others). Thus, ATF6 activates the transcription of both CHOP and XBP-1, while XBP-1 can also upregulate the expression of CHOP.
ER stress also stimulates transmembrane protein IRE1α activity. Upon activation, IRE1α splices the XBP-1 mRNA introns to produce a mature and active XBP-1 protein, that upregulates CHOP expression IRE1α also stimulates the activation of the apoptotic-signaling kinase-1 (ASK1), which then activates the downstream kinases, Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK), which participate in apoptosis induction along with CHOP. The P38 MAP kinase family phosphorylates Ser78 and Ser81 of CHOP, which induces cell apoptosis. Moreover, research studies found that the JNK inhibitors can suppress CHOP upregulation, indicating that JNK activation is also involved in the modulation of CHOP levels.
Downstream apoptotic pathways
Mitochondria-dependent
As a transcription factor, CHOP can regulate the expression of many anti-apoptotic and pro-apoptotic genes, including genes encoding the BCL2-family proteins, GADD34 and TRB-3. In the CHOP-induced apoptotic pathway, CHOP regulates the expression of BCL2 protein family, that includes anti-apoptotic proteins (BCL2, BCL-XL, MCL-1, and BCL-W) and pro-apoptotic proteins (BAK, BAX, BOK, BIM, PUMA and others).
Under ER stress, CHOP can function as either a transcriptional activator or repressor. It forms heterodimers with other C/EBP family transcription factors via bZIP-domain interactions to inhibit the expression of genes responsive to C/EBP family transcription factors, while enhancing the expression of other genes containing a specific 12–14 bp DNA cis-acting element. CHOP can downregulate the expressions of anti-apoptotic BCL2 proteins, and upregulate the expression of proapoptotic proteins (BIM, BAK and BAX expression). BAX-BAK oligomerization causes cytochrome c and apoptosis-inducing factor (AIF) release from mitochondria, eventually causing cell death.
TRB3 pseudokinase is upregulated by the ER stress-inducible transcriptional factor, ATF4-CHOP. CHOP interacts with TRB3, which contributes to the induction of apoptosis. The expression of TRB3 has a pro-apoptotic capacity. Therefore, CHOP also regulates apoptosis by upregulating the expression of the TRB3 gene.
Death-receptor dependent
Death receptor-mediated apoptosis occurs via activation of death ligands (Fas, TNF, and TRAIL) and death receptors. Upon activation, the receptor protein, Fas-associated death domain protein, forms a death-inducing signaling complex, which activates the downstream caspase cascade to induce apoptosis.
The PERK-ATF4-CHOP pathway can induce apoptosis by binding to the death receptors and upregulating the expression of death receptor 4 (DR4) and DR5. CHOP also interacts with the phosphorylated transcription factor JUN to form a complex that binds to the promoter region of DR4 in lung cancer cells. The N-terminal domain of CHOP interacts with phosphorylated JUN to form a complex that regulates the expression of DR4 and DR5. CHOP also upregulates the expression of DR5 by binding to the 5′-region of the DR5 gene.
Under prolonged ER stress conditions, activation of the PERK-CHOP pathway will permit DR5 protein levels to rise, which accelerates the formation of the death-inducing signaling complex (DISC) and activates caspase-8, leading to apoptosis
Other downstream pathways
In addition, CHOP also mediates apoptosis through increasing the expression of the ERO1α (ER reductase) gene, which catalyzes the production of H2O2 in the ER. The highly oxidized state of the ER results in H2O2 leakage into the cytoplasm, inducing the production of reactive oxygen species (ROS) and a series of apoptotic and inflammatory reactions.
The overexpression of CHOP can lead to cell cycle arrest and result in cell apoptosis. At the same time, CHOP-induced apoptosis can also trigger cell death by inhibiting the expression of cell cycle regulatory protein, p21. The p21 protein inhibits the G1 phase of the cell cycle as well as regulates the activity of pre-apoptotic factors. Identified CHOP-p21 relationship may play a role in changing the cell state from adapting to ER stress towards pre-apoptotic activity.
Under most conditions, CHOP can directly bind to the promoters of downstream related genes. However, under specific conditions, CHOP can cooperate with other transcription factors to affect apoptosis. Recent studies have shown that Bcl-2-associated athanogene 5 (Bag5) is over-expressed in prostate cancer and inhibits ER stress-induced apoptosis. Overexpression of Bag5 results in decreased CHOP and BAX expression, and increased Bcl-2 gene expression. Bag5 overexpression inhibited ER stress-induced apoptosis in the unfolded protein response by suppressing PERK-eIF2-ATF4 and enhancing the IRE1-Xbp1 activity.
In general, the downstream targets of CHOP regulate the activation of apoptotic pathways, however, the molecular interaction mechanisms behind those processes remain to be discovered.
Interactions
DNA damage-inducible transcript 3 has been shown to interact with [proteins]:
ATF3,
C-Fos,
C-jun and
CEBPB,
CSNK2A1,
JunD, and
RPS3A.
Clinical significance
Role in fatty liver and hyperinsulinemia
Chop gene deletion has been demonstrated protective against diet induced metabolic syndromes in mice. Mice with germline Chop gene knockout have better glycemic control despite unchanged obesity. A plausible explanation for the observed dissociation between obesity and insulin resistance is that CHOP promotes insulin hypersecretion from pancreatic β cells.
Furthermore, Chop depletion by a GLP1-ASO delivery system was shown to have therapeutic effects of insulin reduction and fatty liver correction, in preclinical mouse models.
Role in microbial infection
CHOP-induced apoptosis pathways had been identified in cells infected by
Porcine circovirus type 2 (PERK-eIF2α-ATF4 -CHOP-BCL2 pathway)
HIV (XBP-1-CHOP-Caspase 3/9 pathway)
Infectious bronchitis virus (PERK-eIF2α-ATF4/PKR-eIF2α-ATF4 pathway)
M. tuberculosis (PERK-eIF2α-CHOP pathway)
Helicobacter pylori (PERK-CHOP or PKR-eIF2α-ATF4 pathway)
Escherichia coli (CHOP-DR5-Caspase 3/8 pathway)
Shigella dysenteriae (p38-CHOP-DR5 pathway)
Since CHOP has an important role of apoptosis induction during infection, it is an important target for further research that will help deepen the current understanding of pathogenesis and potentially provide an opportunity for invention of new therapeutic approaches. For example, small molecule inhibitors of CHOP expression may act as therapeutic options to prevent ER stress and microbial infections. Research had shown that small molecule inhibitors of PERK-eIF2α pathway limit PCV2 virus replication.
Role in other diseases
The regulation of CHOP expression plays an important role in metabolic diseases and in some cancers through its function in mediating apoptosis. The regulation of CHOP expression could be a potential approach to affecting cancer cells through the induction of apoptosis. In the intestinal epithelium, CHOP has been demonstrated to be downregulated under inflammatory conditions (in inflammatory bowel diseases and experimental models of colitis). In this context, CHOP seems to rather regulate the cell cycle than apoptotic processes.
Mutations or fusions of CHOP (e.g. with FUS to form FUS-CHOP) can cause Myxoid liposarcoma.
References
Further reading
External links
Transcription factors
Oncogenes | DNA damage-inducible transcript 3 | [
"Chemistry",
"Biology"
] | 2,458 | [
"Induced stem cells",
"Gene expression",
"Transcription factors",
"Signal transduction"
] |
14,723,101 | https://en.wikipedia.org/wiki/Todd%20Siler | Todd Siler (born August 23, 1953) is an American multimedia artist, author, educator, and inventor. A graduate of Bowdoin College, he became the first visual artist to be granted a PhD from MIT (interdisciplinary studies in Psychology and Art, 1986). Siler began advocating the full integration of the arts and sciences in the 1970s and is the founder of the ArtScience Program and movement.
Creativity research
In the early 1980s, Siler made an extensive study of genius across numerous disciplines to see what, if anything, such highly creative people as Albert Einstein and Sergei Rachmaninoff have, or more importantly do, in common. Although such inquiries are standard, Siler's work went further than any work before or since in examining how methods used by highly creative people might work on the neurological and cellular level. "Creativity is any unconditioned response," is typical of Siler's approach, which both validates and challenges the work of luminaries in the field such as Howard Gardner, Mihaly Csikszentmihalyi and Robert Root-Bernstein (Encyclopedia of Creativity, 1999). These theories were elaborated in two books, Breaking The Mind Barrier: The ArtScience of Neurocosmology (Simon & Schuster, 1990; Touchstone Books, 1992), which is largely intended for scholars, and Think Like A Genius (Bantam Books, 1997; Transworld, 1998) written for the general reader. Siler has developed these theories into proprietary programs which are used extensively in schools and corporations.
Visual arts
The son of an aspiring concert pianist and bio-medical researcher, as a child, Siler was a prodigy in the fine arts, often using highly detailed drawings to express his ideas on integrating the arts and sciences. He studied art as an undergraduate, spending a year "apprenticed" in the studio of American artist Leonard Baskin. In his 20s Siler was part of the same SoHo art scene which launched Julian Schnabel, Francesco Clemente and David Salle. Today, Siler's artworks are in numerous public collections including the Solomon R. Guggenheim Museum, The Metropolitan Museum of Art (20th Century Collection), The Museum of Modern Art in New York City, the Pushkin Museum of Fine Arts in Moscow, and The Israel Museum in Jerusalem.
In 2006, Siler's multimedia exhibition at New York's Ronald Feldman Gallery showed off his artwork relating to what he described as a nature-inspired "Fractal Reactor", a nuclear fusion reactor based on fractal geometry.
Education and invention
As an artist who has championed the study of science, Siler worked with the Cherry Creek School District (Colorado) to pioneer experiential learning methodologies based on the understanding and creation of systems of metaphor.
Siler was instrumental in developing the interdisciplinary curriculum for The Israel Arts and Science Academy (IASA) in Jerusalem.
These programs have become popular with Fortune 500 companies as a way of promoting out-of-the-box thinking.
In addition to being an artist and scholar, Siler holds a number of patents on a wide range of inventions, including a widely used computer-graphics input device and textile printing machinery.
Awards
In 2011, Siler received the Leonardo da Vinci World Award of Arts in recognition of his contributions to contemporary and visual arts, for stimulating creativity, inspiring innovation, and uniting art and science to enrich the experience of creative learning.
References
External links
Siler's works at Feldman Gallery
Todd Siler Metaphorming Minds Artist's Book
Website for Siler's book Think Like A Genius
1953 births
Living people
Creativity researchers
American installation artists
Bowdoin College alumni
American inventors
20th-century American painters
American male painters
21st-century American painters
21st-century American male artists
American self-help writers
American science writers
American education writers
Nuclear technology
20th-century American sculptors
20th-century American male artists
American male sculptors
American contemporary painters | Todd Siler | [
"Physics"
] | 795 | [
"Nuclear technology",
"Nuclear physics"
] |
14,723,147 | https://en.wikipedia.org/wiki/PTPN22 | Protein tyrosine phosphatase non-receptor type 22 (PTPN22) is a cytoplasmatic protein encoded by gene PTPN22 and a member of PEST family of protein tyrosine phosphatases. This protein is also called "PEST-domain Enriched Phosphatase" ("PEP") or "Lymphoid phosphatase" ("LYP"). The name LYP is used strictly for the human protein encoded by PTPN22, but the name PEP is used only for its mouse homolog. However, both proteins have similar biological functions and show 70% identity in amino acid sequence. PTPN22 functions as a negative regulator of T cell receptor (TCR) signaling, which maintains homeostasis of T cell compartment.
Gene
Gene PTPN22 is located on the p arm of the human chromosome 1. It is nearly 58 000 base pairs long and contains 21 exons. In the case of mouse genome, it is located on the q arm of the chromosome 3. It is nearly 55 700 base pairs long and contains 23 exons.
Structure
PTPN22 is composed from 807 amino acids, and it weighs 91,705 kDa. On its N terminus it possesses catalytic domain, which shows the highest level of conservation between human and mouse proteins. Other parts of PTPN22 are less conserved. After catalytic domain PTPN22 has approximately 300 amino acids long domain called "Interdomain". On the C terminus of PTPN22 there are 4 proline-rich motifs (P1 - P4), which can mediate interactions with other proteins. P1 motif is the most important among them, because it is crucial for binding of CSK kinase, and allele encoding PTPN22 with mutated P1 motif is associated with increased risk of numerous autoimmune diseases.
Function
Regulation of T cell receptor signaling
A T cell receptor activation by a cognate peptide triggers a signaling pathway activating a T cell. The first event of this pathway is activation of the SRC family kinase LCK by a dephosphorylation of its C terminal inhibition tyrosine (Y505) and by a phosphorylation of its activation tyrosine (Y394). LCK then phosphorylate tyrosines in the CD3 complex creating a docking site for the SH2 domain of the SYK family kinase ZAP70, which is there phosphorylated too. The Phosphorylated ZAP70 then propagate a signal from a TCR, phosphorylating other proteins and creating a multi-protein complex, which activates downstream signaling pathways. PTPN22 possess the ability to dephosphorylate proteins included in proximal events of the TCR signaling and serves as an important negative regulator of a T cell activation. PTPN22 is able to bind the LCK with phosphorylated Y394, the phosphorylated ZAP70 and the phosphorylated ζ chain of CD3 complex. Thus, it binds molecules of a proximal TCR signaling only after their activation. PTPN22 can dephosphorylate those proteins and decrease the activating signal obtained by a T cell. Dephosphorylation of kinases LCK and ZAP70 by a PTPN22 is specific concerning the phosphorylated tyrosine in those proteins – only the Y394 of LCK and the Y493 of ZAP70 are dephosphorylated. In the absence of PTPN22, an activated T cell receive a stronger activation signal, which is reflected by a greater influx of Ca2+ cations into the cytosol, bigger phosphorylation of an LCK, ZAP70 and ERK and larger expansion of those cells. The inhibitory effect on a TCR signaling was also verified with the usage of PTPN22 inhibitor on a Jurkat T cell line and on human primary T cells, and also with the experiments of PTPN22 overexpression in vitro. The expression of PTPN22 is upregulated after an activation of T cells and an antigen-experienced T cell have higher expression of PTPN22 than a naive T cell.
The regulatory function of PTPN22 is particularly important during an activation by low affinity peptides. In the absence of PTPN22, T cell cannot discriminate between strong and weak antigens sufficiently and those T cells become more responsive, which can be detected like increased upregulation of transcription factors and CD69, increased ERK phosphorylation, increased ability to expand in vivo and to produce cytokines. Increased responsiveness can also break the tolerance against low affinity self-antigens and is well visible, when PTPN22-deficient T cells get into a lymphopenic environment.
Regulation of regulatory T cells
One particular population of T cells, which is influenced by a PTPN22 deficiency is the population of regulatory T cells (Treg cells). PTPN22-deficient mice contain higher amount of Treg cells in lymph nodes and spleens and this difference is more visible with increasing age of mice. There is also a change of the effector Treg cells : central Treg cells ratio in favor of the effector Treg cells. PTPN22 deficiency increases abilities of Treg cells to survive, differentiation of Treg cells from naive T cells, but not the ability to proliferate in vivo, and it also supports transition of central Treg cells to effector Treg cells. One of the reasons, of the increased survival of PTPN22-deficient Treg cells, is that those cells have upregulated expression of GITR, which increases their expansion in vivo. Treatment of PTPN22-deficient mice with an anti-GITR-L blocking antibody suppresses the expansion of Treg cells. PTPN22 deficiency does not impair the suppressive function of Treg cells. Actually there are some articles suggesting that PTPN22-deficient Treg cells possess an enhanced suppressive function or have a bigger ability to obtain an effector phenotype.
Regulation of adhesiveness and motility
Next to a TCR signaling PTPN22 regulates an adhesiveness and a motility of T cells. PTPN22-deficient T cells have a prolonged interval of contact with an antigen presenting cell, which present a low affinity peptide. With a high affinity peptide the difference is not detectable. Part of the reason of the increased adhesiveness of those T cells is that enhanced TCR signaling results in a higher activation of the RAP1 and a boosted inside-out signaling to activate the adhesive molecule LFA-1. In migrating T cells we can see the polarized localization of the PTPN22 at the leading edge of a migrating T cell, where it colocalizes with its substrates LCK and ZAP70. A downregulation of the PTPN22 increases motility, adhesivity and levels of phosphorylated LCK and phosphorylated ZAP70 in those cells. On the contrary, an overexpression of the PTPN22, but not the catalytically inactive PTPN22, increases motility of migrating T cells. An association of the PTPN22, but not its disease associated mutant form, with the LFA-1 results in a decreased LFA-1 clustering and a decreased adhesion. The role of the PTPN22 in the regulation of LFA-1-mediated adhesion and motility is also supported by the observation of increased LFA-1 expression in PTPN22-/- Treg cells.
Interaction partners
The C-terminal part of the PTPN22 bare proline-rich motifs providing binding sites for putative interaction partners. One of those interaction partners is the cytoplasmatic tyrosine kinase CSK, which is a negative regulator of SRC family kinases and a TCR signaling as well as the PTPN22. CSK binds two prolin-rich motifs (P1 and P2) in the structure of PTPN22 through its SH3 domain and the P1 motif is more important in this interaction. A deletion of the P1 motif greatly diminish the inhibitory effect of the PTPN22 on a TCR signaling. The Interaction of those enzymes is needed for their optimal function and the inhibition of TCR signaling. It was also proposed that the interaction of PTPN22 and CSK regulate a localization of the PTPN22 and a dissociation of this complex enables translocation of the PTPN22 to lipid rafts of a plasma membrane, where it can inhibit a TCR signaling. The mutant PTPN22, which is unable to bind CSK, is effectively recruited to a plasma membrane.
Another interaction partner of the PTPN22 is TRAF3. This protein bind the PTPN22 and regulate its translocalization to a plasma membrane, in the absence of TRAF3 there is a bigger amount of the PTPN22 localized at a plasma membrane.
Regulation of PTPN22
It was revealed that PTPN22 is regulated by a phosphorylation. PTPN22 is phosphorylated on the serine in the position 751 by the protein PKC (most probably isoform PKCα) after activation of a T cell. This phosphorylation negatively regulates the TCR-suppressing function of the PTPN22. It also suppresses the polyubiquitination of PTPN22, which targets this protein for degradation, and by this mean, it prolongs half-life of the PTPN22. Phosphorylared PTPN22 interacts better with the CSK which hold PTPN22 away from a plasma membrane, where it can dephosphorylate proteins of a TCR signaling pathway. PTPN22 with the mutated serine 751 has shorter half-life, enhanced recruitment to plasma membrane and reduced interaction with CSK.
PTPN22-deficient mice
Young PTPN22-deficient mice do not display any abnormality in peripheral lymphoid organs, but older PTPN22-deficient mice (older than 6 months) develop a splenomegaly and a lymphadenopathy. In these older mice we can see an increased number of the T cells with phenotype of the effector/memory T cells (CD44hi, CD62Llo), which have higher expression of the PTPN22 than naive T cells in Wild Type mice. The expansion of those T cells is supported by the PTPN22 deficiency. A compartment of Treg cell is also influenced by the PTPN22 deficiency in vivo. Same as with the effector/memory T cells, PTPN22-deficient mice contain a bigger amount of Treg cells in lymph nodes and spleens and this difference is more visible with increasing age of mice. There is also a change of the effector Treg cells : central Treg cells ratio in favor of the effector Treg cells. Influence of the PTPN22 deficiency on Treg cells number is consistent with the higher expression of PTPN22 in Treg cells than in naive T cells. Another abnormality of PTPN22-deficient mice is a spontaneous formation of large germinal centers in spleens and peyer's patches. This formation of germinal centers is dependent on the costimulation molecule CD40L and it is another consequence of the T cell dysregulation. PTPN22-deficient mice have increased levels of antibodies. However, there is no increase in levels of autoantibodies. Despite those effects of the PTPN22 deficiency on a T cell compartment and an antibody production, PTPN22-deficient mice do not show signs of any autoimmune disease.
Disease associated variant of PTPN22
In 2004, Bottini et al. discovered the single-nucleotide polymorphism in the PTPN22 gene at nucleotide 1858. In this variant of the gene, normally occurring cytosine is substituted by thymine (C1858T). This cytosine encodes the codon for an amino acid arginine in the position 620 of the linear protein structure, but the mutation to thymine cause change of an arginine to a tryptophan (R620W). The amino acid 620 is placed in the P1 motif, which is involved in the association with CSK and the mutation to tryptophan diminish the ability of the PTPN22 to bind CSK. The article reporting the existence of this variant also discovered that it is more frequent in Diabetes mellitus type 1 patients. The association of C1858T allele with type 1 diabetes was then confirmed by other studies. In addition, C1858T allele of PTPN22 is associated with other autoimmune diseases including Rheumatoid arthritis, systemic lupus erythematosus, juvenile idiopathic arthritis, anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis, Graves’ disease, myasthenia gravis, Addison's disease. The contribution of the C1858T PTPN22 allele to those diseases was confirmed by more robust meta-analysis. On the other hand, this allele is not linked to autoimmune diseases like multiple sclerosis, Ulcerative colitis, pephigus vulgaris and others. The exact way how the function of the PTPN22 is influenced by this mutation is still unknown. Throughout past years there were appearing evidences supporting that C1858T mutation is a loss-of-function mutation, but also evidences supporting that it is a gain-of-function mutation.
References
Further reading
External links
Proteins
Immune system
T cells | PTPN22 | [
"Chemistry",
"Biology"
] | 2,968 | [
"Biomolecules by chemical classification",
"Immune system",
"Organ systems",
"Molecular biology",
"Proteins"
] |
14,723,251 | https://en.wikipedia.org/wiki/RUNX1T1 | Protein CBFA2T1 is a protein that in humans is encoded by the RUNX1T1 gene.
Function
The protein encoded by this gene is a putative zinc finger transcription factor and oncoprotein. In acute myeloid leukemia, especially in the M2 subtype, the t(8;21)(q22;q22) translocation is one of the most frequent karyotypic abnormalities. The translocation produces a chimeric gene made up of the 5'-region of the RUNX1 gene fused to the 3'-region of this gene. The chimeric protein is thought to associate with the nuclear corepressor/histone deacetylase complex to block hematopoietic differentiation. Several transcript variants encoding multiple isoforms have been found for this gene.
Interactions
RUNX1T1 has been shown to interact with:
CBFA2T2,
CBFA2T3,
Calcitriol receptor
GFI1,
Nuclear receptor co-repressor 1,
Nuclear receptor co-repressor 2,
PRKAR2A, and
Zinc finger and BTB domain-containing protein 16.
References
Further reading
Transcription factors | RUNX1T1 | [
"Chemistry",
"Biology"
] | 243 | [
"Induced stem cells",
"Gene expression",
"Transcription factors",
"Signal transduction"
] |
14,723,308 | https://en.wikipedia.org/wiki/Myocyte-specific%20enhancer%20factor%202A | Myocyte-specific enhancer factor 2A is a protein that in humans is encoded by the MEF2A gene. MEF2A is a transcription factor in the Mef2 family. In humans it is located on chromosome 15q26. Certain mutations in MEF2A cause an autosomal dominant form of coronary artery disease and myocardial infarction.
Function
The process of differentiation from mesodermal precursor cells to myoblasts has led to the discovery of a variety of tissue-specific factors that regulate muscle gene expression. The myogenic basic helix-loop-helix proteins, including myoD (MIM 159970), myogenin (MIM 159980), MYF5 (MIM 159990), and MRF4 (MIM 159991) are 1 class of identified factors. A second family of DNA binding regulatory proteins is the myocyte-specific enhancer factor-2 (MEF2) family. Each of these proteins binds to the MEF2 target DNA sequence present in the regulatory regions of many, if not all, muscle-specific genes. The MEF2 genes are members of the MADS gene family (named for the yeast mating type-specific transcription factor MCM1, the plant homeotic genes 'agamous' and 'deficiens' and the human serum response factor SRF (MIM 600589)), a family that also includes several homeotic genes and other transcription factors, all of which share a conserved DNA-binding domain.[supplied by OMIM]
Interactions
Myocyte-specific enhancer factor 2A has been shown to interact with:
ASCL1,
EP300,
HDAC4,
HDAC9,
Histone deacetylase 5,
MAPK14,
MEF2D,
Mothers against decapentaplegic homolog 2, and
Thyroid hormone receptor alpha and
References
Further reading
External links
Transcription factors
Human proteins | Myocyte-specific enhancer factor 2A | [
"Chemistry",
"Biology"
] | 404 | [
"Induced stem cells",
"Gene expression",
"Transcription factors",
"Signal transduction"
] |
14,723,387 | https://en.wikipedia.org/wiki/SOX9 | Transcription factor SOX-9 is a protein that in humans is encoded by the SOX9 gene.
Function
SOX-9 recognizes the sequence CCTTGAG along with other members of the HMG-box class DNA-binding proteins. It is expressed by proliferating but not hypertrophic chondrocytes that is essential for differentiation of precursor cells into chondrocytes and, with steroidogenic factor 1, regulates transcription of the anti-Müllerian hormone (AMH) gene.
SOX-9 also plays a pivotal role in male sexual development; by working with Sf1, SOX-9 can produce AMH in Sertoli cells to inhibit the creation of a female reproductive system. It also interacts with a few other genes to promote the development of male sexual organs. The process starts when the transcription factor testis determining factor (encoded by the sex-determining region SRY of the Y chromosome) activates SOX-9 activity by binding to an enhancer sequence upstream of the gene. Next, SOX9 activates FGF9 and forms feedforward loops with FGF9 and PGD2. These loops are important for producing SOX-9; without these loops, SOX-9 would run out and the development of a female would almost certainly ensue. Activation of FGF9 by SOX-9 starts vital processes in male development, such as the creation of testis cords and the multiplication of Sertoli cells. The association of SOX-9 and Dax1 actually creates Sertoli cells, another vital process in male development. In the brain development, its murine ortholog Sox-9 induces the expression of Wwp1, Wwp2, and miR-140 to regulate cortical plate entry of newly born nerve cells, and regulate axon branching and axon formation in cortical neurons.
Sox9, also known as SRY-Box Transcription Factor 9, is an important gene is sex determination. The SOX family of genes are all transcription factors for the Y chromosomal sex-determining factor SRY. The SRY gene encodes the SOX transcription factor while it upregulates Sox9. Sox9 then activates Fgf9, Fibroblast growth factor 9, which is another integral transcription factor in the formation of the male gonads. Fgf9 up-regulates Sox9 in a positive feedforward cascade, this causes the differentiation of sertoli cells leading to the formation of the testis.
SOX-9 is a target of the Notch signaling pathway, as well as the Hedgehog pathway, and plays a role in the regulation of neural stem cell fate. In vivo and in vitro studies show that SOX-9 negatively regulates neurogenesis and positively regulates gliogenesis and stem cell survival.
In adult articular chondrocytes, siRNA-mediated knockdown of SOX-9 or RTL3 results in the downregulation of the other and reduced type II collagen (COL2A1) mRNA and protein expression.
Clinical significance
Mutations lead to the skeletal malformation syndrome campomelic dysplasia, frequently with autosomal sex-reversal and cleft palate.
SOX9 sits in a gene desert on 17q24 in humans. Deletions, disruptions by translocation breakpoints and a single point mutation of highly conserved non-coding elements located > 1 Mb from the transcription unit on either side of SOX9 have been associated with Pierre Robin Sequence, often with a cleft palate.
The SOX9 protein has been implicated in both initiation and progression of multiple solid tumors. Its role as a master regulator of morphogenesis during human development makes it an ideal candidate for perturbation in malignant tissues. Specifically, SOX9 appears to induce invasiveness and therapy-resistance in prostate, colorectal, breast and other cancers, and therefore promotes lethal metastasis. Many of these oncogenic effects of SOX9 appear dose-dependent.
SOX9 localization and dynamics
SOX9 is mostly localized in the nucleus and it is highly mobile. Studies in chondrocyte cell line has revealed nearly 50% of SOX9 is bound to DNA and it is directly regulated by external factors. Its half-time of residence on DNA is ~14 seconds.
Role in Sexual Differentiation
SOX9 helps channel SRY activation in sexual differentiation. Mutations in SOX9 or any associated genes can cause a reversal of sex. If FGF9, which is activated by SOX9, is not present, a fetus with both X and Y chromosomes will become female. the same is true if DAX1 is not present. The related phenomena can be caused by unusual activity of the SRY in XX male syndrome, usually when it's translocated onto the X-chromosome and its activity is only activated in some cells. Mutation or deletion of SOX9 could cause an XY fetus to be female because SOX9 is a critical effector gene that works because of the SRY gene to differentiate Sertoli cells and drive testis formation in males.
Interactions
SOX9 has been shown to interact with steroidogenic factor 1, MED12, MAF, SWI/SNF, MLL3 and MLL4.
Knock out models
Loss of function mutations with Sox9 can lead to campomelic dysplasia(CD), due to mutations affecting protein functions and translocations that disrupt gene expression. There have been Sox9 knockout mice that have shown improved stroke recovery, especially when inhibiting inhibitors of axonal sprouting such as NOGO and chondroitin sulfate proteoglycans (CSPGs). Sox9 ablation leads to decreased levels of CSPG, which increases tissue sparing and improved post-stroke neurological recovery. These Sox9 knockout mice promote reparative axonal sprouting, neuroprotection and recovery after stroke.
See also
SOX genes
Further reading
References
External links
Transcription factors | SOX9 | [
"Chemistry",
"Biology"
] | 1,219 | [
"Induced stem cells",
"Gene expression",
"Transcription factors",
"Signal transduction"
] |
14,723,421 | https://en.wikipedia.org/wiki/Transforming%20growth%20factor%2C%20beta%203 | Transforming growth factor beta-3 is a protein that in humans is encoded by the gene.
It is a type of protein, known as a cytokine, which is involved in cell differentiation, embryogenesis and development. It belongs to a large family of cytokines called the Transforming growth factor beta superfamily, which includes the TGF-β family, Bone morphogenetic proteins (BMPs), growth and differentiation factors (GDFs), inhibins and activins.
TGF-β3 is believed to regulate molecules involved in cellular adhesion and extracellular matrix (ECM) formation during the process of palate development. Without TGF-β3, mammals develop a deformity known as a cleft palate. This is caused by failure of epithelial cells in both sides of the developing palate to fuse. TGF-β3 also plays an essential role in controlling the development of lungs in mammals, by also regulating cell adhesion and ECM formation in this tissue, and controls wound healing by regulating the movements of epidermal and dermal cells in injured skin.
Interactions
Transforming growth factor, beta 3 has been shown to interact with TGF beta receptor 2.
Clinical research
After successful phase I/II trials, human recombinant TGF-β3 (avotermin, planned trade name Juvista) failed in Phase III trials.
References
Further reading
External links
GeneReviews/NCBI/NIH/UW entry on Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy, Autosomal Dominant
OMIM entries on Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy, Autosomal Dominant
Proteins
TGFβ domain | Transforming growth factor, beta 3 | [
"Chemistry"
] | 362 | [
"Biomolecules by chemical classification",
"Proteins",
"Molecular biology"
] |
14,723,432 | https://en.wikipedia.org/wiki/NK2%20homeobox%201 | NK2 homeobox 1 (NKX2-1), also known as thyroid transcription factor 1 (TTF-1), is a protein which in humans is encoded by the NKX2-1 gene.
Function
Thyroid transcription factor-1 (TTF-1) is a protein that regulates transcription of genes specific for the thyroid, lung, and diencephalon. It is also known as thyroid specific enhancer binding protein. It is used in anatomic pathology as a marker to determine if a tumor arises from the lung or thyroid. NKX2.1 can be induced by activin A via SMAD2 signaling in a human embryonic stem cell differentiation model.
NKX2.1 is key to the fetal development of lung structures. The dorsal-ventral pattern of NKX2.1 expression forms the ventral boundary in the anterior foregut. NKX2.1 is expressed only in select cells in the ventral wall of the anterior foregut, and is not expressed in the dorsal wall, where the esophagus will emerge from. NKX2.1 knockout in mice results in the development of a shortened trachea which is fused to the esophagus, with the bronchi directly connecting this shared tube to the lungs. This resembles a complete tracheoesophageal fistula, which is a rare congenital condition in humans. Furthermore, distal lung structures do not develop in these knockout mice. Branching of the lungs in these mice did not occur past the main-stem bronchi, resulting in lungs that were smaller in size by about 50% compared to the wild-type mice. The epithelial lining of these distal structures did not show evidence of differentiation into specialized cells. This lining is composed of columnar epithelial cells and scattered ciliated epithelial cells. The proximal epithelium of the lungs showed normal differentiation, indicating that proximal differentiation is independent of NKX2.1. NKX2.1 is initially expressed in the entire epithelium, but is suppressed in a proximal-distal pattern as the lung continues to develop.
Clinical significance
TTF-1 positive cells are found in the lung as type II pneumocytes and club cells. In the thyroid, follicular and parafollicular cells are also positive for TTF-1.
For lung cancers, adenocarcinomas are usually positive, while squamous cell carcinomas and large cell carcinomas are rarely positive. Small cell carcinomas (of any primary site) are usually positive. TTF1 is more than merely a clinical marker of lung adenocarcinoma. It plays an active role in sustaining lung cancer cells in view of the experimental observation that it is mutated in lung cancer.
It has been observed that a loss of Nkx2-1 allows for deregulation of transcription factors FOXA1/2 (by relaxing histone deacetylation and methylation-mediated repression of Foxa1/2 by Nkx2-1) causing reactivation of an embryonic gastric differentiation program in pulmonary cells. This results in mucinous lung adenocarcinoma, a source of poor clinical outcomes for patients.
However others have found that TTF-1 staining is often positive in pulmonary adenocarcinomas, large cell carcinomas, small-cell lung carcinomas, neuroendocrine tumors other than small-cell lung carcinomas and extrapulmonary small-cell carcinomas.
It is also positive in thyroid cancers and is used for monitoring for metastasis and recurrence.
Interactions
NK2 homeobox 1 has been shown to interact with calreticulin and PAX8.
References
Further reading
External links
Transcription factors
Anatomical pathology
Proteins | NK2 homeobox 1 | [
"Chemistry",
"Biology"
] | 782 | [
"Biomolecules by chemical classification",
"Gene expression",
"Signal transduction",
"Induced stem cells",
"Molecular biology",
"Proteins",
"Transcription factors"
] |
14,723,619 | https://en.wikipedia.org/wiki/Cyclin-dependent%20kinase%20inhibitor%201C | Cyclin-dependent kinase inhibitor 1C (p57, Kip2), also known as CDKN1C, is a protein which in humans is encoded by the CDKN1C imprinted gene.
Function
Cyclin-dependent kinase inhibitor 1C is a tight-binding inhibitor of several G1 cyclin/Cdk complexes and a negative regulator of cell proliferation. Mutations of CDKN1C are implicated in sporadic cancers and Beckwith-Wiedemann syndrome suggesting that it is a tumor suppressor candidate.
CDKN1C is a tumor suppressor human gene on chromosome 11 (11p15) and belongs to the cip/kip gene family. It encodes a cell cycle inhibitor that binds to G1 cyclin-CDK complexes. Thus p57KIP2 causes arrest of the cell cycle in G1 phase.
CDKN1C was found to lead to cancer cell dormancy; its gene expression is regulated through the activity of glucocorticoid receptors (GRs) through chromatin remodelling mediated by SWI/SNF.
Research Methods
Since it has been identified that mutation to this tumor suppressing gene can have dramatic effects in a newborn such as macroglossia there has been great research to determine the genetic significance. CDKN1C is prone to error during the process of gene imprinting. The process of gene imprinting is in concert with DNA methylation. This goes makes the gene become transcriptionally silent from the paternal side allowing the maternal gene to be active. If this gene fails to be properly methylated, or obtains a mutation, there will be a lack of cell cycle suppression leading to the pediatric tumor growth.
Research methods for this gene have involved different sequencing methods such as Sanger Sequencing. This sequencing method is a three step process that involves PCR, Gel Electrophoresis, and computer analysis to determine DNA sequences. Sequencing can be helpful in identifying base pair mutations. A study done to assess the phenotypic effects that mutations to this gene will have taken genetic sequencing of a cohort of individuals known to be effected by a mutation on this gene. In this study, they found 37 mutations associated with 38 different pedigrees. This went to prove that mutations to the CDKN1C on chromosome 11 would in fact have phenotypic effects on individuals. These effects are further discussed through the different clinical cases that can occur.
Clinical significance
A mutation of this gene may lead to loss of control over the cell cycle leading to uncontrolled cellular proliferation. p57KIP2 has been associated with Beckwith-Wiedemann syndrome (BWS) which is characterized by increased risk of tumor formation in childhood. Loss-of-function mutations in this gene have also been shown associated to the IMAGe syndrome (Intrauterine growth restriction, Metaphyseal dysplasia, Adrenal hypoplasia congenita, and Genital anomalies). Complete hydatidiform moles consist only of paternal DNA, and thus the cells lack p57 expression as the gene is paternally imprinted (silenced). Immunohistochemical stains for p57 can aid with the diagnosis of hydatidiform moles.
Interactions
Cyclin-dependent kinase inhibitor 1C has been shown to interact with:
LIMK1,
MYBL2,
MyoD, and
PCNA.
References
Further reading
External links
GeneReviews/NIH/NCBI/UW entry on Beckwith-Wiedemann Syndrome
Cell cycle
Tumor suppressor genes | Cyclin-dependent kinase inhibitor 1C | [
"Biology"
] | 740 | [
"Cell cycle",
"Cellular processes"
] |
14,723,646 | https://en.wikipedia.org/wiki/GATA3 | GATA3 is a transcription factor that in humans is encoded by the GATA3 gene. Studies in animal models and humans indicate that it controls the expression of a wide range of biologically and clinically important genes.
The GATA3 transcription factor is critical for the embryonic development of various tissues as well as for inflammatory and humoral immune responses and the proper functioning of the endothelium of blood vessels. GATA3 plays central role in allergy and immunity against worm infections. GATA3 haploinsufficiency (i.e. loss of one or the two inherited GATA3 genes) results in a congenital disorder termed the Barakat syndrome.
Current clinical and laboratory research is focusing on determining the benefits of directly or indirectly blocking the action of GATA3 in inflammatory and allergic diseases such as asthma. It is also proposed to be a clinically important marker for various types of cancer, particularly those of the breast. However, the role, if any, of GATA3 in the development of these cancers is under study and remains unclear.
Gene
The GATA3 gene is located close to the end of the short arm of chromosome 10 at position p14. It consists of 8 exons, and codes for two variants viz., GATA3, variant 1, and GATA3, variant 2. Expression of GATA3 may be regulated in part or at times by the antisense RNA, GATA3-AS1, whose gene is located close to the GATA3 gene on the short arm of chromosome 10 at position p14. Various types of mutations including point mutations as well as small- and large-scale deletional mutations cause an autosomal dominant genetic disorder, the Barakat syndrome (also termed hypoparathyroidism, deafness, and renal dysplasia syndrome). The location of GATA3 borders that of other critical sites on chromosome 10, particularly a site located at 10p14-p13. Mutations in this site cause the congenital disorder DiGeorge syndrome/velocardiofacial syndrome complex 2 (or DiGeorge syndrome 2). Large-scale deletions in GATA3 may span into the DiGeorge syndrome 2 area and thereby cause a complex syndrome with features of the Barakat syndrome combined with some of those of the DiGeorge syndrome 2. Knockout of both GATA3 genes in mice is fatal: these animals die at embryonic days 11 and 12 due to internal bleeding. They also exhibit gross deformities in the brain and spine as well as aberrations in fetal liver hematopoiesis.
Protein
GATA3 variant 1 is a linear protein consisting of 444 amino acids. GATA3 variant 2 protein is an identically structured isoform of, but 1 amino acid shorter than, GATA3 variant 1. Differences, if any, in the functions of these two variants have not been reported. With respect to the best studied variant, variant 1, but presumably also variant 2, one of the zinc finger structural motifs, ZNF2, is located at the protein's C-terminus and binds to specific gene promoter DNA sequences to regulate the expression of the genes controlled by these promoters. The other zinc finger, ZNF1, is at the protein's N-terminus and interacts with various nuclear factors, including Zinc finger protein 1 (i.e. ZFPM1, also termed Friends of GATA1 [i.e. FOG-1]) and ZFPM2 (i.e. FOG-2), that modulate GATA3's gene-stimulating actions.
Pathophysiology
The GATA3 transcription factor regulates the expression of genes involved in the development of various tissues as well as genes involved in physiological as well as pathological humoral inflammatory and allergic responses.
Function
GATA3 belongs to the GATA family of transcription factors. Gene-deletion studies in mice indicate that Gata3 (mouse gene equivalent to GATA3) is critical for the embryonic development and/or function of various cell types (e.g. fat cells, neural crest cells, lymphocytes) and tissues (e.g. kidney, liver, brain, spinal cord, mammary gland). Studies in humans implicate GATA3 in the following:
1) GATA3 is required for the development of the parathyroid gland, sensory components of the auditory system, and the kidney in animals and humans. It may also contribute to the development of the vagina and uterus in humans.
2) In humans, GATA3 is required for the development and/or function of innate lymphoid cells (ILCs), particularly Group 2 ILCs as well as for the development of T helper cells,(Th cells), particularly Th2 cells. Group 2 ILCs and Th2 cells, and thereby GATA3, are critical for the development of allergic and humoral immune responses in humans. Comparable studies in animals implicate GATA3 in the development of lymphocytes that mediate allergic and humoral immunity as well as allergic and humoral immune responses.
3) GATA3 promotes the secretion of IL-4, IL-5, and IL-13 from Th2 cells in humans and has similar actions on comparable mouse lymphocytes. All three of these interleukins serve to promote allergic responses,
4) GATA3 induces the maturation of precursor cells into breast epithelial cells and maintains these cells in their mature state in mice and possibly humans.
5) In mice, GATA3 is responsible for the normal development of various tissues including the skin, fat cells, the thymus, and the nervous system.
Clinical significance
Mutations
Inactivating mutations in one of the two parental GATA3 genes cause the congenital disorder of hypoparathyroidism with sensorineural deafness and kidney malformations, i.e. the Barakat syndrome. This rare syndrome may occur in families or as a new mutation in an individual from a family with no history of the disorder. Mutations in GATA3 cause variable degrees of hypoparathyroidism, deafness, and kidney disease birth defects because of 1) individual differences in the penetrance of the mutation, 2) a sporadic, and as yet unexplained, association with malformation of uterus and vagina, and 3) mutations which extend beyond the GATA3 gene into chromosomal areas where mutations are responsible for developing other types of abnormalities which are characteristics of the DeGeorge syndrome 2. The Barakat syndrome is due to a haploinsufficiency in GATA3 levels, i.e. levels of the transcription factor that are insufficient for the normal development of the cited tissues during embryogenesis.
Allergy
Mouse studies indicate that inhibiting the expression of GATA3 using antisense RNA methods suppresses allergic inflammation. The protein is overexpressed in the afflicted tissues of individuals with various forms of allergy including asthma, rhinitis, nasal polyps, and atopic eczema. This suggests that it may have a role in promoting these disorders. In a phase IIA clinical study of individuals suffering allergen-induced asthma, inhalation of Deoxyribozyme ST010, which specifically inactivates GATA3 messenger RNA, for 28 days reduced early and late immune lung responses to inhaled allergen. The clinical benefit of inhibiting GATA3 in this disorder is thought to be due to interfering with the function of Group 2 ILCs and Th2 cells by, for example, reducing their production of IL-4, IL-13, and especially IL-5. Reduction in these eosinophil-stimulating interleukins, it is postulated, reduces this cells ability to promote allergic reactivity and responses. For similar reasons, this treatment might also prove to be clinical useful for treating other allergic disorders.
Tumors
Breast tumors
Development
GATA3 is one of the three genes mutated in >10% of breast cancers (Cancer Genome Atlas). Studies in mice indicate that the gene is critical for the normal development of breast tissue and directly regulates luminal cell (i.e. cells lining mammary ducts) differentiation in experimentally induced breast cancer. Analytic studies of human breast cancer tissues suggest that GATA3 is required for specific type of low risk breast cancer (i.e. luminal A), is integral to the expression of estrogen receptor alpha, and (in estrogen receptor negative/androgen receptor positive cancers) androgen receptor signaling. These studies suggest that GATA3 is involved in the development of at least certain types of breast cancer in humans. However, there is disagreement on this, with some studies suggesting that the expression of the GATA3 acts to inhibit and other studies suggesting that it acts to promote the development, growth, and/or spread of this cancer. Further studies are needed to elucidate the role, if any, of GATA3 in the development of breast cancer.
Marker
Immuocytochemical analysis of GATA3 protein in breast cells is a valuable marker for diagnosing primary breast cancer, being tested as positive in up to 94% of cases. It is especially valuable for estrogen receptor positive breast cancers but is less sensitive (435-66% elevated), although still more valuable than many other markers, for diagnosing triple-negative breast cancers. This analysis is widely used as a clinically valuable marker for breast cancer.
Other tumor types
Similar to breast tumors, the role of GATA3 in the genesis of other tumor types is unclear but detection of its transcription factor product may be diagnostically useful. Immuocytochemical analysis of GATA3 protein is considered a valuable marker for certain types of urinary bladder and urethral cancers as well as for parathyroid gland tumors (cancerous or benign), Single series reports suggest that this analysis might also be of value for diagnosing salivary gland tumors, salivary duct carcinomas, mammary analog secretory carcinomas, benign ovarian Brenner tumors, benign Walthard cell rests, and paragangliomas.
Interactions
GATA3 has been shown to interact with the following transcription factor regulators: ZFPM1 and ZFPM2; LMO1; and FOXA1. These regulators may promote or inhibit GATA3 in stimulating the expression of its target genes.
See also
GATA transcription factors
References
Attribution
Further reading
External links
Transcription factors | GATA3 | [
"Chemistry",
"Biology"
] | 2,183 | [
"Induced stem cells",
"Gene expression",
"Transcription factors",
"Signal transduction"
] |
14,723,656 | https://en.wikipedia.org/wiki/Granulin | Granulin is a protein that in humans is encoded by the GRN gene. Each granulin protein is cleaved from the precursor progranulin, a 593 amino-acid-long and 68.5 kDa protein. While the function of progranulin and granulin have yet to be determined, both forms of the protein have been implicated in development, inflammation, cell proliferation and protein homeostasis. The 2006 discovery of the GRN mutation in a population of patients with frontotemporal dementia has spurred much research in uncovering the function and involvement in disease of progranulin in the body. While there is a growing body of research on progranulin's role in the body, studies on specific granulin residues are still limited.
Progranulin
Progranulin is the precursor protein for granulin. Cleavage of progranulin produces a variety of active 6 kDa granulin peptides. These smaller cleavage products are named granulin A, granulin B, granulin C, etc. Epithelins 1 and 2 are synonymous with granulins A and B, respectively. Cleavage of progranulin into granulin occurs either in the extracellular matrix or the lysosome. Elastase, proteinase 3 and matrix metalloproteinase are proteases capable of cleaving progranulin into individual granulin peptides. Progranulin and granulin can be further differentiated by their hypothesized opposing roles in the cell. While progranulin is associated with anti-inflammation, cleaved granulin peptides have been implicated in pro-inflammatory behavior. A C. elegans study showed that granulin peptides may also participate in toxic activity.
Expression
Progranulin is expressed in a wide variety of cell types both in the periphery and in the central nervous system. Progranulin expression is low in early development, but increases as cells mature. Cell types expressing progranulin include neurons, microglia, astrocytes and endothelial cells. Progranulin has been found to be highly expressed in microglia and up-regulated during injury Within the brain, progranulin mRNA is highly expressed in pyramidal, hippocampal and Purkinje cells cells.
Structure
Each individual granulin domain peptide is 60 amino acids in length. Granulin peptides are cysteine rich and capable of forming 6 disulfide bonds per residue. The disulfide bonds form a central rod-like core that shuttles each individual granulin peptide into a stacked β-sheet configuration. The structure of the granulin protein is similar to the structure of proteins from protein families that consist of hormones, growth factors, ion channel modulators and enzyme inhibitors. Because of progranulin's structural similarities to these proteins, much research was done to interrogate progranulin's potential role as a growth factor. When progranulin is secreted into the extracellular matrix, it is often glycosylated at four confirmed and one tentative N-linked glycosylation sites. The n-terminus of progranulin is hypothesized to be involved in the secretion of progranulin via secretory vesicles. Specifically, progranulin may be involved in regulating exosome excretion. The C-terminus of progranulin is hypothesized to be the primary binding partner of SORT1, a receptor of extracellular progranulin. The structural differences between each individual granulin peptide have yet to be characterized.
Interactive partners
In the extracellular matrix, progranulin binds to receptors on several cell types resulting in either activation of a signal transduction pathway or engulfment into the cell. Several studies have shown progranulin's involvement in the binding of SORT1 and the subsequent trafficking of bounded progranulin to the lysosome. One recent study has shown that progranulin may actually mediate prosaposin trafficking to the lysosome via SORT1. However, the absence of SORT1 does not prevent exogenous progranulin from promoting neurite outgrowth or enhancing cell survival of GRN knockout cells, suggesting that other receptors are involved in mediating extracellular progranulin function For example, SORT1 -/- neuronal cells are still able to bind progranulin. Other studies have suggested tumor necrosis factor and EPH receptor A2 as potential progranulin facilitators. After binding to the receptor, progranulin may induce and modulate signaling pathways such as MAPK/ERK, PI3K/Akt, and FAK. Gene ontology enrichment analysis reveals an association between progranulin and notch receptor signaling. Granulin has also been shown to interact with Cyclin T1 and TRIB3.
Function
Development
Although progranulin expression increases as cells mature, they are still involved in the development of multiple cell types. Progranulin is hypothesized to be a neurotrophic factor involved in corticogenisis. Induced pluripotent stem cell lines (IPSC) harboring the GRN mutation show a decrease in cortical neuronal differentiation ability. A recent mice study suggests that progranulin may be involved in regulating the early development of cerebellar tissue by selecting for individual climbing fibers as they intersect and form synapses with Purkinje cells. In addition, several studies implicate progranulin in synaptic pruning, a microglial process that occurs during development of the neural network. Cytokines, a neuronal marker for synapse elimination, is found to be upregulated in neurons with the GRN mutation. Increased cytokine tagging results in an increase in microglial density and activity around synapses. Progranulin may also be involved in sexual determination during embryonic development.
Inflammation and wound healing
Progranulin levels are elevated when tissue is inflamed. After wounding, keratinocytes, macrophages and neutrophils increase production of progranulin. Neutrophils are capable of secreting elastase into the extracellular matrix that is capable of cleaving progranulin into granulin peptides, that promote further promote inflammation. SLPI, inhibitors of elastase, are also released by neutrophils and macrophages to modulate progranulin cleavage. Addition of granulin B in cultured epithelial cells causes cells to secrete IL-8, a chemical that attracts monocytes and neutrophils, which further suggests the involvement of granulin peptides in promoting inflammation. The addition of exogenous SLPI and progranulin is able to alleviate the enhanced inflammatory response of mice that are unable to inhibit the cleavage of progranulin.
Cell proliferation
Progranulin is highly expressed in cells that are highly proliferative in nature. Several studies implicate progranulin in tumorigenesis and neuronal outgrowth. Progranulin promotes mitogenesis in epithelial cultures. When two epithelial lines were cultured in media with recombinant PGRN, proliferation was stimulated. Knockout of both progranulin homologues in a zebrafish model reduces axonal outgrowth. In primary cortical and motor neurons, progranulin regulates neuronal outgrowth and survival. In primary motor neurons, progranulin has been shown to increase neurite outgrowth by regulating the glycogen synthase kinase-3 beta. Progranulin may function as an autocrine growth factor in tumorigenesis.
Lysosomal function
The discovery of a GRN mutation leading to lysosomal storage disorder led to many studies that explored progranulin's role in regulating protein homeostasis via the lysosomal pathway. Transcriptional gene network interference study suggests that progranulin is highly involved in lysosomal function and organization. Imaging studies have shown co-localization of progranulin and lysosomal marker LAMP-1. Progranulin expression is regulated by TFEB, a transcription factor that mediates proteins involved in lysosomal biosynthesis. Progranulin may be involved in regulating protease activity. Proteases that could be regulated by progranulin include prosaposin, which is cleaved into saposin peptides in the lysosome, and cathepsin D, the primary protease involved in protein aggregate break down. GRN mutation shares similar neuropathology and clinical phenotype with CHMP2B and VCP mutations, genes that are both involved in the trafficking and breakdown of proteins involved in lysosomal function.
Clinical significance
Frontotemporal dementia
Heterozygous mutation of the GRN gene leading to progranulin haploinsufficiency causes frontotemporal dementia. These mutations include frameshift, splice site, nonsense signal peptide, Kozak sequence disruptions and missense mutations, which result in either nonsense-mediated decay or the production of non-functional protein. Patients with GRN caused FTD (GRN-FTD) exhibit asymmetric brain atrophy, although age of onset, disease progression and clinical symptoms vary, suggesting that other genetic or environmental factors may be involved in disease expression. Pathological indicators include cytosolic ubiquitin deposits enriched in hyperphosphorylated TAR DNA-binding protein 43 (TDP-43), autophagy-related protein aggregates, ubiquitin-binding protein p62, lentiform intranuclear inclusions, dystrophic neurites and inflammation. Patients with the heterozygote mutation exhibit a reduction of 70–80% serum progranulin levels when compared to controls. Reprogrammed stem cells restore GRN mRNA levels to 50%, further suggesting that some other genetic or environmental factor is involved in regulating FTD disease expression. Mice exhibit reduced autophagic flux and autophagy-dependent clearance. Human FTLD-GRN derived fibroblasts show decrease lysosomal protease activity and lymphoblasts containing neuronal ceroid lipofuscinosis-like storage material. FTLD-GRN IPSC cortical Neurons have enlarged vesicles, lipofuscin accumulation and cathepsin D deficiency.
Neuronal ceroid lipofuscinosis
Homozygous mutation of the GRN gene causes neuronal ceroid lipofuscinosis (NCL) characterized by an accumulation of autofluorescent lipofuscin, enlarged vacuoles, impairment in lysosomal activity, retinal and brain degeneration, exaggerated inflammatory responses, microgliosis, astrogliosis and behavioral dysfunction such as OCD-like and disinhibition-like behavior. Aged GRN double mutant mice have lipofuscin deposits and enlarge lysosomes, while one group found phosphorylated TDP-43.
Other diseases
Progranulin may also be involved in cancer development, atherosclerosis and other metabolic disease, Alzheimer's disease, amyotrophic lateral sclerosis (ALS) and limbic predominant age-related TDP-43 encephalopathy (LATE).
Progranulin can promote cyclin D1 expression in breast cancer lines and phosphorylation of proteins through extracellular regulated kinase signaling pathways. Progranulin is highly expressed in ovarian, adrenal carcinomas and immortalized epithelial cells. There is a correlation between progranulin concentration and cancer severity. Granulin release by macrophages has been associated with fibrotic hepatic metastasis in pancreatic cancer. The human liver fluke Opisthorchis viverrini contributes to the development of bile duct (liver) cancer by secreting a granulin-like growth hormone.
Progranulin may also be involved in promoting the progression of atherosclerosis. While progranulin may be anti-atherogenic, granulins may be pro-atherogenic. Increased serum and plasma progranulin levels in patients with type 2 diabetes and visceral obesity implicating progranulin in metabolic diseases.
A recent genome-wide association study (GWAS) has found that genetic variations in GRN are associated with late-onset sporadic Alzheimer’s disease (LOAD). These genetic variations change the degradation pathways of misfolded protein contributing misfolded β-amyloid accumulation and plaque formation.
References
Further reading
External links
GeneReviews/NCBI/NIH/UW entry on GRN-Related Frontotemporal Dementia
Protein families
Precursor proteins | Granulin | [
"Biology"
] | 2,691 | [
"Protein families",
"Protein classification"
] |
14,723,666 | https://en.wikipedia.org/wiki/MAP3K1 | Mitogen-activated protein kinase kinase kinase 1 (MAP3K1) is a signal transduction enzyme that in humans is encoded by the autosomal MAP3K1 gene.
Function
MAP3K1 (or MEKK1) is a serine/threonine kinase and ubiquitin ligase that performs a pivotal role in a network of enzymes integrating cellular receptor responses to a number of mitogenic and metabolic stimuli, including: TNF receptor superfamily (TNFRs), T-cell receptor (TCR), Epidermal growth factor receptor (EGFR), and TGF beta receptor (TGFβR). Mitogen-activated protein kinase kinases (MAP2Ks) are substrates for direct phosphorylation by the MAP3K1 protein kinase. The MAP3K1 kinase domain may also be a modest activator of IκB kinase activation. The MAP3K1 E3 ubiquitin ligase recruits a ubiquitin-conjugating enzyme (including UBE2D2, UBE2D3, and UBE2N:UBE2V1) that has been loaded with ubiquitin, interacts with its substrates, and facilitates the transfer of ubiquitin from the ubiquitin-conjugating enzyme onto its substrates. Genetics has revealed that MAP3K1 is important in: embryonic development, tumorigenesis, cell growth, cell migration, cytokine production, and humoral immunity. MAP3K1 mutants were identified in breast cancer by GWAS.
Structure
MAP3K1 contains a protein kinase domain, PHD finger (which has a RING finger domain-like structure) that serves as an E3 ubiquitin ligase, and scaffold protein regions that mediate protein–protein interactions.
Genetic analyses in murine and avian models
MAP3K1 is highly conserved in Euteleostomi. The spontaneous recessive lidgap-Gates mutation (deletion of Map3k1 exons 2–9, initially described in the 1960s) identified on the SELH/Bc mouse strain causes the same open-eyelids-at-birth mutational phenotype as the gene knockout mutations of the mouse (but not human) MAP3K1 homolog (Map3k1) and also co-maps to distal Chromosome 13. MAP3K1 was analysed genetically by targeted mutagenesis using transgenic mice (C57BL/6 and C57BL/6 × 129 backgrounds), embryonic stem cells, and the DT40 cell line to identify genetic traits.
Mechanism of MAPK activation by MAP3K1
MAP3K1 contains multiple amino acid sites that are phosphorylated and ubiquitinated. Early biochemical analysis demonstrated that triple co-expression of MAP3K1, MAP2K and MAPK in bacterial cells was sufficient for the activation of MAPK. Later analysis of syngenic mice that harbour mutations in TRAF2, UBE2N, Map3k1 and Map3k7 identified critical regulators of cytokine-induced MAPK signal transduction in B cells. Cytokine signaling through MAP3K1 utilises two-stage cell signaling to recruit the signal transduction mechanism to cytokine receptors and then release the signal transduction components, altered by post-translational modification, from the cellular membrane to activate MAPKs. Genetic analysis has demonstrated that the E3 Ub ligase and the kinase domains of MAP3K1 are required for MAPK activation.
Cancers, other diseases and therapeutic targeting
MAP3K1 is a biomarker mutated in 3.24% of all human cancers. MAP3K1 has been associated with several diseases in non-syngeneic human populations, including: breast cancer, adenocarcinoma of the prostate, sarcomatoid hepatocellular carcinoma, acute respiratory distress syndrome, Langerhans cell histiocytosis, and 46,XY disorders of sex development. E6201 is an enzyme inhibitor of MAP3K1 that shows cross-specificity with MAP2K1.
Interaction partners
MAP3K1 has been shown to interact with a number of proteins, including:
AXIN1,
C-Raf, MAP2K1, MAPK1,
Grb2,
MAPK8,
TRAF2,
UBE2I.
TAB1, TNIP1, TNIP2. Signal transducing adaptor molecule,
Transforming protein RhoA,
RAC1, CDC42,
ARHGAP4,
MAP2K4, and
PTK2.
References
Further reading
Mitogen-activated protein kinases
EC 2.7.11
Biomarkers | MAP3K1 | [
"Biology"
] | 985 | [
"Biomarkers"
] |
14,723,679 | https://en.wikipedia.org/wiki/MED1 | Mediator of RNA polymerase II transcription subunit 1 also known as DRIP205 or Trap220 is a subunit of the Mediator complex and is a protein that in humans is encoded by the MED1 gene. MED1 functions as a nuclear receptor coactivator.
Function
The activation of gene transcription is a multistep process that is triggered by factors that recognize transcriptional enhancer sites in DNA. These factors work with co-activators to direct transcriptional initiation by the RNA polymerase II apparatus. The mediator of RNA polymerase II transcription subunit 1 protein is a subunit of the CRSP (cofactor required for SP1 activation) complex, which, along with TFIID, is required for efficient activation by SP1. This protein is also a component of other multisubunit complexes [e.g., thyroid hormone receptor-(TR-) associated proteins that interact with TR and facilitate TR function on DNA templates in conjunction with initiation factors and cofactors]. It also regulates p53-dependent apoptosis and it is essential for adipogenesis. This protein is known to have the ability to self-oligomerize.
Interactions
MED1 has been shown to interact with:
Androgen receptor,
Calcitriol receptor,
Cyclin-dependent kinase 8,
Estrogen receptor alpha,
Glucocorticoid receptor,
Hepatocyte nuclear factor 4 alpha,
P53,
PPARGC1A,
TGS1, and
Thyroid hormone receptor alpha.
Protein family
This entry represents subunit Med1 of the Mediator complex. The Med1 forms part of the Med9 submodule of the Srb/Med complex. It is one of three subunits essential for viability of the whole organism via its role in environmentally-directed cell-fate decisions.
References
Further reading
Protein domains
Transcription coregulators | MED1 | [
"Biology"
] | 383 | [
"Protein domains",
"Protein classification"
] |
14,723,733 | https://en.wikipedia.org/wiki/USF1 | Upstream stimulatory factor 1 is a protein that in humans is encoded by the USF1 gene.
Gene
The upstream stimulatory factor gene encodes a transcription factor USF that belongs to the proto-oncogene MYC family and is featured by a basic helix-loop-helix leucine zipper (bHLH-LZ) motif in the protein structure. USF was originally identified to regulate the major late promoters of adenovirus, and recent research has further revealed its role in tissue protection. The bHLH-LZ motif enables the transactivation capacity of the USF protein through interacting with the Initiator element (Inr) and E-box motif on the bound DNA. In the context of insulin and glucose-induced USF activities, those E-box motifs can act as a glucose-responsive element (GRE) and a part of the carbohydrate response element (ChoRE) to interact with transcription factors.
Isoforms
USF comprises two major isoforms: USF1 and USF2. USF1 gene locates on the chromosome region 1q22-q23 in both human and mice; USF2 gene locates on the chromosome 19q13 in human and chromosome 19q7 in mice, respectively. Both USF1 and USF2 transcripts comprise 10 exons and can undergo exon 4-excision during alternative splicing. From an auto-regulation perspective, these exon 4-excision products act as dominant negative regulators and are found to suppress USF-dependent gene expression.
Protein
Although USF1 and USF2 share 70% of the amino acid sequence in their bHLH-LZ region, only 40% of similarity is found in their full-length proteins. In addition, USF1 and USF2 exhibit different protein abundances in a cell type-specific manner. It has been found that USF1 and USF2 expression increases during the differentiation of erythroid cells. Despite the ubiquitous expression of both isoforms, USF1 and USF2 mediate different biological processes and functions in cells. While USF1 modulates metabolism, immune response, and tissue protection, USF2 primarily controls embryonic development, brain function, iron metabolism, and fertility. Structurally, the highly conserved bHLH-LZ structure on the C-terminus of USF yields high binding specificity and promotes the formation of USF1 homodimers or USF1-USF2 heterodimers for DNA binding. The USF-specific region (USR) on the N-terminal region, on the other hand, facilitates the nuclear translocation and activation of USF1.
Function
This gene encodes a member of the basic helix-loop-helix leucine zipper family and can function as a cellular transcription factor. The encoded protein can activate transcription through pyrimidine-rich initiator (Inr) elements and E-box motifs. This gene has been linked to familial combined hyperlipidemia (FCHL). Two transcript variants encoding distinct isoforms have been identified for this gene.
A study of mice suggested reduced USF1 levels increase metabolism in brown fat.
Regulation
Modulation of DNA binding affinity
The symmetrical E-box motif is the main target of bHLH-LZ transcription factors, and USF1 has a high binding affinity for the core sequence CACGTG in the motif. USF1-DNA binding activity can be modulated by cell type-specific DNA methylation and acetylation on the E-box motif or by post-transcriptional modifications of the USF1 protein. For example, CpG methylation on the central E-box motif inhibits the complex formation of USF1 with its co-transcription factors and therefore decreases the corresponding gene expression in mouse lymphosarcoma cells. In contrast, phosphorylation of USF1 by p38 mitogen-activated protein kinases, protein kinase A or protein kinase C increases its binding to the E-box motif and activate gene transcription.
Phosphorylation
Mitogen-activated protein kinase (MAPKs) phosphorylates serine and threonine residues of substrate proteins and convert extracellular signals induced by growth factors, mitogens or cytokines into intracellular phosphorylation cascades, which regulate cell proliferation, differentiation, stress responses and apoptosis (programmed cell death).
Phosphorylation by MAPKs induces a conformational change of the USF protein and exposes its DNA-binding domain for interaction. This increased structural exposure enhances DNA binding and therefore the transcriptional activity of USF.
ERK1 (also known as MAPK3) and ERK2 (also known as MAPK1) phosphorylate USF1 in response to TFG-β signaling in vascular smooth muscle cells. SMAD2 and SMAD3 signaling following the TFG-β receptor activation can also cooperate with EGFR / ERK pathways to activate USF1, which in turn regulates the gene expression of plasminogen activator inhibitor-1 (PAI-1), a significant biomarker and predictor of cardiovascular disease-related death and a marker of poor prognosis in breast cancer.
Casein kinase 2 or CK-II (CK2) is a tetrameric enzyme composed of two catalytic and two regulatory subunits. In pancreatic cells, CK2 phosphorylates USF1, PDX1 and MST1 to suppress insulin expression.
Gene transcription
Transforming growth factor β 1 (TGF beta 1) is encoded by the TFGB1 gene that contains an E-box within the promoter region and has been implicated in excessive extracellular matrix accumulation under a high-glucose condition. Overexpression of either USF1 or USF2 is found to elevate the TFGB1 promoter activity in human embryonic kidney cells. However, only USF1 overexpression leads to increased TGF-β1 secretion.
Thrombospondin 1 (TSP1) is involved in the development of diabetic nephropathy. USF1/2 binds to the E-box motif (CAGATG) on the human THBS1 promoter and regulates high-glucose-induced TSP1 expression in mesangial cells. USF2 overexpression has been found to augment THBS1 promoter activity and TSP1 expression. The resulting increase in TSP1 expression further promotes the formation of active TGF-β.
AP-1 transcription factor (AP-1) refers to a complex of dimeric transcription factors composed of c-Jun, c-Fos or activating transcriptionfactor (ATF) that bind to the AP-1 binding site on DNA. cJun-cJun / cJun-cFos dimers preferentially bind to the phorbol 12-O-Tetradecanoylphorbol-13-acetate (TPA)-responsive element (TRE region, TGACTCA), whereas cJun-ATF dimers and ATF homodimers preferentially bind to the cAMP-responsive element (CRE, TGACGTCA). The AP-1 complex becomes activated in response to high glucose, oxidative stress, low-density lipoprotein(LDL) and oxidised LDL. It has been reported that a high glucose level upregulates USF and AP-1 binding activities, as well as the protein level of cFos.
Interaction between USF1 and other transcription factors, including SP1, PEA3 (also known as ETV4) and MTF1, also leads to cooperative transcriptional regulation. For instance, the leucine zipper motif of USF1 recruits PEA3 to form a ternary complex and co-regulates the transcription of BAX, an apoptosis regulator. Another USF1-regulated target is topoisomerase III (hTOP3⍺), which catalyzes the topological changes of DNA, modifies DNA supercoil structures, and increases the chromatin accessibility for gene expression. Similar interactions exist between USF1 and JMJD1C or H3K9 demethylase, in which the molecular interactions change chromatin accessibility and elevate the transcription of a series of lipogenic genes, including FASN, ACC, ACLY, and SREBP1.
Chromosome boundary by USF
Chromosomes are generally classified into euchromatin and heterochromatin with distinct histone modifications, compaction levels, and the resulting gene expression patterns. Heterochromatin is a tightly condensed and transcriptionally repressed chromatin domain that is characterized by distinct combinations of histone post-translational modifications. Heterochromatin is required for genome stability and gene expression regulation. However, it can spread into neighboring DNA regions and inactivate gene expression. Chromosome boundary elements are thus necessary to block such stochastic spreads of heterochromatin and maintain stable gene expression. USF1 and USF2 have been found to recruit various histone-modifying complexes, including the histone H3 methyltransferase Set1 complex and the H4 arginine 3 methyltransferase PRMT1, with the latter known to establish active chromatin domains. USF1/USF2 binding deposits a high level of activating histone modifications on adjacent nucleosomes and thus prevents the propagation of chromatin silencing modifications from the heterochromatin, such as H3K9 and K27 methylation.
Other USF1/USF2-related chromatin modifications include the recruitment of the E3 ubiquitin ligase, RNF20, to moniubiquitinate histone H2B. The loss of RNF20 is found to cause an extension of the silencing modifications from the 16 kb heterochromatic domain into the β-globin locus. Moreover, USF1 and USF2 can bind to the 5' DNase I hypersensitive site HS4 and recruit an H3 acetyltransferase, PCAF, which blocks the heterochromatin spread into the β-globin locus.
FASN transactivates for lipogenesis
USF is known to bind the L-type pyruvate kinase promoter on DNA at high glucose and insulin levels. Excessive insulin activates kinases and phosphatases that post-translationally modify USF, sterol regulatory element-binding protein 1C (SREBP1C), Carbohydrate-responsive element-binding protein (ChREBP), and Liver X receptor (LXRs). With insulin stimulation, USF1 and USF2 bind to the E-boxes at -332 and -65 in the promoter region of FASN that encodes Fatty acid synthase (FAS) for lipogenesis.
Various post-translational modifications of USF1 determine its activity and signaling pathways and can affect the lipogenesis process. An abnormal increase in the USF-mediated de novo fatty acid synthesis is found to cause intracellular fatty acid accumulation and deregulate gene expression and cellular processes like tumor cell survival.
Lipogenic pathways
In response to insulin elevation, DNA-protein kinase (DNA-PK) involved in DNA damage repair becomes dephosphorylated and activated. The active form of DNA-PK indirectly phosphorylates USF1 at S262 through AMP-activated protein kinase (AMPK). The S262 phosphorylation increases USF1 interaction with SREBP1C near the sterol regulatory element (SRE) and facilitates the synergistic activation of SREBP1C and transcription of the downstream lipogenic genes.
USF1 S262 phosphorylation also recruits PCAF to acetylate USF1 at the site K237. Both S262 phosphorylation and K237 acetylation enhance USF1 activities and the subsequent transcriptional activation of the fatty acid synthase gene (FASN). Fatty acid synthase (FAS), together with Acetyl-CoA carboxylase (ACC), produces malonyl-CoA, converts it to long-chain fatty acids, and promotes the de novo fatty-acid synthesis for energy provision and protein lipidation.
USF1 modified with S262 phosphorylation an K237 acetylation also recruits BGR1 (also known as SMARCA4)-associated factor 60c (BAF60c). BAF60c is then phosphorylated by atypical protein kinase C (aPKC) at S257, allowing it to form a LipoBAF complex at promoters of lipogenic genes to regulate chromatin structure and gene transcription.
In contrast, HDAC9 deacetylates USF1 during cell fasting, prevents the recruitment of USF1-interacting factors, and suppresses the transcriptional activation of lipogenic genes.
In early embryonic development
USF1 transcription undergoes active dynamics during cell meiosis, in which the USF1 mRNA first increases significantly during 2-8 cells and then decreases to an undetectable level at the blastocyst stage, indicating its role in the embryo genome activation. USF1 siRNA knockout has been shown to compromise the blastocyst rate and deregulate the transcripts of twist-related protein 2 (increased), growth differentiation factor-9 and follistatin (decreased) by affecting their promoter-binding element E-box region during oocyte maturation.
Clinical significance
Diabetic kidney disease
Diabetic kidney disease (DKD) (or Diabetic nephropathy) is a progressive microalbuminuria disease with a slight loss of albumin in the urine (30–300 mg per day); DKD has been viewed as a diabetic complication-related microvascular disorder in a renal manifestation. In kidney biopsy, DKD is characterized by glomerular and tubular basement thickening, mesangial expansion, glomerulosclerosis, podocyte effacement (histology) and nephron loss. DKD occurs in 30%-50% of the diabetic patient population and leads to kidney failures in up to 20% of the type 1 diabetic patients. However, a substantial portion of DKD patients do not manifest albuminuria. DKD pathogenesis is attributed to the dysregulated glucose transport at a higher glucose level and the excessive influx of intracellular glucose into endothelial cells. The elevated glucose level is sustained along with multiple metabolic phenotypes such as excess fatty acids and oxidative stress, as well as shear stresses induced by hypertension and hyperfusion, and can lead to microvascular rarefaction, hypoxia and maladaptation in glomerular neoangiogenesis.
USF1 as an insulin-sensitive transcription factor that becomes active in response to a high glucose level promotes the transactivation of genes involved in lipid metabolism, including hepatic lipase (LIPC), hepatocyte nuclear factor 4 alpha (HNF4A), Apolipoprotein AI (APOA1), Apolipoprotein L1 (APOL1) and Haptoglobin-related protein (HPR). Especially, APOL1 is known to complex with APOA-I and HDL to facilitate cell autophagy in response to injuries and prevent glomerular diseases; however, an APOL1 risk variant specific to podocyte inhibits cell autophagy and can trigger kidney disease.
Cancer
Increased FASN-mediated de novo lipid synthesis
Cancer cells exhibit a set of phenotypes, including a highlighted increase in aerobic glycolysis, lactic acid production (known as the Warburg effect), elevated protein and DNA synthesis, and increased de novo or endogenous fatty acid synthesis by fatty acid synthase (FAS). FAS synthesizes primarily palmitate from malonyl-CoA, which is further esterified to triglycerides for energy storage. Normally, FASN is active during embryogenesis and in fetal lungs for lubricant production; however, it is physiologically low-expressed in non-cancerous adult cells. In contrast, abnormal FASN overexpression is detected in multiple cancer types, spanning breast cancer, colorectal cancer, prostate cancer, pancreatic cancer and ovarian cancer. FASN-mediated de novo lipid synthesis accounts for more than 93% of triglycerides in tumor cells. Specifically, tumor cells prefer glycolysis over oxidation for energy consumption and re-direct the glycolytic products towards de novo fatty acid synthesis to supply lipids for membrane production and protein lipidation for fast cell proliferation. For example, PI3K-AKT pathway is found to increase in LNCaP prostate cancer cells to stimulate FASN overexpression. Concurrently, fatty acid synthase overexpression is also post-translationally sustained by USP2a-mediated ubiquitination reduction, stabilizing FAS for constitutive signal transduction. In addition to de novo lipogenesis, FAS promotes the localization of VEGFR-2 to the lipid raft of the endothelial cell membrane and thus enhances angiogenesis in tumor development. Meanwhile, mutual activation between FAS and ERBB2 (HER2) signaling also potentiates tumorigenesis, in which ERBB2 amplification is associated with elevated survival and proliferation of cancer cells and poor prognosis in breast and gastric cancers; an ERBB2 increase, especially, contributes to 18-25% of breast cancers. In prostate cancer cells and promyelocytic leukemia cells, USF1 activation also attains a high-level of PAI-1 expression and inhibits spontaneous or camptothecin-induced apoptosis.
Decreased USF1-p53 interaction and increased p53 instability
The poor prognosis of gastric cancers is associated with low expression of USF1 and p53. Among gastric cancer patients, 88% of the patients are diagnosed with H. pylori infection, and half of the patients show lower USF1 expression in tumor tissues. Mechanistically, H. pylori induces DNA hypermethylation in the promoter regions of USF1 and USF2 and inhibits expression. Decreased expression reduces the interaction between USF1 and p53 when DNA damage occurs, rendering p53 to associate more frequently with the E3-ubiquitin ligase HDM2 (also known as MDM2) and increasing p53 instability in cancer cells.
Familial combined hyperlipidemia
Familial combined hyperlipidemia (FCHL) was first used to describe lipid abnormalities in 47 Seattle pedigree-containing members with hypercholesterolemia and hypertriglyceridemia. The core FCHL lipid profiles feature high serum cholesterol/triglyceride, apolipoprotein B (APOB) and LDL levels. Genetic evidence has suggested a FCHL-related locus on the human chromosome 1q21-q23, which is linked to metabolic syndromes. Fine-mapping of those linked regions identifies USF1 as the first positionally cloned gene for FCHL and a target for FCHL treatment. In addition, hepatocyte nuclear factor 4 alpha (HNF4A) is also implicated in high lipid levels and metabolic syndromes. Cooperative effects of USF1 and HNF4A have been shown to regulate the expression of apolipoprotein A-II (APOA2) and apolipoprotein C-III (APOC3). Mutations in USF1, HNF4A and apolipoproteins also increase patients' susceptibility to FCHL. Additional genes subjected to USF1 regulation and involved in glucose/lipid metabolism include apolipoprotein A5 (APOA5), apolipoprotein E (APOE), hormone-sensitive lipase (LIPE), hepatic lipase (LIPC), glucokinase (GCK), islet-specific glucose-6-phosphatase catalytic-subunit-related protein (IGRP), insulin, glucagon receptor (GCGR) and ATP-binding cassette transporter A1 (ABCA1).
Interactions
USF1 (human gene) has been shown to interact with USF2, FOSL1 and GTF2I.
References
Further reading
External links
Transcription factors | USF1 | [
"Chemistry",
"Biology"
] | 4,380 | [
"Induced stem cells",
"Gene expression",
"Transcription factors",
"Signal transduction"
] |
14,723,767 | https://en.wikipedia.org/wiki/BCL10 | B-cell lymphoma/leukemia 10 is a protein that in humans is encoded by the BCL10 gene. Like BCL2, BCL3, BCL5, BCL6, BCL7A, and BCL9, it has clinical significance in lymphoma.
Function
Bcl10 was identified by its translocation in a case of mucosa-associated lymphoid tissue (MALT) lymphoma. The protein encoded by this gene contains a caspase recruitment domain (CARD), and has been shown to activate NF-κB. This protein is reported to interact with other CARD and coiled coil domain containing proteins including CARD9, -10, -11 and -14, which are thought to function as upstream regulators in NF-κB signaling. This protein is found to form a complex with the paracaspase MALT1, a protein encoded by another gene known to be translocated in MALT lymphoma. MALT1 and Bcl10 thought to synergize in the activation of NF-κB, and the deregulation of either of them may contribute to the same pathogenetic process that leads to the malignancy. Bcl10 is evolutionary conserved since cnidaria and has been shown to be functionally conserved all the way back to zebrafish. Notably, just like the upstream CARD-CC family, Bcl10 is absent in insects and nematodes, and the correlated phylogenetic distribution of Bcl10 and CARD-CC proteins indicate a conserved complex.
Interactions
BCL10 has been shown to interact with:
CARD10,
CARD11,
CARD14,
CARD9
CRADD,
IKBKG,
MALT1, and
TRAF2.
References
External links
Further reading
Proteins
Tumor_suppressor_genes | BCL10 | [
"Chemistry"
] | 378 | [
"Biomolecules by chemical classification",
"Proteins",
"Molecular biology"
] |
14,723,883 | https://en.wikipedia.org/wiki/HLA-DRB3 | HLA class II histocompatibility antigen, DRB3-1 beta chain is a protein that in humans is encoded by the HLA-DRB3 gene.
Function
The protein encoded by this gene belongs to the HLA class II beta chain paralogues. The class II molecule is a heterodimer consisting of an alpha (DRA) and a beta chain (DRB), both anchored in the membrane. It plays a central role in the immune system by presenting peptides derived from extracellular proteins. Class II molecules are expressed in antigen-presenting cells (APC: B lymphocytes, dendritic cells, macrophages).
Gene structure and polymorphisms
The beta chain is approximately 26–28 kDa. It is encoded by 6 exons, exon one encodes the leader peptide, exons 2 and 3 encode the two extracellular domains, exon 4 encodes the transmembrane domain and exon 5 encodes the cytoplasmic tail. Within the DR molecule the beta chain contains all the polymorphisms specifying the peptide binding specificities. Typing for these polymorphisms is routinely done for bone marrow and kidney transplantation.
Gene expression
DRB1 is expressed at a level five times higher than its paralogues DRB3, DRB4 and DRB5. DRB1 is present in all individuals. Allelic variants of DRB1 are linked with either none or one of the genes DRB3, DRB4 and DRB5. There are 4 related pseudogenes: DRB2, DRB6, DRB7, DRB8 and DRB9.
See also
HLA-DR
References
Further reading
Genes
Human proteins | HLA-DRB3 | [
"Chemistry"
] | 358 | [
"Biochemistry stubs",
"Protein stubs"
] |
14,723,907 | https://en.wikipedia.org/wiki/Calcium-activated%20potassium%20channel%20subunit%20alpha-1 | Calcium-activated potassium channel subunit alpha-1 also known as large conductance calcium-activated potassium channel, subfamily M, alpha member 1 (KCa1.1), or BK channel alpha subunit, is a voltage gated potassium channel encoded by the KCNMA1 gene and characterized by their large conductance of potassium ions (K+) through cell membranes.
Function
BK channels are activated (opened) by changes in membrane electrical potential and/or by increases in concentration of intracellular calcium ion (Ca2+). Opening of BK channels allows K+ to passively flow through the channel, down the electrochemical gradient. Under typical physiological conditions, this results in an efflux of K+ from the cell, which leads to cell membrane hyperpolarization (a decrease in the electrical potential across the cell membrane) and a decrease in cell excitability (a decrease in the probability that the cell will transmit an action potential).
BK channels are essential for the regulation of several key physiological processes including smooth muscle tone and neuronal excitability. They control the contraction of smooth muscle and are involved with the electrical tuning of hair cells in the cochlea. BK channels also contribute to the behavioral effects of ethanol in the worm C. elegans under high concentrations (> 100 mM, or approximately 0.50% BAC). It remains to be determined if BK channels contribute to intoxication in humans.
Structure
BK channels have a tetrameric structure. Each monomer of the channel-forming alpha subunit is the product of the KCNMA1 gene. Modulatory beta subunits (encoded by KCNMB1, KCNMB2, KCNMB3, or KCNMB4) can associate with the tetrameric channel. Alternatively spliced transcript variants encoding different isoforms have been identified.
Each BK channel alpha subunit consists of (from N- to C-terminal):
A unique transmembrane domain (S0) that precedes the 6 transmembrane domains (S1-S6) conserved in all voltage-dependent K+ channels.
A voltage sensing domain (S1-S4).
A K+ channel pore domain (S5, selectivity filter, and S6).
A cytoplasmic C-terminal domain (CTD) consisting of a pair of RCK domains that assemble into an octameric gating ring on the intracellular side of the tetrameric channel. The CTD contains four primary binding sites for Ca2+, called "calcium bowls", encoded within the second RCK domain of each monomer.
Available X-ray structures include:
– Open structure of the BK channel gating ring
– Crystal structure of the human BK gating apparatus
– Structure of the intracellular gating ring from the human high-conductance Ca2+ gated K+ channel (BK Channel)
Pharmacology
BK channels are pharmacological targets for the treatment of stroke. Various pharmaceutical companies developed synthetic molecules activating these channels in order to prevent excessive neurotoxic calcium entry in neurons. But BMS-204352 (MaxiPost) a molecule developed by Bristol-Myers Squibb failed to improve clinical outcome in stroke patients compared to placebo. BK channels have also been found to be activated by exogenous pollutants and endogenous gasotransmitters carbon monoxide and hydrogen sulphide.
BK channels are blocked by tetraethylammonium (TEA), paxilline and iberiotoxin.
Related conditions
Researchers have identified a rare disease in humans caused by mutations in the gene. KCNMA1-linked channelopathy can cause neurological conditions like seizures and movement disorders. An episode of the Diagnosis TV show, based on a column in the New York Times, was about a young girl with a KCNMA1 disorder that caused transient episodes of muscle weakness.
See also
BK channel
Calcium-activated potassium channel
Voltage-gated potassium channel
References
Further reading
External links
Meredith Lab
Ion channels | Calcium-activated potassium channel subunit alpha-1 | [
"Chemistry"
] | 827 | [
"Neurochemistry",
"Ion channels"
] |
14,724,003 | https://en.wikipedia.org/wiki/Placental%20growth%20factor | Placental growth factor (PlGF) is a protein that in humans is encoded by the PGF gene.
Placental growth factor (PGF) is a member of the VEGF (vascular endothelial growth factor) sub-family - a key molecule in angiogenesis and vasculogenesis, in particular during embryogenesis. The main source of PGF during pregnancy is the placental trophoblast. PGF is also expressed in many other tissues, including the villous trophoblast.
The placental growth factor (PGF) gene is a protein-coding gene and a member of the vascular endothelial growth factor (VEGF) family. The PGF gene is expressed only in human umbilical vein endothelial cells (HUVE) and the placenta. PGF is ultimately associated with angiogenesis. Specifically, PGF plays a role in trophoblast growth and differentiation. Trophoblast cells, specifically extravillous trophoblast cells, are responsible for invading the uterine wall and the maternal spiral arteries. The extravillous trophoblast cells produce a blood vessel of larger diameter for the developing fetus that is independent of maternal vasoconstriction. This is essential for increased blood flow and reduced resistance. Proper development of blood vessels in the placenta is crucial for the higher blood requirement of the fetus later in pregnancy.
Under normal physiologic conditions, PGF is also expressed at a low level in other organs including the heart, lung, thyroid, and skeletal muscle.
Isoform tissue specificity
There are three isoforms of this protein: PGF-1, PGF-2, PGF-3. PGF-1 is specifically found in the colon as well as mammary carcinomas, while PGF-2 is only found in early placenta up until the 8th week of development. PGF-2 is the only isoform able to bind to heparin. PGF-3 is found mainly in placental tissues.
Clinical significance
Placental growth factor-expression within human atherosclerotic lesions is associated with plaque inflammation and neovascular growth.
Serum levels of PGF and sFlt-1 (soluble fms-like tyrosine kinase-1, also known as soluble VEGF receptor-1) are altered in women with preeclampsia. Studies show that in both early and late onset preeclampsia, maternal serum levels of sFlt-1 are higher and PGF lower in women presenting with preeclampsia. In addition, placental sFlt-1 levels were significantly increased and PGF decreased in women with preeclampsia as compared to those with uncomplicated pregnancies. This suggests that placental concentrations of sFlt-1 and PGF mirror the maternal serum changes. This is consistent with the view that the placenta is the main source of sFlt-1 and PGF during pregnancy.1
PGF is a potential biomarker for preeclampsia, a condition in which blood vessels in the placenta are too narrow, resulting in high blood pressure. As mentioned before, extravillous trophoblast cells invade maternal arteries. Improper differentiation may result in hypo-invasion of these arteries and thus failure to widen enough. Studies have found low levels of PGF in women who were diagnosed with preeclampsia later in their pregnancy.
Associated diseases
Placental insufficiency, otherwise known as uteroplacental vascular insufficiency, results from insufficient blood supply to the placenta. This disease is characterized by an alteration in the PGF gene and its GPCR and ERK signaling pathways. Alterations in the PGF and the PGF receptor mRNA expression prevent the normal development of placental vasculature.
Twin-to-twin transfusion syndrome is another disease associated with the PGF gene. This is a rare disease occurring primarily in identical twins where blood from one twin is transferred to the other. Typically, the twin whose blood is being transferred is born smaller and with anemia while the other twin is born larger with too much blood and at increased risk for heart failure. The PGF gene pathways primarily affected are the TGF-Beta pathway and AKT signaling pathway.
References
Further reading
Placenta
Angiology
Growth factors | Placental growth factor | [
"Chemistry"
] | 901 | [
"Growth factors",
"Signal transduction"
] |
14,724,063 | https://en.wikipedia.org/wiki/ZFP36 | Tristetraprolin (TTP), also known as zinc finger protein 36 homolog (ZFP36), is a protein that in humans, mice and rats is encoded by the ZFP36 gene. It is a member of the TIS11 (TPA-induced sequence) family, along with butyrate response factors 1 and 2.
TTP binds to AU-rich elements (AREs) in the 3'-untranslated regions (UTRs) of the mRNAs of some cytokines and promotes their degradation. For example, TTP is a component of a negative feedback loop that interferes with TNF-alpha production by destabilizing its mRNA. Mice deficient in TTP develop a complex syndrome of inflammatory diseases.
Interactions
ZFP36 has been shown to interact with 14-3-3 protein family members, such as YWHAH, and with NUP214, a member of the nuclear pore complex.
Regulation
Post-transcriptionally, TTP is regulated in several ways. The subcellular localization of TTP is influenced by interactions with protein partners such as the 14-3-3 family of proteins. These interactions and, possibly, interactions with target mRNAs are affected by the phosphorylation state of TTP, as the protein can be posttranslationally modified by a large number of protein kinases. There is some evidence that the TTP transcript may also be targeted by microRNAs, such as miR-29a.
References
Further reading | ZFP36 | [
"Chemistry"
] | 313 | [
"Biochemistry stubs",
"Protein stubs"
] |
14,724,105 | https://en.wikipedia.org/wiki/Primal%20Pictures | Primal Pictures is a business established in 1991 that provides 3D graphic renderings of human anatomy, built using real scan data from the Visible Human Project, for use by healthcare students, educators, and medical professionals. It operates the Anatomy.tv online platform. In one study, Anatomy.tv was deemed the greatest value in undergraduate anatomy education "since it had highest scores for effectiveness as well as the lowest scores for cost."
Development
The representation of the body in Primal's software is derived from medical scan data that has been interpreted by a team of Primal anatomists and translated into three-dimensional images by graphics specialists. The interactive anatomy visuals are accompanied by animations that demonstrate:
Disease and conditions
Function
Biomechanics
Surgical procedures.
History
In 2012, Informa acquired all of the company, previously owning 10 percent. In 2022, as part of Informa's sale of its Pharma Intelligence business, Primal Pictures became part of private equity firm Warburg Pincus. Later that year, Pharma Intelligence changed its name to Citeline and merged with pharmaceutical technology company Norstella.
References
Medical education
Anatomy
Anatomy websites
History of anatomy
Software companies of the United Kingdom
Anatomical simulation
Software companies based in London
1991 establishments in England
Software companies established in 1991
3D computer graphics
Warburg Pincus companies
External websites
PrimalPictures.com
Anatomy.tv | Primal Pictures | [
"Biology"
] | 272 | [
"Anatomy"
] |
14,724,244 | https://en.wikipedia.org/wiki/Meredith%20Thring | Meredith Wooldridge Thring (17 December 1915 – 15 September 2006) was a British inventor, engineer, futurologist, professor and author.
Education and career
Thring was born in Melbourne, Australia, but moved to England when he was four years old. His school was Malvern College. He obtained a double first class degree in Mathematics and Physics at Trinity College, Cambridge in 1937. He then joined the British Coal Utilisation Research Association, becoming Head of its Combustion Research Laboratory. In 1940, he married Margaret Hooley (died 1986), and they had two sons and one daughter.
In 1946, Thring became head of the newly formed Physics Research group of the British Iron and Steel Research Association. In 1950, he moved to the University of Sheffield, becoming professor and head of the Department of Fuel Technology and Chemical Engineering in 1953. In 1964, he took up the position of head of the Department of Mechanical Engineering at Queen Mary College of the University of London, where he remained until his retirement in 1981. He died in Exmouth, Devon.
Honours
Thring was awarded the Student Medal of the Institute of Fuel in 1938, and the Hadfield Medal of the Iron and Steel Institute. From 1962 to 1963 he was President of the Institute of Fuel. In 1964 he was awarded a ScD degree from University of Cambridge. He was a Fellow of the Institute of Physics (FInstP), the Energy Institute (FEI), the Institution of Mechanical Engineers (FIMechE), the Institution of Engineering and Technology (FIET), and the Institution of Chemical Engineers (FIChemE). He was one of the first Fellows of the Royal Academy of Engineering (FREng).
Work
Thring was a visionary who changed from science to engineering "because he wanted to make the world a better place". In his 1977 book How to Invent, he wrote "One can envisage a society in which man lives in near-equilibrium with his environment, with the minimum use of raw materials by fuel economy, complete recycling of all metals, no throw-away goods, all consumer goods built to last many decades, and near zero pollution." In the same book he describes domestic and gardening tools, Intermediate Technology for less developed countries and robots to take the place of people in dangerous situations. However, these were not just imagining. At the University of Sheffield and Queen Mary College he was actively involved in robotics. He produced a stair-climbing robot, an autonomous fire-fighting robot, and one for clearing a table. After his retirement he founded a charity called Power Aid to help developing countries. In 1969 he predicted a future in which factories would be largely automatic, controlled by a central computer, and supposed that this would reduce the human working week to 10 or 20 hours.
He studied combustion and other forms of energy generation, and was one of the founders of the International Flame Research Foundation. This knowledge of energy was shown in his 1974 book Energy and Humanity which called essentially for a more rational and sustainable approach, with control of pollution. He was also known as a teacher, and for his belief that engineers had an ethical obligation to improve life for all, but notably the underprivileged and disabled.
Books
The domestic open fire: a survey of research prior to 1937 M.W. Thring (London : Combustion Appliance Makers' Assn.) 1938.
The influence of port design on open-hearth furnace flames J.H. Chesters & M.W. Thring (London : Iron and Steel Institute) 1946.
Air Pollution. Based on papers given at a conference held at the University of Sheffield, September 1956. Edited by M. W. Thring (London: Butterworths Scientific Publications) 1957
Pilot plants, models, and scale-up methods in chemical engineering R. E. Johnstone & M. W. Thring (New York : McGraw-Hill) 1957.
The science of flames and furnaces M.W. Thring (London, Chapman & Hall) 1952.
Nuclear propulsion edited by M.W. Thring (London : Butterworths) 1960.
Pulsating combustion : the collected works of F.H. Reynst edited by M.W. Thring (Oxford : Pergamon) 1961.
The science of flames and furnaces, 2nd edition M.W. Thring (London, Chapman & Hall) 1962.
The principles of applied science M. W. Thring (Oxford, Pergamon) 1964.
Engineering: An outline for the intending student M. W. Thring, 1972
Man, machines and tomorrow M.W. Thring, 1973
Energy and Humanity M. W. Thring & R. J. Crookes, 1974
Machines, masters or slaves of man? M.W. Thring, 1974,
Strategy for Energy M. W. Thring, 1975
How to invent M.W. Thring, 1977.
The engineer's conscience M.W. Thring & E. R. Laithwaite, 1980
Robots and telechirs : manipulators with memory, remote manipulators, machine limbs for the handicapped M.W. Thring, 1983
Quotations from G.I.Gurdjieff's Teaching: A Personal Companion M. W. Thring, 1998
Patents
British Patents
GB Patent 535576 (1941) Gas producers
GB Patent 549142 (1942) Refractory material
GB Patent 553753 (1943) Electrostatic gas cleaner
GB Patent 572380 (1945) Crucible and the like furnaces
GB Patent 579324 (1946) Combustion of solid fuel
GB Patent 579823 (1946) Carbonization of coal and combustion of the carbonised residue
GB Patent 587821 (1947) Transportable heating unit
GB Patent 587823 (1947) Controlling the air supply in furnaces and like heating appliances
GB Patent 610950 (1948) Recording gas constituents
GB Patent 760430 (1956) Control of combustion processes
GB Patent 803528 (1958) Smoke-consuming domestic stoves
GB Patent 818718 (1959) Rotary regenerative heat exchangers
GB Patent 842024 (1960) Utilising the waste heat of furnace gases and in cleansing thereof
GB Patent 870446 (1961) The generation of electricity
GB Patent 877779 (1961) Devices to facilitate the lighting of domestic fires
GB Patent 895534 (1962) Electric-arc steel furnaces
GB Patent 896639 (1962) Open-hearth furnaces
GB Patent 985625 (1965) Continuous casting of metals
GB Patent 1023817 (1966) Sampling and analysis of steel
GB Patent 1127443 (1968) Fire detection and fighting apparatus
GB Patent 1111869 (1968) Continuous steel-making
GB Patent 1131233 (1968) Automatic equipment for detecting fires
GB Patent 2167542 (1986) Furnace for industrial waste
US Patents
US Patent 2515545 (1950) Controlling the combustion rate and composition of the combustion gases in the burning of coal
US Patent 2663272 (1953) Controlling the air supply in furnaces and like heating appliances
US Patent 3171877 (1965) Apparatus for Continuous Steel Making
US Patent 3201622 (1965) Generation of Electricity
US Patent 3312230 (1967) Dish-Washing Machines
US Patent 3522859 (1970) Walking Machine
US Patent 3764667 (1973) Process for producing pigment-quality titanium dioxide
References
The Guardian Obituary: Meredith Thring, 10 November 2006
The Independent Obituary: Professor M. W. Thring, 30 September 2006
1915 births
2006 deaths
20th-century British inventors
People educated at Malvern College
Alumni of Trinity College, Cambridge
Academics from Melbourne
Futurologists
British chemical engineers
Engineering academics
Academics of the University of Sheffield
Academics of Queen Mary University of London
Fellows of the Institute of Physics
Fellows of the Institution of Engineering and Technology
Fellows of the Institution of Mechanical Engineers
Fellows of the Royal Academy of Engineering | Meredith Thring | [
"Engineering"
] | 1,614 | [
"Institution of Engineering and Technology",
"Fellows of the Institution of Engineering and Technology"
] |
14,724,536 | https://en.wikipedia.org/wiki/Bicifadine | Bicifadine (DOV-220,075) is a serotonin-norepinephrine-dopamine reuptake inhibitor (SNDRI) discovered at American Cyanamid as an analgesic drug candidate, and licensed to DOV Pharmaceutical in 1998 after American Cyanamid was acquired by Wyeth.
In January 2007, Dov licensed the rights to bicifadine to XTL Biopharmaceuticals after bicifadine failed in a Phase III clinical trial for chronic lower back pain. XTL ran a PhaseIIb clinical trial for pain caused by diabetic neuropathy, which failed in 2008; XTL terminated the agreement in 2010. In 2010 Dov was acquired by Euthymics Bioscience which intended to continue development of other candidates from Dov's portfolio.
Bicifadine has a non-opioid, non-NSAID mechanism for the treatment of pain, which should have less abuse potential than opioid drugs and less propensity to cause gastric ulcers than NSAID drugs. While the drug is purported to be a serotonin (SERT) and noradrenaline transporter (NET) inhibitor, it also has effects at the dopamine transporter (DAT), effectively making it a broad-spectrum monoamine transporter inhibitor or "triple reuptake inhibitor."
See also
DOV-216,303
References
Abandoned drugs
Analgesics
Cyclopropanes
Pyrrolidines
Serotonin–norepinephrine–dopamine reuptake inhibitors
4-Tolyl compounds | Bicifadine | [
"Chemistry"
] | 340 | [
"Drug safety",
"Abandoned drugs"
] |
14,724,743 | https://en.wikipedia.org/wiki/Webots | Webots is a free and open-source 3D robot simulator used in industry, education and research.
The Webots project started in 1996, initially developed by Dr. Olivier Michel at the Swiss Federal Institute of Technology (EPFL) in Lausanne, Switzerland and then from 1998 by Cyberbotics Ltd. as a proprietary licensed software. Since December 2018, it is released under the free and open-source Apache 2 license.
Webots includes a large collection of freely modifiable models of robots, sensors, actuators and objects. In addition, it is also possible to build new models from scratch or import them from 3D CAD software. When designing a robot model, the user specifies both the graphical and the physical properties of the objects. The graphical properties include the shape, dimensions, position and orientation, colors, and texture of the object. The physical properties include the mass, friction factor, as well as the spring and damping constants. Simple fluid dynamics is present in the software.
Webots uses a fork of the ODE (Open Dynamics Engine) for detecting of collisions and simulating rigid body dynamics. The ODE library allows one to accurately simulate physical properties of objects such as velocity, inertia and friction.
Webots includes a set of sensors and actuators frequently used in robotic experiments, e.g. lidars, radars, proximity sensors, light sensors, touch sensors, GPS, accelerometers, cameras, emitters and receivers, servo motors (rotational & linear), position and force sensor, LEDs, grippers, gyros, compass, IMU, etc.
The robot controller programs can be written outside of Webots in C, C++, Python, ROS, Java and MATLAB using a simple API.
Webots offers the possibility to take screenshots and record simulations. Webots worlds are stored in cross-platform *.wbt files whose format is based on the VRML language. One can also import and export Webots worlds and objects in the VRML format. Users can interact with a running simulation by moving robots and other objects with the mouse. Webots can also stream a simulation on web browsers using WebGL.
Web interface
Since August 18, 2017, the robotbenchmark.net website has offered free access to a series of robotics benchmarks based on Webots simulations through the Webots web interface. Webots instances are running in the cloud and the 3D views are displayed in the user browser. From this web interface, users can program robots in Python and learn robot control in a step-by-step procedure.
Controller programming example
This is a simple example of C/C++ controller programming with Webots: a trivial collision avoidance behavior. Initially, the robot runs forwards, then when an obstacle is detected it rotates around itself for a while and then resumes the forward motion.
#include <webots/robot.h>
#include <webots/motor.h>
#include <webots/distance_sensor.h>
#define TIME_STEP 64
int main() {
// initialize Webots
wb_robot_init();
// get handle and enable distance sensor
WbDeviceTag ds = wb_robot_get_device("ds");
wb_distance_sensor_enable(ds, TIME_STEP);
// get handle and initialize the motors
WbDeviceTag left_motor = wb_robot_get_device("left_motor");
WbDeviceTag right_motor = wb_robot_get_device("right_motor");
wb_motor_set_position(left_motor, INFINITY);
wb_motor_set_position(right_motor, INFINITY);
wb_motor_set_velocity(left_motor, 0.0);
wb_motor_set_velocity(right_motor, 0.0);
// control loop
while (1) {
// read sensors
double v = wb_distance_sensor_get_value(ds);
// if obstacle detected
if (v > 512) {
// turn around
wb_motor_set_velocity(left_motor, -600);
wb_motor_set_velocity(right_motor, 600);
}
else {
// go straight
wb_motor_set_velocity(left_motor, 600);
wb_motor_set_velocity(right_motor, 600);
}
// run a simulation step
wb_robot_step(TIME_STEP);
}
wb_robot_cleanup();
return 0;
}
Main fields of application
Fast prototyping of wheeled and legged robots
Research on robot locomotion
Swarm intelligence (Multi-robot simulations)
Artificial life and evolutionary robotics
Simulation of adaptive behaviour
Self-Reconfiguring Modular Robotics
Experimental environment for computer vision
Teaching and robot programming contests
Included robot models
A complete and up-to-date list is provided in the Webots user guide.
AIBO ERS7 and ERS210, Sony Corporation
BIOLOID (dog), Robotis
Boe-Bot
DARwIn-OP, Robotis
E-puck
Hemisson
HOAP-2, Fujitsu Limited
iCub, RobotCub Consortium
iRobot Create, iRobot
Katana IPR, Neuronics AG
Khepera mobile robot I, II, III, K-Team Corporation
KHR-2HV, KHR-3HV, Kondo
Koala, K-Team Corporation
Lego Mindstorms (RCX Rover model)
Magellan
Nao V2, V3, Aldebaran Robotics
MobileRobots Inc Pioneer 2, Pioneer 3-DX, Pioneer 3-AT
Puma 560, Unimate
Scout 2
Shrimp III, BlueBotics SA
Surveyor SRV-1, Surveyor Corporation
youBot, KUKA
Cross compilation and remote control support
E-puck
DARwIn-OP and Robotis OP2
NAO
Thymio II
See also
ROS
E-puck
References
External links
Cyberbotics
Robotics simulation software
1996 software
1996 in robotics
Driving simulators | Webots | [
"Technology"
] | 1,248 | [
"Driving simulators",
"Real-time simulation"
] |
14,725,468 | https://en.wikipedia.org/wiki/Sirtuin%201 | Sirtuin 1, also known as NAD-dependent deacetylase sirtuin-1, is a protein that in humans is encoded by the SIRT1 gene.
SIRT1 stands for sirtuin (silent mating type information regulation 2 homolog) 1 (S. cerevisiae), referring to the fact that its sirtuin homolog (biological equivalent across species) in yeast (Saccharomyces cerevisiae) is Sir2. SIRT1 is an enzyme located primarily in the cell nucleus that deacetylates transcription factors that contribute to cellular regulation (reaction to stressors, longevity).
Function
Sirtuin 1 is a member of the sirtuin family of proteins, homologs of the Sir2 gene in S. cerevisiae. Members of the sirtuin family are characterized by a sirtuin core domain and grouped into four classes. The functions of human sirtuins have not yet been determined; however, yeast sirtuin proteins are known to regulate epigenetic gene silencing and suppress recombination of rDNA. The protein encoded by this gene is included in class I of the sirtuin family.
Sirtuin 1 is downregulated in cells that have high insulin resistance. Furthermore, SIRT1 was shown to de-acetylate and affect the activity of both members of the PGC1-alpha/ERR-alpha complex, which are essential metabolic regulatory transcription factors.
In vitro, SIRT1 has been shown to deacetylate and thereby deactivate the p53 protein, and may have a role in activating T helper 17 cells.
Selective ligands
Activators
Lamin A is a protein that had been identified as a direct activator of Sirtuin 1 during a study on progeria.
Resveratrol has been claimed to be an activator of sirtuin 1, but this effect has been disputed based on the fact that the initially used activity assay, using a non-physiological substrate peptide, can produce artificial results. Resveratrol increases the expression of SIRT1, meaning that it does increase the activity of SIRT1, though not necessarily by direct activation. However, resveratrol was later shown to directly activate Sirtuin 1 against non-modified peptide substrates. Resveratrol also enhances the binding between Sirtuin 1 and Lamin A. In addition to resveratrol, a range of other plant-derived polyphenols have also been shown to interact with SIRT1.
SRT-1720 was also claimed to be an activator, but this now has been questioned.
Methylene blue by increasing NADH/NAD+ ratio.
Metformin activates both PRKA and SIRT1.
Although neither resveratrol or SRT1720 directly activate SIRT1, resveratrol, and probably SRT1720, indirectly activate SIRT1 by activation of AMP-activated protein kinase (AMPK), which increases NAD+ levels (which is the cofactor required for SIRT1 activity). Elevating NAD+ is a more direct and reliable way to activate SIRT1.
Interactions
Sirtuin 1 has been shown in vitro to interact with ERR-alpha and AIRE.
Human Sirt1 has been reported having 136 direct interactions in interactomic studies involved in numerous processes.
Yeast homolog
Sir2 (whose homolog in mammals is known as SIRT1) was the first of the sirtuin genes to be found. It was found in budding yeast, and, since then, members of this highly conserved family have been found in nearly all organisms studied. Sirtuins are hypothesized to play a key role in an organism's response to stresses (such as heat or starvation) and to be responsible for the lifespan-extending effects of calorie restriction.
The three letter yeast gene symbol Sir stands for Silent Information Regulator while the number 2 is representative of the fact that it was the second SIR gene discovered and characterized.
In the roundworm, Caenorhabditis elegans, Sir-2.1 is used to denote the gene product most similar to yeast Sir2 in structure and activity.
Method of action and observed effects
Sirtuins act primarily by removing acetyl groups from lysine residues within proteins in the presence of NAD+; thus, they are classified as "NAD+-dependent deacetylases" and have EC number 3.5.1. They add the acetyl group from the protein to the ADP-ribose component of NAD+ to form O-acetyl-ADP-ribose. The HDAC activity of Sir2 results in tighter packaging of chromatin and a reduction in transcription at the targeted gene locus. The silencing activity of Sir2 is most prominent at telomeric sequences, the hidden MAT loci (HM loci), and the ribosomal DNA (rDNA) locus (RDN1) from which ribosomal RNA is transcribed.
Limited overexpression of the Sir2 gene results in a lifespan extension of about 30%, if the lifespan is measured as the number of cell divisions the mother cell can undergo before cell death. Concordantly, deletion of Sir2 results in a 50% reduction in lifespan. In particular, the silencing activity of Sir2, in complex with Sir3 and Sir4, at the HM loci prevents simultaneous expression of both mating factors which can cause sterility and shortened lifespan. Additionally, Sir2 activity at the rDNA locus is correlated with a decrease in the formation of rDNA circles. Chromatin silencing, as a result of Sir2 activity, reduces homologous recombination between rDNA repeats, which is the process leading to the formation of rDNA circles. As accumulation of these rDNA circles is the primary way in which yeast are believed to "age", then the action of Sir2 in preventing accumulation of these rDNA circles is a necessary factor in yeast longevity.
Starving of yeast cells leads to a similarly extended lifespan, and indeed starving increases the available amount of NAD+ and reduces nicotinamide, both of which have the potential to increase the activity of Sir2. Furthermore, removing the Sir2 gene eliminates the life-extending effect of caloric restriction. Experiments in the nematode Caenorhabditis elegans and in the fruit fly Drosophila melanogaster support these findings. , experiments in mice are underway.
However, some other findings call the above interpretation into question. If one measures the lifespan of a yeast cell as the amount of time it can live in a non-dividing stage, then silencing the Sir2 gene actually increases lifespan Furthermore, calorie restriction can substantially prolong reproductive lifespan in yeast even in the absence of Sir2.
In organisms more complicated than yeast, it appears that Sir2 acts by deacetylation of several other proteins besides histones.
In the fruit fly Drosophila melanogaster, the Sir2 gene does not seem to be essential; loss of a sirtuin gene has only very subtle effects. However, mice lacking the SIRT1 gene (the sir2 biological equivalent) were smaller than normal at birth, often died early or became sterile.
Inhibition of SIRT1
Human aging is characterized by a chronic, low-grade inflammation level, and the pro-inflammatory transcription factor NF-κB is the main transcriptional regulator of genes related to inflammation. SIRT1 inhibits NF-κB-regulated gene expression by deacetylating the RelA/p65 subunit of NF-κB at lysine 310. But NF-κB more strongly inhibits SIRT1. NF-κB increases the levels of the microRNA miR-34a (which inhibits nicotinamide adenine dinucleotide NAD+ synthesis) by binding to its promoter region. resulting in lower levels of SIRT1.
Both the SIRT1 enzyme and the poly ADP-ribose polymerase 1 (PARP1) enzyme require NAD+ for activation. PARP1 is a DNA repair enzyme, so in conditions of high DNA damage, NAD+ levels can be reduced 20–30% thereby reducing SIRT1 activity.
Homologous recombination
SIRT1 protein actively promotes homologous recombination (HR) in human cells, and likely promotes recombinational repair of DNA breaks. SIRT1-mediated HR requires the WRN protein. WRN protein functions in double-strand break repair by HR. WRN protein is a RecQ helicase, and in its mutated form gives rise to Werner syndrome, a genetic condition in humans characterized by numerous features of premature aging. These findings link SIRT1 function to HR, a DNA repair process that is likely necessary for maintaining the integrity of the genome during aging.
References
External links
Corante weblog by Derek Lowe about sir2 and SIRT1 research.
EC 3.5.1
Aging-related proteins
Aging-related enzymes | Sirtuin 1 | [
"Biology"
] | 1,884 | [
"Senescence",
"Aging-related proteins",
"Aging-related enzymes"
] |
14,725,503 | https://en.wikipedia.org/wiki/Alpha-2-HS-glycoprotein | alpha-2-HS-glycoprotein (AHSG, Alpha-2-Heremans-Schmid Glycoprotein) also known as fetuin-A is a protein that in humans is encoded by the AHSG gene. Fetuin-A belongs to the fetuin class of plasma binding proteins and is more abundant in fetal than adult blood.
Function
Alpha2-HS glycoprotein, a glycoprotein present in the serum, is synthesized by hepatocytes and adipocytes. The AHSG molecule consists of two polypeptide chains, which are both cleaved from a proprotein encoded from a single mRNA. It is involved in several functions, such as endocytosis, brain development and the formation of bone tissue. The protein is commonly present in the cortical plate of the immature cerebral cortex and bone marrow hemopoietic matrix, and it has therefore been postulated that it participates in the development of the tissues. However, its exact significance is still obscure.
The choroid plexus is an established extrahepatic expression site. The mature circulating AHSG molecule consists of two polypeptide chains, which are both cleaved from a proprotein encoded from a single mRNA. Multiple post-translational modifications have been reported. Thus AHSG is a secreted partially phosphorylated glycoprotein with complex proteolytic processing that circulates in blood and extracellular fluids. In the test tube AHSG can bind multiple ligands and therefore has been claimed to be involved in several functions, such as endocytosis, brain development and the formation of bone tissue. Most of these functions await confirmation in vivo.
Clinical significance
Fetuins are carrier proteins like albumin. Fetuin-A forms soluble complexes with calcium and phosphate and thus is a carrier of otherwise insoluble calcium phosphate. Thus fetuin-A is a potent inhibitor of pathological calcification, in particular Calciphylaxis. Mice deficient in fetuin-A show systemic calcification of soft tissues. Fetuin-A can inhibit calcification, and inhibits osteogenesis in bone. Fetuin-A appears to promote calcification in coronary artery disease, but oppose calcification in peripheral artery disease.
High levels of Fetuin-A are associated with obesity and insulin resistance. Fetuin-A promotes insulin resistance by enhancing the binding of free fatty acids to TLR4. In adipose tissue, Fetuin-A downregulates the expression of adiponectin, thereby increasing inflammation and insulin resistance. Also in adipose tissue, Fetuin-A reduces lipogenesis and increases lipolysis, thereby increasing obesity and insulin resistance.
Supervised exercise (that is not associated with weight reduction) reduces Fetuin-A.
See also
Fetuin-B
References
External links
Further reading
Glycoproteins | Alpha-2-HS-glycoprotein | [
"Chemistry"
] | 621 | [
"Glycoproteins",
"Glycobiology"
] |
14,725,514 | https://en.wikipedia.org/wiki/Anaplastic%20lymphoma%20kinase | Anaplastic lymphoma kinase (ALK) also known as ALK tyrosine kinase receptor or CD246 (cluster of differentiation 246) is an enzyme that in humans is encoded by the ALK gene.
Identification
Anaplastic lymphoma kinase (ALK) was originally discovered in 1994 in anaplastic large-cell lymphoma (ALCL) cells. ALCL is caused by a (2;5)(p23:q35) chromosomal translocation that generates the fusion protein NPM-ALK, in which the kinase domain of ALK is fused to the amino-terminal part of the nucleophosmin (NPM) protein. Dimerization of NPM constitutively activates the ALK kinase domain.
The full-length protein ALK was identified in 1997 by two groups. The deduced amino acid sequences revealed that ALK was a novel receptor tyrosine kinase (RTK), having an extracellular ligand-binding domain, a transmembrane domain, and an intracellular tyrosine kinase domain. While the tyrosine kinase domain of human ALK shares a high degree of similarity with that of the insulin receptor, its extracellular domain is unique among the RTK family in containing two MAM domains (meprin, A5 protein and receptor protein tyrosine phosphatase mu), an LDLa domain (low-density lipoprotein receptor class A) and a glycine-rich region. Based on overall homology, ALK is closely related to the leukocyte receptor tyrosine kinase (LTK) and, together with the insulin receptor, forms a subgroup in the RTK superfamily. The human ALK gene encodes a protein 1,620 amino acids long with a molecular weight of 180 kDa.
Since the original discovery of the receptor in mammals, several orthologs of ALK have been identified: dAlk in the fruit fly (Drosophila melanogaster) in 2001, scd-2 in the nematode (Caenorhabditis elegans) in 2004, and DrAlk in the zebrafish (Danio rerio) in 2013.
The ligands of the human ALK/LTK receptors were identified in 2014: FAM150A (AUGβ) and FAM150B (AUGα), two small secreted peptides that strongly activate ALK signaling. In invertebrates, ALK-activating ligands are Jelly belly (Jeb) in Drosophila, and hesitation behaviour 1 (HEN-1) in C. elegans. No such ligands have been reported yet in zebrafish or other vertebrates.
Mechanism
Following binding of the ligand, the full-length receptor ALK dimerizes, changes conformation, and autoactivates its own kinase domain, which in turn phosphorylates other ALK receptors in trans on specific tyrosine amino acid residues. ALK phosphorylated residues serve as binding sites for the recruitment of several adaptor and other cellular proteins, such as GRB2, IRS1, Shc, Src, FRS2, PTPN11/Shp2, PLCγ, PI3K, and NF1. Other reported downstream ALK targets include FOXO3a, CDKN1B/p27kip, cyclin D2, NIPA, RAC1, CDC42, p130CAS, SHP1, and PIKFYVE.
Phosphorylated ALK activates multiple downstream signal transduction pathways, including MAPK-ERK, PI3K-AKT, PLCγ, CRKL-C3G, and JAK-STAT.
Function
The receptor ALK plays a pivotal role in cellular communication and in the normal development and function of the nervous system. This observation is based on the extensive expression of ALK messenger RNA (mRNA) throughout the nervous system during mouse embryogenesis. In vitro functional studies have demonstrated that ALK activation promotes neuronal differentiation of PC12 or neuroblastoma cell lines.
ALK is critical for embryonic development in Drosophila. Flies lacking the receptor die due to failure of founder cell specification in embryonic visceral muscle. However, while ALK knockout mice exhibit defects in neurogenesis and testosterone production, they remain viable, suggesting that ALK is not critical to their developmental processes.
ALK regulates retinal axon targeting, growth and size, synapse development at the neuromuscular junction, behavioral responses to ethanol, and sleep. It restricts and constrains learning and long-term memory and small-molecule inhibitors of the ALK receptor can improve learning, long-term memory, and extend healthy lifespan. ALK is also a candidate thinness gene, as its genetic deletion leads to resistance to diet- and leptin-mutation-induced obesity.
Pathology
The ALK gene can be oncogenic in three ways – by forming a fusion gene with any of several other genes, by gaining additional gene copies or with mutations of the actual DNA code for the gene itself.
Anaplastic large-cell lymphoma
The 2;5 chromosomal translocation is associated with approximately 60% of anaplastic large-cell lymphomas (ALCLs), type ALK-positive anaplastic large cell lymphoma and very rare cases of ALCL type primary cutaneous anaplastic large cell lymphoma. The translocation creates a fusion gene consisting of the ALK (anaplastic lymphoma kinase) gene and the nucleophosmin (NPM) gene: the 3' half of ALK, derived from chromosome 2 and coding for the catalytic domain, is fused to the 5' portion of NPM from chromosome 5. The product of the NPM-ALK fusion gene is oncogenic.
In a smaller fraction of ALCL patients, the 3' half of ALK is fused to the 5' sequence of TPM3 gene, encoding for tropomyosin 3. In rare cases, ALK is fused to other 5' fusion partners, such as TFG, ATIC, CLTC1, TPM4, MSN, ALO17, MYH9.
Adenocarcinoma of the lung
The EML4-ALK fusion gene is responsible for approximately 3-5% of non-small-cell lung cancer (NSCLC). The vast majority of cases are adenocarcinomas. Patients with this ALK rearrangement have the following clinicopathologic characteristics: Young age at diagnosis (median 50 years), female gender, nonsmoker/light smoker, adenocarcinoma histology with specific morphologic patterns such as cribriform and solid signet ring, expression of thyroid transcription factor 1, tendency to metastasize to pleura or pericardium, frequently with more metastases than other molecular types, and predominantly metastases to the central nervous system. The standard test used to detect this gene in tumor samples is fluorescence in situ hybridization (FISH) by a US FDA approved kit. Recently Roche Ventana obtained approval in China and European Union countries to test this mutation by immunohistochemistry. Other techniques like reverse-transcriptase PCR (RT-PCR) can also be used to detect lung cancers with an ALK gene fusion but not recommended. ALK lung cancers are found in patients of all ages, although on average these patients tend to be younger. ALK lung cancers are more common in light cigarette smokers or nonsmokers, but a significant number of patients with this disease are current or former cigarette smokers. EML4-ALK-rearrangement in NSCLC is exclusive and not found in EGFR- or KRAS-mutated tumors.
Gene rearrangements and overexpression in other tumours
Familial cases of neuroblastoma
Inflammatory myofibroblastic tumor
Adult and pediatric renal cell carcinomas
Esophageal squamous cell carcinoma
Breast cancer, notably the inflammatory subtype
Colonic adenocarcinoma
Glioblastoma multiforme
Anaplastic thyroid cancer
ALK inhibitors
Xalkori (crizotinib), produced by Pfizer, was approved by the FDA for treatment of late stage lung cancer on August 26, 2011. Early results of an initial Phase I trial with 82 patients with ALK induced lung cancer showed an overall response rate of 57%, a disease control rate at 8 weeks of 87% and progression free survival at 6 months of 72%.
In patients affected by relapsed or refractory ALK+ Anaplastic Large Cell Lymphoma, crizotinib produced objective response rates ranging from 65% to 90% and 3 year progression free survival rates of 60-75%. No relapse of the lymphoma was ever observed after the initial 100 days of treatment. Treatment must be continued indefinitely at present.
Ceritinib was approved by the FDA in April 2014 for the treatment of patients with anaplastic lymphoma kinase (ALK)-positive metastatic non-small cell lung cancer (NSCLC) who have progressed on or are intolerant to crizotinib.
Entrectinib (RXDX-101) is a selective tyrosine kinase inhibitor developed by Ignyta, Inc., with specificity, at low nanomolar concentrations, for all of three Trk proteins (encoded by the three NTRK genes, respectively) as well as the ROS1, and ALK receptor tyrosine kinases. An open label, multicenter, global phase 2 clinical trial called STARTRK-2 is currently underway to test the drug in patients with ROS1/NTRK/ALK gene rearrangements.
See also
Cluster of differentiation
Notes and references
Notes
References
Further reading
External links
ALK Correlations, Experiments, Publications and Clinical Trials
GeneReviews/NCBI/NIH/UW entry on ALK-Related Neuroblastoma Susceptibility
OMIM entries on ALK-Related Neuroblastoma Susceptibility
Clusters of differentiation
Tyrosine kinase receptors | Anaplastic lymphoma kinase | [
"Chemistry"
] | 2,165 | [
"Tyrosine kinase receptors",
"Signal transduction"
] |
14,725,529 | https://en.wikipedia.org/wiki/CAMP%20responsive%20element%20modulator | cAMP responsive element modulator is a protein that in humans is encoded by the CREM gene, and it belongs to the cAMP-responsive element binding protein family. It has multiple isoforms, which act either as repressors or activators. CREB family is important for in regulating transcription in response to various stresses, metabolic and developmental signals. CREM transcription factors also play an important role in many physiological systems, such as cardiac function, circadian rhythms, locomotion and spermatogenesis.
Function
This gene encodes a bZIP transcription factor that binds to the cAMP responsive element found in many viral and cellular promoters. It is an important component of cAMP-mediated signal transduction during the spermatogenetic cycle, as well as other complex processes. Alternative promoter and translation initiation site usage allows this gene to exert spatial and temporal specificity to cAMP responsiveness. Multiple alternatively spliced transcript variants encoding several different isoforms have been found for this gene, with some of them functioning as activators and some as repressors of transcription.
Gene location
The chromosomal location of CREM gene is at 10p11.21, where it starts at 35415769 and ends at 35501886 bp from pter ( according to hg19-Feb_2009)
Interactions
CAMP responsive element modulator has been shown to interact with FHL5.
Disease relevance of CREM
Panic disorder
One study reported the DNA sequence variations in the gene for CREM in panic disorder patients. It showed a significant excess of the shorter eight-repeat allele and of genotypes containing the eight-repeat allele in panic disorder patients. The observed associations were limited to panic disorder without agoraphobia, and they were more prominent in females. But, the independent Italian and Spanish samples in this study did not support their results. Another family-based study showed little evidence of any susceptibility locus for panic disorder either within the CREM gene or in a nearby region on chromosome 10p11
Spermiogenesis deficiency
CREM has been shown to be a master-switch regulator in testis. It plays an important role in the regulation of the expression of post-meiotic genes, and this has been supported by several studies using CREM-mutation mice. The results showed the first step in the process of sperm formation would be blocked if the germ cell development in mice CREM gene were disrupted. The cAMP response element sites can be found in the promoter region of some postmeiotic genes, so that the CREM can target and regulate these genes.
Two studies proved that treatment of rats with Salvia hypoleuca and Alpina galanga can significantly increased the CREM gene expression.
Systemic lupus erythematousus
Less IL-2 will be produced from T cells in humans or mice with systemic lupus erythematousus (SLE). Some studies showed that an increased level CREM was presented in the nucleus of T lymphocytes from SLE patients. The CREM bound to the -180 site of the IL-2 promoter to repress its transcription.
References
Further reading
External links
Transcription factors | CAMP responsive element modulator | [
"Chemistry",
"Biology"
] | 640 | [
"Induced stem cells",
"Gene expression",
"Transcription factors",
"Signal transduction"
] |
14,725,565 | https://en.wikipedia.org/wiki/Homeobox%20A10 | Homeobox protein Hox-A10 is a protein that in humans is encoded by the HOXA10 gene.
Function
In vertebrates, the genes encoding the class of transcription factors called homeobox genes are found in clusters named A, B, C, and D on four separate chromosomes. Expression of these proteins is spatially and temporally regulated during embryonic development. This gene is part of the A cluster on chromosome 7 and encodes a DNA-binding transcription factor that may regulate gene expression, morphogenesis, and differentiation. More specifically, it may function in fertility, embryo viability, and regulation of hematopoietic lineage commitment. Alternatively spliced transcript variants encoding different isoforms have been described.
Downregulation of HOXA10 is observed in the human and baboon decidua after implantation and this downregulation promotes trophoblast invasion by activating STAT3.
Interactions
Homeobox A10 has been shown to interact with PTPN6.
See also
Homeobox
References
Further reading
External links
Transcription factors | Homeobox A10 | [
"Chemistry",
"Biology"
] | 222 | [
"Induced stem cells",
"Gene expression",
"Transcription factors",
"Signal transduction"
] |
14,725,606 | https://en.wikipedia.org/wiki/INSL3 | Insulin-like 3 is a protein that in humans is encoded by the INSL3 gene.
Function
The protein encoded by this gene is an insulin like hormone produced mainly in gonadal tissues in males and females. Studies of the mouse counterpart suggest that this gene may be involved in the development of urogenital tract and female fertility. INSL-3 initiates meiotic progression in follicle-enclosed oocytes by mediating a reduction in intra-oocyte cAMP concentration by activating leucine-rich repeat-containing G protein-coupled receptor 8 (LGR8). It may also act as a hormone to regulate growth and differentiation of gubernaculum, and thus mediating intra-abdominal testicular descent. The mutations in this gene may lead to, but not a frequent cause of, cryptorchidism.
References
Further reading | INSL3 | [
"Chemistry"
] | 176 | [
"Biochemistry stubs",
"Protein stubs"
] |
14,725,651 | https://en.wikipedia.org/wiki/Protein%20SET | Protein SET, also known as Protein SET 1, is a protein that in humans is encoded by the SET gene.
Interactions
Protein SET has been shown to interact with:
Acidic leucine-rich nuclear phosphoprotein 32 family member A,
CDK5R1,
KLF5,
NME1, and
TAF1A.
References
Further reading
Histone Acetyltransferase Inhibitor | Protein SET | [
"Chemistry"
] | 85 | [
"Biochemistry stubs",
"Protein stubs"
] |
14,725,773 | https://en.wikipedia.org/wiki/List%20of%20group-0%20ISBN%20publisher%20codes | A list of publisher codes for (978) International Standard Book Numbers with a group code of zero.
Assignation
The group-0 publisher codes are assigned as follows:
2-digit publisher codes
3-digit publisher codes
(Note: the status of codes not listed in this table is unclear; please help fill the gaps.)
4-digit publisher codes
(Note: many codes are not yet listed in this table; please help fill the gaps.)
5-digit publisher codes
(Note: many codes are not yet listed in this table; please help fill the gaps.)
6-digit publisher codes
(Note: many codes are not yet listed in this table; please help fill the gaps.)
7-digit publisher codes
(Note: many codes are not yet listed in this table; please help fill the gaps.)
See also
List of group-1 ISBN publisher codes
List of ISBN identifier groups
References
External links
https://www.isbn-international.org/range_file_generation
http://www.books-by-isbn.com/
List of 2 and 3-digit publisher codes for ISBNs that start with a 0 from http://blog.openlibrary.org/2009/07/20/isbn-publisher-codes/ where there is also a complete list of publisher codes for ISBNs that start with a 0 or 1.
Book publishing
Bookselling
Book terminology
Checksum algorithms
Identifiers
International Standard Book Number
0
Unique identifiers | List of group-0 ISBN publisher codes | [
"Mathematics"
] | 303 | [
"Mathematical objects",
"Numbers",
"Number-related lists"
] |
14,725,847 | https://en.wikipedia.org/wiki/PTPRA | Receptor-type tyrosine-protein phosphatase alpha is an enzyme that in humans is encoded by the PTPRA gene.
Function
The protein encoded by this gene is a member of the receptor tyrosine phosphatases (RTP), a family of protein tyrosine phosphatases. RTPs are known to be signaling molecules that regulate a variety of cellular processes including cell growth, differentiation, mitotic cycle, and oncogenic transformation. This RTP contains an extracellular domain, a single transmembrane segment and two tandem intracytoplasmic catalytic domains, and thus represents a receptor-type RTP. This RTP has been shown to dephosphorylate and activate Src family tyrosine kinases, and is implicated in the regulation of integrin signaling, cell adhesion and proliferation. Three alternatively spliced variants of this gene, which encode two distinct isoforms, have been reported.
Interactions
PTPRA has been shown to interact with Grb2 and KCNA2.
References
Further reading | PTPRA | [
"Chemistry"
] | 222 | [
"Biochemistry stubs",
"Protein stubs"
] |
14,725,973 | https://en.wikipedia.org/wiki/EPH%20receptor%20B4 | Ephrin type-B receptor 4 is a protein that in humans is encoded by the EPHB4 gene.
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 binds to ephrin-B2 and plays an essential role in vascular development.
References
Further reading
Tyrosine kinase receptors | EPH receptor B4 | [
"Chemistry"
] | 219 | [
"Tyrosine kinase receptors",
"Signal transduction"
] |
14,726,000 | https://en.wikipedia.org/wiki/RBPJ | Recombination signal binding protein for immunoglobulin kappa J region is a protein that in humans is encoded by the RBPJ gene.
RBPJ also known as CBF1, is the human homolog for the Drosophila gene Suppressor of Hairless. Its promoter region is classically used to demonstrate Notch1 signaling.
Interactions
RBPJ has been shown to interact with:
NOTCH1
NCOR2,
PCAF,
SND1,
SNW1,
SOX18, and
HIF1a.
References
Further reading
External links
Transcription factors | RBPJ | [
"Chemistry",
"Biology"
] | 119 | [
"Induced stem cells",
"Gene expression",
"Transcription factors",
"Signal transduction"
] |
14,726,193 | https://en.wikipedia.org/wiki/Carlos%20Arias%20Ortiz | Carlos Federico Arias Ortiz is a Mexican biochemist specialized in rotaviruses. Along his wife, Susana López Charretón, he has been a co-recipient of both the 2001 Carlos J. Finlay Prize for Microbiology and the 2008 TWAS Prize in Biology.
Arias Ortiz holds a bachelor's degree in Pharmacology and both a master's and a doctorate degree in basic biomedical research from the National Autonomous University of Mexico (UNAM). Currently, he works for the Institute of Biotechnology of the same university.
From 1991 to 2006 he was a Howard Hughes Medical Institute International Research Scholar.
See also
List of people from Morelos, Mexico
External links
Profile at the Howard Hughes Medical Institute
Personal web page at the Institute of Biotechnology – UNAM (in Spanish).
References
Mexican biochemists
Members of the Mexican Academy of Sciences
National Autonomous University of Mexico alumni
Academic staff of the National Autonomous University of Mexico
Living people
Year of birth missing (living people)
People from Cuernavaca
TWAS laureates
21st-century Mexican scientists
20th-century Mexican scientists | Carlos Arias Ortiz | [
"Chemistry"
] | 218 | [
"Biochemistry stubs",
"Biochemists",
"Biochemist stubs"
] |
14,726,291 | https://en.wikipedia.org/wiki/GPS%20satellite%20blocks | GPS satellite blocks are the various production generations of the Global Positioning System (GPS) used for satellite navigation. The first satellite in the system, Navstar 1, was launched by the United States Air Force on 22 February 1978. The GPS satellite constellation is now operated by the 2nd Space Operations Squadron (2SOPS) of Space Delta 8, United States Space Force.
The GPS satellites circle the Earth at an altitude of about 20,000 km (12,427 miles) and complete two full orbits every day.
Satellites by block
Block I satellites
Rockwell International was awarded a contract in 1974 to build the first eight Block I satellites. In 1978, the contract was extended to build an additional three Block I satellites. Beginning with Navstar 1 in 1978, ten "Block I" GPS satellites were successfully launched. One satellite, "Navstar 7", was lost due to an unsuccessful launch on 18 December 1981.
The Block I satellites were launched from Vandenberg Air Force Base using Atlas rockets that were converted intercontinental ballistic missiles. The satellites were built by Rockwell International at the same plant in Seal Beach, California where the S-II second stages of the Saturn V rockets were built.
The Block I series consisted of the concept validation satellites and reflected various stages of system development. Lessons learned from the 10 satellites in the series were incorporated into the fully operational Block II series.
Dual solar arrays supplied over 400 watts of power, charging nickel–cadmium batteries for operations in Earth's shadow. S-band communications were used for control and telemetry, while an UHF channel provided cross-links between spacecraft. A hydrazine propulsion system was used for orbital correction. The payload included two L-band navigation signals at 1575.42 MHz (L1) and 1227.60 MHz (L2).
The final Block I launch was conducted on 9 October 1985, but the last Block I satellite was not taken out of service until 18 November 1995, well past its 5-year design life.
Block II satellites
The Block II satellites were the first full scale operational GPS satellites, designed to provide 14 days of operation without any contact from the control segment. The prime contractor was Rockwell International, which built a SVN 12 qualification vehicle after an amendment to the Block I contract. In 1983, the company was awarded an additional contract to build 28 Block II/IIA satellites.
Block II spacecraft were three-axis stabilized, with ground pointing using reaction wheels. Two solar arrays supplied 710 watts of power, while S-band communications were used for control and telemetry. A UHF channel was used for cross-links between spacecraft. A hydrazine propulsion system was used for orbital correction. The payload included two L-band GPS signals at 1575.42 MHz (L1) and 1227.60 MHz (L2). Each spacecraft carried two rubidium and two cesium clocks, as well as nuclear detonation detection sensors, leading to a mass of .
The first of the nine satellites in the initial Block II series was launched on 14 February 1989; the last was launched on 1 October 1990. The final satellite of the series to be taken out of service was decommissioned on 15 March 2007, well past its 7.5 year design life.
Block IIA series
The Block IIA satellites were slightly improved versions of the Block II series, designed to provide 180 days of operation without contact from the control segment. However, the mass increased to .
Nineteen satellites in the Block IIA series were launched, the first on 26 November 1990 and the last on 6 November 1997. Two of the satellites in this series, numbers 35 and 36, were equipped with laser retro-reflectors, allowing them to be tracked independently of their radio signals, providing unambiguous separation of clock and ephemeris errors.
SVN-34, the last Block IIA satellite, broadcast on the PRN 18 signal. It was removed from service on 9 October 2019 but kept as an on-orbit spare until April 2020.
Block IIR series
The Block IIR series are "replenishment" (replacement) satellites developed by Lockheed Martin. Each satellite weighs at launch and once on orbit. The first attempted launch of a Block IIR satellite failed on 17 January 1997 when the Delta II rocket exploded 12 seconds into flight. The first successful launch was on 23 July 1997. Twelve satellites in the series were successfully launched. At least ten satellites in this block carried an experimental S-band payload for search and rescue, known as Distress Alerting Satellite System.
Block IIR-M series
The Block IIR-M satellites include a new military signal and a more robust civil signal, known as L2C. There are eight satellites in the Block IIR-M series, which were built by Lockheed Martin. The first Block IIR-M satellite was launched on 26 September 2005. The final launch of a IIR-M was on 17 August 2009.
Block IIF series
The Block IIF series are "follow-on" satellites developed by Boeing. The satellite has a mass of and a design life of 12 years. The first Block IIF space vehicle was launched in May 2010 on a Delta IV rocket. The twelfth and final IIF launch was on 5 February 2016.
Block III satellites
Block III series
GPS Block III is the first series of third-generation GPS satellites, incorporating new signals and broadcasting at higher power levels. In September 2016, the United States Air Force awarded Lockheed Martin a contract option for two more Block III satellites, setting the total number of GPS III satellites to ten. On 23 December 2018, the first GPS III satellite was launched aboard a SpaceX Falcon 9 Full Thrust. On 22 August 2019, the second GPS III satellite was launched aboard a Delta IV. The third GPS III satellite was launched on 30 June 2020, aboard a SpaceX Falcon 9 launch vehicle. The fourth GPS III satellite launched on 5 November 2020, also aboard a Falcon 9.
Block IIIF series
The Block IIIF series is the second set of GPS Block III satellites, which will consist of up to 22 space vehicles. Block IIIF launches are expected to begin no earlier than 2026 and continue through 2034.
See also
List of GPS satellites
References
Global Positioning System
Satellites of the United States | GPS satellite blocks | [
"Technology",
"Engineering"
] | 1,266 | [
"Wireless locating",
"GPS satellites",
"Aircraft instruments",
"Aerospace engineering",
"Global Positioning System"
] |
14,726,322 | https://en.wikipedia.org/wiki/Complex%20network%20zeta%20function | Different definitions have been given for the dimension of a complex network or graph. For example, metric dimension is defined in terms of the resolving set for a graph. Dimension has also been defined based on the box covering method applied to graphs. Here we describe the definition based on the complex network zeta function. This generalises the definition based on the scaling property of the volume with distance. The best definition depends on the application.
Definition
One usually thinks of dimension for a set which is dense, like the points on a line, for example. Dimension makes sense in a discrete setting, like for graphs, only in the large system limit, as the size tends to infinity. For example, in Statistical Mechanics, one considers discrete points which are located on regular lattices of different dimensions. Such studies have been extended to arbitrary networks, and it is interesting to consider how the definition of dimension can be extended to cover these cases. A very simple and obvious way to extend the definition of dimension to arbitrary large networks is to consider how the volume (number of nodes within a given distance from a specified node) scales as the distance (shortest path connecting two nodes in the graph) is increased. For many systems arising in physics, this is indeed a useful approach. This definition of dimension could be put on a strong mathematical foundation, similar to the definition of Hausdorff dimension for continuous systems. The mathematically robust definition uses the concept of a zeta function for a graph. The complex network zeta function and the graph surface function were introduced to characterize large graphs. They have also been applied to study patterns in Language Analysis. In this section we will briefly review the definition of the functions and discuss further some of their properties which follow from the definition.
We denote by the distance from node to node , i.e., the length of the shortest path connecting the first node to the second node. is if there is no path from node to node . With this definition, the nodes of the complex network become points in a metric space. Simple generalisations of this definition can be studied, e.g., we could consider weighted edges. The graph surface function, , is defined as the number of nodes which are exactly at a distance from a given node, averaged over all nodes of the network. The complex network zeta function is defined as
where is the graph size, measured by the number of nodes. When is zero all nodes contribute equally to the sum in the previous equation. This means that is , and it diverges when . When the exponent tends to infinity, the sum gets contributions only from the nearest neighbours of a node. The other terms tend to zero. Thus, tends to the average degree for the graph as .
The need for taking an average over all nodes can be avoided by using the concept of supremum over nodes, which makes the concept much easier to apply for formally infinite graphs. The definition can be expressed as a weighted sum over the node distances. This gives the Dirichlet series relation
This definition has been used in the shortcut model to study several processes and their dependence on dimension.
Properties
is a decreasing function of , , if . If the average degree of the nodes (the mean coordination number for the graph) is finite, then there is exactly one value of , , at which the complex network zeta function transitions from being infinite to being finite. This has been defined as the dimension of the complex network. If we add more edges to an existing graph, the distances between nodes will decrease. This results in an increase in the value of the complex network zeta function, since will get pulled inward. If the new links connect remote parts of the system, i.e., if the distances change by amounts which do not remain finite as the graph size , then the dimension tends to increase. For regular discrete d-dimensional lattices with distance defined using the norm
the transition occurs at . The definition of dimension using the complex network zeta function satisfies properties like monotonicity (a subset has a lower or the same dimension as its containing set), stability (a union of sets has the maximum dimension of the component sets forming the union) and Lipschitz invariance, provided the operations involved change the distances between nodes only by finite amounts as the graph size goes to . Algorithms to calculate the complex network zeta function have been presented.
Values for discrete regular lattices
For a one-dimensional regular lattice the graph surface function is exactly two for all values of (there are two nearest neighbours, two next-nearest neighbours, and so on). Thus, the complex network zeta function is equal to , where is the usual Riemann zeta function. By choosing a given axis of the lattice and summing over cross-sections for the allowed range of distances along the chosen axis the recursion relation below can be derived
From combinatorics the surface function for a regular lattice can be written as
The following expression for the sum of positive integers raised to a given power will be useful to calculate the surface function for higher values of :
Another formula for the sum of positive integers raised to a given power is
as .
The Complex network zeta function for some lattices is given below.
:
:
: )
:
: (for near the transition point.)
Random graph zeta function
Random graphs are networks having some number of vertices, in which each pair is connected with probability , or else the pair is disconnected. Random graphs have a diameter of two with probability approaching one, in the infinite limit (). To see this, consider two nodes and . For any node different from or , the probability that is not simultaneously connected to both and is . Thus, the probability that none of the nodes provides a path of length between nodes and is . This goes to zero as the system size goes to infinity, and hence most random graphs have their nodes connected by paths of length at most . Also, the mean vertex degree will be . For large random graphs almost all nodes are at a distance of one or two from any given node, is , is , and the graph zeta function is
References
Algebraic graph theory
Network theory | Complex network zeta function | [
"Mathematics"
] | 1,228 | [
"Graph theory",
"Network theory",
"Mathematical relations",
"Algebra",
"Algebraic graph theory"
] |
14,726,522 | https://en.wikipedia.org/wiki/HD%20190228 | HD 190228 is a star with an orbiting substellar companion in the northern constellation of Vulpecula. Its apparent magnitude is 7.30 – too faint to be seen with the naked eye – and the absolute magnitude is 3.34. Based on parallax measurements, it is located at a distance of from the Sun. The system is drifting closer with a radial velocity of −50 km/s.
The spectrum of HD 190228 presents as a subgiant star with a stellar classification of G5 IV, indicating it has exhausted the supply of hydrogen at its core and is evolving off the main sequence. The star is older than the Sun with an age over 5 billion years with a projected rotational velocity of 1.4 km/s. A metal-poor star, it has 18% more mass than the Sun and has grown to 2.4 times the Sun's girth. The star is radiating roughly 4.6 times the luminosity of the Sun from its photosphere at an effective temperature of 5,311 K.
Planetary system
In 2000, it was announced that a giant exoplanet was orbiting the star with a minimum mass of 5 Jupiter masses, designated HD 190228 b. The planetary nature of the object was questioned because of the low metal content of the star: giant planets are more likely to be found around high-metallicity stars, so it was argued that the object was more likely to be a brown dwarf. A 2011 study using astrometric measurements from Hipparcos found that, with 95% confidence, HD 190228 b is in fact a brown dwarf of Jupiter masses in a nearly face-on orbit.
However, later studies in 2022 and 2023 using both Hipparcos and Gaia astrometry found much lower true masses, close to the minimum mass. While the former study notes that their inclination measurement is poorly constrained, and that further study should better constrain the mass, the latter says that the low-mass solution is preferred given the relatively large uncertainty in the Hipparcos data. Thus, it seems likely that HD 190228 b is an exoplanet. It takes 3.1 years to orbit the star, and its orbit is elliptical with an eccentricity of 0.55.
References
G-type subgiants
Planetary systems with one confirmed planet
Vulpecula
BD+27 3593
190228
098714 | HD 190228 | [
"Astronomy"
] | 489 | [
"Vulpecula",
"Constellations"
] |
14,726,567 | https://en.wikipedia.org/wiki/List%20of%20build%20automation%20software | This page lists notable software build automation tools and systems.
Sequencing
These tools sequence build operations often based on dependencies sometimes running tasks in parallel.
; uses XML format for configuration files
; written in Python
; written in Clojure
Boost boost.build For C++ projects, cross-platform, based on Perforce Jam
; written in Rust, using Starlark (BUILD file syntax) as Bazel
; Python-based
D Dub Official package and build manager of the D Language
; with a Groovy-based domain specific language (DSL), combining features of Apache Ant and Apache Maven with more features like a reliable incremental build
; for Clojure projects
; one of the earliest build automation tools; many variants
; from Microsoft
; based on Ant
Perforce Jam Build tool by Perforce, inspired by Make
; Python-based
; Python-based
Meta build
Called meta-build tools, these generate configuration files for other build tools such as those listed above.
; very popoular; integrated with IDEs such as Qt Creator, KDevelop and GNOME Builder
; superseded by GN which generates files for ninja and other tools
OpenMake Software Meister
; integrated with GNOME Builder
; written in Lua
Continuous integration
Continuous integration systems automate build operations at a relatively high level via features including: scheduling and triggering builds, storing build log and output files and integrating with version control systems.
Bitbucket Pipelines and Deployments Continuous integration for Bitbucket hosted repositories
Go continuous delivery Open source, cross-platform
GitLab Runner Continuous integration
GitHub Actions Free continuous integration service for open-source projects
; Hudson fork
Spinnaker Open source multi-cloud continuous delivery service from Netflix and Google
Others
Licensing
See also
Make variants Tools based on or very similar to Unix make
References
Build automation
build automation | List of build automation software | [
"Technology"
] | 372 | [
"Computing-related lists",
"Lists of software"
] |
14,726,626 | https://en.wikipedia.org/wiki/HD%20196050 | HD 196050 is a triple star system located in the southern constellation of Pavo. This system has an apparent magnitude of 7.50 and the absolute magnitude is 4.01. It is located at a distance of from the Sun based on parallax, and is drifting further away with a radial velocity of +61 km/s. It is also called by the Hipparcos designation HIP 101806.
Characteristics
The primary component is a G-type main-sequence star with a stellar classification of G3V. It has a quiescent chromosphere and does not appear to be variable. The star has 18% more mass than the Sun and a 46% greater size. It is around 2.5 billion years old with a higher than solar metallicity, and is spinning with a projected rotational velocity of 3 km/s. The star is radiating 2.21 times the luminosity of the Sun from its photosphere at an effective temperature of 5,834 K.
A faint co-moving companion star, designated component B, was detected based on observations during 2003–2004, located to the south of the primary component. This corresponds to a projected separation of . The star is magnitude 10.62 A third companion, component C, was discovered in 2007, located about from component B. It has a visual magnitude of 15.6.
Planetary system
In 2002, the Anglo-Australian Planet Search team announced the discovery of an extrasolar planet orbiting the star. The discovery was independently confirmed by the Geneva Extrasolar Planet Search team. In 2023, the inclination and true mass of HD 196050 b were determined via astrometry.
See also
HD 190228
HD 195019
List of extrasolar planets
References
Further reading
G-type main-sequence stars
M-type main-sequence stars
Planetary systems with one confirmed planet
Triple stars
Pavo (constellation)
PD-61 06497
196050
101806 | HD 196050 | [
"Astronomy"
] | 389 | [
"Constellations",
"Pavo (constellation)"
] |
14,726,693 | https://en.wikipedia.org/wiki/HD%20212301 | HD 212301 is a binary star system in the south circumpolar constellation of Octans. This star is also called HIP 110852. With an apparent visual magnitude of 7.76, it is too faint to be visible to the naked eye. The system is located at a distance of 177 light years from the Sun based on parallax, and is drifting further away with a radial velocity of +4.7 km/s. It has an absolute magnitude of 4.06.
The primary, component A, is an F-type main-sequence star with a stellar classification of F8V. It has 20% greater mass than the Sun and a 23% larger radius. Its age is about the same as the Sun and it is spinning with a projected rotational velocity of 5.4 km/s. It is a metal-rich star with 50% more metals than the Sun has. The star is radiating 1.9 times the luminosity of the Sun from its photosphere at an effective temperature of 6,169 K.
A secondary companion was announced in 2009. This faint star is located at an angular separation of to the northwest of the primary, corresponding to a projected separation of . This is a red dwarf with an estimated class of M3V and a mass equal to around 35% of the mass of the Sun. The pair share a common proper motion.
A hot jupiter candidate exoplanet was discovered orbiting the primary, based on radial velocity observations taken in 2003 and 2005.
See also
HD 213240
List of extrasolar planets
References
External links
F-type main-sequence stars
M-type main-sequence stars
Planetary systems with one confirmed planet
Binary stars
Octans
Durchmusterung objects
212301
110852 | HD 212301 | [
"Astronomy"
] | 358 | [
"Octans",
"Constellations"
] |
14,726,779 | https://en.wikipedia.org/wiki/HD%20213240 | HD 213240 is a possible binary star system in the constellation Grus. It has an apparent visual magnitude of 6.81, which lies below the limit of visibility for normal human sight. The system is located at a distance of 133.5 light years from the Sun based on parallax. The primary has an absolute magnitude of 3.77.
This is an ordinary G-type main-sequence star with a stellar classification of G0/G1V. It is a metal-rich star with an age that has been calculated as being anywhere from 2.7 to 4.6 billion years. The star has 1.6 times the mass of the Sun and 1.56 times the Sun's radius. It is spinning with a projected rotational velocity of 3.5 km/s. The star is radiating 2.69 times the luminosity of the Sun from its photosphere at an effective temperature of 5,921 K.
A red dwarf companion star was detected in 2005 with a projected separation of 3,898 AU.
Planetary system
The Geneva extrasolar planet search team discovered a planet orbiting this star in 2001. Since this planet was discovered by radial velocity, only its minimum mass was initially known, and there was a 5% chance of it being massive enough to be a brown dwarf. In 2023, the inclination and true mass of HD 213240 b were determined via astrometry, confirming its planetary nature.
See also
HD 212301
List of extrasolar planets
References
G-type main-sequence stars
Planetary systems with one confirmed planet
Binary stars
Grus (constellation)
CD-50 13701
213240
111143 | HD 213240 | [
"Astronomy"
] | 337 | [
"Grus (constellation)",
"Constellations"
] |
14,727,286 | https://en.wikipedia.org/wiki/List%20of%20C%2B%2B%20multi-threading%20libraries | List of cross-platform multi-threading libraries for the C++ programming language.
Apache Portable Runtime
Boost.Thread
C++ Standard Library Thread
Concurrencpp
Dlib
HPX
IPP
OpenMP
OpenThreads
Parallel Patterns Library
POCO C++ Libraries Threading
POSIX Threads
Qt QThread
Rogue Wave SourcePro Threads Module
Stapl
Taskflow
TBB
C++ libraries
C++ Multi-threading libraries
Multi-threading libraries | List of C++ multi-threading libraries | [
"Technology"
] | 101 | [
"Computing-related lists",
"Lists of software"
] |
14,730,177 | https://en.wikipedia.org/wiki/Glass%20production | Glass production involves two main methods – the float glass process that produces sheet glass, and glassblowing that produces bottles and other containers. It has been done in a variety of ways during the history of glass.
Glass container production
Broadly, modern glass container factories are three-part operations: the "batch house", the "hot end", and the "cold end". The batch house handles the raw materials; the hot end handles the manufacture proper—the forehearth, forming machines, and annealing ovens; and the cold end handles the product-inspection and packaging equipment.
Batch processing system (batch house)
Batch processing is one of the initial steps of the glass-making process. The batch house simply houses the raw materials in large silos (fed by truck or railcar), and holds anywhere from 1–5 days of material. Some batch systems include material processing such as raw material screening/sieve, drying, or pre-heating (i.e. cullet). Whether automated or manual, the batch house measures, assembles, mixes, and delivers the glass raw material recipe (batch) via an array of chutes, conveyors, and scales to the furnace. The batch enters the furnace at the "dog house" or "batch charger". Different glass types, colours, desired quality, raw material purity/availability, and furnace design will affect the batch recipe.
Hot end
The hot end of a glassworks is where the molten glass is manufactured into glass products. The batch enters the furnace, then passes to the forming process, internal treatment, and annealing.
The following table lists common viscosity fixpoints, applicable to large-scale glass production and experimental glass melting in the laboratory:
Furnace
The batch is fed into the furnace at a slow, controlled rate by the batch processing system. The furnaces are natural gas- or fuel oil-fired, and operate at temperatures up to . The temperature is limited only by the quality of the furnace’s superstructure material and by the glass composition. Types of furnaces used in container glass making include "end-port" (end-fired), "side-port", and "oxy-fuel". Typically, furnace size is classified by metric tons per day (MTPD) production capability.
Modern furnaces use electric heating methods that improve energy efficiency compared to traditional fossil fuel systems, contributing to reduced pollution and emissions. Electrodes made from molybdenum, graphite, or alloys are used in glass furnaces to conduct electricity and generate energy.
Forming process
There are currently two primary methods of making glass containers: the "blow and blow" method for narrow-neck containers only, and the "press and blow" method used for jars and tapered narrow-neck containers.
In both methods, a stream of molten glass at its plastic temperature () is cut with a shearing blade to form a solid cylinder of glass, called a "gob". The gob is of predetermined weight just sufficient to make a bottle. Both processes start with the gob falling, by gravity, and guided, through troughs and chutes, into the blank moulds, two halves of which are clamped shut and then sealed by the "baffle" from above.
In the "blow and blow" process, the glass is first blown through a valve in the baffle, forcing it down into the three-piece "ring mould" which is held in the "neckring arm" below the blanks, to form the "finish". The term "finish" describes the details (such as cap sealing surface, screw threads, retaining rib for a tamper-proof cap, etc.) at the open end of the container. Then compressed air is blown through the glass, which results in a hollow and partly formed container. Compressed air is then blown again at the second stage to give final shape.
Containers are made in two major stages. The first stage moulds all the details ("finish") around the opening, but the body of the container is initially made much smaller than its final size. These partly manufactured containers are called "parisons", and quite quickly, they are blow-molded into final shape.
The "rings" are sealed from below by a short plunger. After the "settleblow" finishes, the plunger retracts slightly, to allow the skin that's formed to soften. "Counterblow" air then comes up through the plunger, to create the parison. The baffle rises and the blanks open. The parison is inverted in an arc to the "mould side" by the "neckring arm", which holds the parison by the "finish".
As the neckring arm reaches the end of its arc, two mould halves close around the parison. The neckring arm opens slightly to release its grip on the "finish", then reverts to the blank side. "Final blow", applied through the "blowhead", blows the glass out, expanding into the mould, to make the final container shape.
In the press and blow process, the parison is formed by a long metal plunger which rises up and presses the glass out, in order to fill the ring and blank moulds. The process then continues as before, with the parison being transferred to the final-shape mould, and the glass being blown out into the mould.
The container is then picked up from the mould by the "take-out" mechanism, and held over the "deadplate", where air cooling helps cool down the still-soft glass. Finally, the bottles are swept onto a conveyor by the "push out paddles" that have air pockets to keep the bottles standing after landing on the "deadplate"; they're now ready for annealing.
Forming machines
The forming machines hold and move the parts that form the container. The machine consists of 19 basic mechanisms in operation to form a bottle and generally powered by compressed air (high pressure – 3.2 bar and low pressure – 2.8 bar), the mechanisms are electronically timed to coordinate all movements of the mechanisms. The most widely used forming machine arrangement is the individual section machine (or IS machine). This machine has a bank of 5–20 identical sections, each of which contains one complete set of mechanisms to make containers. The sections are in a row, and the gobs feed into each section via a moving chute, called the gob distributor. Sections make either one, two, three or four containers simultaneously (referred to as "single", "double", "triple" and "quad" gob). In the case of multiple gobs, the "shears" cut the gobs simultaneously, and they fall into the blank moulds in parallel.
Forming machines are largely powered by compressed air and a typical glass works will have several large compressors (totaling 30k–60k cfm) to provide the necessary compressed air. However in recent times servo drives have been implemented in the machines which achieve a better digital control of the forming process. It is one step to initialize industries 2.0 in this branch.
Furnaces, compressors, and forming machines generate large quantities of waste heat which are generally cooled by water. Hot glass which is not used in the forming machine is diverted and this diverted glass (called "cullet") is generally cooled by water, and sometimes even processed and crushed in a water bath arrangement. Often cooling requirements are shared over banks of cooling towers arranged to allow for backup during maintenance.
Internal treatment
After the forming process, some containers—particularly those intended for alcoholic spirits—undergo a treatment to improve the chemical resistance of the inside, called "internal treatment" or dealkalization. This is usually accomplished through the injection of a sulfur- or fluorine-containing gas mixture into bottles at high temperatures. The gas is typically delivered to the container either in the air used in the forming process (that is, during the final blow of the container), or through a nozzle directing a stream of the gas into the mouth of the bottle after forming. The treatment renders the container more resistant to alkali extraction, which can cause increases in product pH, and in some cases container degradation.
Annealing
As glass cools, it shrinks and solidifies. Uneven cooling may make glass more susceptible to fracture due to internal stresses: the surface cools first, then as the interior cools and contracts it creates tension. Even cooling is achieved by annealing. An annealing oven (known in the industry as a lehr) heats the container to about , then cools it, depending on the glass thickness, over a 20 – 60 minute period.
Cold end
The role of the cold end of glass container production is to complete the final tasks in the manufacturing process: spray on a polyethylene coating for abrasion resistance and increased lubricity, inspect the containers for defects, label the containers, and package the containers for shipment.
Coatings
Glass containers typically receive two surface coatings, one at the hot end, just before annealing and one at the cold end just after annealing. At the hot end a very thin layer of tin(IV) oxide is applied either using a safe organic compound or inorganic stannic chloride. Tin based systems are not the only ones used, although the most popular. Titanium tetrachloride or organo titanates can also be used. In all cases the coating renders the surface of the glass more adhesive to the cold end coating. At the cold end a layer of typically, polyethylene wax, is applied via a water based emulsion. This makes the glass slippery, protecting it from scratching and stopping containers from sticking together when they are moved on a conveyor. The resultant invisible combined coating gives a virtually unscratchable surface to the glass. Due to reduction of in-service surface damage, the coatings often are described as strengtheners, however a more correct definition might be strength-retaining coatings.
Inspection equipment
Glass containers are 100% inspected; automatic machines, or sometimes persons, inspect every container for a variety of faults. Typical faults include small cracks in the glass called "checks" and foreign inclusions called "stones" which are pieces of the refractory brick lining of the melting furnace that break off and fall into the pool of molten glass, or more commonly oversized silica granules (sand) that have failed to melt and which subsequently are included in the final product. These are especially important to select out due to the fact that they can impart a destructive element to the final glass product. For example, since these materials can withstand large amounts of thermal energy, they can cause the glass product to sustain thermal shock resulting in explosive destruction when heated. Other defects include bubbles in the glass called "blisters" and excessively thin walls. Another defect common in glass manufacturing is referred to as a "tear". In the "press and blow" forming, if a plunger and mould are out of alignment, or heated to an incorrect temperature, the glass will stick to either item and become torn. In addition to rejecting faulty containers, inspection equipment gathers statistical information and relays it to the forming machine operators in the hot end. Computer systems collect fault information and trace it to the mould that produced the container. This is done by reading the mould number on the container, which is encoded (as a numeral, or a binary code of dots) on the container by the mould that made it. Operators carry out a range of checks manually on samples of containers, usually visual and dimensional checks.
Secondary processing
Sometimes container factories will offer services such as "labelling". Several labelling technologies are available. Unique to glass is the Applied Ceramic Labelling process (ACL). This is screen-printing of the decoration onto the container with a vitreous enamel paint, which is then baked on. An example of this is the original Coca-Cola bottle.
Packaging
Glass containers are packaged in various ways. Popular in Europe are bulk pallets with between 1000 and 4000 containers each. This is carried out by automatic machines (palletisers) which arrange and stack containers separated by layer sheets. Other possibilities include boxes and even hand-sewn sacks. Once packed, the new "stock units" are labelled, warehoused, and ultimately shipped.
Marketing
Glass container manufacture in the developed world is a mature market business. World demand for flat glass was approximately 52 million tonnes in 2009. The United States, Europe and China account for 75% of demand, with China's consumption having increased from 20% in the early 1990s to 50%. Glass container manufacture is also a geographical business; the product is heavy and large in volume, and the major raw materials (sand, soda ash and limestone) are generally readily available. Therefore production facilities need to be located close to their markets. A typical glass furnace holds hundreds of tonnes of molten glass, and so it is simply not practical to shut it down every night, or in fact in any period short of a month. Factories therefore run 24 hours a day 7 days a week. This means that there is little opportunity to either increase or decrease production rates by more than a few percent. New furnaces and forming machines cost tens of millions of dollars and require at least 18 months of planning. Given this fact, and the fact that there are usually more products than machine lines, products are sold from stock. The marketing/production challenge is therefore to predict demand both in the short 4- to 12-week term and over the 24- to 48-month-long term. Factories are generally sized to service the requirements of a city; in developed countries there is usually a factory per 1–2 million people. A typical factory will produce 1–3 million containers a day.
Despite its positioning as a mature market product, glass does enjoy a high level of consumer acceptance and is perceived as a "premium" quality packaging format.
Lifecycle impact
Glass containers are wholly recyclable and the glass industries in many countries have a policy, sometimes required by government regulations, of maintaining a high price on cullet to ensure high return rates. Return rates of 95% are not uncommon in the Nordic countries (Sweden, Norway, Denmark and Finland). Return rates of less than 50% are usual in other countries.
Of course glass containers can also be reused, and in developing countries this is common, however the environmental impact of washing containers as against remelting them is uncertain. Factors to consider here are the chemicals and fresh water used in the washing, and the fact that a single-use container can be made much lighter, using less than half the glass (and therefore energy content) of a multiuse container. Also, a significant factor in the developed world's consideration of reuse are producer concerns over the risk and consequential product liability of using a component (the reused container) of unknown and unqualified safety.
How glass containers compare to other packaging types (plastic, cardboard, aluminium) is hard to say; conclusive lifecycle studies are yet to be produced.
Float glass process
Float glass is a sheet of glass made by floating molten glass on a bed of molten metal, typically tin, although lead and various low melting point alloys were used in the past. This method gives the sheet uniform thickness and very flat surfaces. Modern windows are made from float glass. Most float glass is soda–lime glass, but relatively minor quantities of special borosilicate and flat panel display glass are also produced using the float glass process. The float glass process is also known as the Pilkington process, named after the British glass manufacturer Pilkington, who pioneered the technique (invented by Sir Alastair Pilkington) in the 1950s.
Local environmental impacts
As with all highly concentrated industries, glassworks suffer from moderately high local environmental impacts. Compounding this is that because they are mature market businesses, they often have been located on the same site for a long time and this has resulted in residential encroachment. The main impacts on residential housing and cities are noise, fresh water use, water pollution, NOx and SOx air pollution, and dust.
Noise is created by the forming machines. Operated by compressed air, they can produce noise levels of up to 106dBA. How this noise is carried into the local neighborhood depends heavily on the layout of the factory. Another factor in noise production is truck movements. A typical factory will process 600 T of material a day. This means that some 600 T of raw material has to come onto the site and the same off the site again as finished product.
Water is used to cool the furnace, compressor and unused molten glass. Water use in factories varies widely; it can be as little as one tonne water used per melted tonne of glass. Of the one tonne, roughly half is evaporated to provide cooling, the rest forms a wastewater stream.
Most factories use water containing an emulsified oil to cool and lubricate the gob cutting shear blades. This oil-laden water mixes with the water outflow stream, thus polluting it. Factories usually have some kind of water processing equipment that removes this emulsified oil to various degrees of effectiveness.
Nitrogen oxides are a natural product of the burning of gas in air and are produced in large quantities by gas-fired furnaces. Some factories in cities with particular air pollution problems will mitigate this by using liquid oxygen, however the logic of this given the cost in carbon of (1) not using regenerators and (2) having to liquefy and transport oxygen is highly questionable. Sulfur oxides are produced as a result of the glass melting process. Manipulating the batch formula can effect some limited mitigation of this; alternatively exhaust plume scrubbing can be used.
The raw materials for glass-making are all dusty material and are delivered either as a powder or as a fine-grained material. Systems for controlling dusty materials tend to be difficult to maintain, and given the large amounts of material moved each day, only a small amount has to escape for there to be a dust problem. Cullet (broken or waste glass) is also moved about in a glass factory and tends to produce fine glass particles when shovelled or broken.
See also
Mirrors
Blow moulding
Borosilicate glass
Boston round (bottle)
Drinkware
Float glass
Glass disease
Glass Queen
Glassmakers' symbol
History of glass
Irving Wightman Colburn
Packaging and labelling
Wine bottle
Cage cup
References
External links
Containers | Glass production | [
"Materials_science",
"Engineering"
] | 3,802 | [
"Glass engineering and science",
"Glass production"
] |
17,562,270 | https://en.wikipedia.org/wiki/Kielder%20Forest%20Star%20Camp | The Kielder Forest Star Camp is an annual star party, held each autumn and spring in Kielder Forest in northern England. The area is known for its dark skies.
The five night event is based on the Kielder Campsite. Free talks on astronomy are held at nearby Kielder Castle on the Saturday. The event started in October 2003.
See also
List of astronomical societies
References
External links
Kielder Forest Star Camp Web Site
British astronomy organisations
Star parties
Tourist attractions in Northumberland
North East England
Science and technology in Northumberland
Science events in the United Kingdom | Kielder Forest Star Camp | [
"Astronomy"
] | 110 | [
"Star parties",
"British astronomy organisations",
"Astronomy events",
"History of astronomy",
"Astronomy stubs",
"Astronomy organizations"
] |
17,562,889 | https://en.wikipedia.org/wiki/2%2C3-Dimethylbutane | 2,3-Dimethylbutane is an isomer of hexane. It has the chemical formula (CH3)2CHCH(CH3)2. It is a colorless liquid which boils at 57.9 °C.
References
Alkanes | 2,3-Dimethylbutane | [
"Chemistry"
] | 57 | [
"Organic compounds",
"Alkanes"
] |
17,563,810 | https://en.wikipedia.org/wiki/Structural%20abuse | Structural abuse is the process by which an individual or group is dealt with unfairly by a social or cultural system or authority. This unfairness manifests itself as abuse in a psychological, financial, physical or spiritual form, and victims often are unable to protect themselves from harm. An individual's inability to protect themselves may lead to their entrapment in the system, preventing them from seeking justice or recompense for crimes endured and damages incurred, creating a feeling of isolation or helplessness.
Systems containing abusive structures are primarily designed to control individuals or manipulate them for material gain. Most social systems contain at least one structure that induces structural abuse. These structures, when allowed to exist, create a cycle of abuse, wherein the abuse is repetitive or contagious in nature, and may become acceptable in other parts of the system.
Structural abuse differs to structural violence in terms of scale – structural violence is a process occurring within an entire society, such as racism or classism, while structural abuse refers to a specific element of society, or a specific system within society. Abuse occurring on this smaller scale is not necessarily endorsed by wider society, such as modern witch hunts, which have been condemned in South Africa, regardless of deaths that still occur in areas retaining anti-Pagan social structures. Structural abuse can be found on a very small scale, such as in instances of bullying involving more than one perpetrator, or in cases of malfeasance, a common example of which is individual police officers conducting investigations without direct evidence, or ignoring formal complaints made by victims.
Process
Types
There are three types of structural abuse:
Structural interference with an individual's personal health; psychological, social, emotional, physical or spiritual.
Structural interference with an individual's relationships; compromising the ability to establish and maintain social relationships – intimate or platonic.
Structural interference with an individual's liberties and rights; compromising the ability to establish and maintain employment, practicing hobbies or executing other liberties and legal rights.
Affected Groups
Structural abuse is often indirect. As such it can affect vulnerable groups, such as:
Children
Young adults
Adults with disabilities
The elderly
Nature
Structural abuses often "survive" on heuristics of fallacies and distortions of logic.
See also
Accumulation by dispossession
Causes of poverty
Conflict theories
Cultural reproduction
Civil Rights Movement
Cycle of abuse
Cycle of poverty
Discrimination
Economic abuse
Economic violence
Extermination through labour
Freak show
Frog pond effect
Global inequality
Global policeman
Golden Rule
Hate-watching
Human zoo
Imperialism
Institutional abuse
Institutional racism
Iron cage
Judicial murder
Kangaroo court
Peacebuilding
Political repression
Privilege hazard
Slow violence
Social conflict
Social exclusion
Social inequality
Social murder
Structural violence
Subsistence crisis
Suicide among LQBTQIA+ people
Symbolic violence
Toxic masculinity
War on Drugs
Washington consensus
Witch-hunts
References
Further reading
Antisocial Supply -- An educational resource to help others identify emotional and psychological abuse -- antiss.net
Psychological abuse
Abuse | Structural abuse | [
"Biology"
] | 587 | [
"Abuse",
"Behavior",
"Aggression",
"Human behavior"
] |
17,564,368 | https://en.wikipedia.org/wiki/Arctic%20Sun%20medical%20device | The Arctic Sun Temperature Management System is a non-invasive targeted temperature management system. It modulates patient temperature by circulating chilled water in pads directly adhered to the patient's skin. Using varying water temperatures and a computer algorithm, a patient's body temperature can be better controlled. It is produced by Medivance, Inc. of Louisville, Colorado.
Background
Body temperature, which is systematically measured and reported as a vital sign, contributes to maintenance of normal physiology and affects the processes that lead to recovery after illness. Complete and proper functioning of the body is dependent on maintaining a core temperature between . A core temperature above 41.5 °C, or below 33.5 °C, causes a fast decline in proper functioning of the body and may result in injury or death. Intentional manipulation of body temperature has been studied as a treatment strategy for head injuries since the 1900s. In the 1980s, the use of hypothermia on dogs after cardiac arrest demonstrated positive outcomes, including neurological status and survival. In 2005, the American Heart Association implemented recommendations and guidelines for mild hypothermia in post-resuscitation support after cardiac arrest with return of spontaneous circulation.
One of the most common practices of targeted temperature management is to reduce body temperature to a “mild hypothermic state” (per the AHA guidelines is 33 °C (91.4 °F) for 12–24 hours and then slowly re-warm the body back to normal 37 °C (98.6 °F). The purpose of this is to slow the metabolic processes and the chemical cascade that occurs when the brain goes without oxygen for a period of time. A study conducted in 2002-2004 showed that treatment with therapeutic hypothermia for patients resuscitated after cardiac arrest due to ventricular fibrillation led to a positive outcome (Glasgow-Pittsburgh Cerebral Performance category 1 or 2) in 24 of 43 patients compared to only 11 of 43 patients in the standard resuscitation group where no hypothermia was used in treatment.
Therapeutic hypothermia, which lowers the patient's body temperature to levels between , is used to help reduce the risk of the ischemic injury to the brain following a period of insufficient blood flow. Periods of insufficient blood flow may be caused by cardiac arrest, stroke, or brain trauma. Non-invasively induced therapeutic hypothermia has been shown to reduce mortality of successfully resuscitated cardiac arrest victims by 35 percent and increase the chance of a good neurologic outcome by 39 percent.
Device description
The Arctic Sun can be explained as dry water immersion. It is a non-invasive temperature management system that is used to induce hypothermia in comatose patients that have suffered from Sudden Cardiac Arrest (SCA) and patients at risk for ischemic brain damage. Because of the Arctic Sun's noninvasive nature, treatment can be delivered without the host of adverse events associated with invasive procedures such as cooling catheters. The Arctic Sun has adhesive gel pads which stick to a patient's body, and cover only a portion of a patient's body to leave most of the body free for augmenting medical procedures. The device operates under negative pressure and circulates water through the adhesive pads at a temperature between . By controlling the temperature of the water running through the gel pads, the Arctic Sun can help regulate a patient's body temperature. Controlled rewarming has been cited in the literature as beneficial in preventing reperfusion injury.
A complaint levied against the Arctic Sun is the risk of skin injury. A study published in 2007 found that the Arctic Sun caused "skin erythema during the cooling period... in almost all patients," but that no pressure ulcers or frostbite was noted.
Invasive cooling catheter companies have claimed that catheters can lower body temperature at a faster rate, which is relevant because most of the clinical data suggests that the sooner cooling initiates the better a patient's outcome. However, there exists a 75-minute delay on average between admittance and catheter insertion. Even with a physician readily available to place the cooling catheter, the device setup takes a minimum of 11 minutes. When objectively evaluating the published data the average cooling rate for cooling catheters is 2.06 °C. Treatment with the Arctic Sun can be administered within 10 minutes by unsupervised nursing professionals.
Historically, clinicians reported that catheters cool at a quicker rate, however, a 2011 study published in the Society of Critical Care Medicine where 167 patients treated either with the Arctic Sun or the Alsius Coolgard Catheter demonstrated time from cardiac arrest to achieving mild therapeutic hypothermia was equal with both devices. In this study, there was no significant difference in survival with good neurologic function.
See also
Medical equipment
Resuscitation
Therapeutic hypothermia
References
External links
Device specifications
Medical equipment | Arctic Sun medical device | [
"Biology"
] | 1,012 | [
"Medical equipment",
"Medical technology"
] |
17,564,957 | https://en.wikipedia.org/wiki/Zinc%20protoporphyrin | Zinc protoporphyrin (ZPP) refers to coordination complexes of zinc and protoporphyrin IX. It is a red-purple solid that is soluble in water. The complex and related species are found in red blood cells when heme production is inhibited by lead and/or by lack of iron.
Clinical utility
Measurement of zinc protoporphyrin in red cells has been used for screening for lead poisoning.
and for iron deficiency.
Zinc protoporphyrin levels can be elevated as the result of a number of conditions, for instance:
lead poisoning
iron deficiency
sickle cell anemia
sideroblastic anemia
anemia of chronic disease
vanadium exposure
erythropoietic protoporphyria
Diverse types of cancer
The virtue of elevated ZPP testing as a screen is that all of these conditions can be considered worth discovering.
The fluorescent properties of ZPP in intact red cells allows the ZPP/heme molar ratio to be measured quickly, at low cost, and in a small sample volume.
ZnPP is finding a new use as a drug in combined cancer therapies.
History
Porphyrin complexes of zinc have been known since the 1930s. In 1974 ZPP was identified as a major non-heme porphyrin formed in red cells as the result of lead poisoning or iron deficiency., It was already known at this time that non-heme protoporphyrin IX levels were elevated in these conditions, but prior investigators had used acidic extraction methods in their assays that converted ZPP to unbound Protoporphyrin IX. The early literature on quantifying zinc-PP levels may be unreliable.
For cancer therapy
ZnPP has been investigated for cancer therapies.
ZnPP is a competitive inhibitor of heme oxygenase. Heme oxygenase is a cytoprotective enzyme that copes with oxidative stress on a cell and shows higher expression in cancerous tissues. ZnPP suppression of heme oxygenase reduces cell viability of cancer cells and increases cytotoxicity in cancer cells. ZnPP works in combination with anticancer drugs to increase cytotoxicity. ZnPP inhibits tumor growth especially solid tumors. Tumors from brain cancer, colon cancer, prostate cancer, renal cell cancer, oral squamous cell cancer, and leukemia all show a susceptibility to ZnPP due to increase expression of heme oxygenase. The inhibition of heme oxygenase leads to an increase of reactive oxidative species in the cell which sensitizes the cells to chemotherapeutic agents. Increased reactive oxidative species can cause apoptosis in cancer cells and reduce drug resistance when exposed to ZnPP due to loss of the heme oxygenase coping mechanism. The combination of these two therapies is highly effective in treating cancer in experiments thus far, and is a possible new method for overcoming drug resistance. The reduced coping ability of tissues treated with ZnPP also increases radiosensitivity. Cells treated with ZnPP and radiation as opposed to simply one of the two are less viable and more likely to stay in G1 phase of the cell cycle, rather than progress to the G2 phase. ZnPP and radiation combination therapy shows more apoptosis than the same amount of radiation displaying that ZnPP puts stress on cancerous tissue. ZnPP have been injected in a number of trials on solid tumors, but can be utilized more broadly when effectively delivered to cancer cells and not healthy cells. A targeted delivery system is needed to fully exploit the uses of ZnPP as a therapeutic agent and heme oxygenase inhibitor due to the potential side effects of free ZnPP on healthy tissue. Reducing the anti-oxidant capability of healthy cells can reduce effects that would have been favorable. However ZnPP have been encapsulated in nanoparticles with specialized coating for drug delivery inside the body. ZnPP did not show any reduce inhibitory potential on heme oxygenase when loaded into nanoparticles. Similarly ZnPP loaded into nanoparticles has a higher cytotoxicity than free ZnPP after two days due to a more favorable release rate as well as better biodistribution and internalization. The possible negative effects on major organs were not seen and blood distribution is more desirable in ZnPP loaded nanoparticles than free ZnPP. The specific inhibition of heme oxygenase using nanoparticles with encapsulated ZnPP reduces side effects and is likely the future method of administering ZnPP treatment.
Structural chemistry
Zinc porphyrins are always five- or six-coordinate. Because the axial ligands are labile, these complexes are often depicted with planar structures. Planar zinc(II) complexes are unknown.
References
Porphyrins
Blood cells | Zinc protoporphyrin | [
"Chemistry"
] | 994 | [
"Porphyrins",
"Biomolecules"
] |
17,565,049 | https://en.wikipedia.org/wiki/Clean%20feed%20%28television%29 | In television technology, a clean feed is a video signal that does not have added graphics and text. This video signal is used in sport production to allow different television stations to add their own digital on-screen graphic image on a common signal, or in news broadcasting to produce two or more different streams, each one with the same picture but in different languages.
A clean feed is a signal which has not come from the main output of the video switcher, such as the output of a vision mixer before the downstream keyer stage - the clean feed is identical to the main program output but without any captions keyed into it. Modern production equipment can actually put different keys on multiple outputs, allowing them to go to the clean feed or not. The most sophisticated vision mixers (or production switchers, according to the American nomenclature) can generate a clean feed output for any of their mix/effects (ME) buses.
The term clean feed is also used to refer to backhaul feeds of television programming sent via communication satellite or other transport (such as a national fiber-optic network) sent from another TV station or remote television production truck on-location, which does not carry any television advertisements or break bumpers, or in some cases, lower-third graphics or superimposed chyron text.
See also
Mix-minus
Television technology
Television terminology | Clean feed (television) | [
"Technology"
] | 274 | [
"Information and communications technology",
"Television technology"
] |
17,565,253 | https://en.wikipedia.org/wiki/Colorado%20River%20Storage%20Project | The Colorado River Storage Project is a United States Bureau of Reclamation project designed to oversee the development of the upper basin of the Colorado River. The project provides hydroelectric power, flood control and water storage for participating states along the upper portion of the Colorado River and its major tributaries.
Since its inception in 1956, the project has grown to include the participation of several related water management projects throughout the river's basin. The project's original scope, and primary focus, are the upper Colorado River itself, the Green River, the San Juan River, and the Gunnison River.
Participating states are Arizona, Utah, New Mexico, Colorado and Wyoming.
History
Attempts at managing the water supply in the upper Colorado River basin were first recorded in 1854 at Fort Supply in Wyoming, when water was diverted from Blacks Fork to irrigate local lands. Subsequent diversions of the waters in the Colorado basin led to preliminary investigations of means to develop the system as early as 1902 when the Bureau of Reclamation, then known as the Reclamation Service, was established.
Serious consideration for the project began when the Colorado River Compact was signed in 1922 by the participating states, as well as the lower Colorado River states, California and Nevada. As a stipulation of that compact, the upper basin states were required to ensure an annual flow of no less than be delivered to the lower basin states. However, the annual flow of the Colorado River at Lee's Ferry in Arizona, the established dividing point, was extremely erratic, ranging from to . This led to an inability of the upper basin states to meet the minimum delivery requirements to the lower states in dry years, and a loss of significant surpluses in wet years.
In order to regulate the flow of the Colorado and ensure compliance with the compact, a study was undertaken that determined a series of dams and reservoirs on the river and its tributaries would be necessary. A joint effort between the Upper Colorado River Commission, the Bureau of Reclamation and other federal agencies delivered a report with proposed projects to the United States Congress in 1950.
Among the proposed projects was a dam to be constructed on the Green River in Echo Park, in Dinosaur National Monument in Colorado. The proposal for Echo Park Dam created controversy and sparked the ire of Sierra Club director David Brower, who embarked on a national campaign to rescue the park. As part of a compromise, the proposed dam was stricken from the project and replaced with another dam in Glen Canyon, Arizona. Brower, who had not personally visited Glen Canyon prior to the compromise, later lamented the deal, describing it as "the worst mistake of his career" and "'the biggest sin I ever committed'".
A revised, and slightly pared down, version of the plan was passed into law by Congress in 1956. The legislation called for the construction of dams, reservoirs and related works at Curecanti in Colorado, Flaming Gorge in Wyoming, Navajo in New Mexico and Glen Canyon in Arizona. All but the Navajo project were to include power generation capabilities; the Navajo project was intended as flood control only. Also included in the legislation were several related projects in the Colorado River basin.
Project scope
The Colorado River Storage Project is made up of four separate units, spread along the upper Colorado basin and its major tributaries. Also included are several participating projects located throughout the system.
As a whole, the system provides a storage capacity of approximately of water. This capacity is released to meet the Colorado River Compact's delivery requirements during periods of low flow in the system. Additionally, three of the units provide hydroelectric power to major markets in the southwest.
Lee's Ferry in Arizona serves as the southern boundary point for the project, which encompasses the Colorado River upstream from this point and all tributaries.
Glen Canyon Unit
The Glen Canyon Unit, which consists of the Glen Canyon Dam, Lake Powell and the Glen Canyon Powerplant, is the largest and most important unit of the system. While the dam is located near Page in northern Arizona, the majority of Lake Powell resides in southern Utah. With a total storage capacity of of water in Lake Powell, the Glen Canyon Unit accounts for over 64% of the system's overall water storage capacity. The 1,296 megawatt capacity of the dam's hydroelectric generators accounts for almost 75% of the overall generating capacity of the project.
In spite of its importance to the system, the Glen Canyon Unit has also been the source of controversy even before it began operating in 1964. Sierra Club director David Brower, who was partially responsible for the location of the dam as part of a compromise, later regretted the decision. Former Arizona Senator Barry Goldwater, who was a proponent of the dam in the beginning, later recanted his opinion and admitted that he had regretted supporting the project. Recent calls for the draining of Lake Powell and the restoration of Glen Canyon by environmental groups such as Sierra Club have resulted in the founding of several advocacy groups for the cause such as Living Rivers and Friends of Glen Canyon, as well as opposition groups such as Friends of Lake Powell. Given the importance of the unit to the project as well as its impact as a tourist destination to the region, restoration efforts face significant opposition and there currently exist no plans to cease operations at Glen Canyon.
Not directly a part of the project but built as a direct result of it, the Glen Canyon Dam Bridge was constructed over the river in 1959. At the time of its completion it was the highest arch bridge in the world. It currently serves as one of only two bridges to cross the Colorado River between Lake Mead and Lake Powell, carrying the majority of the traffic between northern Arizona and southern Utah.
Flaming Gorge Unit
The Flaming Gorge Unit consists of the Flaming Gorge Dam and the Flaming Gorge Reservoir, and the dam's powerplant. The dam impounds the Green River near Dutch John, Utah. Portions of the reservoir spill over into Southern Wyoming near the city of Green River.
Completed in 1964, the dam provides water storage and hydroelectric generation, as well as flood control on the Green River, the primary tributary to the Colorado. The powerplant in the dam has a capacity of 153 megawatts or about 8.5% of the entire system.
Navajo Unit
The Navajo Unit consists of the Navajo Dam and the Navajo Lake reservoir. The dam impounds the San Juan River near Farmington, New Mexico.
The dam was completed in 1963, and was actually the first of the units in the project to be completed. Unlike the subsequent dams, Navajo Dam did not have any power generating capacity when built. A small plant with a capacity of 32 MW was installed in 1983 in conjunction with the city of Farmington to generate local power.
Aspinall Unit
The Aspinall Unit consists of 3 dams and reservoirs on the Gunnison River in Colorado. It is the only unit in the project to be made up of more than one dam or reservoir.
The Aspinall Unit was originally named the Curecanti Unit, but was renamed for former congressman Wayne N. Aspinall in 1980. Aspinall had been a strong proponent of water reclamation projects in Colorado and the western US in general, and was seen as a key opponent to David Brower in the fight to enact the Colorado River Storage Project. Brower was known to have fought regularly with Aspinall, going so far as to state that he had seen "dream after dream dashed on the stony continents of Wayne Aspinall".
As a whole, the Aspinall Unit has a generating capacity of about 290 megawatts, or about 17% of the entire Colorado River Storage Project, making it the second most productive unit after Glen Canyon.
Blue Mesa Dam
The Blue Mesa Dam impounds the Gunnison River upstream of the Morrow Point Dam forming the Blue Mesa Reservoir, making it the first dam the river passes through. The dam was completed in 1966 and has an electric generating capacity of 86,400 kilowatts, or about 30% of the Aspinall Unit's generating capacity.
Morrow Point Dam
The Morrow Point Dam impounds the Gunnison River downstream from the Blue Mesa Dam but upstream of the Crystal Dam, forming the Morrow Point Reservoir, putting it in the center of the Aspinall Unit. Completed in 1968, Morrow Point is the largest and most productive of the Aspinall dams. Morrow Point has a generating capacity of 173,334 kilowatts, making it the second most productive dam in the entire Colorado River Storage Project system. It provides about 60% of the Aspinall Unit's generating capacity.
Additionally, the Morrow Point Dam is the first thin-arch concrete dam to be built in the Colorado River Storage Project system.
Crystal Dam
The Crystal Dam impounds the Gunnison River about 6 miles (10 km) downstream from the Morrow Point Dam, making it the final dam in the Aspinall Unit. Completed in 1976, it is the last dam in both the Aspinall Unit and the Colorado River Storage Project to be completed, marking the final completion of the system as a whole.
Crystal Dam forms the Crystal Reservoir and has the smallest capacity of the hydroelectric dams in the system, providing some 31,500 kilowatts capacity, or just over 1% of the Aspinall Unit's capacity.
Participating projects
A number of water management projects in various locations of the upper Colorado River basin are considered participating projects in the Colorado River Storage Project. These projects are financially related to the CRSP but are not considered a part of the project itself.
Eleven projects were included as participating projects in the 1956 legislation. These projects include:
Central Utah Project, numerous dams and reservoirs in central Utah
Emery County Project, covering dams in Emery County, Utah
Florida Project, on the Florida River in southwestern Colorado
Hammond Project, on the San Juan River in northeastern New Mexico
La Barge Project in Wyoming
Lyman Project, on the Blacks Fork and Smiths Fork of the Green River, primarily in Wyoming
Paonia Project in west-central Colorado
Pine River Project in western Colorado
Seedskadee Project on the upper Green River Basin in Wyoming
Silt Project in west-central Colorado
Smith Fork Project in west-central Colorado
Wyoming's Eden Project was authorized independently in 1949. It was tied to the Colorado River Storage Project by the terms of its own authorization.
An amendment to the legislation in 1962 added two projects to the participants list:
San Juan–Chama Project, diverting water from the San Juan River basin out to the Rio Grande basin
Navajo Indian Irrigation Project, performed on behalf of the Bureau of Indian Affairs
A 1964 amendment added three more projects:
Bostwick Park Project, involving Cimarron Creek, a tributary of the Gunnison River
Fruitland Mesa Project in Colorado
Savery-Pot Hook Project in Colorado and Wyoming
The Colorado River Basin Project Act in 1968 added a final five projects to the participants list:
Animas-La Plata Water Project in Colorado and New Mexico
Dallas Creek Project, a tributary of the Uncompahgre River, in turn a tributary of the Gunnison River
Dolores Project in southwestern Colorado
San Miguel Project, Colorado
West Divide Project, Colorado
Four projects, the Fruitland Mesa, Savery-Pot Hook, San Miguel and West Divide Projects, were later found to be infeasible and removed from the list. Fruitland Mesa & Savery-Pot Hook Projects were cut by the United States Senate in the Public Works appropriations bill of July 1977.
Project impact
Power, water, and recreational impact
The four primary units of the Colorado River Storage Project have a maximum output of 1,813 megawatts of hydroelectric power at any given time, comparable to a large coal-fired generating station such as the Navajo Generating Station.
The Blue Mesa and Navajo Dams, built primarily to function for flood control purposes, have saved approximately $10 million in flood-related costs up to the year 1999.
Additionally, the various units of the project have created significant recreational opportunities throughout the otherwise arid southwest regions.
Environmental impact
The project has changed the ecosystem in the Colorado River, including in Grand Canyon National Park. Glen Canyon Dam in particular has been the subject of much environmental criticism.
Water trapped behind the dams cools and drops its sediment load in the reservoirs. Natural floods of warm sediment-rich water flowing down the Colorado River, through the Grand Canyon, and on to the Colorado River Delta created sandbars and beaches along the river's course and throughout its canyons. These floods have been replaced with metered releases of cold, sediment-free water which has led to the erosion of sandbars in the Grand Canyon that are crucial for wildlife and has altered the food web within the river with natural species being displaced by invasive species. Attempts to simulate natural flood cycles were started in the 2000s but have thus far failed to restore the natural environment in the canyon.
The project has changed the topography of the river with the heavy loads of silt trapped behind the dams deposited in the upper reaches of the reservoirs. These silt loads have filled up the inundated canyons and are now coming to the surface as the water levels in the reservoirs drop.
The creation of large reservoirs and irrigation systems along the river as part of the project has increased the surface area of the Colorado River and the length of time the water is held in the basin which in turn increases the amount of water lost to evaporation. Some estimates indicate that 8.5 million acre feet of water is being lost each year, equivalent to the average amount of water released from Lake Powell to Lake Mead.
Water from the Colorado River rarely reaches the Colorado River Delta anymore due to usage and evaporative loss within the Project. This has reduced the size of the estuary at the mouth of the river from 3,000 square miles to fewer than 250 square miles. Invasive species have become dominant in the Delta and the loss of this habitat has had wider implications for marine life in the Gulf of California.
References
External links
Colorado River Storage Project
CRSP Management Site – Archived site
Colorado River
History of the American West
United States Bureau of Reclamation | Colorado River Storage Project | [
"Engineering"
] | 2,816 | [
"Colorado River Storage Project"
] |
17,565,856 | https://en.wikipedia.org/wiki/Parthasarathy%27s%20theorem | In mathematics – and in particular the study of games on the unit square – Parthasarathy's theorem is a generalization of Von Neumann's minimax theorem. It states that a particular class of games has a mixed value, provided that at least one of the players has a strategy that is restricted to absolutely continuous distributions with respect to the Lebesgue measure (in other words, one of the players is forbidden to use a pure strategy).
The theorem is attributed to Thiruvenkatachari Parthasarathy.
Theorem
Let and stand for the unit interval ; denote the set of probability distributions on (with defined similarly); and denote the set of absolutely continuous distributions on (with defined similarly).
Suppose that is bounded on the unit square and that is continuous except possibly on a finite number of curves of the form (with ) where the are continuous functions. For , define
Then
This is equivalent to the statement that the game induced by has a value. Note that one player (WLOG ) is forbidden from using a pure strategy.
Parthasarathy goes on to exhibit a game in which
which thus has no value. There is no contradiction because in this case neither player is restricted to absolutely continuous distributions (and the demonstration that the game has no value requires both players to use pure strategies).
References
T. Parthasarathy 1970. On Games over the unit square, SIAM, volume 19, number 2.
Game theory
Theorems in discrete mathematics
Theorems in measure theory | Parthasarathy's theorem | [
"Mathematics"
] | 303 | [
"Theorems in mathematical analysis",
"Mathematical theorems",
"Theorems in measure theory",
"Discrete mathematics",
"Theorems in discrete mathematics",
"Game theory",
"Mathematical problems"
] |
17,567,181 | https://en.wikipedia.org/wiki/Bromous%20acid | Bromous acid is the inorganic compound with the formula of HBrO2. It is an unstable compound, although salts of its conjugate base – bromites – have been isolated. In acidic solution, bromites decompose to bromine.
Discovery
In 1905, Richards A. H. proved the existence of bromous acid through a series of experiments involving silver nitrate (AgNO3) and bromine. The reaction of excess cold aqueous to form hypobromous acid (HBrO), silver bromide (AgBr) and nitric acid (HNO3):
Br2 + AgNO3 + H2O → HBrO + AgBr + HNO3
Richards discovered that the effect of adding excess liquid bromine in a concentrated silver nitrate (AgNO3) resulted in a different reaction mechanism. From numbers of equivalent portions of acid bromine formed from the previous reaction, the ratio between oxygen and bromine was calculated, with the exact value of O:Br (0.149975:0.3745), suggesting the acid compound contains two oxygen atom to one bromine atom. Thus, the chemical structure of the acid compound was deducted as HBrO2.
According to Richards, hypobromous acid (HBrO) arises by the reaction of bromine and silver nitrate solution:
Br2 + AgNO3 + H2O → HBrO + AgBr + HNO3
2 AgNO3 + HBrO + Br2 + H2O → HBrO2 + 2 AgBr + 2 HNO3
Isomerism
The molecule HBrO2 has a bent structure with ∠(H−O−Br) angles of 106.1°. HOBrO also adopts a non-planar conformation with one isomer structure (2a) adopting a dihedral angle ∠(H−O−Br−O) of 74.2°. Moreover, the planar structures of two other isomers (2b-cis and 2c-trans) are transition state for fast enantiomerization.
Another study identified three isomers: HOOBr, HOBrO, and HBr(O)O.
Synthesis
A oxidation reaction between hypobromous acid (HBrO) and hypochlorous acid (HClO) can be used to produce bromous acid (HBrO2) and hydrochloric acid (HCl).
HBrO + HClO → HBrO2 + HCl
A redox reaction of hypobromous acid (HBrO) can form bromous acid (HBrO2) as its product:
HBrO + H2O − 2e− → HBrO2 + 2H+
The disproportionation reaction of two equivalents hypobromous acid (HBrO) results in the formation of both bromous acid (HBrO2) and hydrobromic acid (HBr):
2 HBrO → HBrO2 + HBr
A rearrangement reaction, which results from the syn-proportion of bromic acid (HBrO3) and hydrobromic acid (HBr) gives bromous acid (HBrO2):
2 HBrO3 + HBr → 3 HBrO2
Salts
The salts NaBrO2·3H2O and Ba(BrO2)2·H2O have been crystallized. Upon treatment of these aqueous solutions with salts of Pb2+, Hg2+, and Ag+, the corresponding heavy metal bromites precipitate as solids.
Belousov–Zhabotinsky reaction
Bromous acid is a product of the Belousov–Zhabotinsky reaction resulting from the combination of potassium bromate, cerium(IV) sulfate, propanedioic acid and citric acid in dilute sulfuric acid. Bromous acid is an intermediate stage of the reaction between bromate ion ( ) and bromine (Br−):
+ 2 Br− → HBrO2 + HBrO
Other relevant reactions in such oscillating reactions are:
HBrO2 + + H+ → 2 + H2O
2 HBrO2 → + HOBr + H+
Bromites reduce permanganates to manganates (VI):
2 + + OH− → 2 + + H2O
pKa measurement
The acid dissociation constant of bromous acid, Ka = , was determined using different methods.
The value of the pKa for bromous acid was estimated in research studying the decomposition of bromites. The research measured the rate of bromite decomposition as a function of hydrogen and bromite ion concentrations. The experimental data of the log of the initial velocity were plotted against pH. Using this method, the estimated pKa value for bromous acid was 6.25.
Using another method, the pKa for bromous acid was measured based on the initial velocity of the reaction between sodium bromites and potassium iodine in a pH range of 2.9–8.0, at 25 °C and ionic strength of 0.06 M. The first order dependence of the initial velocity of this disproportionation reaction on [H+] in a pH range of 4.5–8.0. The value of acid dissociation constant measured by this method is Ka = and pKa = .
Reactivity
In comparison to other oxygen-centered oxidants (hypohalites, anions of peroxides) and in line with its low basicity, bromite is a rather weak nucleophile. Rate constants of bromite towards carbocations and acceptor-substituted olefins are by 1–3 orders of magnitude lower than the ones measured with hypobromite.
References
Further reading
Bromites
Halogen oxoacids
Oxidizing acids | Bromous acid | [
"Chemistry"
] | 1,198 | [
"Acids",
"Oxidizing acids",
"Oxidizing agents"
] |
17,567,758 | https://en.wikipedia.org/wiki/BeRTOS | BeRTOS is a real-time operating system designed for embedded systems.
It is free and open-source software released under the GNU General Public License, version 2 (GPLv2) or later, with a special exception granting proprietary applications the right to keep their source code closed while keeping the base BeRTOS code open.
It has a very modular design, that allows running it on different architectures, ranging from tiny 8-bit microcontrollers such as Atmel AVR microcontrollers up to the 32-bit ARM architecture, and on hosted environments such as Linux and Microsoft Windows. BeRTOS is written in ANSI C, and supported by popular embedded Secure Sockets Layer (SSL) and successor Transport Layer Security (TLS) libraries such as wolfSSL.
BeRTOS preemptive multitasking kernel implements many inter-process communication (IPC) primitives, including: signals, semaphores, and messages.
In addition to the kernel, BeRTOS provides a hardware abstraction layer (HAL) that includes many peripheral device drivers (timer, serial, analog-to-digital converter (ADC), motors, liquid-crystal display (LCD), NTC sensors, keyboard, buzzer, memories), algorithms (hash table, cyclic redundancy check (CRC), MD2, entropy pool, run-length encoding (RLE)), communication protocols, and a graphic windowing subsystem for small display devices.
References
External links
Real-time operating systems
Embedded operating systems
Free software operating systems
ARM operating systems
Microkernel-based operating systems
Microkernels
IA-32 operating systems
X86-64 operating systems | BeRTOS | [
"Technology"
] | 345 | [
"Operating system stubs",
"Computing stubs",
"Real-time computing",
"Real-time operating systems"
] |
17,568,082 | https://en.wikipedia.org/wiki/Soil-structure%20interaction | Ground–structure interaction (SSI) consists of the interaction between soil (ground) and a structure built upon it. It is primarily an exchange of mutual stress, whereby the movement of the ground-structure system is influenced by both the type of ground and the type of structure. This is especially applicable to areas of seismic activity. Various combinations of soil and structure can either amplify or diminish movement and subsequent damage. A building on stiff ground rather than deformable ground will tend to suffer greater damage. A second interaction effect, tied to mechanical properties of soil, is the sinking of foundations, worsened by a seismic event. This phenomenon is called soil liquefaction.
Most of the civil engineering structures involve some type of structural element with direct contact with ground. When the external forces, such as earthquakes, act on these systems, neither the structural displacements nor the ground displacements, are independent of each other. The process in which the response of the soil influences the motion of the structure and the motion of the structure influences the response of the soil is termed as soil-structure interaction (SSI).
Conventional structural design methods neglect the SSI effects. Neglecting SSI is reasonable for light structures in relatively stiff soil such as low rise buildings and simple rigid retaining walls. The effect of SSI, however, becomes prominent for heavy structures resting on relatively soft soils for example nuclear power plants, high-rise buildings and elevated-highways on soft soil.
Damage sustained in recent earthquakes, such as the 1995 Kobe earthquake, have also highlighted that the seismic behavior of a structure is highly influenced not only by the response of the superstructure, but also by the response of the foundation and the ground as well. Hence, the modern seismic design codes, such as Standard Specifications for Concrete Structures: Seismic Performance Verification JSCE 2005 stipulate that the response analysis should be conducted by taking into consideration a whole structural system including superstructure, foundation and ground.
Effect of (Soil-structure interaction) SSI and SSI provisions of seismic design codes on structural responses
It is conventionally believed that SSI is a purely beneficial effect, and it can conveniently be neglected for conservative design. SSI provisions of seismic design codes are optional and allow designers to reduce the design base shear of buildings by considering soil-structure interaction (SSI) as a beneficial effect. The main idea behind the provisions is that the soil-structure system can be replaced with an equivalent fixed-base model with a longer period and usually a larger damping ratio. Most of the design codes use oversimplified design spectra, which attain constant acceleration up to a certain period, and thereafter decreases monotonically with period. Considering soil-structure interaction makes a structure more flexible and thus, increasing the natural period of the structure compared to the corresponding rigidly supported structure. Moreover, considering the SSI effect increases the effective damping ratio of the system. The smooth idealization of design spectrum suggests smaller seismic response with the increased natural periods and effective damping ratio due to SSI, which is the main justification of the seismic design codes to reduce the design base shear when the SSI effect is considered. The same idea also forms the basis of the current common seismic design codes such as ASCE 7-10 and ASCE 7-16. Although the mentioned idea, i.e. reduction in the base shear, works well for linear soil-structure systems, it is shown that it cannot appropriately capture the effect of SSI on yielding systems. More recently, Khosravikia et al. evaluated the consequences of practicing the SSI provisions of ASCE 7-10 and those of 2015 National Earthquake Hazards Reduction Program (NEHRP), which form the basis of the 2016 edition of the seismic design standard provided by the ASCE. They showed that SSI provisions of both NEHRP and ASCE 7-10 result in unsafe designs for structures with surface foundation on moderately soft soils, but NEHRP slightly improves upon the current provisions for squat structures. For structures on very soft soils, both provisions yield conservative designs where NEHRP is even more conservative. Finally, both provisions yield near-optimal designs for other systems.
Detrimental effects
Using rigorous numerical analyses, Mylonakis and Gazetas have shown that increase in natural period of structure due to SSI is not always beneficial as suggested by the simplified design spectrums. Soft soil sediments can significantly elongate the period of seismic waves and the increase in natural period of structure may lead to the resonance with the long period ground vibration. Additionally, the study showed that ductility demand can significantly increase with the increase in the natural period of the structure due to SSI effect. The permanent deformation and failure of soil may further aggravate the seismic response of the structure.
When a structure is subjected to an earthquake excitation, it interacts with the foundation and the soil, and thus changes the motion of the ground. Soil-structure interaction broadly can be divided into two phenomena: a) kinematic interaction and b) inertial interaction. Earthquake ground motion causes soil displacement known as free-field motion. However, the foundation embedded into the soil will not follow the free field motion. This inability of the foundation to match the free field motion causes the kinematic interaction. On the other hand, the mass of the superstructure transmits the inertial force to the soil, causing further deformation in the soil, which is termed as inertial interaction.
At low level of ground shaking, kinematic effect is more dominant causing the lengthening of period and increase in radiation damping. However, with the onset of stronger shaking, near-field soil modulus degradation and soil-pile gapping limit radiation damping, and inertial interaction becomes predominant causing excessive displacements and bending strains concentrated near the ground surface resulting in pile damage near the ground level.
Observations from recent earthquakes have shown that the response of the foundation and soil can greatly influence the overall structural response. There are several cases of severe damages in structures due to SSI in the past earthquakes. Yashinsky cites damage in number of pile-supported bridge structures due to SSI effect in the Loma Prieta earthquake in San Francisco in 1989. Extensive numerical analysis carried out by Mylonakis and Gazetas have attributed SSI as one of the reasons behind the dramatic collapse of Hanshin Expressway in 1995 Kobe earthquake.
Design
The main types of foundations, based upon several building characteristics, are:
Isolated plinths (currently not feasible)
Plinths connected by foundations beams
Reverse beams
A plate (used for low-quality grounds)
The filing of foundations grounds takes place according to the mechanical properties of the grounds themselves: in Italy, for instance, according to the new earthquake-proof norm – Ordinanza 3274/2003 – you can identify the following categories:
Category A: homogeneous rock formations
Category B: compact granular or clayey soil
Category C: quite compact granular or clayey soil
Category D: not much compact granular or clayey soil
Category E: alluvial surface layer grounds (very low quality soil)
The type of foundations is selected according to the type of ground; for instance, in the case of homogeneous rock formations connected plinths are selected, while in the case of very low quality grounds plates are chosen.
For further information about the various ways of building foundations see foundation (architecture).
Both grounds and structures can be more or less deformable; their combination can or cannot cause the amplification of the seismic effects on the structure.
Ground, in fact, is a filter with respect to all the main seismic waves, as stiffer soil fosters high-frequency seismic waves while less compact soil accommodates lower frequency waves. Therefore, a stiff building, characterized by a high fundamental frequency, suffers amplified damage when built on stiff ground and then subjected to higher frequencies.
For instance, suppose there are two buildings that share the same high stiffness. They stand on two different soil types: the first, stiff and rocky—the second, sandy and deformable. If subjected to the same seismic event, the building on the stiff ground suffers greater damage.
The second interaction effect, tied to mechanical properties of soil, is about the lowering (sinking) of foundations, worsened by the seismic event itself, especially about less compact grounds. This phenomenon is called soil liquefaction.
Mitigation
The methods most used to mitigate the problem of the ground-structure interaction consist of the employment of the before-seen isolation systems and of some ground brace techniques, which are adopted above all on the low-quality ones (categories D and E).
The most diffused techniques are the jet grouting technique and the pile work technique.
The jet-grouting technique consists of injecting in the subsoil some liquid concrete by means of a drill. When this concrete hardens it forms a sort of column that consolidates the surrounding soil. This process is repeated on all areas of the structure.
The pile work technique consists of using piles, which, once inserted in the ground, support the foundation and the building above, by moving the loads or the weights towards soil layers that are deeper and therefore more compact and movement-resistant.
References
External links
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Seismic soil-structure interaction
Structural engineering
Earthquake and seismic risk mitigation
Earthquake engineering
Foundations (buildings and structures)
Soil mechanics
Structural analysis
Geotechnical structures | Soil-structure interaction | [
"Physics",
"Engineering"
] | 1,925 | [
"Structural engineering",
"Applied and interdisciplinary physics",
"Structural analysis",
"Soil mechanics",
"Foundations (buildings and structures)",
"Construction",
"Civil engineering",
"Mechanical engineering",
"Aerospace engineering",
"Earthquake engineering",
"Earthquake and seismic risk mit... |
17,569,127 | https://en.wikipedia.org/wiki/Medard%20W.%20Welch%20Award | The Medard W. Welch Award is given to scientists who demonstrated outstanding research in the fields pertinent to the focus areas of the American Vacuum Society, which are "the basic science, technology development, and commercialization of materials, interfaces, and processing." It was established in 1969 in memory of Medard W. Welch, a founder of the American Vacuum Society.
List of recipients
See also
List of physics awards
References
Physics awards | Medard W. Welch Award | [
"Technology"
] | 89 | [
"Science and technology awards",
"Physics awards"
] |
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