Kiss-and-run fusion

Kiss-and-run fusion is a type of synaptic vesicle release where the vesicle opens and closes transiently. In this form of exocytosis, the vesicle docks and transiently fuses at the presynaptic membrane and releases its neurotransmitters across the synapse, after which the vesicle can then be reused.
Kiss-and-run differs from full fusion, where the vesicle collapses fully into the plasma membrane and is then later retrieved by a clathrin-coat-dependent process. The idea that neurotransmitter might be released in "quanta" by the fusion of synaptic vesicles with the presynaptic membrane was first introduced by Bernard Katz and Jose del Castillo in 1955, when the first EM images of nerve terminals first appeared. The possibility of transient fusion and rapid retrieval of vesicle membrane was proposed by Bruno Ceccarelli in 1973, after examining in the electron microscope strongly stimulated frog neuromuscular junctions, and indirectly supported by the work of his group in the following years, using electrophysiology, electron microscopy and quick freezing techniques. The actual term, kiss-and-run, was introduced by Ceccarelli's collaborators after the first studies of simultaneous membrane capacitance and amperometric transmitter release measurements were performed and indicated that secretory products could actually be released during transient vesicle fusion.
Today, there is back and forth debate over full fusion and kiss-and-run fusion and which model portrays a more accurate picture of the mechanisms behind synaptic release. The increased accumulation of partially empty secretory vesicles following secretion, observed in electron micrographs are the most compelling evidence in favor of the kiss-and-run model. Accumulation of partially empty vesicles following secretion suggests that during the secretory process, only a portion of the vesicular contents are able to exit the cell, which could only be possible if secretory vesicles were to temporarily establish continuity with the cell plasma membrane, expel a portion of their contents, then detach and reseal.
Discovery.
Transient vesicle fusion was hypothesized by Katz and del Castillo in 1955. However, the first systematic studies were conducted by Ceccarelli et al. in 1973. Ceccarelli et al. studied frog neuromuscular junctions, stimulating them with markers such as horseradish peroxidase to identify endocytosed organelles, and using either mild stimulation (2 Hz) or strong stimulation (10 Hz) protocols for periods ranging from 20 minutes to 4 hours. At low stimulation for a period of 4 hours, Ceccarelli et al. found that there was an increase in horseradish peroxidase labeled vesicles over time, and no increases in large organelles, indicative of the vesicles fusing quickly with the presynaptic membrane and then separating from it after releasing its neurotransmitters. They hypothesized that at low frequencies of stimulation, most of the vesicles are quickly re-formed from the presynaptic membrane during and after stimulation. Further studies in Ceccarelli's lab accumulated evidence on the hypothesis of transient fusion by comparing electrophysiological and morphological data. In particular, images of vesicle fusions were examined on freeze-fractured presynaptic membranes and on electron-microscope images obtained from terminals quick-frozen few ms after the delivery of a single shock to the nerve. In 1993 Alvarez de Toledo and colleagues directly demonstrated the occurrence of secretory product release during the momentary opening of a transiently fusing vesicle, by combining the measurement of membrane capacitance (that monitors changes in surface area) with amperometric detection of the release of mediators. This led Fesce et al. to recapitulate all the indirect evidence in favor of transient fusion and coin the term kiss-and-run. The most compelling evidence for transient or kiss-and-run fusion has come from the discovery of the porosome, a permanent cup-shaped lipoprotein structure at the cell plasma membrane, where secretory vesicles transiently dock and fuse to release intra-vesicular contents from the cell.
Evidence for kiss-and-run.
With the discovery of the kiss-and-run mechanism by Ceccarelli et al., there have been many subsequent studies done that give evidence supporting kiss-and-run fusion. All studies have suggested that there are two main advantages kiss-and-run fusion has over full fusion: 1) kiss-and-run enables more efficient vesicle recycling and 2) kiss-and-run can limit how much neurotransmitter is released due to a smaller fusion pore and a shorter time during which neurotransmitters can actually be released. One of the major problems of kiss-and-run evidence, and subsequently the basis for many counterarguments against kiss-and-run, is that because fusion is so short, it is very hard to capture an actual kiss-and-run event. However, accumulation of partially empty vesicles following secretion strongly favors the kiss-and-run mechanism, suggesting that during the secretory process, only a portion of the vesicular contents are able to exit the cell, which could only be possible if secretory vesicles were to temporarily establish continuity with the cell plasma membrane, expel a portion of their contents, then detach and reseal. Since porosomes are permanent structures at the cell plasma membrane measuring just a fraction of the secretory vesicle size, demonstrates that secretory vesicles "transiently" dock and establish continuity, as opposed to complete collapse.
Rat pancreatic beta cells.
Rat pancreatic beta cells release neurotransmitters through kiss-and-run fusion. In endocrine and neuroendocrine cells, synaptic-like vesicles (SLVs) undergo kiss-and-run, but it's been controversial whether large dense-core vesicles (LDCVs) also undergo kiss-and-run. Studies have shown that LDCVs do undergo kiss-and-run exocytosis. MacDonald et al. used multiple approaches to test for kiss-and-run exocytosis in rat beta cells. By monitoring membrane patches of intact rat beta cells in the presence of 10 mM glucose and 5 mM forskolin, MacDonald et al. found that some vesicles underwent kiss-and-run, as seen by an exocytotic event followed by an endocytotic event of a similar magnitude. Kiss-and-run events accounted for 25% of LDCV exocytosis and 28% of SLV exocytosis. While LDCV kiss-and-run occurred 25% of the time in the presence of forskolin, in the absence of forskolin, LDCV kiss-and-run fusion occurred only 7% of the time. Because forskolin raises cyclic AMP (cAMP) levels, cAMP seemingly plays a very important role in the mechanism in LDCV kiss-and-run fusion in rat pancreatic beta cells.
SLV (pore diameter: 0.8 +/- 0.1 nm) and LDCV (pore diameter: 1.4 +/- 0.1 nm) fusion pores during kiss-and-run have been shown to be big enough to allow for efflux of gamma-aminobutyric acid (GABA) and adenosine triphosphate (ATP), but are too small to release insulin in rat pancreatic beta cells. Thus, the kiss-and-run mechanism could be implicated in medical complications involving insulin.
Hippocampal synapses.
Kiss-and-run exocytosis has been shown to occur at the synapses of neurons located in the hippocampus. Studies using FM1-43, an amphiphile dye inserted into the vesicles or membrane as a marker, have been instrumental in supporting kiss-and-run in hippocampal synapses. In hippocampal synapses, vesicles have been shown to allow the normal release of glutamate, an excitatory neurotransmitter in the brain, without permitting FM1-43 dye to enter or escape from the vesicle, indicating a transient mechanism suggestive of kiss-and-run. Increases in osmolarity have also been shown to permit less dye release in hippocampal synapses. In varying hypertonic solutions, 70% more FM1-43 dye was released from vesicles stimulated in 0.5 osM than from vesicles stimulated in 1.5 osM. Vesicles located in hypertonic regions of the body therefore might be more likely to undergo a kiss-and-run mode of exocytosis.
Mitochondria.
Mitochondria demonstrate kiss-and-run fusion in exchanging inner membrane materials. Studies using mitochondrial matrix-targeted green-photoactivated, red-fluorescent KFP and cyan-photoactivated, green-fluorescence PAGFP in rat cells have shown interactions where the KFP and PAGFP were transferred from one mitochondrion to another mitochondrion through transient fusion, suggesting a kiss-and-run mechanism. Unlike full fusion of mitochondria, which resulted in a single organelle, transient kiss-and-run fusion of two mitochondria resulted in two distinct membranes.
Manipulation of the optic atrophy 1 (Opa1) gene had interesting effects on fusion between mitochondria. Silencing the Opa1 gene decreased full fusion activity of mitochondria after 24 hours, and full fusion activity was completely eliminated after the Opa1 gene was silenced for 48 hours. Transient kiss-and-run fusion activity remained the same after 24 hours of Opa1 silencing. Kiss-and-run fusion is most common with low levels of Opa1 gene expression and extremely high levels of Opa1 gene expression. As a result, Opa1 expression governs fusion in mitochondria with regard to kiss-and-run.
Kiss-and-run fusion in mitochondria help to keep mitochondria in a reduced motility state for shorter period of time compared to full fusion. Liu et al. tested both kiss-and-run and full fusion and their effects on mitochondrial motility, and found that both forms of fusion resulted in decreased mitochondrial motility at first, but kiss-and-run fusion restored, and even increased, mitochondrial motility immediately after the kiss-and-run event was over. Kiss-and-run fusion provides a better mechanism to control mitochondrial bioenergetics than full fusion.
Regulation.
Calcium-dependent actin coating.
Kiss-and-run fusion has been thought to be stabilized by an actin coating of vesicles. Testing for the vesicle uptake of FM1-43 to note when vesicles fused with the membrane allowed researchers to notice that actin coating is a necessary step for the kiss-and-run mechanism. Vesicles labelled with the Beta-actin-green fluorescent protein (GFP) fluoresced seconds after fusing with the presynaptic membrane (as shown by FM1-43 uptake), but non-fused vesicles never fluoresced, suggesting that an actin coating is required for kiss-and-run. This actin coating came from the polymerization of actin monomers.
The actin coating process necessary for transient kiss-and-run fusion is mediated by calcium. Actin coating of vesicles was inhibited by BAPTA-AM, which removes calcium. With the absence of calcium through the use of BAPTA-AM, all fused vesicles remained attached to the presynaptic membrane but did not release its neurotransmitters, suggesting that calcium is required to make the actin coating, and that the actin coating is responsible in the mechanism for vesicle unloading or vesicle release.
Myosin II.
Kiss-and-run exocytosis is regulated by myosin II. Studies using total internal reflection fluorescence microscopy (TIRFM) in neuroendocrine PC12 cells showed that myosin II regulates fusion pore dynamics during kiss-and-run exocytosis. Over-expression of normal myosin II regulatory light chain (RLC) in mRFP (monomeric red fluorescent protein) tagged tissue and Venus-tagged brain tissue resulted in prolonged release kinetics, while over-expression of a mutant form of myosin II RLC short shortened release kinetics. Prolonged release kinetics is indicative of a slower closing of the fusion pore, so myosin II also regulates how much neurotransmitter is released during kiss-and-run exocytosis.
SNAREs.
Much scholarly debate exists over the role of SNARE proteins in kiss-and-run exocytosis. SNARE proteins mediate vesicle fusion - the exocytosis of vesicles with the presynaptic membrane at the fusion pore. When a vesicle fuses with the presynaptic membrane, a SNARE transition occurs from a trans position to a cis position, followed by SNARE dissociation. This process was thought to be irreversible. If kiss-and-run exocytosis occurs, however, then it would suggest that reversible association of SNARE proteins occurs and mediates the kiss-and-run mode of exocytosis. Manipulation of the SNARE proteins during kiss-and-run may give more insight to how the two relate, and more scholarly research is required.


Bernstein Network

The Bernstein Network Computational Neuroscience is a research network in the field of computational neuroscience; this field brings together experimental approaches in neurobiology with theoretical models and computer simulations. It unites different scientific disciplines, such as physics, biology, mathematics, medical science, psychology, computer science, engineering and philosophy in the endeavor to understand how the brain functions. The close combination of neurobiological experiments with theoretical models and computer simulations allows scientists of the Bernstein Network to pursue innovative approaches with regard to one of the most complex structures nature has created in the course of evolution: the natural brain.
The network started in 2004 with a funding initiative of the Federal Ministry of Education and Research (BMBF) to develop and interconnect research structures in computational neuroscience throughout Germany and to promote the transfer of theoretical insight into clinical and technical applications.
It is named after the German physiologist and biophysicist Julius Bernstein (1839-1917). His "membrane hypothesis" provided the first biophysical explanation of how nerve cells transmit and process information via electrical currents. Generating a mathematical description, he also paved the way to simulate neural brain processes in the computer. Today, the Bernstein Network consists of more than 200 research groups worldwide.
History.
In 2004, the Bernstein Network started off as the "Nationales Bernstein Netzwerk Computational Neuroscience" (NNCN)) as a funding initiative of the Federal Ministry of Education and Research (BMBF). The aim of the initiative was the long-term establishment of the research discipline Computational Neuroscience in Germany. As part of the high-tech strategy of the German government, the Bernstein Network has been supported with a total of about 170 million euros until now. The network includes over 200 research groups at more than 25 locations nationwide. The participating research groups were located at universities and non-university research institutes (Fraunhofer, Helmholtz, Leibniz and Max Planck institutes). Using a BMBF initial financing, 22 new professorships in the area of Computational Neuroscience were established at German universities within the framework of the Bernstein Network, which were cnsoblidated by the federal states.
Scientific members of the network were involved in study programs and courses and collaborated with numerous industry partners to develop specific biomedical or technological applications (e.g. brain computer interface, retinal implant, cochlear implant, prosthesis, advanced driver-assistance systems, neuromorphic chips). They also worked (and still do) on new diagnostic methods, therapeutic approaches, or tools for neurological or psychiatric disorders in collaboration with clinical researchers (e.g. epilepsy, tinnitus, amyotrophic lateral sclerosis, Parkinson's disease, stroke, depression, schizophrenia).
Structure.
Six Bernstein Centers (in Berlin, Freiburg, Göttingen, Heidelberg-Mannheim, Munich and Tübingen) form the basic structure of the Bernstein Network. As additional local structural elements, five Bernstein groups have been established (in Bochum, Bremen, Heidelberg, Jena, and Magdeburg). Eleven Bernstein Collaborations link the Bernstein Centers with diverse research groups widely distributed over Germany.
Since 2006, the BMBF has annually allocated the Bernstein Award to an outstanding young scientist in the research field of Computational Neuroscience. The award is endowed with up to 1,25 million euros over five years, and allows to establish an independent junior research group at a German research institution.
Since 2008 and 2009, respectively, the Bernstein Network comprehends two research foci, which explore the first steps towards applications. The" Bernstein Focus: Neurotechnology" includes 4 local collaborative projects (in Berlin, Göttingen, Frankfurt and Freiburg-Tübingen); the" Bernstein Focus: Neuronal Basis of Learning" comprises eight collaborative projects.
Integration into the international research landscape.
The German INCF Node (G-Node) connects the Bernstein Network with the international network of the International Neuroinformatics Coordinating Facility.
Since 2010, the BMBF promotes German-American cooperation projects in the field of computational neuroscience within the framework of the Bernstein Network and the CRCNS program in cooperation with the National Science Foundation (NSF) and the National Institutes of Health (NIH).
In a cooperation between the BMBF, German Research Foundation (DFG), and the Japan Science and Technology Agency (JST), German-Japan Collaboration projects have been launched in 2012.
Bernstein Conference.
The Bernstein Conference is the largest annual Computational Neuroscience conference in Europe attracting an international audience from across the world. Until 2017, it was organized by members of the Bernstein Network at annually changing locations. In the years 2018 - 2022, the Bernstein Conferences takes place in Berlin. The conference offers a broad overview over the topics of Computational Neuroscience and Neurotechnology.
Membership.
In 2009, members of the Bernstein Network founded a non-profit association, the Bernstein Association Computational Neuroscience, aiming at promoting science, research, and teaching in Computational Neuroscience and the communication of research contents and results to the public. The Bernstein Network Computational Neuroscience is open to all researchers in the field or related subjects. Individual membership must be supported by two active Bernstein members. Further information.


Dickie Davis (cricketer)

Richard Peter Davis (18 March 1966 – 29 December 2003) was an English cricketer. Davis was a right-handed batsman, who bowled slow left-arm orthodox. He was born at Westbrook, Kent.
Early life and Kent.
Davis grew up in East Kent and was educated firstly at King Ethelbert School in Birchington-on-Sea and later at Thanet Technical College on the Isle of Thanet. He was coached at county level throughout his life, eventually making his first-class cricket debut for Kent in 1986 against Warwickshire. Despite making his first-class debut for the county at the age of just 20, Davis faced a challenge to remain within the team; he was expected to succeed Derek Underwood, one of the finest left-arm spinners. This following the most successful period in the history of the county and with pitches at Canterbury which were not conducive to slow bowling.
Nonetheless, between 1986 and 1993, he represented Kent in 125 first-class matches with his final appearance for the county coming against the touring Australians. Despite the nature of the pitches at Canterbury, Davis was a successful bowler for the county. In 125 matches, he took 320 wickets at a bowling average of 35.02, with 13 five wicket hauls and 2 ten wicket hauls in a match. His best bowling figures were 7/64, which came in 1992, his best with the ball. During the 1992 season, he took 74 wickets at an average of 21.74, with those best figures coming against Durham at Eastwood Gardens. Up to this time, he had also developed into a handy lower order batsman for the county. In his 125 matches, he scored 1,795 runs at a batting average of 15.74, with 4 half centuries and a high score of 67 which came against Hampshire in the 1989 County Championship. Davis also made his debut in List-A cricket for Kent against Worcestershire. A tidy bowler with a good economy rate, Davis played 106 List-A matches for the county, during which time he took 103 wickets an average of 31.71, which included his only List-A five wicket haul of 5/52 against Somerset. At the end of the 1993 season, the emergence of Min Patel led Davis not to extend his Kent contract.
Moves to Warwickshire and Gloucestershire.
Leaving Kent, Davis moved to Warwickshire who at the time were coached by Bob Woolmer. Woolmer believed Davis could improve as a cricketer if he had more self-belief, even believing he had it in him to represent England at a time when spin bowling was a declining art. He made his first-class debut for the county against Mashonaland during Warwickshire's pre-season tour to Zimbabwe. From 1994 to 1995, he represented Warwickshire in 20 first-class matches and 12 List-A matches. In 20 first-class matches, he took 54 wickets at an average of 31.01, with 3 five wicket hauls and best figures of 6/94. In his 12 List-A matches, he took 13 wickets at an average of 22.23, with best figures of 3/19. In his first season with Warwickshire, he tasted instant success as the team went on to win Warwickshire's first county cricket's first treble – Championship, Benson and Hedges Cup and AXA Equity & Law League. Held in high regard by Woolmer, then Warwickshire captain Dermot Reeve did not share Woolmer's high regard of Davis and with the emergence of the young Ashley Giles, Davis left Warwickshire at the end of the 1995 season. While at the county, Woolmer had also encouraged Davis to take up coaching later in his career, calling him a "deep thinker".
Joining Gloucestershire in 1996, he made his first-class debut for the county against Middlesex at Lord's. Between 1996 and 1997, he represented Gloucestershire in 24 first-class matches, the last of which came against Lancashire. He also played 20 List-A matches for the county, the last of which came against Kent. In his 24 first-class matches for Gloucestershire he took 40 wickets at an average of 41.50, with best figures of 4/35. In his 20 List-A matches for the county he took 20 wickets at an average of 37.30, with best figures of 3/42. After two seasons at Bristol he left to join Sussex.
Sussex and retirement.
Joining Sussex for the 1998 season, he represented the county exclusively in List-A cricket. During that season he played 4 List-A matches for the county in the AXA League and Benson and Hedges Cup against Lancashire, Middlesex and Essex twice. During his 4 match stint with the county, he took just a single wicket at a cost of 118.00, in what ultimately proved to be an unsuccessful spell. With this came his retirement from cricket at the end of 1998 season. In the following years he took up numerous coaching positions, with a successful career as a coach seemingly beckoning. During this time he became the cricket development officer for Greater London.
Berkshire and Leicestershire.
In 2001, Davis came out of retirement to play as the player-coach for Berkshire. His debut in the Minor Counties Championship for the county came against Shropshire. During the 2001 season, he represented the county in 6 Minor Counties Championship matches, the last of which came against Dorset. He also made his debut in the MCCA Knockout Trophy for the county against Dorset. He represented Berkshire in 4 Trophy matches, the last of which came against the Channel Islands. Davis also represented Berkshire in List-A matches, the first of which came when Berkshire played the Middlesex Cricket Board and Essex in the 2001 Cheltenham & Gloucester Trophy. His final List-A match for Berkshire and in his career, came against Lincolnshire in the 1st round of the 2002 Cheltenham & Gloucester Trophy which was played in 2001. It was in this match that he scored his maiden and only List-A half century, with a score of 56.
2001 saw one of the most extraordinary chapters of his career, when on a coaching course in Northampton he was asked by Leicestershire to play a one-off County Championship match; this was due to Leicestershire's injury crisis at the time. Making a single appearance against Northamptonshire, he scored his final first-class half century, by making 51 runs, before being dismissed by Monty Panesar. To expand his fairy tale end of his first-class career, he took figures of 6/73; his wickets included those of Graeme Swann and Michael Hussey.
Career summary.
Davis was considered an able batsman, in his entire first-class career he scored 2,503 runs at an average of 15.26, with 5 half centuries and a high score of 67. A spinner who often did not get too much spin on a cricket ball, Davis was notable for his ability to bowl accurately and to tie up and end. As such he was a bowler whose style was more to defend the run rate than to actively seek to dismiss the batsman. Though, with the ball he took 421 wickets at an average of 34.92, with 17 five wicket hauls and 2 ten wicket hauls in a match, his best figures were 7/64. An able slip fielder, he took 157 catches. In his 145 List-A matches, he scored 457 runs at an average of 10.15, with a single half century high score of 56. With the ball he took 141 wickets at an average of 32.04, a single five wicket haul of 5/52. In the field he toom 57 catches in one-day cricket.
Something of a journeyman, Davis was the first cricketer to have represented five different first-class counties.
Death.
Two weeks after playing for Leicestershire and while acting as assistant coach of the England women's cricket team, Davis suffered a seizure. The cause of this seizure was discovered to be a low-grade brain tumour. During that season's winter, he underwent radiotherapy and chemotherapy while still coaching Kent Women and England Women. With the treatment having little success in fighting the cancer, he underwent surgery in 2002, but his health continued to deteriorate. In 2003, while attending a match at Canterbury he was awarded a numbered county cap by his former club. Ten days before his death, his wife's sister married the then Kent captain David Fulton. Davis died at Blean in Kent on 29 December 2003. He was buried in his Kent blazer.


Hugo Ballesteros Reyes

Hugo Eugenio Ballesteros Reyes (3 January 1931 – 7 April 2019) was a Chilean politician and diplomat.
Born in Santiago, he studied law at the Universidad de Chile's campus in Valparaíso. He served as a member of the Chamber of Deputies (1957–1969) and the Senate (1969–1973). In 1964 he was also a member of his country's delegation to the United Nations General Assembly.
Ballesteros Reyes died of brain cancer in Valparaíso, at the age of 88.


Tuber of vermis

The tuber of vermis, the most posterior division of the inferior vermis, is of small size, and laterally spreads out into the large inferior semilunar lobules, which comprise at least two-thirds of the inferior surface of the hemisphere.


Smash and Grab (biology)

Smash and Grab is the name given to a technique developed by Charles S. Hoffman and Fred Winston used in molecular biology to rescue plasmids from yeast transformants into "Escherichia coli", also known as E. coli, in order to amplify and purify them. In addition, it can be used to prepare yeast genomic DNA (and DNA from tissue samples) for Southern blot analyses or polymerase chain reaction (PCR).


Parabrachial nuclei

The parabrachial nuclei, also known as the parabrachial complex, are a group of nuclei in the dorsolateral pons that surrounds the superior cerebellar peduncle as it enters the brainstem from the cerebellum. They are named from the Latin term for the superior cerebellar peduncle, the "brachium conjunctivum". In the human brain, the expansion of the superior cerebellar peduncle expands the parabrachial nuclei, which form a thin strip of grey matter over most of the peduncle. The parabrachial nuclei are typically divided along the lines suggested by Baxter and Olszewski in humans, into a medial parabrachial nucleus and lateral parabrachial nucleus. These have in turn been subdivided into a dozen subnuclei: the superior, dorsal, ventral, internal, external and extreme lateral subnuclei; the lateral crescent and subparabrachial nucleus (Kolliker-Fuse nucleus) along the ventrolateral margin of the lateral parabrachial complex; and the medial and external medial subnuclei
Components.
The main parabrachial nuclei are the medial parabrachial nucleus, the lateral parabrachial nucleus and the subparabrachial nucleus.
The medial parabrachial nucleus is one of the three main nuclei in the parabrachial area at the junction of the midbrain and the pons. It relays information from the taste area of the solitary nucleus to the ventral posteromedial nucleus of the thalamus.
The lateral parabrachial nucleus is one of three main parabrachial nuclei, located at the junction of the midbrain and pons. It receives information from the caudal solitary tract and transmits signals mainly to the medial hypothalamus but also to the lateral hypothalamus and many of the nuclei targeted by the medial parabrachial nucleus.
The subparabrachial nucleus, also known as the Kölliker-Fuse nucleus and diffuse reticular nucleus, is one of the three parabrachial nuclei between the midbrain and the pons. The subparabrachial nucleus regulates the breathing rate. It receives signals from the caudal, cardio-respiratory part of the solitary nucleus and sends signals to the lower medulla oblongata, the spinal cord, the amygdala and the lateral hypothalamus.
The parabrachial nuclei receive visceral afferent information from a variety of sources in the brainstem, including much input from the solitary nucleus, which brings taste information and information about the remainder of the body. The external, dorsal, internal and superior lateral subnuclei also receive input from the spinal and trigeminal dorsal horn, mainly concerned with pain and other visceral sensations. Outputs from the parabrachial nucleus originate from specific subnuclei and target forebrain sites involved in autonomic regulation, including the lateral hypothalamic area, ventromedial, dorsomedial, and arcuate hypothalamic nuclei, the median and lateral preoptic nuclei, the substantia innominate, the ventroposterior parvicellular and intralaminar thalamic nuclei, the central nucleus of the amygdala, and the insular and infralimbic cortex. The subparabrachialnucleus and lateral crescent send efferents to the nucleus of the solitary tract, ventrolateral medulla, and spinal cord, where they target many respiratory and autonomic cell groups. Many of these same brainstem and forebrain areas send efferents back to the parabrachial nucleus as well.
Function.
Arousal.
Many subsets of neurons in the parabrachial complex that target specific forebrain or brainstem cell groups contain specific neuropeptides, and appear to carry out distinct functions. For example, a population of neurons in the external lateral parabrachial subnucleus that contain the neurotransmitter calcitonin gene-related peptide (CGRP) appears to be critical for relaying information about hypoxia or hypercapnia (e.g., if one is being suffocated during sleep, such as by sleep apnea) to forebrain sites to wake up the brain, and prevent asphyxia.
Recent data indicate that glutamatergic neurons in the medial and lateral parabrachial nuclei, along with glutamatergic neurons in the pedunculopontine tegmental nucleus, provide a critical node in the brainstem for producing a waking state. Lesions of these neurons cause irreversible coma.
Blood sugar control.
Other neurons in the superior lateral parabrachial nucleus that contain cholecystokinin have been found to prevent hypoglycemia.
Thermoregulation.
Other neurons in the dorsal lateral parabrachial nucleus that contain dynorphin sense skin temperature from spinal afferents, and send that information to neurons in the preoptic area involved in thermoregulation. A study in 2017, has shown this information to be relayed through the lateral parabrachial nucleus rather than the thalamus, which drives thermoregulatory behaviour.
Taste.
Parabrachial neurons in rodents that relay taste information to the ventroposterior parvocellular (taste) nucleus of the thalamus are mainly CGRP neurons in the external medial parabrachial nucleus and they project predominantly contralaterally, as well as a smaller number in the ventral lateral nucleus, which project mainly ipsilaterally.
Neurons that mediate the sensation of itching, connect to the parabrachial nucleus by way of glutamatergic spinal projection neurons. This pathway triggers scratching in mice.
Pleasure.
The parabrachial nucleus relays satiety and pain-related signals to higher brain regions; when inhibited, this can produce "liking" responses to certain pleasurable stimuli, such as sweet taste.


Kevin Berry

Kevin John Berry, OAM, (10 April 1945 – 7 December 2006) was an Australian butterfly swimmer of the 1960s who won the gold medal in the 200-metre butterfly at the 1964 Summer Olympics in Tokyo. He set twelve world records in his career. After his swimming career ended, he became the Pictorial Editor of "The Sydney Morning Herald" and later the head of ABC Sport.
Biography.
Berry, the second of seven children, was born in Sydney and grew up in the western suburb of Marrickville, in a family with no prior sporting background. His father Frederick had arrived in Australia in the 1920s and had worked as a bar manager to support the family. He was taught to swim by his elder sister Colleen along with his younger siblings at Botany Bay. His younger brother Paul was a promising youth swimmer who defeated dual Olympic gold medallist Michael Wenden, and later became a professional rugby league footballer. Berry was educated at De La Salle College, and represented the school in athletics and rugby league, with moderate success. Berry joined the Pyrmont Club, which trained at Victoria Park Swimming Pool, under Eric Hayes, and swam from 1956 until 1958 as a freestyler, with reasonable age group success. In 1958 he won a butterfly race, and despite winning more races, Hayes did not think that he was suited to butterfly. Berry switched coaches to Don Talbot, training at Bankstown, New South Wales by the end of the year.
In 1959, at the under-14 New South Wales Championships, Berry came first, second and third in the breaststroke, backstroke and butterfly respectively. Talbot encouraged him, predicting that he would do well the following year. Berry's parents were surprised when Talbot told them at the end of the year that Berry had a chance of making the 1960 Summer Olympics team for Rome, even though he had never entered an Australian Championship before. At the end of the year, he came second to Neville Hayes, a fellow Talbot swimmer, defeating Harry Turner, who had been expected to be Australia's second butterflier at the Olympics.
At the New South Wales championships in January 1960, he came second to Hayes in both the 110-yard and 220-yard butterfly, and repeated this at the Australian Championships, earning himself Olympic selection at the age of 14. He was sent on a training camp with the Australian team to Townsville, Queensland to prepare for the Olympics. Arriving in Rome, Berry swam in the heats of the 4×100-metre medley relay, before being replaced by Hayes in the final, who combined with David Theile, Terry Gathercole and Geoff Shipton to claim silver behind the United States. Under the rules of the era, heat swimmers were not entitled to medals. In the 200-metre butterfly, Berry qualified fifth fastest, but came home in sixth in the final, six seconds behind the American winner Mike Troy. Hayes finished second. Troy, who was impressed by Berry, sent him an autographed postcard, implying that he could be the next Olympic champion.
In 1961 Hayes again won the State and National titles, relegating Berry to second. Berry also finished his high schooling that year, and had a disrupted preparation for an international meet at the end of the year against a Japanese team and the 1962 Commonwealth Games the following year. In the four bilateral meets at Brisbane, Sydney, Melbourne and Hobart, Berry managed to beat Hayes in the last race, making a psychological breakthrough. At the following New South Wales Championships, he broke both the 220-yard and 110-yard butterfly world records, breaking Hayes' dominance. He again lowered the 220-yard record at the Australian Championships in qualifying for the Commonwealth Games. At the Games in Perth, he set Commonwealth records in both events to record his first international victories, and then combined with Julian Carroll, Ian O'Brien and David Dickson to add a third gold in the 4x110-yard medley relay.
In 1963, Berry successfully defended both of his butterfly titles, and then made a European tour with the Australian team, and then passed the entry examinations to Indiana University, and moved to the United States on a swimming scholarship under Doc Counsilman. He was defeated in the US Championships that year by Carl Robie, who later captured his world records. Berry trained amongst high calibre swimmers at Indiana, as his teammates included Tom Stock, Chet Jastremski and Ted Stickles, holders of every backstroke, breaststroke and medley world record respectively.
In 1964, Berry returned to Australia to qualify for the 1964 Summer Olympics in Tokyo, Japan, breaking world records in both the 100-metre and 200-metre butterfly. Due to financial difficulties, he took a job as a petrol station attendant, and washing dishes for a steakhouse. In one case, the Australian team were hosted for a reception at the steakhouse meaning that he had to prepare and clean up despite being one of the guests. Berry attended a training camp in Ayr, Queensland under Talbot, who was the national head coach. During the week before the 200-metre event in Tokyo, Berry, the favourite for the gold medal, swam an extremely slow time trial during practice, in the view of opposition swimmers, leaving doubts in Talbot's mind. Robie broke the Olympic record in both the heat and semifinal. In the final, Berry was one of only two swimmers to have had previous Olympic experience and decided to deliberately false start in order to unsettle his opponents. He then set a time of 2:06.6, 0.3 of a second faster than his previous world record to claim gold. He later combined with Dickson, O'Brien and Peter Reynolds to claim bronze in the 4×100-metre medley relay.
Berry returned to the United States, but was unable to match his previous form, and exchanged regular wins and defeats with Robie, who swam for the University of Michigan. He was selected for the 1966 Commonwealth Games in Kingston, Jamaica, but withdrew after his father's death and returned to Australia. He retired the following year and married, but continued his university education, initially studying business, but later switching to radio and television, and then photography. He worked as a photographer for two years in the United States before switching to "The Sydney Morning Herald" in Australia, where he later became the Pictorial Editor. He served as the ABC head of sport from 1985 until 1987, before starting his own private sports business. He was inducted into the International Swimming Hall of Fame as an "Honor Swimmer" in 1980.
External links.


Brain Research

Brain Research is a peer-reviewed scientific journal focusing on several aspects of neuroscience. It publishes research reports and "minireviews". The editor-in-chief is Matthew J. LaVoie.
Until 2011, full reviews were published in Brain Research Reviews, which is now integrated into the main section, albeit with independent volume numbering. In 2006, four other previously established semi-independent journal sections ("Cognitive Brain Research, Developmental Brain Research, Molecular Brain Research," and "Brain Research Protocols") were merged with "Brain Research".
The journal has nine main subsections:
Abstracting and indexing.
"Brain Research" is abstracted and indexed in:


Glomerulus (olfaction)

The glomerulus (plural glomeruli) is a spherical structure located in the olfactory bulb of the brain where synapses form between the terminals of the olfactory nerve and the dendrites of mitral, periglomerular and tufted cells. Each glomerulus is surrounded by a heterogeneous population of juxtaglomerular neurons (that include periglomerular, short axon, and external tufted cells) and glial cells.
All glomeruli are located near the surface of the olfactory bulb. The olfactory bulb also includes a portion of the anterior olfactory nucleus, the cells of which contribute fibers to the olfactory tract. They are the initial sites for synaptic processing of odor information coming from the nose. A glomerulus is made up of a globular tangle of axons from the olfactory receptor neurons, and dendrites from the mitral and tufted cells, as well as, from cells that surround the glomerulus such as the external tufted cells, periglomerular cells, short axon cells, and astrocytes. In mammals, glomeruli typically range between 50-120 µm in diameter and number between 1100 and 2400 depending on the species, with roughly between 1100 and 1200 in humans. The number of glomeruli in a human decreases with age; in humans that are over 80 they are nearly absent. Each glomerulus is composed of two compartments, the olfactory nerve zone and the non-olfactory nerve zone. The olfactory nerve zone is composed of preterminals and terminals of the olfactory nerve and is where the olfactory receptor cells make synapses on their targets. The non-olfactory nerve zone is composed of the dendritic processes of intrinsic neurons and is where dendrodendritic interactions between intrinsic neurons occur.
Anatomy.
Glomeruli are important waystations in the pathway from the nose to the olfactory cortex and have been found to be critical for odorant signal transduction. The olfactory receptor neurons (ORN), which originate in the nasal epithelium express only one type of olfactory receptor (OR). These ORNs then project their axons to the olfactory bulb. In the olfactory bulb, the ORNs synapse with termination in the glomeruli. Each glomerulus receives input from olfactory receptor neurons expressing only one type of olfactory receptor. The glomerular activation patterns within the olfactory bulb are thought to represent the quality of the odor being detected. These activation patterns of glomeruli can change due to changes in airflow rate and odor concentration in the mucus layer of the nasal cavity. A certain odorant can activate a glomeruli strongly whilst affecting others with less efficiency to very little at all. Linda Buck and Richard Axel were awarded a Nobel prize in 2004 for heavily influencing the working out of the genetic basis for this Olfactory coding.
The current dogma is that axons from all ORNs expressing the same receptor converge onto one or two glomeruli of a possible 1800 glomeruli in each olfactory bulb. As the axons of the ORNs migrate towards their specific glomeruli they often overshoot into neighboring glomeruli. Thus, a glomerulus representing a specific OR develops slowly and involves considerable axonal reorganization in order to achieve the highly topographical projection observed in adult mice.
Function.
The glomerulus is the basic unit in the odor map of the olfactory bulb. Each odor activates a different pattern of glomeruli, such that, simply by analyzing the different sets of activated glomeruli, one could, in theory, decode the identity of the odor. This odor map, however, is modified by the circuitry within the olfactory bulb so that the spiking pattern of the second-order mitral cells is usually different from that of the olfactory sensory neurons.
Other species.
Glomerulus in Dogs.
The glomerulus process in dogs is divided in 3 parts. signal acquisition, signal transduction, and signal processing. Some dogs have as many as 100 times more ORNs than humans do, producing a correspondingly sharpened ability to detect and discriminate among millions of odors. Characteristics of these stages include: the role of olfactory plume and sniffing, the continuous renewal of Glomerulus receptors throughout the life cycle, and the relationship between the olfactory neuron and the glomerulus, and finally, the synthetic nature of glomerulus coding.
Glomerulus in Fish.
One of the most distinctive features of fish olfaction is that it takes place entirely in the aquatic environment. The carrier of stimulant is water and therefore the chemicals must be soluble in water. The olfactory epithelium of fish consists of three cell types, like other vertebrates. These three cell types are the receptor cells, supporting cells and basal cells.
Fish glomerulus differs from the mammalian glomerulus in terms of the number of dendrites that it receives from the mitral cells. In a mammalian olfactory system, a single dendrite from a mitral cell enters a single glomerulus. However, in fish, one or more dendrites from mitral cells enter one or more glomerulus.


Reversible reaction

A reversible reaction is a reaction in which the conversion of reactants to products and the conversion of products to reactants occur simultaneously.
A and B can react to form C and D or, in the reverse reaction, C and D can react to form A and B. This is distinct from a reversible process in thermodynamics.
Weak acids and bases undergo reversible reactions. For example, carbonic acid:
The concentrations of reactants and products in an equilibrium mixture are determined by the analytical concentrations of the reagents (A and B or C and D) and the equilibrium constant, "K". The magnitude of the equilibrium constant depends on the Gibbs free energy change for the reaction. So, when the free energy change is large (more than about 30 kJ mol−1), then the equilibrium constant is large (log K > 3) and the concentrations of the reactants at equilibrium are very small. Such a reaction is sometimes considered to be an irreversible reaction, although small amounts of the reactants are still expected to be present in the reacting system. A truly irreversible chemical reaction is usually achieved when one of the products exits the reacting system, for example, as does carbon dioxide (volatile) in the reaction
History.
The concept of a reversible reaction was introduced by Berthollet in 1803, after he had observed the formation of sodium carbonate crystals at the edge of a salt lake (one of the natron lakes in Egypt, in limestone):
He recognized this as the reverse of the familiar reaction
Until then, chemical reactions were thought to always proceed in one direction. Berthollet reasoned that the excess of salt in the lake helped push the "reverse" reaction towards the formation of sodium carbonate.
In 1864, Waage and Guldberg formulated their law of mass action which quantified Berthollet's observation. Between 1884 and 1888, Le Chatelier and Braun formulated Le Chatelier's principle, which extended the same idea to a more general statement on the effects of factors other than concentration on the position of the equilibrium.
Reaction kinetics.
For the reversible reaction A⇌B, the forward step A→B has a rate constant formula_1 and the backwards step B→A has a rate constant formula_2. The concentration of A obeys the following differential equation:
If we consider that the concentration of product B at anytime is equal to the concentration of reactants at time zero minus the concentration of reactants at time formula_3, we can set up the following equation:
Combining and , we can write
Separation of variables is possible and using an initial value formula_5, we obtain:
and after some algebra we arrive at the final kinetic expression:
The concentration of A and B at infinite time has a behavior as follows:
Thus, the formula can be linearized in order to determine formula_12:
To find the individual constants formula_1 and formula_2, the following formula is required:


Extrastriate cortex

The extrastriate cortex is the region of the occipital cortex of the mammalian brain located next to the primary visual cortex. Primary visual cortex (V1) is also named striate cortex because of its striped appearance in the microscope. The extrastriate cortex encompasses multiple functional areas, including V3, V4, V5/MT, which is sensitive to motion, or the extrastriate body area (EBA) used in the perception of human bodies.
Anatomy.
In terms of Brodmann areas, the extrastriate cortex comprises Brodmann area 18 and Brodmann area 19, while the striate cortex comprises Brodmann area 17.
In primates, the extrastriate cortex includes visual area V3, visual area V4, and visual area MT (sometimes called V5), while V1 corresponds to the striate cortex, and V2 to the prestriate cortex.


Paramedian reticular nucleus

The paramedian reticular nucleus (in Terminologia Anatomica, or paramedian medullary reticular group in NeuroNames) sends its connections to the spinal cord in a mostly ipsilateral manner, although there is some decussation.
It projects to the vermis in the anterior lobe, the pyramis and the uvula.
The paramedian nucleus also projects to the contralateral PRN, the gigantocellular nucleus, and the nucleus ambiguous.
The paramedian reticular formation is adjacent to the abducens (VI)nucleus in the pons and adjacent to the oculomotor nucleus(III) in the midbrain.
The paramedian nucleus receives afferents mostly from the fastigial nucleus in the cerebellum and the cerebral cortex; however, the projections from the spinal cord are very sparse.
The descending afferent connections come mostly from the frontal and parietal lobes; however the pontine reticular formation also sends projections to the paramedian reticular nucleus.
There are also very sparse innervations from the superior colliculus.
Lesions in the paramedian reticular nucleus have been shown to cause a stereotyped increase in the random patterns of motion in rats. The paramedian nuclei on either side of the brain stem have been shown to mediate the horizontal eye movements on their ipsilateral sides. It seems possible that the random motion patterns of the above rats were caused by an inability to mediate their horizontal eye movements.


Progesterone 3-acetyl enol ether

Progesterone 3-acetyl enol ether, also known as progesterone acetate, as well as 3-acetoxypregna-3,5-dien-20-one, is a progestin which was never marketed. It was reported to possess similar potency to progesterone and hydroxyprogesterone caproate in the rabbit endometrial carbonic anhydrase test, a bioassay of progestogenic activity. In addition, it was able to maintain pregnancy in animals. Progesterone 3-acetyl enol ether is closely related to quingestrone, which is also known as progesterone 3-cyclopentyl enol ether and was formerly marketed as an oral contraceptive.
The 3-acetyl ether may be cleaved from progesterone 3-acetyl enol ether "in vivo" and, based on its chemical structure, this may result in the transformation of progesterone 3-acetyl enol ether into 3α-dihydroprogesterone and/or 3β-dihydroprogesterone. 3β-Dihydroprogesterone has been reported to possess about the same progestogenic potency as progesterone in the Clauberg test, whereas 3α-dihydroprogesterone was not assessed.
The C3 enol ethers of progesterone are less suited for use via depot injection relative to progestogen esters like hydroxyprogesterone caproate due to their susceptibility to oxidative metabolism.


Methestrol dipropionate

Methestrol dipropionate or methoestrol dipropionate (brand name Meprane Dipropionate), also known as promethestrol dipropionate or promethoestrol dipropionate or as dimethylhexestrol dipropionate, is a synthetic nonsteroidal estrogen of the stilbestrol group related to diethylstilbestrol that is or was used clinically. It is the dipropionate form of methestrol (or promethestrol), which, in contrast to methestrol dipropionate, was never marketed.


Smound

Smound is a perception or sense experience created from the convergence of scents and sounds in the brain. The word is a portmanteau of smell and sound.
Research by Wesson and Wilson.
The smound concept is based on a study done by Daniel Wesson, PhD and Donald Wilson, PhD, researchers at the Nathan S. Kline Institute for Psychiatric Research (NKI) in New York City.
The study, which was published in "The Journal of Neuroscience", traced extracellular recordings from the olfactory tubercles of anesthetized mice. They found that 65% of single tubercle units responded to odours and 19% responded to auditory tones. When the tubercles were subjected to both odour and tone, 29% displayed supraadditive or suppressive responses. The authors of the study have suggested that this shows some cross-modulation between the two senses.
Applications.
"Scientific American" has suggested that the results of this study could have a major impact on the study of synesthesia. The researchers plan to patent a device for sniffer dogs that would link inhaled scents with a sound, making the operations of these animals more efficient and effective.
History of the concept.
The idea that sounds and scents may be linked in the brain was suggested in 1862 by G. W. Septimus Piesse, who said, "Scents, like sounds, appear to influence the olfactory nerve in certain definite degrees." Piesse also suggested that there may be an octave of odour.


Monatepil

Monatepil is a calcium channel blocker and α1-adrenergic receptor antagonist used as an antihypertensive.


Roger Ebert Should Lay Off the Fatty Foods

"Roger Ebert Should Lay Off the Fatty Foods" is the eleventh episode of the second season of the American animated television series "South Park". The 24th episode of the series overall, it originally aired on Comedy Central in the United States on September 2, 1998. The episode was written by series co-creator Trey Parker, along with David Goodman, and directed by Parker. It spoofs the "" episode "Dagger of the Mind". In the episode, the boys visit a planetarium; they soon discover that the operator has sinister intentions involving brainwashing. Meanwhile, Cartman auditions to sing on the Cheesy Poofs advertisement.
Despite the title, the episode has nothing to do with Roger Ebert (who had given "Orgazmo" and "BASEketball" negative reviews, despite being complimentary of the show "South Park"), aside from a brief joke about a fictional "Roger Ebert constellation" during the tour of the planetarium, and another joke, obscured by other characters speaking over it, comparing the hot gas that composes stars to "what comes out of Roger Ebert's mouth when he speaks".
Plot.
The class goes on a bus trip to the local planetarium. Once arriving, Cartman is tempted by a Cheesy Poofs truck parked outside, auditioning kids to sing the Cheesy Poofs song on their next television advertisement. The kids all think they will hate the planetarium, but after watching the star show, they want to go back again after the field trip. Not only do they go back, but they all also start volunteering to work at the planetarium. This turns out to be because the director, Dr. Adams, is using a brainwashing device on them. While doing so, he describes how stars are made up of hot gas, "which also comes out of Roger Ebert's mouth".
Cartman sings the Cheesy Poofs song and gets selected to sing it on television, after cheating and browbeating his way past the other contestants. Cartman bursts into the classroom to tell his friends that he was selected to sing on the commercial, only to be confronted by Kyle as Kyle creates an on-the-spot Haiku poem about Cartman's chances. Kyle says "I bet you don't win, They don't let big fat asses, perform on TV" in perfect Haiku form (which the children were studying at the time), to which Mr Garrison exclaims "very good Kyle!". Stan and Kyle become concerned about the planetarium's star show. When they have Kenny go and witness the show while Stan and Kyle examine the controls, they casually increase the star projector's power, unexpectedly causing Kenny's head to explode. Stan and Kyle tell Officer Barbrady what has happened; Barbrady is skeptical but accompanies them to question Dr. Adams. Because of this, Dr. Adams brainwashes Barbrady to believe that he is Elvis Presley; he then reveals his brainwashing scheme to the boys: to have people work at the planetarium because nobody finds planetariums interesting.
Meanwhile, school counselor Mr. Mackey and school nurse Nurse Gollum have learned of the mind control device through a child who earlier escaped the planetarium. They race to stop Dr. Adams, and a showdown occurs at the planetarium, with Stan, Kyle, Mr. Mackey, and Nurse Gollum against Dr. Adams and Barbrady. The boys, Mackey, and Nurse Gollum are quickly captured, tied down, and brainwashed into forgetting everything they found out.
However, in the middle of the process, Cartman, upon discovering the other boys missed his commercial, angrily kicks the star projector, sending the full blast of the mind control machine into Dr. Adams' brain. Dr. Adams becomes a mindless shell collapsed against a wall. Cartman is elated that he not only was on television but saved everyone as well. His mother chastizes him for picking his nose again.
Home media.
All 18 episodes of the second season, including "Roger Ebert Should Lay Off the Fatty Foods", were released on a DVD box set on June 3, 2003.


List of Thai language idioms

Idioms in the Thai language are usually derived from various natural or cultural references. Many include rhyming and/or alliteration, and their distinction from aphorisms and proverbs are not always clear. This is a list of such idioms.


Dick Brown (baseball)

Richard Ernest Brown (January 17, 1935 – April 17, 1970) was an American professional baseball catcher who played in Major League Baseball (MLB) for the Cleveland Indians, Chicago White Sox, Detroit Tigers and Baltimore Orioles. The native of Shinnston, West Virginia, attended Florida State University. He threw and batted right-handed and was listed as tall and . His brother Larry Brown had a 12-year MLB career (1963–74) as an infielder with four American League teams.
Originally signed by the Indians in 1953, Dick Brown made his big league debut on June 20, 1957 against the Boston Red Sox at the age of 22. After three seasons with the Indians, he was traded to the Chicago White Sox on December 6, 1959, along with Don Ferrarese, Minnie Miñoso and Jake Striker for Norm Cash, Bubba Phillips and Johnny Romano.
Brown caught for six pitchers who would eventually be inducted into the Baseball Hall of Fame. He played in 636 games over nine seasons, hitting .244 with 62 home runs and 223 runs batted in. His best two seasons were the two he spent with Detroit: he hit 16 home runs in 1961 and 12 home runs in 1962. He had a career .989 fielding percentage. Career highlights include back-to-back-to-back home runs he hit with Norm Cash and Steve Boros on May 23, 1961. He hit a grand slam less than one month earlier on April 29.
He played his final game on October 3, 1965. He had been expected to continue as the Orioles' starting catcher entering the 1966 season, but the discovery of a brain tumor early in spring training necessitated surgery to remove it on March 7. Additional surgery weeks later revealed another brain tumor, an inoperable one that effectively ended Brown's playing career and cost him his life. He served as a scout for the Orioles until his death at age 35 in Baltimore in 1970. He is buried in Pinecrest Cemetery in Lake Worth, Florida.


Perineurium

The perineurium is a protective sheath that surrounds a nerve fascicle. This bundles together axons targeting the same anatomical location. The perineurium is composed from fibroblasts.
In the peripheral nervous system, the myelin sheath of each axon in a nerve is wrapped in a delicate protective sheath known as the endoneurium. Fascicles, bundles of neurons, are surrounded by the perineurium. Several fascicles may be in turn bundled together with a blood supply and fatty tissue within yet another sheath, the epineurium. This grouping structure is analogous to the muscular organization system of epimysium, perimysium and endomysium.
Structure.
The perineurium is composed of connective tissue, which has a distinctly lamellar arrangement consisting of one to several concentric layers. The perineurium is composed of perineurial cells, which are epithelioid myofibroblasts. Perineurial cells are sometimes referred to as myoepithelioid due to their epithelioid and myofibroblastoid properties including tight junctions, gap junctions, external laminae and contractility. The tight junctions provide selective barrier to chemical substances.
The perineurium is a smooth, transparent tubular membrane which may be easily separated from the fibers it encloses. In contrast, the epineurium is a tough and mechanically resistant tissue which is not easily penetrated by a needle.


Sakes alive

Sakes Alive! is an old-fashioned mild oath, popular in the 1930s, 40s and 50s. Derives from "Land(s) sakes (alive)", with "Lands" standing for "Lord’s". Equivalent to today's “My Goodness”, “Good Lord”, “Oh my God” or the most closely related "For God's Sake."


Myotonia congenita

Myotonia congenita is a congenital neuromuscular channelopathy that affects skeletal muscles (muscles used for movement). It is a genetic disorder. The hallmark of the disease is the failure of initiated contraction to terminate, often referred to as delayed relaxation of the muscles (myotonia) and rigidity. Symptoms include delayed relaxation of the muscles after voluntary contraction (myotonia), and may also include stiffness, hypertrophy (enlargement), transient weakness in some forms of the disorder (from certain genetic mutations), severe masseter spasm, and cramping. The condition is sometimes referred to as fainting goat syndrome, as it is responsible for the eponymous 'fainting' seen in fainting goats when presented with a sudden stimulus. Of note, myotonia congenita has no association with malignant hyperthermia (MH).
Symptoms and signs.
The prolonged muscle contractions, which occur most commonly in the leg muscles in recessive mutations, and more commonly in the hands, face, and eyelids in dominant mutations, are often enhanced by inactivity, and in some forms are relieved by repetitive movement known as "the warm-up effect". This effect often diminishes quickly with rest. Some individuals with myotonia congenita are prone to falling as a result of hasty movements or an inability to stabilize themselves after a loss of balance. During a fall, a person with myotonia congenita may experience partial or complete rigid paralysis that will quickly resolve once the event is over. However, a fall into cold water may render the person unable to move for the duration of submergence. As with myotonic goats, children are more prone to falling than adults, due to their impulsivity.
The two major types of myotonia congenita are distinguished by the severity of their symptoms and their patterns of inheritance. Becker disease usually appears later in childhood than Thomsen disease, and causes more severe myotonia, muscle stiffness and transient weakness. Although myotonia in itself is not normally associated with pain, cramps or myalgia may develop. People with Becker disease often experience temporary attacks of muscle weakness, particularly in the arms and hands, brought on by movement after periods of rest. They may also develop mild, permanent muscle weakness over time. This muscle weakness is not observed in people with Thomsen disease. However, in recent times, as more of the individual mutations that cause myotonia congenita are identified, these limited disease classifications are becoming less widely used.
Early symptoms in a child may include:
Possible complications may include:
Phenotypic variability.
Both Thomsen and Becker myotonia have high phenotype variability. Severity of symptoms can vary greatly between individuals and throughout the lives of the individuals themselves. This may be partly because there are over 130 currently known different mutations that can cause the disorder, each with their own specifics, and also because myotonia congenita is an ion channel disorder, and ion channels are sensitive to internal and external environmental factors. It has been shown that pregnancy and the use of diuretics aggravate myotonia, and both these conditions are linked to the loss of divalent cations such as magnesium and calcium. It has further been shown that in pharmacological induced myotonia in isolated rat muscle, myotonia could be dampened by increasing the magnesium and calcium content of the extracellular medium. This has also been shown for isolated human muscle.
Adrenaline/epinephrine is well known to make myotonia worse in most individuals with the disorder, and a person with myotonia congenita may experience a sudden increase in difficulty with mobility in a particularly stressful situation during which adrenaline is released.
Due to the invisible nature of the disorder, the fact that those with myotonia congenita often appear very fit and able bodied, the general lack of knowledge about the disorder by the general and medical community, and often by the individual themselves, and the potential for inconsistency with the symptoms, many people with myotonia congenita have experienced a degree of social persecution at one time or another because of the effects of their disorder.
Temperature.
Many patients report that temperature may affect the severity of symptoms, especially cold as being an aggravating factor. However, there is some scientific debate on this subject, and some even report that cold may alleviate symptoms.
The warm-up phenomenon.
This phenomenon was described along with the disease by Thomsen in 1876 but its etiology remains unclear.
Patients report that myotonia congenita may present itself in the following ways (this is from first hand experience). If the person is sedentary and then decides to walk up a set of stairs, by the third or fourth step their leg muscles begin to stiffen significantly, requiring them to slow down almost to a complete stop. But as the muscles loosen up, a few steps later, they can once again begin to climb the steps at a normal pace. If this person plays any kind of a sport, a good warm-up is mandatory. Otherwise if they need to quickly and intensively use their muscles, such as in a sprint race or a basketball game, their muscles will freeze up, causing them to slow down or almost come to a complete stop. But once the muscles are warmed up, they can once again function normally. This can happen in various muscles, even in muscles such as the tongue. For example, if a person has not spoken for awhile and then wants to speak, their tongue may be stiff at first causing the words to come out a little garbled, but after a few seconds of trying to speak, the tongue muscle will loosen up and then they can speak normally for the remainder of the time that they are conversing.
Patients report that repeated contraction of muscle alleviates present myotonia with each contraction, such that myotonia is almost absent after a few contractions of the same muscle. The effect lasts about five minutes. There have been several proposed mechanisms for this phenomenon, but none have been conclusive; one theory is that the Na+/K+-ATPase is stimulated during the myotonic activity by increased intracellular Na+ in the cytosol of the muscle cell, increasing the activity of the Na+/K+-ATPase. However, in experiments with patients where the Na+/K+-ATPase had been blocked in the underarm by infusion of the Na+/K+-ATPase-blocker Ouabain, no effect on warm-up was observed. Another theory is that the few remaining functional chloride channels in muscle may become more active with increased muscle activity. However, this is not widely recognized.
It has been proposed that inactivation of Na+ channel 1.4 that resides in skeletal muscle, could play an important role in the warm-up phenomenon. In particular slow-inactivation of the channel is believed to have a spatial and temporal extend that is correlated to warm-up and therefore may provide a plausible cause.
Causes.
The disorder is caused by mutations in part of a gene (CLCN1) encoding the ClC-1 chloride channel, resulting in muscle fiber membranes having an unusually exaggerated response to stimulation (hyperexcitability).
Three cases have been reported who were diagnosed with Thomsen's myotonia and proved on genetic testing not to have mutations in the chloride gene but rather in the alpha-subunit of the voltage gated sodium channel (SCN4A). Like chloride channel mutations, patients with sodium channel mutations may have a very varied phenotype, making a diagnosis more difficult.
Mechanisms.
Myotonia congenita is caused in humans by loss-of-function mutations in the gene "CLCN1". This is the gene encoding the protein CLCN1, that forms the ClC-1 chloride channel, critical for the normal function of skeletal muscle cells. This gene is also associated with the condition in horses, goats, and dogs. In short, in lack of sufficient functional chloride channels, the muscle fiber membrane becomes hyper-excitable and continues to be electrically active (firing action potentials) when stimulated, for longer periods of time, than a normal muscle fiber. This results in prolonged contraction/delayed relaxation of the muscle.
The dysfunctional Cl− channels are located in the muscle fiber membrane and do not affect the motor nerve innervating the muscle. However, many studies have shown that denervation of muscle fibers alter the resting membrane conductance, but whether this affects myotonia in the muscle has been subject to heavy debate, and results from experiments are inconclusive.
In skeletal muscle fibers, a large transverse tubule system with a high surface-area to volume ratio exists. The onset of skeletal muscle activity is associated with the initiation and propagation of action potentials again associated with an efflux of K+ to the extracellular fluid and transverse tubule system. When many action potentials are elicited subsequently more K+ is expelled from the cell into the transverse tubular system. As K+ accumulates in the transverse tubular system the equilibrium potential for K+ (EK+) normally around -80 mV, becomes more depolarized (depolarization), according to the Nernst equation. In skeletal muscle fibers the equilibrium potential for Cl− is around -80 mV, equal to that of K+ at rest. Cl− moves towards its equilibrium potential around -80 mV, while potassium moves towards its equilibrium potential more depolarized than -80 mV during activity. This results in a slightly more depolarized membrane potential of the fiber during repeated action potentials, see Goldman equation. The Na+ conductance is only elevated shortly compared to the K+ conductance during each action potential, which is why K+ largely determines the membrane potential (Cl− is passively distributed during rest).
In the case of myotonia congenita, the chloride channels that allow Cl− to move across the membrane towards its equilibrium potential are defective, thus K+ is the only ion determining the membrane potential, and as more and more K+ accumulates in the transverse tubular system with each subsequent action potential the fiber depolarizes until the membrane potential comes close enough to the action potential threshold for spontaneous activity to ensue
Spontaneous action potentials can arise for several seconds, leading to the delayed relaxation that is the hallmark of myotonia. Cessation of spontaneous activity is associated with sodium channel inactivation (Nav1.4).
Diagnosis.
Types.
Two types of myotonia congenita exist, an autosomal dominant form and an autosomal recessive form. Autosomal dominant myotonia congenita (OMIM #160800) is also called Thomsen disease, after Danish/German physician Asmus Julius Thomas Thomsen (1815–1896), who himself had the disease and who wrote the first description of it in the medical literature (in 1876). Autosomal recessive myotonia congenita (OMIM #255700) is also called generalized myotonia, recessive generalized myotonia (RGM), Becker disease, and Becker myotonia, after the German professor Peter Emil Becker, who discovered its recessive nature.
The term "congenital" in its sense of "clinically apparent from birth" applies only to Thomsen disease, as the clinical onset of Becker myotonia may be delayed up to the age of 4 to 6 years. But in either form of myotonia congenita, the term's strictest sense reflects that the disease is genetically present from birth, although the clinical onset may be delayed.
With the advent of genetic testing, it has recently been found that some typically recessive mutations may occur in a dominant fashion in some individuals. The reason for this is not known.
Because several CLCN1 mutations can cause either Becker disease or Thomsen disease, doctors usually rely on characteristic signs and symptoms to distinguish the two forms of myotonia congenita. However, myotonia caused by CLCN1 mutations can occasionally be clinically indistinguishable from myotonia caused by sodium channel mutations (SCN4A mutations) resulting in the similar disease paramyotonia congenita.
A so-called Finnish heritage disease, congenital myotonia is more common in Finland and among ethnic Finns. A molecular study of the CLCN1 gene in 24 families in northern Finland, including 46 affected individuals, showed that although the inheritance appeared to be dominant (Thomsen type), in fact it is recessive (Becker type).
Differential diagnosis.
Sodium channel myotonias (SCN4A)
Dystrophies
Potassium channel disorders (KCNJ2)
Other disorders
Treatment.
Some cases of myotonia congenita do not require treatment, or it is determined that the risks of the medication outweigh the benefits. If necessary, however, symptoms of the disorder may be relieved with quinine, ranolazine, procainamide, flecainide, phenytoin, carbamazepine, mexiletine and other anticonvulsant drugs. Physical therapy and other rehabilitative measures may also be used to help muscle function. Genetic counseling is available.
Epidemiology.
In northern Scandinavia, the prevalence of myotonia congenita has been estimated at 1:10,000.
Myotonia congenita is estimated to affect 1 in 100,000 people worldwide.
Research.
Myotonia can be achieved in preparations of intact isolated muscle by the administration of 9-Anthracenecarboxylic acid, a blocker of chloride channels. It is also possible to achieve myotonia in preparations of intact isolated muscle by greatly lowering or removing the extracellular content of chloride in the bathing medium.
During the 1970s several murine models of myotonia appeared. One in particular has been used widely, the "adr" mouse or "arrested development of righting response". This model is often used in scientific work with muscular dystrophy, and displays myotonia due to lack of functional chloride channels.


Larry Bogdanow

Larry Bogdanow (February 24, 1947 – June 29, 2011) was an American restaurant architect.
Early life and education.
Born in Houston, Texas, Bogdanow graduated from Washington University in St. Louis, Missouri, in 1970.
He moved to New York City and studied architecture at the Pratt Institute in Brooklyn, New York, where he earned a bachelor's degree in 1977.
Career.
He began his career working for the architectural firm Beyer Blinder Belle, but quickly left to establish his own firm, New City Designs, in 1978. That firm eventually became Bogdanow Partners Architects.
His firm became known for designing the architecture for several well-known restaurants in New York City, including the Union Square Cafe and many others including Savoy, Cub Room, Atlas, Follonico, Kelley & Ping, City Hall, Kin Khao, Union Pacific and The Screening Room. Outside of New York, his firm was responsible for the design of Rubicon in San Francisco, Lexington Square Cafe in Westchester and Adagio in Chicago.
Death.
Bogdanow died of a brain tumor on June 29, 2011 in Manhattan, aged 64.


Limbic lobe

The limbic lobe is an arc-shaped region of cortex on the medial surface of each cerebral hemisphere of the mammalian brain, consisting of parts of the frontal, parietal and temporal lobes. The term is ambiguous, with some authors including the paraterminal gyrus, the subcallosal area, the cingulate gyrus, the parahippocampal gyrus, the dentate gyrus, the hippocampus and the subiculum; while the Terminologia Anatomica includes the cingulate sulcus, the cingulate gyrus, the isthmus of cingulate gyrus, the fasciolar gyrus, the parahippocampal gyrus, the parahippocampal sulcus, the dentate gyrus, the fimbrodentate sulcus, the fimbria of hippocampus, the collateral sulcus, and the rhinal sulcus, and omits the hippocampus.
History.
Broca named the limbic lobe in 1878, identifying it with the cingulate and parahippocampal gyri, and associating it with the sense of smell - Treviranus having earlier noted that, between species, the size of the parahippocampal gyrus varies with the size of the olfactory nerve. In 1937 Papez theorized that a neural circuit (the Papez circuit) including the hippocampal formation and the cingulate gyrus constitutes the neural substrate of emotional behavior, and Klüver and Bucy reported that, in monkeys, resection involving the hippocampal formation and the amygdaloid complex has a profound effect on emotional responses. As a consequence of these publications, the idea that the entire limbic lobe is dedicated to olfaction receded, and a direct connection between emotion and the limbic lobe was established.


Shokuiku

Shokuiku (Kanji: 食育) is the Japanese term for "food education". The law defines it as the "acquisition of knowledge about food and nutrition, as well as the ability to make appropriate decisions through practical experience with food, with the aim of developing people's ability to live on a healthy diet".
It was initiated by Sagen Ishizuka, a famous military doctor and pioneer of the macrobiotic diet. Following the introduction of Western fast food in the late 20th century, the Japanese government mandated education in nutrition and food origins, starting with the Basic Law of Shokuiku in 2005, and followed with the School Health Law in 2008. Universities have established programs to teach shokuiku in public schools, as well as investigating its effectiveness through academic study.
Major concerns that led to the development of shokuiku law include schoolchildren skipping breakfast, children purchasing meals at a convenience store instead of eating with their parents, and families not eating meals together.
Classes in shokuiku study the processes of making food like farming and fermentation, how additivess create flavor, and where food comes from.


Sociome

The Sociome is a concept used by scientists in Biology and Sociology referring to the dimensions of existence that are social. The term is also an indication of the convergence of systems biology and the study of society as a complex system that has begun to occur among early 21st Century scientists. Just as the "phenome" is typically thought of as the set of expressed phenotypes of an organism, the sociome can be thought of as the set of observed characteristics of societies. For example, while all societies consisting of humans might be thought of as having the potential to become egalitarian social democracies, not all observed societies are egalitarian or social democracies. Thus, the sociome can also be thought of indirectly as an ideal type of the unrealized potential of any given organization of social beings.
Origin of term.
The first known usage of the term "sociome" was in 2001 by Daichi Kamiyama. The term has also been utilized by sociologist Adam Thomas Perzynski. The two scientists differ in their usage. Kamiyama's study describes a new scientific "era of the sociome (Sociology[+ome])" characterized by the study of the social activities of molecules. This usage is an anthropomorphism of social behavior, wherein molecules are described as having the ability to socialize. Perzynski's social scientific usage varies from this considerably. While Sociology is the study of society, behavior and social relationships, the sociome is the characterization and quantification of patterns, variables, activities, relationships and attributes across all societies that exist and can be studied. The suffix -ome has been used primarily in biology, as in genome, proteome, microbiome, metabolome and phenome. Basu and colleagues have used the term "sociome" to refer to a sort of standardized approach to the characterization of geocoded social attributes (e.g. neighborhood level). In 2014, Del Savio and colleagues discussed the blurring of the boundaries between disciplines, and increased enthusiasm for the "sociome" concept and its importance for research in social science, epigenetics and epidemiology, with cautionary advice about the risks rooted in the marred history of Sociobiology
Still other authors have referred to sociomics as the bidirectional interplay between the field of Science and Technology Studies and all other "-omics" fields.
The -omics Wikipedia entry had previously listed sociome as a proposed new name for sociology, although it is unclear whether this has ever actually been proposed by any credible source. Still others have proposed that sociome is the object of study of Sociometry.


Synfire chain

A synfire chain (synchronous firing chain) is a feed-forward network of neurons with multiple layers or pools. In a synfire chain, neural impulses propagate synchronously back and forth from layer to layer. Each neuron in one layer feeds excitatory connections to neurons in the next, while each neuron in the receiving layer is excited by neurons in the previous layer.
Activity.
Activity along a synfire chain propagates in a synchronous or an asynchronous mode. In the asynchronous mode, an elevated firing rate in one pool will accumulate, and increase the firing rate in the next layer. In the synchronous mode, a volley of spikes in one layer will elicit a synchronous volley in the other, after one synaptic delay. It has been argued that the only stable mode of transmission is the synchronous mode.
History.
The term synfire chain was first used by Moshe Abeles in 1982, to account for the appearance of synchronous firing sequences with long inter-spike delays, which resisted explanation in terms of the known properties of cortical physiology. This structure, with every neuron in one pool exciting all neurons in the second pool, was suggested by Griffith as a structure that can guarantee a fixed level of activity in a network of excitatory neurons. He called this structure a “complete transmission line”. Griffith did not study its properties in any detail.


Alloclamide

Alloclamide (Pectex, Tuselin) is an antitussive and antihistamine drug marketed in Finland and Spain. It has never been marketed in the US.
It is sold as an oral solution, containing 6.25 mg/mL alloclamide. The recommended dosage for adults is 25 mg three to four times daily. Adverse effects include constipation and sedation.


Proper fasciculi

The proper fasciculi, or spinospinal fasciculi, or propriospinal tracts, are groups of short fibres, ascending and descending, and crossed and uncrossed, within the spinal cord. These fibres are grouped into anterior, posterior, and lateral regions and make up a spinal pathway. Descending dorsal root collaterals are often included in the pathway.
Components.
The anterior proper fasciculus consists of longitudinal intersegmental fibres which arise from cells in the grey matter, more especially from those of the medial group of the anterior column, and, after a longer or shorter course, re-enter the gray substance; and fibres which cross in the anterior white commissure from the grey matter of the opposite side.
The lateral proper fasciculus is made up of the remainder of the lateral column, and is continuous in front with the anterior proper fasciculus. It consists chiefly of intersegmental fibres which arise from cells in the grey matter, and, after a longer or shorter course, re-enter the grey matter and ramify in it. Some of its fibers are, also continued upward into the brain in the medial longitudinal fasciculus.
The posterior proper fasciculus arises from cells in the posterior column; their axons bifurcate (fork) into ascending and descending branches which occupy the ventral part of the funiculus close to the grey column. They are intersegmental and run for varying distances sending off collaterals and terminals to the grey matter.


Marc Brackett

Marc A. Brackett is a research psychologist and the Founding Director of the Yale Center for Emotional Intelligence and Professor in the Child Study Center at Yale University.
Biography.
Brackett earned his Ph.D. in psychology from the University of New Hampshire in 2003, where he was supervised by emotional intelligence scholar John D. Mayer. He was a postdoctoral fellow at Yale University with Mayer's collaborator, Peter Salovey.
Academic career.
Brackett's research focuses on the role of emotional intelligence in learning, decision making, relationship quality, and mental health; the measurement of emotional intelligence; best practices for bringing emotional intelligence into schools and organizations; and the influences of emotional intelligence training on student and educator effectiveness, bullying prevention, and school climate.
He is the author, co-author, and editor of over 125 scholarly publications and the developer of two university courses on emotional intelligence. His most recent book is "Permission to Feel: Unlocking the Power of Emotions to Help Our Kids, Ourselves, and Our Society Thrive".
RULER.
Brackett is the lead developer of RULER, an evidence-based approach to social emotional learning that has been approved by CASEL (Collaborative for Academic, Social, and Emotional Learning). The acronym RULER refers to the five key emotion skills of Recognizing, Understanding, Labeling, Expressing, and Regulating emotions. RULER intends to increase personal wellbeing, effective teaching and leadership, academic achievement, and classroom emotional climate change. An essential aspect of RULER is that it involves training for educational leaders, teachers, support staff, students and families. To date, RULER has been adopted by 2009 schools across the globe, reaching over 1,000,000 students.
Recognition.
Much of Brackett's research is being extended to different cultures, including England, Spain, Italy, Australia, and China. In 2009, his work on social emotional learning (SEL) earned him the Joseph E. Zins Award. He received the 2004/2007 award for Excellence in Research, MENSA Education and Research Foundation. In 2017 he was awarded an honorary doctorate from Manhattanville College.
Currently, he is a consultant to Facebook on a large-scale research project designed to both prevent and decrease online bullying.


Small intensely fluorescent cell

Small intensely fluorescent cells (SIF cells) are the interneurons of the sympathetic ganglia (postganglionic neurons) of the Sympathetic division of the autonomic nervous system (ANS). The neurotransmitter for these cells is dopamine. They are a neural crest derivative and share a common sympathoadrenal precursor cell with sympathetic neurons and chromaffin cells (adrenal medulla).
Although an autonomic ganglion is the site where pregangllonlc fibers synapse on postganglionic neurons, the presence of small interneurons has been recognized. These cells exhibit catecholamine fluorescence and are referred to as small intensely fluorescent (SIF) cells. In some ganglia, these intemeurons receive preganglionic cholinergic fibers and may modulate ganglionic transmission. In other ganglia, they receive collateral branches and may serve some Integrative function. Many SIF cells contain dopamine, which Is thought to be their transmitter.[1]
[1] < https://shop.lww.com/Snell-s-Clinical-Neuroanatomy/p/9781496346759 >


Hewer

A hewer ( or "Häuer") is a miner who loosens rock and minerals in a mine. In medieval mining in Europe a "Hauer" was the name given to a miner who had passed his test ("Hauerprüfung") as a hewer.
Training.
In Europe in former times, before he could become a hewer, the miner had to learn to be a "sorter boy" ("Scheidejunge"), identifying ores and separating the ore from the gangue. After that he would continue his training in the pit itself. Here, he had to learn further skills, initially as a putter ("Hundtstößer" literally "truck pusher"), transporting material around the mine in wagons. Only afterwards could he learn the skills, as an apprentice hewer ("Lehrhäuer"), that he would later need as a hewer. This form of training, the acquisition of knowledge by experience, was practised in mining until the First World War.
From the 1920s, the training of hewers was legally regulated as a result of union demands. Because, in the meantime, many skills required special knowledge, other tradesmen were gradually employed in mining and in the pits: initially metalworkers and, later, electricians. Following training and passing exams, the craftsman had to gain practical experience in order to sit for his hewer examination. This comprised a theoretical and a practical element.
The hewer exam could be taken once the miner was 20 years old. Between his apprenticeship as a sorter boy and the exam, the trainee hewer thus had at least two years of practical experience. After passing the hewer's exam there was a "graduation" event ("Lossprechung").
Hierarchy.
An apprentice hewer was placed under a hewer and had to work under his direction. In the dressing area of the mine, old, former hewers were responsible for supervising the sorter boys. The hewer reported to the mine foreman or supervisor, the "Steiger", also called the "Dinghauer" in some mines, or in smaller pits, the "Hutmann".
The hewer was held in particular esteem, by the other miners in the pit, even though he actually had no authority over them. The "Steiger", who were important officials in the early days of state mining, later became just ordinary employees.
Promotion.
Depending on diligence, skill and suitability, a hewer could be promoted to "Hutmann" or "Steiger". Even an appointment as shift foreman ("Schichtmeister"), to the council of aldermen or jurats ("Berggeschworenen") or as mine manager ("Bergmeister") was possible. At the end of the 18th century, pit and operational officials were legally required to undertake engineering training at a mining academy or mining school. For this reason, the training of a "Steiger" could no longer be carried out simply through on the job training.
Hewers with many years of experience, the ability to lead men and who had sufficient mining and technical skills, could be promoted to the rank of supervisor ("Aufsichtshauer") or senior hewer ("Oberhauer"). They were not, however, supervisory staff in the mining legal sense, but had the role of a team foreman.
If a hewer proved to be particularly expert, he would be appointed as a "master hewer" ("Meisterhauer"). He was then responsible for the technical training of junior miners. For this, the master hewer, was specially trained in a preparatory course, which culminated with an in-house examination. Master hewers reported to the mining authority.
A particularly experienced hewer who had worked for over 10 years and was at least 35 years old, could, if suitable, be appointed as a "leading hewer" ("Fahrhauer"). In order to achieve this he had to be deemed professionally suitable. His professional suitability was assessed on a so-called leading hewer's course ("Fahrhauerkurs"), which also acted as a certificate of proficiency. Leading hewers were responsible persons in the sense of the Federal Mining Law ("Bundesberggesetz") and were given a written order of authority ("Bestellschreiben").
Hours of work and wages.
The working hours of the hewers varied from region to region and ranged between 10–12 hours, but the time taking entering and leaving the mine was not counted. For one week of hired work in 1617 a hewer was paid just 18 "Mariengroschen". This week's wages would not even buy a pound of butter at that time. Until the beginning of the 1950s, they worked 5½ days a week comprising 50 hours. Today, the hewer works 7 hours a day without coming to the surface.


Interstitiospinal tract

The interstitiospinal tract is one of ten descending neuronal tracts in humans that provides motor control to specific upper cervical somatic segments. The origin of this uncrossed tract is in the interstitial nucleus of Cajal (related to the oculomotor nucleus) which is subsequently found in the Edinger-Westphal nucleus of the midbrain. This tract also contributes to the make-up of the medial longitudinal fasciculus (MLF). Within the terminal segments of the upper cervical segments the interstitiospinal tract synapses in rexed laminae VII and VIII. It is believed to function in head and neck reflex movements in response to primarily visual and possibly vestibular stimuli.


Murexide test

The murexide test is an analytical technique to identify the presence of caffeine and other purine derivatives in a sample. These compounds do not respond to the common alkaloid detecting tests such as Dragendorff's reagent. In this test the alkaloids are mixed with a tiny amount of potassium chlorate and a drop of hydrochloric acid. The sample is then evaporated to dryness and the resulting residue is exposed to ammonia vapour. Purine alkaloids produce a pink color in this test. Murexide (ammonium purpurate) with a purple color is also produced in this test.
Uses.
Murexide test is a color test for uric acid and some other purines. The (solid) sample is first treated with conc. nitric acid, which is slowly evaporated away; subsequent addition of ammonia solution (NH4OH) gives a purple color if uric acid was present, due to formation of murexide, or a yellow color that turns to red on heating if a xanthine is present.