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Fungivore Bracket fungi have been found in their droppings throughout the year, and Simpson in the "Australasian Mycological Newsletter" suggested it is likely they also eat species of Agaricales and Pezizales but these have not been found in their droppings since they disintegrate when they are eaten. Emus ("Dromaius novaehollandiae") will eat immature "Lycoperdon" and "Bovista" fungi if presented to them as will brush turkeys ("Alectura lathami") if offered "Mycena", suggesting that species of Megapodiidae may feed opportunistically on mushrooms. Mycoparasitism occurs when any fungus feeds on other fungi, a form of parasitism, our knowledge of it in natural environments is very limited. "Collybia" grow on dead mushrooms. The fungal genus, "Trichoderma" produces enzymes such as chitinases which degrade the cell walls of other fungi. They are able to detect other fungi and grow towards them, they then bind to the hyphae of other fungi using lectins on the host fungi as a receptor, forming an appressorium. Once this is formed, "Trichoderma" inject toxic enzymes into the host and probably peptaibol antibiotics, which create holes in the cell wall, allowing "Trichoderma" to grow inside of the host and feed. "Trichoderma" are able to digest sclerotia, durable structures which contain food reserves, which is important if they are to control pathogenic fungi in the long term | Biology | https://en.wikipedia.org/wiki?curid=18320085 | Fungivore | 139,963 |
Fungivore "Trichoderma" species have been recorded as protecting crops from "Botrytis cinerea", "Rhizoctonia solani", "Alternaria solani", "Glomerella graminicola", "Phytophthora capsici", "Magnaporthe grisea" and "Colletotrichum lindemuthianum"; although this protection may not be entirely due to "Trichoderma" digesting these fungi, but by them improving plant disease resistance indirectly. Bacterial mycophagy was a term coined in 2005, to describe the ability of some bacteria to "grow at the expense of living fungal hyphae". In a 2007 review in the "New Phytologist" this definition was adapted to only include bacteria which play an active role in gaining nutrition from fungi, excluding those that feed off passive secretions by fungi, or off dead or damaged hyphae. The majority of our knowledge in this area relates to interactions between bacteria and fungi in the soil and in or around plants, little is known about interactions in marine and freshwater habitats, or those occurring on or inside animals. It is not known what effects bacterial mycophagy has on the fungal communities in nature. There are three mechanisms by which bacteria feed on fungi; they either kill fungal cells, cause them to secrete more material out of their cells or enter into the cells to feed internally and they are categorised according to these habits. Those that kill fungal cells are called nectrotrophs, the molecular mechanisms of this feeding are thought to overlap considerably with bacteria that feed on fungi after they have died naturally | Biology | https://en.wikipedia.org/wiki?curid=18320085 | Fungivore | 139,964 |
Fungivore Necrotrophs may kill the fungi through digesting their cell wall or by producing toxins which kill fungi, such as tolaasin produced by "Pseudomonas tolaasii". Both of these mechanisms may be required since fungal cell walls are highly complex, so require many different enzymes to degrade them, and because experiments demonstrate that bacteria that produce toxins cannot always infect fungi. It is likely that these two systems act synergistically, with the toxins killing or inhibiting the fungi and exoenzymes degrading the cell wall and digesting the fungus. Examples of necrotrophs include "Staphylococcus aureus" which feed on "Cryptococcus neoformans", "Aeromonas caviae" which feed on "Rhizoctonia solani", "Sclerotium rolfsii" and "Fusarium oxysporum", and some myxobacteria which feed on "Cochliobolus miyabeanus" and "Rhizoctonia solani". Bacteria which manipulate fungi to produce more secretions which they in turn feed off are called extracellular biotrophs; many bacteria feed on fungal secretions, but do not interact directly with the fungi and these are called saprotrophs, rather than biotrophs. Extracellular biotrophs could alter fungal physiology in three ways; they alter their development, the permeability of their membranes (including the efflux of nutrients) and their metabolism. The precise signalling molecules that are used to achieve these changes are unknown, but it has been suggested that auxins (better known for their role as a plant hormone) and quorum sensing molecules may be involved | Biology | https://en.wikipedia.org/wiki?curid=18320085 | Fungivore | 139,965 |
Fungivore Bacteria have been identified that manipulate fungi in these ways, for example mycorrhiza helper bacteria (MHBs) and "Pseudomonas putida", but it remains to be demonstrated whether the changes they cause are directly beneficial to the bacteria. In the case of MHBs, which increase infection of plant roots by mycorrhizal fungi, they may benefit, because the fungi gain nutrition from the plant and in turn the fungi will secrete more sugars. The third group, that enter into living fungal cells are called endocellular biotrophs. Some of these are transmitted vertically whereas others are able to actively invade and subvert fungal cells. The molecular interactions involved in these interactions are mostly unknown. Many endocellular biotrophs, for example some "Burkholderia" species, belong to the β-proteobacteria which also contains species which live inside the cells of mammals and amoeba. Some of them, for example "Candidatus" Glomeribacter gigasporarum, which colonises the spores of "Gigaspora margarita", have reduced genome sizes indicating that they have become entirely dependent on the metabolic functions of the fungal cells in which they live. When all the endocellular bacteria inside "G. margarita" were removed, the fungus grew differently and was less fit, suggesting that some bacteria may also provide services to the fungi they live in. The ciliate family Grossglockneridae, including the species "Grossglockneria acuta", feed exclusively on fungi. "G | Biology | https://en.wikipedia.org/wiki?curid=18320085 | Fungivore | 139,966 |
Fungivore acuta" first attaches themselves to a hyphae or sporangium via a feeding tube and then a ring-shaped structure, around 2 μm in diameter is observed to appear on the fungus, possibly consisting of degraded cell wall material. "G. acuta" then feeds through the hole in the cell wall for, on average, 10 minutes, before detaching itself and moving away. The precise mechanism of feeding is not known, but it conceivably involves enzymes including acid phosphatases, cellulases and chitinases. Microtubules are visible in the feeding tube, as are possible reserves of cell membrane, which may be used to form food vacuoles filled with the cytoplasm of the fungus, via endocytosis, which are then transported back into "G. acuta". The holes made by "G. acuta" bear some similarities to those made by amoeba, but unlike amoeba "G. acuta" never engulfs the fungus. Around 90% of land plants live in symbiosis with mycorrhizal fungi, where fungi gain sugars from plants and plants gain nutrients from the soil via the fungi. Some species of plant have evolved to manipulate this symbiosis, so that they no longer give fungi sugars that they produce and instead gain sugars from the fungi, a process called myco-heterotrophy. Some plants are only dependent on fungi as a source of sugars during the early stages of their development, these include most of the orchids as well as many ferns and lycopods | Biology | https://en.wikipedia.org/wiki?curid=18320085 | Fungivore | 139,967 |
Fungivore Others are dependent on this food source for their entire lifetime, including some orchids and Gentianaceae, and all species of Monotropaceae and Triuridaceae. Those that are dependent on fungi, but still photosynthesise are called mixotrophs since they gain nutrition in more than one way, by gaining a significant amount of sugars from fungi, they are able to grow in the deep shade of forests. Examples include the orchids "Epipactis", "Cephalanthera" and "Plantanthera" and the tribe Pyroleae of the family Ericaceae. Others, such as "Monotropastrum humile", no longer photosynthesise and are totally dependent on fungi for nutrients. Around 230 such species exist, and this trait is thought to have evolved independently on five occasions outside of the orchid family. Some individuals of the orchid species "Cephalanthera damasonium" are mixotrophs, but others do not photosynthesise. Because the fungi that myco-heterotrophic plants gain sugars from in turn gain them from plants that do photosynthesise, they are considered indirect parasites of other plants. The relationship between orchids and orchid mycorrhizae has been suggested to be somewhere between predation and parasitism. The precise mechanisms by which these plants gain sugars from fungi are not known and has not been demonstrated scientifically | Biology | https://en.wikipedia.org/wiki?curid=18320085 | Fungivore | 139,968 |
Fungivore Two pathways have been proposed; they may either degrade fungal biomass, particularly the fungal hyphae which penetrate plant cells in a similar manner to in arbuscular mycorrhizae, or absorb sugars from the fungi by disrupting their cell membranes, through mass flow. To prevent the sugars returning to the fungi, they must compartmentalise the sugars or convert them into forms which the fungi cannot use. Three insect lineages, the beetles, ants and termites, independently evolved the ability to farm fungi between 40 and 60 million years ago. In a similar way to the way that human societies became more complex after the development of plant-based agriculture, the same occurred in these insect lineages when they evolved this ability and these insects are now of major importance in ecosystems. The methods that insects use to farm fungi share fundamental similarities with human agriculture. Firstly, insects inoculate a particular habitat or substrate with fungi, much in the same as humans plant seeds in fields. Secondly, they cultivate the fungi by regulating the growing environment to try to improve the growth of the fungus, as well as protecting it from pests and diseases. Thirdly they harvest the fungus when it is mature and feed on it. Lastly they are dependent on the fungi they grow, in the same way that humans are dependent on crops. Ambrosia beetles, for example "Austroplatypus incompertus", farm ambrosia fungi inside of trees and feed on them | Biology | https://en.wikipedia.org/wiki?curid=18320085 | Fungivore | 139,969 |
Fungivore The mycangia (organs which carry fungal spores) of ambrosia beetles contain various species of fungus, including species of "Ambrosiomyces", "Ambrosiella", "Ascoidea", "Ceratocystis", "Dipodascus", "Diplodia", "Endomycopsis", "Monacrosporium" and "Tuberculariella". The ambrosia fungi are only found in the beetles and their galleries, suggesting that they and the beetles have an obligate symbiosis. Around 330 species of termites in twelve genera of the subfamily Macrotermitinae cultivate a specialised fungus in the genus "Termitomyces". The fungus is kept in a specialised part of the nest in fungus cones. Worker termites eat plant matter, producing faecal pellets which they continuously place on top of the cone. The fungus grows into this material and soon produces immature mushrooms, a rich source of protein, sugars and enzymes, which the worker termites eat. The nodules also contain indigestible asexual spores, meaning that the faecal pellets produced by the workers always contain spores of the fungus that colonise the plant material that they defaecate. The "Termitomyces" also fruits, forming mushrooms above ground, which mature at the same time that the first workers emerge from newly formed nests. The mushrooms produce spores that are wind dispersed, and through this method, new colonies acquire a fungal strain. In some species, the genetic variation of the fungus is very low, suggesting that spores of the fungus are transmitted vertically from nest to nest, rather than from wind dispersed spores | Biology | https://en.wikipedia.org/wiki?curid=18320085 | Fungivore | 139,970 |
Fungivore Around 220 described species, and more undescribed species of ants in the tribe Attini cultivate fungi. They are only found in the New World and are thought to have evolved in the Amazon Rainforest, where they are most diverse today. For these ants, farmed fungi are the only source of food on which their larvae are raised on and are also an important food for adults. Queen ants carry a small part of fungus in small pouches in their mouthparts when they leave the nest to mate, allowing them to establish a new fungus garden when they form a new nest. Different lineages cultivate fungi on different substrates, those that evolved earlier do so on a wide range of plant matter, whereas leaf cutter ants are more selective, mainly using only fresh leaves and flowers. The fungi are members of the families Lepiotaceae and Pterulaceae. Other fungi in the genus "Escovopsis" parasitise the gardens and antibiotic-producing bacteria also inhabit the gardens. The marine snail "Littoraria irrorata", which lives in the salt marshes of the southeast of the United States feeds on fungi that it encourages to grow. It creates and maintains wounds on the grass, "Spartina alterniflora" which are then infected by fungi, probably of the genera "Phaeosphaeria" and "Mycosphaerella", which are the preferred diet of the snail. They also deposit faeces on the wounds that they create, which encourage the growth of the fungi because they are rich in nitrogen and fungal hyphae | Biology | https://en.wikipedia.org/wiki?curid=18320085 | Fungivore | 139,971 |
Fungivore Juvenile snails raised on uninfected leaves do not grow and are more likely to die, indicating the importance of the fungi in the diet of "L. irrorata". | Biology | https://en.wikipedia.org/wiki?curid=18320085 | Fungivore | 139,972 |
Pandemic (board game) Pandemic is a cooperative board game designed by Matt Leacock and first published by Z-Man Games in the United States in 2008. "Pandemic" is based on the premise that four diseases have broken out in the world, each threatening to wipe out a region. The game accommodates two to four players, each playing one of seven possible specialists: dispatcher, medic, scientist, researcher, operations expert, Contingency Planner, or quarantine specialist. Through the combined effort of all the players, the goal is to discover all four cures before any of several game-losing conditions are reached. Three expansions, "Pandemic: On the Brink", "Pandemic: In the Lab", and "Pandemic: State of Emergency", co-designed by Matt Leacock and Tom Lehmann, each add several new roles and special events, as well as rule adjustments to allow a fifth player or to play in teams. In addition, several rule expansions are included, referred to as "challenge kits". "Pandemic" is considered one of the most successful cooperative games that has reached mainstream market sales, condensing the type of deep strategy offered by earlier cooperative games, like "Arkham Horror", into a game that can be played in a limited time by a wider range of players. Aside from expansions several spinoffs have been released. Most notably "Pandemic Legacy: Season 1" which adds an ongoing storyline and permanent changes to the game, has been for some time rated highly by the website Board Game Geek on its board game rankings | Biology | https://en.wikipedia.org/wiki?curid=18320834 | Pandemic (board game) | 139,973 |
Pandemic (board game) Leacock began designing the game in 2004, after realizing that competitive games were damaging his relationship with his wife; he based it on the 2002–2004 SARS outbreak. The goal of "Pandemic" is for the players, in their randomly selected roles, to work cooperatively to stop the spread of four diseases and cure them before a pandemic occurs. "Pandemic" setup consists of a game board representing a network connecting 48 cities on the map of the earth, two decks of cards (Player cards and Infection cards), four colors of cubes (each representing a different disease), six Research Stations, and a pawn for each player. The Player cards include cards with each city name (the same as those on the board); Special Event cards, which can be played at specific times to take beneficial actions; and Epidemic cards. Infection cards consist of one card for each city on the board and a color of the disease that will start there. At the start of the game, Infection cards are randomly drawn to populate the board with infections, from 1 to 3 cubes for a number of cities. Players start at Atlanta, the home of the Centers for Disease Control, and are given a random role and a number of Player cards. On each turn, a player can take 4 actions, consisting of any combination of the following: Other Actions, as per the following four options: On conclusion of the turn, the player draws two Player cards, reducing their hand down to seven cards by discarding Player cards and/or immediately playing Special Event cards | Biology | https://en.wikipedia.org/wiki?curid=18320834 | Pandemic (board game) | 139,974 |
Pandemic (board game) If either draw is an Epidemic card, the player draws a card from the bottom of the Infection deck and places three cubes on that city, puts that card into the Infection discard pile, reshuffles the discard pile, and places it back on top of the Infection deck. After the two Player cards are drawn (epidemic or otherwise), a number of Infection cards are revealed, and one cube of the indicated color is placed on each city drawn. Should a city already have three cubes and a new cube is to be added, an Outbreak occurs, and each interconnected city gains one cube of that colour. This can create a chain reaction across many cities if several already have three disease cubes on them. The game is over if any of the following occur: To aid in winning the game, players are given roles that allow them to alter the above rules. Five roles were introduced with the core game, but additional roles were added through the game's expansion. For example, the Medic is able to treat all cubes in a city with one action or, once a cure for a disease is found, can remove cubes of that color without spending an action, while the Scientist needs only four cards of the same color to discover the cure. The players are also helped by the Special Event cards, which allow for similar one-time actions, such as direct removal of a few infection tokens or immediate construction of a research lab | Biology | https://en.wikipedia.org/wiki?curid=18320834 | Pandemic (board game) | 139,975 |
Pandemic (board game) "Pandemic" requires the players to coordinate their efforts to win the game, specifically in gathering and sharing the necessary cards to discover cures while moving in coordination around the board and preventing Outbreaks in an efficient manner. In 2009 the first official expansion was released, featuring several new roles, rules variants for a fifth player, new Special Event cards, and new challenges for the players. There are eight Role Cards in this expansion, including a revised Operation Expert card and a Bio-Terrorist card, which pits one player against the rest of the team. The challenges include a fifth disease, Mutation, which must be cured or not present at the game board when the players score for victory. Another challenge is the Virulent Strain, which makes one disease particularly deadly, replacing standard Epidemic cards with new ones. Each such card represents a special nasty effect that this particular epidemic has on the game play. This is the second expansion, released in the summer of 2013, with a new game board that allows players to research disease cures in a laboratory. The goal of this activity is the same as in the base game—to find cures for diseases—but this time with an added research aspect. Players can also use new characters and new special events included with the expansion. In addition, it added a one-player mode and a team play mode, in which teams of two compete to be the most effective team | Biology | https://en.wikipedia.org/wiki?curid=18320834 | Pandemic (board game) | 139,976 |
Pandemic (board game) "In the Lab" requires both "Pandemic" and "On the Brink" to play, and also requires replacement decks if using the first editions of "Pandemic" and "On the Brink". A third expansion, released in March 2015, adds new roles and events and three new challenges: The Hinterlands, where animals spread diseases to human; Emergency Events, in which unpredicted events have a negative effect on the game; and Superbug, where a fifth disease is introduced that cannot be treated. The expansion is compatible with the two previous expansions, but neither is required. The purple disease cubes included with "State of Emergency" make the set included in "On the Brink" redundant. Z-man Games has released free-to-download scenarios, with changes to the base game. Various scenarios are set to be released. , scenarios "Isolation" and "Government Shutdown" have been published. A second edition of "Pandemic" was released in 2013, with new artwork and two new characters: the Contingency Planner and the Quarantine Specialist. Some prints of the second edition had an error with a missing line between Lagos and São Paulo and edge-to-edge printing on cards. A second edition of the "On the Brink" expansion was released in 2013. In July 2018 it was announced that a 10-year Anniversary Edition will be released in Q4 2018. This edition will include detailed miniatures representing the individual roles, updated role cards, a larger board, and wooden disease cubes | Biology | https://en.wikipedia.org/wiki?curid=18320834 | Pandemic (board game) | 139,977 |
Pandemic (board game) All components will be contained in a metal box made to represent a first aid kit from the early 20th century. This edition will be a remake of the original game, but will include additional room within the box to hold expansions. The "Pandemic base replacement deck" updates the first edition of "Pandemic" to its second edition. "Compatibility pack #2" updates the first edition of the "On the Brink" expansion to its second edition. The "In the Lab" expansion (released after the second editions of "Pandemic" and "On the Brink") requires the second edition(s), or the first edition(s) along with its compatibility pack(s). Six spinoffs or alternate versions of "Pandemic" have been released by Z-Man Games, all of which are stand-alone games and are not compatible with the original or with each other. Released in 2014, "Pandemic: The Cure" is a dice-based game that uses a similar rule set to the original board game but strips down the number of cities and leaves the outcome of turns up to chance via dice rolls. An expansion to the game, "Pandemic: The Cure - Experimental Meds", was released in November 2016, adding a fifth disease and a new hot zone mechanism. "Pandemic: Contagion" is a card-based version of the game, first released at Spiel 2014, that puts players in the role of the diseases and, unlike the base game is non-cooperative. The object of the game is to eradicate the human race by spreading infections | Biology | https://en.wikipedia.org/wiki?curid=18320834 | Pandemic (board game) | 139,978 |
Pandemic (board game) Released in October 2015 and designed by Matt Leacock and Rob Daviau, "Pandemic Legacy: Season 1" is a legacy version of the base game released by Z-Man Games, similar to "Risk Legacy", in which the game added an ongoing storyline to the basic game, meaning the game board and rules change permanently after each game. Each game represents one month of time in a campaign which simulates the passage of one year. If the players win the first game, they move on to the next month, and if they lose, they try again, but move on to the next month regardless of what happens in the second game. New rules and components are included in packages that remain sealed until certain events take place, such as completing the game for a given month, or losing a certain number of games in a row. Released in October 2017 and designed by the same pair of designers Matt Leacock and Rob Daviau was a logical continuation from the original Season 1. The board game is set in a devastated earth 71 years after Season 1. This version changes the base rules of "Pandemic" enough to where a prologue tutorial game is included in the campaign so that players can learn the new mechanics. Instead of diseases being represented by cubes, and the goal being to minimize the number of cubes placed, cubes represent supplies, and disease starts spreading if supplies dwindle too low. "Pandemic: Reign of Cthulhu", designed by Matt Leacock and Chuck Yager, was released at GenCon 2016 | Biology | https://en.wikipedia.org/wiki?curid=18320834 | Pandemic (board game) | 139,979 |
Pandemic (board game) In this version of the game, players battle against occultists to prevent the summoning of the monster Cthulhu. "Pandemic Survival" is not a single game, but instead a series of separate historical games covering a local area instead of the entire globe. "Pandemic: Iberia" is the first game of the "Pandemic Survival" series, released in the fall of 2016 and designed by Matt Leacock and Jesus Torres Castro, "Pandemic Iberia" is set on the Iberian peninsula in 1848. It introduced developing railroads and purifying water as new mechanics. In addition, players could play to cure four specific historical diseases: malaria, typhus, yellow fever, and cholera. "Pandemic: Rising Tide" is the second game of the "Pandemic Survival" series, released in the last quarter of 2017. "Pandemic Rising Tide" is set in the Netherlands, where players cooperate to prevent flooding of the country by the rising waters. "Pandemic: Fall of Rome" was released in the last quarter of 2018. "Pandemic: Fall of Rome" takes players back in history to the time of Rome when a weakened military has left the borders open to invasion from countless tribes. Players must recruit armies, fortify cities, forge alliances, and find peace with their neighboring peoples. "Pandemic: Rapid Response" is a real-time cooperative game set in the "Pandemic" universe, released in 2019 and designed by Kane Klenko | Biology | https://en.wikipedia.org/wiki?curid=18320834 | Pandemic (board game) | 139,980 |
Pandemic (board game) In "Rapid Response," players take on the role of an international crisis response team tasked with delivering essential supplies to cities affected by natural disasters. Players roll dice and allocate the results to various actions, including producing resources, piloting the plane towards affected cities, recycling the waste created by producing resources, and dropping off finished supplies in the cities that need them. The game takes place in real time, with the game briefly pausing and a new city being added after a two-minute timer expires. Players win by delivering relief to all cities and lose by running out of time or creating too much waste. "Pandemic Legacy: Season 1" has been generally received very positively. It has been described as a "leap forward in modern board game design", and "the best board game ever created", quickly becoming the highest rated board game of all time on the influential Board Game Geek website | Biology | https://en.wikipedia.org/wiki?curid=18320834 | Pandemic (board game) | 139,981 |
Pandemic (board game) The Guardian has claimed that "this may be the best board game ever created", BoardGameTheories stresses that its strategic depth is increased significantly because players have to balance the interest of the current game with that of the overall campaign while making decisions, and Board Games Land described the game as "smart, dramatic and thematic, designed to create those memorable moments full of emotional highs and lows only a handful board games can match" As of the first quarter 2019, "Pandemic Legacy: Season 1" is the second highest user-rated game on BoardGameGeek, while "Pandemic Legacy: Season 2" (#32), "Pandemic" (#74), and "Pandemic: Iberia" (#79) also fall within the top 100. In 2013, an iOS version entitled Pandemic: The Board Game was released by Asmodee Digital. The digital game was ported to PC five years later and released via Steam. | Biology | https://en.wikipedia.org/wiki?curid=18320834 | Pandemic (board game) | 139,982 |
SAT Subject Test in Biology E/M The SAT Subject Test in Biology is the name of a one-hour multiple choice test given on biology by the College Board. A student chooses whether to take the test depending upon college entrance requirements for the schools in which the student is planning to apply. Until 1994, the SAT Subject Tests were known as Achievement Tests; and from 1995 until January 2005, they were known as SAT IIs. Of all SAT subject tests, the Biology E/M test is the only SAT II that allows the test taker a choice between the ecological or molecular tests. A set of 60 questions is taken by all test takers for Biology and a choice of 20 questions is allowed between either the E or M tests. This test is graded on a scale between 200 and 800. The average for Molecular is 630 while Ecological is 591. This test has 80 multiple-choice questions that are to be answered in one hour. All questions have five answer choices. Students receive one point for each correct answer, lose ¼ of a point for each incorrect answer, and receive 0 points for questions left blank. The student's score is based entirely on his or her performance in answering the multiple-choice questions. The questions cover a broad range of topics in general biology. There are more specific questions related respectively on ecological concepts (such as population studies and general Ecology) on the E test and molecular concepts such as DNA structure, translation, and biochemistry on the M test | Biology | https://en.wikipedia.org/wiki?curid=18322812 | SAT Subject Test in Biology E/M | 139,983 |
SAT Subject Test in Biology E/M The College Board suggests a year-long course in biology at the college preparatory level, as well as a one-year course in algebra, and lab experience as preparation for the test. The test requires understanding of biological data and concepts, science-related terms, and the ability to effectively synthesize and interpret data from charts, maps, and other visual media. However, most questions from this test are derived from, or are similar to, the pre-2012 AP Biology multiple choice questions. By taking an AP class or a class with similar rigor, one's chances at doing well on this test should improve. | Biology | https://en.wikipedia.org/wiki?curid=18322812 | SAT Subject Test in Biology E/M | 139,984 |
MEDUSA (weapon) MEDUSA (Mob Excess Deterrent Using Silent Audio) is a directed-energy non-lethal weapon designed by WaveBand Corporation in 2003-2004 for temporary personnel incapacitation. The weapon is based on the microwave auditory effect resulting in a strong sound sensation in the human head when it is subject to certain kinds of pulsed/modulated microwave radiation. The developers claimed that through the combination of pulse parameters and pulse power, it is possible to raise the auditory sensation to a “discomfort” level, deterring personnel from entering a protected perimeter or, if necessary, temporarily incapacitating particular individuals. In 2005, Sierra Nevada Corporation acquired WaveBand Corporation. | Biology | https://en.wikipedia.org/wiki?curid=18327191 | MEDUSA (weapon) | 139,985 |
Mulde event The was an anoxic event, and marked the second of three relatively minor mass extinctions (the Ireviken, Mulde, and Lau events) during the Silurian period. It coincided with a global drop in sea level, and is closely followed by an excursion in geochemical isotopes. Its onset is synchronous with the deposition of the Fröel formation in Gotland. Perceived extinction in the conodont fauna, however, likely represent a change in the depositional environment of sedimentary sequences rather than a genuine biological extinction. The Ireviken, Mulde, and Lau events were all closely followed by isotopic excursions. | Biology | https://en.wikipedia.org/wiki?curid=18327306 | Mulde event | 139,986 |
Sialome In biochemistry, the term sialome may refer to two distinct concepts: | Biology | https://en.wikipedia.org/wiki?curid=18334913 | Sialome | 139,987 |
Neural correlates of consciousness The neural correlates of consciousness (NCC) constitute the minimal set of neuronal events and mechanisms sufficient for a specific conscious percept. Neuroscientists use empirical approaches to discover neural correlates of subjective phenomena; that is, neural changes which necessarily and regularly correlate with a specific experience. The set should be "minimal" because, under the assumption that the brain is sufficient to give rise to any given conscious experience, the question is which of its components is necessary to produce it. A science of consciousness must explain the exact relationship between subjective mental states and brain states, the nature of the relationship between the conscious mind and the electro-chemical interactions in the body (mind–body problem). Progress in neuropsychology and neurophilosophy has come from focusing on the body rather than the mind. In this context the neuronal correlates of consciousness may be viewed as its causes, and consciousness may be thought of as a state-dependent property of some undefined complex, adaptive, and highly interconnected biological system. Discovering and characterizing neural correlates does not offer a theory of consciousness that can explain how particular systems experience anything at all, or how and why they are associated with consciousness, the so-called hard problem of consciousness, but understanding the NCC may be a step toward such a theory | Biology | https://en.wikipedia.org/wiki?curid=18345264 | Neural correlates of consciousness | 139,988 |
Neural correlates of consciousness Most neurobiologists assume that the variables giving rise to consciousness are to be found at the neuronal level, governed by classical physics, though a few scholars have proposed theories of quantum consciousness based on quantum mechanics. There is great apparent redundancy and parallelism in neural networks so, while activity in one group of neurons may correlate with a percept in one case, a different population might mediate a related percept if the former population is lost or inactivated. It may be that every phenomenal, subjective state has a neural correlate. Where the NCC can be induced artificially the subject will experience the associated percept, while perturbing or inactivating the region of correlation for a specific percept will affect the percept or cause it to disappear, giving a cause-effect relationship from the neural region to the nature of the percept. What characterizes the NCC? What are the commonalities between the NCC for seeing and for hearing? Will the NCC involve all the pyramidal neurons in the cortex at any given point in time? Or only a subset of long-range projection cells in the frontal lobes that project to the sensory cortices in the back? Neurons that fire in a rhythmic manner? Neurons that fire in a synchronous manner? These are some of the proposals that have been advanced over the years. The growing ability of neuroscientists to manipulate neurons using methods from molecular biology in combination with optical tools (e.g., Adamantidis et al | Biology | https://en.wikipedia.org/wiki?curid=18345264 | Neural correlates of consciousness | 139,989 |
Neural correlates of consciousness 2007) depends on the simultaneous development of appropriate behavioral assays and model organisms amenable to large-scale genomic analysis and manipulation. It is the combination of such fine-grained neuronal analysis in animals with ever more sensitive psychophysical and brain imaging techniques in humans, complemented by the development of a robust theoretical predictive framework, that will hopefully lead to a rational understanding of consciousness, one of the central mysteries of life. There are two common but distinct dimensions of the term "consciousness", one involving "arousal" and "states of consciousness" and the other involving "content of consciousness" and "conscious states". To be conscious "of" anything the brain must be in a relatively high state of arousal (sometimes called "vigilance"), whether in wakefulness or REM sleep, vividly experienced in dreams although usually not remembered. Brain arousal level fluctuates in a circadian rhythm but may be influenced by lack of sleep, drugs and alcohol, physical exertion, etc. Arousal can be measured behaviorally by the signal amplitude that triggers some criterion reaction (for instance, the sound level necessary to evoke an eye movement or a head turn toward the sound source). Clinicians use scoring systems such as the Glasgow Coma Scale to assess the level of arousal in patients. High arousal states are associated with conscious states that have specific content, seeing, hearing, remembering, planning or fantasizing about something | Biology | https://en.wikipedia.org/wiki?curid=18345264 | Neural correlates of consciousness | 139,990 |
Neural correlates of consciousness Different levels or states of consciousness are associated with different kinds of conscious experiences. The "awake" state is quite different from the "dreaming" state (for instance, the latter has little or no self-reflection) and from the state of deep sleep. In all three cases the basic physiology of the brain is affected, as it also is in "altered states of consciousness", for instance after taking drugs or during meditation when conscious perception and insight may be enhanced compared to the normal waking state. Clinicians talk about "impaired states of consciousness" as in "the comatose state", "the persistent vegetative state" (PVS), and "the minimally conscious state" (MCS). Here, "state" refers to different "amounts" of external/physical consciousness, from a total absence in coma, persistent vegetative state and general anesthesia, to a fluctuating and limited form of conscious sensation in a minimally conscious state such as sleep walking or during a complex partial epileptic seizure. The repertoire of conscious states or experiences accessible to a patient in a minimally conscious state is comparatively limited. In brain death there is no arousal, but it is unknown whether the subjectivity of experience has been interrupted, rather than its observable link with the organism | Biology | https://en.wikipedia.org/wiki?curid=18345264 | Neural correlates of consciousness | 139,991 |
Neural correlates of consciousness Functional neuroimaging have shown that parts of the cortex are still active in vegetative patients that are presumed to be unconscious; however, these areas appear to be functionally disconnected from associative cortical areas whose activity is needed for awareness. The potential "richness of conscious experience" appears to increase from deep sleep to drowsiness to full wakefulness, as might be quantified using notions from complexity theory that incorporate both the dimensionality as well as the granularity of conscious experience to give an integrated-information-theoretical account of consciousness. As behavioral arousal increases so does the range and complexity of possible behavior. Yet in REM sleep there is a characteristic atonia, low motor arousal and the person is difficult to wake up, but there is still high metabolic and electric brain activity and vivid perception. Many nuclei with distinct chemical signatures in the thalamus, midbrain and pons must function for a subject to be in a sufficient state of brain arousal to experience anything at all. These nuclei therefore belong to the enabling factors for consciousness. Conversely it is likely that the specific content of any particular conscious sensation is mediated by particular neurons in cortex and their associated satellite structures, including the amygdala, thalamus, claustrum and the basal ganglia. The possibility of precisely manipulating visual percepts in time and space has made vision a preferred modality in the quest for the NCC | Biology | https://en.wikipedia.org/wiki?curid=18345264 | Neural correlates of consciousness | 139,992 |
Neural correlates of consciousness Psychologists have perfected a number of techniques – masking, binocular rivalry, continuous flash suppression, motion induced blindness, change blindness, inattentional blindness – in which the seemingly simple and unambiguous relationship between a physical stimulus in the world and its associated percept in the privacy of the subject's mind is disrupted. In particular a stimulus can be perceptually suppressed for seconds or even minutes at a time: the image is projected into one of the observer's eyes but is invisible, not seen. In this manner the neural mechanisms that respond to the subjective percept rather than the physical stimulus can be isolated, permitting visual consciousness to be tracked in the brain. In a "perceptual illusion", the physical stimulus remains fixed while the percept fluctuates. The best known example is the "Necker cube" whose 12 lines can be perceived in one of two different ways in depth. A perceptual illusion that can be precisely controlled is "binocular rivalry". Here, a small image, e.g., a horizontal grating, is presented to the left eye, and another image, e.g., a vertical grating, is shown to the corresponding location in the right eye. In spite of the constant visual stimulus, observers consciously see the horizontal grating alternate every few seconds with the vertical one. The brain does not allow for the simultaneous perception of both images | Biology | https://en.wikipedia.org/wiki?curid=18345264 | Neural correlates of consciousness | 139,993 |
Neural correlates of consciousness Logothetis and colleagues recorded a variety of visual cortical areas in awake macaque monkeys performing a binocular rivalry task. Macaque monkeys can be trained to report whether they see the left or the right image. The distribution of the switching times and the way in which changing the contrast in one eye affects these leaves little doubt that monkeys and humans experience the same basic phenomenon. In the primary visual cortex (V1) only a small fraction of cells weakly modulated their response as a function of the percept of the monkey while most cells responded to one or the other retinal stimulus with little regard to what the animal perceived at the time. But in a high-level cortical area such as the inferior temporal cortex along the ventral stream almost all neurons responded only to the perceptually dominant stimulus, so that a "face" cell only fired when the animal indicated that it saw the face and not the pattern presented to the other eye. This implies that NCC involve neurons active in the inferior temporal cortex: it is likely that specific reciprocal actions of neurons in the inferior temporal and parts of the prefrontal cortex are necessary. A number of fMRI experiments that have exploited binocular rivalry and related illusions to identify the hemodynamic activity underlying visual consciousness in humans demonstrate quite conclusively that activity in the upper stages of the ventral pathway (e.g | Biology | https://en.wikipedia.org/wiki?curid=18345264 | Neural correlates of consciousness | 139,994 |
Neural correlates of consciousness , the fusiform face area and the parahippocampal place area) as well as in early regions, including V1 and the lateral geniculate nucleus (LGN), follow the percept and not the retinal stimulus. Further, a number of fMRI and DTI experiments suggest V1 is necessary but not sufficient for visual consciousness. In a related perceptual phenomenon, "flash suppression", the percept associated with an image projected into one eye is suppressed by flashing another image into the other eye while the original image remains. Its methodological advantage over binocular rivalry is that the timing of the perceptual transition is determined by an external trigger rather than by an internal event. The majority of cells in the inferior temporal cortex and the superior temporal sulcus of monkeys trained to report their percept during flash suppression follow the animal's percept: when the cell's preferred stimulus is perceived, the cell responds. If the picture is still present on the retina but is perceptually suppressed, the cell falls silent, even though primary visual cortex neurons fire. Single-neuron recordings in the medial temporal lobe of epilepsy patients during flash suppression likewise demonstrate abolishment of response when the preferred stimulus is present but perceptually masked | Biology | https://en.wikipedia.org/wiki?curid=18345264 | Neural correlates of consciousness | 139,995 |
Neural correlates of consciousness Given the absence of any accepted criterion of the minimal neuronal correlates necessary for consciousness, the distinction between a persistently vegetative patient who shows regular sleep-wave transitions and may be able to move or smile, and a minimally conscious patient who can communicate (on occasion) in a meaningful manner (for instance, by differential eye movements) and who shows some signs of consciousness, is often difficult. In global anesthesia the patient should not experience psychological trauma but the level of arousal should be compatible with clinical exigencies. Blood-oxygen-level-dependent fMRI have demonstrated normal patterns of brain activity in a patient in a vegetative state following a severe traumatic brain injury when asked to imagine playing tennis or visiting rooms in his/her house. Differential brain imaging of patients with such global disturbances of consciousness (including akinetic mutism) reveal that dysfunction in a widespread cortical network including medial and lateral prefrontal and parietal associative areas is associated with a global loss of awareness. Impaired consciousness in epileptic seizures of the temporal lobe was likewise accompanied by a decrease in cerebral blood flow in frontal and parietal association cortex and an increase in midline structures such as the mediodorsal thalamus. Relatively local bilateral injuries to midline (paramedian) subcortical structures can also cause a complete loss of awareness | Biology | https://en.wikipedia.org/wiki?curid=18345264 | Neural correlates of consciousness | 139,996 |
Neural correlates of consciousness These structures therefore "enable" and control brain arousal (as determined by metabolic or electrical activity) and are necessary neural correlates. One such example is the heterogeneous collection of more than two dozen nuclei on each side of the upper brainstem (pons, midbrain and in the posterior hypothalamus), collectively referred to as the reticular activating system (RAS). Their axons project widely throughout the brain. These nuclei – three-dimensional collections of neurons with their own cyto-architecture and neurochemical identity – release distinct neuromodulators such as acetylcholine, noradrenaline/norepinephrine, serotonin, histamine and orexin/hypocretin to control the excitability of the thalamus and forebrain, mediating alternation between wakefulness and sleep as well as general level of behavioral and brain arousal. After such trauma, however, eventually the excitability of the thalamus and forebrain can recover and consciousness can return. Another enabling factor for consciousness are the five or more intralaminar nuclei (ILN) of the thalamus. These receive input from many brainstem nuclei and project strongly, directly to the basal ganglia and, in a more distributed manner, into layer I of much of the neocortex. Comparatively small (1 cm or less) bilateral lesions in the thalamic ILN completely knock out all awareness. Many actions in response to sensory inputs are rapid, transient, stereotyped, and unconscious | Biology | https://en.wikipedia.org/wiki?curid=18345264 | Neural correlates of consciousness | 139,997 |
Neural correlates of consciousness They could be thought of as cortical reflexes and are characterized by rapid and somewhat stereotyped responses that can take the form of rather complex automated behavior as seen, e.g., in complex partial epileptic seizures. These automated responses, sometimes called "zombie behaviors", could be contrasted by a slower, all-purpose conscious mode that deals more slowly with broader, less stereotyped aspects of the sensory inputs (or a reflection of these, as in imagery) and takes time to decide on appropriate thoughts and responses. Without such a consciousness mode, a vast number of different zombie modes would be required to react to unusual events. A feature that distinguishes humans from most animals is that we are not born with an extensive repertoire of behavioral programs that would enable us to survive on our own ("physiological prematurity"). To compensate for this, we have an unmatched ability to learn, i.e., to consciously acquire such programs by imitation or exploration. Once consciously acquired and sufficiently exercised, these programs can become automated to the extent that their execution happens beyond the realms of our awareness. Take, as an example, the incredible fine motor skills exerted in playing a Beethoven piano sonata or the sensorimotor coordination required to ride a motorcycle along a curvy mountain road. Such complex behaviors are possible only because a sufficient number of the subprograms involved can be executed with minimal or even suspended conscious control | Biology | https://en.wikipedia.org/wiki?curid=18345264 | Neural correlates of consciousness | 139,998 |
Neural correlates of consciousness In fact, the conscious system may actually interfere somewhat with these automated programs. From an evolutionary standpoint it clearly makes sense to have both automated behavioral programs that can be executed rapidly in a stereotyped and automated manner, and a slightly slower system that allows time for thinking and planning more complex behavior. This latter aspect may be one of the principal functions of consciousness. Other philosophers, however, have suggested that consciousness would not be necessary for any functional advantage in evolutionary processes. No one has given a causal explanation, they argue, of why it would not be possible for a functionally equivalent non-conscious organism (i.e., a philosophical zombie) to achieve the very same survival advantages as a conscious organism. If evolutionary processes are blind to the difference between function "F" being performed by conscious organism "O" and non-conscious organism "O*", it is unclear what adaptive advantage consciousness could provide. As a result, an exaptive explanation of consciousness has gained favor with some theorists that posit consciousness did not evolve as an adaptation but was an exaptation arising as a consequence of other developments such as increases in brain size or cortical rearrangement. Consciousness in this sense has been compared to the blind spot in the retina where it is not an adaption of the retina, but instead just a by-product of the way the retinal axons were wired | Biology | https://en.wikipedia.org/wiki?curid=18345264 | Neural correlates of consciousness | 139,999 |
Neural correlates of consciousness Several scholars including Pinker, Chomsky, Edelman, and Luria have indicated the importance of the emergence of human language as an important regulative mechanism of learning and memory in the context of the development of higher-order consciousness. It seems possible that visual zombie modes in the cortex mainly use the dorsal stream in the parietal region. However, parietal activity can affect consciousness by producing attentional effects on the ventral stream, at least under some circumstances. The conscious mode for vision depends largely on the early visual areas (beyond V1) and especially on the ventral stream. Seemingly complex visual processing (such as detecting animals in natural, cluttered scenes) can be accomplished by the human cortex within 130–150 ms, far too brief for eye movements and conscious perception to occur. Furthermore, reflexes such as the oculovestibular reflex take place at even more rapid time-scales. It is quite plausible that such behaviors are mediated by a purely feed-forward moving wave of spiking activity that passes from the retina through V1, into V4, IT and prefrontal cortex, until it affects motorneurons in the spinal cord that control the finger press (as in a typical laboratory experiment). The hypothesis that the basic processing of information is feedforward is supported most directly by the short times (approx. 100 ms) required for a selective response to appear in IT cells | Biology | https://en.wikipedia.org/wiki?curid=18345264 | Neural correlates of consciousness | 140,000 |
Neural correlates of consciousness Conversely, conscious perception is believed to require more sustained, reverberatory neural activity, most likely via global feedback from frontal regions of neocortex back to sensory cortical areas that builds up over time until it exceeds a critical threshold. At this point, the sustained neural activity rapidly propagates to parietal, prefrontal and anterior cingulate cortical regions, thalamus, claustrum and related structures that support short-term memory, multi-modality integration, planning, speech, and other processes intimately related to consciousness. Competition prevents more than one or a very small number of percepts to be simultaneously and actively represented. This is the core hypothesis of the global workspace theory of consciousness. In brief, while rapid but transient neural activity in the thalamo-cortical system can mediate complex behavior without conscious sensation, it is surmised that consciousness requires sustained but well-organized neural activity dependent on long-range cortico-cortical feedback. The neurobiologist Christfried Jakob (1866-1956) argued that the only conditions which must have neural correlates are direct sensations and reactions; these are called "intonations". Neurophysiological studies in animals provided some insights on the neural correlates of conscious behavior. Vernon Mountcastle, in the early 1960s, set up to study this set of problems, which he termed "the Mind/Brain problem", by studying the neural basis of perception in the somatic sensory system | Biology | https://en.wikipedia.org/wiki?curid=18345264 | Neural correlates of consciousness | 140,001 |
Neural correlates of consciousness His labs at Johns Hopkins were among the first, along with Edward V.Evarts at NIH, to record neural activity from behaving monkeys. Struck with the elegance of SS Stevens approach of magnitude estimation, Mountcastle's group discovered three different modalities of somatic sensation shared one cognitive attribute: in all cases the firing rate of peripheral neurons was linearly related to the strength of the percept elicited. More recently, Ken H. Britten, William T. Newsome, and C. Daniel Salzman have shown that in area MT of monkeys, neurons respond with variability that suggests they are the basis of decision making about direction of motion. They first showed that neuronal rates are predictive of decisions using signal detection theory, and then that stimulation of these neurons could predictably bias the decision. Such studies were followed by Ranulfo Romo in the somatic sensory system, to confirm, using a different percept and brain area, that a small number of neurons in one brain area underlie perceptual decisions. Other lab groups have followed Mountcastle's seminal work relating cognitive variables to neuronal activity with more complex cognitive tasks. Although monkeys cannot talk about their perceptions, behavioral tasks have been created in which animals made nonverbal reports, for example by producing hand movements. Many of these studies employ perceptual illusions as a way to dissociate sensations ("i.e.", the sensory information that the brain receives) from perceptions ("i.e | Biology | https://en.wikipedia.org/wiki?curid=18345264 | Neural correlates of consciousness | 140,002 |
Neural correlates of consciousness ", how the consciousness interprets them). Neuronal patterns that represent perceptions rather than merely sensory input are interpreted as reflecting the neuronal correlate of consciousness. Using such design, Nikos Logothetis and colleagues discovered perception-reflecting neurons in the temporal lobe. They created an experimental situation in which conflicting images were presented to different eyes ("i.e.", binocular rivalry). Under such conditions, human subjects report bistable percepts: they perceive alternatively one or the other image. Logothetis and colleagues trained the monkeys to report with their arm movements which image they perceived. Temporal lobe neurons in Logothetis experiments often reflected what the monkeys' perceived. Neurons with such properties were less frequently observed in the primary visual cortex that corresponds to relatively early stages of visual processing. Another set of experiments using binocular rivalry in humans showed that certain layers of the cortex can be excluded as candidates of the neural correlate of consciousness. Logothetis and colleagues switched the images between eyes during the percept of one of the images. Surprisingly the percept stayed stable. This means that the conscious percept stayed stable and at the same time the primary input to layer 4, which is the input layer, in the visual cortex changed. Therefore layer 4 can not be a part of the neural correlate of consciousness | Biology | https://en.wikipedia.org/wiki?curid=18345264 | Neural correlates of consciousness | 140,003 |
Neural correlates of consciousness Mikhail Lebedev and their colleagues observed a similar phenomenon in monkey prefrontal cortex. In their experiments monkeys reported the perceived direction of visual stimulus movement (which could be an illusion) by making eye movements. Some prefrontal cortex neurons represented actual and some represented perceived displacements of the stimulus. Observation of perception related neurons in prefrontal cortex is consistent with the theory of Christof Koch and Francis Crick who postulated that neural correlate of consciousness resides in prefrontal cortex. Proponents of distributed neuronal processing may likely dispute the view that consciousness has a precise localization in the brain. Francis Crick wrote a popular book, "The Astonishing Hypothesis," whose thesis is that the neural correlate for consciousness lies in our nerve cells and their associated molecules. Crick and his collaborator Christof Koch have sought to avoid philosophical debates that are associated with the study of consciousness, by emphasizing the search for "correlation" and not "causation". There is much room for disagreement about the nature of this correlate ("e.g.", does it require synchronous spikes of neurons in different regions of the brain? Is the co-activation of frontal or parietal areas necessary?) | Biology | https://en.wikipedia.org/wiki?curid=18345264 | Neural correlates of consciousness | 140,004 |
Neural correlates of consciousness The philosopher David Chalmers maintains that a neural correlate of consciousness, unlike other correlates such as for memory, will fail to offer a satisfactory explanation of the phenomenon; he calls this the hard problem of consciousness. | Biology | https://en.wikipedia.org/wiki?curid=18345264 | Neural correlates of consciousness | 140,005 |
Darwinian Demon A is a hypothetical organism that would result if there were no biological constraints on evolution. Such an organism would maximize all aspects of fitness simultaneously and would exist if there were no limitations from available variation or physiological constraints. It is named for Charles Darwin. Such organisms would reproduce directly after being born, produce infinitely many offspring, and live indefinitely. Even though no such organisms exist, biologists use Darwinian Demons in thought experiments to understand different life history strategies among different organisms. | Biology | https://en.wikipedia.org/wiki?curid=18349854 | Darwinian Demon | 140,006 |
Gallery forest Gallery forests are forests that form as corridors along rivers or wetlands and project into landscapes that are otherwise only sparsely treed such as savannas, grasslands, or deserts. Gallery forests are able to exist where the surrounding landscape does not support forests for a number of reasons. The riparian zones in which they grow offer greater protection from fire which would kill tree seedlings. In addition, the alluvial soils of the gallery habitat are often of higher fertility and have better drainage than the soils of the surrounding landscape with a more reliable water supply at depth. As a result, the boundary between gallery forest and the surrounding woodland or grassland is usually abrupt, with the ecotone being only a few metres wide. Gallery forests have shrunk in extent worldwide as a result of human activities, including domestic livestock's preventing tree seedling establishment and the construction of dams and weirs causing flooding or interfering with natural stream flow. In addition to these disturbances, gallery forests are also threatened by many of the same processes that threaten savannas. | Biology | https://en.wikipedia.org/wiki?curid=18359501 | Gallery forest | 140,007 |
Seasoning (colonialism) Seasoning, or The Seasoning, is the term applied to the period of adjustment that was undertaken by African slaves and European immigrants following their first attack of tropical disease, during the colonisation of the Americas. Malaria was the chief adversary of colonists and slaves. Death rates dramatically differed between regions in the Americas. Those who survived were known as "Seasoned", and for slaves, this would command a higher price. The term arose during the period when newly arrived slaves in American plantations died at varying but high rates. For instance, in Cuba, deaths in the single year were between 7 and 12 percent while the mortality rate reached as high as 33 percent in Jamaica. The term has also been applied to a period of preparation that covered adjustment to new sociocultural, labor, and geographic environments. The goal was to erase the slaves' memories prior to slavery so that their history begins and ends with their usefulness to their owners. It usually involved an older slave breaking in new ones using approaches such as less severe forms of punishment (e.g. restriction on food). Other variations involved harsher and more physically forceful procedure. This is demonstrated in the case of slave owners who believed that adaptation must begin at the earliest stage with the immediate removal of the element of subjective resistance by instilling fear and breaking the slave's spirit. | Biology | https://en.wikipedia.org/wiki?curid=18373301 | Seasoning (colonialism) | 140,008 |
Active recall is a principle of efficient learning, which claims the need to actively stimulate memory during the learning process. It contrasts with passive review, in which the learning material is processed passively (e.g. by reading, watching, etc.). For example, reading a text about George Washington, with no further action, is a passive review. Answering the question "Who was the first US President?", is active recall. There are several variations of active recall as a strategy and these include the 3R (read-recite-review) method by McDaniel et al. and Scott Young's Feynman technique. exploits the psychological testing effect and is very efficient in consolidating long-term memory. Research revealed that it is the quickest, most efficient, and effective way to study written materials, at least for factual and problem-solving tests. Aside from passive review, it is said to be better than mindmapping and note-taking since it is extremely efficient for committing details and ideas into one's memory. It is also suggested that the neocortex has an active recall that can use episodic information to build new semantic memories, which could mean the hippocampus plays a role in the way memories are consolidated in the neocortex. A study done by J.D. Karpicke and H.L. Roediger, III (2008) lent support to the idea that practicing information retrieval is integral to learning. They had college students study 40 pairs of foreign language words on flash cards | Biology | https://en.wikipedia.org/wiki?curid=18374763 | Active recall | 140,009 |
Active recall One group learned the words by going through the deck of cards each time until they could recall all the words. The other group's subjects dropped a card whenever they successfully recalled its paired word on the reverse side. Both groups alternated between study and test trials. Furthermore, half of the subjects were tested on the entire list during each test trial, while the other half were only tested on words they failed to recall on previous test trials. The results of a follow-up test on the entire list a week later clearly showed that those who were tested on the entire list during learning were able to recall a greater percentage of the word pairs (~80% as opposed to ~30% for the partial-list tested subjects). Results didn't depend on how the students studied (entire list or only unrecalled pairs), only how they were tested. The authors concluded that more rigorous testing leads to better retrieval in the future. Karpicke and Janell R. Blunt (2011) followed up in this finding and questioned whether elaborative studying with concept mapping or retrieval-heavy studying was more effective. 200 Subjects who had studied various scientific concepts using more retrieval techniques did 50% better than the other group when tested a week later on their comprehension and ability to infer. Retrieval-heavy studiers performed better than concept-mappers in every measured way, even on questions requiring the creation of concept maps | Biology | https://en.wikipedia.org/wiki?curid=18374763 | Active recall | 140,010 |
Active recall Thus, they concluded that retrieval techniques aid learning more than elaborative studying. Karpicke believes the next step is to discover better ways to use retrieval in learning. McDaniel et al. (2009) came up with the 3R (read-recite-review) method for learning from textbooks. They conducted two experiments that compared the 3R strategy to rereading and note-taking ones. Their results from one of the experiments showed that 3R improved both immediate and delayed (one week) free recall of information. The other one involved more complexity, and its results showed 3R studiers did better than those who reread and as well as note-takers, though the note-takers studied for longer than the 3R group. Thus there is much support that active recall is better than rereading text for enhancing learning. In fact, Karpicke, et al. (2009) believe that students get "illusions of competence" from rereading their notes and textbook. One reason for this illusion is that the text contains all the information, so it is easy to glance over it and feel as if it is known well, when that is not the case at all. Better put: in the text, the cue and corresponding target are both present, which is not the case during testing. The results of their study showed that retrieval as a study strategy is rare among students. They prefer to reread instead. Some critics of active recall claim that using retrieval techniques only improves learning a specific response. However, Karpicke et al | Biology | https://en.wikipedia.org/wiki?curid=18374763 | Active recall | 140,011 |
Active recall (2009) and Butler (2010) proved that at the very least, information is better remembered. | Biology | https://en.wikipedia.org/wiki?curid=18374763 | Active recall | 140,012 |
Somatic evolution in cancer Somatic evolution is the accumulation of mutations and epimutations in somatic cells (the cells of a body, as opposed to germ plasm and stem cells) during a lifetime, and the effects of those mutations and epimutations on the fitness of those cells. This evolutionary process has first been shown by the studies of Bert Vogelstein in colon cancer. Somatic evolution is important in the process of aging as well as the development of some diseases, including cancer. Cells in pre-malignant and malignant neoplasms (tumors) evolve by natural selection. This accounts for how cancer develops from normal tissue and why it has been difficult to cure. There are three necessary and sufficient conditions for natural selection, all of which are met in a neoplasm: Cells in neoplasms compete for resources, such as oxygen and glucose, as well as space. Thus, a cell that acquires a mutation that increases its fitness will generate more daughter cells than competitor cells that lack that mutation. In this way, a population of mutant cells, called a clone, can expand in the neoplasm. Clonal expansion is the signature of natural selection in cancer. Cancer therapies act as a form of artificial selection, killing sensitive cancer cells, but leaving behind resistant cells. Often the tumor will regrow from those resistant cells, the patient will relapse, and the therapy that had been previously used will no longer kill the cancer cells | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,013 |
Somatic evolution in cancer This selection for resistance is similar to the repeatedly spraying crops with a pesticide and selecting for resistant pests until the pesticide is no longer effective. Modern descriptions of biological evolution will typically elaborate on major contributing factors to evolution such as the formation of local micro-environments, mutational robustness, molecular degeneracy, and cryptic genetic variation. Many of these contributing factors in evolution have been isolated and described for cancer. Cancer is a classic example of what evolutionary biologists call multilevel selection: at the level of the organism, cancer is usually fatal so there is selection for genes and the organization of tissues that suppress cancer. At the level of the cell, there is selection for increased cell proliferation and survival, such that a mutant cell that acquires one of the hallmarks of cancer (see below), will have a competitive advantage over cells that have not acquired the hallmark. Thus, at the level of the cell there is selection for cancer. The earliest ideas about neoplastic evolution come from Boveri who proposed that tumors originated in chromosomal abnormalities passed on to daughter cells. In the decades that followed, cancer was recognized as having a clonal origin associated with chromosomal aberrations. Early mathematical modeling of cancer, by Armitage and Doll, set the stage for the future development of the somatic evolutionary theory of cancer | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,014 |
Somatic evolution in cancer Armitage and Doll explained the cancer incidence data, as a function of age, as a process of the sequential accumulation of somatic mutations (or other rate limiting steps). Advances in cytogenetics facilitated discovery of chromosome abnormalities in neoplasms, including the Philadelphia chromosome in chronic myelogenous leukemia and translocations in acute myeloblastic leukemia. Sequences of karyotypes replacing one another in a tumor were observed as it progressed. Researchers hypothesized that cancer evolves in a sequence of chromosomal mutations and selection and that therapy may further select clones. In 1971, Knudson published the 2-hit hypothesis for mutation and cancer based on statistical analysis of inherited and sporadic cases of retinoblastoma. He postulated that retinoblastoma developed as a consequence of two mutations; one of which could be inherited or somatic followed by a second somatic mutation. Cytogenetic studies localized the region to the long arm of chromosome 13, and molecular genetic studies demonstrated that tumorigenesis was associated with chromosomal mechanisms, such as mitotic recombination or non-disjunction, that could lead to homozygosity of the mutation. The retinoblastoma gene was the first tumor suppressor gene to be cloned in 1986 | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,015 |
Somatic evolution in cancer Cairns hypothesized a different, but complementary, mechanism of tumor suppression in 1975 based on tissue architecture to protect against selection of variant somatic cells with increased fitness in proliferating epithelial populations, such as the intestine and other epithelial organs. He postulated that this could be accomplished by restricting the number of stem cells for example at the base of intestinal crypts and restraining the opportunities for competition between cells by shedding differentiated intestinal cells into the gut. The essential predictions of this model have been confirmed although mutations in some tumor suppressor genes, including CDKN2A (p16), predispose to clonal expansions that encompass large numbers of crypts in some conditions such as Barrett's esophagus. He also postulated an immortal DNA strand that is discussed at Immortal DNA strand hypothesis. Nowell synthesized the evolutionary view of cancer in 1976 as a process of genetic instability and natural selection. Most of the alterations that occur are deleterious for the cell, and those clones will tend to go extinct, but occasional selectively advantageous mutations arise that lead to clonal expansions. This theory predicts a unique genetic composition in each neoplasm due to the random process of mutations, genetic polymorphisms in the human population, and differences in the selection pressures of the neoplasm's microenvironment. Interventions are predicted to have varying results in different patients | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,016 |
Somatic evolution in cancer What is more important, the theory predicts the emergence of resistant clones under the selective pressures of therapy. Since 1976, researchers have identified clonal expansions and genetic heterogeneity within many different types of neoplasms. There are multiple levels of genetic heterogeneity associated with cancer, including single nucleotide polymorphism (SNP), sequence mutations, Microsatellite shifts and instability, loss of heterozygosity (LOH), Copy number variation (detected both by comparative genomic hybridization (CGH), and array CGH,) and karyotypic variations including chromosome structural aberrations and aneuploidy. Studies of this issue have focused mainly at the gene mutation level, as copy number variation, LOH and specific chromosomal translocations are explained in the context of gene mutation. It is thus necessary to integrate multiple levels of genetic variation in the context of complex system and multilevel selection. System instability is a major contributing factor for genetic heterogeneity. For the majority of cancers, genome instability is reflected in a large frequency of mutations in the whole genome DNA sequence (not just the protein coding regions that are only 1.5% of the genome). In whole genome sequencing of different types of cancers, large numbers of mutations were found in two breast cancers (about 20,000 point mutations), 25 melanomas (9,000 to 333,000 point mutations) and a lung cancer (50,000 point mutations and 54,000 small additions and deletions) | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,017 |
Somatic evolution in cancer Genome instability is also referred to as an enabling characteristic for achieving endpoints of cancer evolution. Many of the somatic evolutionary studies have traditionally been focused on clonal expansion, as recurrent types of changes can be traced to illustrate the evolutionary path based on available methods. Recent studies from both direct DNA sequencing and karyotype analysis illustrate the importance of the high level of heterogeneity in somatic evolution. For the formation of solid tumors, there is an involvement of multiple cycles of clonal and non-clonal expansion. Even at the typical clonal expansion phase, there are significant levels of heterogeneity within the cell population, however, most are under-detected when mixed populations of cells are used for molecular analysis. In solid tumors, a majority of gene mutations are not recurrent types, and neither are the karyotypes. These analyses offer an explanation for the findings that there are no common mutations shared by most cancers. The state of a cell may be changed epigenetically, in addition to genetic alterations. The best-understood epigenetic alterations in tumors are the silencing or expression of genes by changes in the methylation of CG pairs of nucleotides in the promoter regions of the genes. These methylation patterns are copied to the new chromosomes when cells replicate their genomes and so methylation alterations are heritable and subject to natural selection | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,018 |
Somatic evolution in cancer Methylation changes are thought to occur more frequently than mutations in the DNA, and so may account for many of the changes during neoplastic progression (the process by which normal tissue becomes cancerous), in particular in the early stages. For instance, when loss of expression of the DNA repair protein MGMT occurs in a colon cancer, it is caused by a mutation only about 4% of the time, while in most cases the loss is due to methylation of its promoter region. Similarly, when loss of expression of the DNA repair protein PMS2 occurs in colon cancer, it is caused by a mutation about 5% of the time, while in most cases loss of expression is due to methylation of the promoter of its pairing partner MLH1 (PMS2 is unstable in the absence of MLH1). Epigenetic changes in progression interact with genetic changes. For example, epigenetic silencing of genes responsible for the repair of mispairs or damages in the DNA (e.g. MLH1 or MSH2) results in an increase of genetic mutations. Deficiency of DNA repair proteins PMS2, MLH1, MSH2, MSH3, MSH6 or BRCA2 can cause up to 100-fold increases in mutation frequency Epigenetic deficiencies in DNA repair gene protein expression have been found in many cancers, though not all deficiencies have been evaluated in all cancers. Epigeneticically deficient DNA repair proteins include BRCA1, WRN, MGMT, MLH1, MSH2, ERCC1, PMS2, XPF, P53, PCNA and OGG1, and these are found to be deficient at frequencies of 13% to 100% in different cancers | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,019 |
Somatic evolution in cancer (Also see Frequencies of epimutations in DNA repair genes.) In addition to well studied epigenetic promoter methylation, more recently there have been substantial findings of epigenetic alterations in cancer due to changes in histone and chromatin architecture and alterations in the expression of microRNAs (microRNAs either cause degradation of messenger RNAs or block their translation) For instance, hypomethylation of the promoter for microRNA miR-155 increases expression of miR-155, and this increased miR-155 targets DNA repair genes MLH1, MSH2 and MSH6, causing each of them to have reduced expression. In cancers, loss of expression of genes occurs about 10 times more frequently by transcription silencing (caused by somatically heritable promoter hypermethylation of CpG islands) than by mutations. As Vogelstein et al. point out, in a colorectal cancer there are usually about 3 to 6 driver mutations and 33 to 66 hitchhiker or passenger mutations. In contrast, in colon tumors compared to adjacent normal-appearing colonic mucosa, there are about 600 to 800 somatically heritable heavily methylated CpG islands in promoters of genes in the tumors while these CpG islands are not methylated in the adjacent mucosa. Methylation of the cytosine of CpG dinucleotides is a somatically heritable and conserved regulatory mark that is generally associated with transcriptional repression. CpG islands keep their overall un-methylated state (or methylated state) extremely stably through multiple cell generations | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,020 |
Somatic evolution in cancer One common feature of neoplastic progression is the expansion of a clone with a genetic or epigenetic alteration. This may be a matter of chance, but is more likely due to the expanding clone having a competitive advantage (either a reproductive or survival advantage) over other cells in the tissue. Since clones often have many genetic and epigenetic alterations in their genomes, it is often not clear which of those alterations cause a reproductive or survival advantage and which other alterations are simply hitchhikers or passenger mutations (see Glossary below) on the clonal expansion. Clonal expansions are most often associated with the loss of the p53 (TP53) or p16 (CDKN2A/INK4a) tumor suppressor genes. In lung cancer, a clone with a p53 mutation was observed to have spread over the surface of one entire lung and into the other lung. In bladder cancer, clones with loss of p16 were observed to have spread over the entire surface of the bladder. Likewise, large expansions of clones with loss of p16 have been observed in the oral cavity and in Barrett's esophagus. Clonal expansions associated with inactivation of p53 have also appear in skin, Barrett's esophagus, brain, and kidney. Further clonal expansions have been observed in the stomach, bladder, colon, lung, hematopoietic (blood) cells, and prostate. These clonal expansions are important for at least two reasons | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,021 |
Somatic evolution in cancer First, they generate a large target population of mutant cells and so increase the probability that the multiple mutations necessary to cause cancer will be acquired within that clone. Second, in at least one case, the size of the clone with loss of p53 has been associated with an increased risk of a pre-malignant tumor becoming cancerous. It is thought that the process of developing cancer involves successive waves of clonal expansions within the tumor. The term "field cancerization" was first used in 1953 to describe an area or "field" of epithelium that has been preconditioned by (at that time) largely unknown processes so as to predispose it towards development of cancer. Since then, the terms "field cancerization" and "field defect" have been used to describe pre-malignant tissue in which new cancers are likely to arise. Field defects, for example, have been identified in most of the major areas subject to tumorigenesis in the gastrointestinal (GI) tract. Cancers of the GI tract that are shown to be due, to some extent, to field defects include head and neck squamous cell carcinoma (HNSCC), oropharyngeal/laryngeal cancer, esophageal adenocarcinoma and esophageal squamous-cell carcinoma, gastric cancer, bile duct cancer, pancreatic cancer, small intestine cancer and colon cancer. In the colon, a field defect probably arises by natural selection of a mutant or epigenetically altered cell among the stem cells at the base of one of the intestinal crypts on the inside surface of the colon | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,022 |
Somatic evolution in cancer A mutant or epigenetically altered stem cell, if it has a selective advantage, could replace the other nearby stem cells by natural selection. This can cause a patch of abnormal tissue, or field defect. The figure in this section includes a photo of a freshly resected and lengthwise-opened segment of the colon that may represent a large field defect in which there is a colon cancer and four polyps. The four polyps, in addition to the cancer, may represent sub-clones with proliferative advantages. The sequence of events giving rise to this possible field defect are indicated below the photo. The schematic diagram shows a large area in yellow indicating a large patch of mutant or epigenetically altered cells that formed by clonal expansion of an initial cell based on a selective advantage. Within this first large patch, a second such mutation or epigenetic alteration may have occurred so that a given stem cell acquired an additional selective advantage compared to the other stem cells within the patch, and this altered stem cell expanded clonally forming a secondary patch, or sub-clone, within the original patch. This is indicated in the diagram by four smaller patches of different colors within the large yellow original area | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,023 |
Somatic evolution in cancer Within these new patches (sub-clones), the process may have been repeated multiple times, indicated by the still smaller patches within the four secondary patches (with still different colors in the diagram) which clonally expanded, until a stem cell arose that generated either small polyps (which may be benign neoplasms) or else a malignant neoplasm (cancer). These neoplasms are also indicated, in the diagram below the photo, by 4 small tan circles (polyps) and a larger red area (cancer). The cancer in the photo occurred in the cecal area of the colon, where the colon joins the small intestine (labeled) and where the appendix occurs (labeled). The fat in the photo is external to the outer wall of the colon. In the segment of colon shown here, the colon was cut open lengthwise to expose the inner surface of the colon and to display the cancer and polyps occurring within the inner epithelial lining of the colon. Phylogenetics may be applied to cells in tumors to reveal the evolutionary relationships between cells, just as it is used to reveal evolutionary relationships between organisms and species. Shibata, Tavare and colleagues have exploited this to estimate the time between the initiation of a tumor and its detection in the clinic. Louhelainen "et al." have used parsimony to reconstruct the relationships between biopsy samples based on loss of heterozygosity | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,024 |
Somatic evolution in cancer Phylogenetic trees should not be confused with oncogenetic trees, which represent the common sequences of genetic events during neoplastic progression and do not represent the relationships of common ancestry that are essential to a phylogeny. For an up-to-date review in this field, see Bast 2012. An adaptive landscape is a hypothetical topological landscape upon which evolution is envisioned to take place. It is similar to Wright's fitness landscape in which the location of each point represents the genotype of an organism and the altitude represents the fitness of that organism in the current environment. However, unlike Wright's rigid landscape, the adaptive landscape is pliable. It readily changes shape with changes in population densities and survival/reproductive strategies used within and among the various species. Wright's shifting balance theory of evolution combines genetic drift (random sampling error in the transmission of genes) and natural selection to explain how multiple peaks on a fitness landscape could be occupied or how a population can achieve a higher peak on this landscape. This theory, based on the assumption of density-dependent selection as the principal forms of selection, results in a fitness landscape that is relatively rigid. A rigid landscape is one that does not change in response to even large changes in the position and composition of strategies along the landscape | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,025 |
Somatic evolution in cancer In contrast to the fitness landscape, the adaptive landscape is constructed assuming that both density and frequency-dependent selection is involved (selection is frequency-dependant when the fitness of a species depends not only on that species strategy but also on the strategy of all other species). As such, the shape of the adaptive landscape can change drastically in response to even small changes in strategies and densities. The flexibility of adaptive landscapes provide several ways for natural selection to cross valleys and occupy multiple peaks without having to make large changes in their strategies. Within the context of differential or difference equation models for population dynamics, an adaptive landscape may actually be constructed using a fitness generating function. If a given species is able to evolve, it will, over time, "climb" the adaptive landscape toward a fitness peak through gradual changes in its mean phenotype according to a strategy dynamic that involves the slope of the adaptive landscape. Because the adaptive landscape is not rigid and can change shape during the evolutionary process, it is possible that a species may be driven to maximum, minimum, or saddle point on the adaptive landscape. A population at a global maximum on the adaptive landscape corresponds an evolutionarily stable strategy (ESS) and will become dominant, driving all others toward extinction | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,026 |
Somatic evolution in cancer Populations at a minimum or saddle point are not resistant to invasion, so that the introduction of a slightly different mutant strain may continue the evolutionary process toward unoccupied local maxima. The adaptive landscape provides a useful tool for studying somatic evolution as it can describe the process of how a mutant cell evolves from a small tumor to an invasive cancer. Understanding this process in terms of the adaptive landscape may lead to the control of cancer through external manipulation of the shape of the landscape. In their landmark paper, "The Hallmarks of Cancer", Hanahan and Weinberg suggest that cancer can be described by a small number of underlying principles, despite the complexities of the disease. The authors describe how tumor progression proceeds via a process analogous to Darwinian evolution, where each genetic change confers a growth advantage to the cell. These genetic changes can be grouped into six "hallmarks", which drive a population of normal cells to become a cancer. The six hallmarks are: Genetic instability is defined as an "enabling characteristic" that facilitates the acquisition of other mutations due to defects in DNA repair. The hallmark "self-sufficiency in growth signals" describes the observation that tumor cells produce many of their own growth signals and thereby no longer rely on proliferation signals from the micro-environment | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,027 |
Somatic evolution in cancer Normal cells are maintained in a nondividing state by antigrowth signals, which cancer cells learn to evade through genetic changes producing "insensitivity to antigrowth signals". A normal cell initiates programmed cell death (apoptosis) in response to signals such as DNA damage, oncogene overexpression, and survival factor insufficiency, but a cancer cell learns to "evade apoptosis", leading to the accumulation of aberrant cells. Most mammalian cells can replicate a limited number of times due to progressive shortening of telomeres; virtually all malignant cancer cells gain an ability to maintain their telomeres, conferring "limitless replicative potential". As cells cannot survive at distances of more than 100 μm from a blood supply, cancer cells must initiate the formation of new blood vessels to support their growth via the process of "sustained angiogenesis". During the development of most cancers, primary tumor cells acquire the ability to undergo "invasion and metastasis" whereby they migrate into the surrounding tissue and travel to distant sites in the body, forming secondary tumors. The pathways that cells take toward becoming malignant cancers are variable, and the order in which the hallmarks are acquired can vary from tumor to tumor. The early genetic events in tumorigenesis are difficult to measure clinically, but can be simulated according to known biology | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,028 |
Somatic evolution in cancer Macroscopic tumors are now beginning to be described in terms of their underlying genetic changes, providing additional data to refine the framework described in The Hallmarks of Cancer. The theory about the monoclonal origin of cancer states that, in general, neoplasms arise from a single cell of origin. While it is possible that certain carcinogens may mutate more than one cell at once, the tumor mass usually represents progeny of a single cell, or very few cells. A series of mutations is required in the process of carcinogenesis for a cell to transition from being normal to pre-malignant and then to a cancer cell. The mutated genes usually belong to classes of caretaker, gatekeeper, landscaper or several other genes. Mutation ultimately leads to acquisition of the ten hallmarks of cancer. The first malignant cell, that gives rise to the tumor, is often labeled a cancer stem cell. The cancer stem-cell hypothesis relies on the fact that a lot of tumors are heterogeneous – the cells in the tumor vary by phenotype and functions. Current research shows that in many cancers there is apparent hierarchy among cells. in general, there is a small population of cells in the tumor – about 0.2%–1% – that exhibits stem cell-like properties. These cells have the ability to give rise to a variety of cells in tumor tissue, self-renew indefinitely, and upon transfer can form new tumors. According to the hypothesis, cancer stem cells are the only cells capable of tumorigenesis – initiation of a new tumor | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,029 |
Somatic evolution in cancer Cancer stem cell hypothesis might explain such phenomena as metastasis and remission. The monoclonal model of cancer and the cancer stem-cell model are not mutually exclusive. Cancer stem cell arises by clonal evolution as a result of selection for the cell with the highest fitness in the neoplasm. This way, the heterogeneous nature of neoplasm can be explained by two processes – clonal evolution, or the hierarchical differentiation of cells, regulated by cancer stem cells. All cancers arise as a result of somatic evolution, but only some of them fit the cancer stem cell hypothesis. The evolutionary processes do not cease when a population of cancer stem cells arises in a tumor. Cancer treatment drugs pose a strong selective force on all types of cells in tumors, including cancer stem cells, which would be forced to evolve resistance to the treatment. Cancer stem cells do not always have to have the highest resistance among the cells in the tumor to survive chemotherapy and re-emerge afterwards. The surviving cells might be in a special microenvironment, which protects them from adverse effects of treatment. It is currently unclear as to whether cancer stem cells arise from adult stem cell transformation, a maturation arrest of progenitor cells, or as a result of dedifferentiation of mature cells. Therapeutic resistance has been observed in virtually every form of therapy, from the beginning of cancer therapy. In most cases, therapies appear to select for mutations in the genes or pathways targeted by the drug | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,030 |
Somatic evolution in cancer Some of the first evidence for a genetic basis of acquired therapeutic resistance came from studies of methotrexate. Methotrexate inhibits the dihydrofolate reductase (DHFR) gene. However, methotrexate therapy appears to select for cells with extra copies (amplification) of DHFR, which are resistant to methotrexate. This was seen in both cell culture and samples from tumors in patients that had been treated with methotrexate. A common cytotoxic chemotherapy used in a variety of cancers, 5-fluorouracil (5-FU), targets the TYMS pathway and resistance can evolve through the evolution of extra copies of TYMS, thereby diluting the drug's effect. In the case of Gleevec (Imatinib), which targets the BCR-ABL fusion gene in chronic myeloid leukemia, resistance often develops through a mutation that changes the shape of the binding site of the drug. Sequential application of drugs can lead to the sequential evolution of resistance mutations to each drug in turn. Gleevec is not as selective as was originally thought. It turns out that it targets other tyrosine kinase genes and can be used to control gastrointestinal stromal tumors (GISTs) that are driven by mutations in c-KIT. However, patients with GIST sometimes relapse with additional mutations in c-KIT that make the cancer cells resistant to Gleevec. Gefitinib(Iressa) and Erlotinib (Tarceva) are epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors used for non-small cell lung cancer patients whose tumors have somatic mutations in EGFR | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,031 |
Somatic evolution in cancer However, most patients' tumors eventually become resistant to these drugs. Two major mechanisms of acquired resistance have been discovered in patients who have developed clinical resistance to Gefitinib or Erlotinib: point mutations in the EGFR gene targeted by the drugs, and amplification of MET, another receptor tyrosine kinase, which can bypass EGFR to activate downstream signaling in the cell. In an initial study, 22% of tumors with acquired resistance to Gefitinib or Erlotinib had MET amplification. To address these issues, clinical trials are currently assessing irreversible EGFR inhibitors (which inhibit growth even in cell lines with mutations in EGFR), the combination of EGFR and MET kinase inhibitors, and Hsp90 inhibitors (EGFR and MET both require Hsp90 proteins to fold properly). In addition, taking repeated tumor biopsies from patients as they develop resistance to these drugs would help to understand the tumor dynamics. Selective estrogen receptor modulators (SERMs) are a commonly used adjuvant therapy in estrogen-receptor positive (ERα+) breast cancer and a preventive treatment for women at high risk of the disease. There are several possible mechanisms of SERM resistance, though the relative clinical importance of each is debated. These include: Most prostate cancers derive from cells that are stimulated to proliferate by androgens. Most prostate cancer therapies are therefore based on removing or blocking androgens | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,032 |
Somatic evolution in cancer Mutations in the androgen receptor (AR) have been observed in anti-androgen resistant prostate cancer that makes the AR hypersensitive to the low levels of androgens that remain after therapy. Likewise, extra copies of the AR gene (amplification) have been observed in anti-androgen resistant prostate cancer. These additional copies of the gene are thought to make the cell hypersensitive to low levels of androgens and so allow them to proliferate under anti-androgen therapy. Resistance to radiotherapy is also commonly observed. However, to date, comparisons of malignant tissue before and after radiotherapy have not been done to identify genetic and epigenetic changes selected by exposure to radiation. In gliomas, a form of brain cancer, radiation therapy appears to select for stem cells, though it is unclear if the tumor returns to the pre-therapy proportion of cancer stem cells after therapy or if radiotherapy selects for an alteration that keeps the glioma cells in the stem cell state. Cancer drugs and therapies commonly used today are evolutionary inert and represent a strong selection force, which leads to drug resistance. A possible way to avoid that is to use a treatment agent that would co-evolve alongside cancer cells. Anoxic bacteria could be used as competitors or predators in hypoxic environments within tumors. Scientists have been interested in the idea of using anoxic bacteria for over 150 years, but until recently there has been little progress in that field | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,033 |
Somatic evolution in cancer According to Jain and Forbes, several requirements have to be met by the cells to qualify as efficient anticancer bacterium: 1.The bacterium cannot be toxic to the host 2.Its population should be restricted to the tumor mass 3.It should be able to disperse evenly throughout the neoplasm 4.At the end of the treatment bacterium should be easily eliminated from the host 5.It should not be causing severe immune response 6.It should be able to cause tumor cells death through competition for nutrients. In the process of the treatment, cancer cells are most likely to evolve some form of resistance to the bacterial treatment. However, being a living organism, bacteria would coevolve with tumor cells, potentially eliminating the possibility of resistance. Since bacteria prefer an anoxic environment, they are not efficient at eliminating cells on the periphery of the tumor, where oxygen supply is efficient. A combination of bacterial treatment with chemical drugs will increase chances of destroying the tumor. Oncolytic viruses are engineered to infect cancerous cells. Limitations of that method include immune response to the virus and the possibility of the virus evolving into a pathogen. By manipulating the tumor environment, it is possible to create favorable conditions for the cells with least resistance to chemotherapy drugs to become more fit and outcompete the rest of the population. The chemotherapy, administered directly after, should wipe out the predominant tumor cells | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,034 |
Somatic evolution in cancer Mapping between common terms from cancer biology and evolutionary biology | Biology | https://en.wikipedia.org/wiki?curid=18398577 | Somatic evolution in cancer | 140,035 |
Naturhistorieselskabet - the Society for Natural History - was a private society that was the only institution to offer education in natural history in Denmark in the late 18th century. The spirit of the Age of Enlightenment and an escalating agricultural crisis, led the king and the Danish elite to call foreign experts on economy, including botany and silviculture, to the country. The autonomous University of Copenhagen, on the other hand, was reluctant to employ foreign experts in little-established disciplines. was formed in 1788 in order to ensure education in botany, zoology and mineralogy based on private funds. For example, Martin Vahl lectured in botany. After the appointment in 1795 of a professor in geology and in 1797 one in botany, the society gradually lost its importance. It was soon abolished and its collections donated to the state (much later united with the university collections). Wagner, P.H. 2001. Institutionaliseringen af botanik og geologi i Danmark-Norge i det 18. århundrede (colloquium). Institut for Videnskabshistorie. | Biology | https://en.wikipedia.org/wiki?curid=18400577 | Naturhistorieselskabet | 140,036 |
Quantum Aspects of Life Quantum Aspects of Life, a book published in 2008 with a foreword by Roger Penrose, explores the open question of the role of quantum mechanics at molecular scales of relevance to biology. The book contains chapters written by various world-experts from a 2003 symposium and includes two debates from 2003–2004; giving rise to a mix of both sceptical and sympathetic viewpoints. The book addresses questions of quantum physics, biophysics, nanoscience, quantum chemistry, mathematical biology, complexity theory, and philosophy that are inspired by the 1944 seminal book "What Is Life?" by Erwin Schrödinger. Section 1: "Emergence and Complexity" Section 2: "Quantum Mechanisms in Biology" Section 3: "The Biological Evidence" Section 4: "Artificial Quantum Life" Section 5: "The Debate" | Biology | https://en.wikipedia.org/wiki?curid=18404729 | Quantum Aspects of Life | 140,037 |
WolfQuest is a 3D wildlife simulation video game originally developed by the Minnesota Zoo and game developer company Eduweb, and developed solely by Eduweb since 2013. The game's main purpose is to help players understand wolves and the roles they play in nature by being virtually incarnated as a gray wolf themselves. "WolfQuest" challenges players to learn about wolf ecology by living the life of a wild wolf in Yellowstone National Park and is a family-friendly, fun game for people of all ages. The game was originally funded by grants from the National Science Foundation, Best Buy, and other foundations and donors and distributed as a free download for Mac and Windows computer. In November 2015, Eduweb released a "2.7", an improved and expanded version of the game for purchase. While the old, free version of the game remains available, development efforts are now focused on new versions, particularly "3: Anniversary Edition," a complete remake and expansion of the game. Gameplay is divided into two parts – single player, where players are able to play in a "story mode" type adventure, and multiplayer, where players are able to play in real-time with up to 7 other people in a player-created game server. "WolfQuest" was initially developed episodically, and these episodes now form the main single-player game arc: In single player, the player must survive as a dispersal gray wolf in Yellowstone National Park. To do so they must hunt elk, moose, and hares, or feed off elk carcasses | Biology | https://en.wikipedia.org/wiki?curid=18409681 | WolfQuest | 140,038 |
WolfQuest They must also avoid dangers such as grizzly bears, coyotes, and non-dispersal wolves. However, it is possible to fight off the bears and coyotes by chasing them, and fight off other wolves. They have the option to find a mate, which, when successful, will follow and aid the player throughout the rest of the game. In order to find a mate, the player must first earn 800 experience points, mainly by hunting elk, and then search for a mate which can be found in all territories. When creating their wolf character, players are free to choose the gender, fur coloration, stats, and name of their wolf. There are a variety of pelts to choose from (organized by packs), with two sliders that let players change the tints of the guard hairs and undercoat of the wolf. "2.7" added many new customization features, including more pelts as well as injuries and a radio collar. Just like real wolves, males are larger in size than females. Upon leaving Amethyst Mountain, players (with their mate) enter the Slough Creek map and search for a den to raise pups in a new location, Slough Creek. However, after finding a densite, the player must scent mark the area around the den to make it safe from predators and stranger wolves. After completion, the player will obtain pups. Ravenous bears, coyotes, eagles, cougars, and wolves roam the earth, posing a new threat to young pups as they wait to snatch one up under a novice parent's nose | Biology | https://en.wikipedia.org/wiki?curid=18409681 | WolfQuest | 140,039 |
WolfQuest At the end, you, your mate, and your surviving pups must make a journey for the summer den in the Douglas fir forests. But the player, the player's mate, and pups will run into grizzlies, coyotes, eagles and drowning. The only way pups can get across the river is by finding a shallow sandbar. Wolf territories will also expand, so the player cannot take an easy way out. In the game, players have the opportunity (though not a mandatory option) to raid a cattle ranch for extra food in the Night Mission. The player sneaks around in the dark at a cow ranch, and searches for the calf to kill and feed to his/her pups. However, doing so is extremely dangerous and can result in being shot - a warning that the player is close to being shot, is hearing dogs barking. The player has approximately a minute to find the calf and kill it and consume it. In multiplayer, the objectives of the game are the same with two exceptions. The player co-operates with a maximum of 8 wolves including themselves, and can have no game-sanctioned mate. (Regardless, some players still say that other players are their mates.) Public multiplayer games allow anyone to join. Private games require a game-name and password and allow text and voice chats. (Text chats are filtered through a standard badwords list.) Players are encouraged to report any behavior that breaks the multiplayer rules. Players in multiplayer can start rallies and hunt bull elk and moose. Bull elk have more meat than female elk and are many times harder to kill | Biology | https://en.wikipedia.org/wiki?curid=18409681 | WolfQuest | 140,040 |
WolfQuest Moose are far more difficult to hunt than any of the elk, and will take some time to kill, but the reward of meat is greater. Players may bite elk in the neck or back legs while hunting. "2.7" added a multiplayer mode to the Slough Creek mission arc, so players can raise pups together and journey to the rendezvous site. A new map was included with "2.7." Called Lost River, it depicts a fictional valley outside the boundaries of Yellowstone National Park and features both wilderness and urban areas. Humans have abandoned the valley but left clues about some sort of catastrophe. Players are left to speculate what might have happened. This map is available for both single-player and multiplayer games. In August 2010, held an "idea contest" via the Community Forum, which can be found here - Index page. The winner for the "Big Idea" section of the contest was Exiah, with her idea "Time and Weather", which affects hunting with weather and time. The winner for the "Game Enhancement" section was Cama, with his idea "I need a rest!", where players can make their wolves sit or lie down to regain stamina faster than they would standing still. "Survival of the Pack: Deluxe" was released on October 5, 2011 with several new features added to it, as well as "I need a rest", weather and time was also added. It includes both episodes: Amethyst Mountain and Slough Creek. Players can press "R" to sit, and pressing it again, to cause their wolf to lie down | Biology | https://en.wikipedia.org/wiki?curid=18409681 | WolfQuest | 140,041 |
WolfQuest The "Z" button will cause a dialogue box to appear, asking the player which time of day they would like to sleep until (Dawn, Day, Dusk, and Night). Weather includes snow: rain, lightning and fire, and affects scents seen in scent-view. Shortly after the "Survival of the Pack: Deluxe" release, the version, 2.5.1 came out on October 11, 2011, and was a minor bug fix update to "2.5" (which added weather effects, changing times of day, a new phrase chat, improved lexicon chat safeguards, and more). This version fixed bugs with female wolf choice in single-player, seeing other wolves sit and lie down in multi-player, and a few other minor bugs. Between 2011 and January 2014, there were no plans for further development for several years. originally planned to make an episode 3 and an episode 4, as stated in the site's frequently asked questions page, located at FAQ - WolfQuest. However, on November 28, 2011, the following was announced on the Community Forums: "We're glad so many people were so excited for the release of episode 2.5 (WolfQuest: Survival of the Pack Deluxe), and we're hoping everyone is enjoying it. But of course, along with a new release always comes the question: what's next?? As you all should be aware, development is determined by funding. While we continue to discuss possible options for expansion of the game and community, we (the Team) are not currently working on any new releases. If that changes, we will be sure to let you all know | Biology | https://en.wikipedia.org/wiki?curid=18409681 | WolfQuest | 140,042 |
WolfQuest Thank you all for playing the game and conversing on these forums; we hope to continue adding new forum content and game updates if more funding becomes available." In spring 2014, Eduweb announced that a tablet version of the game was under development, to be released in the near future. Development took more time than anticipated, and platform support was expanded to include Mac and Windows computer. This new version, called *"2.7", released in November 2015 for Mac and Windows and in September 2016 for phones and tablets. This version includes the entire game, plus many enhancements and new features. Following Eduweb's plans to continue with the project's development, the community forums and website will remain online and freely accessible for the foreseeable future, rendering the 2012 announcement null and void as of 2014. It has been stated that with strong sales of version 2.7, a third episode may be a possibility. On December 31st, 2016 the game dev announced that they were beginning work on another episode. There is currently no official release date (it was stated to be <nowiki>"not anytime soon"</nowiki>). In August 2017, Eduweb announced that development of *"3: Anniversary Edition" was underway. This new version, a complete remake and expansion of the original game, serves as the foundation for new chapters such as Tower Fall. Eduweb released the first episode as early access on July 25, 2019 for PC/Mac | Biology | https://en.wikipedia.org/wiki?curid=18409681 | WolfQuest | 140,043 |
WolfQuest 3: Anniversary Edition includes: On September 2006, The National Science Foundation awarded the Minnesota Zoo and Eduweb a US$508,253 informal education grant to develop "WolfQuest". This makes it the first video game funded by the National Science Foundation, under grant number 0610427. "WolfQuest" won a few awards at Unite 2008, a developer's conference. It received Special Recognition Awards in two different categories, Best Serious Game and Best Multiplayer. "WolfQuest" also won the Education Award from the Association of Zoos and Aquariums (AZA) and a Bronze MUSE Award from the American Association of Museums. "The Association of Zoos and Aquariums recognizes outstanding achievement in educational program design judging programs on their ability to promote conservation knowledge, attitudes and behavior, show innovation, and measure success." "WolfQuest" was cited by Senator Tom Coburn in his "Wastebook 2010" report about government spending: • The National Science Foundation (NSF) awarded over $600,000 to the Minnesota Zoo to create a wolf "avatar" video game called "WolfQuest." Eduweb released the first episode of Wolf Quest: Anniversary Edition (Amethyst Mountain) as early access for PC/Mac on 25th July, 2019 on Steam and itch.io. While in Early Access, Eduweb is updating the game frequently with more features, multiplayer, and ultimately the Slough Creek episode with pups. The mobile version will come after the game is completed on PC/Mac platforms | Biology | https://en.wikipedia.org/wiki?curid=18409681 | WolfQuest | 140,044 |
WolfQuest Also in development, new episode/map called Tower Fall which will continue life with pups. The Tower Fall expansion will be an in-game purchase (DLC) and released after WolfQuest: Anniversary Edition. | Biology | https://en.wikipedia.org/wiki?curid=18409681 | WolfQuest | 140,045 |
List of countries by forest area This article is a list of countries by forest area. Types of places listed include the entire planet, continents, regions, countries, provinces, states, and territories. Percentage data was calculated using information from the CIA's World Factbook 2011. | Biology | https://en.wikipedia.org/wiki?curid=18410438 | List of countries by forest area | 140,046 |
Power graph analysis In computational biology, power graph analysis is a method for the analysis and representation of complex networks. is the computation, analysis and visual representation of a power graph from a graph (networks). can be thought of as a lossless compression algorithm for graphs. It extends graph syntax with representations of cliques, bicliques and stars. Compression levels of up to 95% have been obtained for complex biological networks. Hypergraphs are a generalization of graphs in which edges are not just couples of nodes but arbitrary n-tuples. Power graphs are not another generalization of graphs, but instead a novel representation of graphs that proposes a shift from the "node and edge" language to one using cliques, bicliques and stars as primitives. Graphs are drawn with circles or points that represent nodes and lines connecting pairs of nodes that represent edges. Power graphs extend the syntax of graphs with power nodes, which are drawn as a circle enclosing nodes or "other power nodes", and power edges, which are lines between power nodes. Bicliques are two sets of nodes with an edge between every member of one set and every member of the other set. In a power graph, a biclique is represented as an edge between two power nodes. Cliques are a set of nodes with an edge between every pair of nodes. In a power graph, a clique is represented by a power node with a loop. Stars are a set of nodes with an edge between every member of that set and a single node outside the set | Biology | https://en.wikipedia.org/wiki?curid=18411966 | Power graph analysis | 140,047 |
Power graph analysis In a power graph, a star is represented by a power edge between a regular node and a power node. Given a graph formula_1 where formula_2 is the set of nodes and formula_3 is the set of edges, a power graph formula_4 is a graph defined on the power set formula_5 of power nodes connected to each other by power edges: formula_6. Hence power graphs are defined on the power set of nodes as well as on the power set of edges of the graph formula_7. The semantics of power graphs are as follows: if two power nodes are connected by a power edge, this means that all nodes of the first power node are connected to all nodes of the second power node. Similarly, if a power node is connected to itself by a power edge, this signifies that all nodes in the power node are connected to each other by edges. The following two conditions are required: The Fourier analysis of a function can be seen as a rewriting of the function in terms of harmonic functions instead of formula_8 pairs. This transformation changes the point of view from time domain to frequency domain and enables many interesting applications in signal analysis, data compression, and filtering. Similarly, Power Graph Analysis is a rewriting or decomposition of a network using bicliques, cliques and stars as primitive elements (just as harmonic functions for Fourier analysis). It can be used to analyze, compress and filter networks. There are, however, several key differences | Biology | https://en.wikipedia.org/wiki?curid=18411966 | Power graph analysis | 140,048 |
Power graph analysis First, in Fourier analysis the two spaces (time and frequency domains) are the same function space - but stricto sensu, power graphs are not graphs. Second, there is not a unique power graph representing a given graph. Yet a very interesting class of power graphs are minimal power graphs which have the least number of power edges and power nodes necessary to represent a given graph. In general, there is no unique minimal power graph for a given graph. In this example (right) a graph of four nodes and five edges admits two minimal power graphs of two power edges each. The main difference between these two minimal power graphs is the higher nesting level of the second power graph as well as a loss of symmetry with respect to the underlying graph. Loss of symmetry is only a problem in small toy examples since complex networks rarely exhibit such symmetries in the first place. Additionally, one can minimize the nesting level but even then, there is in general not a unique minimal power graph of minimal nesting level. The power graph greedy algorithm relies on two simple steps to perform the decomposition: The first step identifies candidate power nodes through a hierarchical clustering of the nodes in the network based on the similarity of their neighboring nodes. The similarity of two sets of neighbors is taken as the Jaccard index of the two sets. The second step performs a greedy search for possible power edges between candidate power nodes | Biology | https://en.wikipedia.org/wiki?curid=18411966 | Power graph analysis | 140,049 |
Power graph analysis Power edges abstracting the most edges in the original network are added first to the power graph. Thus bicliques, cliques and stars are incrementally replaced with power edges, until all remaining single edges are also added. Candidate power nodes that are not the end point of any power edge are ignored. Modular decomposition can be used to compute a power graph by using the strong modules of the modular decomposition. Modules in modular decomposition are groups of nodes in a graph that have identical neighbors. A Strong Module is a module that does not overlap with another module. However, in complex networks strong modules are more the exception than the rule. Therefore, the power graphs obtained through modular decomposition are far from minimality. The main difference between modular decomposition and power graph analysis is the emphasis of power graph analysis in decomposing graphs not only using modules of nodes but also modules of edges (cliques, bicliques). Indeed, power graph analysis can be seen as a loss-less simultaneous clustering of both nodes and edges. Power Graph Analysis has been shown to be useful for the analysis of several types of biological networks such as Protein-protein interaction networks, domain-peptide binding motifs, Gene regulatory networks and Homology/Paralogy networks. Also a network of significant disease-trait pairs have been recently visualized and analyzed with Power Graphs | Biology | https://en.wikipedia.org/wiki?curid=18411966 | Power graph analysis | 140,050 |
Power graph analysis Network compression, a new measure derived from Power Graphs, has been proposed as a quality measure for protein interaction networks. Power Graphs have been also applied to the analysis of drug-target-disease networks for Drug repositioning. Power Graphs have been applied to large-scale data in social networks, for community mining or for modeling author types. | Biology | https://en.wikipedia.org/wiki?curid=18411966 | Power graph analysis | 140,051 |
Arthur Galston Arthur W. Galston (April 21, 1920 – June 15, 2008) was an American botanist and bioethicist. As a plant biologist, Galston studied the effects of light on plant development. He identified riboflavin and other flavins as photoreceptors involved in phototropism, the bending of plants toward light, challenging the prevailing view that carotene was responsible. As a graduate student in 1943, Galston studied the use of 2,3,5-triiodobenzoic acid (TIBA) to encourage the flowering of soybeans, and noted that high levels had a defoliant effect. The British and U.S. military later developed TIBA into Agent Orange which was employed extensively in Malaya and Vietnam. Galston became a bioethicist, and spoke out against such uses of science. As chairman of Yale's botany department, Galston's ethical objections led President Nixon to end the use of Agent Orange. Galston was the youngest child of Hyman and Freda Galston. He grew up in a Jewish family in Brooklyn, impoverished during the Great Depression. Inspired by doctors like microbiologist Paul de Kruif but unable to afford medical school, Galston enrolled at Cornell's Agricultural College which was free for citizens of New York State. He played saxophone in jazz and swing bands to earn living expenses. Galston's original intention was to attend Cornell Veterinary School after his freshman year. However, under the influence of botany professor Loren C. Petry he came to love botany, turned down an acceptance to Cornell Veterinary School, and earned a B.S | Biology | https://en.wikipedia.org/wiki?curid=18417495 | Arthur Galston | 140,052 |
Arthur Galston in botany from Cornell instead in 1940. The University of Illinois offered Galston a teaching assistantship for graduate work, so he went to Champaign-Urbana to study botany and biochemistry. He worked with plant physiologist Harry J. Fuller and botanist Oswald Tippo. Fuller, although nominally his advisor, was sent to South America on war-related research and was unavailable much of the time. Galston completed his M.Sc. in 1942 and his Ph.D. in 1943. It was a wartime requirement that the doctorate be completed in three years. Galston's Ph.D. dissertation was titled "Physiology of flowering, with especial reference to floral initiation in soybeans" (1943). His research focused on finding a chemical means to make soybeans flower and fruit earlier, so that they could mature before the end of the growing season. He discovered both that 2,3,5-triiodobenzoic acid (TIBA) would speed up the flowering of soybeans. He also noted that in higher concentrations it would defoliate the soybeans by causing them to release ethylene. During World War II, the Imperial Japanese Army captured most of the world's rubber plantations in British Malaya, causing a natural rubber shortage for the Allied armies. Natural rubber came from the rubber tree, Hevea brasiliensis, a native of South America that was commercially grown in Southeast Asia. The United States government established a research program to develop synthetic rubber, and also encouraged research into botanical alternatives | Biology | https://en.wikipedia.org/wiki?curid=18417495 | Arthur Galston | 140,053 |
Arthur Galston Guayule, whose sap could be used to produce latex, was considered a possible substitute for rubber. Galston was recommended to James F. Bonner by H. E. Carter, and spent a year working with Bonner at Caltech in Pasadena, California to develop rubber tires from guayule. By the end of 1944, the U.S. had achieved success with synthetic, petroleum-based rubber, and interest in guayule research lessened. In July 1944, Galston was drafted into the U.S. Navy as an enlisted man. He ultimately served as Natural Resources officer in Naval Military Government on Okinawa until his discharge in 1946. After a year as an instructor at Yale University in 1946-1947, Galston returned to the California Institute of Technology to work with James Bonner as a senior research fellow. While at Caltech, Galston made an important discovery. He identified riboflavin as a photoreceptor involved in the bending of plants toward light. This overturned a commonly held belief that carotene was the photoreceptor involved in phototropism. In 1950 Galston accepted a Guggenheim Fellowship to spend a year working with Hugo Theorell at the Karolinska Institute in Stockholm, Sweden. Upon his return to Caltech in 1951, Galston became tenured as an associate professor. His supporters included Bonner and Frits Warmolt Went, both of whom were senior plant biology researchers at Caltech. He co-taught classes in biology with George Beadle, who was then chairman of the biology department | Biology | https://en.wikipedia.org/wiki?curid=18417495 | Arthur Galston | 140,054 |
Arthur Galston In 1955, Galston was offered a full professorship at Yale University by Oswald Tippo, chair of the botany department. In addition to a significant increase in salary and position, it was an opportunity for leadership in an expanding department. Yale, in New Haven, Connecticut, was also closer to family members in New York City and work opportunities for Galston's wife, Dale Judith Kuntz. Galston accepted the offer, and taught at Yale from 1955 onwards. At Yale, Galston continued to do research in the areas of auxin physiology, photobiology, plant hormones, protoplasts and polyamines. Using microspectrophotometric measurements, he was the first researcher to report that phytochromes were located in plant nuclei, a result that would be confirmed using molecular techniques over 30 years later. At Yale, increasing amounts of Galston's time were spent in administrative roles. He served as chair of the Departments of Botany and Biology, the university-wide Course of Study Committee, and the Committee on Teaching and Learning. He was also director of the Biological Sciences Division. Following mandatory retirement from the biology department in 1990, he became the Eaton Professor Emeritus in the Department of Molecular, Cellular and Developmental Biology as well as professor emeritus in the School of Forestry & Environmental Studies. He continued to lecture and write after his retirement, in his second career as a bioethicist | Biology | https://en.wikipedia.org/wiki?curid=18417495 | Arthur Galston | 140,055 |
Arthur Galston He was president of the Botanical Society of America and of the American Society of Plant Physiologists (1962-1963). Galston supervised 24 Ph.D. and 67 postdoctoral students from around the world. He authored more than 320 papers and several books on plant physiology, as well as co-editing two books on bioethics. In 1951, biological warfare scientists at Fort Detrick, Maryland began investigating defoliants based upon Galston's Ph.D. discoveries with TIBA. They eventually produced the toxic defoliant Agent Orange used by the British Air Force during the Malayan Emergency and the U.S. Air Force during the Vietnam War. Galston was deeply affected by this development of his research. In 1972, he described his viewpoint: While the United States government argued that herbicides like Agent Orange did not qualify as chemical weapons, Galston asserted that their use was a violation of the United Nations Resolution of December 5, 1966 against the wartime use of “asphyxiating, poisonous or other gases” and “analogous liquids, materials or devices”. He was clear about the devastating impact of their use on the environment, and warned of the likelihood that they were harmful to animals and humans as well as plants. Galston visited Vietnam and China, viewing the environmental damage in Vietnam first-hand. Beginning in 1965, Galston lobbied both his scientific colleagues and the government to stop using Agent Orange. Galston and U.S. geneticist Matthew S. Meselson appealed to the U. S | Biology | https://en.wikipedia.org/wiki?curid=18417495 | Arthur Galston | 140,056 |
Arthur Galston Department of Defense to investigate the human toxicology of Agent Orange. The research conducted by the Department of Defense led to the discovery that Agent Orange caused birth defects in laboratory rats. In 1971 this information led to U.S. President Richard M. Nixon banning the use of the substance. Later research showed that Agent Orange contained high levels of teratogenic dioxins. With Ethan Signer of MIT, Galston was one of the first two American scientists invited to visit the People's Republic of China. In 1971, he met Chou En-lai, then Prime Minister, as well as King Norodom Sihanouk of Cambodia, who then resided in Shanghai. The visit was reported in "The New York Times". Galston's experiences on visits to China led him to write "Daily life in people's China" (1973). Galston taught bioethics to Yale undergraduates from 1977 to 2004. In 2003-2004 his introductory bioethics course attracted 460 students, making it one of the most popular courses in Yale College. After his retirement as a biologist in 1990, he became affiliated with Yale's Institution for Social & Policy Studies, where he helped to found the Interdisciplinary Center for Bioethics. Galston also co-founded the National Senior Conservation Corps (Grey is Green), a non-profit organization dedicated to helping older Americans to create positive environmental change and lead more sustainable lives. In 1966, Galston successfully nominated Duke Ellington to receive an honorary doctorate from Yale | Biology | https://en.wikipedia.org/wiki?curid=18417495 | Arthur Galston | 140,057 |
Arthur Galston The Duke received the honor in 1967, but Galston was unable to attend, and did not meet him until 1972. died of congestive heart failure on June 15, 2008, in Hamden, Connecticut. | Biology | https://en.wikipedia.org/wiki?curid=18417495 | Arthur Galston | 140,058 |
Geysers on Mars Martian geysers (or jets) are putative sites of small gas and dust eruptions that occur in the south polar region of Mars during the spring thaw. "Dark dune spots" and "spiders" – or araneiforms – are the two most visible types of features ascribed to these eruptions. Martian geysers are distinct from geysers on Earth, which are typically associated with hydrothermal activity. These are unlike any terrestrial geological phenomenon. The reflectance (albedo), shapes and unusual spider appearance of these features have stimulated a variety of hypotheses about their origin, ranging from differences in frosting reflectance, to explanations involving biological processes. However, all current geophysical models assume some sort of jet or geyser-like activity on Mars. Their characteristics, and the process of their formation, are still a matter of debate. These features are unique to the south polar region of Mars in an area informally called the 'cryptic region', at latitudes 60° to 80° south and longitudes 150°W to 310°W; this 1 meter deep carbon dioxide (CO) ice transition area—between the scarps of the thick polar ice layer and the permafrost—is where clusters of the apparent geyser systems are located | Biology | https://en.wikipedia.org/wiki?curid=18418502 | Geysers on Mars | 140,059 |
Geysers on Mars The seasonal frosting and defrosting of carbon dioxide ice results in the appearance of a number of features, such dark dune spots with spider-like rilles or channels below the ice, where spider-like radial channels are carved between the ground and the carbon dioxide ice, giving it an appearance of spider webs, then, pressure accumulating in their interior ejects gas and dark basaltic sand or dust, which is deposited on the ice surface and thus, forming dark dune spots. This process is rapid, observed happening in the space of a few days, weeks or months, a growth rate rather unusual in geology – especially for Mars. However, it would seem that multiple years would be required to carve the larger spider-like channels. There is no direct data on these features other than images taken in the visible and infrared spectra. The geological features informally called dark dune spots and spiders were separately discovered on images acquired by the MOC camera on board the Mars Global Surveyor during 1998–1999. At first it was generally thought they were unrelated features because of their appearance, so from 1998 through 2000 they were reported separately on different research publications ( and -respectively). "Jet" or "geyser" models were proposed and refined from 2000 onwards. The name 'spiders' was coined by Malin Space Science Systems personnel, the developers of the camera. One of the first and most interesting spider photos was found by Greg Orme in October 2000 | Biology | https://en.wikipedia.org/wiki?curid=18418502 | Geysers on Mars | 140,060 |
Geysers on Mars The unusual shape and appearance of these 'spider webs' and spots caused a lot of speculation about their origin. The first years' surveillance showed that during the following Martian years, 70% of the spots appear at exactly the same place, and a preliminary statistical study obtained between September 1999 and March 2005, indicated that dark dune spots and spiders are related phenomena as functions of the cycle of carbon dioxide (CO) condensing as “dry ice” and sublimating. It was also initially suggested that the dark spots were simply warm patches of bare ground, but thermal imaging during 2006 revealed that these structures were as cold as the ice that covers the area, indicating they were a thin layer of dark material lying on top of the ice and kept chilled by it. However, soon after their first detection, they were discovered to be negative topographical features – i.e. radial troughs or channels of what today are thought to be geyser-like vent systems. The geysers' two most prominent features (dark dune spots and spider channels) appear at the beginning of the Martian spring on dune fields covered with carbon dioxide (CO or 'dry ice'), mainly at the ridges and slopes of the dunes; by the beginning of winter, they disappear. Dark spots' shape is generally round, on the slopes it is usually elongated, sometimes with streams—possibly of water—that accumulate in pools at the bottom of the dunes. Dark dune spots are typically 15 to 46 metres (50 to 150 feet) wide and spaced several hundred feet apart | Biology | https://en.wikipedia.org/wiki?curid=18418502 | Geysers on Mars | 140,061 |
Geysers on Mars The size of spots varies, and some are as small as 20 m across,—however, the smaller size seen is limited by imaging resolution—and can grow and coalesce into formations several kilometres wide. Spider features, when viewed individually, form a round lobed structure reminiscent of a spider web radiating outward in lobes from a central point. Its radial patterns represent shallow channels or ducts in the ice formed by the flow of the sublimation gas toward the vents. The entire spider channel network is typically 160–300 m across, although there are large variations. Each geyser's characteristic form appears to depend on a combination of such factors as local fluid or gas composition and pressure, ice thickness, underlying gravel type, local climate and meteorological conditions. The geysers' boundary does not seem to correlate with any other properties of the surface such as elevation, geological structure, slope, chemical composition or thermal properties. The geyser-like system produce low-albedo spots, fans and blotches, with small radial spider-like channel networks most often associated with their location. At first, the spots seem to be grey, but later their centres darken because they gradually get covered with dark ejecta, thought to be mainly basaltic sand. Not all dark spots observed in early spring are associated with spider landforms, however, a preponderance of dark spots and streaks on the cryptic terrain are associated with the appearance of spiders later in the season | Biology | https://en.wikipedia.org/wiki?curid=18418502 | Geysers on Mars | 140,062 |