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Ahmed (1919–1974) was a Kenyan elephant with unusually large tusks. He spent some of his time in the area of Mount Marsabit, and was the first elephant to be protected under Kenyan presidential decree. He was the subject of a Google Doodle on 6 December 2023. Little is known about Ahmed the elephant's early life, but he gained his reputation in the 1960s after being spotted by hikers in the Northern Kenya mountains. Known as “The King Of Marsabit,” spotters claimed Ahmed’s tusks were so large they scraped the ground. The legend took hold across Kenya. In 1970, Ahmed became the subject of many television projects, including an ABC series and a documentary. His rise in pop culture inspired school children to campaign for Ahmed’s protection from poachers. After they sent letters to Kenya’s first President Mzee Jomo Kenyatta, he placed Ahmed under his protection by Presidential Decree. Two professional hunters watched over him day and night to preserve his life. After Ahmed died of natural causes at age 55, Kenya celebrated his legacy. President Kenyatta ordered taxidermists to preserve Ahmed for future generations at the Nairobi National Museum. He can still be seen there today. == See also == Isilo (elephant) Satao (elephant) == References ==
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Ytterbium fluoride may refer to: Ytterbium(II) fluoride (ytterbium difluoride), YbF2 Ytterbium(III) fluoride (ytterbium trifluoride), YbF3
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"title": "Ytterbium fluoride"
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Attention or focus, is the concentration of awareness on some phenomenon to the exclusion of other stimuli. It is the selective concentration on discrete information, either subjectively or objectively. William James (1890) wrote that "Attention is the taking possession by the mind, in clear and vivid form, of one out of what seem several simultaneously possible objects or trains of thought. Focalization, concentration, of consciousness are of its essence." Attention has also been described as the allocation of limited cognitive processing resources. Attention is manifested by an attentional bottleneck, in terms of the amount of data the brain can process each second; for example, in human vision, less than 1% of the visual input data stream of 1MByte/sec can enter the bottleneck, leading to inattentional blindness. Attention remains a crucial area of investigation within education, psychology, neuroscience, cognitive neuroscience, and neuropsychology. Areas of active investigation involve determining the source of the sensory cues and signals that generate attention, the effects of these sensory cues and signals on the tuning properties of sensory neurons, and the relationship between attention and other behavioral and cognitive processes, which may include working memory and psychological vigilance. A relatively new body of research, which expands upon earlier research within psychopathology, is investigating the diagnostic symptoms associated with traumatic brain injury and its effects on attention. Attention also varies across cultures. For example, people from cultures that center around collectivism pay greater attention to the big picture in the image given to them, rather than specific elements of the image. On the other hand, those involved in more individualistic cultures tend to pay greater attention to the most noticeable portion of the image. The relationships between attention and consciousness are complex enough that they have warranted philosophical exploration. Such exploration is both ancient and continually relevant,
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as it can have effects in fields ranging from mental health and the study of disorders of consciousness to artificial intelligence and its domains of research. == Contemporary definition and research == Prior to the founding of psychology as a scientific discipline, attention was studied in the field of philosophy. Thus, many of the discoveries in the field of attention were made by philosophers. Psychologist John B. Watson calls Juan Luis Vives the father of modern psychology because, in his book De Anima et Vita (The Soul and Life), he was the first to recognize the importance of empirical investigation. In his work on memory, Vives found that the more closely one attends to stimuli, the better they will be retained. By the 1990s, psychologists began using positron emission tomography (PET) and later functional magnetic resonance imaging (fMRI) to image the brain while monitoring tasks involving attention. Considering this expensive equipment was generally only available in hospitals, psychologists sought cooperation with neurologists. Psychologist Michael Posner (then already renowned for his influential work on visual selective attention) and neurologist Marcus Raichle pioneered brain imaging studies of selective attention. Their results soon sparked interest from the neuroscience community, which until then had been focused on monkey brains. With the development of these technological innovations, neuroscientists became interested in this type of research that combines sophisticated experimental paradigms from cognitive psychology with these new brain imaging techniques. Although the older technique of electroencephalography (EEG) had long been used to study the brain activity underlying selective attention by cognitive psychophysiologists, the ability of the newer techniques to measure precisely localized activity inside the brain generated renewed interest by a wider community of researchers. A growing body of such neuroimaging research has identified a frontoparietal attention network which appears to be responsible for control of
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attention. A definition of a psychological construct forms a research approach to its study. In scientific works, attention often coincides and substitutes the notion of intentionality due to the extent of semantic uncertainty in the linguistic explanations of these notions' definitions. Intentionality has in turn been defined as "the power of minds to be about something: to represent or to stand for things, properties and states of affairs". Although these two psychological constructs (attention and intentionality) appear to be defined by similar terms, they are different notions. To clarify the definition of attention, it would be correct to consider the origin of this notion to review the meaning of the term given to it when the experimental study on attention was initiated. It is thought that the experimental approach began with famous experiments with a 4 x 4 matrix of sixteen randomly chosen letters – the experimental paradigm that informed Wundt's theory of attention. Wundt interpreted the experimental outcome introducing the meaning of attention as "that psychical process, which is operative in the clear perception of the narrow region of the content of consciousness." These experiments showed the physical limits of attention threshold, which were 3-6 letters observing the matrix during 1/10 s of their exposition. "We shall call the entrance into the large region of consciousness - apprehension, and the elevation into the focus of attention - apperception." Wundt's theory of attention postulated one of the main features of this notion that attention is an active, voluntary process realized during a certain time. In contrast, neuroscience research shows that intentionality may emerge instantly, even unconsciously; research reported to register neuronal correlates of an intentional act that preceded this conscious act (also see shared intentionality). Therefore, while intentionality is a mental state (“the power of the mind to be about
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something”, arising even unconsciously), the description of the construct of attention should be understood in the dynamical sense as the ability to elevate the clear perception of the narrow region of the content of consciousness and to keep in mind this state for a time. The attention threshold would be the period of minimum time needed for employing perception to clearly apprehend the scope of intention. From this perspective, a scientific approach to attention is relevant when it considers the difference between these two concepts (first of all, between their statical and dynamical statuses). The growing body of literature shows empirical evidence that attention is conditioned by the number of elements and the duration of exposition. Decades of research on subitizing have supported Wundt's findings about the limits of a human ability to concentrate awareness on a task. Latvian prof. Sandra Mihailova and prof. Igor Val Danilov drew an essential conclusion from the Wundtian approach to the study of attention: the scope of attention is related to cognitive development. As the mind grasps more details about an event, it also increases the number of reasonable combinations within that event, enhancing the probability of better understanding its features and particularity. For example, three items in the focal point of consciousness have six possible combinations (3 factorial), and four items have 24 (4 factorial) combinations. This number of combinations becomes significantly prominent in the case of a focal point with six items with 720 possible combinations (6 factorial). Empirical evidence suggests that the scope of attention in young children develops from two items in the focal point at age up to six months to five or more items in the focal point at age about five years. As follows from the most recent studies in relation to teaching activities in school, “attention”
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should be understood as “the state of concentration of an individual's consciousness on the process of selecting by his own psyche the information he requires and on the process of choosing an algorithm for response actions, which involves the intensification of sensory and intellectual activities”. == Selective and visual == In cognitive psychology there are at least two models which describe how visual attention operates. These models may be considered metaphors which are used to describe internal processes and to generate hypotheses that are falsifiable. Generally speaking, visual attention is thought to operate as a two-stage process. In the first stage, attention is distributed uniformly over the external visual scene and processing of information is performed in parallel. In the second stage, attention is concentrated to a specific area of the visual scene (i.e., it is focused), and processing is performed in a serial fashion. The first of these models to appear in the literature is the spotlight model. The term "spotlight" was inspired by the work of William James, who described attention as having a focus, a margin, and a fringe. The focus is an area that extracts information from the visual scene with a high-resolution, the geometric center of which being where visual attention is directed. Surrounding the focus is the fringe of attention, which extracts information in a much more crude fashion (i.e., low-resolution). This fringe extends out to a specified area, and the cut-off is called the margin. The second model is called the zoom-lens model and was first introduced in 1986. This model inherits all properties of the spotlight model (i.e., the focus, the fringe, and the margin), but it has the added property of changing in size. This size-change mechanism was inspired by the zoom lens one might find on a camera, and any
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change in size can be described by a trade-off in the efficiency of processing. The zoom-lens of attention can be described in terms of an inverse trade-off between the size of focus and the efficiency of processing: because attention resources are assumed to be fixed, then it follows that the larger the focus is, the slower processing will be of that region of the visual scene, since this fixed resource will be distributed over a larger area. It is thought that the focus of attention can subtend a minimum of 1° of visual angle, however the maximum size has not yet been determined. A significant debate emerged in the last decade of the 20th century in which Treisman's 1993 Feature Integration Theory (FIT) was compared to Duncan and Humphrey's 1989 attentional engagement theory (AET).: 5–7 FIT posits that "objects are retrieved from scenes by means of selective spatial attention that picks out objects' features, forms feature maps, and integrates those features that are found at the same location into forming objects." Treismans's theory is based on a two-stage process to help solve the binding problem of attention. These two stages are the preattentive stage and the focused attention stage. Preattentive Stage: The unconscious detection and separation of features of an item (color, shape, size). Treisman suggests that this happens early in cognitive processing and that individuals are not aware of the occurrence due to the counter intuitiveness of separating a whole into its part. Evidence shows that preattentive focuses are accurate due to illusory conjunctions. Focused Attention Stage: The combining of all feature identifiers to perceive all parts as one whole. This is possible through prior knowledge and cognitive mapping. When an item is seen within a known location and has features that people have knowledge of, then prior knowledge
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will help bring features all together to make sense of what is perceived. The case of R.M's damage to his parietal lobe, also known as Balint's syndrome, shows the incorporation of focused attention and combination of features in the role of attention. Through sequencing these steps, parallel and serial search is better exhibited through the formation of conjunctions of objects. Conjunctive searches, according to Treismans, are done through both stages in order to create selective and focused attention on an object, though Duncan and Humphrey would disagree. Duncan and Humphrey's AET understanding of attention maintained that "there is an initial pre-attentive parallel phase of perceptual segmentation and analysis that encompasses all of the visual items present in a scene. At this phase, descriptions of the objects in a visual scene are generated into structural units; the outcome of this parallel phase is a multiple-spatial-scale structured representation. Selective attention intervenes after this stage to select information that will be entered into visual short-term memory.": 5–7 The contrast of the two theories placed a new emphasis on the separation of visual attention tasks alone and those mediated by supplementary cognitive processes. As Rastophopoulos summarizes the debate: "Against Treisman's FIT, which posits spatial attention as a necessary condition for detection of objects, Humphreys argues that visual elements are encoded and bound together in an initial parallel phase without focal attention, and that attention serves to select among the objects that result from this initial grouping.": 8 == Neuropsychological model == In the twentieth century, the pioneering research of Lev Vygotsky and Alexander Luria led to the three-part model of neuropsychology defining the working brain as being represented by three co-active processes listed as Attention, Memory, and Activation. A.R. Luria published his well-known book The Working Brain in 1973 as a concise adjunct volume
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to his previous 1962 book Higher Cortical Functions in Man. In this volume, Luria summarized his three-part global theory of the working brain as being composed of three constantly co-active processes which he described as the; (1) Attention system, (2) Mnestic (memory) system, and (3) Cortical activation system. The two books together are considered by Homskaya's account as "among Luria's major works in neuropsychology, most fully reflecting all the aspects (theoretical, clinical, experimental) of this new discipline." The product of the combined research of Vygotsky and Luria have determined a large part of the contemporary understanding and definition of attention as it is understood at the start of the 21st-century. == Multitasking and divided attention == Multitasking can be defined as the attempt to perform two or more tasks simultaneously; however, research shows that when multitasking, people make more mistakes or perform their tasks more slowly. Attention must be divided among all of the component tasks to perform them. In divided attention, individuals attend or give attention to multiple sources of information at once or perform more than one task at the same time. Older research involved looking at the limits of people performing simultaneous tasks like reading stories, while listening and writing something else, or listening to two separate messages through different ears (i.e., dichotic listening). Generally, classical research into attention investigated the ability of people to learn new information when there were multiple tasks to be performed, or to probe the limits of our perception (cf. Donald Broadbent). There is also older literature on people's performance on multiple tasks performed simultaneously, such as driving a car while tuning a radio or driving while being on the phone. The vast majority of current research on human multitasking is based on performance of doing two tasks simultaneously, usually that involves
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driving while performing another task, such as texting, eating, or even speaking to passengers in the vehicle, or with a friend over a cellphone. This research reveals that the human attentional system has limits for what it can process: driving performance is worse while engaged in other tasks; drivers make more mistakes, brake harder and later, get into more accidents, veer into other lanes, and/or are less aware of their surroundings when engaged in the previously discussed tasks. There has been little difference found between speaking on a hands-free cell phone or a hand-held cell phone, which suggests that it is the strain of attentional system that causes problems, rather than what the driver is doing with his or her hands. While speaking with a passenger is as cognitively demanding as speaking with a friend over the phone, passengers are able to change the conversation based upon the needs of the driver. For example, if traffic intensifies, a passenger may stop talking to allow the driver to navigate the increasingly difficult roadway; a conversation partner over a phone would not be aware of the change in environment. There have been multiple theories regarding divided attention. One, conceived by cognitive scientist Daniel Kahneman, explains that there is a single pool of attentional resources that can be freely divided among multiple tasks. This model seems oversimplified, however, due to the different modalities (e.g., visual, auditory, verbal) that are perceived. When the two simultaneous tasks use the same modality, such as listening to a radio station and writing a paper, it is much more difficult to concentrate on both because the tasks are likely to interfere with each other. The specific modality model was theorized by Cognitive Psychologists David Navon and Daniel Gopher in 1979. However, more recent research using well controlled dual-task
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paradigms points at the importance of tasks. As an alternative, resource theory has been proposed as a more accurate metaphor for explaining divided attention on complex tasks. Resource theory states that as each complex task is automatized, performing that task requires less of the individual's limited-capacity attentional resources. Other variables play a part in our ability to pay attention to and concentrate on many tasks at once. These include, but are not limited to, anxiety, arousal, task difficulty, and skills. == Simultaneous == Simultaneous attention is a type of attention, classified by attending to multiple events at the same time. Simultaneous attention is demonstrated by children in Indigenous communities, who learn through this type of attention to their surroundings. Simultaneous attention is present in the ways in which children of indigenous backgrounds interact both with their surroundings and with other individuals. Simultaneous attention requires focus on multiple simultaneous activities or occurrences. This differs from multitasking, which is characterized by alternating attention and focus between multiple activities, or halting one activity before switching to the next. Simultaneous attention involves uninterrupted attention to several activities occurring at the same time. Another cultural practice that may relate to simultaneous attention strategies is coordination within a group. Indigenous heritage toddlers and caregivers in San Pedro were observed to frequently coordinate their activities with other members of a group in ways parallel to a model of simultaneous attention, whereas middle-class European-descent families in the U.S. would move back and forth between events. Research concludes that children with close ties to Indigenous American roots have a high tendency to be especially wide, keen observers. This points to a strong cultural difference in attention management. == Alternative topics and discussions == === Overt and covert orienting === Attention may be differentiated into "overt" versus "covert" orienting. Overt
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orienting is the act of selectively attending to an item or location over others by moving the eyes to point in that direction. Overt orienting can be directly observed in the form of eye movements. Although overt eye movements are quite common, there is a distinction that can be made between two types of eye movements; reflexive and controlled. Reflexive movements are commanded by the superior colliculus of the midbrain. These movements are fast and are activated by the sudden appearance of stimuli. In contrast, controlled eye movements are commanded by areas in the frontal lobe. These movements are slow and voluntary. Covert orienting is the act of mentally shifting one's focus without moving one's eyes. Simply, it is changes in attention that are not attributable to overt eye movements. Covert orienting has the potential to affect the output of perceptual processes by governing attention to particular items or locations (for example, the activity of a V4 neuron whose receptive field lies on an attended stimuli will be enhanced by covert attention) but does not influence the information that is processed by the senses. Researchers often use "filtering" tasks to study the role of covert attention of selecting information. These tasks often require participants to observe a number of stimuli, but attend to only one. The current view is that visual covert attention is a mechanism for quickly scanning the field of view for interesting locations. This shift in covert attention is linked to eye movement circuitry that sets up a slower saccade to that location. There are studies that suggest the mechanisms of overt and covert orienting may not be controlled separately and independently as previously believed. Central mechanisms that may control covert orienting, such as the parietal lobe, also receive input from subcortical centres involved in overt orienting.
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In support of this, general theories of attention actively assume bottom-up (reflexive) processes and top-down (voluntary) processes converge on a common neural architecture, in that they control both covert and overt attentional systems. For example, if individuals attend to the right hand corner field of view, movement of the eyes in that direction may have to be actively suppressed. Covert attention has been argued to reflect the existence of processes "programming explicit ocular movement". However, this has been questioned on the grounds that N2, "a neural measure of covert attentional allocation—does not always precede eye movements". However, the researchers acknowledge, "it may be impossible to definitively rule out the possibility that some kind of shift of covert attention precedes every shift of overt attention". === Exogenous and endogenous orienting === Orienting attention is vital and can be controlled through external (exogenous) or internal (endogenous) processes. However, comparing these two processes is challenging because external signals do not operate completely exogenously, but will only summon attention and eye movements if they are important to the subject. Exogenous (from Greek exo, meaning "outside", and genein, meaning "to produce") orienting is frequently described as being under control of a stimulus. Exogenous orienting is considered to be reflexive and automatic and is caused by a sudden change in the periphery. This often results in a reflexive saccade. Since exogenous cues are typically presented in the periphery, they are referred to as peripheral cues. Exogenous orienting can even be observed when individuals are aware that the cue will not relay reliable, accurate information about where a target is going to occur. This means that the mere presence of an exogenous cue will affect the response to other stimuli that are subsequently presented in the cue's previous location. Several studies have investigated the influence of valid
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and invalid cues. They concluded that valid peripheral cues benefit performance, for instance when the peripheral cues are brief flashes at the relevant location before the onset of a visual stimulus. Psychologists Michael Posner and Yoav Cohen (1984) noted a reversal of this benefit takes place when the interval between the onset of the cue and the onset of the target is longer than about 300 ms. The phenomenon of valid cues producing longer reaction times than invalid cues is called inhibition of return. Endogenous (from Greek endo, meaning "within" or "internally") orienting is the intentional allocation of attentional resources to a predetermined location or space. Simply stated, endogenous orienting occurs when attention is oriented according to an observer's goals or desires, allowing the focus of attention to be manipulated by the demands of a task. In order to have an effect, endogenous cues must be processed by the observer and acted upon purposefully. These cues are frequently referred to as central cues. This is because they are typically presented at the center of a display, where an observer's eyes are likely to be fixated. Central cues, such as an arrow or digit presented at fixation, tell observers to attend to a specific location. When examining differences between exogenous and endogenous orienting, some researchers suggest that there are four differences between the two kinds of cues: exogenous orienting is less affected by cognitive load than endogenous orienting; observers are able to ignore endogenous cues but not exogenous cues; exogenous cues have bigger effects than endogenous cues; and expectancies about cue validity and predictive value affects endogenous orienting more than exogenous orienting. There exist both overlaps and differences in the areas of the brain that are responsible for endogenous and exogenous orientating. Another approach to this discussion has been covered under
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the topic heading of "bottom-up" versus "top-down" orientations to attention. Researchers of this school have described two different aspects of how the mind focuses attention to items present in the environment. The first aspect is called bottom-up processing, also known as stimulus-driven attention or exogenous attention. These describe attentional processing which is driven by the properties of the objects themselves. Some processes, such as motion or a sudden loud noise, can attract our attention in a pre-conscious, or non-volitional way. We attend to them whether we want to or not. These aspects of attention are thought to involve parietal and temporal cortices, as well as the brainstem. More recent experimental evidence support the idea that the primary visual cortex creates a bottom-up saliency map, which is received by the superior colliculus in the midbrain area to guide attention or gaze shifts. The second aspect is called top-down processing, also known as goal-driven, endogenous attention, attentional control or executive attention. This aspect of our attentional orienting is under the control of the person who is attending. It is mediated primarily by the frontal cortex and basal ganglia as one of the executive functions. Research has shown that it is related to other aspects of the executive functions, such as working memory, and conflict resolution and inhibition. === Influence of processing load === A "hugely influential" theory regarding selective attention is the perceptual load theory, which states that there are two mechanisms that affect attention: cognitive and perceptual. The perceptual mechanism considers the subject's ability to perceive or ignore stimuli, both task-related and non task-related. Studies show that if there are many stimuli present (especially if they are task-related), it is much easier to ignore the non-task related stimuli, but if there are few stimuli the mind will perceive the irrelevant stimuli
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as well as the relevant. The cognitive mechanism refers to the actual processing of the stimuli. Studies regarding this showed that the ability to process stimuli decreased with age, meaning that younger people were able to perceive more stimuli and fully process them, but were likely to process both relevant and irrelevant information, while older people could process fewer stimuli, but usually processed only relevant information. Some people can process multiple stimuli, e.g. trained Morse code operators have been able to copy 100% of a message while carrying on a meaningful conversation. This relies on the reflexive response due to "overlearning" the skill of morse code reception/detection/transcription so that it is an autonomous function requiring no specific attention to perform. This overtraining of the brain comes as the "practice of a skill [surpasses] 100% accuracy," allowing the activity to become autonomic, while your mind has room to process other actions simultaneously. Based on the primary role of the perceptual load theory, assumptions regarding its functionality surrounding that attentional resources are that of limited capacity which signify the need for all of the attentional resources to be used. This performance, however, is halted when put hand in hand with accuracy and reaction time (RT). This limitation arises through the measurement of literature when obtaining outcomes for scores. This affects both cognitive and perceptual attention because there is a lack of measurement surrounding distributions of temporal and spatial attention. Only a concentrated amount of attention on how effective one is completing the task and how long they take is being analyzed making a more redundant analysis on overall cognition of being able to process multiple stimuli through perception. === Clinical model === Attention is best described as the sustained focus of cognitive resources on information while filtering or ignoring extraneous information. Attention
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is a very basic function that often is a precursor to all other neurological/cognitive functions. As is frequently the case, clinical models of attention differ from investigation models. One of the most used models for the evaluation of attention in patients with very different neurologic pathologies is the model of Sohlberg and Mateer. This hierarchic model is based in the recovering of attention processes of brain damage patients after coma. Five different kinds of activities of growing difficulty are described in the model; connecting with the activities those patients could do as their recovering process advanced. Focused attention: The ability to respond discretely to specific sensory stimuli. Sustained attention (vigilance and concentration): The ability to maintain a consistent behavioral response during continuous and repetitive activity. Selective attention: The ability to maintain a behavioral or cognitive set in the face of distracting or competing stimuli. Therefore, it incorporates the notion of "freedom from distractibility." Alternating attention: The ability of mental flexibility that allows individuals to shift their focus of attention and move between tasks having different cognitive requirements. Divided attention: This refers to the ability to respond simultaneously to multiple tasks or multiple task demands. This model has been shown to be very useful in evaluating attention in very different pathologies, correlates strongly with daily difficulties and is especially helpful in designing stimulation programs such as attention process training, a rehabilitation program for neurological patients of the same authors. == Other descriptors for types of attention == Mindfulness: Mindfulness has been conceptualized as a clinical model of attention. Mindfulness practices are clinical interventions that emphasize training attention functions. Vigilant attention: Remaining focused on a non-arousing stimulus or uninteresting task for a sustained period is far more difficult than attending to arousing stimuli and interesting tasks, and requires a specific type of
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attention called 'vigilant attention'. Thereby, vigilant attention is the ability to give sustained attention to a stimulus or task that might ordinarily be insufficiently engaging to prevent our attention being distracted by other stimuli or tasks. === Neural correlates === Most experiments show that one neural correlate of attention is enhanced firing. If a neuron has a different response to a stimulus when an animal is not attending to a stimulus, versus when the animal does attend to the stimulus, then the neuron's response will be enhanced even if the physical characteristics of the stimulus remain the same. In a 2007 review, Professor Eric Knudsen describes a more general model which identifies four core processes of attention, with working memory at the center: Working memory temporarily stores information for detailed analysis. Competitive selection is the process that determines which information gains access to working memory. Through top-down sensitivity control, higher cognitive processes can regulate signal intensity in information channels that compete for access to working memory, and thus give them an advantage in the process of competitive selection. Through top-down sensitivity control, the momentary content of working memory can influence the selection of new information, and thus mediate voluntary control of attention in a recurrent loop (endogenous attention). Bottom-up saliency filters automatically enhance the response to infrequent stimuli, or stimuli of instinctive or learned biological relevance (exogenous attention). Neurally, at different hierarchical levels spatial maps can enhance or inhibit activity in sensory areas, and induce orienting behaviors like eye movement. At the top of the hierarchy, the frontal eye fields (FEF) and the dorsolateral prefrontal cortex contain a retinocentric spatial map. Microstimulation in the FEF induces monkeys to make a saccade to the relevant location. Stimulation at levels too low to induce a saccade will nonetheless enhance cortical responses to
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stimuli located in the relevant area. At the next lower level, a variety of spatial maps are found in the parietal cortex. In particular, the lateral intraparietal area (LIP) contains a saliency map and is interconnected both with the FEF and with sensory areas. Exogenous attentional guidance in humans and monkeys is by a bottom-up saliency map in the primary visual cortex. In lower vertebrates, this saliency map is more likely in the superior colliculus (optic tectum). Certain automatic responses that influence attention, like orienting to a highly salient stimulus, are mediated subcortically by the superior colliculi. At the neural network level, it is thought that processes like lateral inhibition mediate the process of competitive selection. In many cases attention produces changes in the EEG. Many animals, including humans, produce gamma waves (40–60 Hz) when focusing attention on a particular object or activity. Another commonly used model for the attention system has been put forth by researchers such as Michael Posner. He divides attention into three functional components: alerting, orienting, and executive attention that can also interact and influence each other. Alerting is the process involved in becoming and staying attentive toward the surroundings. It appears to exist in the frontal and parietal lobes of the right hemisphere, and is modulated by norepinephrine. Orienting is the directing of attention to a specific stimulus. Executive attention is used when there is a conflict between multiple attention cues. It is essentially the same as the central executive in Baddeley's model of working memory. The Eriksen flanker task has shown that the executive control of attention may take place in the anterior cingulate cortex === Cultural variation === Children appear to develop patterns of attention related to the cultural practices of their families, communities, and the institutions in which they participate. In 1955,
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Jules Henry suggested that there are societal differences in sensitivity to signals from many ongoing sources that call for the awareness of several levels of attention simultaneously. He tied his speculation to ethnographic observations of communities in which children are involved in a complex social community with multiple relationships. Many Indigenous children in the Americas predominantly learn by observing and pitching in. There are several studies to support that the use of keen attention towards learning is much more common in Indigenous Communities of North and Central America than in a middle-class European-American setting. This is a direct result of the Learning by Observing and Pitching In model. Keen attention is both a requirement and result of learning by observing and pitching-in. Incorporating the children in the community gives them the opportunity to keenly observe and contribute to activities that were not directed towards them. It can be seen from different Indigenous communities and cultures, such as the Mayans of San Pedro, that children can simultaneously attend to multiple events. Most Maya children have learned to pay attention to several events at once in order to make useful observations. One example is simultaneous attention which involves uninterrupted attention to several activities occurring at the same time. Another cultural practice that may relate to simultaneous attention strategies is coordination within a group. San Pedro toddlers and caregivers frequently coordinated their activities with other members of a group in multiway engagements rather than in a dyadic fashion. Research concludes that children with close ties to Indigenous American roots have a high tendency to be especially keen observers. This learning by observing and pitching-in model requires active levels of attention management. The child is present while caretakers engage in daily activities and responsibilities such as: weaving, farming, and other skills necessary for survival.
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Being present allows the child to focus their attention on the actions being performed by their parents, elders, and/or older siblings. In order to learn in this way, keen attention and focus is required. Eventually the child is expected to be able to perform these skills themselves. In one study, it was found that when looking at a picture, Americans focus more on the center figure than Japanese do, especially after 1 second has passed. Japanese individuals spent larger amounts of time focusing on parts in the background. Miyamoto et al. compared pictures of landscapes in Japan and the US, noting that Japanese scenes contained more boundaries and edges than the American ones. === Modelling === In the domain of computer vision, efforts have been made to model the mechanism of human attention, especially the bottom-up intentional mechanism and its semantic significance in classification of video contents. Both spatial attention and temporal attention have been incorporated in such classification efforts. Generally speaking, there are two kinds of models to mimic the bottom-up salience mechanism in static images. One is based on the spatial contrast analysis. For example, a center–surround mechanism has been used to define salience across scales, inspired by the putative neural mechanism. It has also been hypothesized that some visual inputs are intrinsically salient in certain background contexts and that these are actually task-independent. This model has established itself as the exemplar for salience detection and consistently used for comparison in the literature; the other kind of model is based on the frequency domain analysis. This method was first proposed by Hou et al.. This method was called SR. Then, the PQFT method was also introduced. Both SR and PQFT only use the phase information. In 2012, the HFT method was introduced, and both the amplitude and the
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"page_id": 68753,
"source": null,
"title": "Attention"
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phase information are made use of. The Neural Abstraction Pyramid is a hierarchical recurrent convolutional model, which incorporates bottom-up and top-down flow of information to iteratively interpret images. === Hemispatial neglect === Hemispatial neglect, also called unilateral neglect, often occurs when people have damage to the right hemisphere of their brain. This damage often leads to a tendency to ignore the left side of one's body or even the left side of an object that can be seen. Damage to the left side of the brain (the left hemisphere) rarely yields significant neglect of the right side of the body or object in the person's local environments. The effects of spatial neglect, however, may vary and differ depending on what area of the brain was damaged. Damage to different neural substrates can result in different types of neglect. Attention disorders (lateralized and nonlaterized) may also contribute to the symptoms and effects. Much research has asserted that damage to gray matter within the brain results in spatial neglect. New technology has yielded more information, such that there is a large, distributed network of frontal, parietal, temporal, and subcortical brain areas that have been tied to neglect. This network can be related to other research as well; the dorsal attention network is tied to spatial orienting. The effect of damage to this network may result in patients neglecting their left side when distracted about their right side or an object on their right side. === Attention in social contexts === Social attention is one special form of attention that involves the allocation of limited processing resources in a social context. Previous studies on social attention often regard how attention is directed toward socially relevant stimuli such as faces and gaze directions of other individuals. In contrast to attending-to-others, a different line of
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"page_id": 68753,
"source": null,
"title": "Attention"
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researches has shown that self-related information such as own face and name automatically captures attention and is preferentially processed comparing to other-related information. These contrasting effects between attending-to-others and attending-to-self prompt a synthetic view in a recent Opinion article proposing that social attention operates at two polarizing states: In one extreme, individual tends to attend to the self and prioritize self-related information over others', and, in the other extreme, attention is allocated to other individuals to infer their intentions and desires. Attending-to-self and attending-to-others mark the two ends of an otherwise continuum spectrum of social attention. For a given behavioral context, the mechanisms underlying these two polarities might interact and compete with each other in order to determine a saliency map of social attention that guides our behaviors. An imbalanced competition between these two behavioral and cognitive processes will cause cognitive disorders and neurological symptoms such as autism spectrum disorders and Williams syndrome. === Distracting factors === According to Daniel Goleman's book, Focus: The Hidden Driver of Excellence, there are two types of distracting factors affecting focus – sensory and emotional. A sensory distracting factor would be, for example, while a person is reading this article, they are neglecting the white field surrounding the text. An emotional distracting factor would be when someone is focused on answering an email, and somebody shouts their name. It would be almost impossible to neglect the voice speaking it. Attention is immediately directed toward the source. Positive emotions have also been found to affect attention. Induction of happiness has led to increased response times and an increase in inaccurate responses in the face of irrelevant stimuli. Two possible theories as to why emotions might make one more susceptible to distracting stimuli is that emotions take up too much of one's cognitive resources and make
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{
"page_id": 68753,
"source": null,
"title": "Attention"
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it harder to control your focus of attention. The other theory is that emotions make it harder to filter out distractions, specifically with positive emotions due to a feeling of security. Another distracting factor to attention processes is insufficient sleep. Sleep deprivation is found to impair cognition, specifically performance in divided attention. Divided attention is possibly linked with the circadian processes. === Failure to attend === Inattentional blindness was first introduced in 1998 by Arien Mack and Irvic Rock. Their studies show that when people are focused on specific stimuli, they often miss other stimuli that are clearly present. Though actual blindness is not occurring here, the blindness that happens is due to the perceptual load of what is being attended to. Based on the experiment performed by Mack and Rock, Ula Finch and Nilli Lavie tested participants with a perceptual task. They presented subjects with a cross, one arm being longer than the other, for 5 trials. On the sixth trial, a white square was added to the top left of the screen. The results conclude that out of 10 participants, only 2 (20%) actually saw the square. This would suggest that when a higher focus was attended to the length of the crossed arms, the more likely someone would altogether miss an object that was in plain sight. Change blindness was first tested by Rensink and coworkers in 1997. Their studies show that people have difficulty detecting changes from scene to scene due to the intense focus on one thing, or lack of attention overall. This was tested by Rensink through a presentation of a picture, and then a blank field, and then the same picture but with an item missing. The results showed that the pictures had to be alternated back and forth a good number of
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{
"page_id": 68753,
"source": null,
"title": "Attention"
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times for participants to notice the difference. This idea is greatly portrayed in films that have continuity errors. Many people do not pick up on differences when in reality, the changes tend to be significant. == History of the study == === Philosophical period === Psychologist Daniel E. Berlyne credits the first extended treatment of attention to philosopher Nicolas Malebranche in his work "The Search After Truth". "Malebranche held that we have access to ideas, or mental representations of the external world, but not direct access to the world itself." Thus in order to keep these ideas organized, attention is necessary. Otherwise we will confuse these ideas. Malebranche writes in "The Search After Truth", "because it often happens that the understanding has only confused and imperfect perceptions of things, it is truly a cause of our errors.... It is therefore necessary to look for means to keep our perceptions from being confused and imperfect. And, because, as everyone knows, there is nothing that makes them clearer and more distinct than attentiveness, we must try to find the means to become more attentive than we are". According to Malebranche, attention is crucial to understanding and keeping thoughts organized. Philosopher Gottfried Wilhelm Leibniz introduced the concept of apperception to this philosophical approach to attention. Apperception refers to "the process by which new experience is assimilated to and transformed by the residuum of past experience of an individual to form a new whole." Apperception is required for a perceived event to become a conscious event. Leibniz emphasized a reflexive involuntary view of attention known as exogenous orienting. However, there is also endogenous orienting which is voluntary and directed attention. Philosopher Johann Friedrich Herbart agreed with Leibniz's view of apperception; however, he expounded on it in by saying that new experiences had to be
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"page_id": 68753,
"source": null,
"title": "Attention"
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tied to ones already existing in the mind. Herbart was also the first person to stress the importance of applying mathematical modeling to the study of psychology. Throughout the philosophical era, various thinkers made significant contributions to the field of attention studies, beginning with research on the extent of attention and how attention is directed. In the beginning of the 19th century, it was thought that people were not able to attend to more than one stimulus at a time. However, with research contributions by Sir William Hamilton, 9th Baronet this view was changed. Hamilton proposed a view of attention that likened its capacity to holding marbles. You can only hold a certain number of marbles at a time before it starts to spill over. His view states that we can attend to more than one stimulus at once. William Stanley Jevons later expanded this view and stated that we can attend to up to four items at a time. === 1860–1909 === This period of attention research took the focus from conceptual findings to experimental testing. It also involved psychophysical methods that allowed measurement of the relation between physical stimulus properties and the psychological perceptions of them. This period covers the development of attentional research from the founding of psychology to 1909. Wilhelm Wundt introduced the study of attention to the field of psychology. Wundt measured mental processing speed by likening it to differences in stargazing measurements. Astronomers in this time would measure the time it took for stars to travel. Among these measurements when astronomers recorded the times, there were personal differences in calculation. These different readings resulted in different reports from each astronomer. To correct for this, a personal equation was developed. Wundt applied this to mental processing speed. Wundt realized that the time it takes to
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"page_id": 68753,
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see the stimulus of the star and write down the time was being called an "observation error" but actually was the time it takes to switch voluntarily one's attention from one stimulus to another. Wundt called his school of psychology voluntarism. It was his belief that psychological processes can only be understood in terms of goals and consequences. Franciscus Donders used mental chronometry to study attention and it was considered a major field of intellectual inquiry by authors such as Sigmund Freud. Donders and his students conducted the first detailed investigations of the speed of mental processes. Donders measured the time required to identify a stimulus and to select a motor response. This was the time difference between stimulus discrimination and response initiation. Donders also formalized the subtractive method which states that the time for a particular process can be estimated by adding that process to a task and taking the difference in reaction time between the two tasks. He also differentiated between three types of reactions: simple reaction, choice reaction, and go/no-go reaction. Hermann von Helmholtz also contributed to the field of attention relating to the extent of attention. Von Helmholtz stated that it is possible to focus on one stimulus and still perceive or ignore others. An example of this is being able to focus on the letter u in the word house and still perceiving the letters h, o, s, and e. One major debate in this period was whether it was possible to attend to two things at once (split attention). Walter Benjamin described this experience as "reception in a state of distraction." This disagreement could only be resolved through experimentation. In 1890, William James, in his textbook The Principles of Psychology, remarked: Everyone knows what attention is. It is the taking possession by the mind,
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"page_id": 68753,
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"title": "Attention"
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in clear and vivid form, of one out of what seem several simultaneously possible objects or trains of thought. Focalization, concentration, of consciousness are of its essence. It implies withdrawal from some things in order to deal effectively with others, and is a condition which has a real opposite in the confused, dazed, scatterbrained state which in French is called distraction, and Zerstreutheit in German. James differentiated between sensorial attention and intellectual attention. Sensorial attention is when attention is directed to objects of sense, stimuli that are physically present. Intellectual attention is attention directed to ideal or represented objects; stimuli that are not physically present. James also distinguished between immediate or derived attention: attention to the present versus to something not physically present. According to James, attention has five major effects. Attention works to make us perceive, conceive, distinguish, remember, and shorten reactions time. === 1910–1949 === During this period, research in attention waned and interest in behaviorism flourished, leading some to believe, like Ulric Neisser, that in this period, "There was no research on attention". However, Jersild published very important work on "Mental Set and Shift" in 1927. He stated, "The fact of mental set is primary in all conscious activity. The same stimulus may evoke any one of a large number of responses depending upon the contextual setting in which it is placed". This research found that the time to complete a list was longer for mixed lists than for pure lists. For example, if a list was names of animals versus a list of the same size with names of animals, books, makes and models of cars, and types of fruits, it takes longer to process the second list. This is task switching. In 1931, Telford discovered the psychological refractory period. The stimulation of neurons is followed
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"page_id": 68753,
"source": null,
"title": "Attention"
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by a refractory phase during which neurons are less sensitive to stimulation. In 1935 John Ridley Stroop developed the Stroop Task which elicited the Stroop Effect. Stroop's task showed that irrelevant stimulus information can have a major impact on performance. In this task, subjects were to look at a list of colors. This list of colors had each color typed in a color different from the actual text. For example, the word Blue would be typed in Orange, Pink in Black, and so on. Example: Blue Purple Red Green Purple Green Subjects were then instructed to say the name of the ink color and ignore the text. It took 110 seconds to complete a list of this type compared to 63 seconds to name the colors when presented in the form of solid squares. The naming time nearly doubled in the presence of conflicting color words, an effect known as the Stroop Effect. === 1950–1974 === In the 1950s, research psychologists renewed their interest in attention when the dominant epistemology shifted from positivism (i.e., behaviorism) to realism during what has come to be known as the "cognitive revolution". The cognitive revolution admitted unobservable cognitive processes like attention as legitimate objects of scientific study. Modern research on attention began with the analysis of the "cocktail party problem" by Colin Cherry in 1953. At a cocktail party how do people select the conversation that they are listening to and ignore the rest? This problem is at times called "focused attention", as opposed to "divided attention". Cherry performed a number of experiments which became known as dichotic listening and were extended by Donald Broadbent and others.: 112 In a typical experiment, subjects would use a set of headphones to listen to two streams of words in different ears and selectively attend to one
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"page_id": 68753,
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stream. After the task, the experimenter would question the subjects about the content of the unattended stream. Broadbent's Filter Model of Attention states that information is held in a pre-attentive temporary store, and only sensory events that have some physical feature in common are selected to pass into the limited capacity processing system. This implies that the meaning of unattended messages is not identified. Also, a significant amount of time is required to shift the filter from one channel to another. Experiments by Gray and Wedderburn and later Anne Treisman pointed out various problems in Broadbent's early model and eventually led to the Deutsch–Norman model in 1968. In this model, no signal is filtered out, but all are processed to the point of activating their stored representations in memory. The point at which attention becomes "selective" is when one of the memory representations is selected for further processing. At any time, only one can be selected, resulting in the attentional bottleneck.: 115–116 This debate became known as the early-selection vs. late-selection models. In the early selection models (first proposed by Donald Broadbent), attention shuts down (in Broadbent's model) or attenuates (in Treisman's refinement) processing in the unattended ear before the mind can analyze its semantic content. In the late selection models (first proposed by J. Anthony Deutsch and Diana Deutsch), the content in both ears is analyzed semantically, but the words in the unattended ear cannot access consciousness. Lavie's perceptual load theory, however, "provided elegant solution to" what had once been a "heated debate". == See also == == References == == Further reading == "Attention" . Encyclopædia Britannica. Vol. III (9th ed.). 1878. p. 52. Goleman D (2013). Focus: The Hidden Driver of Excellence. Harper. ISBN 978-0062114860. Ward LM (2008). "PDF". Scholarpedia. 3 (10): 1538. doi:10.4249/scholarpedia.1538.
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"page_id": 68753,
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Pickled fruit refers to fruit that has been pickled. Pickling is the process of food preservation by either anaerobic fermentation in brine or immersion in vinegar. Many types of fruit are pickled. Some examples include peaches, apples, crabapples, pears, plums, grapes, currants, tomatoes and olives. Vinegar may also be prepared from fruit, such as apple cider vinegar. For thousands of years in many parts of the world, pickles have been used as the main method to preserve fruits and other foods. There is evidence that thousands of years ago in Mesopotamia, Egypt, Greece, Rome and China people pickled different foods for preservation. Mayan culture in America used tobacco to preserve food, specifically to make pickled peppers. In ancient times the different cultures used salt that was found naturally and water to make the brine, which they used to pickle foods that cannot be eaten naturally, such as olives and some grains. == Peaches == Pickled peaches may be prepared from medium-sized, non-melting clingstone peaches that are small-seeded. In the United States prior to around 1960, some were prepared from small, unripe freestone peaches. Flavour may be added to the pickle using 'sweet spices', such as cinnamon, cloves and allspice, or savoury pickling spices, such as peppercorns and coriander. Pickled peaches may be used to accompany meats and in salads, and also have other uses. == Pears == Pickled pears may be prepared with sugar, cinnamon, cloves and allspice to add flavor, and may be referred to as spiced pears. They may be prepared from underripe pears. Pickled pears may be used to accompany dishes such as roasts and salads, among others. == Grapes == To pickle grapes it is necessary to use white wine vinegar, water, kosher salt, sugar, cloves garlic, rosemary and dried chili flakes. Garlic, chili flakes and
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"page_id": 46402706,
"source": null,
"title": "Pickled fruit"
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some other species make grapes a unique flavor. == Cantaloupe == The cantaloupe is a summer season fruit, which can be pickled and refrigerated to be able to eat it during the rest of the year. The cantaloupe can be pickled using champagne vinegar, hot water, granulated sugar, ice, mustard seed, celery seed, Aleppo pepper and cinnamon stick. == List of pickled fruits == Pickled fruits == By country == In Malaysia, some fruits are pickled when they are unripe, such as belimbing, kedondong, chermai, lime, pineapple, papaya, mango and nutmeg. In Mexico, there are two phrases to describe a pickle: the term "escabechar" or "encurtir" is used when food is pickled by vinegar; whereas it is called "escabeche" or "salmuera" when salt is the main pickling agent. The word "vinegar" is of French origin (Vin - Aigre), comprising "vino-agrio" in Spanish and literally "wine-sour" in English. At its origin, vinegar was obtained as the result from the fermentation of wine which was sour. In Mexico, vinegar is obtained in large part from the fermentation of fruits such as pineapple and apple; people use this naturally sourced vinegar to pickle fruits and vegetables in the home. With many various peppers, the pickle pepper is very popular in Mexico — the pepper being one of the main products made both at home and by the pickling industry. Some states in Mexico such as Oaxaca and Puebla use homemade fermented pineapple-vinegar or sour brine to pickle fruits such as mangoes, membrillos and some cactus — the resulting pickles are then used as ingredients in traditional cooking. == See also == == References ==
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"page_id": 46402706,
"source": null,
"title": "Pickled fruit"
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Much insight in quantum mechanics can be gained from understanding the closed-form solutions to the time-dependent non-relativistic Schrödinger equation. It takes the form H ^ ψ ( r , t ) = [ − ℏ 2 2 m ∇ 2 + V ( r ) ] ψ ( r , t ) = i ℏ ∂ ψ ( r , t ) ∂ t , {\displaystyle {\hat {H}}\psi {\left(\mathbf {r} ,t\right)}=\left[-{\frac {\hbar ^{2}}{2m}}\nabla ^{2}+V{\left(\mathbf {r} \right)}\right]\psi {\left(\mathbf {r} ,t\right)}=i\hbar {\frac {\partial \psi {\left(\mathbf {r} ,t\right)}}{\partial t}},} where ψ {\displaystyle \psi } is the wave function of the system, H ^ {\displaystyle {\hat {H}}} is the Hamiltonian operator, and t {\displaystyle t} is time. Stationary states of this equation are found by solving the time-independent Schrödinger equation, [ − ℏ 2 2 m ∇ 2 + V ( r ) ] ψ ( r ) = E ψ ( r ) , {\displaystyle \left[-{\frac {\hbar ^{2}}{2m}}\nabla ^{2}+V{\left(\mathbf {r} \right)}\right]\psi {\left(\mathbf {r} \right)}=E\psi {\left(\mathbf {r} \right)},} which is an eigenvalue equation. Very often, only numerical solutions to the Schrödinger equation can be found for a given physical system and its associated potential energy. However, there exists a subset of physical systems for which the form of the eigenfunctions and their associated energies, or eigenvalues, can be found. These quantum-mechanical systems with analytical solutions are listed below. == Solvable systems == The two-state quantum system (the simplest possible quantum system) The free particle The one-dimensional potentials The particle in a ring or ring wave guide The delta potential The single delta potential The double-well delta potential The steps potentials The particle in a box / infinite potential well The finite potential well The step potential The rectangular potential barrier The triangular potential The quadratic potentials The quantum harmonic oscillator The quantum harmonic oscillator
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"page_id": 9505941,
"source": null,
"title": "List of quantum-mechanical systems with analytical solutions"
}
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with an applied uniform field The Inverse square root potential The periodic potential The particle in a lattice The particle in a lattice of finite length The Pöschl–Teller potential The quantum pendulum The three-dimensional potentials The rotating system The linear rigid rotor The symmetric top The particle in a spherically symmetric potential The hydrogen atom or hydrogen-like atom e.g. positronium The hydrogen atom in a spherical cavity with Dirichlet boundary conditions The Mie potential The Hooke's atom The Morse potential The Spherium atom Zero range interaction in a harmonic trap Multistate Landau–Zener models The Luttinger liquid (the only exact quantum mechanical solution to a model including interparticle interactions) == Solutions == == See also == List of quantum-mechanical potentials – a list of physically relevant potentials without regard to analytic solubility List of integrable models WKB approximation Quasi-exactly-solvable problems == References == == Reading materials == Mattis, Daniel C. (1993). The Many-Body Problem: An Encyclopedia of Exactly Solved Models in One Dimension. World Scientific. ISBN 978-981-02-0975-9.
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{
"page_id": 9505941,
"source": null,
"title": "List of quantum-mechanical systems with analytical solutions"
}
|
"The Parable of the Sunfish" is an anecdote with which Ezra Pound opens ABC of Reading, a 1934 work of literary criticism. Pound uses this anecdote to emphasize an empirical approach for learning about art, in contrast to relying on commentary rooted in abstraction. While the parable is based on students' recollections of Louis Agassiz's teaching style, Pound's retelling diverges from these sources in several respects. The parable has been used to illustrate the benefits of scientific thinking, but more recent literary criticism has split on whether the parable accurately reflects the scientific process and calls into question Pound's empirical approach to literature. == The Parable == The text of the parable below is excerpted from Pound's ABC of Reading. == Context == === ABC of Reading === Pound opens ABC of Reading with the following pronouncement: The proper METHOD for studying poetry and good letters is the method of contemporary biologists, that is careful first-hand examination of the matter, and continual COMPARISON of one 'slide' or specimen with another. No man is equipped for modern thinking until he has understood the anecdote of Agassiz and the sunfish.: 17, emphasis in original In the parable, a graduate student is sent to noted biologist Louis Agassiz to complete his education, and Agassiz asks the student three times to describe a sunfish specimen. The student replies with, in turn, the common name of the fish, a brief summary of the species, and a four-page essay on the species. Agassiz finally tells the student to "look at the fish" and "[a]t the end of three weeks the fish was in an advanced state of decomposition, but the student knew something about it.": 18 The text of the parable itself spans 131 words over sixteen lines and is often reproduced in full when cited.
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"page_id": 36506774,
"source": null,
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Pound contrasts this empiricism against knowledge gained through increasingly abstract definitions. As an example, Pound relates what might happen if a European is asked to define "red". After the initial response that red is a color, Pound imagines asking for a definition of color and having it described in terms of vibration, with vibration then defined in terms of energy, and that successive abstractions eventually reach a level where language has lost its power.: 19 Returning to empiricism, Pound reminds the reader that the progress of science increased rapidly once "Bacon had suggested the direct examination of phenomena, and after Galileo and others had stopped discussing things so much, and had begun really to look at them".: 20 Pound provides several other examples of the same contrasting ideas throughout the first chapter, ranging over topics as diverse as chemistry, Chinese writing, and Stravinsky. At the end of the chapter he summarizes his argument by claiming abstraction does not expand knowledge.: 26 === Literary essays === Pound subsequently refers to the parable in two essays: "The Teacher's Mission" and "Mr Housman at Little Bethel". Both were republished in The Literary Essays of Ezra Pound and reference Agassiz without including details of the parable. "The Teacher's Mission" in particular provides a straightforward explanation of how Pound wished the parable to be interpreted. ==== "Mr Housman at Little Bethel" ==== In January 1934, Pound published a critique of A. E. Housman's The Name and Nature of Poetry in the Criterion. As part of the critique, Pound offers an emendation to Housman's claim that "the intelligence" of the eighteenth century involved "some repressing and silencing of poetry".: 68 Pound replies that the root cause was the tendency towards abstract statements, which came about in part because eighteenth century authors "hadn't heard about Professor Agassiz's
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{
"page_id": 36506774,
"source": null,
"title": "Parable of the Sunfish"
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fish.": 68 ==== "The Teacher's Mission" ==== Also in 1934, Pound published an essay critiquing existing methods for teaching literature in general and university-level instruction methods in particular. He identifies the root of the problem as abstraction and uses the word "liberty" as an example of a term where a specific, concrete meaning has been lost. Pound finds this situation "inexcusable AFTER the era of 'Agassiz and the fish'" and demands an approach to general education that "parallels ... biological study based on EXAMINATION and COMPARISON of particular specimens.": 60, emphasis in original == Sources == Louis Agassiz was a Swiss-born scientist at Harvard University who, by 1896, had established a reputation for "lock[ing] a student up in a room full of turtle-shells, or lobster-shells, or oyster-shells, without a book or a word to help him, and not let[ting] him out till he had discovered all the truths which the objects contained." Several students of Agassiz who went on to prominence recorded this rite of passage, including Henry Blake, David Starr Jordan, Addison Emery Verrill, and Burt Green Wilder. American literary critic Robert Scholes traces the parable's source to two narratives in particular: those of former students Nathaniel Southgate Shaler and Samuel Hubbard Scudder. Their anecdotes were reprinted in Lane Cooper's Louis Agassiz as a Teacher: Illustrative Extracts on his Method of Instruction.: 655–6 Their separate accounts differ markedly from Pound's: both students provide oral reports with a wealth of detail after being initially forbidden from consulting outside sources. === Shaler's Autobiography === Nathaniel Shaler left his humanist studies and joined Agassiz's lab at Harvard University, having already read Agassiz's introductory essay on classification. His autobiography details his initial interactions with Agassiz. With regard to his first assignment, Shaler recorded that Agassiz brought him a small fish to study with
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"page_id": 36506774,
"source": null,
"title": "Parable of the Sunfish"
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the stipulation that Shaler not discuss it with anyone or read anything on the topic until Agassiz had given him permission. When Shaler asked Agassiz for more explicit instructions, Agassiz replied that he could not be more explicit than saying "[f]ind out what you can without damaging the specimen".: 98 After the first hours, Shaler thought he had "compassed that fish," but despite Agassiz always being "within call" he was not asked to present his conclusions.: 98 During the course of the following week, Shaler recorded the details of "how the scales went in series, their shape, the form and placement of the teeth, etc.": 98 At length on the seventh day, came the question "Well?" and my disgorge of learning to him as he sat on the edge of my table puffing his cigar. At the end of the hour's telling, he swung off and away, saying "That is not right.": 98 Shaler concluded Agassiz was testing him to see if he was capable of "doing hard, continuous work without the support of a teacher" and redoubled his efforts, starting from scratch and, over the course of seven ten-hour days, managed to describe the specimen to Agassiz's satisfaction.: 99 === Scudder's "Look at your fish!" === Samuel Hubbard Scudder recorded a similar experience, first published in 1874 as "Look at Your Fish" in Every Saturday magazine. Agassiz again starts his new student off with a fish preserved in alcohol and instructs the student to "look at it", and promises "by and by I will ask what you have seen".: 2 As opposed to Pound's decomposing sunfish, Scudder's account emphasizes the care taken to keep the specimen in good condition: I was to keep the fish before me in a tin tray, and occasionally moisten the surface with alcohol from
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{
"page_id": 36506774,
"source": null,
"title": "Parable of the Sunfish"
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the jar ... In ten minutes I had seen all that could be seen in that fish, and started in search of the Professor – who had, however, left the Museum; and when I returned, after lingering over some of the odd animals stored in the upper apartment, my specimen was dry all over. I dashed the fluid over the fish as if to resuscitate the beast from a fainting fit, and looked with anxiety for a return of the normal sloppy appearance. This little excitement over, nothing was done but to return to a steadfast gaze at my mute companion.: 2 Scudder provides the additional detail that "instruments of all kinds were interdicted", including any magnifying glass.: 3 After several hours Agassiz asks for a report and Scudder describes "the fringed gill-arches and moveable operculum; the pores of the head, fleshy lips and lidless eyes; the lateral line, the spinous fins and forked tail; the compressed and arched body".: 3 Disappointed, Agassiz informs his student that he has failed to observe "the most conspicuous features of the animal" and commands him to "look again, look again!": 3 The mortified Scudder is eventually asked to consider overnight what he has seen, and is able to report to Agassiz the following morning that "the fish has symmetrical sides with paired organs", which was the observation Agassiz was looking for.: 4 However, when Scudder then asked what he should do next, Agassiz replied, "Oh, look at your fish!" which Scudder did for another two full days.: 4 === Cooper's Louis Agassiz as a Teacher === In 1917, English professor Lane Cooper from Cornell University published a collection of reminiscences of Agassiz. The book included notes from several notable contributors, including Scudder and Cooper, William James, Professor Addison Emery Verrill ("[Agassiz's] plan was
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"page_id": 36506774,
"source": null,
"title": "Parable of the Sunfish"
}
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to make young students depend on natural objects rather than on statements in books"),: 27 and Professor Edward S. Morse, who wrote that Agassiz's method was "simply to let the student study intimately one object at a time.": 48 (footnote) Cooper prefigures Pound's interest by remarking on the "close, though not obvious, relation between investigation in biology or zoology and the observation and comparison of these organic forms which we call form of literature and works of art",: 2–3 concluding that "We study a poem, the work of man's art, in the same way that Agassiz made Shaler study a fish.": 4 Critic Robert Scholes concludes that Pound had access to this book and used the material within it as the source for the parable that opens ABC of Reading.: 655–6 == Interpretation and criticism == === Agassiz === Science historian Mary P. Winsor provides extensive commentary on Agassiz's initial assignments for his students. The solution to the "riddle",: 14 as she calls it, lies in a similar anecdote given by Agassiz in his Essay on Classification:Suppose that the innumerable articulated animals, which are counted by tens of thousands, nay, perhaps by hundreds of thousands, had never made their appearance upon the surface of the globe, with one single exception: that, for instance, our Lobster (Homarus americanus) were the only representative of that extraordinarily diversified type,—how should we introduce that species of animals in our systems?: 5, quoted in : 14–15 Agassiz provides several potential solutions: the species of lobster could have a single genus "by the side of all the other classes with their orders, families, etc.",: 5 or a family with one genus and one species, or a class with one order and one genus, etc. Agassiz concludes a single species is sufficient to derive the entirety of
|
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"page_id": 36506774,
"source": null,
"title": "Parable of the Sunfish"
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the hierarchy: at the time, this would have been "a distinct genus, a distinct family, a distinct class, a distinct branch.": 7–8 The point of the sunfish is not observing characteristics that distinguish individuals, species and genus, but rather characteristics that are held in common higher up the taxonomic hierarchy. Scudder's observation that finally satisfies Agassiz is that the sunfish has bilateral, paired organs; a characteristic that Winsor notes is common to all vertebrates.: 14 === Pound === Pound, echoing Cooper, opens ABC of Reading by stating that the correct method for the study of poetry is "the method of contemporary biologists" and that "No man is equipped for modern thinking until he has understood the anecdote of Agassiz and the fish." Commentators have summarized Pound's position with the term empiricism, but have divided over whether the parable endorses or indicts the idea. The simplest interpretations in scientific writing, history of science, and literary criticism take the parable at face value, accepting empiricism and observation as legitimate techniques. For example, when writing about stellar atmospheres, Dimitri Mihalas states that "it is specimens, not facts, that are the ultimate empirical currency that we must use if we wish to purchase a valid theory" before beginning a discussion of Pound's sunfish.: emphasis in original Moving from acceptance of empiricism to an understanding of its limitations, Christopher Tilley emphasizes in his comments on "scientific archeology" that Pound's student "was not simply learning about 'reality', the sunfish, but a way of approaching that reality – a discourse bound up in a particular thought tradition (empiricism)".: 76 Robert Scholes reaches a similar conclusion, noting that the student "seems to be reporting about a real and solid world in a perfectly transparent language, but actually he is learning how to produce a specific kind of discourse,
|
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"page_id": 36506774,
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controlled by a particular scientific paradigm".: 654 Author Bob Perelman takes the suspicion of empiricism one step further in his 1994 The Trouble With Genius: Reading Pound, Joyce, Stein, and Zukofsky. Perelman discusses the parable as one of two anecdotes in ABC of Reading that frame Pound's discussion of Chinese ideograms. The former describes attendance at two hypothetical concerts: one of Debussy and another of Ravel. Pound states that a person who attended both concerts knows more about the composers than someone who has only read "ALL of the criticisms that have ever been written of both".: 24, emphasis in original Perelman considers the contradiction between "everyone" and "knowledge" to be the key to Pound's thinking: only a gifted or lucky few are able to apprehend the truth (whether by attending the concert or observing the specimen); the rest can only make do with "a fog of clichés, received ideas, second-hand and second-rate opinions, written darkness.": 52 With regard to the parable, Perelman observes the lack of "scientific institutions, pedagogic procedures, or communicable terminologies" where any mediating written descriptions ("sunfish", "diplodokus") only serve to obscure knowledge. Knowledge ultimately resides within Agassiz rather than the world, and "[w]hat looks initially like a commitment to empiricism has led instead to an authoritarian idealism.": 53 Two critics have also commented on the parable's implications in describing the nature of knowledge in terms of the decay of Pound's fish. Celeste Goodridge notes that Marianne Moore's 1934 review of Pound's Cantos uses a detailed metaphor of a grasshopper wing to describe the conversations therein. In Goodridge's opinion, Moore's "microscopic examination" both undercuts the work as well as "pays homage, in its precision, to Pound's reverence for 'the applicability of scientific method to literary criticism.'": 73 Goodridge then reproduces the parable in full and comments, "Agassiz
|
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"page_id": 36506774,
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"title": "Parable of the Sunfish"
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teaches Pound that all knowledge is necessarily fragmented and does not constitute a whole.": 74 Knowledge of the fish cannot begin until decay has commenced, reducing the specimen to its constituent parts. Peter Nicholas Baker reaches a fundamentally different conclusion. He begins the discussion of the parable by first quoting Pound on the topic of genius: The genius can pay in nugget and in lump gold; it is not necessary that he bring up his knowledge into the mint of consciousness, stamp it either into the coin of conscientiously analyzed form-detail knowledge or into the paper money of words before he transmit it.: emphasis in original Baker finds the most striking feature of the parable to be the absence of description of the fish. Baker asks: "Do readers of this anecdote learn about the fish, or rather about a certain kind of authoritarian teaching practice?": 79 Baker claims that Pound's images of coining metal are just as unrealistic as his ideas regarding science and the scientific method. The reader, following Pound's student, reaches knowledge through intuition alone; the decomposing fish, so far as epistemology is concerned, has become "transparent".: 80 == Notes == == References ==
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The following is a partial list of the "C" codes for Medical Subject Headings (MeSH), as defined by the United States National Library of Medicine (NLM). This list continues the information at List of MeSH codes (C15). Codes following these are found at List of MeSH codes (C17). For other MeSH codes, see List of MeSH codes. The source for this content is the set of 2006 MeSH Trees from the NLM. == MeSH C16 – congenital, hereditary, and neonatal diseases and abnormalities == === MeSH C16.131 – abnormalities === ==== MeSH C16.131.042 – abnormalities, drug-induced ==== ==== MeSH C16.131.077 – abnormalities, multiple ==== MeSH C16.131.077.065 – Alagille syndrome MeSH C16.131.077.095 – Angelman syndrome MeSH C16.131.077.112 – Bardet–Biedl syndrome MeSH C16.131.077.130 – basal-cell nevus syndrome MeSH C16.131.077.133 – Beckwith–Wiedemann syndrome MeSH C16.131.077.137 – Bloom syndrome MeSH C16.131.077.208 – branchio-oto-renal syndrome MeSH C16.131.077.250 – Cockayne syndrome MeSH C16.131.077.262 – cri du chat syndrome MeSH C16.131.077.272 – De Lange syndrome MeSH C16.131.077.327 – Down syndrome MeSH C16.131.077.350 – ectodermal dysplasia MeSH C16.131.077.350.398 – Ellis–van Creveld syndrome MeSH C16.131.077.350.424 – focal dermal hypoplasia MeSH C16.131.077.350.712 – neurocutaneous syndromes MeSH C16.131.077.393 – Gardner's syndrome MeSH C16.131.077.410 – holoprosencephaly MeSH C16.131.077.445 – incontinentia pigmenti MeSH C16.131.077.509 – Laurence–Moon syndrome MeSH C16.131.077.525 – Leopard syndrome MeSH C16.131.077.550 – Marfan syndrome MeSH C16.131.077.578 – Möbius syndrome MeSH C16.131.077.606 – nail–patella syndrome MeSH C16.131.077.661 – oculocerebrorenal syndrome MeSH C16.131.077.677 – orofaciodigital syndromes MeSH C16.131.077.703 – POEMS syndrome MeSH C16.131.077.730 – Prader–Willi syndrome MeSH C16.131.077.740 – proteus syndrome MeSH C16.131.077.745 – prune belly syndrome MeSH C16.131.077.790 – rubella syndrome, congenital MeSH C16.131.077.804 – Rubinstein–Taybi syndrome MeSH C16.131.077.850 – Short rib – polydactyly syndrome MeSH C16.131.077.860 – Smith–Lemli–Opitz syndrome MeSH C16.131.077.938 – Waardenburg syndrome MeSH C16.131.077.951 – Wolfram syndrome MeSH C16.131.077.970 – Zellweger syndrome ==== MeSH C16.131.080 – abnormalities, radiation-induced
|
{
"page_id": 5115037,
"source": null,
"title": "List of MeSH codes (C16)"
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|
==== ==== MeSH C16.131.240 – cardiovascular abnormalities ==== MeSH C16.131.240.110 – arterio-arterial fistula MeSH C16.131.240.150 – arteriovenous malformations MeSH C16.131.240.150.125 – arteriovenous fistula MeSH C16.131.240.150.295 – intracranial arteriovenous malformations MeSH C16.131.240.275 – central nervous system vascular malformations MeSH C16.131.240.400 – heart defects, congenital MeSH C16.131.240.400.090 – aortic coarctation MeSH C16.131.240.400.145 – arrhythmogenic right ventricular dysplasia MeSH C16.131.240.400.200 – cor triatriatum MeSH C16.131.240.400.210 – coronary vessel anomalies MeSH C16.131.240.400.220 – crisscross heart MeSH C16.131.240.400.280 – dextrocardia MeSH C16.131.240.400.280.500 – Kartagener syndrome MeSH C16.131.240.400.340 – ductus arteriosus, patent MeSH C16.131.240.400.395 – Ebstein's anomaly MeSH C16.131.240.400.450 – Eisenmenger complex MeSH C16.131.240.400.560 – heart septal defects MeSH C16.131.240.400.560.098 – aortopulmonary septal defect MeSH C16.131.240.400.560.350 – endocardial cushion defects MeSH C16.131.240.400.560.375 – heart septal defects, atrial MeSH C16.131.240.400.560.375.518 – Lutembacher's syndrome MeSH C16.131.240.400.560.375.702 – Trilogy of Fallot MeSH C16.131.240.400.560.540 – heart septal defects, ventricular MeSH C16.131.240.400.625 – hypoplastic left heart syndrome MeSH C16.131.240.400.685 – Leopard syndrome MeSH C16.131.240.400.701 – levocardia MeSH C16.131.240.400.720 – Marfan syndrome MeSH C16.131.240.400.849 – Tetralogy of Fallot MeSH C16.131.240.400.915 – transposition of great vessels MeSH C16.131.240.400.915.300 – double outlet right ventricle MeSH C16.131.240.400.920 – tricuspid atresia MeSH C16.131.240.400.929 – truncus arteriosus, persistent MeSH C16.131.240.670 – pulmonary atresia MeSH C16.131.240.700 – scimitar syndrome ==== MeSH C16.131.260 – chromosome disorders ==== MeSH C16.131.260.040 – Angelman syndrome MeSH C16.131.260.080 – Beckwith–Wiedemann syndrome MeSH C16.131.260.090 – branchio-oto-renal syndrome MeSH C16.131.260.190 – cri du chat syndrome MeSH C16.131.260.210 – De Lange syndrome MeSH C16.131.260.260 – Down syndrome MeSH C16.131.260.380 – holoprosencephaly MeSH C16.131.260.700 – Prader–Willi syndrome MeSH C16.131.260.790 – Rubinstein–Taybi syndrome MeSH C16.131.260.800 – sex chromosome disorders MeSH C16.131.260.800.240 – ectodermal dysplasia MeSH C16.131.260.800.240.350 – focal dermal hypoplasia MeSH C16.131.260.800.300 – fragile X syndrome MeSH C16.131.260.800.340 – gonadal dysgenesis, 46,xy MeSH C16.131.260.800.345 – gonadal dysgenesis, mixed MeSH C16.131.260.800.490 – Klinefelter syndrome MeSH C16.131.260.800.670 – orofaciodigital syndromes
|
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"page_id": 5115037,
"source": null,
"title": "List of MeSH codes (C16)"
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MeSH C16.131.260.800.870 – Turner syndrome MeSH C16.131.260.940 – WAGR syndrome MeSH C16.131.260.970 – Williams syndrome ==== MeSH C16.131.300 – DiGeorge syndrome ==== ==== MeSH C16.131.314 – digestive system abnormalities ==== MeSH C16.131.314.094 – anus, imperforate MeSH C16.131.314.125 – biliary atresia MeSH C16.131.314.184 – choledochal cyst MeSH C16.131.314.184.500 – Caroli disease MeSH C16.131.314.244 – diaphragmatic eventration MeSH C16.131.314.330 – esophageal atresia MeSH C16.131.314.439 – Hirschsprung's disease MeSH C16.131.314.466 – intestinal atresia MeSH C16.131.314.556 – Meckel's diverticulum ==== MeSH C16.131.384 – eye abnormalities ==== MeSH C16.131.384.079 – aniridia MeSH C16.131.384.079.950 – WAGR syndrome MeSH C16.131.384.159 – anophthalmos MeSH C16.131.384.190 – blepharophimosis MeSH C16.131.384.282 – coloboma MeSH C16.131.384.405 – ectopia lentis MeSH C16.131.384.480 – hydrophthalmos MeSH C16.131.384.666 – microphthalmos MeSH C16.131.384.784 – retinal dysplasia ==== MeSH C16.131.482 – lymphatic abnormalities ==== MeSH C16.131.482.500 – lymphangiectasis, intestinal ==== MeSH C16.131.581 – monsters ==== MeSH C16.131.581.197 – anencephaly MeSH C16.131.581.806 – twins, conjoined ==== MeSH C16.131.621 – musculoskeletal abnormalities ==== MeSH C16.131.621.077 – arthrogryposis MeSH C16.131.621.207 – craniofacial abnormalities MeSH C16.131.621.207.207 – cleidocranial dysplasia MeSH C16.131.621.207.231 – craniofacial dysostosis MeSH C16.131.621.207.231.427 – Hallermann's syndrome MeSH C16.131.621.207.231.480 – hypertelorism MeSH C16.131.621.207.231.576 – mandibulofacial dysostosis MeSH C16.131.621.207.231.576.410 – goldenhar syndrome MeSH C16.131.621.207.240 – craniosynostoses MeSH C16.131.621.207.240.100 – acrocephalosyndactylia MeSH C16.131.621.207.410 – holoprosencephaly MeSH C16.131.621.207.525 – Leopard syndrome MeSH C16.131.621.207.540 – maxillofacial abnormalities MeSH C16.131.621.207.540.170 – cherubism MeSH C16.131.621.207.540.460 – jaw abnormalities MeSH C16.131.621.207.540.460.185 – cleft palate MeSH C16.131.621.207.540.460.457 – micrognathism MeSH C16.131.621.207.540.460.606 – Pierre Robin syndrome MeSH C16.131.621.207.540.460.655 – prognathism MeSH C16.131.621.207.540.460.813 – retrognathism MeSH C16.131.621.207.620 – microcephaly MeSH C16.131.621.207.690 – Noonan syndrome MeSH C16.131.621.207.700 – orofaciodigital syndromes MeSH C16.131.621.207.715 – plagiocephaly, nonsynostotic MeSH C16.131.621.207.720 – platybasia MeSH C16.131.621.207.850 – Rubinstein–Taybi syndrome MeSH C16.131.621.386 – funnel chest MeSH C16.131.621.417 – gastroschisis MeSH C16.131.621.445 – Hajdu–Cheney syndrome MeSH C16.131.621.449 – hip dislocation, congenital MeSH C16.131.621.551 – Klippel–Feil syndrome
|
{
"page_id": 5115037,
"source": null,
"title": "List of MeSH codes (C16)"
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|
MeSH C16.131.621.585 – limb deformities, congenital MeSH C16.131.621.585.350 – ectromelia MeSH C16.131.621.585.380 – foot deformities, congenital MeSH C16.131.621.585.425 – hand deformities, congenital MeSH C16.131.621.585.512 – lower extremity deformities, congenital MeSH C16.131.621.585.600 – polydactyly MeSH C16.131.621.585.600.750 – short rib – polydactyly syndrome MeSH C16.131.621.585.620 – proteus syndrome MeSH C16.131.621.585.800 – syndactyly MeSH C16.131.621.585.800.100 – acrocephalosyndactylia MeSH C16.131.621.585.800.756 – Poland syndrome MeSH C16.131.621.585.984 – thanatophoric dysplasia MeSH C16.131.621.585.988 – upper extremity deformities, congenital MeSH C16.131.621.906 – synostosis MeSH C16.131.621.906.364 – craniosynostoses MeSH C16.131.621.906.364.100 – acrocephalosyndactylia MeSH C16.131.621.906.819 – syndactyly MeSH C16.131.621.906.819.100 – acrocephalosyndactylia MeSH C16.131.621.906.819.756 – Poland syndrome ==== MeSH C16.131.666 – nervous system malformations ==== MeSH C16.131.666.142 – central nervous system cyst MeSH C16.131.666.142.100 – arachnoid cyst MeSH C16.131.666.190 – central nervous system vascular malformations MeSH C16.131.666.190.200 – hemangioma, cavernous, central nervous system MeSH C16.131.666.190.600 – central nervous system venous angioma MeSH C16.131.666.190.800 – sinus pericranii MeSH C16.131.666.205 – Dandy–Walker syndrome MeSH C16.131.666.300 – hereditary motor and sensory neuropathies MeSH C16.131.666.300.200 – Charcot–Marie–Tooth disease MeSH C16.131.666.300.780 – Refsum disease MeSH C16.131.666.300.820 – spastic paraplegia, hereditary MeSH C16.131.666.310 – hereditary sensory and autonomic neuropathies MeSH C16.131.666.310.309 – dysautonomia, familial MeSH C16.131.666.410 – holoprosencephaly MeSH C16.131.666.450 – hydranencephaly MeSH C16.131.666.460 – intracranial arteriovenous malformations MeSH C16.131.666.680 – neural tube defects MeSH C16.131.666.680.196 – anencephaly MeSH C16.131.666.680.291 – Arnold–Chiari malformation MeSH C16.131.666.680.488 – encephalocele MeSH C16.131.666.680.598 – meningocele MeSH C16.131.666.680.610 – meningomyelocele MeSH C16.131.666.680.800 – spinal dysraphism MeSH C16.131.666.680.800.730 – spina bifida cystica MeSH C16.131.666.680.800.750 – spina bifida occulta MeSH C16.131.666.845 – septo-optic dysplasia ==== MeSH C16.131.740 – respiratory system abnormalities ==== MeSH C16.131.740.195 – bronchogenic cyst MeSH C16.131.740.214 – bronchopulmonary sequestration MeSH C16.131.740.271 – choanal atresia MeSH C16.131.740.290 – cystic adenomatoid malformation of lung, congenital MeSH C16.131.740.501 – kartagener syndrome MeSH C16.131.740.815 – scimitar syndrome MeSH C16.131.740.830 – tracheobronchomegaly ==== MeSH C16.131.810 –
|
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"page_id": 5115037,
"source": null,
"title": "List of MeSH codes (C16)"
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situs inversus ==== MeSH C16.131.810.250 – dextrocardia MeSH C16.131.810.250.500 – kartagener syndrome MeSH C16.131.810.700 – levocardia ==== MeSH C16.131.831 – skin abnormalities ==== MeSH C16.131.831.066 – acrodermatitis MeSH C16.131.831.150 – dyskeratosis congenita MeSH C16.131.831.350 – ectodermal dysplasia MeSH C16.131.831.350.398 – Ellis–van Creveld syndrome MeSH C16.131.831.350.424 – focal dermal hypoplasia MeSH C16.131.831.350.712 – neurocutaneous syndromes MeSH C16.131.831.428 – Ehlers–Danlos syndrome MeSH C16.131.831.493 – epidermolysis bullosa MeSH C16.131.831.493.080 – epidermolysis bullosa acquisita MeSH C16.131.831.493.160 – epidermolysis bullosa dystrophica MeSH C16.131.831.493.170 – epidermolysis bullosa, junctional MeSH C16.131.831.493.180 – epidermolysis bullosa simplex MeSH C16.131.831.512 – ichthyosis MeSH C16.131.831.512.400 – ichthyosiform erythroderma, congenital MeSH C16.131.831.512.400.375 – hyperkeratosis, epidermolytic MeSH C16.131.831.512.400.410 – ichthyosis, lamellar MeSH C16.131.831.512.410 – ichthyosis vulgaris MeSH C16.131.831.512.420 – ichthyosis, x-linked MeSH C16.131.831.512.723 – Sjögren–Larsson syndrome MeSH C16.131.831.580 – incontinentia pigmenti MeSH C16.131.831.675 – port-wine stain MeSH C16.131.831.766 – pseudoxanthoma elasticum MeSH C16.131.831.775 – Rothmund–Thomson syndrome MeSH C16.131.831.812 – sclerema neonatorum MeSH C16.131.831.936 – xeroderma pigmentosum ==== MeSH C16.131.850 – stomatognathic system abnormalities ==== MeSH C16.131.850.500 – maxillofacial abnormalities MeSH C16.131.850.500.460 – jaw abnormalities MeSH C16.131.850.500.460.185 – cleft palate MeSH C16.131.850.500.460.457 – micrognathism MeSH C16.131.850.500.460.606 – Pierre Robin syndrome MeSH C16.131.850.500.460.655 – prognathism MeSH C16.131.850.500.460.813 – retrognathism MeSH C16.131.850.525 – mouth abnormalities MeSH C16.131.850.525.164 – cleft lip MeSH C16.131.850.525.185 – cleft palate MeSH C16.131.850.525.304 – fibromatosis, gingival MeSH C16.131.850.525.480 – macrostomia MeSH C16.131.850.525.520 – microstomia MeSH C16.131.850.525.955 – velopharyngeal insufficiency MeSH C16.131.850.800 – tooth abnormalities MeSH C16.131.850.800.065 – amelogenesis imperfecta MeSH C16.131.850.800.065.300 – dental enamel hypoplasia MeSH C16.131.850.800.100 – anodontia MeSH C16.131.850.800.250 – dens in dente MeSH C16.131.850.800.260 – dentin dysplasia MeSH C16.131.850.800.270 – dentinogenesis imperfecta MeSH C16.131.850.800.370 – fused teeth MeSH C16.131.850.800.600 – odontodysplasia MeSH C16.131.850.800.850 – tooth, supernumerary ==== MeSH C16.131.894 – thyroid dysgenesis ==== MeSH C16.131.894.500 – lingual thyroid MeSH C16.131.894.500.500 – lingual goiter ==== MeSH C16.131.939 – urogenital abnormalities
|
{
"page_id": 5115037,
"source": null,
"title": "List of MeSH codes (C16)"
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|
==== MeSH C16.131.939.132 – bladder exstrophy MeSH C16.131.939.258 – cryptorchidism MeSH C16.131.939.374 – epispadias MeSH C16.131.939.445 – frasier syndrome MeSH C16.131.939.516 – hypospadias MeSH C16.131.939.629 – multicystic dysplastic kidney MeSH C16.131.939.742 – nephritis, hereditary MeSH C16.131.939.842 – sex differentiation disorders MeSH C16.131.939.842.260 – freemartinism MeSH C16.131.939.842.309 – gonadal dysgenesis MeSH C16.131.939.842.309.193 – gonadal dysgenesis, 46,xx MeSH C16.131.939.842.309.388 – gonadal dysgenesis, 46,xy MeSH C16.131.939.842.309.391 – gonadal dysgenesis, mixed MeSH C16.131.939.842.309.872 – turner syndrome MeSH C16.131.939.842.316 – hermaphroditism MeSH C16.131.939.842.316.313 – hermaphroditism, true MeSH C16.131.939.842.316.627 – pseudohermaphroditism MeSH C16.131.939.842.316.627.109 – androgen insensitivity syndrome MeSH C16.131.939.842.316.627.220 – Denys–Drash syndrome MeSH C16.131.939.842.425 – Kallmann syndrome MeSH C16.131.939.842.454 – Klinefelter syndrome MeSH C16.131.939.921 – WAGR syndrome === MeSH C16.300 – fetal diseases === ==== MeSH C16.300.030 – chorioamnionitis ==== ==== MeSH C16.300.060 – erythroblastosis, fetal ==== MeSH C16.300.060.480 – hydrops fetalis ==== MeSH C16.300.080 – fetal alcohol syndrome ==== ==== MeSH C16.300.100 – fetal hypoxia ==== ==== MeSH C16.300.390 – fetal growth retardation ==== ==== MeSH C16.300.570 – fetal macrosomia ==== ==== MeSH C16.300.580 – meconium aspiration syndrome ==== === MeSH C16.320 – genetic diseases, inborn === ==== MeSH C16.320.033 – adrenal hyperplasia, congenital ==== ==== MeSH C16.320.070 – anemia, hemolytic, congenital ==== MeSH C16.320.070.095 – anemia, dyserythropoietic, congenital MeSH C16.320.070.100 – anemia, hemolytic, congenital nonspherocytic MeSH C16.320.070.150 – anemia, sickle cell MeSH C16.320.070.150.440 – hemoglobin SC disease MeSH C16.320.070.150.670 – sickle cell trait MeSH C16.320.070.365 – elliptocytosis, hereditary MeSH C16.320.070.480 – glucosephosphate dehydrogenase deficiency MeSH C16.320.070.480.370 – favism MeSH C16.320.070.490 – hemoglobin c disease MeSH C16.320.070.785 – spherocytosis, hereditary MeSH C16.320.070.875 – thalassemia MeSH C16.320.070.875.100 – alpha-thalassemia MeSH C16.320.070.875.150 – beta-thalassemia ==== MeSH C16.320.077 – anemia, hypoplastic, congenital ==== MeSH C16.320.077.090 – anemia, Diamond–Blackfan MeSH C16.320.077.280 – fanconi anemia ==== MeSH C16.320.080 – ataxia telangiectasia ==== ==== MeSH C16.320.099 – blood coagulation disorders, inherited
|
{
"page_id": 5115037,
"source": null,
"title": "List of MeSH codes (C16)"
}
|
==== MeSH C16.320.099.037 – activated protein C resistance MeSH C16.320.099.056 – afibrinogenemia MeSH C16.320.099.075 – antithrombin III deficiency MeSH C16.320.099.080 – Bernard–Soulier syndrome MeSH C16.320.099.300 – factor V deficiency MeSH C16.320.099.310 – factor VII deficiency MeSH C16.320.099.320 – factor X deficiency MeSH C16.320.099.325 – factor XI deficiency MeSH C16.320.099.330 – factor XII deficiency MeSH C16.320.099.335 – factor XIII deficiency MeSH C16.320.099.500 – hemophilia A MeSH C16.320.099.510 – hemophilia B MeSH C16.320.099.515 – Hermansky–Pudlak syndrome MeSH C16.320.099.550 – hypoprothrombinemias MeSH C16.320.099.690 – protein C deficiency MeSH C16.320.099.820 – thrombasthenia MeSH C16.320.099.900 – Von Willebrand disease MeSH C16.320.099.970 – Wiskott–Aldrich syndrome ==== MeSH C16.320.129 – CADASIL ==== ==== MeSH C16.320.160 – cardiomyopathy, hypertrophic, familial ==== ==== MeSH C16.320.170 – cherubism ==== ==== MeSH C16.320.180 – chromosome disorders ==== MeSH C16.320.180.040 – angelman syndrome MeSH C16.320.180.080 – Beckwith–Wiedemann syndrome MeSH C16.320.180.090 – branchio-oto-renal syndrome MeSH C16.320.180.190 – cri du chat syndrome MeSH C16.320.180.210 – De Lange syndrome MeSH C16.320.180.260 – Down syndrome MeSH C16.320.180.380 – holoprosencephaly MeSH C16.320.180.700 – Prader–Willi syndrome MeSH C16.320.180.790 – Rubinstein–Taybi syndrome MeSH C16.320.180.800 – sex chromosome disorders MeSH C16.320.180.800.240 – ectodermal dysplasia MeSH C16.320.180.800.240.350 – focal dermal hypoplasia MeSH C16.320.180.800.300 – fragile X syndrome MeSH C16.320.180.800.340 – gonadal dysgenesis, 46,xy MeSH C16.320.180.800.345 – gonadal dysgenesis, mixed MeSH C16.320.180.800.490 – Klinefelter syndrome MeSH C16.320.180.800.670 – orofaciodigital syndromes MeSH C16.320.180.800.870 – Turner syndrome MeSH C16.320.180.940 – WAGR syndrome MeSH C16.320.180.970 – Williams syndrome ==== MeSH C16.320.190 – cystic fibrosis ==== ==== MeSH C16.320.240 – dwarfism ==== MeSH C16.320.240.500 – achondroplasia MeSH C16.320.240.562 – cockayne syndrome MeSH C16.320.240.625 – congenital hypothyroidism MeSH C16.320.240.750 – laron syndrome MeSH C16.320.240.875 – mulibrey nanism ==== MeSH C16.320.290 – eye diseases, hereditary ==== MeSH C16.320.290.040 – albinism MeSH C16.320.290.040.090 – albinism, ocular MeSH C16.320.290.040.100 – albinism, oculocutaneous MeSH C16.320.290.040.100.400 – Hermansky–Pudlak syndrome MeSH C16.320.290.040.600 –
|
{
"page_id": 5115037,
"source": null,
"title": "List of MeSH codes (C16)"
}
|
piebaldism MeSH C16.320.290.078 – aniridia MeSH C16.320.290.078.950 – WAGR syndrome MeSH C16.320.290.142 – choroideremia MeSH C16.320.290.162 – corneal dystrophies, hereditary MeSH C16.320.290.162.410 – Fuchs' endothelial dystrophy MeSH C16.320.290.235 – Duane retraction syndrome MeSH C16.320.290.468 – gyrate atrophy MeSH C16.320.290.564 – optic atrophies, hereditary MeSH C16.320.290.564.400 – optic atrophy, hereditary, leber MeSH C16.320.290.564.500 – optic atrophy, autosomal dominant MeSH C16.320.290.564.980 – Wolfram syndrome MeSH C16.320.290.660 – retinal dysplasia MeSH C16.320.290.684 – retinitis pigmentosa MeSH C16.320.290.684.500 – Usher syndromes ==== MeSH C16.320.306 – familial Mediterranean fever ==== ==== MeSH C16.320.322 – genetic diseases, x-linked ==== MeSH C16.320.322.061 – androgen insensitivity syndrome MeSH C16.320.322.092 – choroideremia MeSH C16.320.322.108 – dyskeratosis congenita MeSH C16.320.322.124 – fabry disease MeSH C16.320.322.186 – focal dermal hypoplasia MeSH C16.320.322.201 – glycogen storage disease type IIb MeSH C16.320.322.217 – glycogen storage disease type VIII MeSH C16.320.322.233 – granulomatous disease, chronic MeSH C16.320.322.241 – ichthyosis, x-linked MeSH C16.320.322.360 – hemophilia B MeSH C16.320.322.500 – mental retardation, x-linked MeSH C16.320.322.500.124 – adrenoleukodystrophy MeSH C16.320.322.500.249 – Coffin–Lowry syndrome MeSH C16.320.322.500.500 – fragile X syndrome MeSH C16.320.322.500.625 – Lesch–Nyhan syndrome MeSH C16.320.322.500.687 – Menkes kinky hair syndrome MeSH C16.320.322.500.750 – mucopolysaccharidosis II MeSH C16.320.322.500.875 – pyruvate dehydrogenase complex deficiency disease MeSH C16.320.322.500.937 – Rett syndrome MeSH C16.320.322.562 – muscular dystrophy, Duchenne MeSH C16.320.322.625 – muscular dystrophy, Emery–Dreifuss MeSH C16.320.322.750 – oculocerebrorenal syndrome MeSH C16.320.322.906 – Pelizaeus–Merzbacher disease MeSH C16.320.322.937 – Wiskott–Aldrich syndrome ==== MeSH C16.320.338 – genetic diseases, y-linked ==== ==== MeSH C16.320.355 – Hajdu–Cheney syndrome ==== ==== MeSH C16.320.365 – hemoglobinopathies ==== MeSH C16.320.365.155 – anemia, sickle cell MeSH C16.320.365.155.440 – hemoglobin sc disease MeSH C16.320.365.155.668 – sickle cell trait MeSH C16.320.365.463 – hemoglobin c disease MeSH C16.320.365.826 – thalassemia MeSH C16.320.365.826.100 – alpha-thalassemia MeSH C16.320.365.826.100.350 – hydrops fetalis MeSH C16.320.365.826.150 – beta-thalassemia ==== MeSH C16.320.400 – heredodegenerative disorders, nervous system ====
|
{
"page_id": 5115037,
"source": null,
"title": "List of MeSH codes (C16)"
}
|
MeSH C16.320.400.024 – Alexander disease MeSH C16.320.400.050 – amyloid neuropathies, familial MeSH C16.320.400.150 – Canavan disease MeSH C16.320.400.200 – Cockayne syndrome MeSH C16.320.400.330 – dystonia musculorum deformans MeSH C16.320.400.350 – Gerstmann–Sträussler–Scheinker disease MeSH C16.320.400.375 – Hallervorden–Spatz syndrome MeSH C16.320.400.387 – hepatolenticular degeneration MeSH C16.320.400.393 – hereditary central nervous system demyelinating diseases MeSH C16.320.400.400 – hereditary motor and sensory neuropathies MeSH C16.320.400.400.200 – Charcot–Marie–Tooth disease MeSH C16.320.400.400.780 – Refsum disease MeSH C16.320.400.400.820 – spastic paraplegia, hereditary MeSH C16.320.400.415 – hereditary sensory and autonomic neuropathies MeSH C16.320.400.415.309 – dysautonomia, familial MeSH C16.320.400.430 – Huntington disease MeSH C16.320.400.480 – Lafora disease MeSH C16.320.400.500 – Lesch–Nyhan syndrome MeSH C16.320.400.520 – Menkes kinky hair syndrome MeSH C16.320.400.525 – mental retardation, x-linked MeSH C16.320.400.525.124 – adrenoleukodystrophy MeSH C16.320.400.525.249 – Coffin–Lowry syndrome MeSH C16.320.400.525.500 – fragile X syndrome MeSH C16.320.400.525.625 – Lesch–Nyhan syndrome MeSH C16.320.400.525.687 – Menkes kinky hair syndrome MeSH C16.320.400.525.750 – mucopolysaccharidosis II MeSH C16.320.400.525.875 – pyruvate dehydrogenase complex deficiency disease MeSH C16.320.400.525.937 – Rett syndrome MeSH C16.320.400.540 – myotonia congenita MeSH C16.320.400.542 – myotonic dystrophy MeSH C16.320.400.560 – neurofibromatosis MeSH C16.320.400.560.400 – neurofibromatosis 1 MeSH C16.320.400.560.700 – neurofibromatosis 2 MeSH C16.320.400.600 – neuronal ceroid-lipofuscinosis MeSH C16.320.400.630 – optic atrophies, hereditary MeSH C16.320.400.630.400 – optic atrophy, hereditary, leber MeSH C16.320.400.630.500 – optic atrophy, autosomal dominant MeSH C16.320.400.630.980 – Wolfram syndrome MeSH C16.320.400.700 – Rett syndrome MeSH C16.320.400.765 – spinal muscular atrophies of childhood MeSH C16.320.400.780 – spinocerebellar degenerations MeSH C16.320.400.780.200 – Friedreich's ataxia MeSH C16.320.400.780.500 – myoclonic cerebellar dyssynergia MeSH C16.320.400.780.750 – olivopontocerebellar atrophies MeSH C16.320.400.780.875 – spinocerebellar ataxias MeSH C16.320.400.780.875.500 – Machado–Joseph disease MeSH C16.320.400.820 – Tourette syndrome MeSH C16.320.400.880 – tuberous sclerosis MeSH C16.320.400.940 – Unverricht–Lundborg syndrome ==== MeSH C16.320.427 – hyperthyroxinemia, familial dysalbuminemic ==== ==== MeSH C16.320.455 – Jervell and Lange-Nielsen syndrome ==== ==== MeSH C16.320.467 – kallmann syndrome ==== ==== MeSH
|
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"page_id": 5115037,
"source": null,
"title": "List of MeSH codes (C16)"
}
|
C16.320.480 – kartagener syndrome ==== ==== MeSH C16.320.540 – marfan syndrome ==== ==== MeSH C16.320.565 – metabolism, inborn errors ==== MeSH C16.320.565.066 – amino acid metabolism, inborn errors MeSH C16.320.565.066.102 – albinism MeSH C16.320.565.066.102.090 – albinism, ocular MeSH C16.320.565.066.102.100 – albinism, oculocutaneous MeSH C16.320.565.066.102.100.400 – Hermansky–Pudlak syndrome MeSH C16.320.565.066.102.600 – piebaldism MeSH C16.320.565.066.187 – alkaptonuria MeSH C16.320.565.066.210 – aminoaciduria, renal MeSH C16.320.565.066.210.250 – cystinuria MeSH C16.320.565.066.210.490 – Hartnup disease MeSH C16.320.565.066.275 – carbamoyl-phosphate synthase I deficiency disease MeSH C16.320.565.066.340 – citrullinemia MeSH C16.320.565.066.470 – homocystinuria MeSH C16.320.565.066.475 – hyperargininemia MeSH C16.320.565.066.477 – hyperglycinemia, nonketotic MeSH C16.320.565.066.480 – hyperhomocysteinemia MeSH C16.320.565.066.544 – hyperlysinemias MeSH C16.320.565.066.608 – maple syrup urine disease MeSH C16.320.565.066.620 – multiple carboxylase deficiency MeSH C16.320.565.066.620.100 – biotinidase deficiency MeSH C16.320.565.066.620.380 – holocarboxylase synthetase deficiency MeSH C16.320.565.066.729 – ornithine carbamoyltransferase deficiency disease MeSH C16.320.565.066.766 – phenylketonurias MeSH C16.320.565.066.766.500 – phenylketonuria, maternal MeSH C16.320.565.066.880 – tyrosinemias MeSH C16.320.565.088 – amino acid transport disorders, inborn MeSH C16.320.565.088.400 – Hartnup disease MeSH C16.320.565.088.600 – oculocerebrorenal syndrome MeSH C16.320.565.100 – amyloidosis, familial MeSH C16.320.565.100.050 – amyloid neuropathies, familial MeSH C16.320.565.100.160 – cerebral amyloid angiopathy, familial MeSH C16.320.565.150 – brain diseases, metabolic, inborn MeSH C16.320.565.150.050 – abetalipoproteinemia MeSH C16.320.565.150.162 – carbamoyl-phosphate synthase I deficiency disease MeSH C16.320.565.150.168 – cerebral amyloid angiopathy, familial MeSH C16.320.565.150.175 – citrullinemia MeSH C16.320.565.150.320 – galactosemias MeSH C16.320.565.150.355 – Hartnup disease MeSH C16.320.565.150.360 – hepatolenticular degeneration MeSH C16.320.565.150.365 – homocystinuria MeSH C16.320.565.150.370 – hyperargininemia MeSH C16.320.565.150.375 – hyperglycinemia, nonketotic MeSH C16.320.565.150.380 – hyperlysinemias MeSH C16.320.565.150.412 – Leigh disease MeSH C16.320.565.150.425 – Lesch–Nyhan syndrome MeSH C16.320.565.150.435 – lysosomal storage diseases, nervous system MeSH C16.320.565.150.435.295 – fucosidosis MeSH C16.320.565.150.435.340 – glycogen storage disease type II MeSH C16.320.565.150.435.590 – mucolipidoses MeSH C16.320.565.150.435.810 – sialic acid storage disease MeSH C16.320.565.150.435.825 – sphingolipidoses MeSH C16.320.565.150.435.825.200 – Fabry disease MeSH C16.320.565.150.435.825.300 – gangliosidoses MeSH C16.320.565.150.435.825.300.300 –
|
{
"page_id": 5115037,
"source": null,
"title": "List of MeSH codes (C16)"
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|
gangliosidoses GM2 MeSH C16.320.565.150.435.825.300.300.800 – Sandhoff disease MeSH C16.320.565.150.435.825.300.300.840 – Tay–Sachs disease MeSH C16.320.565.150.435.825.300.300.920 – Tay–Sachs disease, AB variant MeSH C16.320.565.150.435.825.300.400 – gangliosidosis GM1 MeSH C16.320.565.150.435.825.400 – Gaucher disease MeSH C16.320.565.150.435.825.590 – leukodystrophy, globoid cell MeSH C16.320.565.150.435.825.594 – leukodystrophy, metachromatic MeSH C16.320.565.150.435.825.700 – Niemann–Pick diseases MeSH C16.320.565.150.520 – maple syrup urine disease MeSH C16.320.565.150.535 – MELAS syndrome MeSH C16.320.565.150.540 – Menkes kinky hair syndrome MeSH C16.320.565.150.545 – MERRF syndrome MeSH C16.320.565.150.640 – oculocerebrorenal syndrome MeSH C16.320.565.150.650 – ornithine carbamoyltransferase deficiency disease MeSH C16.320.565.150.680 – peroxisomal disorders MeSH C16.320.565.150.680.100 – adrenoleukodystrophy MeSH C16.320.565.150.680.760 – Refsum disease MeSH C16.320.565.150.680.970 – Zellweger syndrome MeSH C16.320.565.150.687 – phenylketonurias MeSH C16.320.565.150.687.500 – phenylketonuria, maternal MeSH C16.320.565.150.725 – pyruvate carboxylase deficiency disease MeSH C16.320.565.150.750 – pyruvate dehydrogenase complex deficiency disease MeSH C16.320.565.150.875 – tyrosinemias MeSH C16.320.565.202 – carbohydrate metabolism, inborn errors MeSH C16.320.565.202.125 – carbohydrate-deficient glycoprotein syndrome MeSH C16.320.565.202.251 – fructose metabolism, inborn errors MeSH C16.320.565.202.251.221 – fructose-1,6-diphosphatase deficiency MeSH C16.320.565.202.251.271 – Hereditary fructose intolerance MeSH C16.320.565.202.303 – fucosidosis MeSH C16.320.565.202.355 – galactosemias MeSH C16.320.565.202.449 – glycogen storage disease MeSH C16.320.565.202.449.448 – glycogen storage disease type I MeSH C16.320.565.202.449.500 – glycogen storage disease type II MeSH C16.320.565.202.449.510 – glycogen storage disease type IIb MeSH C16.320.565.202.449.520 – glycogen storage disease type III MeSH C16.320.565.202.449.540 – glycogen storage disease type IV MeSH C16.320.565.202.449.560 – glycogen storage disease type V MeSH C16.320.565.202.449.580 – glycogen storage disease type VI MeSH C16.320.565.202.449.600 – glycogen storage disease type VII MeSH C16.320.565.202.449.620 – glycogen storage disease type VIII MeSH C16.320.565.202.460 – hyperoxaluria, primary MeSH C16.320.565.202.589 – lactose intolerance MeSH C16.320.565.202.607 – mannosidase deficiency diseases MeSH C16.320.565.202.607.500 – alpha-mannosidosis MeSH C16.320.565.202.607.750 – beta-mannosidosis MeSH C16.320.565.202.670 – mucolipidoses MeSH C16.320.565.202.715 – mucopolysaccharidoses MeSH C16.320.565.202.715.640 – mucopolysaccharidosis I MeSH C16.320.565.202.715.645 – mucopolysaccharidosis II MeSH C16.320.565.202.715.650 – mucopolysaccharidosis III MeSH C16.320.565.202.715.655 – mucopolysaccharidosis IV MeSH C16.320.565.202.715.670 –
|
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"page_id": 5115037,
"source": null,
"title": "List of MeSH codes (C16)"
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|
mucopolysaccharidosis VI MeSH C16.320.565.202.715.675 – mucopolysaccharidosis VII MeSH C16.320.565.202.720 – multiple carboxylase deficiency MeSH C16.320.565.202.720.100 – biotinidase deficiency MeSH C16.320.565.202.720.380 – holocarboxylase synthetase deficiency MeSH C16.320.565.202.742 – nesidioblastosis MeSH C16.320.565.202.765 – persistent hyperinsulinemia hypoglycemia of infancy MeSH C16.320.565.202.810 – pyruvate metabolism, inborn errors MeSH C16.320.565.202.810.444 – Leigh disease MeSH C16.320.565.202.810.666 – pyruvate carboxylase deficiency disease MeSH C16.320.565.202.810.766 – pyruvate dehydrogenase complex deficiency disease MeSH C16.320.565.240 – cytochrome-c oxidase deficiency MeSH C16.320.565.390 – glucosephosphate dehydrogenase deficiency MeSH C16.320.565.437 – hyperbilirubinemia, hereditary MeSH C16.320.565.437.281 – Crigler–Najjar syndrome MeSH C16.320.565.437.528 – Gilbert disease MeSH C16.320.565.499 – jaundice, chronic idiopathic MeSH C16.320.565.556 – lipid metabolism, inborn errors MeSH C16.320.565.556.475 – hypercholesterolemia, familial MeSH C16.320.565.556.480 – hyperlipidemia, familial combined MeSH C16.320.565.556.480.390 – hypercholesterolemia, familial MeSH C16.320.565.556.480.395 – hyperlipoproteinemia type IV MeSH C16.320.565.556.483 – hyperlipoproteinemia type III MeSH C16.320.565.556.487 – hyperlipoproteinemia type IV MeSH C16.320.565.556.493 – hyperlipoproteinemia type V MeSH C16.320.565.556.500 – hypolipoproteinemia MeSH C16.320.565.556.500.220 – abetalipoproteinemia MeSH C16.320.565.556.500.440 – hypobetalipoproteinemia MeSH C16.320.565.556.500.448 – lecithin acyltransferase deficiency MeSH C16.320.565.556.500.724 – Tangier disease MeSH C16.320.565.556.641 – lipoidosis MeSH C16.320.565.556.641.201 – cholesterol ester storage disease MeSH C16.320.565.556.641.391 – lipoidproteinosis MeSH C16.320.565.556.641.509 – neuronal ceroid-lipofuscinosis MeSH C16.320.565.556.641.643 – refsum disease MeSH C16.320.565.556.641.723 – sjogren-larsson syndrome MeSH C16.320.565.556.641.803 – sphingolipidoses MeSH C16.320.565.556.641.803.300 – Fabry disease MeSH C16.320.565.556.641.803.350 – gangliosidoses MeSH C16.320.565.556.641.803.350.300 – gangliosidoses GM2 MeSH C16.320.565.556.641.803.350.300.700 – Sandhoff disease MeSH C16.320.565.556.641.803.350.300.850 – Tay–Sachs disease MeSH C16.320.565.556.641.803.350.300.925 – Tay–Sachs disease, AB variant MeSH C16.320.565.556.641.803.350.360 – gangliosidosis GM1 MeSH C16.320.565.556.641.803.441 – Gaucher disease MeSH C16.320.565.556.641.803.585 – leukodystrophy, globoid cell MeSH C16.320.565.556.641.803.594 – leukodystrophy, metachromatic MeSH C16.320.565.556.641.803.730 – Niemann–Pick diseases MeSH C16.320.565.556.641.803.850 – sea-blue histiocyte syndrome MeSH C16.320.565.556.641.923 – Wolman disease MeSH C16.320.565.556.645 – lipoprotein lipase deficiency, familial MeSH C16.320.565.556.750 – peroxisomal disorders MeSH C16.320.565.556.750.025 – acatalasia MeSH C16.320.565.556.750.112 – adrenoleukodystrophy MeSH C16.320.565.556.750.200 – chondrodysplasia punctata, rhizomelic MeSH C16.320.565.556.750.760 – Refsum disease MeSH
|
{
"page_id": 5115037,
"source": null,
"title": "List of MeSH codes (C16)"
}
|
C16.320.565.556.750.970 – Zellweger syndrome MeSH C16.320.565.556.850 – Smith–Lemli–Opitz syndrome MeSH C16.320.565.556.925 – xanthomatosis, cerebrotendinous MeSH C16.320.565.580 – lysosomal storage diseases MeSH C16.320.565.580.201 – cholesterol ester storage disease MeSH C16.320.565.580.554 – lysosomal storage diseases, nervous system MeSH C16.320.565.580.554.295 – fucosidosis MeSH C16.320.565.580.554.340 – glycogen storage disease type II MeSH C16.320.565.580.554.590 – mucolipidoses MeSH C16.320.565.580.554.810 – sialic acid storage disease MeSH C16.320.565.580.554.825 – sphingolipidoses MeSH C16.320.565.580.554.825.200 – Fabry disease MeSH C16.320.565.580.554.825.300 – gangliosidoses MeSH C16.320.565.580.554.825.300.300 – gangliosidoses GM2 MeSH C16.320.565.580.554.825.300.300.800 – Sandhoff disease MeSH C16.320.565.580.554.825.300.300.840 – Tay–Sachs disease MeSH C16.320.565.580.554.825.300.300.920 – Tay–Sachs disease, AB variant MeSH C16.320.565.580.554.825.300.400 – gangliosidosis GM1 MeSH C16.320.565.580.554.825.400 – Gaucher disease MeSH C16.320.565.580.554.825.590 – leukodystrophy, globoid cell MeSH C16.320.565.580.554.825.594 – leukodystrophy, metachromatic MeSH C16.320.565.580.554.825.700 – Niemann–Pick diseases MeSH C16.320.565.580.577 – mannosidase deficiency diseases MeSH C16.320.565.580.577.500 – alpha-mannosidosis MeSH C16.320.565.580.577.750 – beta-mannosidosis MeSH C16.320.565.580.600 – mucopolysaccharidoses MeSH C16.320.565.580.600.640 – mucopolysaccharidosis I MeSH C16.320.565.580.600.645 – mucopolysaccharidosis II MeSH C16.320.565.580.600.650 – mucopolysaccharidosis III MeSH C16.320.565.580.600.655 – mucopolysaccharidosis IV MeSH C16.320.565.580.600.670 – mucopolysaccharidosis VI MeSH C16.320.565.580.600.675 – mucopolysaccharidosis VII MeSH C16.320.565.580.803 – sphingolipidoses MeSH C16.320.565.580.803.300 – Fabry disease MeSH C16.320.565.580.803.350 – gangliosidoses MeSH C16.320.565.580.803.350.300 – gangliosidoses GM2 MeSH C16.320.565.580.803.350.300.700 – Sandhoff disease MeSH C16.320.565.580.803.350.300.850 – Tay–Sachs disease MeSH C16.320.565.580.803.350.300.925 – Tay–Sachs disease, AB variant MeSH C16.320.565.580.803.441 – Gaucher disease MeSH C16.320.565.580.803.585 – leukodystrophy, globoid cell MeSH C16.320.565.580.803.594 – leukodystrophy, metachromatic MeSH C16.320.565.580.803.730 – niemann-pick diseases MeSH C16.320.565.580.803.850 – sea-blue histiocyte syndrome MeSH C16.320.565.580.923 – Wolman disease MeSH C16.320.565.618 – metal metabolism, inborn errors MeSH C16.320.565.618.337 – hemochromatosis MeSH C16.320.565.618.403 – hepatolenticular degeneration MeSH C16.320.565.618.482 – hypophosphatasia MeSH C16.320.565.618.544 – hypophosphatemia, familial MeSH C16.320.565.618.590 – Menkes kinky hair syndrome MeSH C16.320.565.618.711 – paralyses, familial periodic MeSH C16.320.565.618.711.550 – hypokalemic periodic paralysis MeSH C16.320.565.618.711.600 – paralysis, hyperkalemic periodic MeSH C16.320.565.618.711.600.500 – Andersen syndrome MeSH C16.320.565.618.815 – pseudohypoparathyroidism MeSH C16.320.565.618.815.815 – pseudopseudohypoparathyroidism MeSH C16.320.565.731 –
|
{
"page_id": 5115037,
"source": null,
"title": "List of MeSH codes (C16)"
}
|
porphyria, erythropoietic MeSH C16.320.565.735 – porphyrias, hepatic MeSH C16.320.565.735.074 – coproporphyria, hereditary MeSH C16.320.565.735.150 – porphyria, acute intermittent MeSH C16.320.565.735.250 – porphyria cutanea tarda MeSH C16.320.565.735.437 – porphyria, hepatoerythropoietic MeSH C16.320.565.735.625 – porphyria, variegate MeSH C16.320.565.735.812 – protoporphyria, erythropoietic MeSH C16.320.565.769 – progeria MeSH C16.320.565.798 – purine–pyrimidine metabolism, inborn errors MeSH C16.320.565.798.368 – gout MeSH C16.320.565.798.368.410 – arthritis, gouty MeSH C16.320.565.798.594 – Lesch–Nyhan syndrome MeSH C16.320.565.851 – renal tubular transport, inborn errors MeSH C16.320.565.851.093 – acidosis, renal tubular MeSH C16.320.565.851.191 – aminoaciduria, renal MeSH C16.320.565.851.191.250 – cystinuria MeSH C16.320.565.851.191.457 – Hartnup disease MeSH C16.320.565.851.368 – cystinosis MeSH C16.320.565.851.368.210 – Fanconi syndrome MeSH C16.320.565.851.532 – glycosuria, renal MeSH C16.320.565.851.647 – hypophosphatemia, familial MeSH C16.320.565.851.750 – oculocerebrorenal syndrome MeSH C16.320.565.851.770 – pseudohypoaldosteronism MeSH C16.320.565.925 – steroid metabolism, inborn errors MeSH C16.320.565.925.249 – adrenal hyperplasia, congenital MeSH C16.320.565.925.500 – mineralocorticoid excess syndrome, apparent MeSH C16.320.565.925.750 – ichthyosis, x-linked MeSH C16.320.565.925.875 – Smith–Lemli–Opitz syndrome ==== MeSH C16.320.577 – muscular dystrophies ==== MeSH C16.320.577.074 – distal myopathies MeSH C16.320.577.149 – glycogen storage disease type VII MeSH C16.320.577.280 – muscular dystrophies, limb-girdle MeSH C16.320.577.300 – muscular dystrophy, Duchenne MeSH C16.320.577.350 – muscular dystrophy, Emery–Dreifuss MeSH C16.320.577.400 – muscular dystrophy, facioscapulohumeral MeSH C16.320.577.450 – muscular dystrophy, oculopharyngeal MeSH C16.320.577.500 – myotonic dystrophy ==== MeSH C16.320.590 – myasthenic syndromes, congenital ==== ==== MeSH C16.320.600 – nail–patella syndrome ==== ==== MeSH C16.320.700 – neoplastic syndromes, hereditary ==== MeSH C16.320.700.100 – adenomatous polyposis coli MeSH C16.320.700.100.393 – Gardner's syndrome MeSH C16.320.700.175 – basal-cell nevus syndrome MeSH C16.320.700.250 – colorectal neoplasms, hereditary nonpolyposis MeSH C16.320.700.305 – dysplastic nevus syndrome MeSH C16.320.700.330 – exostoses, multiple hereditary MeSH C16.320.700.435 – hamartoma syndrome, multiple MeSH C16.320.700.600 – Li–Fraumeni syndrome MeSH C16.320.700.630 – multiple endocrine neoplasia MeSH C16.320.700.630.500 – multiple endocrine neoplasia type 1 MeSH C16.320.700.630.505 – multiple endocrine neoplasia type 2a MeSH C16.320.700.630.510 –
|
{
"page_id": 5115037,
"source": null,
"title": "List of MeSH codes (C16)"
}
|
multiple endocrine neoplasia type 2b MeSH C16.320.700.642 – Wilms' tumor MeSH C16.320.700.642.220 – Denys–Drash syndrome MeSH C16.320.700.642.950 – WAGR syndrome MeSH C16.320.700.645 – Neurofibromatosis MeSH C16.320.700.645.650 – neurofibromatosis 1 MeSH C16.320.700.645.655 – neurofibromatosis 2 MeSH C16.320.700.705 – Peutz–Jeghers syndrome MeSH C16.320.700.852 – Sturge–Weber syndrome ==== MeSH C16.320.737 – osteogenesis imperfecta ==== ==== MeSH C16.320.775 – pain insensitivity, congenital ==== ==== MeSH C16.320.800 – Romano–Ward syndrome ==== ==== MeSH C16.320.850 – skin diseases, genetic ==== MeSH C16.320.850.080 – albinism MeSH C16.320.850.080.090 – albinism, ocular MeSH C16.320.850.080.100 – albinism, oculocutaneous MeSH C16.320.850.080.100.400 – Hermansky–Pudlak syndrome MeSH C16.320.850.080.600 – piebaldism MeSH C16.320.850.180 – cutis laxa MeSH C16.320.850.210 – dermatitis, atopic MeSH C16.320.850.235 – dyskeratosis congenita MeSH C16.320.850.250 – ectodermal dysplasia MeSH C16.320.850.250.398 – Ellis–van Creveld syndrome MeSH C16.320.850.250.424 – focal dermal hypoplasia MeSH C16.320.850.250.712 – neurocutaneous syndromes MeSH C16.320.850.260 – Ehlers–Danlos syndrome MeSH C16.320.850.275 – epidermolysis bullosa MeSH C16.320.850.275.160 – epidermolysis bullosa dystrophica MeSH C16.320.850.275.170 – epidermolysis bullosa, junctional MeSH C16.320.850.275.180 – epidermolysis bullosa simplex MeSH C16.320.850.400 – ichthyosiform erythroderma, congenital MeSH C16.320.850.400.375 – hyperkeratosis, epidermolytic MeSH C16.320.850.400.410 – ichthyosis, lamellar MeSH C16.320.850.405 – ichthyosis vulgaris MeSH C16.320.850.408 – ichthyosis, x-linked MeSH C16.320.850.420 – incontinentia pigmenti MeSH C16.320.850.475 – keratoderma, palmoplantar MeSH C16.320.850.475.440 – keratoderma, palmoplantar, diffuse MeSH C16.320.850.475.600 – Papillon–Lefèvre disease MeSH C16.320.850.490 – keratosis follicularis MeSH C16.320.850.700 – pemphigus, benign familial MeSH C16.320.850.730 – porokeratosis MeSH C16.320.850.738 – porphyria, erythropoietic MeSH C16.320.850.742 – porphyrias, hepatic MeSH C16.320.850.742.074 – coproporphyria, hereditary MeSH C16.320.850.742.150 – porphyria, acute intermittent MeSH C16.320.850.742.250 – porphyria cutanea tarda MeSH C16.320.850.742.437 – porphyria, hepatoerythropoietic MeSH C16.320.850.742.625 – porphyria, variegate MeSH C16.320.850.742.812 – protoporphyria, erythropoietic MeSH C16.320.850.750 – pseudoxanthoma elasticum MeSH C16.320.850.765 – Rothmund–Thomson syndrome MeSH C16.320.850.820 – Sjögren–Larsson syndrome MeSH C16.320.850.970 – xeroderma pigmentosum ==== MeSH C16.320.925 – Werner syndrome ==== === MeSH C16.614 – infant, newborn, diseases
|
{
"page_id": 5115037,
"source": null,
"title": "List of MeSH codes (C16)"
}
|
=== ==== MeSH C16.614.042 – amniotic band syndrome ==== ==== MeSH C16.614.053 – anemia, neonatal ==== MeSH C16.614.053.344 – fetofetal transfusion MeSH C16.614.053.511 – fetomaternal transfusion ==== MeSH C16.614.092 – asphyxia neonatorum ==== ==== MeSH C16.614.131 – birth injuries ==== MeSH C16.614.131.587 – paralysis, obstetric ==== MeSH C16.614.213 – cystic fibrosis ==== ==== MeSH C16.614.258 – epilepsy, benign neonatal ==== ==== MeSH C16.614.304 – erythroblastosis, fetal ==== MeSH C16.614.304.502 – kernicterus ==== MeSH C16.614.378 – hemorrhagic disease of newborn ==== ==== MeSH C16.614.390 – hernia, umbilical ==== ==== MeSH C16.614.414 – hydrocephalus ==== MeSH C16.614.414.200 – Dandy–Walker syndrome ==== MeSH C16.614.438 – hydrophthalmos ==== ==== MeSH C16.614.451 – hyperbilirubinemia, neonatal ==== MeSH C16.614.451.500 – jaundice, neonatal MeSH C16.614.451.500.250 – jaundice, chronic idiopathic ==== MeSH C16.614.465 – hyperostosis, cortical, congenital ==== ==== MeSH C16.614.492 – ichthyosis ==== MeSH C16.614.492.400 – ichthyosiform erythroderma, congenital MeSH C16.614.492.400.375 – hyperkeratosis, epidermolytic MeSH C16.614.492.400.410 – ichthyosis, lamellar MeSH C16.614.492.420 – ichthyosis, x-linked MeSH C16.614.492.723 – Sjögren–Larsson syndrome ==== MeSH C16.614.521 – infant, premature, diseases ==== MeSH C16.614.521.125 – bronchopulmonary dysplasia MeSH C16.614.521.450 – leukomalacia, periventricular MeSH C16.614.521.563 – respiratory distress syndrome, newborn MeSH C16.614.521.563.475 – hyaline membrane disease MeSH C16.614.521.731 – retinopathy of prematurity ==== MeSH C16.614.580 – meconium aspiration syndrome ==== ==== MeSH C16.614.595 – Möbius syndrome ==== ==== MeSH C16.614.610 – neonatal abstinence syndrome ==== ==== MeSH C16.614.643 – nystagmus, congenital ==== ==== MeSH C16.614.677 – ophthalmia neonatorum ==== ==== MeSH C16.614.694 – persistent fetal circulation syndrome ==== ==== MeSH C16.614.716 – persistent hyperinsulinemia hypoglycemia of infancy ==== ==== MeSH C16.614.760 – Rothmund–Thomson syndrome ==== ==== MeSH C16.614.810 – sclerema neonatorum ==== ==== MeSH C16.614.815 – severe combined immunodeficiency ==== ==== MeSH C16.614.868 – syphilis, congenital ==== ==== MeSH C16.614.890 – thanatophoric dysplasia ==== ==== MeSH C16.614.909 – toxoplasmosis, congenital ==== ==== MeSH
|
{
"page_id": 5115037,
"source": null,
"title": "List of MeSH codes (C16)"
}
|
C16.614.947 – Wolman disease ==== The list continues at List of MeSH codes (C17).
|
{
"page_id": 5115037,
"source": null,
"title": "List of MeSH codes (C16)"
}
|
The New Zealand Fungarium (PDD): Te Kohinga Hekaheka o Aotearoa is the major collection of New Zealand fungi. It is one of the largest collections in the Southern Hemisphere. The Fungarium is designated a Nationally Significant Collection by the Ministry of Business, Innovation and Employment. == History == The accessioning of collections that led to the establishment of the New Zealand Fungarium (PDD): Te Kohinga Hekaheka o Aotearoa began with the appointment of G.H. Cunningham in 1919 by the Department of Agriculture. Cunningham and the collection were transferred to the Department of Science and Industrial Research's Plant Diseases Division in 1936. This is the origin of the PDD acronym. The DSIR was disestablished and reorganised into a number of Crown Research Institutes (CRIs) in 1992 and the Fungarium is now part of and maintained by the Manaaki Whenua Landcare Research CRI. == Collections == The Fungarium houses the collections of R.E. Beever (Agaricales, Boletales), G.H. Cunningham (Aphyllophorales, Gasteromycetes, Uredinales), J.M. Dingley (Ascomycetes), E. Horak (Agaricales), S.J. Hughes (Hyphomycetes, sooty moulds), R.F.R. McNabb (Agaricales, Boletaceae, Dacrymycetaceae, Strobilomycetaceae, Tremellaceae), R.H. Petersen (Clavariaceae), G.J. Samuels (Ascomycetes), and K. Curtis. Fungal specimens from the herbarium of the Plant Health and Diagnostic Station, Levin (LEV) have been incorporated into PDD. The study of the New Zealand native mushrooms and other larger fungi was pioneered by Greta Stevenson, Marie Taylor, and Barbara Segedin from the late 1940s until the 1990s. Collectively they described over 250 new species of New Zealand fungi. All these are available through the Biota of New Zealand or Systematics Collections Data internet portals. The Fungarium has over 2,900 Type specimens – these are the specimens on which the species descriptions are based. These include over 17,000 New Zealand primary Types. Fungarium staff undertook an assessment in 2019 to identify native fungi that
|
{
"page_id": 78318750,
"source": null,
"title": "New Zealand Fungarium"
}
|
are endangered. As a result, 30 species were added to the International Union for Conservation of Nature's Red List. == References == == External links == Meet Maj Padamsee, curator of the New Zealand Fungarium (2022) Meet Adrienne Stanton, collection manager at the NZ Fungarium | Te Kohinga Hekaheka o Aotearoa (2022) Peter Buchanan introduces the New Zealand Fungarium | Te Kohinga Hekaheka o Aotearoa (2022)
|
{
"page_id": 78318750,
"source": null,
"title": "New Zealand Fungarium"
}
|
The Cotton effect in physics, is the characteristic change in optical rotatory dispersion and/or circular dichroism in the vicinity of an absorption band of a substance. In a wavelength region where the light is absorbed, the absolute magnitude of the optical rotation at first varies rapidly with wavelength, crosses zero at absorption maxima and then again varies rapidly with wavelength but in the opposite direction. This phenomenon was discovered in 1895 by the French physicist Aimé Cotton (1869–1951). The Cotton effect is called positive if the optical rotation first increases as the wavelength decreases (as first observed by Cotton), and negative if the rotation first decreases. A protein structure such as a beta sheet shows a negative Cotton effect. == See also == Cotton–Mouton effect == References ==
|
{
"page_id": 2952350,
"source": null,
"title": "Cotton effect"
}
|
The Aston–Greenburg rearrangement is a name reaction in organic chemistry. It allows for the generation of tertiary α-alkylesters from corresponding α-haloketones through a 1,2-rearrangement, with the use of an alkoxide. == Mechanism == == References ==
|
{
"page_id": 71306402,
"source": null,
"title": "Aston–Greenburg rearrangement"
}
|
The International Conference on Bioinformatics (InCoB) is a scientific conference on bioinformatics aimed at scientists in the Asia Pacific region. It has been held annually since 2002. Originally organised by coordination between the Asia Pacific Bioinformatics Network (APBioNet) and the Thailand National Center for Genetic Engineering and Biotechnology (BIOTEC) in 2002, the meeting has since been the flagship conference of the APBioNet, where APBioNet's Annual General Meeting is held. == Scientific publications == Since 2006, InCoB has been partnering with BMC Bioinformatics to publish an InCoB Special Conference Issue of top papers presented at the conference. In 2007, an additional tie-up with the Bioinformation journal was established in addition to the BMC Bioinformatics issue. == Technological placeshifting == Since 2007, InCoB held in Hong Kong University of Science and Technology, has been placeshifted in an additional location in a developing country venue, namely the Vietnam National University, Hanoi (VNU) through the advanced videoconferencing project of APAN and TEIN2. In 2015, InCoB was organised jointly with the International Conference on Genome Informatics in an attempt to increase effectiveness and scalability. == Satellite training workshops == Since 2007, at the VNU site coordinated by the Institute of Biotechnology Hanoi (IBT), InCoB coordinated with the International Union for Biochemists and Molecular Biologists (IUBMB), the Federation of Asian Oceanian Biochemists and Molecular Biologists (FAOBMB) and APBioNet to hold a two-week bioinformatics training course with course faculty from Karolinska Institutet, NCBI and National University of Singapore, supported by the S* Alliance for Bioinformatics Education and BioSlax, a software development project hosted at NUS as part of an ASEAN SubCommittee on Biotechnology (SCB) project. This collaboration with IUBMB and FAOBMB continues in 2008 with a bioinformatics education workshop in Taipei, Taiwan, where the main meeting of InCoB 2008 will be situated. == Past and present conferences
|
{
"page_id": 12848292,
"source": null,
"title": "International Conference on Bioinformatics"
}
|
== == External links == APBioNet Website InCoB Website == References ==
|
{
"page_id": 12848292,
"source": null,
"title": "International Conference on Bioinformatics"
}
|
Segmented filamentous bacteria or Candidatus Savagella are members of the gut microbiota of rodents, fish and chickens, and have been shown to potently induce immune responses in mice. They form a distinct lineage within the Clostridiaceae and the name Candidatus Savagella has been proposed for this lineage. They were previously named Candidatus Arthromitus because of their morphological resemblance to bacterial filaments previously observed in the guts of insects by Joseph Leidy. Despite the fact that they have been widely referred to as segmented filamentous bacteria, this term is somewhat problematic as it does not allow one to distinguish between bacteria that colonize various hosts or even if segmented filamentous bacteria are actually several different bacterial species. In mice, these bacteria grow primarily in the terminal ileum in close proximity to the intestinal epithelium where they are thought to help induce T helper 17 cell responses. Intriguingly, Segmented Filamentous Bacteria were found to expand in AID-deficient mice, which lack the ability to mount an appropriate humoral immune response because of impaired somatic hypermutation; parabiotic experiments revealed the importance of IgA in eliminating Segmented Filamentous Bacteria. This goes hand in hand with an earlier study demonstrating the ability of monocolonization with Segmented Filamentous Bacteria to dramatically increase mucosal IgA levels. Segmented Filamentous Bacteria are species specific, and may be important to immune development. == See also == List of bacteria genera List of bacterial orders == References == Gut Immune Maturation Depends on Colonization with a Host-Specific Microbiota (Cell Volume 149, Issue 7 2012 1578 – 1593) == Further reading == At least 50 scholarly articles on the subject at Google scholar. Two review articles Ivanov II; Littman DR (May 2010). "Segmented filamentous bacteria take the stage". Mucosal Immunol. 3 (3): 209–12. doi:10.1038/mi.2010.3. PMC 3010405. PMID 20147894. Klaasen HL; Koopman JP; Poelma
|
{
"page_id": 29363365,
"source": null,
"title": "Segmented filamentous bacteria"
}
|
FG; Beynen AC (June 1992). "Intestinal, segmented, filamentous bacteria". FEMS Microbiol. Rev. 8 (3–4): 165–80. doi:10.1016/0378-1097(92)90801-t. PMID 1515159.
|
{
"page_id": 29363365,
"source": null,
"title": "Segmented filamentous bacteria"
}
|
The molecular formula C22H31N3O2 (molar mass: 369.50 g/mol, exact mass: 369.2416 u) may refer to: Solvent Yellow 124 Piboserod
|
{
"page_id": 32181415,
"source": null,
"title": "C22H31N3O2"
}
|
Invasion genetics is the area of study within biology that examines evolutionary processes in the context of biological invasions. Invasion genetics considers how genetic and demographic factors affect the success of a species introduced outside of its native range, and how the mechanisms of evolution, such as natural selection, mutation, and genetic drift, operate in these populations. Researchers exploring these questions draw upon theory and approaches from a range of biological disciplines, including population genetics, evolutionary ecology, population biology, and phylogeography. Invasion genetics, due to its focus on the biology of introduced species, is useful for identifying potential invasive species and developing practices for managing biological invasions. It is distinguished from the broader study of invasive species because it is less directly concerned with the impacts of biological invasions, such as environmental or economic harm. In addition to applications for invasive species management, insights gained from invasion genetics also contribute to a broader understanding of evolutionary processes such as genetic drift and adaptive evolution. == History == === Descriptions of invasive species === Charles Elton formed the basis for examining biological invasions as a unified issue in his 1958 monograph, The Ecology of Invasions by Animals and Plants, drawing together case studies of species introductions. Other important events in the study of invasive species include a series of issues published by the Scientific Committee on Problems of the Environment in the 1980s and the founding of the journal Biological Invasions in 1999. Much of the research motivated by Elton's monograph is generally identified with invasion ecology, and focuses on the ecological causes and impacts of biological invasions. === The Genetics of Colonizing Species === The evolutionary modern synthesis in the early 20th century brought together Charles Darwin's theory of evolution by natural selection and classical genetics through the development of
|
{
"page_id": 63048872,
"source": null,
"title": "Invasion genetics"
}
|
population genetics, which provided the conceptual basis for studying how evolutionary processes shape variation in populations. This development was crucial to the emergence of invasion genetics, which is concerned with the evolution of populations of introduced species. The beginning of invasion genetics as a distinct study has been identified with a symposium held at Asilomar in 1964 which included a number of major contributors to the modern synthesis, including Theodosius Dobzhansky, Ernst Mayr, and G. Ledyard Stebbins, as well as scientists with experience working in areas of weed and pest control. Stebbins, working with another botanist, Herbert G. Baker, collected a series of articles which emerged from the Asilomar symposium and published a volume titled The Genetics of Colonizing Species in 1965. This volume introduced many of the questions which continue to motivate research in invasion genetics today, including questions about the characteristics of successful invaders, the importance of a species' mating system in colonization success, the relative importance of genetic variation and phenotypic plasticity in adaptation to new environments, and the effect of population bottlenecks on genetic variation. === Terminology of invasion genetics === Since its publication in 1965, The Genetics of Colonizing Species helped to motivate research which would provide a theoretical and empirical foundation for invasion genetics. However, the term invasion genetics only first appeared in the literature in 1998, and the first published definition appeared in 2005. The success of introduced species is quite variable, consequently researchers have sought to develop terminology which allows distinguishing different levels of success. These approaches rely on describing invasion as a biological process. == Process of biological invasion == === Background === Researchers have proposed a number of different methods for describing biological invasions. In 1992, the ecologists Mark Williamson and Alastair Fitter divided the process of biological invasion into
|
{
"page_id": 63048872,
"source": null,
"title": "Invasion genetics"
}
|
three stages: escaping, establishing, and becoming a pest. Since then, there has been an expanding effort to develop a framework for categorizing biological invasions in terms that are neutral with respect to a species' environmental and economic impacts. This approach has allowed biologists to focus on the processes which facilitate or inhibit the spread of introduced species. David M. Richardson and colleagues describe how introduced species must pass a series of barriers prior to becoming naturalized or invasive in a new range. Alternatively, the stages of an invasion may be separated by filters, as described by Robert I. Colautti and Hugh MacIsaac, so that invasion success would depend on the rate of introduction (propagule pressure) as well as the traits possessed by the organism. === Description === The most recent systematic effort to describe the steps of a biological invasion was made by Tim Blackburn and colleagues in 2011, which combined the concepts of barriers and stages. According to this framework, there are four stages of an invasion: transport, introduction, establishment, and spread. Each of these stages is accompanied by one or more barriers. === Application of invasion genetics to different stages of invasion === Invasion genetics can be used to understand the processes involved at each stage of a biological invasion. Many of the foundational questions of invasion genetics focused on processes involved during establishment and spread. As early as 1955, Herbert G. Baker proposed that self-fertilization would be a favourable trait for colonizing species because successful establishment would not require the simultaneous introduction of two individuals of opposite sexes. Baker subsequently elaborated a series of "ideal weed characteristics" in an article in The Genetics of Colonizing Species, which included traits such as the ability to tolerate environmental variation, dispersal ability, and the ability to tolerate generalist herbivores and
|
{
"page_id": 63048872,
"source": null,
"title": "Invasion genetics"
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|
pathogens. While some of the traits, such as ease of germination, may aid a species in transport or introduction, most of the traits Baker identified were primarily conducive to establishment and spread. Advances in the study of molecular evolution may help biologists to understand better the processes of transport and introduction. Genomicist Melania Cristescu and her colleagues examined mitochondrial DNA of the fishhook waterflea introduced into the Great Lakes, tracing the source of the invasive populations to the Baltic Sea. More recently, Cristescu has argued for expanding the use of phylogenetic and phylogenomic approaches, as well as applying metabarcoding and population genomics, to understand how species are introduced and identify "failed invasions" where introduction does not lead to establishment. == Factors influencing invasion success == === Propagule pressure === Propagule pressure describes the number of individuals introduced into an area in which they are not native, and can strongly affect the ability of species to reach a later stage of invasion. Factors which may influence the rate of transport and introduction into a novel environment include the species' abundance in its native range, as well as its tendency to co-occur with or be deliberately moved by humans. The likelihood of reaching establishment is also highly dependent on the number of individuals introduced. Small populations can be limited by Allee effects, as individuals may have difficulty finding suitable mates and populations are vulnerable to demographic stochasticity. Small populations may also suffer from inbreeding depression. Species that are introduced in larger numbers are more likely to establish in different environments, and high propagule pressure will introduce more genetic diversity into a population. These factors can help a species adapt to different environmental conditions during establishment as well as during subsequent spread in a new range. === Traits of successful invaders === Herbert
|
{
"page_id": 63048872,
"source": null,
"title": "Invasion genetics"
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|
G. Baker's list of 14 "ideal weed characteristics", published in the 1965 volume The Genetics of Colonizing Species, has been the basis for investigation into characteristics which could contribute to invasion success of plants. Since Baker first proposed this list, researchers have debated whether or not particular traits could be linked to the "invasiveness" of a species. Mark van Kleunen, in revisiting the question, proposed examining the traits of candidate invaders in the context of the process of biological invasion. According to this approach, particular traits might be useful for introduced species because they would allow them to pass through a filter associated with a particular stage of an invasion. === Genetic variation === A population of introduced species exhibiting higher genetic variation could be more successful during establishment and spread, due to the higher likelihood of possessing a suitable genotype for the novel environment. However, populations of a species in an introduced range are likely to exhibit lower genetic variation compared to populations in the native range due to population bottlenecks and founder effects experienced during introduction. A classic study on population bottlenecks, conducted by Masatoshi Nei, described a genetic signature of bottlenecks on introduced populations of Drosophila pseudoobscura in Colombia. The ecological success of many invaders despite these apparent genetic limitations suggests a "genetic paradox of invasion", for which a number of answers have been proposed. One of the possible resolutions for the genetic paradox of invasion is that most bottlenecks experienced by introduced species are typically not severe enough to have a strong effect on genetic variation. As well, a species may be introduced multiple times from multiple sources, resulting in genetic admixture which could compensate for lost genetic variation. The evolutionary ecologist Katrina Dlugosch has noted that the relationship between genetic variation and capacity for adaptation
|
{
"page_id": 63048872,
"source": null,
"title": "Invasion genetics"
}
|
is nonlinear and may depend on factors such as the effect size of adaptive loci (in quantitative genetics, effect size refers to the magnitude of change in a phenotypic trait value associated with a particular locus) and the presence of cryptic variation. === Phenotypic plasticity === Phenotypic plasticity is the expression of different traits (or phenotypes), such as morphology or behaviour, in response to different environments. Plasticity allows organisms to cope with environmental variation without necessitating genetic evolution. Herbert G. Baker proposed that the possession of "general purpose" genotypes which were tolerant of a range of environments could be advantageous for species introduced into new areas. General purpose genotypes could help introduced species encountering environmental variation during establishment and spread, in part because introduced species should have less genetic variation than native species. However, it remains disputed whether or not invasive species exhibit higher plasticity than native and non-invasive species. == Evolution during biological invasions == === Genetic consequences of range expansion === Range expansion is the process by which an organism spreads and establishes new populations across a geographic scale, so it is part of a biological invasion. During a range expansion, there exists an expanding wave front, where rapidly-growing populations are established by a relatively small number of individuals. Under these demographic conditions, the phenomenon of gene surfing can lead to the accumulation of deleterious mutations. This reduces the fitness of individuals at the wave front, and is described as an expansion load (see also: mutation load). These mutations can limit the rate of range expansion and, in the absence of effective recombination and natural selection which would remove such mutations, can have severe and persisting negative effects on populations. === Local adaptation === Invasive species may encounter environments which differ either from those experienced in their natural
|
{
"page_id": 63048872,
"source": null,
"title": "Invasion genetics"
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|
range or where they are introduced. In these environments natural selection can act on these introduced populations, provided that there is sufficient genetic variation present in the population, which may lead to local adaptation. Such adaptation can facilitate both the establishment and spread of an introduced species. Local adaptation can, however, be inhibited by genetic admixture between populations. Admixture can result in hybrid breakdown by breaking up beneficial gene linkages and introducing maladapted alleles. Admixture can also facilitation species introductions by increasing genetic variation, thereby limiting the cost of inbreeding in small populations. Through heterosis, the increased quality of hybrid offspring, admixture has also been shown to increase the vigour of introduced populations of common yellow monkeyflower. === Hybridization === Hybridization broadly refers to breeding between individuals from genetically isolated populations, and may therefore be within a species (intraspecific) or between species (interspecific). When offspring are distinct from either parent, hybridization can be a source of evolutionary novelty. Hybridization can also lead to gene flow between populations or species through the mechanism of introgression. Hybridization and its contribution to evolution was a subject of interest for G. Ledyard Stebbins, who noted in a 1959 review that the introduction of European species of the genus Tragopogon to North America had led to hybrid speciation; this example was also discussed by Herbert G. Baker in The Genetics of Colonizing Species. The first systematic review of the role of invasive plant species in interspecific hybridization appeared in 1992, and the phenomenon has also been explored in fish and aquatic invertebrates. Hybridization may increase the invasiveness of introduced species, either by introducing genetic variation, heterosis, or by creating novel genotypes which perform better in a given environment. Gene flow between introduced and native species can also result in the loss of biodiversity through genetic
|
{
"page_id": 63048872,
"source": null,
"title": "Invasion genetics"
}
|
pollution. === Evolutionary responses of native species to invaders === Because biological invasions can have a profound impact on the invaded environment, it is expected that the arrival of invasive species creates new selective pressures on native organisms, typically through competitive or predatory interactions. Through adaptive evolution, species in affected ecological communities could evolve to tolerate invasive species. This means that biological invasions potentially have both ecological and evolutionary consequences for native species. However, many studies have failed to detect an adaptive response of native species to ecological disruptions. The ecologists Jennifer Lau and Casey terHorst have pointed to this absence of an evolutionary response as an important consideration for understanding how invasive species disrupt ecological communities and the multiple challenges faced by native populations. == See also == == References == == Further reading == Barrett, Spencer C.H.; Colautti, Robert I.; Dlugosch, Katrina M.; Rieseberg, Loren H., eds. (2016). Invasion genetics: The Baker and Stebbins legacy. Hoboken, NJ: John Wiley & Sons. ISBN 9781118922163. WorldCat == External links == Spencer Barrett on the Foundation of Invasion Genetics (YouTube link)
|
{
"page_id": 63048872,
"source": null,
"title": "Invasion genetics"
}
|
The molecular formula C18H12O4 (molar mass: 292.28 g/mol, exact mass: 292.0736 u) may refer to: Karanjin Polyporic acid
|
{
"page_id": 26348712,
"source": null,
"title": "C18H12O4"
}
|
In optics, optical rotatory dispersion is the variation of the specific rotation of a medium with respect to the wavelength of light. Usually described by German physicist Paul Drude's empirical relation: [ α ] λ T = ∑ n = 0 ∞ A n λ 2 − λ n 2 {\displaystyle [\alpha ]_{\lambda }^{T}=\sum _{n=0}^{\infty }{\frac {A_{n}}{\lambda ^{2}-\lambda _{n}^{2}}}} where [ α ] λ T {\displaystyle [\alpha ]_{\lambda }^{T}} is the specific rotation at temperature T {\displaystyle T} and wavelength λ {\displaystyle \lambda } , and A n {\displaystyle A_{n}} and λ n {\displaystyle \lambda _{n}} are constants that depend on the properties of the medium. Optical rotatory dispersion has applications in organic chemistry regarding determining the structure of organic compounds. == Principles of operation == When white light passes through a polarizer, the extent of rotation of light depends on its wavelength. Short wavelengths are rotated more than longer wavelengths, per unit of distance. Because the wavelength of light determines its color, the variation of color with distance through the tube is observed. This dependence of specific rotation on wavelength is called optical rotatory dispersion. In all materials the rotation varies with wavelength. The variation is caused by two quite different phenomena. The first accounts in most cases for the majority of the variation in rotation and should not strictly be termed rotatory dispersion. It depends on the fact that optical activity is actually circular birefringence. In other words, a substance which is optically active transmits right circularly polarized light with a different velocity from left circularly polarized light. In addition to this pseudodispersion which depends on the material thickness, there is a true rotatory dispersion which depends on the variation with wavelength of the indices of refraction for right and left circularly polarized light. For wavelengths that are
|
{
"page_id": 2952363,
"source": null,
"title": "Optical rotatory dispersion"
}
|
absorbed by the optically active sample, the two circularly polarized components will be absorbed to differing extents. This unequal absorption is known as circular dichroism. Circular dichroism causes incident linearly polarized light to become elliptically polarized. The two phenomena are closely related, just as are ordinary absorption and dispersion. If the entire optical rotatory dispersion spectrum is known, the circular dichroism spectrum can be calculated, and vice versa. === Chirality === In order for a molecule (or crystal) to exhibit circular birefringence and circular dichroism, it must be distinguishable from its mirror image. An object that cannot be superimposed on its mirror image is said to be chiral, and optical rotatory dispersion and circular dichroism are known as chiroptical properties. Most biological molecules have one or more chiral centers and undergo enzyme-catalyzed transformations that either maintain or invert the chirality at one or more of these centers. Still other enzymes produce new chiral centers, always with a high specificity. These properties account for the fact that optical rotatory dispersion and circular dichroism are widely used in organic and inorganic chemistry and in biochemistry. In the absence of magnetic fields, only chiral substances exhibit optical rotatory dispersion and circular dichroism. In a magnetic field, even substances that lack chirality rotate the plane of polarized light, as shown by Michael Faraday. Magnetic optical rotation is known as the Faraday effect, and its wavelength dependence is known as magnetic optical rotatory dispersion. In regions of absorption, magnetic circular dichroism is observable. == See also == == References ==
|
{
"page_id": 2952363,
"source": null,
"title": "Optical rotatory dispersion"
}
|
Sir William Henry Bragg (2 July 1862 – 12 March 1942) was an English physicist and X-ray crystallographer who uniquely shared a Nobel Prize with his son Lawrence Bragg – the 1915 Nobel Prize in Physics: "for their services in the analysis of crystal structure by means of X-rays". == Biography == === Early years === Bragg was born at Westward, near Wigton, Cumberland, England, the son of Robert John Bragg, a merchant marine officer and farmer, and his wife Mary née Wood, a clergyman's daughter. When Bragg was seven years old, his mother died, and he was raised by his uncle, also named William Bragg, at Market Harborough, Leicestershire. He was educated at the Grammar School there, at King William's College on the Isle of Man and, having won an exhibition (scholarship), at Trinity College, Cambridge. He graduated in 1884 as third wrangler, and in 1885 was awarded a first class honours in the mathematical tripos. === University of Adelaide === In 1885, at the age of 23, Bragg was appointed (Sir Thomas) Elder Professor of Mathematics and Experimental Physics in the University of Adelaide, Australia, and started work there early in 1886. Being a skilled mathematician, at that time he had limited knowledge of physics, most of which was in the form of applied mathematics he had learnt at Trinity. Also at that time, there were only about a hundred students doing full courses at Adelaide, of whom less than a handful belonged to the science school, whose deficient teaching facilities Bragg improved by apprenticing himself to a firm of instrument makers. Bragg was an able and popular lecturer; he encouraged the formation of the student union, and the attendance, free of charge, of science teachers at his lectures. Bragg's interest in physics developed, particularly in the field
|
{
"page_id": 396459,
"source": null,
"title": "William Henry Bragg"
}
|
of electromagnetism. In 1895, he was visited by Ernest Rutherford, en route from New Zealand to Cambridge; this was the commencement of a lifelong friendship. Bragg had a keen interest in the new discovery of X-rays by Wilhelm Röntgen. On 29 May 1896 at Adelaide, Bragg demonstrated before a meeting of local doctors the application of "X-rays to reveal structures that were otherwise invisible". Samuel Barbour, senior chemist of F. H. Faulding & Co., an Adelaide pharmaceutical manufacturer, supplied the necessary apparatus in the form of a Crookes tube, a glass discharge tube. The tube had been obtained at Leeds, England, where Barbour visited the firm of Reynolds and Branson, a manufacturer of photographic and laboratory equipment. Barbour returned to Adelaide in April 1896. Barbour had conducted his own experiments shortly after return to Australia, but results were limited due to limited battery power. At the University, the tube was attached to an induction coil and a battery borrowed from Sir Charles Todd, Bragg's father-in-law. The induction coil was utilized to produce the electric spark necessary for Bragg and Barbour to "generate short bursts of X-rays". The audience was favorably impressed. Bragg availed himself as a test subject, in the manner of Röntgen and allowed an X-ray photograph to be taken of his hand. The image of the fingers in his hand revealed "an old injury to one of his fingers sustained when using the turnip chopping machine on his father's farm in Cumbria". As early as 1895, Bragg was working on wireless telegraphy, though public lectures and demonstrations focussed on his X-ray research which would later lead to his Nobel Prize. In a hurried visit by Rutherford, he was reported as working on a Hertzian oscillator. There were many common practical threads to the two technologies and he was
|
{
"page_id": 396459,
"source": null,
"title": "William Henry Bragg"
}
|
ably assisted in the laboratory by Arthur Lionel Rogers who manufactured much of the equipment. On 21 September 1897 Bragg gave the first recorded public demonstration of the working of wireless telegraphy in Australia during a lecture meeting at the University of Adelaide as part of the Public Teachers' Union conference. Bragg departed Adelaide in December 1897, and spent all of 1898 on a 12-month leave of absence, touring Great Britain and Europe and during this time visited Marconi and inspected his wireless facilities. He returned to Adelaide in early March 1899, and already on 13 May 1899, Bragg and his father-in-law, Sir Charles Todd, were conducting preliminary tests of wireless telegraphy with a transmitter at the Observatory and a receiver on the South Road (about 200 metres). Experiments continued throughout the southern winter of 1899 and the range was progressively extended to Henley Beach. In September the work was extended to two way transmissions with the addition of a second induction coil loaned by Mr. Oddie of Ballarat. It was desired to extend the experiments cross a sea path and Todd was interested in connecting Cape Spencer and Althorpe Island, but local costs were considered prohibitive while the charges for patented equipment from the Marconi Company were exorbitant. At the same time Bragg's interests were leaning towards X-rays and practical work in wireless in South Australia was largely dormant for the next decade. The turning-point in Bragg's career came in 1904 when he gave the presidential address to section A of the Australasian Association for the Advancement of Science at Dunedin, New Zealand, on "Some Recent Advances in the Theory of the Ionization of Gases". This idea was followed up "in a brilliant series of researches" which, within three years, earned him a fellowship of the Royal Society of
|
{
"page_id": 396459,
"source": null,
"title": "William Henry Bragg"
}
|
London. This paper was also the origin of his first book Studies in Radioactivity (1912). Soon after the delivery of his 1904 address, some radium bromide was made available to Bragg for experimentation. In December 1904 his paper "On the Absorption of α Rays and on the Classification of the α Rays from Radium" appeared in the Philosophical Magazine, and in the same issue a paper "On the Ionization Curves of Radium", written in collaboration with his student Richard Kleeman, also appeared. At the end of 1908, Bragg returned to England. During his 23 years in Australia "he had seen the number of students at the University of Adelaide almost quadruple, and had a full share in the development of its excellent science school." He had returned to England on the maiden voyage of the SS Waratah, a ship which vanished at sea on its second voyage the next year. He had been alarmed at the ship's tendency to list during his voyage, and had concluded that the ship's metacentre was just below her centre of gravity. In 1911, he testified his belief that the Waratah was unstable at the Inquiry into the ship's disappearance. There is a bust of William Bragg in North Terrace, Adelaide, South Australia. === University of Leeds === Bragg occupied the Cavendish chair of physics at the University of Leeds from 1909 until 1915. He continued his work on X-rays with much success. He invented the X-ray spectrometer and with his son, Lawrence Bragg, then a research student at Cambridge, founded the new science of X-ray crystallography, the analysis of crystal structure using X-ray diffraction. === World War I === Both of his sons (Lawrence and Robert) were called into the army after war broke out in 1914 . The following year he was appointed
|
{
"page_id": 396459,
"source": null,
"title": "William Henry Bragg"
}
|
Quain Professor of Physics at University College London. He had to wait for almost a year to contribute to the war effort: finally, in July 1915, he was appointed to the Board of Invention and Research set up by the Admiralty. In September, his younger son Robert died of wounds at Gallipoli. In November, he shared the Nobel Prize in Physics with elder son William Lawrence. The Navy was struggling to prevent sinkings by unseen, submerged U boats. The scientists recommended that the best tactic was to listen for the submarines. The Navy had a hydrophone research establishment at Aberdour Scotland, staffed with navy men. In November 1915, two young physicists were added to its staff. Bowing to outside pressure to use science, in July 1916, the Admiralty appointed Bragg as scientific director at Aberdour, assisted by three additional young physicists. They developed an improved directional hydrophone, which finally convinced the Admiralty of their usefulness. Late in 1916, Bragg with his small group moved to Harwich, where the staff was enlarged and they had access to a submarine for tests. In France, where scientists had been mobilized since the beginning of the war, the physicist Paul Langevin made a major stride with echolocation, generating intense sound pulses with quartz sheets oscillated at high frequency, which were then used as microphones to listen for echoes. Quartz was usable when vacuum tubes became available at the end of 1917 to amplify the faint signals. The British made sonar practicable by using mosaics of small quartz bits rather than slices from a large crystal. In January 1918, Bragg moved into the Admiralty as head of scientific research in the anti-submarine division. By war's end British vessels were being equipped with sonar manned by trained listeners. Inspired by William Lawrence's methods for locating enemy
|
{
"page_id": 396459,
"source": null,
"title": "William Henry Bragg"
}
|
guns by the sound of their firing, the output from six microphones miles apart along the coast were recorded on moving photographic film. Sound ranging is much more accurate in the sea than in the turbulent atmosphere. They were able to localize the sites of distant explosions, which were used to obtain the precise positions of British warships and of minefields. === University College London === After the war Bragg returned to University College London, where he continued to work on crystal analysis. === Royal Institution === From 1923, he was Fullerian Professor of Chemistry at the Royal Institution and director of the Davy Faraday Research Laboratory. This institution was practically rebuilt in 1929–30 and, under Bragg's directorship many valuable papers were issued from the laboratory. In 1919, 1923, 1925 and 1931 he was invited to deliver the Royal Institution Christmas Lecture on The World of Sound; Concerning the Nature of Things, Old Trades and New Knowledge and The Universe of Life respectively. === The Royal Society and the coming war === Bragg was elected president of the Royal Society in 1935. The physiologist A. V. Hill was biological secretary and soon A. C. G. Egerton became physical secretary. During World War I all three had stood by for frustrating months before their skills were employed for the war effort. Now the cause of science was strengthened by the report of a high-level Army committee on lessons learned in the last war; their first recommendation was to "keep abreast of modern scientific developments". Anticipating another war, the Ministry of Labour was persuaded to accept Hill as a consultant on scientific manpower. The Royal Society compiled a register of qualified men. They proposed a small committee on science to advise the Committee on Imperial Defence, but this was rejected. Finally in
|
{
"page_id": 396459,
"source": null,
"title": "William Henry Bragg"
}
|
1940, as Bragg's term ended, a scientific advisory committee to the War Cabinet was appointed. Bragg was among the 2,300 names of prominent persons listed on the Nazis' Special Search List, of those who were to be arrested on the invasion of Great Britain and turned over to the Gestapo. Bragg died in 1942. == Honours and awards == Bragg was joint winner with his son, Lawrence Bragg, of the Nobel Prize in Physics in 1915: "For their services in the analysis of crystal structure by means of X-ray". Bragg was elected Fellow of the Royal Society in 1907, vice-president in 1920, and served as President of the Royal Society from 1935 to 1940. He was elected an International Member of the United States National Academy of Sciences in 1939 and an International Member of the American Philosophical Society. He was elected as a member of the Royal Academy of Science, Letters and Fine Arts of Belgium on 1 June 1946. He was appointed Commander of the Order of the British Empire (CBE) in 1917 and Knight Commander (KBE) in the 1920 civilian war honours. He was admitted to the Order of Merit in 1931. Matteucci Medal (1915) Rumford Medal (1916) Copley Medal (1930) Franklin Medal (1930) John J. Carty Award of the National Academy of Sciences (1939) The current Electoral district of Bragg, in the South Australian House of Assembly, was created in 1970, and was named after both William and Lawrence Bragg. == Private life == In 1889, in Adelaide, Bragg married Gwendoline Todd, a skilled water-colour painter, and daughter of astronomer, meteorologist and electrical engineer Sir Charles Todd. They had three children, a daughter, Gwendolen and two sons, William Lawrence, born in 1890 in North Adelaide, and Robert. Gwendolen married the English architect Alban Caroe, Bragg taught
|
{
"page_id": 396459,
"source": null,
"title": "William Henry Bragg"
}
|
William at the University of Adelaide, and Robert was killed in the Battle of Gallipoli. Bragg's wife, Gwendoline, died in 1929. Bragg played tennis and golf, and as a founding member of the North Adelaide and Adelaide University Lacrosse Clubs, contributed to the introduction of lacrosse to South Australia and was also the secretary of the Adelaide University Chess Association. Bragg died in 1942 in England and was survived by his daughter Gwendolen and his son, Lawrence. == Legacy == The lecture theatre of King William's College (KWC) is named in memory of Bragg; the Sixth-Form invitational literary debating society at KWC, the Bragg Society, is also named in his memory. One of the school "Houses" at Robert Smyth School, Market Harborough, Leicester, is named "Bragg" in memory of him being a student there. Since 1992, the Australian Institute of Physics has awarded The Bragg Gold Medal for Excellence in Physics for the best PhD thesis by a student at an Australian university. The two sides of the medal contain the images of Sir William Henry and his son Sir Lawrence Bragg. The Experimental Technique Centre at Brunel University is named the Bragg Building. The Sir William Henry Bragg Building at the University of Leeds opened in 2021. In 1962, the Bragg Laboratories were constructed at the University of Adelaide to commemorate 100 years since the birth of Sir William H. Bragg. The Australian Bragg Centre for Proton Therapy and Research also in Adelaide, Australia was completed in late 2023. It is named for both father and son and offers radiation therapy for cancer patients. In August 2013, Bragg's relative, the broadcaster Melvyn Bragg, presented a BBC Radio 4 programme "Bragg on the Braggs" on the 1915 Nobel Prize in Physics winners. == Publications == William Henry Bragg, William Lawrence
|
{
"page_id": 396459,
"source": null,
"title": "William Henry Bragg"
}
|
Bragg, "X Rays and Crystal Structure", G. Bell & Son, London, 1915. William Henry Bragg, The World of Sound (1920) William Henry Bragg, The Crystalline State – The Romanes Lecture for 1925. Oxford, 1925. William Henry Bragg, Concerning the Nature of Things (1925) William Henry Bragg, Old Trades and New Knowledge (1926) William Henry Bragg, An Introduction to Crystal Analysis (1928) William Henry Bragg, The Universe of Light (1933) == See also == George Gamow – has 1931 photograph with Bragg, location unspecified. List of Nobel laureates in Physics List of presidents of the Royal Society == References == == Further reading == "[a] most valuable record of his work and picture of his personality is the excellent obituary written by Professor Andrade of London University for the Royal Society of London." Statement made by Sir Kerr Grant, in: "The Life and work of Sir William Bragg", the John Murtagh Macrossan Memorial Lecture for 1950, University of Queensland. Written and presented by Sir Kerr Grant, Emeritus Professor of Physics, University of Adelaide. Reproduced as pages 5–37 of Bragg Centenary, 1886–1986, University of Adelaide. "William and Lawrence Bragg, Father and Son: The Most Extraordinary Collaboration in Science", John Jenkin, Oxford University Press 2008. Ross, John F. A History of Radio in South Australia 1897–1977 (J. F. Ross, 1978) [1] == External links == "Annotated Bibliography for William Henry Bragg from the Alsos Digital Library for Nuclear Issues". 4 August 2010. Archived from the original on 4 August 2010. "Cambridge Physicists: William Lawrence Bragg (biography)". Archived from the original on 21 October 2012. Retrieved 2 July 2024. Data from the University of Leeds Archived 18 November 2007 at the Wayback Machine Fullerian Professorships Nobelprize.org – The Nobel Prize for Physics in 1915 William Henry Bragg on Nobelprize.org Works by William Henry Bragg
|
{
"page_id": 396459,
"source": null,
"title": "William Henry Bragg"
}
|
at LibriVox (public domain audiobooks)
|
{
"page_id": 396459,
"source": null,
"title": "William Henry Bragg"
}
|
The molecular formula C24H36O2 (molar mass: 356.54 g/mol, exact mass: 356.2715 u) may refer to: JWH-138 JWH-359 Nisinic acid
|
{
"page_id": 40176820,
"source": null,
"title": "C24H36O2"
}
|
The molecular formula C28H48O6 (molar mass: 480.69 g/mol, exact mass: 480.3451 u) may refer to: Brassinolide 24-Epibrassinolide
|
{
"page_id": 25693365,
"source": null,
"title": "C28H48O6"
}
|
Evolution Without Evidence: Charles Darwin and "The Origin of Species" is a 1982 book by historian Barry G. Gale. Contrary to the title, the book is not on the Creation–evolution controversy. Gale attempts to explain why Charles Darwin waited twenty years to publish his theory of natural selection and how his theory evolved during this period. The book heavily relies on Darwin's letters, notebooks, essays and papers. Darwin's private correspondences with Asa Gray and Joseph Hooker are cited. == Evolution Without Evidence: Charles Darwin and "The Origin of Species" == Gale explores Darwin's inexperience in botany and zoology as they pertain to his theory. This allowed him to convince others of Darwin's theory. Gale also discusses how Darwin uses social skills to get information and help for his theories and others. Lastly, Gale mentions Darwin's failure to convince important experts in the field and why he was forced to publish his theory prematurely. == Summary of Darwin's theory == Charles Darwin was an English naturalist who came up with the theory of Darwinism. Darwinism embedded the theory of biological evolution. He claimed that all species of organisms develop through natural selection. Darwin's theory of natural selection is, "the differential survival and reproduction of individuals due to differences in phenotype." == Criticism of Darwin's theory == Reception of Darwin's theory of evolution was met with mixed views particularly in the religious community. Specifically the church of England spoke out against the book, while liberal Anglicans supported his theory as an instrument used by God. During this time, Darwin's excitement seemed to grow as he utilized his correspondents to gain more support for his theory. == Darwin's correspondents == Asa Gray was a well renowned American botanist who authored Gray's Manual. Gray was a supporter of Charles Darwin, even though they had
|
{
"page_id": 48106681,
"source": null,
"title": "Evolution Without Evidence"
}
|
different bases of beliefs. However Gray became a proponent for Darwin's theory and garner support for it by incorporating the theory as an extension of a divine creator. Joseph Hooker was a British botanist famously argued in favor of Darwin's theory against the then bishop of Oxford. In his essay the introductory Introductory Essay to the Flora Tasmaniae, he announced his support for Darwin's theory which marked the first recognizable man of science publicly backing Charles Darwin. Hooker and Darwin exchanged roughly 1400 letters over the course of 40 years during their friendship. == Reception to Gale's book == The book has received positive reviews, but the title has been criticized as misleading. Muriel L. Blaisdell a professor of interdisciplinary studies praised the research of the book and described it as "easily accessible to the general reader... A new portrait of Darwin with its distinctively modern styling." Historian of science Philip F. Rehbock positively reviewed the book, stating it "will prove most useful to those who are looking for a direct path into the mountain of Darwinian literature. They will find Gale's route clearly articulated, heavily documented, adequately indexed, and unburdened by technical terminology." Biologist Richard Lewontin commented in a review "What is appealing in Gale’s work is a picture of a life in the social community of science that corresponds to our everyday experience of how careers are built." Biologist Gert Korthof has reviewed the book in depth. He felt that the book seemed to present unbiased, well researched evaluation of Darwin's theory and shed light on the lack of evidence behind it. The book does not say that Darwin did not have evidence in order to support his theory of Evolution. == References == == Further reading == Reiskind, Jonathan. (1985). That Fateful Friday: Darwin Between the Beagle
|
{
"page_id": 48106681,
"source": null,
"title": "Evolution Without Evidence"
}
|
and the Origin. The Florida Entomologist. Vol. 68, No. 1. pp. 11–17. Wyhe, John van. (2007). Mind the Gap: Did Darwin Avoid Publishing His Theory for Many Years? Notes and Records of the Royal Society of London. Vol. 61, No. 2. pp. 177–205.
|
{
"page_id": 48106681,
"source": null,
"title": "Evolution Without Evidence"
}
|
Isinglass ( EYE-zing-gla(h)ss) is a form of collagen obtained from the dried swim bladders of fish. The English word origin is from the obsolete Dutch huizenblaas – huizen is a kind of sturgeon, and blaas is a bladder, or German Hausenblase, meaning essentially the same. The bladders, once removed from the fish, processed, and dried, are formed into various shapes for use. It is used mainly for the clarification or fining of some beer and wine. It can also be cooked into a paste for specialised gluing purposes. Although originally made exclusively from sturgeon, especially beluga, in 1795 an invention by William Murdoch facilitated a cheap substitute using cod. This was extensively used in Britain in place of Russian isinglass, and in the US hake was important. In modern British brewing all commercial isinglass products are blends of material from a limited range of tropical fish. == Foods and drinks == Before the inexpensive production of gelatin and other competing products, isinglass was used in confectionery and desserts such as fruit jelly and blancmange. Isinglass finings are widely used as a processing aid in the British brewing industry to accelerate the fining, or clarification, of beer. It is used particularly in the production of cask-conditioned beers, although many cask ales are available which are not fined using isinglass. The finings flocculate the live yeast in the beer into a jelly-like mass, which settles to the bottom of the cask. Left undisturbed, beer will clear naturally; the use of isinglass finings accelerates the process. Isinglass is sometimes used with an auxiliary fining, which further accelerates the process of sedimentation. Non-cask beers that are destined for kegs, cans, or bottles are often pasteurised and filtered. The yeast in these beers tends to settle to the bottom of the storage tank naturally, so
|
{
"page_id": 265407,
"source": null,
"title": "Isinglass"
}
|
the sediment from these beers can often be filtered without using isinglass. However, some breweries still use isinglass finings for non-cask beers, especially when attempting to repair bad batches. Many vegetarians consider beers that are processed with these finings (such as most cask-conditioned ales in the UK) to be unsuitable for vegetarian diets (although acceptable for pescetarians). According to global data in 2018, along with low-calorie beer and gluten-free beer, beers that are acceptable for strict vegetarians are expected to grow in demand in the coming years. The demand increase is attributed to millennial consumers, and some companies have introduced vegetarian friendly options or done away with isinglass use. A beer-fining agent that is suitable for vegetarians is Irish moss, a type of red algae containing the polymer chemical carrageenan. However, carrageenan-based products (used in both the boiling process and after fermentation) primarily reduce hazes caused by proteins, but isinglass is used at the end of the brewing process, after fermentation, to remove yeast. Since the two fining agents act differently (on different haze-forming particles), they are not interchangeable, and some beers use both. Isinglass finings are also used in the production of kosher wines, although for reasons of kashrut, they are not derived from the beluga sturgeon, because this fish is not kosher. Whether the use of a nonkosher isinglass renders a beverage nonkosher is a matter of debate in Jewish law. Rabbi Yehezkel Landau, in Noda B'Yehuda, first edition, Yore Deah 26, for example, permits such beverages. This is the position followed by many kashrut-observant Jews today. The similar-sounding names has resulted in confusion between isinglass and waterglass, especially as both have been used to preserve eggs. A solution of isinglass was applied to eggs and allowed to dry, sealing their pores. Waterglass is sodium silicate. Eggs were
|
{
"page_id": 265407,
"source": null,
"title": "Isinglass"
}
|
submerged in solutions of waterglass, and a gel of silicic acid formed, also sealing the pores of the eggshell. == Conservation == Isinglass is also used as an adhesive to repair parchment, stucco and damage to paintings on canvas. Pieces of the best Russian isinglass are soaked overnight to soften and swell the dried material. Next, it is cooked slowly in a double boiler at 45 °C while being stirred. A small amount of gum tragacanth dissolved in water is added to the strained isinglass solution to act as an emulsifier. When repairing paint that is flaking from parchment, isinglass can be applied directly to an area which has been soaked with a small amount of ethanol. It is typically applied as a very tiny drop that is then guided, with the help of a binocular microscope, under the edges of flaking paint. It can also be used to coat tissue or goldbeater's skin. On paintings this can be used as a temporary backing to either canvas patches or filler until dried. Here, isinglass is similar to parchment size and other forms of gelatin, but it is unique in that as a dried film the adhesive can be reactivated with moisture. For this use, the isinglass is cooked with a few drops of glycerin or honey. This adhesive is advantageous in situations where minimal use of water is desired for the parchment as the isinglass can be reactivated with an ethanol-water mixture. It also has a greater adhesive strength than many other adhesives used for parchment repair. == In popular culture == In the musical Oklahoma!, the song "The Surrey With the Fringe on Top" describes the surrey as having "isinglass curtains you can roll right down" although here the term refers to mica, commonly used for windows in vehicle
|
{
"page_id": 265407,
"source": null,
"title": "Isinglass"
}
|
side screens (but totally inflexible). Mentioned several times in chapter 68 of Moby Dick by Herman Melville, in a discussion of whale skin and blubber. Mentioned in The Book of Life by Deborah Harkness, "her scales fell like isinglass", in reference to the scales of a fire drake named Corra, and in Mark Twain's The Gilded Age where he describes a furnace door which "framed a small square of isinglass..." (chapter seven). It is also mentioned in the first paragraph of Willa Cather’s The Song of the Lark: “the isinglass sides of the hard-coal burner were aglow.” == References == == Further reading == Davidson, Alan (1999). "Isinglass". Oxford Companion to Food. Oxford University Press. p. 407. ISBN 0-19-211579-0. Woods, Chris (1995). "Conservation Treatments for Parchment Documents", Journal of the Society of Archivists, Vol. 16, Issue 2, pp. 221–239. Chemozyme Archived 21 September 2018 at the Wayback Machine
|
{
"page_id": 265407,
"source": null,
"title": "Isinglass"
}
|
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