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Interval order	Interval order	More formally, a countable poset P=(X,≤) is an interval order if and only if there exists a bijection from X to a set of real intervals, so xi↦(ℓi,ri) such that for any xi,xj∈X we have xi<xj in P exactly when ri<ℓj Such posets may be equivalently characterized as those with no induced subposet isomorphic to the pair of two-element chains, in other words as the (2+2) -free posets . Fully written out, this means that for any two pairs of elements a>b and c>d one must have a>d or c>b The subclass of interval orders obtained by restricting the intervals to those of unit length, so they all have the form (ℓi,ℓi+1) , is precisely the semiorders.
Interval order	Interval order	The complement of the comparability graph of an interval order ( X , ≤) is the interval graph (X,∩) Interval orders should not be confused with the interval-containment orders, which are the inclusion orders on intervals on the real line (equivalently, the orders of dimension ≤ 2).
Interval order	Interval orders and dimension	An important parameter of partial orders is order dimension: the dimension of a partial order P is the least number of linear orders whose intersection is P . For interval orders, dimension can be arbitrarily large. And while the problem of determining the dimension of general partial orders is known to be NP-hard, determining the dimension of an interval order remains a problem of unknown computational complexity.A related parameter is interval dimension, which is defined analogously, but in terms of interval orders instead of linear orders. Thus, the interval dimension of a partially ordered set P=(X,≤) is the least integer k for which there exist interval orders ⪯1,…,⪯k on X with x≤y exactly when x⪯1y,…, and x⪯ky . The interval dimension of an order is never greater than its order dimension.
Interval order	Combinatorics	In addition to being isomorphic to (2+2) -free posets, unlabeled interval orders on [n] are also in bijection with a subset of fixed-point-free involutions on ordered sets with cardinality 2n . These are the involutions with no so-called left- or right-neighbor nestings where, for any involution f on [2n] , a left nesting is an i∈[2n] such that i<i+1<f(i+1)<f(i) and a right nesting is an i∈[2n] such that f(i)<f(i+1)<i<i+1 Such involutions, according to semi-length, have ordinary generating function F(t)=∑n≥0∏i=1n(1−(1−t)i).
Interval order	Combinatorics	The coefficient of tn in the expansion of F(t) gives the number of unlabeled interval orders of size n . The sequence of these numbers (sequence A022493 in the OEIS) begins 1, 2, 5, 15, 53, 217, 1014, 5335, 31240, 201608, 1422074, 10886503, 89903100, 796713190, 7541889195, 75955177642, …
Spreader (railroad)	Spreader (railroad)	A spreader is a type of maintenance equipment designed to spread or shape ballast profiles. The spreader spreads gravel along the railroad ties. The various ploughs, wings and blades of specific spreaders allow them to remove snow, build banks, clean and dig ditches, evenly distribute gravel, as well as trim embankments of brush along the side of the track. Spreaders quickly proved themselves as an extremely economical tool for maintaining trackside drainage ditches and spreading fill dumped beside the track.The operation of the wings was once performed by compressed air and later hydraulics. Besides the MoW-operation spreaders are also used in open cast mines to clean the tracks from overburden tipped from dump cars.
Spreader (railroad)	Jordan spreader history	The Jordan spreader was the creation of Oswald F. Jordan, a Canadian road master who worked in the Niagara, Ontario area on the Canada Southern Railway, later a subsidiary of the New York Central Railroad. He supervised a crew at the St. Thomas Canada Southern shop in the early 1890s. Jordan's first patent, filed in 1890 and listing Robert Potts as co-inventor, covered a single-blade mechanism with the blade height adjustable with a hand crank and gearing.Jordan formed his own company, O.F. Jordan Company, in 1898 and continued construction of Jordan Spreaders. By 1906, the company had moved to Chicago, Jordan was a U.S. Citizen, and the spreader was a far more sophisticated device, with blades on both sides of the car, pneumatic power for raising and lowering each blade, and considerably more rugged construction. By 1909, the spreader was being built on a steel-framed car body instead of the wood used in earlier models, and a plow was mounted on the front, with an extension in front of that for shifting material across the track from side to side. Shortly after this, Jordan added a pneumatic system for rapidly and automatically extending and retracting the side blades. At this point, the primary purpose of the Jordan spreader was spreading ballast along the tracks.
Spreader (railroad)	Jordan spreader history	Following Jordan's death in 1910, Walter Riley took over management of the company and directed it for the next 50 years. Over the years that followed, the Jordan spreader was developed into a multi-purpose MoW vehicle with adjustable blades and ploughs added to the wings. New uses included trackside ditch maintenance and spreading fill dumped beside the track. Over 1,400 spreaders were built. Jordan spreaders are available by special order from Harsco Rail. In 2001, the Jordan Spreader was inducted into the North America Railway Hall of Fame in the "Local:Technical Innovation" category. It shared this selection with another technical innovation, the rotary snowplow.
HD 153201	HD 153201	HD 153201 is a Bp star in the southern constellation of Ara. It is chemically peculiar star that displays an anomalous abundance of the element silicon in its spectrum. This is a suspected variable star of the type known as Alpha² Canum Venaticorum. There is a magnitude 9.86 companion star at an angular separation of 2.30″ along a position angle of 131°.
Osmotic-controlled release oral delivery system	Osmotic-controlled release oral delivery system	The osmotic-controlled release oral delivery system (OROS) is an advanced controlled release oral drug delivery system in the form of a rigid tablet with a semi-permeable outer membrane and one or more small laser drilled holes in it. As the tablet passes through the body, water is absorbed through the semipermeable membrane via osmosis, and the resulting osmotic pressure is used to push the active drug through the laser drilled opening(s) in the tablet and into the gastrointestinal tract. OROS is a trademarked name owned by ALZA Corporation, which pioneered the use of osmotic pumps for oral drug delivery.
Osmotic-controlled release oral delivery system	Rationale	Pros and cons Osmotic release systems have a number of major advantages over other controlled-release mechanisms. They are significantly less affected by factors such as pH, food intake, GI motility, and differing intestinal environments. Using an osmotic pump to deliver drugs has additional inherent advantages regarding control over drug delivery rates. This allows for much more precise drug delivery over an extended period of time, which results in much more predictable pharmacokinetics. However, osmotic release systems are relatively complicated, somewhat difficult to manufacture, and may cause irritation or even blockage of the GI tract due to prolonged release of irritating drugs from the non-deformable tablet.
Osmotic-controlled release oral delivery system	Oral osmotic release systems	Single-layer The Elementary Osmotic Pump (EOP) was developed by ALZA in 1974, and was the first practical example of an osmotic pump based drug release system for oral use. It was introduced to the market in the early 1980s in Osmosin (indomethacin) and Acutrim (phenylpropanolamine), but unexpectedly severe issues with GI irritation and cases of GI perforation led to the withdrawal of Osmosin.Merck & Co. later developed the Controlled-Porosity Osmotic Pump (CPOP) with the intention of addressing some of the issues that led to Osmosin's withdrawal via a new approach to the final stage of the release mechanism. Unlike the EOP, the CPOP had no pre-formed hole in the outer shell for the drug to be expelled out of. Instead, the CPOP's semipermeable membrane was designed to form numerous small pores upon contact with water through which the drug would be expelled via osmotic pressure. The pores were formed via the use of a pH insensitive leachable or dissolvable additive such as sorbitol.
Osmotic-controlled release oral delivery system	Oral osmotic release systems	Multi-layer Both the EOP and CPOP were relatively simple designs, and were limited by their inability to deliver poorly soluble drugs. This led to the development of an additional internal "push layer" composed of material (a swellable polymer) that would expand as it absorbed water, which then pushed the drug layer (which incorporates a viscous polymer for suspension of poorly soluble drugs) out of the exit hole at a controlled rate. Osmotic agents such as sodium chloride, potassium chloride, or xylitol are added to both the drug and push layers to increase the osmotic pressure. The initial design developed in 1982 by ALZA researchers was designated the Push-Pull Osmotic Pump (PPOP), and Procardia XL (nifedipine) was one of the first drugs to utilize this PPOP design.
Osmotic-controlled release oral delivery system	Oral osmotic release systems	In the early 1990s, an ALZA-funded research program began to develop a new dosage form of methylphenidate for the treatment of children with attention deficit hyperactivity disorder (ADHD). Methylphenidate's short half-life required multiple doses to be administered each day to attain long-lasting coverage, which made it an ideal candidate for the OROS technology. Multiple candidate pharmacokinetic profiles were evaluated and tested in an attempt to determine the optimal way to deliver the drug, which was especially important given the puzzling failure of an existing extended-release formulation of methylphenidate (Ritalin SR) to act as expected. The zero-order (flat) release profile that the PPOP was optimal at delivering failed to maintain its efficacy over time, which suggested that acute tolerance to methylphenidate formed over the course of the day. This explained why Ritalin SR was inferior to twice-daily Ritalin IR, and led to the hypothesis that an ascending pattern of drug delivery was necessary to maintain clinical effect. Trials designed to test this hypothesis were successful, and ALZA subsequently developed a modified PPOP design that utilized an overcoat of methylphenidate designed to release immediately and rapidly raise serum levels, followed by 10 hours of first-order (ascending) drug delivery from the modified PPOP design. This design was called the Push-Stick Osmotic Pump (PSOP), and utilized two separate drug layers with different concentrations of methylphenidate in addition to the (now quite robust) push layer.
Glutathione reductase	Glutathione reductase	Glutathione reductase (GR) also known as glutathione-disulfide reductase (GSR) is an enzyme that in humans is encoded by the GSR gene. Glutathione reductase (EC 1.8.1.7) catalyzes the reduction of glutathione disulfide (GSSG) to the sulfhydryl form glutathione (GSH), which is a critical molecule in resisting oxidative stress and maintaining the reducing environment of the cell. Glutathione reductase functions as dimeric disulfide oxidoreductase and utilizes an FAD prosthetic group and NADPH to reduce one molar equivalent of GSSG to two molar equivalents of GSH: The glutathione reductase is conserved between all kingdoms. In bacteria, yeasts, and animals, one glutathione reductase gene is found; however, in plant genomes, two GR genes are encoded. Drosophila and trypanosomes do not have any GR at all. In these organisms, glutathione reduction is performed by either the thioredoxin or the trypanothione system, respectively.
Glutathione reductase	Function	Glutathione plays a key role in maintaining proper function and preventing oxidative stress in human cells. It can act as a scavenger for hydroxyl radicals, singlet oxygen, and various electrophiles. Reduced glutathione reduces the oxidized form of the enzyme glutathione peroxidase, which in turn reduces hydrogen peroxide (H2O2), a dangerously reactive species within the cell. [In the following illustration of redox reeactions, the rightmost arrow is reversed; it should be pointing up not down.] In addition, it plays a key role in the metabolism and clearance of xenobiotics, acts as a cofactor in certain detoxifying enzymes, participates in transport, and regenerates antioxidants such and Vitamins E and C to their reactive forms. The ratio of GSSG/GSH present in the cell is a key factor in properly maintaining the oxidative balance of the cell, that is, it is critical that the cell maintains high levels of the reduced glutathione and a low level of the oxidized glutathione disulfide. This narrow balance is maintained by glutathione reductase, which catalyzes the reduction of GSSG to GSH.
Glutathione reductase	Structure	Glutathione reductase from human erythrocytes is a homodimer consisting of 52Kd monomers, each containing 3 domains. GR exhibits single sheet, double layered topology where an anti-parallel beta-sheet is largely exposed to the solvent on one face while being covered by random coils on the other face. This includes and NADPH-binding Domain, FAD-binding domain(s) and a dimerization domain. Each monomer contains 478 residues and one FAD molecule. GR is a thermostable protein, retaining function up to 65 °C.
Glutathione reductase	Reaction mechanism	Steps: Reductive half The action of GR proceeds through two distinct half reactions, a reductive half mechanism followed by an oxidative half. In the first half, NADPH reduces FAD present in GSR to produce a transient FADH− anion. This anion then quickly breaks a disulfide bond of Cys58 - Cys63, forming a short lived covalent bond a stable charge-transfer complex between the flavin and Cys63. The now oxidized NADP+ is released and is subsequently replaced by a new molecule of NADPH. This is the end of the so-called reductive half of the mechanism.
Glutathione reductase	Reaction mechanism	Oxidative half In the oxidative half of the mechanism, Cys63 nucleophilically attacks the nearest sulfide unit in the GSSG molecule (promoted by His467), which creates a mixed disulfide bond (GS-Cys58) and a GS− anion. His467 of GSR then protonates the GS- anion to release the first molecule of GSH. Next, Cys63 nucleophilically attacks the sulfide of Cys58, releasing a GS− anion, which, in turn, picks up a solvent proton and is released from the enzyme, thereby creating the second GSH. So, for every GSSG and NADPH, two reduced GSH molecules are gained, which can again act as antioxidants scavenging reactive oxygen species in the cell.
Glutathione reductase	Inhibition	In vitro, glutathione reductase is inhibited by low concentrations of sodium arsenite and methylated arsenate metabolites, but in vivo, significant Glutathione Reductase inhibition by sodium arsenate has only been at 10 mg/kg/day. Glutathione reductase is also inhibited by some flavanoids, a class of pigments produced by plants.
Glutathione reductase	Clinical significance	GSH is a key cellular antioxidant and plays a major role in the phase 2 metabolic clearance of electrophilic xenobiotics. The importance of the GSH pathway and enzymes that affect this delicate balance is gaining an increased level of attention in recent years. Although glutathione reductase has been an attractive target for many pharmaceuticals, there have been no successful glutathione reductase related therapeutic compounds created to date. In particular, glutathione reductase appears to be a good target for anti-malarials, as the glutathione reductase of the malaria parasite Plasmodium falciparum has a significantly different protein fold than that of mammalian glutathione reductase. By designing drugs specific to p. falciparum it may be possible to selectively induce oxidative stress in the parasite, while not affecting the host.
Glutathione reductase	Clinical significance	There are two main classes of GR targeting compounds: Inhibitors of GSSG binding, or dimerization: Reactive electrophiles such as gold compounds, and fluoronaphthoquinones.
Glutathione reductase	Clinical significance	Drugs which use glutathione reductase to regenerate, such as redox cyclers. Two examples of these types of compounds are Methylene blue and Naphthoquinone.Clinical trials performed in Burkina Faso have revealed mixed results when treating malaria with Naphthoquinones In cells exposed to high levels of oxidative stress, like red blood cells, up to 10% of the glucose consumption may be directed to the pentose phosphate pathway (PPP) for production of the NADPH needed for this reaction. In the case of erythrocytes, if the PPP is non-functional, then the oxidative stress in the cell will lead to cell lysis and anemia.Lupus is an autoimmune disorder in which patients produce an elevated quantity of antibodies that attack DNA and other cell components. In a recent study, a single nucleotide polymorphism (SNP) in the Glutathione Reductase gene was found to be highly associated with lupus in African Americans in the study. African Americans with lupus have also been shown to express less reduced glutathione in their T cells. The study's authors believe that reduced glutathione reductase activity may contribute to the increased production of reactive oxygen in African Americans with lupus.In mice, glutathione reductase has been implicated in the oxidative burst, a component of the immune response. The oxidative burst is a defense mechanism in which neutrophils produce and release reactive oxidative species in the vicinity of bacteria or fungi to destroy the foreign cells. Glutathione Reductase deficient neutrophils were shown to produce a more transient oxidative burst in response to bacteria than neutrophils that express GR at ordinary levels. The mechanism of Glutathione Reductase in sustaining the oxidative burst is still unknown.
Glutathione reductase	Clinical significance	Deficiency Glutathione reductase deficiency is a rare disorder in which the glutathione reductase activity is absent from erythrocytes, leukocytes or both. In one study this disorder was observed in only two cases in 15,000 tests for glutathione reductase deficiency performed over the course of 30 years. In the same study, glutathione reductase deficiency was associated with cataracts and favism in one patient and their family, and with severe unconjugated hyperbilirubinemia in another patient. It has been proposed that the glutathione redox system (of which glutathione reductase is a part) is almost exclusively responsible for the protecting of eye lens cells from hydrogen peroxide because these cells are deficient in catalase, an enzyme which catalyzes the breakdown of hydrogen peroxide, and the high rate of cataract incidence in glutathione reductase deficient individuals.Some patients exhibit deficient levels of glutathione activity as a result of not consuming enough riboflavin in their diets. Riboflavin is a precursor for FAD, whose reduced form donates two electron to the disulfide bond which is present in the oxidized form of glutathione reductase in order to begin the enzyme's catalytic cycle. In 1999, a study found that 17.8% of males and 22.4% of females examined in Saudi Arabia suffered from low glutathione reductase activity due to riboflavin deficiency.
Glutathione reductase	Clinical significance	Connection to favism In favism, patients lack glucose-6-phosphate dehydrogenase, an enzyme in their pentose phosphate pathway that reduces NADP+ to NADPH while catalyzing the conversion of glucose-6-phosphate to 6-phosphoglucono-δ-lactone. Glucose-6-phosphate dehydrogenase deficient individuals have less NADPH available for the reduction of oxidized glutathione via glutathione reductase. Thus their basal ratio of oxidized to reduced glutathione is significantly higher than that of patients who express glucose-6-phosphate dehydrogenase, normally, making them unable to effectively respond to high levels of reactive oxygen species, which causes cell lysis.
Glutathione reductase	Monitoring glutathione reductase activity	The activity of glutathione reductase is used as indicator for oxidative stress. The activity can be monitored by the NADPH consumption, with absorbance at 340 nm, or the formed GSH can be visualized by Ellman's reagent. Alternatively the activity can be measured using roGFP (redox-sensitive Green Fluorescent Protein).
Glutathione reductase	In plants	As it does in human cells, glutathione reductase helps to protect plant cells from reactive oxygen species. In plants, reduced glutathione participates in the glutathione-ascorbate cycle in which reduced glutathione reduces dehydroascorbate, a reactive byproduct of the reduction of hydrogen peroxide. In particular, glutathione reductase contributes to plants' response to abiotic stress. The enzyme's activity has been shown to be modulated in response to metals, metalloids, salinity, drought, UV radiation and heat induced stress.
Glutathione reductase	History	Glutathione reductase was first purified in 1955 at Yale University by P. Janmeda. Janmeda also identified NADPH as the primary electron donor for the enzyme. Later groups confirmed the presence of FAD and the thiol group, and an initial mechanism was suggested for the mechanism in 1965. The initial (low resolution) structure of glutathione reductase was solved in 1977. This was quickly followed by a 3Å structure by Shulze et al. in 1978. Glutathione reductase has been studied exhaustively since these early experiments, and is subsequently one of the most well characterized enzymes to date.
Glutathione reductase	Interactive pathway map	Interactive pathway can be found here: pathway map
Verilog-to-Routing	Verilog-to-Routing	Verilog-to-Routing (VTR) is an open source CAD flow for FPGA devices. VTR's main purpose is to map a given circuit described in Verilog, a Hardware Description Language, on a given FPGA architecture for research and development purposes; the FPGA architecture targeted could be a novel architecture that a researcher wishes to explore, or it could be an existing commercial FPGA whose architecture has been captured in the VTR input format. The VTR project has many contributors, with lead collaborating universities being the University of Toronto, the University of New Brunswick, and the University of California, Berkeley . Additional contributors include Google, The University of Utah, Princeton University, Altera, Intel, Texas Instruments, and MIT Lincoln Lab.
Verilog-to-Routing	VTR Flow	The VTR design flow usually consists of three main component applications: ODIN II which compiles Verilog code to a circuit in Berkeley Logic Interchange Format (BLIF), a human-readable graph representation of the circuit; ABC which optimizes the BLIF circuit produced by ODIN II; and VPR which packs, places and routes the optimized circuit on the given FPGA architecture. There are some additional optional tools that can process the VTR output further. For example, the FASM FPGA Assembly tool can produce programming bitstreams for some commercial FPGAs (Xilinx Artix and Lattice ice40) at the end of the VTR flow, while the OpenFPGA tool integrates with VTR to produce a standard cell layout of a novel (proposed) FPGA. It is also possible to use different tools for the first (HDL synthesis) stage of the VTR flow; for example the Titan Flow uses Quartus to perform the HDL to logic synthesis stage, and then VPR to perform placement and routing, while Symbiflow uses the Yosys synthesis tool followed by VPR placement and routing.
Verilog-to-Routing	VTR Flow	ODIN II ODIN II is the HDL compiler of the VTR flow. It transforms a given Verilog code to a BLIF circuit, performs code and circuit optimizations, visualizes circuits, and performs partial mapping of logic to available hard blocks of the given architecture. Also, it can simulate the execution of circuits both for validation as well as power, performance and heat analysis. ODIN II is maintained by the University of New Brunswick.
Verilog-to-Routing	VTR Flow	ABC ABC optimizes BLIF circuits by performing logic optimization and technology mapping. ABC is maintained by the University of California, Berkeley. VPR Versatile Place and Route (VPR) is the final component of VTR. Its input is a BLIF circuit, which it packs, places and routes on an input FPGA architecture.
Verilog-to-Routing	VTR Flow	During packing, neighboring and related logic elements of the circuit are clustered together into Logic Blocks matching the hardware of the FPGA. During placement, these logic blocks as well as hard blocks are assigned to the available hardware resources of the FPGA. Finally, during routing the signal connections between blocks are made. VPR is primarily developed by the University of Toronto, with contributions from many other universities and companies.
Verilog-to-Routing	VTR Flow	FASM The FPGA Assembly (genfasm) tool will produce a programming bitstream from a VTR implementation (placement and routing of a circuit) on commercial architectures for which complete VTR architecture files describing the FPGA device have been produced. Currently this includes the Xilinx Artix and Lattice ice40 FPGA families. This tool is primarily developed by Google.
Fascia iliaca block	Fascia iliaca block	Fascia iliaca blocks (FIC, FICB) is a local anesthetic nerve block, a type of regional anesthesia technique, used to provide analgesia or anaesthesia to the hip and thigh. FICB can performed by using ultrasound or with a loss of resistance technique, the latter sometimes referred to as the "two-pop-method". FICB works by affecting the femoral, obturator and the lateral cutaneous nerves with a local anesthetic.
Fascia iliaca block	Technique	When FICB is performed with the loss of resistance technique, the injection site for FICB is found by drawing an imaginary line between the pubic tubercle to the anterior superior iliac spine. The injection site is 1 cm. below the lateral one third and the medial two thirds of this line. Two losses of resistances are felt as the fascia lata and the fascia iliaca is penetrated by a semi-blunt cannula. Aspiration (drawing back the cannula) is performed, after which a local anaesthetic is injected while compressing on the skin distally to increase cranial distribution.
Fascia iliaca block	Technique	FICB can generally be performed with minimally required training and by non-medical practitioners
Fascia iliaca block	Medical uses	FIC can be used to offer pain relief for hip fractures in adults and femoral fractures in children.
Fascia iliaca block	Adverse effects	FIC is generally safe to use and have few adverse effects. There is a 0.09-3.2% risk of hematomas at the injection site and a 0.18% risk of local anaesthetic intoxication. There are also case reports of pneumoretroperitoneum using continuous infusion, bladder puncture with a modified block under very special conditions and postoperative neuropathy.
Fascia iliaca block	History	The block was first described in 1989 as an alternative to 3-in-1 nerve block in children.
Cell surface receptor	Cell surface receptor	Cell surface receptors (membrane receptors, transmembrane receptors) are receptors that are embedded in the plasma membrane of cells. They act in cell signaling by receiving (binding to) extracellular molecules. They are specialized integral membrane proteins that allow communication between the cell and the extracellular space. The extracellular molecules may be hormones, neurotransmitters, cytokines, growth factors, cell adhesion molecules, or nutrients; they react with the receptor to induce changes in the metabolism and activity of a cell. In the process of signal transduction, ligand binding affects a cascading chemical change through the cell membrane.
Cell surface receptor	Structure and mechanism	Many membrane receptors are transmembrane proteins. There are various kinds, including glycoproteins and lipoproteins. Hundreds of different receptors are known and many more have yet to be studied. Transmembrane receptors are typically classified based on their tertiary (three-dimensional) structure. If the three-dimensional structure is unknown, they can be classified based on membrane topology. In the simplest receptors, polypeptide chains cross the lipid bilayer once, while others, such as the G-protein coupled receptors, cross as many as seven times. Each cell membrane can have several kinds of membrane receptors, with varying surface distributions. A single receptor may also be differently distributed at different membrane positions, depending on the sort of membrane and cellular function. Receptors are often clustered on the membrane surface, rather than evenly distributed.
Cell surface receptor	Structure and mechanism	Mechanism Two models have been proposed to explain transmembrane receptors' mechanism of action. Dimerization: The dimerization model suggests that prior to ligand binding, receptors exist in a monomeric form. When agonist binding occurs, the monomers combine to form an active dimer. Rotation: Ligand binding to the extracellular part of the receptor induces a rotation (conformational change) of part of the receptor's transmembrane helices. The rotation alters which parts of the receptor are exposed on the intracellular side of the membrane, altering how the receptor can interact with other proteins within the cell.
Cell surface receptor	Domains	Transmembrane receptors in plasma membrane can usually be divided into three parts.
Cell surface receptor	Domains	Extracellular domains The extracellular domain is just externally from the cell or organelle. If the polypeptide chain crosses the bilayer several times, the external domain comprises loops entwined through the membrane. By definition, a receptor's main function is to recognize and respond to a type of ligand. For example, a neurotransmitter, hormone, or atomic ions may each bind to the extracellular domain as a ligand coupled to receptor. Klotho is an enzyme which effects a receptor to recognize the ligand (FGF23).
Cell surface receptor	Domains	Transmembrane domains Two most abundant classes of transmembrane receptors are GPCR and single-pass transmembrane proteins. In some receptors, such as the nicotinic acetylcholine receptor, the transmembrane domain forms a protein pore through the membrane, or around the ion channel. Upon activation of an extracellular domain by binding of the appropriate ligand, the pore becomes accessible to ions, which then diffuse. In other receptors, the transmembrane domains undergo a conformational change upon binding, which affects intracellular conditions. In some receptors, such as members of the 7TM superfamily, the transmembrane domain includes a ligand binding pocket.
Cell surface receptor	Domains	Intracellular domains The intracellular (or cytoplasmic) domain of the receptor interacts with the interior of the cell or organelle, relaying the signal. There are two fundamental paths for this interaction: The intracellular domain communicates via protein-protein interactions against effector proteins, which in turn pass a signal to the destination. With enzyme-linked receptors, the intracellular domain has enzymatic activity. Often, this is tyrosine kinase activity. The enzymatic activity can also be due to an enzyme associated with the intracellular domain.
Cell surface receptor	Signal transduction	Signal transduction processes through membrane receptors involve the external reactions, in which the ligand binds to a membrane receptor, and the internal reactions, in which intracellular response is triggered.Signal transduction through membrane receptors requires four parts: Extracellular signaling molecule: an extracellular signaling molecule is produced by one cell and is at least capable of traveling to neighboring cells. Receptor protein: cells must have cell surface receptor proteins which bind to the signaling molecule and communicate inward into the cell. Intracellular signaling proteins: these pass the signal to the organelles of the cell. Binding of the signal molecule to the receptor protein will activate intracellular signaling proteins that initiate a signaling cascade. Target proteins: the conformations or other properties of the target proteins are altered when a signaling pathway is active and changes the behavior of the cell.Membrane receptors are mainly divided by structure and function into 3 classes: The ion channel linked receptor; The enzyme-linked receptor; and The G protein-coupled receptor. Ion channel linked receptors have ion channels for anions and cations, and constitute a large family of multipass transmembrane proteins. They participate in rapid signaling events usually found in electrically active cells such as neurons. They are also called ligand-gated ion channels. Opening and closing of ion channels is controlled by neurotransmitters. Enzyme-linked receptors are either enzymes themselves, or directly activate associated enzymes. These are typically single-pass transmembrane receptors, with the enzymatic component of the receptor kept intracellular. The majority of enzyme-linked receptors are, or associate with, protein kinases. G protein-coupled receptors are integral membrane proteins that possess seven transmembrane helices. These receptors activate a G protein upon agonist binding, and the G-protein mediates receptor effects on intracellular signaling pathways.
Cell surface receptor	Signal transduction	Ion channel-linked receptor During the signal transduction event in a neuron, the neurotransmitter binds to the receptor and alters the conformation of the protein. This opens the ion channel, allowing extracellular ions into the cell. Ion permeability of the plasma membrane is altered, and this transforms the extracellular chemical signal into an intracellular electric signal which alters the cell excitability.The acetylcholine receptor is a receptor linked to a cation channel. The protein consists of four subunits: alpha (α), beta (β), gamma (γ), and delta (δ) subunits. There are two α subunits, with one acetylcholine binding site each. This receptor can exist in three conformations. The closed and unoccupied state is the native protein conformation. As two molecules of acetylcholine both bind to the binding sites on α subunits, the conformation of the receptor is altered and the gate is opened, allowing for the entry of many ions and small molecules. However, this open and occupied state only lasts for a minor duration and then the gate is closed, becoming the closed and occupied state. The two molecules of acetylcholine will soon dissociate from the receptor, returning it to the native closed and unoccupied state.
Cell surface receptor	Signal transduction	Enzyme-linked receptors As of 2009, there are 6 known types of enzyme-linked receptors: Receptor tyrosine kinases; Tyrosine kinase associated receptors; Receptor-like tyrosine phosphatases; Receptor serine/threonine kinases; Receptor guanylyl cyclases and histidine kinase associated receptors. Receptor tyrosine kinases have the largest population and widest application. The majority of these molecules are receptors for growth factors such as epidermal growth factor (EGF), platelet-derived growth factor (PDGF), fibroblast growth factor (FGF), hepatocyte growth factor (HGF), nerve growth factor (NGF) and hormones such as insulin.
Cell surface receptor	Signal transduction	Most of these receptors will dimerize after binding with their ligands, in order to activate further signal transductions. For example, after the epidermal growth factor (EGF) receptor binds with its ligand EGF, the two receptors dimerize and then undergo phosphorylation of the tyrosine residues in the enzyme portion of each receptor molecule. This will activate the tyrosine kinase and catalyze further intracellular reactions.
Cell surface receptor	Signal transduction	G protein-coupled receptors G protein-coupled receptors comprise a large protein family of transmembrane receptors. They are found only in eukaryotes. The ligands which bind and activate these receptors include: photosensitive compounds, odors, pheromones, hormones, and neurotransmitters. These vary in size from small molecules to peptides and large proteins. G protein-coupled receptors are involved in many diseases, and thus are the targets of many modern medicinal drugs.There are two principal signal transduction pathways involving the G-protein coupled receptors: the cAMP signaling pathway and the phosphatidylinositol signaling pathway. Both are mediated via G protein activation. The G-protein is a trimeric protein, with three subunits designated as α, β, and γ. In response to receptor activation, the α subunit releases bound guanosine diphosphate (GDP), which is displaced by guanosine triphosphate (GTP), thus activating the α subunit, which then dissociates from the β and γ subunits. The activated α subunit can further affect intracellular signaling proteins or target functional proteins directly.
Cell surface receptor	Membrane receptor-related disease	If the membrane receptors are denatured or deficient, the signal transduction can be hindered and cause diseases. Some diseases are caused by disorders of membrane receptor function. This is due to deficiency or degradation of the receptor via changes in the genes that encode and regulate the receptor protein. The membrane receptor TM4SF5 influences the migration of hepatic cells and hepatoma. Also, the cortical NMDA receptor influences membrane fluidity, and is altered in Alzheimer's disease. When the cell is infected by a non-enveloped virus, the virus first binds to specific membrane receptors and then passes itself or a subviral component to the cytoplasmic side of the cellular membrane. In the case of poliovirus, it is known in vitro that interactions with receptors cause conformational rearrangements which release a virion protein called VP4.The N terminus of VP4 is myristylated and thus hydrophobic【myristic acid=CH3(CH2)12COOH】. It is proposed that the conformational changes induced by receptor binding result in the attachment of myristic acid on VP4 and the formation of a channel for RNA.
Cell surface receptor	Structure-based drug design	Through methods such as X-ray crystallography and NMR spectroscopy, the information about 3D structures of target molecules has increased dramatically, and so has structural information about the ligands. This drives rapid development of structure-based drug design. Some of these new drugs target membrane receptors. Current approaches to structure-based drug design can be divided into two categories. The first category is about determining ligands for a given receptor. This is usually accomplished through database queries, biophysical simulations, and the construction of chemical libraries. In each case, a large number of potential ligand molecules are screened to find those fitting the binding pocket of the receptor. This approach is usually referred to as ligand-based drug design. The key advantage of searching a database is that it saves time and power to obtain new effective compounds. Another approach of structure-based drug design is about combinatorially mapping ligands, which is referred to as receptor-based drug design. In this case, ligand molecules are engineered within the constraints of a binding pocket by assembling small pieces in a stepwise manner. These pieces can be either atoms or molecules. The key advantage of such a method is that novel structures can be discovered.
Cell surface receptor	Structure-based drug design	Other examples Adrenergic receptor Olfactory receptors Receptor tyrosine kinases Epidermal growth factor receptor Insulin Receptor Fibroblast growth factor receptors, High affinity neurotrophin receptors Ephrin receptors Integrins Low Affinity Nerve Growth Factor Receptor NMDA receptor Several Immune receptors Toll-like receptor T cell receptor CD28 SCIMP protein
Hamiltonian coloring	Hamiltonian coloring	Hamiltonian coloring, named after William Rowan Hamilton, is a type of graph coloring. Hamiltonian coloring uses a concept called detour distance between two vertices of the graph. It has many applications in different areas of science and technology.
Hamiltonian coloring	Terminologies	Radio coloring A graph G with diameter D with n nodes that is colored (i.e. has a positive integer assigned to each vertex) with k colors is called a radio k-coloring G if for every pair of vertices a and b, the sum of the distance between them and the difference between their labels ("colors") is greater than k. For example, two nodes labelled 3 and 7 with a distance of 5 is acceptable for a radio 8-coloring, but not for a radio 9-coloring, since (7−3)+5=9 , which is not greater than 9.
Hamiltonian coloring	Terminologies	Antipodal coloring A radio (d-1)-coloring, that is, where k is equal to one less than the graph's diameter, is known as an antipodal coloring because antipodal vertices may be colored the same, but all nodes between them must be different.
Hamiltonian coloring	Terminologies	Detour distance The distance between two vertices in a graph is defined as the minimum of lengths of paths connecting those vertices. The detour distance between two vertices, say, u and v is defined as the length of the longest u-v path in the graph. In the case of a tree the detour distance between any two vertices is same as the distance between the two vertices.
Hamiltonian coloring	Terminologies	Hamiltonian coloring Hamiltonian colorings are a variation on antipodal colorings where, instead of considering the regular distance between nodes, the detour distance is instead considered. Specifically, a Hamiltonian coloring's nodes have the property that the detour distance plus the difference in colors is greater than or equal to one less than n, the number of nodes in the graph. If the graph G is a path, then any Hamiltonian coloring is also an antipodal coloring, which is the inspiration for the definition of Hamiltonian coloring.
Vivisection	Vivisection	Vivisection (from Latin vivus 'alive', and sectio 'cutting') is surgery conducted for experimental purposes on a living organism, typically animals with a central nervous system, to view living internal structure. The word is, more broadly, used as a pejorative catch-all term for experimentation on live animals by organizations opposed to animal experimentation, but the term is rarely used by practising scientists. Human vivisection, such as live organ procurement, has been perpetrated as a form of torture.
Vivisection	Animal vivisection	Research requiring vivisection techniques that cannot be met through other means is often subject to an external ethics review in conception and implementation, and in many jurisdictions use of anesthesia is legally mandated for any surgery likely to cause pain to any vertebrate.In the United States, the Animal Welfare Act explicitly requires that any procedure that may cause pain use "tranquilizers, analgesics, and anesthetics" with exceptions when "scientifically necessary". The act does not define "scientific necessity" or regulate specific scientific procedures, but approval or rejection of individual techniques in each federally funded lab is determined on a case-by-case basis by the Institutional Animal Care and Use Committee, which contains at least one veterinarian, one scientist, one non-scientist, and one other individual from outside the university.In the United Kingdom, any experiment involving vivisection must be licensed by the Home Secretary. The Animals (Scientific Procedures) Act 1986 "expressly directs that, in determining whether to grant a licence for an experimental project, 'the Secretary of State shall weigh the likely adverse effects on the animals concerned against the benefit likely to accrue.'"In Australia, the Code of Practice "requires that all experiments must be approved by an Animal Experimentation Ethics Committee" that includes a "person with an interest in animal welfare who is not employed by the institution conducting the experiment, and an additional independent person not involved in animal experimentation."Anti-vivisectionists have played roles in the emergence of the animal welfare and animal rights movements, arguing that animals and humans have the same natural rights as living creatures, and that it is inherently immoral to inflict pain or injury on another living creature, regardless of the purpose or potential benefit to mankind.
Vivisection	Animal vivisection	Vivisection and anti-vivisection in the 19th century At the turn of the 19th century, medicine was undergoing a transformation. The emergence of hospitals and the development of more advanced medical tools such as the stethoscope are but a few of the changes in the medical field. There was also an increased recognition that medical practices needed to be improved, as many of the current therapeutics were based on unproven, traditional theories that may or may not have helped the patient recover. The demand for more effective treatment shifted emphasis to research with the goal of understanding disease mechanisms and anatomy. This shift had a few effects, one of which was the rise in patient experimentation, leading to some moral questions about what was acceptable in clinical trials and what was not. An easy solution to the moral problem was to use animals in vivisection experiments, so as not to endanger human patients. This, however, had its own set of moral obstacles, leading to the anti-vivisection movement.
Vivisection	Animal vivisection	François Magendie (1783–1855) One polarizing figure in the anti-vivisection movement was François Magendie. Magendie was a physiologist at the Académie Royale de Médecine in France, established in the first half of the 19th century. Magendie made several groundbreaking medical discoveries, but was far more aggressive than some of his other contemporaries with his use of animal experimentation. For example, the discovery of the different functionalities of dorsal and ventral spinal nerve roots was achieved by both Magendie, as well as a Scottish anatomist named Charles Bell. Bell used an unconscious rabbit because of "the protracted cruelty of the dissection", which caused him to miss that the dorsal roots were also responsible for sensory information. Magendie, on the other hand, used conscious, six-week-old puppies for his own experiments. While Magendie's approach was more of an infringement on what would today be referred to as animal rights, both Bell and Magendie used the same rationalization for vivisection: the cost of animal lives and experimentation was well worth it for the benefit of humanity.Many viewed Magendie's work as cruel and unnecessarily torturous. One note is that Magendie carried out many of his experiments before the advent of anesthesia, but even after ether was discovered it was not used in any of his experiments or classes. Even during the period before anesthesia, other physiologists expressed their disgust with how he conducted his work. One such visiting American physiologist describes the animals as "victims" and the apparent sadism that Magendie displayed when teaching his classes. The cruelty in such experiments actually even led to Magendie's role as an important figure in animal-rights legislation, such as his experiments being cited in the drafting of the British Cruelty to Animals Act 1876 and Cruel Treatment of Cattle Act 1822, otherwise known as Martin's Act, with its namesake, Irish MP and well known anti-cruelty campaigner Richard Martin describing Magendle as "disgrace to Society" after one of Magendle's public vivisections, described by Martin as "anatomical theatres", which was widely commented on at the time reportedly involving a greyhound's dissection potentially over two days. Magendle faced widespread opposition in British society, among the general public but also his contemporaries, including William Sharpey who described his experiments aside from cruel as "purposeless" and "without sufficient object", a feeling he claimed was shared among other physiologists.
Vivisection	Animal vivisection	David Ferrier and the Cruelty to Animals Act 1876 The Cruelty to Animals Act, 1876 in Britain determined that one could only conduct vivisection on animals with the appropriate license from the state, and that the work the physiologist was doing had to be original and absolutely necessary. The stage was set for such legislation by physiologist David Ferrier. Ferrier was a pioneer in understanding the brain and used animals to show that certain locales of the brain corresponded to bodily movement elsewhere in the body in 1873. He put these animals to sleep, and caused them to move unconsciously with a probe. Ferrier was successful, but many decried his use of animals in his experiments. Some of these arguments came from a religious standpoint. Some were concerned that Ferrier's experiments would separate God from the mind of man in the name of science. Some of the anti-vivisection movement in England had its roots in Evangelicalism and Quakerism. These religions already had a distrust for science, only intensified by the recent publishing of Darwin's Theory of Evolution in 1859.Neither side was pleased with how the Cruelty to Animals Act 1876 was passed. The scientific community felt as though the government was restricting their ability to compete with the quickly advancing France and Germany with new regulations. The anti-vivisection movement was also unhappy, but because they believed that it was a concession to scientists for allowing vivisection to continue at all. Ferrier would continue to vex the anti-vivisection movement in Britain with his experiments when he had a debate with his German opponent, Friedrich Goltz. They would effectively enter the vivisection arena, with Ferrier presenting a monkey, and Goltz presenting a dog, both of which had already been operated on. Ferrier won the debate, but did not have a license, leading the anti-vivisection movement to sue him in 1881. Ferrier was not found guilty, as his assistant was the one operating, and his assistant did have a license. Ferrier and his practices gained public support, leaving the anti-vivisection movement scrambling. They made the moral argument that given recent developments, scientists would venture into more extreme practices to operating on "the cripple, the mute, the idiot, the convict, the pauper, to enhance the 'interest' of [the physiologist's] experiments".
Vivisection	Human vivisection	It is possible that human vivisection was practised by some Greek anatomists in Alexandria in the 3rd century BC. Celsus in De Medicina states that Herophilos of Alexandria vivisected some criminals sent by the King, and the early Christian writer Tertullian states that Herophilos vivisected at least 600 live prisoners although the accuracy of this claim is disputed by many historians.Andalusian Arab Ibn Tufail in the 12th century elaborated on human vivisection in his treatise called Hayy ibn Yaqzan and Nadia Maftouni, discussing the subject in an extensive article, believes him to be among the early supporters of autopsy and vivisection.Unit 731, a biological and chemical warfare research and development unit of the Imperial Japanese Army, undertook lethal human experimentation during the period that comprised both the Second Sino-Japanese War and the Second World War (1937–1945). In the Filipino island of Mindanao, Moro Muslim prisoners of war were subjected to various forms of vivisection by the Japanese, in many cases without anesthesia.Nazi human experimentation involved many medical experiments on live subjects, such as vivisections by Josef Mengele, usually without anesthesia.
Dimethyldioxirane	Dimethyldioxirane	Dimethyldioxirane (DMDO), also referred to as Murray's reagent in reference to Robert W. Murray, is a dioxirane derived from acetone and can be considered as a monomer of acetone peroxide. It is a powerful yet selective oxidizing agent which finds use in organic synthesis. It is known only in the form of a dilute solution, usually in acetone, and hence the properties of the pure material are largely unknown.
Dimethyldioxirane	Synthesis	DMDO is not commercially available because of its instability. DMDO can be prepared as dilute solutions (~0.1 M) by treatment of acetone with potassium peroxymonosulfate KHSO5, usually in the form of Oxone (2KHSO5·KHSO4·K2SO4).
Dimethyldioxirane	Synthesis	The preparation of DMDO is rather inefficient (typical yields < 3%) and typically only yields a relatively dilute solution in acetone (only up to approximately 0.1 M). This is tolerable as preparation uses inexpensive substances: acetone, sodium bicarbonate, and potassium peroxymonosulfate (commercially known as "oxone"). The solution can be stored at low temperatures and its concentration may be assayed immediately prior to its use.
Dimethyldioxirane	Synthesis	The more active compound methyl(trifluoromethyl)dioxirane (H3C)(F3C)CO2 can be similarly prepared from methyl trifluoromethyl ketone. Stability Solutions are stable under refrigeration (−10 to −20 °C) for up to a week. The rate of decomposition will increase upon exposure to light or heavy metals.
Dimethyldioxirane	Uses	The most common use for DMDO is the oxidation of alkenes to epoxides. One particular advantage of using DMDO is that the only byproduct of oxidation is acetone, a fairly innocuous and volatile compound. DMDO oxidations are particularly mild, sometimes allowing oxidations which might not otherwise be possible. In fact, DMDO is considered the reagent of choice for epoxidation, and in nearly all circumstances is as good as or better than peroxyacids such as meta-chloroperoxybenzoic acid (mCPBA).Despite its high reactivity, DMDO displays good selectivity for olefins. Typically, electron deficient olefins are oxidized more slowly than electron rich ones. DMDO will also oxidize several other functional groups. For example, DMDO will oxidize primary amines to nitro compounds and sulfides to sulfoxides. In some cases, DMDO will even oxidize unactivated C-H bonds: DMDO can also be used to convert nitro compounds to carbonyl compounds (Nef reaction).
Biological pathway	Biological pathway	A biological pathway is a series of interactions among molecules in a cell that leads to a certain product or a change in a cell. Such a pathway can trigger the assembly of new molecules, such as a fat or protein. Pathways can also turn genes on and off, or spur a cell to move. Some of the most common biological pathways are involved in metabolism, the regulation of gene expression and the transmission of signals. Pathways play a key role in advanced studies of genomics.
Biological pathway	Biological pathway	Most common types of biological pathways: Metabolic pathway Genetic pathway Signal transduction pathway
Biological pathway	Pathways databases	KEGG Pathway database is a popular pathway search database highly used by biologists. WikiPathways is a community curated pathway database using the "wiki" concept. All pathways have an open license and can be freely used. Reactome is a free and manually curated online database of biological pathways. NCI-Nature Pathway Interaction Database is a free biomedical database of human cellular signaling pathways (new official name: NCI Nature Pathway Interaction Database: Pathway, synonym: PID). PhosphoSitePlus is a database of observed post-translational modifications in human and mouse proteins; an online systems biology resource providing comprehensive information and tools for the study of protein post-translational modifications (PTMs) including phosphorylation, ubiquitination, acetylation and methylation. BioCyc database collection is an assortment of organism specific Pathway/Genome Databases. Human Protein Reference Database is a centralized platform to visually depict and integrate information pertaining to domain architecture, post-translational modifications, interaction networks and disease association for each protein in the human proteome (the last release was #9 in 2010). PANTHER (Protein ANalysis THrough Evolutionary Relationships) is a large curated biological database of gene/protein families and their functionally related subfamilies that can be used to classify and identify the function of gene products. TRANSFAC (TRANScription FACtor database) is a manually curated database of eukaryotic transcription factors, their genomic binding sites and DNA binding profiles (provided by geneXplain GmbH). MiRTarBase is a curated database of MicroRNA-Target Interactions. DrugBank is a comprehensive, high-quality, freely accessible, online database containing information on drugs and drug targets. esyN is a network viewer and builder that allows to import pathways from the biomodels database or from biogrid, flybase pombase and see what drugs interact with the proteins in your network. Comparative Toxicogenomics Database (CTD) is a public website and research tool that curates scientific data describing relationships between chemicals/drugs, genes/proteins, diseases, taxa, phenotypes, GO annotations, pathways, and interaction modules; CTD illuminates how environmental chemicals affect human health. Pathway commons is a project and database that uses BioPAX language to convert, integrate and query other biological pathway and interaction databases.
Network allocation vector	Network allocation vector	The network allocation vector (NAV) is a virtual carrier-sensing mechanism used with wireless network protocols such as IEEE 802.11 (Wi-Fi) and IEEE 802.16 (WiMax). The virtual carrier-sensing is a logical abstraction which limits the need for physical carrier-sensing at the air interface in order to save power. The MAC layer frame headers contain a duration field that specifies the transmission time required for the frame, in which time the medium will be busy. The stations listening on the wireless medium read the Duration field and set their NAV, which is an indicator for a station on how long it must defer from accessing the medium.
Network allocation vector	Network allocation vector	The NAV may be thought of as a counter, which counts down to zero at a uniform rate. When the counter is zero, the virtual carrier-sensing indication is that the medium is idle; when nonzero, the indication is busy. The medium shall be determined to be busy when the station (STA) is transmitting. In IEEE 802.11, the NAV represents the number of microseconds the sending STA intends to hold the medium busy (maximum of 32,767 microseconds). When the sender sends a Request to Send the receiver waits one SIFS before sending Clear to Send. Then the sender will wait again one SIFS before sending all the data. Again the receiver will wait a SIFS before sending ACK. So NAV is the duration from the first SIFS to the ending of ACK. During this time the medium is considered busy. Wireless stations are often battery-powered, so to conserve power the stations may enter a power-saving mode. A station decrements its NAV counter until it becomes zero, at which time it is awakened to sense the medium again.
Network allocation vector	Network allocation vector	The NAV virtual carrier sensing mechanism is a prominent part of the CSMA/CA MAC protocol used with IEEE 802.11 WLANs. NAV is used in DCF, PCF and HCF.
7-Methylxanthine	7-Methylxanthine	7-Methylxanthine (7-MX), also known as heteroxanthine, is an active metabolite of caffeine (1,3,7-trimethylxanthine) and theobromine (3,7-dimethylxanthine). It is a non-selective antagonist of the adenosine receptors. The compound may slow the progression of myopia (nearsightedness). It is under investigation for this purpose in children with myopia.
7-Methylxanthine	7-Methylxanthine	It is shown that systemic treatment with 7-mx appears to be efficient in retarding axial elongation and myopia progression among myopic children. The treatment is safe and without side effects, and may be continued until 18–20 years of age, when age-related cross-linking of collagen prevents further elongation of the eye. Additionally, further studies show that oral intake of 7-MX was associated with reduced myopia progression and reduced axial elongation in this sample of myopic children from Denmark. Randomised controlled trials are needed to determine whether the association is causal.
7-Methylxanthine	7-Methylxanthine	Further clinical trials will be conducted to ascertain the full efficacy of this new drug for the use of controlling the progression of Myopia.
Stock catalyst	Stock catalyst	A stock catalyst is an event that causes the price of a security to move, often significantly. In a simplified sense, it can be either bad news that unnerves investors or good news to get investors interested in the stock again. Stock catalysts often change investor sentiment and can mark the beginning or end of stock trends. The most common catalysts arise due to unexpected information that triggers the market to re-consider a company's business prospects. Some investors and traders use catalysts in short-term trading strategies to generate a profit.
Stock catalyst	Types	A stock catalyst can be either a sudden catalyst or an anticipated catalyst. Sudden catalysts cannot be anticipated and are announced suddenly by the company during a press release. An example of a sudden catalyst is a company partnership since they are announced without prior notice to investors. Anticipated catalysts are catalysts that investors are aware of before the catalyst even happens. They are generally pre-scheduled and can have a strong affect a company's stock price during the days leading up to and including the event.
Stock catalyst	Examples	The following are examples of stock catalysts: Earnings release Investor Conference Product Release FDA/CDC Approval Economic Event Metric Reveal Court Decision Corporate Action IPO IPO Lockup Expiration Partnership Contracts Analyst Revisions
Stock catalyst	Trading strategies	Buy the Rumor, Sell the News The trading strategy around buying the rumor and selling the news revolves around buying or selling the stock during the 3 weeks leading up to the catalyst event, and selling before the event actually occurs. This strategy can be predicable because the stock market will price in rumors around the catalyst in the days leading up to the event. If the catalyst is expected to be positive, then the company stock is also expected to rise in the weeks leading up to the event.
Stock catalyst	Trading strategies	Trade the Catalyst Another trading strategy related to stock catalysts is buying or selling the stock and maintaining that position during the catalyst event. This is a highly speculative and risky strategy due to the unpredictability of catalyst events such as earnings releases.
MED24	MED24	Mediator of RNA polymerase II transcription subunit 24 is an enzyme that in humans is encoded by the MED24 gene.
MED24	Function	This gene encodes a component of the mediator complex (also known as TRAP, SMCC, DRIP, or ARC), a transcriptional coactivator complex thought to be required for the expression of almost all genes. The mediator complex is recruited by transcriptional activators or nuclear receptors to induce gene expression, possibly by interacting with RNA polymerase II and promoting the formation of a transcriptional pre-initiation complex. Multiple transcript variants encoding different isoforms have been found for this gene.
MED24	Interactions	MED24 has been shown to interact with Estrogen receptor alpha, Cyclin-dependent kinase 8, Calcitriol receptor and BRCA1.
Aiyara cluster	Aiyara cluster	An Aiyara cluster is a low-powered computer cluster specially designed to process Big Data. The Aiyara cluster model can be considered as a specialization of the Beowulf cluster in the sense that Aiyara is also built from commodity hardware, not inexpensive personal computers, but system-on-chip computer boards. Unlike Beowulf, applications of an Aiyara cluster are scoped only for the Big Data area, not for scientific high-performance computing. Another important property of an Aiyara cluster is that it is low-power. It must be built with a class of processing units that produces less heat.
Aiyara cluster	Aiyara cluster	The name Aiyara originally referred to the first ARM-based cluster built by Wichai Srisuruk and Chanwit Kaewkasi at Suranaree University of Technology. The name "Aiyara" came from a Thai word literally an elephant to reflect its underneath software stack, which is Apache Hadoop. Like Beowulf, an Aiyara cluster does not define a particular software stack to run atop it. A cluster normally runs a variant of the Linux operating system. Commonly used Big Data software stacks are Apache Hadoop and Apache Spark.
Aiyara cluster	Development	A report of the Aiyara hardware which successfully processed a non-trivial amount of Big Data was published in the Proceedings of ICSEC 2014. Aiyara Mk-I, the second Aiyara cluster, consists of 22 Cubieboards. It is the first known SoC-based ARM cluster which is able to process Big Data successfully using the Spark and HDFS stack.The Aiyara cluster model, a technical description explaining how to build an Aiyara cluster, was later published by Chanwit Kaewkasi in the DZone's 2014 Big Data Guide.
Aiyara cluster	Development	The further results and cluster optimization techniques, that make the cluster's processing rate boost to 0.9 GB/min while still preserve low-power consumption, were reported in the Proceeding of IEEE's TENCON 2014. The whole architecture of software stack, including the runtime, data integrity verification and data compression, is studied and improved. The work reported in this paper achieved the processing rate at almost 0.9 GB/min, successfully processed the same benchmarks from the previous work by roughly 38 minutes.
Derivation of the Schwarzschild solution	Derivation of the Schwarzschild solution	The Schwarzschild solution describes spacetime under the influence of a massive, non-rotating, spherically symmetric object. It is considered by some to be one of the simplest and most useful solutions to the Einstein field equations .
Derivation of the Schwarzschild solution	Assumptions and notation	Working in a coordinate chart with coordinates (r,θ,ϕ,t) labelled 1 to 4 respectively, we begin with the metric in its most general form (10 independent components, each of which is a smooth function of 4 variables). The solution is assumed to be spherically symmetric, static and vacuum. For the purposes of this article, these assumptions may be stated as follows (see the relevant links for precise definitions): A spherically symmetric spacetime is one that is invariant under rotations and taking the mirror image.
Derivation of the Schwarzschild solution	Assumptions and notation	A static spacetime is one in which all metric components are independent of the time coordinate t (so that ∂∂tgμν=0 ) and the geometry of the spacetime is unchanged under a time-reversal t→−t A vacuum solution is one that satisfies the equation Tab=0 . From the Einstein field equations (with zero cosmological constant), this implies that Rab=0 since contracting Rab−R2gab=0 yields R=0 Metric signature used here is (+,+,+,−).
Derivation of the Schwarzschild solution	Diagonalising the metric	The first simplification to be made is to diagonalise the metric. Under the coordinate transformation, (r,θ,ϕ,t)→(r,θ,ϕ,−t) , all metric components should remain the same. The metric components gμ4 (μ≠4 ) change under this transformation as: gμ4′=∂xα∂x′μ∂xβ∂x′4gαβ=−gμ4 (μ≠4 )But, as we expect gμ4′=gμ4 (metric components remain the same), this means that: gμ4=0 (μ≠4 )Similarly, the coordinate transformations (r,θ,ϕ,t)→(r,θ,−ϕ,t) and (r,θ,ϕ,t)→(r,−θ,ϕ,t) respectively give: gμ3=0 (μ≠3 )gμ2=0 (μ≠2 )Putting all these together gives: gμν=0 (μ≠ν )and hence the metric must be of the form: 11 22 33 44 dt2 where the four metric components are independent of the time coordinate t (by the static assumption).
Derivation of the Schwarzschild solution	Simplifying the components	On each hypersurface of constant t , constant θ and constant ϕ (i.e., on each radial line), 11 should only depend on r (by spherical symmetry). Hence 11 is a function of a single variable: 11 =A(r) A similar argument applied to 44 shows that: 44 =B(r) On the hypersurfaces of constant t and constant r , it is required that the metric be that of a 2-sphere: sin 2⁡θdϕ2) Choosing one of these hypersurfaces (the one with radius r0 , say), the metric components restricted to this hypersurface (which we denote by 22 and 33 ) should be unchanged under rotations through θ and ϕ (again, by spherical symmetry). Comparing the forms of the metric on this hypersurface gives: 22 33 22 sin 2⁡θdϕ2) which immediately yields: 22 =r02 and 33 sin 2⁡θ But this is required to hold on each hypersurface; hence, 22 =r2 and 33 sin 2⁡θ An alternative intuitive way to see that 22 and 33 must be the same as for a flat spacetime is that stretching or compressing an elastic material in a spherically symmetric manner (radially) will not change the angular distance between two points.
Derivation of the Schwarzschild solution	Simplifying the components	Thus, the metric can be put in the form: sin 2⁡θdϕ2+B(r)dt2 with A and B as yet undetermined functions of r . Note that if A or B is equal to zero at some point, the metric would be singular at that point.
Derivation of the Schwarzschild solution	Calculating the Christoffel symbols	Using the metric above, we find the Christoffel symbols, where the indices are (1,2,3,4)=(r,θ,ϕ,t) . The sign ′ denotes a total derivative of a function. sin 2⁡θ/A0000−B′/(2A)] sin cos ⁡θ00000] cot cot ⁡θ000000] Γik4=[000B′/(2B)00000000B′/(2B)000]

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