Glycogen is the immediate form of energy for muscle contraction.
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Most shellfish allergens are proteins that are involved in muscle contraction.
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The extremities don't have much muscle contraction, so there's not much heat produced.
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This creates the pumping action, replacing the muscle contraction of the human heart.
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"A big physiological sign to look for is involuntary muscle contraction," Marin says.
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Any muscle contraction is good because it's pumping blood back up toward your brain.
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It affects the enzymes that control muscle contraction, not hormones that cause muscles to contract.
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The muscles contract and then relax, similar to the regular muscle contraction experienced during normal exercise.
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A jolt of electricity causes a muscle contraction that stimulates ejaculation of sperm through the usual channels.
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It affects the enzymes that control muscle contraction.. Overdoses can cause vomiting, seizures and loss of consciousness.
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It alters the shape of a "sodium channel" that maintains an electric current to stimulate muscle contraction.
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Progressive muscle contraction/relaxation This practice is all about using the mind to speak to the body.
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"Scarring in general affects the muscle's ability to work effectively and efficiently during a muscle contraction," she says.
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In the FES bike race, competitors with paraplegia artificially "pedal" by stimulating motor nerves to cause muscle contraction.
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The pain isn't searing — unlike, say, sticking your finger in a wall socket — but isn't pleasant: a brief muscle contraction, then numbness.
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Stirring from wind, much like a muscle contraction, allows gases to mix and reach important places like a termite nest or human blood.
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"When you keep a muscle contraction for over 60 seconds, it's going to have that effect of really tightening and sculpting the muscle," explains Lagree.
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Neurons are only a portion of what is cumulatively called a "nerve bundle"; they carry the electric impulses that govern muscle contraction or register sensation.
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Pillars were inserted into the muscle fiber during the process to help visualize displacement and create a method for detecting the force that was exerted during muscle contraction.
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They've raised the bar with their latest Nerf creation, however: a bionic gun that can attach to an amputated or missing limb and be fired by muscle contraction.
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"Carbs are the primary fuel for muscle contraction," explains Kelly Pritchett, an associate professor of nutrition and exercise science at Central Washington University and a certified specialist in sports dietetics.
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DeBruler explains that humans are somewhere between 50 to 200 percent stronger on the eccentric phase (resisting force) of muscle contraction than we are on the concentric phase (creating force).
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"When the heels pitch you forward, you adjust the balance of the spine and you need active muscle contraction to stay centered, and some women think that works," says Dr. Lipson.
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Pressurized air inflates and deflates this central chamber, replacing the muscle contraction of the human heart, and this is how the artificial heart is able to pump fluid with comparable viscosity to human blood.
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Eleven different genes showed evidence of mutations occurring over generations that boosted the animal's muscle contraction, stress response and regulation of energy-releasing processes, all of which beefed up the big cat's running prowess.
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Typical medications used to treat long-term hiccups, according to the Mayo Clinic, are the muscle relaxer Baclofen; antipsychotic Chlorpromazine; and Metoclopramide, which increases muscle contraction in the upper digestive tract and is typically used to treat reflux.
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"Though water needs are relatively variable depending on the size and muscle mass, drinking too much water in a short amount of time can actually lead to hyponatremia, meaning the dilution of the amount of sodium in your body," explains Heather Milton, a senior exercise physiologist at NYU Langone Health, adding that sodium is one of the key electrolytes needed for muscle contraction and proper cell function.
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In effect, the thick filament moves or slides along the thin filament, resulting in muscle contraction. This process is known as the sliding filament model of muscle contraction.
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A uterine contraction is a muscle contraction of the uterine smooth muscle.
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Located in the jejunum, N cells release neurotensin, and control smooth muscle contraction.
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The sliding filament theory is a universally accepted explanation of the mechanism that underlies muscle contraction.
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Muscle contraction is the activation of tension-generating sites within muscle fibers. In physiology, muscle contraction does not necessarily mean muscle shortening because muscle tension can be produced without changes in muscle length, such as when holding a heavy book or a dumbbell at the same position. The termination of muscle contraction is followed by muscle relaxation, which is a return of the muscle fibers to their low tension-generating state. Muscle contractions can be described based on two variables: length and tension.
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Calciseptine has been shown to block L-type calcium channels, thus inhibiting smooth muscle contraction and cardiac function.
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Adolf Fick originally discovered in 1882 that "contracting muscle under stretch could produce greater force than a shortening muscle contraction" like in concentric movements. Fifty years later, A.V. Hill determined that "the body had lower energy demand during an eccentric muscle contraction than during a concentric muscle action". Erling Asmussen first introduced eccentric training in 1953 as "excentric", with ex meaning "away from" and centric meaning "center". Hence, the term was coined to mean a muscle contraction that moves away from the center of the muscle.
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These millipedes remain passively locked-up since they need not continued muscle contraction to remain in the rolled-up position.
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Activation of TLR4 in intrauterine infections leads to deregulation of prostaglandin synthesis, leading to uterine smooth muscle contraction [citation needed].
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Pain increases gradually, but it can also be sudden. Cold causes muscle contraction, which leads to increased previously hidden symptoms.
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Thought to have a domain-interface model of binding. In hypertension, the binding of nitrendipine causes a decrease in the probability of open L-type calcium channels and reduces the influx of calcium. The reduced levels of calcium prevent smooth muscle contraction within these muscle cells. Prevention of muscle contraction enables smooth muscle dilation.
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During motor activity, serotonin released in synapses that contact motoneurons promotes muscle contraction. During high level of motor activity, the amount of serotonin released increases and a spillover occurs. Serotonin binds to extrasynaptic receptors located on the axon initial segment of motoneurons with the result that nerve impulse initiation and thereby muscle contraction are inhibited.
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The phosphorylation of MLC will enable the myosin crossbridge to bind to the actin filament and allow contraction to begin (through the crossbridge cycle). Since smooth muscle does not contain a troponin complex, as striated muscle does, this mechanism is the main pathway for regulating smooth muscle contraction. Reducing intracellular calcium concentration inactivates MLCK but does not stop smooth muscle contraction since the myosin light chain has been physically modified through phosphorylation(and not via ATPase activity). To stop smooth muscle contraction this change needs to be reversed.
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It is not understood whether the physical opening of the L-type calcium channels or the presence of calcium causes the ryanodine receptors to open. The outflow of calcium allows the myosin heads access to the actin cross-bridge binding sites, permitting muscle contraction. Muscle contraction ends when calcium ions are pumped back into the sarcoplasmic reticulum, allowing the contractile apparatus and, thus, muscle cell to relax. Upon muscle contraction, the A-bands do not change their length (1.85 micrometer in mammalian skeletal muscle), whereas the I-bands and the H-zone shorten.
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There are repackaged TENS and EMS units marketed as erotic electrostimulation power sources. EMS units are designed to cause muscle contraction.
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A large-scale example of an action performed by the cytoskeleton is muscle contraction. This is carried out by groups of highly specialized cells working together. A main component in the cytoskeleton that helps show the true function of this muscle contraction is the microfilament. Microfilaments are composed of the most abundant cellular protein known as actin.
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Muscle contraction stimulates muscle cells to translocate GLUT4 receptors to their surfaces. This is especially true in cardiac muscle, where continuous contraction increases the rate of GLUT4 translocation; but is observed to a lesser extent in increased skeletal muscle contraction. In skeletal muscle, muscle contractions increase GLUT4 translocation several fold, and this is likely regulated by RAC1 and AMP- activated protein kinase.
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J Appl Physiol. 2005 Jul;99(1):371-2. While this explanation is attractive because it would explain the readily observable tight coupling between muscle contraction and a rapid increase in muscle blood flow, recent evidence has emerged that cast doubts on this theory. Experiments have shown that a strong muscle contraction can occur without a corresponding increase in skeletal muscle blood flow.
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Average level of activity in a tendon organ population is representative of the whole muscle force. The Ib sensory feedback generates spinal reflexes and supraspinal responses which control muscle contraction. Ib afferents synapse with interneurons that are within the spinal cord that also project to the brain cerebellum and cerebral cortex. The autogenic inhibition reflex assists in regulating muscle contraction force.
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Spike potentials are one of the action potentials, which occur in electrical activity of smooth muscle contraction in animals. These are true action potentials.
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In addition, a medical symptom known as "Séguin's signal" is named after him, being described as an involuntary muscle contraction prior to an epileptic attack.
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Gabapentin inhibits neurotransmitter release in the dorsal horn of the spinal cord and various areas of the central nervous system. It helps treat mild symptoms and can be tolerated for longer periods of time compared to other drug treatments. Dantrolene helps combat dystonia and fever by affecting muscle contraction and relaxation cycles. It hinders the release of calcium from the sarcoplasmic reticulum, inhibiting muscle contraction.
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Basically, it limits the effectiveness of octopamine, the neurotransmitter that controls muscle contraction in sudden movements.Jewel Wasps. YouTube. YouTube, 19 Feb. 2009. Web. 10 Dec. 2012.
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Manuel Francisco Morales (July 23, 1919 – November 12, 2009) was a Honduran- born American biophysicist who did pivotal research on the molecular basis of muscle contraction.
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Dephosphorylation of the myosin light chain (and subsequent termination of muscle contraction) occurs through activity of a second enzyme known as myosin light-chain phosphatase (MLCP).
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Focal tonic seizures are characterized by sustained muscle contraction of muscle groups, and thus often appear as abnormal posturing of a single limb or eye deviation.
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The nerve terminates onto the endplate, forming the neuromuscular junction—a structure which is required to transmit nerve impulses to the muscle, and thus initiating muscle contraction.
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Increases in firing frequency improve athletic force by decreasing the time to maximum muscle contraction (also known as reaction time) rather than increasing the maximum force output.
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A hydrostatic skeleton uses hydrostatic pressure generated from muscle contraction against a liquid filled cavity. The liquid filled cavity is commonly referred to as the hydrostatic body. The liquid within the hydrostatic body acts as an incompressible fluid and the body wall of the hydrostatic body provides a passive elastic antagonist to muscle contraction, which in turn generates a force, which in turn creates movement.R. B. Clark and J. B. Cowey.
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Recent research indicates that sphingosine-1-phosphate (S1P) signaling is an important regulator of vascular smooth muscle contraction. When transmural pressure increases, sphingosine kinase 1 phosphorylates sphingosine to S1P, which binds to the S1P2 receptor in plasma membrane of cells. This leads to a transient increase in intracellular calcium, and activates Rac and Rhoa signaling pathways. Collectively, these serve to increase MLCK activity and decrease MLCP activity, promoting muscle contraction.
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Kininogens are precursor proteins for kinins, biologically active polypeptides involved in blood coagulation, vasodilation, smooth muscle contraction, inflammatory regulation, and the regulation of the cardiovascular and renal systems.
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Motor neuron activity precedes muscle contraction, which precedes the movement. Sensory signals also reflect events that have already occurred. Such delays affect the choice of motor program. # Uncertainty.
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This gene encodes a protein with similarity to the Caenorhabditis elegans unc93 protein. The Unc93 protein is involved in the regulation or coordination of muscle contraction in the worm.
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COL22A1 is a human gene encoding for collagen. The associated protein is thought to contribute to the stabilization of myotendinous junctions and strengthen skeletal muscle attachments during muscle contraction.
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The central component of fatigue is triggered by an increase of the level of serotonin in the central nervous system. During motor activity, serotonin released in synapses that contact motoneurons promotes muscle contraction. During high level of motor activity, the amount of serotonin released increases and a spillover occurs. Serotonin binds to extrasynaptic receptors located on the axon initial segment of motoneurons with the result that nerve impulse initiation and thereby muscle contraction are inhibited.
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In biomechanics, Hill's muscle model refers to either Hill's equations for tetanized muscle contraction or to the 3-element model. They were derived by the famous physiologist Archibald Vivian Hill.
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When a sucker attaches itself to an object, the infundibulum mainly provides adhesion while the central acetabulum is free. Sequential muscle contraction of the infundibulum and acetabulum causes attachment and detachment.
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It is also involved in regulation of dopamine pathways. In the periphery, neurotensin is found in enteroendocrine cells of the small intestine, where it leads to secretion and smooth muscle contraction.
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Energy is put into the store at low power by slow but strong muscle contraction, and retrieved from the store at high power by rapid relaxation of the mechanical elastic structures.
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Together they discovered in 1954 the mechanism of muscle contraction, popularly called the "sliding filament theory", which is the foundation of our modern understanding of muscle mechanics. In 1960 he became head of the Department of Physiology at University College London. He was elected a Fellow of the Royal Society in 1955, and President in 1980. The Royal Society awarded him the Copley Medal in 1973 for his collective contributions to the understanding of nerve impulses and muscle contraction.
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During contraction of a muscle, within each muscle cell, myosin molecular motors collectively exert forces on parallel actin filaments. Muscle contraction starts from nerve impulses which then causes increased amounts of calcium to be released from the sarcoplasmic reticulum. Increases in calcium in the cytosol allows muscle contraction to begin with the help of two proteins, tropomyosin and troponin. Tropomyosin inhibits the interaction between actin and myosin, while troponin senses the increase in calcium and releases the inhibition.
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This gradient is the driving force for other transport proteins, such as the sodium-calcium exchanger, which plays an important role in cardiomyocytes. To make muscle contraction possible, a calcium influx from the extracellular fluid into the cell is crucial. After the muscle contraction, the calcium is normally pumped out of the cell and exchanged for sodium. When the sodium gradient is depleted, calcium cannot be pumped back and, as a consequence, accumulates in the cardiomyocyte.
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The intake of sodium and chloride, along with lower relative concentrations of potassium and calcium ions in the seawater allow southern bluefin tuna to generate the action potentials required for muscle contraction.
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69, no. 1, pp. 35–51 (1978). This theory allowed him to explain experimental features of muscle contraction, such as the relation of tension to velocity as described by Hill's muscle model.
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The degree of muscle contraction or extension can be measured on a scale at the back of the model. Other ophthalmotropes were designed later by Landolt, Knapp, Donders, Snellen, Wundt, and others.
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In addition to the eel skin acting as an external tendon, the skin attaches directly to the underlying muscle, which allow for the eel to generate an even greater force per muscle contraction.
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Drugs which affect smooth muscle contraction, such as doxazosin, nitroglycerine, nifedipine and phenoxybenzamine, may provide pain relief. Topical lidocaine patches have been reported to decrease in severity and frequency of pain cutaneous leiomyomas.
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This assumption of a local mechano-chemical transduction is in accord with Tirosh's mechanism of muscle contraction, where the muscle force derives from an integrated action of active streaming created by ATP hydrolysis.
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Because myosin light chain has no inherent phosphate cleaving property over active PKC prevents the dephosphorylation of myosin light protein leaving it in the activated conformation, causing an increase in smooth muscle contraction.
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A muscle contraction is described as isometric if the muscle tension changes but the muscle length remains the same. In contrast, a muscle contraction is isotonic if muscle tension remains the same throughout the contraction. If the muscle length shortens, the contraction is concentric; if the muscle length lengthens, the contraction is eccentric. In natural movements that underlie locomotor activity, muscle contractions are multifaceted as they are able to produce changes in length and tension in a time-varying manner.
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Schwartz–Jampel syndrome is caused by mutations in the HSPG2 gene, which makes the protein perlecan, which is found in muscle and cartilage. Relationships between the disease and perlecan deficiency have been studied. In Schwartz–Jampel syndrome, it is suspected that abnormal perlecan function leads to a deficiency in acetylcholinesterase, an enzyme involved in breaking down the neurotransmitter acetylcholine, which incites muscle contraction. If acetylcholine is not broken down, it can lead to prolonged muscle contraction/stiffening of the muscles (myotonia).
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The Ca2+ ions bind to troponin, what causes the displacement of tropomyosin, a protein that prevents myosin walking along actin. The displacement of tropomyosin exposes the myosin-binding sites on actin, permitting muscle contraction. This way, while muscle contraction is driven by Ca2+ release, muscle relaxation is driven by Ca2+ removal from sarcoplasm. Along with Ca2+ pumps, PV contributes to Ca2+ removal from cytoplasm: PV binds to Ca2+ ions in the sarcoplasm, and then shuttles it to the sarcoplasmic reticulum.
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Which trajectory is best? # Noise. Noise is defined as small fluctuations that are unrelated to a signal, which can occur in neurons and synaptic connections at any point from sensation to muscle contraction. # Delays.
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Botulism prevents muscle contraction by blocking the release of acetylcholine, thereby halting postsynaptic activity of the neuromuscular junction. If its effects reach the respiratory muscles, then it can lead to respiratory failure, leading to death.
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Rolf Nidergerke (30 April 1921 – 27 December 2011) was a German physiologist and physician, and one of the discoverers of the sliding filament theory of muscle contraction. He and Andrew Huxley, complimenting the independent works of Hugh Huxley and Jean Hanson, revealed that muscle contraction is due to shortening of the muscle fibres. He studied medicine throughout the Second World War, and obtained his MD degree as the war ended in 1945. After a brief practise in his hometown, he chose a research career.
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The function of the antagonist muscle contraction is believed to control the amplitude and timing of ballistic movements. Antagonist muscle contraction may serve to prevent injury to joints by preventing the limb from overextending itself and also function to control the distance and time the limb is being moved. Experiments involving ballistic movement of small amplitudes show a marked increase in antagonist muscle activation and experiments where distance moved is not controlled antagonist muscle activation was decreased or absent.Zehr, E.P. and Sale, D.G. (1994).
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When a motor neuron is activated, all of the muscle fibers innervated by the motor neuron are stimulated and contract. The activation of one motor neuron will result in a weak but distributed muscle contraction. The activation of more motor neurons will result in more muscle fibers being activated, and therefore a stronger muscle contraction. Motor unit recruitment is a measure of how many motor neurons are activated in a particular muscle, and therefore is a measure of how many muscle fibers of that muscle are activated.
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The discovery of the axonal reflex found that the axon reflex activates local arterioles causing vasodilation and muscle contraction. This muscle contraction was observed in people with asthma where the released neuropeptides caused the smooth muscle in the airway to contract. Similarly the release of cholinergic agents at sudomotor nerve terminals evokes an axon reflex that stimulates sweat glands inducing the body to sweat in response to heat. The axon reflex is possible through the transmission of signals from the cutaneous receptors on the skin.
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The prokineticin receptor is a G protein-coupled receptor which binds the peptide hormone prokineticin. There are two variants each encoded by a different gene (PROKR1, PROKR2). These receptors mediate gastrointestinal smooth muscle contraction and angiogenesis.
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In vivo mechanics of maximum isometric muscle contraction in man: Implications for modelling-based estimates of muscle specific tension. In Herzog W. (Ed). Skeletal muscle mechanics: from mechanisms to function. Wiley & Sons Ltd, p.267-288.
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EDHF: spreading the influence of the endothelium. British Journal of Pharmacology. 164:3, 839-852. (2011). However, dysfunction within these Ca2+-activated pathways can lead to an increase in tone caused by unregulated smooth muscle contraction.
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In cardiac muscle, the result of CICR is observed as a spatio-temporally restricted Ca2+ spark. The result of CICR across the cell causes the significant increase in cytosolic Ca2+ that is important in activating muscle contraction.
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Actin and myosin The increase of sustained muscle contraction leads to oxygen and ATP depletion with prolonged exposure to calcium. The muscle cell membrane pump may become damaged allowing free form myoglobin to leak into the bloodstream.
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By the end of the 1940s Szent-Györgyi's team had postulated with evidence that contraction of actomyosin was equivalent to muscle contraction as a whole. But the notion was generally opposed, even from the likes of Nobel laureates such as Otto Fritz Meyerhof and Archibald Hill, who adhered to the prevailing dogma that myosin was a structural protein and not a functional enzyme. However, in one of his last contributions to muscle research, Szent-Györgyi demonstrated that actomyosin driven by ATP was the basic principle of muscle contraction.
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Following depolarization, the acetylcholine molecules are then removed from the end plate region and enzymatically hydrolysed by acetylcholinesterase. Normal end plate function can be blocked by two mechanisms. Nondepolarizing agents, such as tubocurarine, block the agonist, acetylcholine, from binding to nicotinic receptors and activating them, thereby preventing depolarization. Alternatively, depolarizing agents, such as succinylcholine, are nicotinic receptor agonists which mimic Ach, block muscle contraction by depolarizing to such an extent that it desensitizes the receptor and it can no longer initiate an action potential and cause muscle contraction.
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Ballistic movement: Muscle activation and neuromuscular adaptation. Canadian Journal of Applied Physiology. 19(4): 363-378. The second agonist muscle activation is suggested to terminate the negative acceleration of the antagonist muscle contraction and thus the ballistic movement.
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A 0 is for no muscle contraction. A 1 is for a flicker or trace of contraction in a muscle. A 2 is for active movement in a muscle with gravity eliminated. A 3 is for movement against gravity.
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The GLUT4 carrier vesicles are either transferrin positive or negative, and are recruited by different stimuli. Transferrin- positive GLUT4 vesicles are utilized during muscle contraction while the transferrin-negative vesicles are activated by insulin stimulation as well as by exercise.
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Botulinum A Toxin (BTX A) is injected into the external sphincter via cystoscopic or ultrasound. Botox blocks the release of acetylcholine, a neurotransmitter that is needed for muscle contraction. With the release of acetylcholine inhibited, muscles will become more relaxed.
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Taking the suggestion of Bernard Katz, he continued his study on cardiac muscle (a specialised muscle of the heart), on which he discovered the role of calcium in muscle contraction (often dubbed the "calcium story") He retired from UCL in 1987.
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Azemiopsin, a toxin obtained from the Azemiops feae viper venom, is a polypeptide that consists of 21 amino acid residues. It does not contain cysteine residues or disulfide bridges. The polypeptide can block skeletal muscle contraction by blocking nicotinic acetylcholine receptors.
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This results in increased intestinal fluid and accelerated transit. By elevating cGMP, linaclotide is also considered to reduce activation of colonic sensory neurons, reducing pain; and activates colonic motor neurons, which increases smooth muscle contraction and thus promotes bowel movements.
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This leads to a reduction in smooth muscle contraction and mucus hyper-secretions, and thus produces a bronchodilatory effect. The terminal half-life of tiotropium in COPD patients following once daily inhalation of 5 mcg tiotropium was approximately 25 hours.
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Hormones like epinephrine and norepinephrine can affect the cardiovascular centre and cause it to increase the rate of impulses sent to the sinoatrial node, or pacemaker, resulting in faster and stronger cardiac muscle contraction and thus increasing the heart rate.
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In heart failure, this mechanism fails, as the ventricle is loaded with blood to the point where heart muscle contraction becomes less efficient. This is due to reduced ability to cross- link actin and myosin filaments in over-stretched heart muscle.
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As the MRC unit was enlarged he was invited back in 1962, with a research fellowship at King's College for five years and then a more permanent one at Churchill College. He became the joint Head of the Structural Studies Division of the LMB in 1975, and its Deputy Director in 1979. In 1969, on the basis of his work over more than 15 years, he finally formulated the "swinging cross-bridge hypothesis" of muscle contraction, which is the molecular basis of muscle contraction. The concept itself became directly fundamental to other types of cell motility.
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It takes multiple reactions between myosin and actin to effectively produce one muscle contraction, and, therefore, the availability of large amounts of ATP is required to produce each muscle contraction. For this reason, biological processes have evolved to produce efficient ways to replenish the potential energy of ATP from ADP. Breaking one of ATP's phosphorus bonds generates approximately 30.5 kilojoules per Mole of ATP (7.3 kcal). ADP can be converted, or powered back to ATP through the process of releasing the chemical energy available in food; in humans, this is constantly performed via aerobic respiration in the mitochondria.
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ParvE101Q is being investigated for side effects, and optimal delivery mechanisms before moving on to experimental trials to treat conditions such as diastolic heart failure. Parvalbumin has diverse effects on cell cycles, second messengers, microtubule organization, cardiac muscle contraction, and the nervous system.
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Cathinone can also affect cholinergic concentrations in the gut and airways by blocking prejunctional adrenergic receptors (a2 adrenergic) and activating 5-HT7 receptors, thereby inhibiting smooth muscle contraction. It can also induce dry mouth, blurred vision and increased blood pressure and heart rate.
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A surgical procedure known as myectomy may also be useful. BEB is a fairly rare disease, affecting only one in every 20,000 people in the United States. The word is from Greek: βλέφαρον / blepharon, eyelid, and σπασμός / spasmos, spasm, an uncontrolled muscle contraction.
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Rho proteins regulate many important cellular processes, including cytokinesis, transcription, smooth muscle contraction, cell growth and transformation. Dysregulation of the Rho signal transduction pathway has been implicated in many forms of cancer. Alternative splicing results in multiple transcript variants encoding different isoforms.
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As the strength of the muscle contraction is increased, more and more muscle fibers produce action potentials. When the muscle is fully contracted, there should appear a disorderly group of action potentials of varying rates and amplitudes (a complete recruitment and interference pattern).
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The extraocular muscles are the six muscles that control movement of the eye and one muscle that controls eyelid elevation (levator palpebrae). The actions of the six muscles responsible for eye movement depend on the position of the eye at the time of muscle contraction.
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Gamma motor neurons, unlike alpha motor neurons, are not directly involved in muscle contraction. The nerves associated with these neurons do not send signals that directly adjust the shortening or lengthening of muscle fibers. However, these nerves are important in keeping muscle spindles taut.
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If the enzyme is inhibited, acetylcholine accumulates and nerve impulses cannot be stopped, causing prolonged muscle contraction. Paralysis occurs and death may result since the respiratory muscles are affected. DFP also inhibits some proteases. It is a useful additive for protein or cell isolation procedure.
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1992 May. 55(5):369-71Lepore FE, Duvoisin RC. Apraxia of eyelid opening: an involuntary levator inhibition. Neurology. 1985 Mar. 35(3):423-7 have shown that ALO may involve either involuntary levator palpebrae superioris muscle inhibition, persistent pretarsal orbicularis oculi muscle contraction, or both.
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The IT arm is anchored to tropomyosin via adjacent segments of cTnT, so it is believed to move as a unit along with tropomyosin throughout the cardiac cycle. In the low calcium environment present during diastole (~100 nM), tropomyosin is anchored into the "blocked" position along the actin thin filament through the binding of the troponin I inhibitory (cTnI128-147) and C-terminal (cTnI160-209) regions. This prevents actin-myosin cross-bridging and effectively shuts off muscle contraction. As the cytoplasmic Ca2+ concentration rises to ~1 μM during systole, Ca2+ binding to the regulatory domain of cardiac troponin C (cNTnC) is the key event that leads to muscle contraction.
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Muscle spindles are innervated by both sensory neurons and motor neurons in order to provide proprioception and make the appropriate movements via firing of motor neurons. There are three types of lower motor neurons involved in muscle contraction: alpha motor neurons, gamma motor neurons, and beta motor neurons. Alpha motor neurons, the most abundant type, are used in the actual force for muscle contraction and therefore innervate extrafusal muscle fibers (muscle fibers outside of the muscle spindle). Gamma motor neurons, on the other hand, innervate only intrafusal muscle fibers (within the muscle spindle), whereas beta motor neurons, which are present in very low amounts, innervate both intrafusal and extrafusal muscle cells.
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The function of TnI is to control striated muscle contraction and relaxation. Troponin I interacts with all major regulatory proteins in the sarcomeric thin filaments of cardiac and skeletal muscles: troponin C, troponin T, tropomyosin and actin. When cytosolic Ca2+ is low, TnI binds the thin filament to block the myosin binding sites on actin. The rise of cytosolic Ca2+ results in binding to the N-terminal domain of troponin C and induces conformational changes in troponin C and the troponin complex, which releases the inhibition of myosin-actin interaction and activates myosin ATPase and cross bridge cycling to generate myosin power strokes and muscle contraction.
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Alpha motor neurons target extrafusal muscle fibers. The motor nerves associated with these neurons innervate extrafusal skeletal muscle fibers and are responsible for muscle contraction. These nerve fibers have the largest diameter of the motor neurons and require the highest conduction velocity of the three types.
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Because myosin II is essential for muscle contraction, defects in muscular myosin predictably cause myopathies. Myosin is necessary in the process of hearing because of its role in the growth of stereocilia so defects in myosin protein structure can lead to Usher syndrome and non-syndromic deafness.
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The discovery of phosphocreatine was reported in 1927. In the 1960s, creatine kinase (CK) was shown to phosphorylate ADP using phosphocreatine (PCr) to generate ATP. It follows that ATP, not PCr is directly consumed in muscle contraction. CK uses creatine to "buffer" the ATP/ADP ratio.
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In between two terminal cisternae is a tubular infolding called a transverse tubule (T tubule). T tubules are the pathways for action potentials to signal the sarcoplasmic reticulum to release calcium, causing a muscle contraction. Together, two terminal cisternae and a transverse tubule form a triad.
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Each of these treatment modalities have primary concerns that they address. For example, botulinum injections paralyze facial muscles. This prevents muscle contraction and subsequent wrinkle formation. Injectable fillers are often used in the nasolabial fold to increase volume and minimize the appearance of sagging or wrinkling.
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SBK3 is statistically predicted to be involved in sarcomere organization, regulation of muscle relaxation, cardiac myofibril assembly, and regulation of cardiac muscle contraction by regulation of the release of sequestered calcium ions. However, the function of SBK3 has yet to be well understood by the scientific community.
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The function of this gene is currently unknown. There is evidence that CCDC78 plays a role in skeletal muscle contraction. This is supported by structural similarities to other muscle proteins and by localization assays. CCDC78's predicted structure was similar to that of tropomyosin (see below).
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Lightbulb sign indicative of posterior shoulder dislocation shown on the left. On the right, the same shoulder after reduction. Posterior dislocations are uncommon, and are typically due to the muscle contraction from electric shock or seizure. They may be caused by strength imbalance of the rotator cuff muscles.
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Serum magnesium is necessary for full secretion of PTH. Without the parathyroid glands, there is no trigger to release calcium into the blood. Another consequence of hypoparathyroidism is the lack of calcium in the blood to trigger muscle contraction. Without calcium present, muscles innervation is unable to take place.
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Some furoquinoline alkaloids have been found to have in vitro pharmacological properties such as antimicrobial, antiviral, mutagenic and cytotoxic activities. They also show antiplatelet aggregation, inhibition of various enzymes, antibacterial, and antifungal activity. Dictamnine has the property of causing smooth muscle contraction. Skimmianine, extracted from Esenbeckia leiocarpa Engl.
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Thus, when O2 partial pressure is low, hemoglobin-bound O2 is more readily transferred to myoglobin. Myoglobin, found in high concentrations in muscle tissue, can then transfer the oxygen to muscle tissue muscle fibers, where it will be used in the generation of energy to fuel muscle contraction.
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In hystricomorphs the medial masseter is enlarged and originates on the side of the rostrum (in extreme cases as far forward as the premaxilla), where it then passes through a greatly enlarged infraorbital foramen to insert on the mandible. This gives an almost horizontal resultant to the muscle contraction.
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Sliding filament theory: A sarcomere in relaxed (above) and contracted (below) positions The sliding filament theory explains the mechanism of muscle contraction based on muscle proteins that slide past each other to generate movement. According to the sliding filament theory, the myosin (thick) filaments of muscle fibers slide past the actin (thin) filaments during muscle contraction, while the two groups of filaments remain at relatively constant length. It was independently introduced in 1954 by two research teams, one consisting of Andrew F. Huxley and Rolf Niedergerke from the University of Cambridge, and the other consisting of Hugh Huxley and Jean Hanson from the Massachusetts Institute of Technology. It was originally conceived by Hugh Huxley in 1953.
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The laptop allows for the crew-member to control and monitor MARES operations, including set-up procedures, experiment steps, data display, data processing, results summaries, and programming of a desired experiment/exercise scenario. The MARES software is designed to clearly guide the subject/operator through all steps with tailored instructions, including text, graphics, and interaction prompts. It is fully programmable, allowing the user to set up complex movements by selecting from a pre-defined set of basic control algorithms for the motor, known as basic motion units (BMUs), and building up a sequence of exercise steps or routines. There is a BMU for each mode of muscle contraction, including: isometric (muscle contraction at a fixed length, i.e.
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In effect, the thick filament moves or slides along the thin filament, resulting in muscle contraction. This process is known as the sliding filament model. The binding of the myosin heads to the muscle actin is a highly regulated process. The thin filament is made of actin, tropomyosin, and troponin.
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The regulation of chloride flow within muscle cells plays a role in controlling muscle contraction and relaxation. The anoctamin-5 protein is also found in other cells including heart (cardiac) muscle cells and bone cells. The anoctamin-5 protein may be important for the development of muscle and bone before birth.
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This cycle occurs in Skeletal muscle myocyte's cytosolic compartment. This reaction helps to dispose AMP produced after following reaction. :ATP → ADP + Pi (Utilisation of ATP for Muscle contraction) 2 ADP → ATP + AMP (Catalysed by Adenylyl kinase/Myokinase) Purine nucleotide cycle occurs during strenuous exercise, fasting or starvation when ATP reservoirs run low.
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In Florence Steno focused on the muscular system and the nature of muscle contraction. He became a member of Accademia del Cimento and had long discussions with Francesco Redi. Like Vincenzo Viviani, Steno proposed a geometrical model of muscles to show that a contracting muscle changes its shape but not its volume.
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Croton nepetifolius (Croton nepetaefolius) is an aromatic species of flowering plant in the spurge family, Euphorbiaceae, that is native to northeastern Brazil. It is commonly known as marmeleiro vermelh (red quince). The plant has been used in folk medicine as a sedative, an orexigenic (appetite enhancer) and an antispasmodic (muscle contraction suppressor).
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Electromyography is the measurement and analysis of the electrical activity in skeletal muscles. This technique is useful for diagnosing the health of the muscle tissue and the nerves that control them.Mayo Clinic Staff, "Electromyography (EMG)". Retrieved 27 July 2012 EMG measures action potentials, called Motor Unit Action Potentials (MUAPs), created during muscle contraction.
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A fasciculation, or muscle twitch, is a spontaneous, involuntary muscle contraction and relaxation, involving fine muscle fibers. They are common, with as much as 70% of people experiencing them. They can be benign, or associated with more serious conditions. When no cause or pathology is identified, they are diagnosed as benign fasciculation syndrome.
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Pumiliotoxin is a toxin found in poison dart frogs (genus Dendrobates and Phyllobates). It affects the calcium channels, interfering with muscle contraction in the heart and skeletal muscle. PTX 251D has several effects. It rapidly induces convulsions and death to mice and insects (LD50 being, respectively, 10 mg/kg and 150 ng/larvae).
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The higher the recruitment the stronger the muscle contraction will be. Motor units are generally recruited in order of smallest to largest (smallest motor neurons to largest motor neurons, and thus slow to fast twitch) as contraction increases. This is known as Henneman's size principle.Henneman, E., Somjen, G. & Carpenter, D. O. (1965).
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Mutations in this protein cause congenital myotonia. CLCN1 is critical for the normal function of skeletal muscle cells. For the body to move normally, skeletal muscles must tense (contract) and relax in a coordinated way. Muscle contraction and relaxation are controlled by the flow of ions into and out of muscle cells.
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ACTC1 encodes cardiac muscle alpha actin. This isoform differs from the alpha actin that is expressed in skeletal muscle, ACTA1. Alpha cardiac actin is the major protein of the thin filament in cardiac sarcomeres, which are responsible for muscle contraction and generation of force to support the pump function of the heart.
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In muscle cells, they regulate muscle contraction by controlling the binding of myosin heads to the actin filament. Mutations in this gene result in autosomal dominant nemaline myopathy, and oncogenes formed by chromosomal translocations involving this locus are associated with cancer. Multiple transcript variants encoding different isoforms have been found for this gene.
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Muscle fibers are in turn composed of myofibrils. The myofibrils are composed of actin and myosin filaments, repeated in units called sarcomeres, which are the basic functional units of the muscle fiber. The sarcomere is responsible for the striated appearance of skeletal muscle and forms the basic machinery necessary for muscle contraction.
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For the action potential to reach the myofibrils, the action potential travels along the transverse tubules (T-tubules) that connects the sarcolemma and center of the fibre. Later, action potential reaches the sarcoplasmic reticulum which stores the Ca2+ needed for muscle contraction and causes Ca2+ to be released from the sarcoplasmic reticulum.
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However, their role is important in keeping muscle spindles taut, thereby allowing the continued firing of alpha neurons, leading to muscle contraction. These neurons also play a role in adjusting the sensitivity of muscle spindles.Burke, D., Skuse, N.F., Stuart, D.G. (1979) "The regularity of muscle spindle discharge in man." Journal of Physiology.
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This means that the calcium used for muscle contraction, is pumped out of the cell, resulting in muscle relaxation. In the sinoatrial node, this phase is also due to the closure of the L-type calcium channels, preventing inward flux of Ca2+ and the opening of the rapid delayed rectifier potassium channels (IKr).
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The word myoclonus uses combining forms of myo- and clonus, indicating muscle contraction dysfunction. It is pronounced or . The prevalence of the variants shows division between American English and British English. The variant stressing the -oc- syllable is the only pronunciation given in a half dozen major American dictionaries (medical and general).
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To make progress on understanding the function of muscle, new ways of observing how the network of filaments behave during contraction were needed. Prior to the war, he had been working on a preliminary design for interference microscopy, which at the time he believed to be original, though it turned out to have been tried 50 years before and abandoned. He, however, was able to make interference microscopy work and to apply it to the problem of muscle contraction with great effect. He was able to view muscle contraction with greater precision than conventional microscopes, and to distinguish types of fiber more easily. By 1953, with the assistance of Rolf Niedergerke, he began to find the features of muscle movement.
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Grade 5: full active range of motion & Normal muscle resistance Grade 4: full active range of motion & Reduced muscle resistance Grade 3: full active range of motion & No muscle resistance Grade 2: Reduced active range of motion & No muscle resistance Grade 1: No active range of motion & Palpable muscle contraction only Grade 0: No active range of motion & No palpable muscle contraction Manual muscle testing, however, has a number of limitations. One limitation is that the MRC scale is an ordinal scale with disproportional distances between grades. Another limitation of the MRC scale is that the scoring depends on the judgment of the examiner. Finally, with the 6-point ordinal MRC scale, it is difficult to identify relatively small but clinically relevant changes in muscle strength.
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The RYR2 protein functions as the major component of a calcium channel located in the sarcoplasmic reticulum that supplies ions to the cardiac muscle during systole. To enable cardiac muscle contraction, calcium influx through voltage-gated L-type calcium channels in the plasma membrane allows calcium ions to bind to RYR2 located on the sarcoplasmic reticulum. This binding causes the release of calcium through RYR2 from the sarcoplasmic reticulum into the cytosol, where it binds to the C domain of troponin, which shifts tropomyosin and allows the myosin ATPase to bind to actin, enabling cardiac muscle contraction. RYR2 channels are associated with many cellular functions, including mitochondrial metabolism, gene expression and cell survival, in addition to their role in cardiomyocyte contraction.
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It also mediates respiratory sinus arrhythmia. When a change of blood pH is detected by central chemoreceptors or by peripheral chemoreceptors in aortic bodies and in carotid bodies, or a change of blood pressure is detected by baroreceptors in the aortic sinuses or carotid sinuses, the cardiovascular centre affects changes to the heart rate by sending a nerve impulse to the cardiac pacemaker (or SA node) via sympathetic fibres (to cause faster and stronger cardiac muscle contraction) and the vagus nerve (to cause slower and less strong cardiac muscle contraction). The cardiovascular centre also increases the stroke volume of the heart (that is, the amount of blood it pumps). These two changes help to regulate the cardiac output, so that a sufficient amount of blood reaches tissue.
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Many experience contractures, which are defined as joints that cannot be stretched or moved. Clonus is another symptom that is characterized by alternating, rapid muscle contraction and relaxation. This presents itself as tremors and scissoring of the limbs. Distonia, or lasting muscle contractions and tightness, is also often experienced by those affected by spastic quadriplegia.
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Thus, the regulatory mechanisms of PhK activity vary somewhat depending on cell type. In general, the enzyme is regulated allosterically and by reversible phosphorylation. Hormones, nerve impulses and muscle contraction stimulate the release of calcium ions. These act as an allosteric activator, binding to the δ subunits of phosphorylase kinase, and partly activating enzyme activity.
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TCP muscles should be under a load to keep the muscle extended. The electrical energy transforms to thermal energy due to electrical resistance, which also known as Joule heating, Ohmic heating, and resistive heating. As the temperature of the TCP muscle increases by Joule heating, the polymer contracts and it causes the muscle contraction.
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The C3a, C4a and C5a components are referred to as anaphylatoxins: they cause smooth muscle contraction, vasodilation, histamine release from mast cells, and enhanced vascular permeability. They also mediate chemotaxis, inflammation, and generation of cytotoxic oxygen radicals. The proteins are highly hydrophilic, with a mainly alpha-helical structure held together by 3 disulfide bridges.
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Pumiliotoxins are much weaker than batrachotoxins, ranging between 100 and 1000 times less poisonous. There are three different types of this toxin: A, B and C, of which toxins A and B are more toxic than C. Pumiliotoxins interfere with muscle contraction by affecting calcium channels, causing partial paralysis, difficulty moving, hyperactivity, or death.
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Doi's sign is a clinical sign in which absent deep tendon reflexes can be elicited after a short period of maximal muscle contraction. This occurs in patients with Eaton-Lambert syndrome, but is not seen in patients with neuropathy.Jane M. Orient, Joseph D. Sapira. Sapira's art & science of bedside diagnosis, 3rd edition, page 610.
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Tensiomyography measurement A tensiomyography measurement consists of four steps: # A special sensor is placed on the muscle to be measured. The sensor contains a tip designed to register muscle's contraction. # Muscle contraction is induced with twitch type (one millisecond) of surface electrical stimulus. # Contraction of muscle under isometric conditions results in a muscle belly displacement.
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Acetylcholine is synthesized in the cytoplasm of the neuron from choline and acetyl-CoA. Choline acyltransferase is the enzyme that synthesizes acetylcholine and is often used as a marker in research relating to acetylcholine production. Neurons that utilize acetylcholine are called cholinergic neurons and they are very important in muscle contraction, memory, and learning.
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Hyoscine butylbromide reduces the stimulation of smooth muscle contraction and the production of respiratory secretions. These are normally stimulated by the parasympathetic nervous system, via the neurotransmitter acetylcholine. As an antimuscarinic, hyoscine butylbromide binds to muscarinic acetylcholine receptors, blocking their effect. It is a quaternary ammonium compound and a semisynthetic derivative of hyoscine hydrobromide (scopolamine).
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VX is an acetylcholinesterase inhibitor. It works by blocking the function of acetylcholinesterase (AChE). Normally, when a motor neuron is stimulated, it releases the neurotransmitter acetylcholine (ACh) into the space between the neuron and an adjacent muscle cell, the synaptic cleft. When acetylcholine is taken up by the muscle cell, it stimulates muscle contraction.
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MLC-2v plays an important role in cross-bridge cycling kinetics and cardiac muscle contraction. MLC-2v phosphorylation at Ser14 and Ser15 increases myosin lever arm stiffness and promotes myosin head diffusion, which altogether slow down myosin kinetics and prolong the duty cycle as a means to fine-tune myofilament Ca2+ sensitivity to force.
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A gamma motor neuron (γ motor neuron), also called gamma motoneuron, is a type of lower motor neuron that takes part in the process of muscle contraction, and represents about 30% of ( Aγ ) fibers going to the muscle.Hunt, C. (1951) "The reflex activity of mammalian small-nerve fibres." Journal of Physiology. 115(4): 456–469.
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Schedl Lab Protocol for gonad dissections In a C. elegans behavioral assay, analyzing the time course of paralysis provides information about the neuromuscular junction. Levamisole acts as an acetylcholine receptor agonist, which leads to muscle contraction. Continuing activation leads to paralysis. The time course of paralysis provides information about the acetylcholine receptors on the muscle.
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The regulation of tissue perfusion occurs in microcirculation. There, arterioles control the flow of blood to the capillaries. Arterioles contract and relax, varying their diameter and vascular tone, as the vascular smooth muscle responds to diverse stimuli. Distension of the vessels due to increased blood pressure is a fundamental stimulus for muscle contraction in arteriolar walls.
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Hirnpotentialänderungen bei Willkürbewegungen und passiven Bewegungen des Menschen: Bereitschaftspotential und reafferente Potentiale. Pflügers Arch 284: 1–17 "Citation Classic" Vaughan, Costa, and Ritter (1968) noted that the readiness potential was larger contralateral to the side of the body where the muscle contraction occurred.Vaughan, H. G., Costa, L. D., Ritter, W., 1967. Topography of the Human Motor Potential.
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Angiotensin II binds to AT1 receptors, increases contraction of vascular smooth muscle, and stimulates aldosterone resulting in sodium reabsorption and increase in blood volume. Smooth muscle contraction occurs due to increased calcium influx through the L-type calcium channels in smooth muscle cells during the plateau component, increasing the intracellular calcium and membrane potential which sustain depolarization and contraction.
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There are multiple mechanisms causing the increased smooth muscle contraction involved in coronary vasospasm, including increased Rho-kinase activity. Increased levels of Rho-kinase inhibit myosin phosphatase activity, leading to increased calcium sensitivity and hypercontraction. Rho-kinase also decreases nitric oxide synthase activity, which reduces nitric oxide concentrations. Lower levels of nitric oxide are present in spastic coronary arteries.
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The conserved domain of this protein possesses the binding activities to Ca++-calmodulin, actin, tropomyosin, myosin, and phospholipids. This protein is a potent inhibitor of the actin-tropomyosin activated myosin MgATPase, and serves as a mediating factor for Ca++-dependent inhibition of smooth muscle contraction. Alternative splicing of this gene results in multiple transcript variants encoding distinct isoforms.
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Alpha motor neurons innervate extrafusal muscle fibers that generate force at neuromuscular junctions at the start of muscle contraction. They have large cell bodies and receive proprioceptive input. They have been shown to reduce in population, but not in size with age. Damage to these cell bodies can lead to severe muscle weakness and loss of reflexes.
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Glycogen branching enzyme is responsible for normal branching of the glycogen molecule. Glycogen is a molecular polymer of glucose used to store energy. It is important for providing energy for skeletal and cardiac muscle contraction, and for maintaining glucose hemostasis in the blood. Molecules of glucose are linked into linear chains by α-1,4-glycosidic bonds.
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Vitamin deficiencies can lead to wide-ranging clinical abnormalities that reflect the diversity of their metabolic roles. Twelve minerals are known to be essential nutrients for cats. Calcium and phosphorus are crucial to strong bones and teeth. Cats need other minerals, such as magnesium, potassium, and sodium, for nerve impulse transmission, muscle contraction, and cell signaling.
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71-76 Kalckar was fortunate to be working at an important period in biochemistry's evolution.Singleton, R. Jr. 2007b The biochemical community was in the process of demonstrating the chemical reactions involved in breakdown of foodstuffs essential for growth. At the same time, physiologists were demonstrating the involvement of some of these reactions various physiological processes, e.g. muscle contraction.
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Fasudil (HA-1077) is a selective RhoA/Rho kinase (ROCK) inhibitor. ROCK is an enzyme that plays an important role in mediating vasoconstriction and vascular remodeling in the pathogenesis of pulmonary hypertension. ROCK induces vasoconstriction by phosphorylating the myosin- binding subunit of myosin light chain (MLC) phosphatase, thus decreasing MLC phosphatase activity and enhancing vascular smooth muscle contraction.
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ROCK1 phosphorylation sites are at RXXS/T or RXS/T. More than 15 ROCK1 substrates have been identified and activation from these substrates most often leads to actin filament formation and cytoskeleton rearrangements. MYPT-1 is involved in a pathway for smooth muscle contraction. When ROCK1 is activated by binding of GTPase RhoA it produces multiple signaling cascades.
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The area composita is a special heart muscle specific mixed type adhering junction connecting single cardiomyocytes. They are responsible for the force transmission during muscle contraction and are believed to be the main component of the mammalian cardiac intercalated discs (see Franke et al. 2006; Pieperhoff and Franke, 2007; Pieperhoff and Franke, 2008; see also Goossens et al., 2007).
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While the muscle fiber does not have smooth endoplasmic cisternae, it contains a sarcoplasmic reticulum. The sarcoplasmic reticulum surrounds the myofibrils and holds a reserve of the calcium ions needed to cause a muscle contraction. Periodically, it has dilated end sacs known as terminal cisternae. These cross the muscle fiber from one side to the other.
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Choline is needed to produce acetylcholine. This is a neurotransmitter which plays a necessary role in muscle contraction, memory and neural development, for example. Nonetheless, there is little acetylcholine in the human body relative to other forms of choline. Neurons also store choline in the form of phospholipids to their cell membranes for the production of acetylcholine.
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Margatoxin blocks potassium channels Kv1.1 Kv1.2 en Kv1.3. Kv1.2 channel regulates neurotransmitter release associated with heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, immunological response and cell volume. Kv1.3 channels are expressed in T and B lymphocytes.KCNA3 Margatoxin irreversibly inhibits the proliferation of human T-cells in a concentration of 20 μM.
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Pacinian corpuscles sense changes in pressure and vibration to monitor the rate of acceleration of movement. They will initiate a sudden relaxatory response if movement happens too fast. Deep fascia can also relax slowly as some mechanoreceptors respond to changes over longer timescales. Unlike the Golgi tendon organs, Golgi receptors report joint position independent of muscle contraction.
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In mammals, when a muscle contracts, a series of reactions occur. Muscle contraction is stimulated by the motor neuron sending a message to the muscles from the somatic nervous system. Depolarization of the motor neuron results in neurotransmitters being released from the nerve terminal. The space between the nerve terminal and the muscle cell is called the neuromuscular junction.
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PV is known to be involved in relaxation of fast-twitch muscle fibers. This function is associated with PV role in calcium sequestration. During muscle contraction, the action potential stimulate voltage-sensitive proteins in T-tubules membrane. These proteins stimulate the opening of Ca2+ channels in the sarcoplasmic reticulum, leading to release of Ca2+ in the sarcoplasm.
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Most myoclonus is caused by a disturbance of the central nervous system. Some are from peripheral nervous system injury. Studies suggest several locations in the brain are involved in myoclonus. One is in the brainstem, close to structures that are responsible for the startle response, an automatic reaction to an unexpected stimulus involving rapid muscle contraction.
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The effect of these different toxins on Carcinus meanas is visually indistinguishable, namely cramp followed by paralysis and death. However, their mode of action differs. Toxin IV of Condylactis aurantiaca causes a repetitive firing of the excitatory axon for several minutes resulting in muscle contraction without causing a detectable change in the amplitude of the excitatory junction potentials (EJPS).
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Myosin essential light chain (ELC), ventricular/cardiac isoform is a protein that in humans is encoded by the MYL3 gene. This cardiac ventricular/slow skeletal ELC isoform is distinct from that expressed in fast skeletal muscle (MYL1) and cardiac atrial muscle (MYL4). Ventricular ELC is part of the myosin molecule and is important in modulating cardiac muscle contraction.
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The patellar tendon reflex is an example of the stretch reflex. The stretch reflex (myotatic reflex) is a muscle contraction in response to stretching within the muscle. The reflex functions to maintain the muscle at a constant length. The term deep tendon reflex is often wrongfully used by many health workers and students to refer to this reflex.
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Such wing movements, hovering, and other aerodynamic feats are only possible because of the flies' asynchronous muscle systems. Their muscle systems are asynchronous because there is not a direct correlation between each muscle contraction and a wing flap. Instead, the muscle contractions cause changes in the shape of the thorax of the midges, which facilitates the extremely fast movements of their wings.
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To compound the problem, impaired sarcoplasmic reticulum calcium release and reduced mitochondrial reuptake limits peak cytosolic levels of the important signaling ion during muscle contraction. Decreased intra- mitochondrial calcium concentration increases dehydrogenase activation and ATP synthesis. So in addition to lower ATP synthesis due to fatty acid oxidation, ATP synthesis is impaired by poor calcium signaling as well, causing cardiac problems for diabetics.
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Both these structures are thick muscles, and are covered with chitinous cuticle to make a protective surface. It is used for grasping substratum, catching prey and for locomotory accessory. When the sucker attaches itself on an object, the infundibulum maily provides adhesion while the central acetabulum is quite free. The sequential muscle contraction the infundibulum and acetabulum causes attachment and detachment.
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For contraction, the myosin molecule is usually bound to two separate filaments and both ends simultaneously "walk" toward their filament's plus end, sliding the actin filaments closer to each other. This results in the shortening, or contraction, of the actin bundle (but not the filament). This mechanism is responsible for muscle contraction and cytokinesis, the division of one cell into two.
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A spasm is a sudden involuntary contraction of a muscle, a group of muscles, or a hollow organ such as the heart. A spasmodic muscle contraction may be caused by many medical conditions, including dystonia. Most commonly, it is a muscle cramp which is accompanied by a sudden burst of pain. A muscle cramp is usually harmless and ceases after a few minutes.
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Pars triangularis has been shown to have a role in cognitive control of memory. There are more ways than one to remember something. When a person remembers, (s)he retrieves information from storage in a memory center of the brain. This information may be the muscle contraction sequence for shoe-tying, the face of a loved one, or anything in between.
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Suxamethonium has a longer duration of effect than acetylcholine, and is not hydrolyzed by acetylcholinesterase. By maintaining the membrane potential above threshold, it does not allow the muscle cell to repolarize. When acetylcholine binds to an already depolarized receptor, it cannot cause further depolarization. Calcium is removed from the muscle cell cytoplasm independent of repolarization (depolarization signaling and muscle contraction are independent processes).
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The bullet strikes and severs the spinal column causing flaccid paralysis and eliminates the possibility of involuntary muscle spasms. The advantage of flaccid paralysis is the subject is rendered incapacitated instantaneously preventing involuntary muscle contraction that may pull the trigger or cause other movements that may injure or kill the hostage. This is a difficult shot even by the best marksmen.
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A concept known as the size principle, allows for a gradation of muscle force during weak contraction to occur in small steps, which then become progressively larger when greater amounts of force are required. Finally, if the frequency of muscle action potentials increases such that the muscle contraction reaches its peak force and plateaus at this level, then the contraction is a tetanus.
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Neuromedin U (or NmU) is a neuropeptide found in the brain of humans and other mammals, which has a number of diverse functions including contraction of smooth muscle, regulation of blood pressure, pain perception, appetite, bone growth, and hormone release. It was first isolated from the spinal cord in 1985, and named after its ability to cause smooth muscle contraction in the uterus.
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Lipase member H is an enzyme that in humans is encoded by the LIPH gene. This gene encodes a membrane-bound member of the mammalian triglyceride lipase family. It catalyzes the production of 2-acyl lysophosphatidic acid (LPA), which is a lipid mediator with diverse biological properties that include platelet aggregation, smooth muscle contraction, and stimulation of cell proliferation and motility.
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The Department of Structural Biochemistry focuses on structural and functional analyses of biologically and medically relevant membrane proteins and macromolecular complexes. Special attention is given to the investigation into the molecular mechanisms of muscle contraction and the infection with bacterial toxins. Furthermore, membrane proteins that play an important role in the synthesis, transport, and homeostasis of cholesterol in the body are examined.
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A tremor is an involuntary, somewhat rhythmic, muscle contraction and relaxation involving to-and-fro movements of one or more body parts. It is the most common of all involuntary movements and can affect the hands, arms, eyes, face, head, vocal cords, trunk, and legs. Most tremors occur in the hands. In some people, tremor is a symptom of another neurological disorder.
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Injection of 50 ng LqhIT2 of per 100 mg body weight is sufficient to paralyze blowfly larvae. This injection causes a short transient muscle contraction a few seconds after application. However, the threshold to increase membrane potential then decreases until the muscle is not electrically excitable anymore. The contraction is followed by flaccid paralysis, which lasts up to five minutes after injection.
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Myokymia is an involuntary, spontaneous, localized quivering of a few muscles, or bundles within a muscle, but which are insufficient to move a joint. One type is superior oblique myokymia. Myokymia is commonly used to describe an involuntary eyelid muscle contraction, typically involving the lower eyelid or less often the upper eyelid. It occurs in normal individuals and typically starts and disappears spontaneously.
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Thyrotoxic myopathy is usually diagnosed by a neurologist who has extensive experience diagnosing neuromuscular disorders. There are many types of neuromuscular disorders that present similar physical symptoms. Extensive clinical tests are performed first to determine if there is a neuromuscular disorder and then to determine which disorder it is. Electromyography is used to diagnose myopathies by comparing muscle contraction responses to electrical stimulus.
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A flexor is a muscle that flexes a joint. In anatomy, flexion (from the Latin verb flectere, to bend) is a joint movement that decreases the angle between the bones that converge at the joint. For example, your elbow joint flexes when you bring your hand closer to the shoulder. Flexion is typically instigated by muscle contraction of a flexor.
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The calcium ions trigger powerful muscle contraction aided by ATP molecules. To prevent cold shortening, a process known as electrical stimulation is carried out, especially in beef carcasses, immediately after slaughter and skinning. In this process, the carcass is stimulated with alternating current, causing it to contract and relax, which depletes the ATP reserve from the carcass and prevents cold shortening.
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Schlesinger 1946 Curare notably functions to inhibit nicotinic acetylcholine receptors at the neuromuscular junction. Normally, these receptor channels allow sodium ions into muscle cells to initiate an action potential that leads to muscle contraction. By blocking the receptors, the neurotoxin is capable of significantly reducing neuromuscular junction signaling, an effect which has resulted in its use by anesthesiologists to produce muscular relaxation.
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Though not universally used, ‘metabolic fatigue’ is a common term for the reduction in contractile force due to the direct or indirect effects of two main factors: # Shortage of fuel (substrates) within the muscle fiber # Accumulation of substances (metabolites) within the muscle fiber, which interfere either with the release of calcium (Ca2+) or with the ability of calcium to stimulate muscle contraction.
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Spasticity () is a feature of altered skeletal muscle performance with a combination of paralysis, increased tendon reflex activity, and hypertonia. It is also colloquially referred to as an unusual "tightness", stiffness, or "pull" of muscles. Clinically, spasticity results from the loss of inhibition of motor neurons, causing excessive velocity-dependent muscle contraction. This ultimately leads to hyperreflexia, an exaggerated deep tendon reflex.
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Symptoms start with slowly developing dysarthria (difficulty speaking) and cerebellar truncal ataxia (unsteadiness) and then the progressive dementia becomes more evident. Loss of memory can be the first symptom of GSS. Extrapyramidal and pyramidal symptoms and signs may occur and the disease may mimic spinocerebellar ataxias in the beginning stages. Myoclonus (spasmodic muscle contraction) is less frequently seen than in Creutzfeldt–Jakob disease.
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Enzymes serve a wide variety of functions inside living organisms. They are indispensable for signal transduction and cell regulation, often via kinases and phosphatases. They also generate movement, with myosin hydrolyzing ATP to generate muscle contraction, and also transport cargo around the cell as part of the cytoskeleton. Other ATPases in the cell membrane are ion pumps involved in active transport.
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Distal stabilisation of muscles is recommended. This allows effective muscle contraction which reduces atrophy, allows functional use of the stump and maintains soft tissue coverage of the remnant bone. The preferred stabilisation technique is myodesis where the muscle is attached to the bone or its periosteum. In joint disarticulation amputations tenodesis may be used where the muscle tendon is attached to the bone.
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ROCK1 has a diverse range of functions in the body. It is a key regulator of actin-myosin contraction, stability, and cell polarity. These contribute to many progresses such as regulation of morphology, gene transcription, proliferation, differentiation, apoptosis and oncogenic transformation. Other functions involve smooth muscle contraction, actin cytoskeleton organization, stress fiber and focal adhesion formation, neurite retraction, cell adhesion and motility.
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Muscarinic M3 receptors are expressed in regions of the brain that regulate insulin homeostasis, such as the hypothalamus and dorsal vagal complex of the brainstem. These receptors are highly expressed on pancreatic beta cells and are critical regulators of glucose homoestasis by modulating insulin secretion. In general, they cause smooth muscle contraction and increased glandular secretions. They are unresponsive to PTX and CTX.
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Current medical science does not precisely describe the causes of dystonia. Misfiring of neurons in the sensorimotor cortex, a thin layer of neural tissue that covers the brain, is thought to cause contractions. This misfiring may result from impaired inhibitory mechanisms during muscle contraction. When the brain tells a given muscle to contract, it simultaneously silences muscles that would oppose the intended movement.
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Research on skeletal muscle properties uses many techniques. Electrical muscle stimulation is used to determine force and contraction speed at different stimulation frequencies, which are related to fiber-type composition and mix within an individual muscle group. In vitro muscle testing is used for more complete characterization of muscle properties. The electrical activity associated with muscle contraction are measured via electromyography (EMG).
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Associated with a breakdown in gut barrier function, necrotizing enterocolitis may be mediated by HB-EGF effects on intestinal mucosa. HB-EGF expressed during skeletal muscle contraction facilitates peripheral glucose removal, glucose tolerance and uptake. The upregulation of HB-EGF with exercise may explain the molecular basis for the decrease in metabolic disorders such as obesity and type 2 diabetes with regular exercise.
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Troponin C, also known as TN-C or TnC, is a protein that resides in the troponin complex on actin thin filaments of striated muscle (cardiac, fast- twitch skeletal, or slow-twitch skeletal) and is responsible for binding calcium to activate muscle contraction. Troponin C is encoded by the TNNC1 gene in humans for both cardiac and slow skeletal muscle.
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The action potentials that cause this also require ion changes: Na influxes during the depolarization phase and K effluxes for the repolarization phase. Cl− ions also diffuse into the sarcoplasm to aid the repolarization phase. During intense muscle contraction, the ion pumps that maintain homeostasis of these ions are inactivated and this (with other ion related disruption) causes ionic disturbances.
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A person with ALO may complain of occasionally being unable to open the eye at will, typically after prolonged closure. Oftentimes, ALO only persists momentarily and the ptosis resolves upon manually lifting the eyelid. During attempted lid opening, there may be forceful frontalis muscle contraction, backward thrusting of the head, or opening of the mouth noted.Ugarte M, Teimory M. Apraxia of lid opening.
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A tremor is an involuntary, somewhat rhythmic, muscle contraction and relaxation involving oscillations or twitching movements of one or more body parts. It is the most common of all involuntary movements and can affect the hands, arms, eyes, face, head, vocal folds, trunk, and legs. Most tremors occur in the hands. In some people, a tremor is a symptom of another neurological disorder.
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This dynamic is called resting pressure and is considered safe and comfortable for long-term treatment. Conversely, the stability of the bandage creates a very high resistance to stretch when pressure is applied through internal muscle contraction and joint movement. This force is called working pressure. Long stretch compression bandages have long stretch properties, meaning their high compressive power can be easily adjusted.
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The Greek word blepharon means "eyelid". Spasm means "uncontrolled muscle contraction". The term blepharospasm ['blef-a-ro-spaz-m] can be applied to any abnormal blinking or eyelid tic or twitch resulting from any cause, ranging from dry eyes to Tourette's syndrome to tardive dyskinesia. The blepharospasm referred to here is officially called benign essential blepharospasm (BEB) to distinguish it from the less serious secondary blinking disorders.
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Phonation is the production of a periodic sound wave by vibration of the vocal folds. Airflow from the lungs, as well as laryngeal muscle contraction, causes movement of the vocal folds. It is the properties of tension and elasticity that allow the vocal folds to be stretched, bunched, brought together and separated. During prephonation, the vocal folds move from the abducted to adducted position.
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Acetylcholine Nicotine Nicotinic acetylcholine receptors, or nAChRs, are receptor polypeptides that respond to the neurotransmitter acetylcholine. Nicotinic receptors also respond to drugs such as the agonist nicotine. They are found in the central and peripheral nervous system, muscle, and many other tissues of many organisms. At the neuromuscular junction they are the primary receptor in muscle for motor nerve-muscle communication that controls muscle contraction.
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Prokineticins are secreted proteins that can promote angiogenesis and induce strong gastrointestinal smooth muscle contraction. The protein encoded by this gene is an integral membrane protein and G protein-coupled receptor for prokineticins. The encoded protein is similar in sequence to GPR73, another G protein-coupled receptor for prokineticins. Mutations in the PROKR2 (also known as KAL3) gene have been implicated in hypogonadotropic hypogonadism and gynecomastia.
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Cerebral vasospasm is one of the complications caused by subarachnoid haemorrhage. It usually happens from the third day after the aneurysm event, and reaches its peak on 5th to 7th day. There are several mechanisms proposed for this complication. Blood products released from subarachnoid haemorrhage stimulates the tyrosine kinase pathway causing the release of calcium ions from intracellular storage, resulting in smooth muscle contraction of cerebral arteries.
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There are several different types of muscle energy techniques: #Postisometric relaxation (direct technique): Treat by engaging the restrictive barrier in all planes. # Reciprocal inhibition: Treat by contracting the antagonistic muscles, which causes the agonist muscle to relax through the reciprocal inhibition reflex arc. There are direct and indirect reciprocal inhibition techniques. # Joint mobilization using muscle force: Use muscle contraction to restore range of motion in a joint.
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Moon jelly (Aurelia aurita) with rhopalia visible in indentations of rim Rhopalia (singular: rhopalium) are small sensory structures of Scyphozoa (typical jellyfish) and Cubozoa (box jellies). In Aurelia they lie in marginal indententions around the bell and are flanked by rhopalial lappets. Specialized structures to sense light (ocelli) and perceive gravity (statoliths) are usually present. They also control the pace of swimming- muscle contraction.
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He worked using Huxley's own interference microscope. Within a year he helped to improve the technique and a research paper on the mechanism of muscle contraction was ready. At that moment almost the same observation was made by Hugh Huxley and Jean Hanson at the Massachusetts Institute of Technology. Authored in pairs their papers were simultaneously published in the 22 May 1954 issue of Nature.
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Myosin, a structural component of muscle, consists of two heavy chains and four light chains. The protein encoded by this gene is a myosin light chain that may regulate muscle contraction by modulating the ATPase activity of myosin heads. The encoded protein binds calcium and is activated by myosin light chain kinase. Two transcript variants encoding different isoforms have been found for this gene.
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The physical characteristics of the tremor and the history of the patient will contribute to the diagnosis of Holmes tremor. A doctor will determine if the tremor is present during rest or voluntary muscle contraction and the frequency of the tremor. A Holmes tremor is generally made worse upon standing and upon intentional movements. Also, a Holmes tremor is not as rhythmic as other tremors.
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Ions are also critical for nerves and muscles, as action potentials in these tissues are produced by the exchange of electrolytes between the extracellular fluid and the cytosol. Electrolytes enter and leave cells through proteins in the cell membrane called ion channels. For example, muscle contraction depends upon the movement of calcium, sodium and potassium through ion channels in the cell membrane and T-tubules.
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In some applications, the nerves are stimulated to generate localized muscle activity, i.e., the stimulation is aimed at generating direct muscle contraction. In other applications, stimulation is used to activate simple or complex reflexes. In other words, the afferent nerves are stimulated to evoke a reflex, which is typically expressed as a coordinated contraction of one or more muscles in response to the sensory nerve stimulation.
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The protein encoded by this gene is a glutathione-independent prostaglandin D synthase that catalyzes the conversion of prostaglandin H2 (PGH2) to prostaglandin D2 (PGD2). PGD2 functions as a neuromodulator as well as a trophic factor in the central nervous system. PGD2 is also involved in smooth muscle contraction/relaxation and is a potent inhibitor of platelet aggregation. This gene is preferentially expressed in brain.
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Jan Swammerdam (February 12, 1637 – February 17, 1680) was a Dutch biologist and microscopist. His work on insects demonstrated that the various phases during the life of an insect—egg, larva, pupa, and adult—are different forms of the same animal. As part of his anatomical research, he carried out experiments on muscle contraction. In 1658, he was the first to observe and describe red blood cells.
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Heavy meromyosin is a protein chain terminating in a globular head portion/cross bridge. HMM consists of two subunits, Heavy Meromyosin Subunit 1 and 2 (HMMS-1 and HMMS-2). The majority of myosin activity is concentrated in HMMS-1. HMMS-1 has an actin binding site and ATP binding site (myosin ATPase) that determines the rate of muscle contraction when muscle is stretched.
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Nerve agents attack the nervous system. All such agents function the same way resulting in cholinergic crisis: they inhibit the enzyme acetylcholinesterase, which is responsible for the breakdown of acetylcholine (ACh) in the synapses between nerves that control muscle contraction. If the agent cannot be broken down, muscles are prevented from relaxing and they are effectively paralyzed. This includes the heart and the muscles used for breathing.
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The animal moves through the water via rhythmic muscle contraction, aided by its side cilia, and a tuft of longer cilia on its back. The organism can also use its musculature to roll up into a ball, and maintain that form for several months. Adults are known to have a symbiotic relationship with bacterial species. Genetic data confirms that its diet includes bivalve mollusks.
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The dynamic interaction between the thick and thin filaments results in muscle contraction. Myosin belongs to a family of motor proteins, and the muscle isoforms of this family comprise the thick filament. The thin filament is made of the skeletal muscle isoforms of actin. Each myosin protein 'paddles' along the thin actin filament, repeatedly binding to myosin-binding sites along the actin filament, ratcheting and letting go.
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Dynamin-like 120 kDa protein, mitochondrial is a protein that in humans is encoded by the OPA1 gene. This protein regulates mitochondrial fusion and cristae structure in the inner mitochondrial membrane (IMM) and contributes to ATP synthesis and apoptosis, and small, round mitochondria. Mutations in this gene have been implicated in dominant optic atrophy (DOA), leading to loss in vision, hearing, muscle contraction, and related dysfunctions.
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Caldesmon is an inhibitor of actinomyosin ATPase and motility, and both actin binding and caldesmon inhibition are greatly enhanced in the presence of tropomyosin. Smooth muscle contraction is initiated by the release of Ca2+. Ca2+ binds to and activates calmodulin, which then binds to caldesmon. This binding causes the caldesmon protein to disengage from the actin filament, exposing the myosin-binding sites on the actin filament.
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The principal cytoplasmic proteins are myosin and actin (also known as "thick" and "thin" filaments, respectively) which are arranged in a repeating unit called a sarcomere. The interaction of myosin and actin is responsible for muscle contraction. Every single organelle and macromolecule of a muscle fiber is arranged to ensure form meets function. The cell membrane is called the sarcolemma with the cytoplasm known as the sarcoplasm.
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At the neuromuscular junction, the nerve fiber is able to transmit a signal to the muscle fiber by releasing ACh (and other substances), causing muscle contraction. Muscles will contract or relax when they receive signals from the nervous system. The neuromuscular junction is the site of the signal exchange. The steps of this process in vertebrates occur as follows:(1) The action potential reaches the axon terminal.
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"The Mechanics of Sprint Running." The Journal of Physiology 217 (1971): 709-21. As the velocity of the runner increases, inertia and air resistance effects become the limiting factors on the sprinter's top speed. It was previously believed that there was an intramuscular viscous force that increased proportionally to the velocity of muscle contraction that opposed the contractile force; this theory has since been disproved.
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Their function is similar in many respects to neurons. Cardiac muscle tissue has autorhythmicity, the unique ability to initiate a cardiac action potential at a fixed rate—spreading the impulse rapidly from cell to cell to trigger the contraction of the entire heart. There are specific proteins expressed in cardiac muscle cells. These are mostly associated with muscle contraction, and bind with actin, myosin, tropomyosin, and troponin.
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This condition differs as it affects both the extrinsic and enteric nervous systems due to the decreased dopamine levels in both. This results in less smooth muscle contraction of the colon, increasing the colon transit time. The reduced dopamine levels also causes dystonia of the striated muscles of the pelvic floor and external anal sphincter. This explains how Parkinson's disease can lead to constipation.
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The cause of OAB is unclear, and indeed there may be multiple causes. It is often associated with overactivity of the detrusor urinae muscle, a pattern of bladder muscle contraction observed during urodynamics. It is also possible that the increased contractile nature originates from within the urothelium and lamina propria, and abnormal contractions in this tissue could stimulate dysfunction in the detrusor or whole bladder.
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Drewes RC, Hedrick MS, Hillman SS, Withers PC. "Unique role of skeletal muscle contraction in vertical lymph movement in anurans." Journal of Experimental Biology 2007 Nov;210(Pt 22):3931-9. A translation by George Haslam of the first two volumes of Die Anatomie des Frosches, including considerable new material, was published under the title The anatomy of the frog in 1889.Ecker, A. Wiedersheim, R. Haslam.
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Comparison of smooth muscle and skeletal muscle contraction Contractions of skeletal muscle fiber are caused due to electrical stimulation. This process is caused by the depolarization of the transverse tubular junctions. Once depolarized the sarcoplasmic reticulm (SR) releases Ca2+ into the myoplasm where it will bind to a number of calcium sensitive buffers. The Ca2+ in the myoplasm will diffuse to Ca2+ regulator sites on the thin filaments.
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As muscles contract, they use ATP. The energy needed to make ATP comes from a variety of different pathways—such as glycolysis or oxidative phosphorylation—that ultimately use glucose as a starting material. In striated skeletal muscle cells, GLUT4 concentration in the plasma membrane can increase as a result of either exercise or muscle contraction. During exercise, the body needs to convert glucose to ATP to be used as energy.
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The three types of muscle (skeletal, cardiac and smooth) have significant differences. However, all three use the movement of actin against myosin to create contraction. In skeletal muscle, contraction is stimulated by electrical impulses transmitted by the nerves, the motoneurons (motor nerves) in particular. Cardiac and smooth muscle contractions are stimulated by internal pacemaker cells which regularly contract, and propagate contractions to other muscle cells they are in contact with.
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Glycine is integral to the formation of alpha-helices in secondary protein structure due to its compact form. For the same reason, it is the most abundant amino acid in collagen triple-helices. Glycine is also an inhibitory neurotransmitter - interference with its release within the spinal cord (such as during a Clostridium tetani infection) can cause spastic paralysis due to uninhibited muscle contraction. Glycine is a colorless, sweet-tasting crystalline solid.
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The purpose is to reduce the mechanical force on the sarcolemma as a result of muscle contraction. In addition to myoclonus dystonia, problems associated with a dysfunctional DAP complex include Duchenne muscular dystrophy. Upwards of 65 mutations of the SGCE gene are thought to cause myoclonus dystonia. The majority of the mutations lead to a truncated protein product that results in the loss-of-function of the epsilon sarcoglycan protein.
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Carnitine shuttle activation occurs due to a need for fatty acid oxidation which is required for energy production. During vigorous muscle contraction or during fasting, ATP concentration decreases and AMP concentration increases leading to the activation of AMP-activated protein kinase (AMPK). AMPK phosphorylates acetyl-CoA carboxylase, which normally catalyzes malonyl-CoA synthesis. This phosphorylation inhibits acetyl-CoA carboxylase, which in turn lowers the concentration of malonyl-CoA.
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Muscle strain is one of the most common injuries in tennis. When an isolated large-energy appears during the muscle contraction and at the same time, bodyweight applies huge amounts of pressure to the lengthened muscle, which can result in the occurrence of muscle strain. Inflammation and bleeding are triggered when muscle strain occur which resulted in redness, pain and swelling. Overuse is also common in tennis players from all levels.
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First, Sodium ions flow into the cell to depolarize it and cause skeletal muscle contraction. Once the action potential is over, potassium ions flow out of the cell due to increased cell membrane permeability to those ions. This high permeability contributes to the rapid repolarization of the membrane potential. This repolarization occurs quickly enough that another action potential can cause depolarization, even before the last action potential has dissipated.
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Types of muscle contractions Muscle contractions can be described based on two variables: force and length. Force itself can be differentiated as either tension or load. Muscle tension is the force exerted by the muscle on an object whereas a load is the force exerted by an object on the muscle. When muscle tension changes without any corresponding changes in muscle length, the muscle contraction is described as isometric.
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MYH7 is a gene encoding a myosin heavy chain beta (MHC-β) isoform (slow twitch) expressed primarily in the heart, but also in skeletal muscles (type I fibers). This isoform is distinct from the fast isoform of cardiac myosin heavy chain, MYH6, referred to as MHC-α. MHC-β is the major protein comprising the thick filament in cardiac muscle and plays a major role in cardiac muscle contraction.
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Isoinertial denotes a type of resistance used in exercise training which maintains a constant inertia throughout the range of motion, facilitating a constant resistance and maximal muscle force in every angle. The term isoinertial derives from the words iso (same) and inertial (resistance), which in one terminology describes the primary concept of the isoinertial system, or expressing the same inertia in both the concentric and the eccentric phases of muscle contraction.
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There are five known functions of intraglomerular mesangial cells: structural support of glomerular capillaries, regulation of the glomerular filtration rate, mesangial matrix formation, phagocytosis, and monitoring of capillary lumen glucose concentration. Intraglomerular mesangial cells have contractile activity. The initiation of contraction of mesangial cells is similar to that of smooth muscle. Contraction of mesangial cells is coupled with contraction of the basement membrane of the endothelium of glomerular capillaries.
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This produces a positive change in membrane potential, known as depolarization, which is propagated throughout the heart and initiates muscle contraction. Pacemaker cells, however, do not have a resting potential. Instead, immediately after repolarization, the membrane potential of these cells begins to depolarise again automatically, a phenomenon known as the pacemaker potential. Once the pacemaker potential reaches a set value, the threshold potential, it produces an action potential.
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The significance of ATP is in its ability to store potential energy within the phosphate bonds. The energy stored between these bonds can then be transferred to do work. For example, the transfer of energy from ATP to the protein myosin causes a conformational change when connecting to actin during muscle contraction. The cycle of synthesis and degradation of ATP; 1 and 2 represent output and input of energy, respectively.
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Muscles and neurons are activated by electrolyte activity between the extracellular fluid or interstitial fluid, and intracellular fluid. Electrolytes may enter or leave the cell membrane through specialized protein structures embedded in the plasma membrane called "ion channels". For example, muscle contraction is dependent upon the presence of calcium (Ca2+), sodium (Na+), and potassium (K+). Without sufficient levels of these key electrolytes, muscle weakness or severe muscle contractions may occur.
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There are four main different types of muscle contraction: twitch, treppe, tetanus and isometric/isotonic. Twitch contraction is the process in which a single stimulus signals for a single contraction. In twitch contraction the length of the contraction may vary depending on the size of the muscle cell. During treppe (or summation) contraction muscles do not start at maximum efficiency; instead they achieve increased strength of contraction due to repeated stimuli.
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Many animal species use paralysing toxins to capture prey, evade predation, or both. It was shown that in stimulated muscles the decrease in frequency of the miniature potentials runs parallel to the decrease in postsynaptic potential as well as to the decrease in muscle contraction. In invertebrates, this clearly indicates that, e.g., Microbracon (wasp genus) venom causes paralysis of the neuromuscular system by acting at a presynaptic site.
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The biceps brachii flex the lower arm. The brachioradialis, in the forearm, and brachialis, located deep to the biceps in the upper arm, are both synergists that aid in this motion. Muscle action that moves the axial skeleton work over a joint with an origin and insertion of the muscle on respective side. The insertion is on the bone deemed to move towards the origin during muscle contraction.
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The Jendrassik maneuver, which entails interlocking of flexed fingers to distract a patient and prime the reflex response, can also be used to accentuate reflexes.Delwaide PJ, Toulouse P. The Jendrassik maneuver: quantitative analysis of reflex reinforcement by remote voluntary muscle contraction. Adv Neurol. 1983;39:661-9. In cases of hyperreflexia, the physician may place his finger on top of the tendon, and tap the finger with the hammer.
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Bottom panel: SEM of campaniform on the base of the haltere of a sarcophagid fly. Campaniform sensilla are a class of mechanoreceptors found in insects, which respond to stress and strain within the animal's cuticle. Campaniform sensilla function as proprioceptors that detect mechanical load as resistance to muscle contraction, similar to mammalian Golgi tendon organs. Sensory feedback from campaniform sensilla is integrated in the control of posture and locomotion.
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However, as ATP is absent, there must be a breakdown of muscle tissue by enzymes (endogenous or bacterial) during decomposition. As part of the process of decomposition, the myosin heads are degraded by the enzymes, allowing the muscle contraction to release and the body to relax. Decomposition of the myofilaments occurs 48 to 60 hours after the peak of rigor mortis, which occurs approximately 13 hours after death.
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The actin filaments here are both pre-existing and new. Cleavage is driven by these motor proteins, actin and myosin, which are the same proteins involved with muscle contraction. During cellular cleavage, the contractile ring tightens around the cytoplasm of the cell until the cytoplasm is pinched into two daughter cells. During the final phase of mitosis, telophase, the furrow forms an intercellular bridge using mitotic spindle fibers.
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The normal relaxed state of the lung and chest is partially empty. Further exhalation requires muscular work. Inhalation is an active process requiring work. Some of this work is to overcome frictional resistance to flow, and part is used to deform elastic tissues, and is stored as potential energy, which is recovered during the passive process of exhalation, Tidal breathing does not require active muscle contraction during exhalation.
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Integrative and Comparative Biology 55: 718-727.Svendsen MBS, Domenici P, Marras S, Krause J, Boswell KM, Rodriguez- Pinto I, Wilson ADM, Kurvers RHJM, Viblanc PE, Finger JS & Steffensen JF (2016) "Maximum swimming speeds of sailfish and other large marine predatory fish species based on muscle contraction time: A myth revisited". Biology Open, 5: 1415-1419. Generally, sailfish do not grow to more than in length and rarely weigh over .
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The binding of ACh to the receptor can depolarize the muscle fiber, causing a cascade that eventually results in muscle contraction. Neuromuscular junction diseases can be of genetic and autoimmune origin. Genetic disorders, such as Duchenne muscular dystrophy, can arise from mutated structural proteins that comprise the neuromuscular junction, whereas autoimmune diseases, such as myasthenia gravis, occur when antibodies are produced against nicotinic acetylcholine receptors on the sarcolemma.
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Muscle strain is one of the most common injuries in tennis. When an isolated large-energy appears during the muscle contraction and at the same time body weight apply huge amount of pressure to the lengthened muscle, muscle strain can occur. Inflammation and bleeding are triggered when muscle strain occurs, which can result in redness, pain and swelling. Overuse is also common in tennis players of all levels.
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Calcium's function in muscle contraction was found as early as 1882 by Ringer. Subsequent investigations were to reveal its role as a messenger about a century later. Because its action is interconnected with cAMP, they are called synarchic messengers. Calcium can bind to several different calcium-modulated proteins such as troponin-C (the first one to be identified) and calmodulin, proteins that are necessary for promoting contraction in muscle.
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Skeletal muscle is composed of long cylindrical cells called muscle fibers. There are two types of muscle fibers, slow twitch or muscle contraction (type I) and fast twitch (type II). Slow twitch fibers are more efficient in using oxygen to generate energy, while fast twitch fibers are less efficient. However, fast twitch fibers fire more rapidly, allowing them to generate more power than slow twitch (type I) fibers.
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These neurons are important for mediating energy-demanding motor behaviors, such as escape-induced jumping and flight. For example, the locust DUMeti neuron releases octopamine onto the extensor tibia muscle to increase muscle tension and increase relaxation rate. These actions promote efficient leg muscle contraction for jumping. During flight, DUM neurons are also active and release octopamine throughout the body to synchronize energy metabolism, respiration, muscle activity and flight interneuron activity.
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By decreasing the concentration of IP3 in the cytoplasm, ITP3K terminates propagation of the calcium signaling pathway. The calcium signaling pathway is involved in a variety of cellular processes including muscle contraction, gamete fertilization, and neurotransmitter release. Since the calcium second messenger has such widespread cellular functionality, it must be tightly regulated. ITP3K, shown in step 6 in the schematic, plays a role in calcium homeostasis by means of signal termination.
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Vitamin A is an essential micro-nutrient for vision, reproduction, cell and tissue differentiation, and immune function. Vitamin D and calcium work together in cases of maintaining homeostasis, creating muscle contraction, transmission of nerve pulses, blood clotting, and membrane structure. A lack of vitamin A, vitamin D, or calcium can cause dryness and brittleness. Insufficient vitamin B12 can lead to excessive dryness, darkened nails, and rounded or curved nail ends.
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Tetany in evoked stimulus, as defined in Morgan & Mikhail's Clinical Anesthesiology as a ~5 seconds of sustained stimulus of between 50 and a 100 Hz. The reaction of muscle tissue to stimulus under no neuromuscular blockade should be equal in intensity throughout the stimulus, The first muscle twitch and last should be of roughly equal magnitude. Clinically it will present as equal muscle contraction throughout the duration of muscle stimulation.
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According to the profile posted at his personal blog, his mission is "to solve the so-called mind-brain problem." After graduating from the University of Tokyo in 1985 with a degree in science and in 1987 with a degree in law, Mogi received in 1992 a Ph.D. with the thesis "Mathematical Model of Muscle Contraction". Ken Mogi was Japan's first TED speaker. He presented in 2012 March.
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Nitric oxide (NO) contributes to vessel homeostasis by inhibiting vascular smooth muscle contraction and growth, platelet aggregation, and leukocyte adhesion to the endothelium. Humans with atherosclerosis, diabetes, or hypertension often show impaired NO pathways. Nitric oxide (NO) is a mediator of vasodilation in blood vessels. It is induced by several factors, and once synthesized by eNOS it results in phosphorylation of several proteins that cause smooth muscle relaxation.
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Muscle cells contract in complex mechanical and chemical processes. If any part of the process or structure is disrupted, dysfunction will likely result, as in the case of those with genetic variations. In those with nemaline myopathy, muscle contraction is adversely affected. At the electron microscopic level, rod-shaped components can often be seen in some of the muscle cells, and when seen, are diagnostic for the condition called nemaline rod myopathy.
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Voltage-dependent calcium channels are important for generating electrical signals in excitable cells like neurons and cardiac or smooth muscle cells. N-type Ca2+ channels are found in neuronal cells, and play an important role in the coupling of nerve excitation and neurotransmitter secretion. L-type calcium channels are present in cardiac and smooth muscle cells, coupling excitation to muscle contraction. Other types of voltage-activated Ca2+-channels include T-type and P-type channels.
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Respiratory arrest should be distinguished from respiratory failure. The former refers to the complete cessation of breathing, while respiratory failure is the inability to provide adequate ventilation for the body's requirements. Without intervention, both may lead to decreased oxygen in the blood (hypoxemia), elevated carbon dioxide level in the blood (hypercapnia), inadequate oxygen perfusion to tissue (hypoxia), and may be fatal. Respiratory arrest is also different from cardiac arrest, the failure of heart muscle contraction.
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Both 3,4-diaminopyridine formulations delay the repolarization of nerve terminals after a discharge, thereby allowing more calcium to accumulate in the nerve terminal. Pyridostigmine decreases the degradation of acetylcholine after release into the synaptic cleft, and thereby improves muscle contraction. An older agent, guanidine, causes many side effects and is not recommended. 4-Aminopyridine (dalfampridine), an agent related to 3,4-aminopyridine, causes more side effects than 3,4-DAP and is also not recommended.
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The threshold for toxicity varies between species of animals: for sheep a threshold value of 1.8 - 2.0 mg/kg was found, and for cattle 1.55 mg/kg. Measuring the lolitrem B concentration in fat tissue can be used to estimate the amount of lolitrem B consumed, and is used to determine the cause of death for cattle that presenting with neurological symptoms. Lolitrem B likely acts synergistically with ergotamine to increase smooth muscle contraction.
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Various kinds of involuntary muscle activity may be referred to as a "spasm". A spasm may be a muscle contraction caused by abnormal nerve stimulation or by abnormal activity of the muscle itself. A series of spasms, or permanent spasms, is called a "spasmism". A spasm may lead to muscle strains or tears in tendons and ligaments if the force of the spasm exceeds the tensile strength of the underlying connective tissue.
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Muscle fatigue is the neuromuscular adaptation to challenges over a period of time. The use of motor units over a period of time can result in changes in the motor command from the brain. Since the force of contraction cannot be changed, the brain instead recruits more motor units to achieve maximal muscle contraction. Recruitment of motor units varies from muscle to muscle depending on the upper limit of motor recruitment in the muscle.
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The young human eye can change focus from distance (infinity) to as near as 6.5 cm from the eye. This dramatic change in focal power of the eye of approximately 15 dioptres (the reciprocal of focal length in metres) occurs as a consequence of a reduction in zonular tension induced by ciliary muscle contraction. This process can occur in as little as 224 ± 30 milliseconds in bright light. The amplitude of accommodation declines with age.
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Mammalian bombesin-like peptides are widely distributed in the central nervous system as well as in the gastrointestinal tract, where they modulate smooth-muscle contraction, exocrine and endocrine processes, metabolism, and behavior. They bind to G protein-coupled receptors on the cell surface to elicit their effects. Bombesin-like peptide receptors include gastrin-releasing peptide receptor, neuromedin B receptor, and bombesin-like receptor-3 (BRS3; this article). BB3 is a G protein-coupled receptor.
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The use of new types of light microscopes led to the important proposal in 1954 of the sliding filament mechanism for muscle contraction. Randall was also successful in integrating the teaching of biosciences at King's College. In 1951 he set up a large multidisciplinary group working under his personal direction to study the structure and growth of the connective tissue protein collagen. Their contribution helped to elucidate the three-chain structure of the collagen molecule.
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He thus has worked on the initiation of muscle contraction, its implications for cellular electrolyte homeostasis, the control of bone resorption under both normal and osteoporotic conditions and cortical spreading depression phenomena in the central nervous system often presaging migraine headache . His current interests are directed towards mechanisms of arrhythmogenesis in genetically modified hearts, studied using biophysical, physiological and molecular biological methods and their implications for the management of atrial fibrillation and sudden cardiac death.
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However, unlike acetylcholine, anatoxin-a is not degradable by cholinesterase, resulting in a persistent muscle contraction. This disruption presents as coordination loss, paralysis, muscle twitching, shortness of breath, and possibly death. Biological toxicity aside, Anabaena circinalis blooms have the potential to disrupt commercial fishing areas, water-treatment facilities, and recreational waterways. Add to this the high cost of toxicity monitoring, and it's apparent that Anabaena circinalis can have a detrimental economic impact as well.
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One explanation for the increased irisin expression with exercise in mouse and man may have evolved as a consequence of muscle contraction during shivering. Muscle secretion of a hormone that activates adipose thermogenesis during this process might provide a broader, more robust defense against hypothermia. The therapeutic potential of irisin is obvious. Exogenously administered irisin induces the browning of subcutaneous fat and thermogenesis, and it presumably could be prepared and delivered as an injectable polypeptide.
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However, the main role played by the muscles and tendons is to withstand the force that is experienced in the landing. This force is withstood in eccentric contraction. When muscle contraction is sufficiently great, it is able to stop the downward movement very quickly. This phase is sometimes called the phase of amortization in which the athlete absorbs some of the force and stops downward movement by the strong eccentric contraction of the muscles.
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Parasympathetic activation of the M3 muscarinic receptors causes ciliary muscle contraction, the effect of contraction is to decrease the diameter of the ring of ciliary muscle. The parasympathetic tone is dominant when a higher degree of accommodation of the lens is required, such as reading a book. The ciliary body is also known to receive sympathetic innervation via long ciliary nerves. When test subjects are startled, their eyes automatically adjust for distance vision.
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Part of the myosin II structure. Atoms in the heavy chain are colored pink (on the left-hand side); atoms in the light chains are colored faded-orange and faded-yellow (also on the left-hand side). Myosins () are a superfamily of motor proteins best known for their roles in muscle contraction and in a wide range of other motility processes in eukaryotes. They are ATP-dependent and responsible for actin-based motility.
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U46619 is a stable synthetic analog of the endoperoxide prostaglandin PGH2 first prepared in 1975, and acts as a thromboxane A2 (TP) receptor agonist. It potently stimulates TP receptor-mediated, but not other prostaglandin receptor-mediated responses in various in vitro preparations. and exhibits many properties similar to thromboxane A2, including shape change and aggregation of platelets and smooth muscle contraction. U46619 is a vasoconstrictor that mimics the hydroosmotic effect of vasopressin.
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Nerve agents are substances that disrupt the chemical communications through the nervous system. One mechanism of disruption, utilized by the G, GV, and V series of chemicals is caused by blocking the acetylcholinesterase, an enzyme that normally destroys and stops the activity of acetylcholine, a neurotransmitter. Poisoning by these nerve agents leads to an accumulation of acetylcholine at the nerve axon, producing a perpetual excited state in the nerve (e.g. constant muscle contraction).
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Muscle energy techniques address somatic dysfunction through stretching and muscle contraction. For example, if a person is unable to fully abduct her arm, the treating physician raises the patient's arm near the end of the patient's range of motion, also called the edge of the restrictive barrier. The patient then tries to lower her arm, while the physician provides resistance. This resistance against the patient's motion allows for isotonic contraction of the patient's muscle.
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James A. Spudich () is an American scientist and professor. He is the Douglass M. and Nola Leishman Professor of Biochemistry and of Cardiovascular Disease at Stanford University and works on the molecular basis of muscle contraction. He was awarded the Albert Lasker Basic Medical Research Award in 2012 with Michael Sheetz and Ronald Vale. He is a Fellow of the American Academy of Arts and Sciences and a Member of the National Academy of Sciences.
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Rice spent most of his academic career from 1955 to 1995 at the Department of Biological Sciences at Carnegie Mellon University in Pittsburgh, Pennsylvania, and served as department head. He was also a scientist-in- residence at the Marine Biological Laboratory at Woods Hole, Massachusetts during the summer months. His research focused on the biochemistry and cellular physiology of muscle contraction and nerve transmission. In retirement he has taken up an interest in genetic genealogy.
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The stretch reflex operates as a feedback mechanism to control muscle length by causing muscle contraction. In contrast, the tendon reflex operates as a negative feedback mechanism to control muscle tension. Although the tendon reflex is less sensitive than the stretch reflex, it can override the stretch reflex when tension is great, for example, causing a person to drop a very heavy weight. Like the stretch reflex, the tendon reflex is ipsilateral.
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Muscle fatigue is the decline in ability of a muscle to generate force. It can be a result of vigorous exercise but abnormal fatigue may be caused by barriers to or interference with the different stages of muscle contraction. There are two main causes of muscle fatigue: the limitations of a nerve’s ability to generate a sustained signal (neural fatigue); and the reduced ability of the muscle fiber to contract (metabolic fatigue).
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The MYH16 gene encodes a protein called myosin heavy chain 16, which is a muscle protein in mammals. At least in primates, it is a specialized muscle protein found only in the temporalis and masseter muscles of the jaw. Myosin heavy chain proteins are important in muscle contraction, and if they are missing, the muscles will be smaller. In non-human primates, MYH16 is functional and the animals have powerful jaw muscles.
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Calsequestrin is a calcium-binding protein that acts as a calcium buffer within the sarcoplasmic reticulum. The protein helps hold calcium in the cisterna of the sarcoplasmic reticulum after a muscle contraction, even though the concentration of calcium in the sarcoplasmic reticulum is much higher than in the cytosol. It also helps the sarcoplasmic reticulum store an extraordinarily high amount of calcium ions. Each molecule of calsequestrin can bind 18 to 50 Ca2+ ions.
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Sequence analysis has suggested that calcium is not bound in distinct pockets via EF-hand motifs, but rather via presentation of a charged protein surface. Two forms of calsequestrin have been identified. The cardiac form Calsequestrin-2 (CASQ2) is present in cardiac and slow skeletal muscle and the fast skeletal form Calsequestrin-1(CASQ1) is found in fast skeletal muscle. The release of calsequestrin-bound calcium (through a calcium release channel) triggers muscle contraction.
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Neuromuscular junction diseases are a result of a malfunction in one or more steps of the above pathway. As a result, normal functioning can be completely or partially inhibited, with the symptoms largely presenting themselves as problems in mobility and muscle contraction as expected from disorders in motor end plates. Neuromuscular junction diseases can also be referred to as end plate diseases or disorders. Among neuromuscular diseases some can be autoimmune disease, or hereditary disorders.
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The myosin heads tilt and drag along the actin filament a small distance (10–12 nm). The heads then release the actin filament and then changes angle to relocate to another site on the actin filament a further distance (10–12 nm) away. They can then re-bind to the actin molecule and drag it along further. This process is called crossbridge cycling and is the same for all muscles (see muscle contraction).
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Meromyosin is a part of myosin (mero meaning "part of"). With regards to human anatomy myosin and actin constitute the basic functional unit of a muscle fiber, called sarcomere, playing a role in muscle contraction. Biochemically viewed meromyosin form subunits of the actin-associated motor protein, myosin, Following proteolysis, two types of meromyosin are formed: heavy meromyosin (HMM) and light meromyosin (LMM). Light meromyosin has a long, straight portion in the “tail” region.
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"Determination of the Chronaxie and Rheobase of Denervated Limb Muscles in Conscious Rabbits". Artificial Organs, Volume 29 Issue 3 Page 212 - March 2005 In Greek, the root rhe translates to "current or flow", and basi means "bottom or foundation": thus the rheobase is the minimum current that will produce an action potential or muscle contraction. Rheobase can be best understood in the context of the strength-duration relationship (Fig. 1).Fleshman et al.
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Part of a Myofibril A neuromuscular junction (or myoneural junction) is a chemical synapse between a motor neuron and a muscle fiber. It allows the motor neuron to transmit a signal to the muscle fiber, causing muscle contraction. Muscles require innervation to function—and even just to maintain muscle tone, avoiding atrophy. In the neuromuscular system nerves from the central nervous system and the peripheral nervous system are linked and work together with muscles.
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Sodium-based action potentials usually last for under one millisecond, but calcium-based action potentials may last for 100 milliseconds or longer. In some types of neurons, slow calcium spikes provide the driving force for a long burst of rapidly emitted sodium spikes. In cardiac muscle cells, on the other hand, an initial fast sodium spike provides a "primer" to provoke the rapid onset of a calcium spike, which then produces muscle contraction.
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The clinical manifestations of tetanus are caused when tetanus toxin blocks inhibitory impulses, by interfering with the release of neurotransmitters, including glycine and gamma-aminobutyric acid. These inhibitory neurotransmitters inhibit the alpha motor neurons. With diminished inhibition, the resting firing rate of the alpha motor neuron increases, producing rigidity, unopposed muscle contraction and spasm. Characteristic features are risus sardonicus (a rigid smile), trismus (commonly known as "lock-jaw"), and opisthotonus (rigid, arched back).
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Myosin heavy chain, α isoform (MHC-α) is a protein that in humans is encoded by the MYH6 gene. This isoform is distinct from the ventricular/slow myosin heavy chain isoform, MYH7, referred to as MHC-β. MHC-α isoform is expressed predominantly in human cardiac atria, exhibiting only minor expression in human cardiac ventricles. It is the major protein comprising the cardiac muscle thick filament, and functions in cardiac muscle contraction.
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It is used in patients with parkinsonism and akathisia, and to reduce the side effects of antipsychotic treatment given for schizophrenia. Procyclidine is also a second-line drug for the treatment of Parkinson's disease. It improves tremor but not rigidity or bradykinesia. Procyclidine is also sometimes used for the treatment of dystonia (but not tardive dyskinesia), a rare disorder that causes abnormal muscle contraction, resulting in twisting postures of limbs, trunk, or face.
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A robotic Leg attaches to an individual who has had a lower extremity amputation—of a portion of a leg or foot. Doctors and technicians measure the remaining limb structure and of the person’s prosthesis to ideally fit the robotic leg.How Prosthetic Limbs Work After they attach the robotic leg, they embed the sensors in the robotic leg that measure the electrical activity created by re-innervated muscle contraction, and existing thigh muscle.
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In addition to condensed matter physics, Tolpygo was also interested in biophysics. He proposed an original microscopic theory of muscle contraction based on the idea that the energy of decomposition of adenosine triphosphate (ATP) molecule is transferred along the chains of hydrogen bonds between actin and myosin polymers causing their mutual motion.Tolpygo K. B. "Possible role of hydrogen-bonds in conformational changes in biopolymers and carrying out their macroscopic displacements." Studia Biophysica, v.
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The influx of calcium ions into the cell can initiate a myriad of calcium-dependent processes including muscle contraction, gene expression, and secretion. Calcium-dependent processes can be halted by lowering intracellular calcium levels, which, for example, can be accomplished by calcium pumps. Voltage-dependent calcium channels are multi- proteins composed of α1, β, α2δ and γ subunits. The major subunit is α1, which forms the selectivity pore, voltage-sensor and gating apparatus of VDCCs.
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Changes in the resting membrane potential involving denervated muscles presents mild depolarization when a muscle contraction stimulus is present. While there is no immediate change involving resting and action potential, there is an increase with membrane resistance. After prolonged denervation, it is revealed that resting membrane potential over time is reduced while action potentials progressively decreased and become slower. Acetylcholine is a neurotransmitter that becomes supersensitive in the presence of denervated muscle.
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In 1895 he succeeded Ewald Hering (1834–1918) as manager of the department of physiology at the University of Prague. Gad is known from his work in experimental physiology. He performed numerous investigations involving electrophysiology, spinal cord functionality, the relationship between lactic acid to muscle contraction, et al. With Edward Flatau (1868–1932), he conducted experiments that were critical of Bastian-Bruns Law in regards to the loss of function following spinal cord injury.
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In contrast to the mouse myotubes calciseptine did not change the reversal potential of the Ca2+ current. In rat muscle fibers after applying calciseptine there were very slight changes found in twitch tension, which shows us that the peptide had very little effect on muscle contraction. Calciseptine also had little effect on frog muscle fibers. There is a small effect of calciseptine during a series of repetitive stimuli which generate a tetanus; calciseptine increased tetanic tension.
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Using this new technology, these two students proposed the Sliding Filament Theory of muscle contraction. Ground breaking research was constantly coming out of his lab. In 1941, Schmitt was recruited by MIT's Karl Compton and Vannevar Bush to lead radically new Department of Biology there that would combine biology, physics, mathematics, and chemistry. Schmitt became an authority on electron microscopy and conducted innovative studies on kidney function, tissue metabolism, and the chemistry, physiology, biochemistry, and electrophysiology of the nerve.
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Respiratory arrest is caused by apnea (cessation of breathing) or respiratory dysfunction severe enough it will not sustain the body (such as agonal breathing). Prolonged apnea refers to a patient who has stopped breathing for a long period of time. If the heart muscle contraction is intact, the condition is known as respiratory arrest. An abrupt stop of pulmonary gas exchange lasting for more than five minutes may damage vital organs especially the brain, possibly permanently.
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Actin participates in many important cellular processes, including muscle contraction, cell motility, cell division and cytokinesis, vesicle and organelle movement, cell signaling, and the establishment and maintenance of cell junctions and cell shape. Many of these processes are mediated by extensive and intimate interactions of actin with cellular membranes. In vertebrates, three main groups of actin isoforms, alpha, beta, and gamma have been identified. The alpha actins, found in muscle tissues, are a major constituent of the contractile apparatus.
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Strychnine is a neurotoxin which acts as an antagonist of glycine and acetylcholine receptors. It primarily affects the motor nerve fibers in the spinal cord which control muscle contraction. An impulse is triggered at one end of a nerve cell by the binding of neurotransmitters to the receptors. In the presence of an inhibitory neurotransmitter, such as glycine, a greater quantity of excitatory neurotransmitters must bind to receptors before there will be an action potential generated.
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Acetylcholine then diffuses across the synaptic cleft. It may be hydrolysed by acetylcholine esterase (AchE) or bind to the nicotinic receptors located on the motor end plate. The binding of two acetylcholine molecules results in a conformational change in the receptor that opens the sodium-potassium channel of the nicotinic receptor. This allows and ions to enter the cell and ions to leave the cell, causing a depolarization of the end plate, resulting in muscle contraction.
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This clinical environment, in combination with the slow speed and improved mechanics, had never been managed before. SuperSlow instructors are also educated with an emphasis on using precise language in exercise. A ten/ten protocol was used in the 1940s by body builders and later in the 1960s by powerlifters as a plateau breaker under the name MC/MM or muscle contraction with measured movement. This similar idea was sometimes advocated by Bob Hoffman of the York Barbell Company.
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Locusts and other grasshoppers (suborder Caelifera) stridulate by rubbing hind legs against pegs on wing surfaces in an up and downward motion. Cicadas (superfamily Cicadoidea) produce sound at much greater volumes than Orthopterans, relying on a pair of organs called tymbals on the base of the abdomen behind the wings. Muscle contraction rapidly deforms the tymbal membrane, emitting several different types of sounds. Insects thus produce a variety of sounds, using various mechanisms distinct from other animals.
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Normally, a human being is able to feel pleasure from an orgasm. Upon reaching a climax, chemicals are released in the brain and motor signals are activated that will cause quick cycles of muscle contraction in the corresponding areas of both males and females. Sometimes, these signals can cause other involuntary muscle contractions such as body movements and vocalization. Finally, during orgasm, upward neural signals go to the cerebral cortex and feelings of intense pleasure are experienced.
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Potassium channels play a role in many cellular processes including the maintenance of the action potential, muscle contraction, hormone secretion, osmotic regulation, and ion flow. This gene encodes the K2P4.1 protein, a lipid-gated ion channel that belongs to the superfamily of potassium channel proteins containing two pore-forming P domains. K2P4.1 homodimerizes and functions as an outwardly rectifying channel. It is expressed primarily in neural tissues and is stimulated by membrane stretch and polyunsaturated fatty acids.
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The temperature of a muscle has a significant effect on the velocity and power of the muscle contraction, with performance generally declining with decreasing temperatures and increasing with rising temperatures. The Q10 coefficient represents the degree of temperature dependence a muscle exhibits as measured by contraction rates. A Q10 of 1.0 indicates thermal independence of a muscle whereas an increasing Q10 value indicates increasing thermal dependence. Values less than 1.0 indicate a negative or inverse thermal dependence, i.e.
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The generation of a transmembrane electrical potential through ion movement across a cell membrane drives biological processes like nerve conduction, muscle contraction, hormone secretion, and sensory processes. By convention, a typical animal cell has a transmembrane electrical potential of -50 mV to -70 mV inside the cell relative to the outside. Electrochemical gradients also play a role in establishing proton gradients in oxidative phosphorylation in mitochondria. The final step of cellular respiration is the electron transport chain.
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Some of Schwann's earliest work in 1835 involved muscle contraction, which he saw as a starting point for "the introduction of calculation to physiology". He developed and described an experimental method to calculate the contraction force of the muscle, by controlling and measuring the other variables involved. His measurement technique was developed and used later by Emil du Bois-Reymond and others. Schwann's notes suggest that he hoped to discover regularities and laws of physiological processes.
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Muscle spindle discharges are sent to the spinal cord through afferent nerve fibers, where they activate monosynaptic and polysynaptic reflex arcs, causing the muscle to contract. The effects of sustained vibratory stimulation on muscle contraction, posture and kinesthetic perceptions are much more complex than merely contraction of the muscle being vibrated. Russian scientists Victor Gurfinkel, Mikhail Lebedev, Andrew Polyakov and Yuri Levick used vibratory stimulation to study human posture control and spectral characteristics of electromyographic (EMG) activity.
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This action facilitates the rate that aqueous humor leaves the eye to decrease intraocular pressure. Paradoxically, when pilocarpine induces this ciliary muscle contraction (known as an accommodative spasm) it causes the eye's lens to thicken and move forward within the eye. This movement causes the iris (which is located immediately in front of the lens) to also move forward, narrowing the Anterior chamber angle. Narrowing of the anterior chamber angle increases the risk of increased intraocular pressure.
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The muscle contraction of a ballistic muscle movement can exhibit a muscle coactivation of concurrent agonist Lee, J.B., Matsumoto, T., Othman, T., Yamauchi, M., Taimura, A., Kaneda, E., Ohwatari, N. and Kosaka, M. (1999) Coactivation of the flexor muscles as a synergist with the extensors during ballistic finger exetension movement in trained kendo and karate athletes. International Journal of Sports Medecine. 20(1): 7-11. and antagonist muscles or the characteristic triphasic agonist/antagonist/agonist muscle activation.
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In this sense the power of the muscles is actually amplified. When energy is produced by muscle contraction, stored in a tendon, then released to increase mechanical energy of the body (or body segment), muscle power is amplified. It is important to note, however, that the term power ‘amplification’ may be deceptive. In animals, elastic mechanisms never add energy to the system; they amplify power in the sense that the energy is released more rapidly than it is stored.
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As the rectum becomes more distended, the sphincters relax and a reflex expulsion of the contents of the rectum occurs. Expulsion occurs through contractions of the muscles of the rectum. The urge to voluntarily defecate occurs after the rectal pressure increases to beyond 18 mmHg; and reflex expulsion at 55 mmHg. In voluntary defecation, in addition to contraction of the rectal muscles and relaxation of the external anal sphincter, abdominal muscle contraction, and relaxation of the puborectalis muscle occurs.
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In addition to extensive teaching activities, the Department of Biochemistry at Eötvös Loránd University did research into the biochemistry of proteins and the biology of muscle contraction. The Department had internationally recognized results in the study of the structure of myosin. The activities of the Biochemistry Research Group and then of the Department of Biochemistry were centered on Bíró's research topics. Bíró published one of his most outstanding research findings together with András Szent-Györgyi jun.
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One of the standard means of assessing functional classification is the bench test, which is used in swimming, lawn bowls and wheelchair fencing. Using the Adapted Research Council (MRC) measurements, muscle strength is tested using the bench press for a variety of spinal cord related injuries with a muscle being assessed on a scale of 0 to 5. A 0 is for no muscle contraction. A 1 is for a flicker or trace of contraction in a muscle.
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One of the standard means of assessing functional classification is the bench test, which is used in swimming, lawn bowls and wheelchair fencing. Using the Adapted Research Council measurements, muscle strength is tested using the bench press for a variety of spinal cord related injuries with a muscle being assessed on a scale of 0 to 5. A 0 is for no muscle contraction. A 1 is for a flicker or trace of contraction in a muscle.
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Skeletal muscle, with terminal cisterna labeled near bottom. Terminal cisternae are enlarged areas of the sarcoplasmic reticulum surrounding the transverse tubules. These discrete regions within the muscle cell store calcium (increasing the capacity of the sarcoplasmic reticulum to release calcium) and release it when an action potential courses down the transverse tubules, eliciting muscle contraction. Because terminal cisternae ensure rapid calcium delivery, they are well developed in muscles that contract quickly, such as fast twitch skeletal muscle.
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T98G is a glioblastoma cell line used in brain cancer research and drug development. The ACTA2 protein, which is involved in muscle contraction, is present in large amounts in the T98G cell line. The T98G cell line was derived from a 61-year-old human male and has a hyperpentaploid chromosome count with a modal number ranging from 128 to 132. The cells are not tumorigenic in mice, but do proliferate with proper anchorage in cell culture.
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The right arm had been severed by someone with knowledge of human anatomy, had been tourniqueted to stem blood flow, and due to the lack of muscle contraction, was removed post- mortem.Autumn of Terror: Jack the Ripper, His Crimes and Times p. 95 It was also revealed that the victim had been wearing a broché satin dress at the time of death. The dress had been manufactured in Bradford, England, from a pattern estimated as three years old.
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Smooth muscle contraction is caused by the sliding of myosin and actin filaments (a sliding filament mechanism) over each other. The energy for this to happen is provided by the hydrolysis of ATP. Myosin functions as an ATPase utilizing ATP to produce a molecular conformational change of part of the myosin and produces movement. Movement of the filaments over each other happens when the globular heads protruding from myosin filaments attach and interact with actin filaments to form crossbridges.
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Viperid venoms typically contain an abundance of protein-degrading enzymes, called proteases, that produce symptoms such as pain, strong local swelling and necrosis, blood loss from cardiovascular damage complicated by coagulopathy, and disruption of the blood-clotting system. Also being vasculotoxic in nature, viperine venom causes vascular endothelial damage and hemolysis. Death is usually caused by collapse in blood pressure. This is in contrast to elapid venoms that generally contain neurotoxins that disable muscle contraction and cause paralysis.
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Interactive animation of the structure of ATP Adenosine triphosphate (ATP) is an organic compound and hydrotrope that provides energy to drive many processes in living cells, e.g. muscle contraction, nerve impulse propagation, condensate dissolution, and chemical synthesis. Found in all known forms of life, ATP is often referred to as the "molecular unit of currency" of intracellular energy transfer. When consumed in metabolic processes, it converts either to adenosine diphosphate (ADP) or to adenosine monophosphate (AMP).
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EMG is a common technique used in many disciplines within the Exercise and Rehab Sciences. Skeletal muscle has two physiological responses: relaxation and contraction.The electrical activity associated with muscle contraction are measured via electromyography (EMG) The mechanisms for which these responses occur generate electrical activity measured by EMG. Specifically, EMG can measure the action potential of a skeletal muscle, which occurs from the hyperpolarization of the motor axons from nerve impulses sent to the muscle (1).
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Of these, Q50R and G159D co- segregated with disease in affected family members, increasing confidence that they are clinically significant mutations. The biochemical consequences of thin filament DCM-associated mutations are less well established than for HCM, although there has been some suggestion that some of the mutations abolish the calcium desensitizing effect of cTnI phosphorylation at Ser22/23. This may be because some mutations disrupt the precise positioning of cNTnC for triggering muscle contraction when cTnI is unphosphorylated.
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The goal of this initiative is to address gaps in existing knowledge about the pathways leading to motor impairment. Gandevia and his team have designed the program to focus mainly on three areas: muscle contraction, fatigue, and impaired balance. With his team, Gandevia has conducted the largest study examining physiological factors contributing to falls in patients diagnosed with multiple sclerosis. He has also compiled the first description of the three- dimensional changes that occur when muscles contract.
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The Michael and Kate Bárány Award for Young Investigators from the Biophysical Society in Rockville, Maryland, "recognizes an outstanding contribution to biophysics by a person who has not achieved the rank of full professor." The award was established in 1992 as the Young Investigator Award and renamed in 1998, when it was endowed by Michael Bárány and Kate Bárány. The Báránys were survivors of The Holocaust who went on to become leading researchers in muscle contraction.
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The diad is a structure in the cardiac myocyte located at the sarcomere Z-line. It is composed of a single t-tubule paired with a terminal cisterna of the sarcoplasmic reticulum. The diad plays an important role in excitation- contraction coupling by juxtaposing an inlet for the action potential near a source of Ca2+ ions. This way, the wave of depolarization can be coupled to calcium-mediated cardiac muscle contraction via the sliding filament mechanism.
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The alpha subunit is a protein of about 268 to 286 amino acid residues and the beta subunit is approximately 280 amino acids, their sequences are well conserved in eukaryotic species. The actin filament system, a prominent part of the cytoskeleton in eukaryotic cells, is both a static structure and a dynamic network that can undergo rearrangements: it is thought to be involved in processes such as cell movement and phagocytosis, as well as muscle contraction.
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Lipogenesis is the metabolic process through which acetyl-CoA is converted to triglyceride for storage in fat. The triglycerides in fat are packaged within cytoplasmic lipid droplets. The process begins with acetyl-CoA, which is an organic compound used to transfer energy from metabolism of carbohydrates, fatty acids, and ethanol. Through the citric acid cycle, acetyl-CoA is broken down to produce ATP, which is then an energy source for many metabolic processes, including protein synthesis and muscle contraction.
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Sea anemone neurotoxin is the name given to neurotoxins produced by sea anemones with related structure and function. Sea anemone neurotoxins can be divided in two functional groups that either specifically target the sodium channel or the potassium channel. A number of proteins belong to the sodium channel toxin family, including calitoxin and anthopleurin. The neurotoxins bind specifically to the sodium channel, thereby delaying its inactivation during signal transduction, resulting in strong stimulation of mammalian cardiac muscle contraction.
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After being stimulated via IL-33 during an infection, they begin to secrete IL-5, leading to an activation of B1 B cells and the production of IgM antibodies. ILC2s are the dominant population of ILC in the lungs. By producing IL-13, they can initiate smooth muscle contraction and mucus secretion, but also goblet cell hyperplasia if the IL-13 is overexpressed. In addition, ILC2s help pulmonary wound healing after influenza infection by secreting amphiregulin.
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Orgasm is the conclusion of the plateau phase of the sexual response cycle and is experienced by both males and females. It is accompanied by quick cycles of muscle contraction in the lower pelvic muscles, which surround both the anus and the primary sexual organs. Women also experience uterine and vaginal contractions. Orgasms are often associated with other involuntary actions, including vocalizations and muscular spasms in other areas of the body and a generally euphoric sensation.
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The TRPV4 (transient receptor potential vanilloid 4) gene, located on chromosome 12, encodes for a protein that serves as an ion channel, typically found in the plasma membrane and is permeable to Ca2+. Abnormal regulation of Ca2+ can lead to inefficient muscle contraction. TRPV4 plays a major role in mechanosensation, as well as osmosensory functions in nerve endings, endothoelia, and alveoli. The TRPV4 protein consists of 871 amino acids with its N- and C- terminals facing intracellularly.
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The first documented experiments dealing with EMG started with Francesco Redi’s works in 1666. Redi discovered a highly specialized muscle of the electric ray fish (Electric Eel) generated electricity. By 1773, Walsh had been able to demonstrate that the eel fish’s muscle tissue could generate a spark of electricity. In 1792, a publication entitled De Viribus Electricitatis in Motu Musculari Commentarius appeared, written by Luigi Galvani, in which the author demonstrated that electricity could initiate muscle contraction.
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Fully functional membrane Destroyed membrane ;Phospholipases :Phospholipase is an enzyme that transforms the phospholipid molecule into a lysophospholipid (soap) -> the new molecule attracts and binds fat and ruptures cell membranes. Phospholipase A2 is one specific type of phospholipases found in snake venom. :Snake example: Okinawan habu (Trimeresurus flavoviridis) ;Cardiotoxins / Cytotoxins :Cardiotoxins are components that are specifically toxic to the heart. They bind to particular sites on the surface of muscle cells and cause depolarisation -> the toxin prevents muscle contraction.
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A more recent technique has been developed called high-frequency irreversible electroporation (H-FIRE). This technique uses electrodes to apply bipolar bursts of electricity at a high frequency, as opposed to unipolar bursts of electricity at a low frequency. This type of procedure has the same tumor ablation success as N-TIRE. However, it has one distinct advantage, H-FIRE does not cause muscle contraction in the patient and therefore there is no need for a paralytic agent.
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Calcium is a ubiquitous second messenger with wide-ranging physiological roles. These include muscle contraction, neuronal transmission (as in an excitatory synapse), cellular motility (including the movement of flagella and cilia), fertilization, cell growth (proliferation), neurogenesis, learning and memory as with synaptic plasticity, and secretion of saliva. High levels of cytoplasmic Ca2+ can also cause the cell to undergo apoptosis. Other biochemical roles of calcium include regulating enzyme activity, permeability of ion channels, activity of ion pumps, and components of the cytoskeleton.
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The integral membrane protein encoded by this gene is a lysophosphatidic acid (LPA) receptor from a group known as EDG receptors. These receptors are members of the G protein-coupled receptor superfamily. Utilized by LPA for cell signaling, EDG receptors mediate diverse biologic functions, including proliferation, platelet aggregation, smooth muscle contraction, inhibition of neuroblastoma cell differentiation, chemotaxis, and tumor cell invasion. Alternative splicing of this gene has been observed and two transcript variants have been described, each encoding identical proteins.
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Non-depolarizing agents A decrease in binding of acetylcholine leads to a decrease in its effect and neuron transmission to the muscle is less likely to occur. It is generally accepted that non-depolarizing agents block by acting as reversible competitive inhibitors. That is, they bind to the receptor as antagonists and that leaves fewer receptors available for acetylcholine to bind. Depolarizing agents Depolarizing agents produce their block by binding to and activating the ACh receptor, at first causing muscle contraction, then paralysis.
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It has been noted that the MYH11 mutation could be responsible for at least 14% of hereditary thoracic aortic aneurisms particularly Type 6. This is because the mutated variant produces an incorrect filamentary assembly and a reduced capacity for vascular smooth muscle contraction. Degradation of the aortic media has been recorded in these individuals, with areas of disorganization and hyperplasia as well as stenosis of the aorta's vasa vasorum. The number of afflictions that the gene is implicated in is increasing.
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Blocking the channels leads to vasoconstriction and to an increase in blood pressure. The BK channel α subunit is expressed in muscle and nerve tissue and the BK channels are abundant in the brain. The BK channels modulate neurotransmitter release, the form of the action potential and repetitive firing. Inhibition of the channels can explain why there would be an increased release in excitatory neurotransmitters resulting in tremors, ataxia, hypersensitivity, increased smooth muscle contraction in the colon and an increased heart rate.
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Publisher: Academic Press, 1995. , two proteins that interact together to produce muscle contraction and relaxation. Myosin II, also known as conventional myosin, has two heavy chains that consist of the head and tail domains and four light chains (two per head) that bind to the heavy chains in the “neck” region. When the muscle needs to contract, calcium ions flow into the cytosol from the sarcoplasmic reticulum, where they activate calmodulin, which in turn activates myosin light-chain kinase (MLC kinase).
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Electromyographical biofeedback or myofeedback could provide patients who suffer from central facial palsy the ability to create myo-electrical potentials that they can interpret. This method provides patients with information about muscle contraction that is normally subliminal. Electromyographical biofeedback enables the patient to regain control of muscles that are involved in facial expression that have been atrophied. Brener’s model was one of the first models to describe the circuitry of the role of feedback for voluntary control of physiological processes.
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The hydantoin derivative dantrolene is a spasmolytic agent with a unique mechanism of action outside of the CNS. It reduces skeletal muscle strength by inhibiting the excitation- contraction coupling in the muscle fiber. In normal muscle contraction, calcium is released from the sarcoplasmic reticulum through the ryanodine receptor channel, which causes the tension-generating interaction of actin and myosin. Dantrolene interferes with the release of calcium by binding to the ryanodine receptor and blocking the endogenous ligand ryanodine by competitive inhibition.
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The legs swing (kip) up and provide momentum to assist in the explosive upward force needed to ascend above the bar. More advanced athletes can perform a strict variation of the muscle-up which is done slowly, without any kip. This variation begins with a swinging dead hang (or by standing still, with feet farther forward than the bar, if the person's feet can touch the ground) and uses muscle contraction to ascend above the bar in an explosive yet controlled fashion.
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The sm-M20 is suggested to play a regulatory role in muscle contraction by binding to MBS. MBS is also encoded by another gene, myosin light chain phosphatase target subunit 1. sm-M20 shows higher binding affinity to this gene product than to myosin light chain phosphatase target subunit 2-MBS even though the two MBS proteins are highly similar. Although both MBSs increase the activity of MLCP, myosin light chain phosphatase target subunit 1-MBS is a more efficient activator.
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It can move freely in a calligraphic stroke, or circumscribe, act as a planar definition, as a mathematical structural element (as in Golden Section) or as a path in motion (when it coordinates kinetic movements such as in muscle contraction). Artist's world is dynamic – in the state of becoming – rather than static. In ‘Dimension and Balance’, the line is related to psychological and social concepts of space. Klee explains subjectivity of our perception by comparing examples of optical illusion with horizon and perspective.
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Sport-specific training routines are used by many competitors. These often specify that the speed of muscle contraction during weight training should be the same as that of the particular sport. Sport- specific training routines also often include variations to both free weight and machine movements that may not be common for traditional weightlifting. Though weight training can stimulate the cardiovascular system, many exercise physiologists, based on their observation of maximal oxygen uptake, argue that aerobics training is a better cardiovascular stimulus.
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Epinephrine (adrenaline) Activation of β1 receptors induces positive inotropic, chronotropic output of the cardiac muscle, leading to increased heart rate and blood pressure, secretion of ghrelin from the stomach, and renin release from the kidneys. Activation of β2 receptors induces smooth muscle relaxation in the lungs, gastrointestinal tract, uterus, and various blood vessels. Increased heart rate and heart muscle contraction are associated with the β1 receptors; however, β2 cause vasodilation in the myocardium. β3 receptors are mainly located in adipose tissue.
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Super Slow is Hutchins trademarked name for the High intensity training approach advocated by Arthur Jones. It is based on ideas from the 1940s and 1960s called 10/10 "muscle contraction with measured movement" and implemented using fixed weight Nautilus machines. In more recent times such "Time Under Load" ideas have seen a renaissance with Dr Doug McGuff's best selling Body by Science. The 10 second lifting, 10 second lowering repetition speed of movement was suggested to Ken Hutchins by Dr. Vincent Bocchicchio.
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Uterine atony is defined as failure of the uterus to contract adequately following delivery. The loss of tone in the uterine musculature is a result of endogenous oxytocin that is released in the course of delivery. Normally, contraction of the uterine muscles during labor compresses the blood vessels and reduces flow, thereby increasing the likelihood of coagulation and preventing hemorrhage. A lack of uterine muscle contraction, however, can lead to an acute hemorrhage, as the uterine blood vessels are not sufficiently compressed.
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In (our recent) study, we report decorin to be differentially expressed and released in response to muscle contraction using different approaches. Decorin is released from contracting human myotubes, and circulating decorin levels are increased in response to acute resistance exercise in humans. Moreover, decorin expression in skeletal muscle is increased in humans and mice after chronic training. Because decorin directly binds myostatin, a potent inhibitor of muscle growth, we investigated a potential function of decorin in the regulation of skeletal muscle growth.
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The predominant symptom of Pisa syndrome is dystonia. Dystonia is a neurological movement disorder characterized by sustained muscle contraction leading to abnormal posture, twisting, and repetitive movement. In Pisa Syndrome specifically there is commonly a tonic flexion of the trunk of the body to one side, leading to a slight lean (reminiscent of the Leaning Tower of Pisa, hence the name "Pisa syndrome"). This is usually associated with a backward axial rotation of the spine and indifferent to markedly abnormal posture.
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Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. Four sequence-related potassium channel genes - shaker, shaw, shab, and shal - have been identified in Drosophila, and each has been shown to have human homolog(s). This gene encodes a member of the potassium channel, voltage-gated, shaker-related subfamily.
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At the active site, a substrate binds to an enzyme to induce a chemical reaction. Substrates, transition states, and products can bind to the active site, as well as any competitive inhibitors. For example, in the context of protein function, the binding of calcium to troponin in muscle cells can induce a conformational change in troponin. This allows for tropomyosin to expose the actin-myosin binding site to which the myosin head binds to form a cross-bridge and induce a muscle contraction.
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Embden conducted studies on carbohydrate metabolism and muscle contraction, and he was the first to discover and link together all the steps involved in the conversion of glycogen to lactic acid. In 1918, Otto Fritz Meyerhof's work on cellular metabolism showed that the process involved the breakdown of glucose to lactic acid. Embden is known for having worked out the precise steps involved in this breakdown. Henceforth, this cellular metabolic sequence from glycogen to lactic acid became known as the Embden–Meyerhof pathway.
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As the disease progresses, the muscular system is debilitated throughout the body, as the brain cannot control the contraction of muscles. Hypotonia (low muscle tone and strength), dystonia (involuntary, sustained muscle contraction), and ataxia (lack of control over movement) are often seen in people with Leigh disease. The eyes are particularly affected; the muscles that control the eyes become weak, paralyzed, or uncontrollable in conditions called ophthalmoparesis (weakness or paralysis) and nystagmus (involuntary eye movements). Slow saccades are also sometimes seen.
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This increase in calcium activates calcium-sensitive contractile proteins that then use ATP to cause cell shortening. The mechanism for muscle contraction evaded scientists for years and requires continued research and updating. The sliding filament theory was independently developed by Andrew F. Huxley and Rolf Niedergerke and by Hugh Huxley and Jean Hanson. Their findings were published as two consecutive papers published in the 22 May 1954 issue of Nature under the common theme "Structural Changes in Muscle During Contraction".
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Troponin C, skeletal muscle is a protein that in humans is encoded by the TNNC2 gene. Troponin (Tn), a key protein complex in the regulation of striated muscle contraction, is composed of 3 subunits. The Tn-I subunit inhibits actomyosin ATPase, the Tn-T subunit binds tropomyosin and Tn-C, while the Tn-C subunit binds calcium and overcomes the inhibitory action of the troponin complex on actin filaments. The protein encoded by this gene is the Tn-C subunit.
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Potassium voltage-gated channel subfamily E member 1 is a protein that in humans is encoded by the KCNE1 gene. Voltage-gated potassium channels (Kv) represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. KCNE1 is one of five members of the KCNE family of Kv channel ancillary or β subunits.
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The transport mechanism for tryptophan is shared with the branched chain amino acids (BCAAs), leucine, isoleucine, and valine. During extended exercise, BCAAs are consumed for skeletal muscle contraction, allowing for greater transport of tryptophan across the blood-brain barrier. None of the components of the serotonin synthesis reaction are saturated under normal physiological conditions,Newsholme, E. A., I. N. Acworth, and E. Bloomstrand. Amino acids, brain neurotransmitters and a functional link between muscle and brain that is important in sustained exercise.
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Tetany or tetanic seizure is a medical sign consisting of the involuntary contraction of muscles, which may be caused by disorders that increase the action potential frequency of muscle cells or the nerves that innervate them. Muscle cramps caused by the disease tetanus are not classified as tetany; rather, they are due to a lack of inhibition to the neurons that supply muscles. Tetanic contractions (physiologic tetanus) are a broad range of muscle contraction types, of which tetany is only one.
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This depolarization voltage spike triggers an action potential which propagates down the postsynaptic membrane leading to muscle contraction. It is important to note that EPPs are not action potentials, but that they trigger action potentials. In a normal muscular contraction, approximately 100-200 acetylcholine vesicles are released causing a depolarization that is 100 times greater in magnitude than a MEPP. This causes the membrane potential to depolarize +40mV (100 x 0.4mV = 40mV) from -100mV to -60mV where it reaches threshold.
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This is similar to a voltage gated calcium channel, but is not actually an ionotropic channel. Instead, it serves to activate Ryanodine, which will let calcium ions pass into the sarcoplasmic reticulum, and triggers calcium release to the muscle fiber itself. A T-tubule surrounded by two terminal cisternae is referred to as a " triad" in physiology. As previously explained, the terminal cisternae along with the transverse tubules are the mechanisms of transduction from a nervous impulse to an actual muscle contraction.
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Swammerdam did not believe the results of his own experiment, suggesting that they were the result of artifact. However, he concluded in his book The Book of Nature II that "motion or irritation of the nerve alone is necessary to produce muscular motion". This idea was an important step toward the current understanding of how nerves actually cause muscle contraction. Balloonist theory took a second hit from Francis Glisson who performed an experiment in which a man flexed a muscle under water.
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Possible biological contributors to dynapenia include the nervous system’s deteriorating control of voluntary skeletal muscle activation and a decreased number of functioning motor units. The nervous system's lowered ability to stimulate a full muscle contraction subsequently leads to loss of muscle strength and power. A study by Harridge et al. also showed that all dynapenic subjects had incomplete voluntary activation during a maximum contraction (69-93%), suggesting that loss of voluntary muscle activation plays an important role in the loss of muscle strength.
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Peripheral nervous system diseases may be further categorized by the type of nerve cell (motor, sensory, or both) affected by the disorder. Effective treatment of these diseases is often prevented by lack of understanding of the underlying molecular and genetic pathology. Epigenetic therapy is being investigated as a method of correcting the expression levels of misregulated genes in neurodegenerative diseases. Neurodengenerative diseases of motor neurons can cause degeneration of motor neurons involved in voluntary muscle control such as muscle contraction and relaxation.
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In 1980, Tansey pursued her undergraduate education at Stanford University in Palo Alto, California. She completed her Bachelors in Biological Sciences and then stayed at Stanford to complete her Master's in Biological Sciences as well. After graduating in 1985, Tansey pursued her graduate studies in Physiology and Cell Cycle Regulation at the University of Texas Southwestern Medical Center. Under the mentorship of James T. Stull, Tansey explored the role of myosin light chain kinase (MLCK) phosphorylation in the regulation of smooth muscle contraction.
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These proteins consist of rod-shaped coiled-coil hetero- or homo-dimers that lie along the α-helical groove of most actin filaments. Interaction occurs along the length of the actin filament, with dimers aligning in a head-to-tail fashion. Tropomyosins are often categorised into two groups, muscle tropomyosin isoforms and nonmuscle tropomyosin isoforms. Muscle tropomyosin isoforms are involved in regulating interactions between actin and myosin in the muscle sarcomere and play a pivotal role in regulated muscle contraction.
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This gene encodes a G-protein coupled receptor that binds sulfated members of the cholecystokinin (CCK) family of peptide hormones. This receptor is a major physiologic mediator of pancreatic enzyme secretion and smooth muscle contraction of the gallbladder and stomach. In the central and peripheral nervous system this receptor regulates satiety and the release of beta- endorphin and dopamine. The extracellular, N-terminal, domain of this protein adopts a tertiary structure consisting of a few helical turns and a disulfide- cross linked loop.
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Potassium channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. Four sequence-related potassium channel genes - shaker, shaw, shab, and shal - have been identified in Drosophila, and each has been shown to have human homolog(s). This gene encodes a member of the potassium channel, voltage-gated, shaker-related subfamily.
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Potassium channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. Four sequence-related potassium channel genes - shaker, shaw, shab, and shal - have been identified in Drosophila, and each has been shown to have human homolog(s). This gene encodes a member of the potassium channel, voltage-gated, shaker-related subfamily.
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KCNB1's regulation and propagation of current provides a means for regulatory control over several physiological functions. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and apoptosis. Voltage-gated potassium channels are essential in regulating neuronal membrane potential, and in contributing to action potential production and firing. In mammalian CNS neurons, KCNB1 is a predominant delayed rectifier potassium current that regulates neuronal excitability, action potential duration, and tonic spiking.
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The ease of ion movement along cardiac muscle fibers axes is such that action potentials are able to travel from one cardiac muscle cell to the next, facing only slight resistance. Each syncytium obeys the all or none law. Intercalated discs are complex adhering structures that connect the single cardiomyocytes to an electrochemical syncytium (in contrast to the skeletal muscle, which becomes a multicellular syncytium during mammalian embryonic development). The discs are responsible mainly for force transmission during muscle contraction.
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The extra-aural (unrelated to hearing) bioeffects on various internal organs and the central nervous system included auditory shifts, vibrotactile sensitivity change, muscle contraction, cardiovascular function change, central nervous system effects, vestibular (inner ear) effects, and chest wall/lung tissue effects. Researchers found that low-frequency sonar exposure could result in significant cavitations, hypothermia, and tissue shearing. No follow up experiments were recommended. Tests performed on mice show the threshold for both lung and liver damage occurs at about 184 dB.
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Researchers once attributed fatigue to a build-up of lactic acid in muscles. However, this is no longer believed. Rather, lactate may stop muscle fatigue by keeping muscles fully responding to nerve signals. The available oxygen and energy supply, and disturbances of muscle ion homeostasis are the main factor determining exercise performance, at least during brief very intense exercise. Each muscle contraction involves an action potential that activates voltage sensors, and so releases Ca2+ ions from the muscle fibre’s sarcoplasmic reticulum.
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Voltage-gated potassium channels (Kv) represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. KCNE3 encodes a member of the five-strong KCNE family of voltage- gated potassium (Kv) channel ancillary or β subunits. KCNE3 is best known for modulating the KCNQ1 Kv α subunit, but it also regulates hERG, Kv2.1, Kv3.
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However, transport of the mature spermatozoa through the remainder of the male reproductive system is achieved via muscle contraction rather than the spermatozoon's motility. A glycoprotein coat over the acrosome prevents the sperm from fertilizing the egg prior to traveling through the male and female reproductive tracts. Capacitation of the sperm by the enzymes FPP (fertilization promoting peptide, produced in the prostate gland) and heparin (in the female reproductive tract) removes this coat and allows sperm to bind to the egg.
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Hypoparathyroidism is decreased function of the parathyroid glands with underproduction of parathyroid hormone. This can lead to low levels of calcium in the blood, often causing cramping and twitching of muscles or tetany (involuntary muscle contraction), and several other symptoms. It is a very rare disease. The condition can be inherited, but it is also encountered after thyroid or parathyroid gland surgery, and it can be caused by immune system- related damage as well as a number of rarer causes.
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The main symptoms of hypoparathyroidism are the result of the low blood calcium level, which interferes with normal muscle contraction and nerve conduction. As a result, people with hypoparathyroidism can experience paresthesia, an unpleasant tingling sensation around the mouth and in the hands and feet, as well as muscle cramps and severe spasms known as "tetany" that affect the hands and feet. Many also report a number of subjective symptoms such as fatigue, headaches, bone pain and insomnia. Crampy abdominal pain may occur.
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Tedisamil also appears to provide specific, single channel blocking of IK-ATP at high concentrations. As the potassium channels are responsible for restoring the resting membrane potential during an action potential, lengthening their inactivation will stop the cycle of fibrillation by preventing muscle contraction until all ion channels are available to open. Regular use of tedisamil will prevent further fibrillation and restore normal electrical rhythm. Tedisamil’s antiarrythmic activity also appears to be supported by inhibiting sodium currents in cardiac muscle.
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Specialized testing called manometry can be performed to evaluate the motor function of the esophagus, which can help identify abnormal patterns of muscle contraction within the esophagus that are suggestive of DES. The treatment of DES consists primarily of medications, such as acid suppressing agents (like proton-pump inhibitors), calcium channel blockers, hyoscine butylbromide, or nitrates. In only extremely rare cases, surgery may be considered. People with DES have higher incidences of gastroesophageal reflux disease (GERD), neuromuscular diseases, and degenerative neurological disorders.
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ALDOA is a key enzyme in the fourth step of glycolysis, as well as in the reverse pathway gluconeogenesis. It catalyzes the reversible conversion of fructose-1,6-bisphosphate to glyceraldehydes-3-phosphate and dihydroxyacetone phosphate by aldol cleavage of the C3–C4 bond. As a result, it is a crucial player in ATP biosynthesis. ALDOA also contributes to other "moonlighting" functions such as muscle maintenance, regulation of cell shape and motility, striated muscle contraction, actin cytoskeleton organization, and regulation of cell proliferation.
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A simple view, that is almost certainly too limited and that dates back to the earliest work on the motor cortex, is that neurons in the motor cortex control movement by a feed- forward direct pathway. In that view, a neuron in the motor cortex sends an axon or projection to the spinal cord and forms a synapse on a motor neuron. The motor neuron sends an electrical impulse to a muscle. When the neuron in the cortex becomes active, it causes a muscle contraction.
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The amplitude of movements are based upon the antagonistic muscles forces and the amount of leverage the antagonistic muscle provides for movement. For the torsion motion, muscles are arranged in helical layers around a hydrostatic body. The fiber angle (the angle the fiber makes with the long axis of the body) plays a critical role in torsion, if the angle is greater than 54°44', during muscle contraction, torsion and elongation will occur. If the fiber angle is less than 54°44', torsion and shortening will occur.
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Biol Bull, 158(1):58–68, February 1980. The two dimensional stiffness allows for the body of the eel to be modeled a pressurized cylinder with the fiber angle of the cross helical arrangement dictating the method by which the eel moves. Eel skin behaves like skin having a fiber angle greater than 45°. In an eel with the cross helical fiber arrangement, muscle contraction in the anterior region bends the fish, and so the skin on the convex side is extended in the longitudinal direction.
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Guanosine is a purine nucleoside comprising guanine attached to a ribose (ribofuranose) ring via a β-N9-glycosidic bond. Guanosine can be phosphorylated to become guanosine monophosphate (GMP), cyclic guanosine monophosphate (cGMP), guanosine diphosphate (GDP), and guanosine triphosphate (GTP). These forms play important roles in various biochemical processes such as synthesis of nucleic acids and proteins, photosynthesis, muscle contraction, and intracellular signal transduction (cGMP). When guanine is attached by its N9 nitrogen to the C1 carbon of a deoxyribose ring it is known as deoxyguanosine.
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Potassium voltage-gated channel subfamily G member 1 is a protein that in humans is encoded by the KCNG1 gene. Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. This gene encodes a member of the potassium channel, voltage- gated, subfamily G. This gene is abundantly expressed in skeletal muscle.
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The pressor and uterine contraction effects of pituitary extracts, in contrast, remained unchanged, as did the effects of adrenaline on the heart and effects of parasympathetic nerve stimulation. Dale clearly saw the specificity of the ″paralytic″ (antagonist) effect of ergot for ″the so- called myoneural junctions connected with the true sympathetic or thoracic- lumbar division of the autonomic nervous system″ – the adrenoceptors. He also saw its specificity for the ″myoneural junctions″ mediating smooth muscle contraction as opposed to those mediating smooth muscle relaxation. But there he stopped.
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Pleurothotonus, commonly known as Pisa syndrome, is a rare neurological disorder which occurs due to prolonged exposure to antipsychotic drugs (which may also be referred to as neuroleptics). It is characterized by dystonia, and abnormal and sustained involuntary muscle contraction. This may cause twisting or jerking movements of the body or a body part. Although Pisa syndrome develops most commonly in those undergoing long-term treatment with antipsychotics, it has been reported less frequently in patients receiving other medications, such as an acetylcholinesterase inhibitor.
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For absorption through the skin the NOAEL is set to 150 mg/kg per day for rabbits, based on the reduction of food consumption. When methiocarb is fed to rats at a dose of 50 ppm, it gives a reduction of brain cholinesterase by 14% and 5% in males and females respectively. When methiocarb is administered as an aerosol to rats, the highest concentration (96 mg/m3 in solvent) showed signs of involuntary muscle contraction (tremors). These signs weren't observed in the other groups.
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In controlled release reversals of such concentric motions, the eccentric movement stretches the muscle with opposing force that is stronger than the muscle force. When myofilaments of the muscle fiber are stretched in such eccentric contractions there can be reduced numbers of detachments of cross bridge myosin and actin links. With more cross bridges remaining attached there is greater force production in the muscle. Examples of activities involving eccentric muscle contraction include walking down a hill or resisting the force of gravity while lowering a heavy object.
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These smooth muscle cells have muscarinic M3 receptors on their membrane. The activation of these receptors by acetylcholine will activate an intracellular G protein, that in turn will activate the phospholipase C pathway, that will end in an increase of intracellular calcium concentrations and therefore contraction of the smooth muscle cell. The muscle contraction will cause the diameter of the bronchus to decrease, therefore increasing its resistance to airflow. Bronchoconstriction is common in people with respiratory problems, such as asthma, COPD, and cystic fibrosis.
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Increases in cytoplasmic Ca2+ levels interfere with muscle contraction, leading to the characteristic symptoms of BD. In some cases of BD, no mutations in ATP2A1 have been observed. Disease transmission in cases of non- ATP2A1 BD have been characterized as autosomal dominant pattern of inheritance. These cases have revealed that the cause of the disease likely exhibits genetic heterogeneity, meaning the disease involves mutations in other locations within the genome (although no other loci have been identified in the development of BD as of now).
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If the muscle length changes while muscle tension remains the same, then the muscle contraction is isotonic. In an isotonic contraction, the muscle length can either shorten to produce a concentric contraction or lengthen to produce an eccentric contraction. In natural movements that underlie locomotor activity, muscle contractions are multifaceted as they are able to produce changes in length and tension in a time-varying manner. Therefore, neither length nor tension is likely to remain constant when the muscle is active during locomotor activity.
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In addition to this, it has already been shown that NO stimulates increased cyclic GMP (cGMP) levels in the smooth muscle cells, inducing a signaling cascade that results in the activation of cGMP-dependent protein kinase (PKG) and an ultimate decrease in smooth muscle Ca concentration. This leads to a decrease in muscle contraction and a subsequent dilation of the blood vessel. Whether the vessels are constricted or dilated dictates the amount of oxygen and glucose that is able to reach the neuronal tissue.
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Potassium voltage-gated channel, Shal-related subfamily, member 1 (KCND1), also known as Kv4.1, is a human gene. Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. Four sequence-related potassium channel genes - shaker, shaw, shab, and shal - have been identified in Drosophila, and each has been shown to have human homolog(s).
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For longer sarcomere lengths, this is the result of there being less overlap of the thin and thick filaments; for shorter sarcomere lengths, the cause is the decreased sensitivity for calcium by the myofilaments. An increase in filling of the ventricle increases the load experienced by each cardiac muscle fiber, stretching the fibers toward their optimal length. The stretching of the muscle fibers augments cardiac muscle contraction by increasing the calcium sensitivity of the myofibrils,Klabunde, Richard E. "Cardiovascular Physiology Concepts". Lippincott Williams & Wilkins, 2011, p. 74.
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Thanks to fusimotor activation, the afferent signal from muscle spindles remains efficient in monitoring large changes of muscle length without turning silent during muscle shortening. On the other hand, very small intramuscular events are monitored as well, thanks to the extreme sensitivity of the sense organ. An example is the small pulsatile component of the muscle contraction which is due to a periodic fluctuation at 8–10 Hz of the motor command. These small variations are insentient but readily monitored by the population of spindle afferents.
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Following his PhD, Huxley continued research on the structure and function of muscle. Since Cambridge did not have electron microscopy, which began to be used for biological studies at the time, he went to Massachusetts Institute of Technology as a postdoctoral fellow on a Commonwealth Fellowship in late summer of 1952. He work in F. O. Schmitt's laboratory where he was joined by Jean Hanson in 1953. Their collaboration proved to be fruitful as they discovered the so-called "sliding filament theory" of muscle contraction.
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Hill made many exacting measurements of the heat released when skeletal muscles contract and relax. A key finding was that heat is produced during contraction, which requires investment of chemical energy, but not during relaxation, which is passive. His earliest measurements used equipment left behind by the Swedish physiologist Magnus Blix, Hill measured a temperature rise of only 0.003 °C. After publication he learned that German physiologists had already reported on heat and muscle contraction and he went to Germany to learn more about their work.
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A cramp is a sudden, involuntary muscle contraction or overshortening; while generally temporary and non-damaging, they can cause significant pain and a paralysis-like immobility of the affected muscle. Onset is usually sudden and it resolves on its own over a period of several seconds, minutes, or hours. Cramps may occur in a skeletal muscle or smooth muscle. Skeletal muscle cramps may be caused by muscle fatigue or a lack of electrolytes such as sodium (a condition called hyponatremia), potassium (called hypokalemia), or magnesium (called hypomagnesemia).
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Functional electric stimulation (FES) is a NMES technique where nerves or muscles affected by stroke receive bursts of low-level electrical current. The goal of FES is to strengthen muscle contraction and improve motor control. It may be effective in reducing subluxation and the pain associated with subluxation. Different slings are available to manage shoulder subluxation. However, the use of slings remains controversial and may increase the risk of adverse effects on symmetry and balance between the left and right shoulders, and can impact peoples’ body image.
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The solution is heated, usually via an external heater/cooler water bath, to an appropriate test temperature for the muscle that is being tested. Muscles are stimulated to contract by applying electric current to either the nerve which innervates the muscle or via platinum electrodes placed in the circulating solution to evoke a response of the entire muscle. The servomotor detects changes in force and/or length due to muscle contraction. Stimulation level is often set to the level which ensures maximal motor unit recruitment.
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Two common stimuli for eliciting smooth muscle contraction are circulating epinephrine and activation of the sympathetic nervous system (through release of norepinephrine) that directly innervates the muscle. These compounds interact with cell surface adrenergic receptors. Such stimuli result in a signal transduction cascade that leads to increased intracellular calcium from the sarcoplasmic reticulum through IP3-mediated calcium release, as well as enhanced calcium entry across the sarcolemma through calcium channels. The rise in intracellular calcium complexes with calmodulin, which in turn activates myosin light-chain kinase.
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The balance between potassium and sodium is maintained by ion transporter proteins in the cell membrane. The cell membrane potential created by potassium and sodium ions allows the cell to generate an action potential—a "spike" of electrical discharge. The ability of cells to produce electrical discharge is critical for body functions such as neurotransmission, muscle contraction, and heart function. Disruption of this balance may thus be fatal: for example, ingestion of large amounts of potassium compounds can lead to hyperkalemia strongly influencing the cardiovascular system.
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According to the recommendations made by the Quebec Task Force, treatment for individuals with whiplash associated disorders grade 1–3 may include non-narcotic analgesics. Non-steroidal anti- inflammatory drugs may also be prescribed in the case of WAD 2 and WAD 3, but their use should be limited to a maximum of three weeks. Botulinum toxin A is used to treat involuntary muscle contraction and spasms. Botulinum toxin type-A is only temporary and repeated injections need to take place in order to feel the effects.
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Neuromuscular junctions are the focal point where a motor neuron attaches to a muscle. Acetylcholine, (a neurotransmitter used in skeletal muscle contraction) is released from the axon terminal of the nerve cell when an action potential reaches the microscopic junction called a synapse. A group of chemical messengers cross the synapse and stimulate the formation of electrical changes, which are produced in the muscle cell when the acetylcholine binds to receptors on its surface. Calcium is released from its storage area in the cell's sarcoplasmic reticulum.
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An impulse from a nerve cell causes calcium release and brings about a single, short muscle contraction called a muscle twitch. If there is a problem at the neuromuscular junction, a very prolonged contraction may occur, such as the muscle contractions that result from tetanus. Also, a loss of function at the junction can produce paralysis. Skeletal muscles are organized into hundreds of motor units, each of which involves a motor neuron, attached by a series of thin finger-like structures called axon terminals.
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Rottlerin has been reported to be a PKCδ inhibitor. PKCδ has been implicated in depressing cardiac function and cell death after ischemia-reperfusion injury as well as promoting vascular smooth muscle contraction and decreasing perfusion. However, the role of rottlerin as a specific PKCδ inhibitor has been questioned. There have been several studies using rottlerin as a PKCδ selective inhibitor based on in vitro studies, but some studies showed it did not block PKCδ activity and did block other kinase and non-kinase proteins in vitro.
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Diacetyl has been shown to alter the amino acid arginine which could interfere with protein structure and function. Additionally diacetyl can bind to DNA and form guanosine adducts which can cause DNA uncoiling and cell death. In vitro studies on human cells also suggest that diacetyl alters the structure and function of the extracellular matrix and modifies epithelial cell responses to growth factors. Human cells exposed to diacetyl also increase secretion of substance P which causes mucus hypersecretion, airway smooth muscle contraction, and edema.
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In absence of external interventions, the umbilical cord occludes physiologically shortly after birth, explained both by a swelling and collapse of Wharton's jelly in response to a reduction in temperature and by vasoconstriction of the blood vessels by smooth muscle contraction. In effect, a natural clamp is created, halting the flow of blood. In air at 18 °C, this physiological clamping will take three minutes or less. In water birth, where the water temperature is close to body temperature, normal pulsation can be 5 minutes and longer.
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Protein kinase C epsilon type (PKCε) is an enzyme that in humans is encoded by the PRKCE gene. PKCε is an isoform of the large PKC family of protein kinases that play many roles in different tissues. In cardiac muscle cells, PKCε regulates muscle contraction through its actions at sarcomeric proteins, and PKCε modulates cardiac cell metabolism through its actions at mitochondria. PKCε is clinically significant in that it is a central player in cardioprotection against ischemic injury and in the development of cardiac hypertrophy.
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The idea that nerve stimulation led to movement had important implications for neuroscience by putting forward the idea that behaviour is based on stimuli. Swammerdam's research had been referenced before its publication by Nicolas Steno, who had visited Swammerdam in Amsterdam. Swammerdam's research concluded after Steno had published the second edition of Elements of Myology in 1669, which is referenced in Biblia Naturae. A letter from Steno to Malpighi from 1675 suggests that Swammerdam's findings on muscle contraction had caused his crisis of consciousness.
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As part of the Troponin complex, the function of cTnT is to regulate muscle contraction. The N-terminal region of TnT that strongly binds actin most likely moves with Tm and actin during strong myosin crossbridge binding and force generation. This region is likely involved in the transduction of cooperativity down the thin filament. The C-terminal region of TnT constitutes part of the globular troponin complex domain, and participates in employing the calcium sensitivity of strong myosin crossbridge binding to the thin filament.
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Tm functions in association with the troponin complex to regulate the calcium-dependent interaction of actin and myosin during muscle contraction. Tm molecules are arranged head-to-tail along the actin thin filament, and are a key component in cooperative activation of muscle. A three state model has been proposed by McKillop and Geeves, which describes the positions of Tm during a cardiac cycle. The blocked (B) state occurs in diastole when intracellular calcium is low and Tm blocks the myosin binding site on actin.
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Latrotoxin (α-Latrotoxin) found in venom of widow spiders also affects the neuromuscular junction by causing the release of acetylcholine from the presynaptic cell. Mechanisms of action include binding to receptors on the presynaptic cell activating the IP3/DAG pathway and release of calcium from intracellular stores and pore formation resulting in influx of calcium ions directly. Either mechanism causes increased calcium in presynaptic cell, which then leads to release of synaptic vesicles of acetylcholine. Latrotoxin causes pain, muscle contraction and if untreated potentially paralysis and death.
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Hydrophobic binding of cNTnC to the "switch" region of troponin I, cTnI148-159, stabilizes the Ca2+-bound open conformation of cNTnC (increasing the Ca2+ binding affinity of cNTnC from about Kd = 5 μM to Kd = 0.8 μM). This binding event removes the adjacent cTnI inhibitory regions from actin and stabilizes tropomyosin in its default "closed" position on the thin filament, allowing actin-myosin cross- bridging and muscle contraction to proceed. Strong actin-myosin interaction can further shift the thin filament into the "open" position.
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An isolated cardiac muscle cell, beating The physiology of cardiac muscle shares many similarities with that of skeletal muscle. The primary function of both muscle types is to contract, and in both cases, a contraction begins with a characteristic flow of ions across the cell membrane known as an action potential. The action potential subsequently triggers muscle contraction by increasing the concentration of calcium within the cytosol. However, the mechanism by which calcium concentrations within the cytosol rise differ between skeletal and cardiac muscle.
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In cardiac muscle, opening of the L-type calcium channel permits influx of calcium into the cell. The calcium binds to the calcium release channels (RYRs) in the SR, opening them; this phenomenon is called "calcium- induced calcium release", or CICR. However the RYRs are opened, either through mechanical-gating or CICR, Ca2+ is released from the SR and is able to bind to troponin C on the actin filaments. The muscles then contract through the sliding filament mechanism, causing shortening of sarcomeres and muscle contraction.
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A tetanic contraction (also called tetanized state, tetanus, or physiologic tetanus, the latter to differentiate from the disease called tetanus) is a sustained muscle contraction evoked when the motor nerve that innervates a skeletal muscle emits action potentials at a very high rate. During this state, a motor unit has been maximally stimulated by its motor neuron and remains that way for some time. This occurs when a muscle's motor unit is stimulated by multiple impulses at a sufficiently high frequency. Each stimulus causes a twitch.
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DAG remains associated with the plasma membrane, while IP3 is released into the cytoplasm. IP3 then diffuses through the cytosol and binds to IP3 receptors on the endoplasmic reticulum or sarcoplasmic reticulum, resulting in the opening of a membrane channel and an influx of calcium ions into the cytoplasm. Calcium serves as a second messenger for various downstream cellular events including glycogen metabolism, muscle contraction, neurotransmitter release, and transcriptional regulation. Therefore, calcium homeostasis is essential for proper cell function and response to extracellular signals.
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PP1 plays an instrumental role in glycogen metabolism through its responsibility for the interconversion between phosphorylase a and b. Protein phosphatase 1 (PP1) belongs to a certain class of phosphatases known as protein serine/threonine phosphatases. This type of phosphatase includes metal-dependent protein phosphatases (PPMs) and aspartate-based phosphatases. PP1 has been found to be important in the control of glycogen metabolism, muscle contraction, cell progression, neuronal activities, splicing of RNA, mitosis, cell division, apoptosis, protein synthesis, and regulation of membrane receptors and channels.
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Numerous in vitro experimental data indicate that calponin 1 functions as an inhibitory regulator of smooth muscle contractility through inhibiting actomyosin interactions. In this regulation, binding of Ca2+-calmodulin and PKC phosphorylation dissociate calponin 1 from the actin filament and facilitate smooth muscle contraction. In vivo data also support the role of calponin 1 as regulator of smooth muscle contractility. While aortic smooth muscle of adult Wistar Kyoto rats, which naturally lacks calponin 1, is fully contractile, it has a decreased sensitivity to norepinephrine activation.
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Gap junction alpha-1 protein (GJA1), also known as connexin 43 (Cx43), is a protein that in humans is encoded by the GJA1 gene on chromosome 6. As a connexin, GJA1 is a component of gap junctions, which allow for gap junction intercellular communication (GJIC) between cells to regulate cell death, proliferation, and differentiation. As a result of its function, GJA1 is implicated in many biological processes, including muscle contraction, embryonic development, inflammation, and spermatogenesis, as well as diseases, including oculodentodigital dysplasia (ODDD), heart malformations, and cancers.
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Voltage-gated potassium channel subunit beta-1 is a protein that in humans is encoded by the KCNAB1 gene. Potassium channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. Four sequence-related potassium channel genes - shaker, shaw, shab, and shal - have been identified in Drosophila, and each has been shown to have human homolog(s).
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This can be quantified using multi-frequency tympanometry. Thus, a high resonant- frequency pathology such as otosclerosis can be differentiated from low resonant-frequency pathologies such as ossicular discontinuity. In the absence of a pathology, a loud sound (generally greater than 70 dB above threshold) causes the stapedius muscle to contract, reducing the admittance of the middle ear and softening the perceived loudness of the sound. If the mobility of the stapes is reduced due to otosclerosis, then stapedius muscle contraction does not significantly decrease the admittance.
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Parabutoxins block Shaker-related voltage-gated potassium channels members 1,2 and 3 (Kv1.1, Kv1.2 and Kv1.3 channels). These channels have different functions that include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction and cell volume. PBTxs have a weak affinity towards Kvα1 channels. The dissociation constants (Kd) for Kv1.1, Kv1.2 and Kv1.3 channels are, respectively, 21.1 μM, 1.0 μM and 0.8 μM in the case of PBTx1 and 79 μM, 500 nM and 500 nM for PBTx3.
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Body heat is generated by metabolism. This refers to the chemical reactions cells use to break down glucose into water and carbon dioxide and, in so doing, generate ATP (adenosine triphosphate), a high-energy compound used to power other cellular processes. Muscle contraction is a type of metabolic process that generates heat energy, and heat is also generated through friction when blood flows through the circulatory system. All organisms metabolize food and other inputs, but some make better use of the output than others.
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Because the presence of calcium in the cytosol is required for muscle contraction, blockers of calcium channels prevent the muscles from building tension. Blockers of the L-type calcium channels, which occur in cardiac and smooth muscles, thus act as smooth muscle relaxants and inhibitors of cardiac contractions. Common blockers of L-type calcium channels are 1,4-dihydropyridines, which are used in treatment of cardiovascular diseases. Because of their activity as a relaxant, they can relax smooth muscles surrounding blood vessels, thus widening them and lowering the blood pressure.
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Also, the inspiration during respiration provides a suction pressure within the lumen. The semilunar valves are directed towards the flow of the lymph and open when the pressure in the first lymphangion is greater than the pressure in the next lymphangion. Pressure in the first lymphangion may increase because of smooth muscle contraction (in lymph vessel) or because of pressure on the walls from outside (in a capillary) result because of. Alternatively, pressure within the next lymphangion may decrease because of negative pressure as a result of inspiration.
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Sotalol non- selectively binds to both β1- and β2-adrenergic receptors preventing activation of the receptors by their stimulatory ligand (catecholamines). Without the binding of this ligand to the receptor, the G-protein complex associated with the receptor cannot activate production of cyclic AMP, which is responsible for turning on calcium inflow channels. A decrease in activation of calcium channels will therefore result in a decrease in intracellular calcium. In heart cells, calcium is important in generating electrical signals for heart muscle contraction, as well as generating force for this contraction.
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There is some evidence that desmin may also connect the sarcomere to the extracellular matrix (ECM) through desmosomes which could be important in signalling between the ECM and the sarcomere which could regulate muscle contraction and movement. Finally, desmin may be important in mitochondria function. When desmin is not functioning properly there is improper mitochondrial distribution, number, morphology and function. Since desmin links the mitochondria to the sarcomere it may transmit information about contractions and energy need and through this regulate the aerobic respiration rate of the muscle cell.
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The arrangement of connective tissue fibers determines the range of motion of a body, and serves as an antagonist against muscle contraction. The most commonly observed connective tissue arrangement for soft bodied animals consists of layers of alternating right and left-handed helices of connective tissue fibers which surround the hydraulic body. This cross helical arrangement is seen in the tube feet starfish, different types of worms and suckers in octopus. This cross helical arrangement allows for the connective tissue layers to evenly distribute force throughout the hydrostatic body.
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The extension in the longitudinal direction produces contraction in the hoop direction as the fiber angle decreases until these dimensional changes are resisted by the body of the eel. The skin becomes skin, and additional longitudinal force(applied by skin) results in force being transmitted along the tail. Therefore, changes in fiber angle of the cross helical arrangement in eel skin allows for the transmission of force through the skin during swimming. The skin act like an external tendon allowing for an eel to generate a greater propulsive force per muscle contraction.
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This peristaltic action is the primary driving force, moving lymph within its vessel walls. The regulation of the frequency and power of contraction is regulated by the sympathetic nervous system. Lymph movement can be influenced by the pressure of nearby muscle contraction, arterial pulse pressure and the vacuum created in the chest cavity during respiration, but these passive forces contribute only a minor percentage of lymph transport. The fluids collected are pumped into continually larger vessels and through lymph nodes, which remove debris and police the fluid for dangerous microbes.
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For suction feeding a system of linked four-bar linkages is responsible for the coordinated opening of the mouth and 3-D expansion of the buccal cavity. Other linkages are responsible for protrusion of the premaxilla. Linkages are also present as locking mechanisms, such as in the knee of the horse, which enables the animal to sleep standing, without active muscle contraction. In pivot feeding, used by certain bony fishes, a four-bar linkage at first locks the head in a ventrally bent position by the alignment of two bars.
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The muscle weakness seen in those with Andersen–Tawil syndrome arises from the depolarisation of the resting membrane potential caused by a decrease in /K1. The depolarised resting membrane potential means that sodium channels which are responsible for initiating action potentials are unable to fully recover from inactivation, leading to a less excitable membrane and less forceful muscle contraction. The mechanisms underlying the skeletal abnormalities seen in Andersen–Tawil syndrome have not been fully explained. Possibilities include impaired function of osteoclasts, cells which regulate bone growth, or disruption of the bone morphogenetic protein signalling cascade.
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Second-degree burn after a high tension line accident Heating due to resistance can cause extensive and deep burns. When applied to the hand, electricity can cause involuntary muscle contraction, producing the "no-let- go" phenomenon, and increasing the risk for serious burns. Voltage levels of 500 to 1000 volts tend to cause internal burns due to the large energy (which is proportional to the duration multiplied by the square of the voltage divided by resistance) available from the source. Damage due to current is through tissue heating and/or electroporation injury.
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Together they discovered the so-called "sliding filament theory", the underpinning idea on muscle contraction. Their publication in the 22 May 1954 issue of Nature became a landmark in muscle physiology. They provided the strong evidence for the theory in 1956, in which they showed electron microscopic details of the shortening and elongation of muscle fibres against each other. Even then the theory was not easily embraced, even in 1960 at a symposium of biomacromolecules held in Pittsburgh, Pasadena, scientists including the Nobel laureate Paul Flory argued against the sliding process.
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Voltage-gated potassium channels (Kv) represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. The KCNE4 gene encodes KCNE4 (originally named MinK-related peptide 3 or MiRP3), a member of the KCNE family of voltage-gated potassium (Kv) channel ancillary or β subunits. KCNE4 is best known for modulating the KCNQ1 Kv α subunit, but it also regulates KCNQ4, Kv1.
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Electrochemotherapy employs lower dosages of chemotherapeutic drugs than standard chemotherapy protocols; thus, the patient's burden usually associated to chemotherapy is not present. In the clinical use of electrochemotherapy, limited side effects related to bleomycin or cisplatin use are recorded. Provided that appropriate anesthesia is used for alleviation of the symptoms associated with application of electric pulses, the control of the pain level during the electrochemotherapy acceptable for the patients. Other than pain, which is limited to the treated tumor and surrounding tissue, muscle contraction during electric pulse delivery is the only other discomfort.
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He unveiled the fast- changing electricity associated with muscle contraction and nerve excitation – the action potentials. At the same time, du Bois-Reymond also reported in detail less fluctuating electricity at wounds – injury current and potential – he made to himself. Figure 5 - Some sample cell types and their resting potentials, revealing that actively proliferating and plastic cells cluster in the depolarized end of the continuum, while terminally-differentiated mature cell types tend to be strongly polarized. Bioelectricity work began in earnest at the beginning of the 20th century.
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This binding partly stabilizes the protein in the active form. The phosphorylase kinase is completely activated when the β and α subunits are phosphorylated by protein kinase A and the delta subunit has bound to calcium ions. In muscle cells, phosphorylation of the α and β subunits by PKA is the result of a cAMP-mediated cell signaling cascade initiated by the binding of epinephrine to β-adrenergic receptors on the cell surface. Additionally, the release of calcium ions from the sarcoplasmic reticulum during muscle contraction inactivates the inhibitory δ subunit and activates PhK fully.
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Onset of PLS usually occurs spontaneously after age 50 and progresses gradually over a number of years, or even decades. The disorder usually begins in the legs, but it may start in the tongue or the hands. Symptoms may include difficulty with balance, weakness and stiffness in the legs, and clumsiness. Other common symptoms are spasticity (involuntary muscle contraction due to the stretching of muscle, which depends on the velocity of the stretch) in the hands, feet, or legs, foot dragging, and speech and swallowing problems due to involvement of the facial muscles.
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Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. KCNE5 encodes a membrane protein, KCNE5 (originally named KCNE1-L) that has sequence similarity to the KCNE1 gene product, a member of the potassium channel, voltage-gated, isk-related subfamily. The KCNE gene family comprises five genes in the human genome, each encoding a type I membrane protein.
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Vitamin D, also coined as the sunshine vitamin, is necessary within a child's diet as it allows body tissues and in particular bone to be properly nourished and mineralized. Vitamin D3, which is gained from dietary nutrients, is also essential for calcium absorption and homeostasis, which ensures standard muscle contraction and the transport of blood throughout the body. Without adequate consumption of vitamin D, children can become predisposed to conditions such as rickets, which is the "softening or weakening of bones". which can only be treated with vitamin D supplements, sunlight and surgery.
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The mentalis is a paired central muscle of the lower lip, situated at the tip of the chin. It originates from the mentum and inserts into the chin soft tissue. The primary effect of the mentalis contraction is the upward-inward movement of the soft tissue complex of the chin, which raises the central portion of the lips in turn. In the setting of lip incompetence (the upper and lower lips do not touch each other at rest), the mentalis muscle contraction can bring temporary but strained oral competence.
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Structure of neuromuscular junction. A neuromuscular junction is a chemical synapse formed by the contact between a motor neuron and a muscle fiber. It is the site in which a motor neuron transmits a signal to a muscle fiber to initiate muscle contraction. The sequence of events that results in the depolarization of the muscle fiber at the neuromuscular junction begins when an action potential is initiated in the cell body of a motor neuron, which is then propagated by saltatory conduction along its axon toward the neuromuscular junction.
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Their conclusion states that the observation: This was the discovery of "Sliding Filament Theory", the first scientific evidence and the basis of modern understanding of muscle contraction. Contrary to scientific view of the time they found that the muscle as a whole do not contract of expand, but it was individual group of the muscle fibres (called I or light bands), while other fibres (A or dark bands) are never changed. The very "hypothesis" was experimentally proved in 1966. Niedergerke moved from Cambridge to London in 1955, joining the Biophysics Department at University College London.
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Skeletal muscle, with myofibrils labeled at upper right and sarcoplasmic reticulum at bottom Muscle contraction begins with the brain setting off action potentials, which are waves in the electrical charges that extend along neurons. The waves travel to a group of cells in a muscle, letting calcium ions out from the cells' sarcoplasmic reticula (SR), which are storage areas for calcium. The released calcium lets myofibrils contract under the power of energy-carrying adenosine triphosphate (ATP) molecules. Meanwhile, the calcium is quickly pumped back into the SR by fast calcium pumps.
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NDO is a dysfunction of the bladder that results from disease or injury in the nervous system. NDO may be related to congenital conditions (often-inherited conditions beginning at or before birth), such as spina bifida (myelomeningocele), or other conditions such as spinal cord injury. With NDO, there is overactivity of the bladder wall muscle, which normally relaxes to allow storage of urine. The bladder wall muscle overactivity results in sporadic bladder muscle contraction, which increases pressure in the bladder and decreases the volume of urine the bladder can hold.
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This prevents moving muscles from working against the contraction force of antagonist muscles. Thus, during voluntary movement, the Ia inhibitory interneurons are used to coordinate muscle contraction. Further, the Ia inhibitory interneurons allow the higher centers to coordinate commands sent to the two muscles working opposite of each other at a single joint via a single command. The interneuron receives the input command from the corticospinal descending axons in such a way that the descending signal, which activates the contraction of one muscle, causes relaxation of the other muscles.
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At low doses it acts through the sympathetic nervous system to increase heart muscle contraction force and heart rate, thereby increasing cardiac output and blood pressure. Higher doses also cause vasoconstriction that further increases blood pressure. Older literature also describes very low doses thought to improve kidney function without other consequences, but recent reviews have concluded that doses at such low levels are not effective and may sometimes be harmful. While some effects result from stimulation of dopamine receptors, the prominent cardiovascular effects result from dopamine acting at α1, β1, and β2 adrenergic receptors.
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Impulses are passed from the central nervous system down neurons until they reach the motor neuron, which releases the neurotransmitter acetylcholine (ACh) into the neuromuscular junction. ACh binds to nicotinic acetylcholine receptors on the surface of the muscle cell and opens ion channels, allowing sodium ions to flow into the cell and potassium ions to flow out; this ion movement causes a depolarization, which allows for the release of calcium ions within the cell. Calcium ions bind to proteins within the muscle cell to allow for muscle contraction; the ultimate consequence of a stimulus.
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It may also include a request for any medications the person is taking. Documentation required may include x-rays, ASIA scale results, or Modified Ashworth Scale scores. One of the standard means of assessing functional classification is the bench test, which is used in swimming, lawn bowls and wheelchair fencing. Using the Adapted Research Council (MRC) measurements, muscle strength is tested using the bench press for a variety of spinal cord related injuries with a muscle being assessed on a scale of 0 to 5. A 0 is for no muscle contraction.
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It may also include a request for any medications the person is taking. Documentation that may be required my include x-rays, ASIA scale results, or Modified Ashworth Scale scores. One of the standard means of assessing functional classification is the bench test, which is used in swimming, lawn bowls and wheelchair fencing. Using the Adapted Research Council (MRC) measurements, muscle strength is tested using the bench press for a variety of spinal cord related injuries with a muscle being assessed on a scale of 0 to 5. A 0 is for no muscle contraction.
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It may also include a request for any medications the person is taking. Documentation that may be required my include X-rays, ASIA scale results, or Modified Ashworth Scale scores. One of the standard means of assessing functional classification is the bench test, which is used in swimming, lawn bowls and wheelchair fencing. Using the Adapted Research Council (MRC) measurements, muscle strength is tested using the bench press for a variety of spinal cord related injuries with a muscle being assessed on a scale of 0 to 5. A 0 is for no muscle contraction.
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It may also include a request for any medications the person is taking. Documentation that may be required my include x-rays, ASIA scale results, or Modified Ashworth Scale scores. One of the standard means of assessing functional classification is the bench test, which is used in swimming, lawn bowls and wheelchair fencing. Using the Adapted Research Council (MRC) measurements, muscle strength is tested using the bench press for a variety of spinal cord related injuries with a muscle being assessed on a scale of 0 to 5. A 0 is for no muscle contraction.
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It may also include a request for any medications the person is taking. Documentation that may be required my include x-rays, ASIA scale results, or Modified Ashworth Scale scores. One of the standard means of assessing functional classification is the bench test, which is used in swimming, lawn bowls and wheelchair fencing. Using the Adapted Research Council (MRC) measurements, muscle strength is tested using the bench press for a variety of spinal cord related injuries with a muscle being assessed on a scale of 0 to 5. A 0 is for no muscle contraction.
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It may also include a request for any medications the person is taking. Documentation that may be required may include X-rays, ASIA scale results, or Modified Ashworth Scale scores. One of the standard means of assessing functional classification is the bench test, which is used in swimming, lawn bowls and wheelchair fencing. Using the Adapted Research Council (MRC) measurements, muscle strength is tested using the bench press for a variety of spinal cord related injuries with a muscle being assessed on a scale of 0 to 5. A 0 is for no muscle contraction.
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The complex of C3b(2)Bb is a protease which cleaves C5 into C5b and C5a. C5 convertase is also formed by the classical pathway when C3b binds C4b and C2b. C5a is an important chemotactic protein, helping recruit inflammatory cells. C3a is the precursor of an important cytokine (adipokine) named ASP (although this is not universally accepted ) and is usually rapidly cleaved by carboxypeptidase B. Both C3a and C5a have anaphylatoxin activity, directly triggering degranulation of mast cells as well as increasing vascular permeability and smooth muscle contraction.
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In this electron micrograph of a cell, the cleavage furrow has nearly completely divided the cell. Cilliate undergoing the last processes of binary fission, with the cleavage furrow being clearly visible. In cell biology, the cleavage furrow is the indentation of the cell's surface that begins the progression of cleavage, by which animal and some algal cells undergo cytokinesis, the final splitting of the membrane, in the process of cell division. The same proteins responsible for muscle contraction, actin and myosin, begin the process of forming the cleavage furrow, creating an actomyosin ring.
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Activated mast cells and basophils undergo a process called degranulation, during which they release histamine and other inflammatory chemical mediators (cytokines, interleukins, leukotrienes, and prostaglandins) from their granules into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve stimulation, and smooth muscle contraction. This results in rhinorrhea, itchiness, dyspnea, and anaphylaxis. Depending on the individual, allergen, and mode of introduction, the symptoms can be system-wide (classical anaphylaxis), or localized to particular body systems; asthma is localized to the respiratory system and eczema is localized to the dermis.
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Generally, when faced with a dangerous stimuli, fish will contract their axial muscle, resulting a C-shaped contraction away from the stimulus. This response occurs in two separate stages: a muscle contraction that allows them to speed away from a stimulus (stage 1), and a sequential contralateral movement (stage 2). This escape is also known as a "fast-start response". The majority of the fish respond to an external stimulus (pressure changes) within 5 to 15 milliseconds, while some will exhibit a slower response taking up to 80 milliseconds.
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The proposed chemical mechanism does not depend on the concentration of the substrates or products in the medium. However, a shift in their concentration mainly causes free energy changes in the first and final steps of the reactions () and () due to the changes in the free energy content of every molecule, whether S or P, in water solution. This approach is in accordance with the following mechanism of muscle contraction. The final step of ATP hydrolysis in skeletal muscle is the product release caused by the association of myosin heads with actin.
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In invertebrate smooth muscle, contraction is initiated with the binding of calcium directly to myosin and then rapidly cycling cross-bridges, generating force. Similar to the mechanism of vertebrate smooth muscle, there is a low calcium and low energy utilization catch phase. This sustained phase or catch phase has been attributed to a catch protein that has similarities to myosin light-chain kinase and the elastic protein-titin called twitchin. Clams and other bivalve mollusks use this catch phase of smooth muscle to keep their shell closed for prolonged periods with little energy usage.
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A coronary catheterization is a minimally invasive procedure to access the coronary circulation and blood filled chambers of the heart using a catheter. It is performed for both diagnostic and interventional (treatment) purposes. Coronary catheterization is one of the several cardiology diagnostic tests and procedures. Specifically, through the injection of a liquid radiocontrast agent and illumination with X-rays, angiocardiography allows the recognition of occlusion, stenosis, restenosis, thrombosis or aneurysmal enlargement of the coronary artery lumens; heart chamber size; heart muscle contraction performance; and some aspects of heart valve function.
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Cardiac muscle troponin T (cTnT) is a protein that in humans is encoded by the TNNT2 gene. Cardiac TnT is the tropomyosin-binding subunit of the troponin complex, which is located on the thin filament of striated muscles and regulates muscle contraction in response to alterations in intracellular calcium ion concentration. The TNNT2 gene is located at 1q32 in the human chromosomal genome, encoding the cardiac muscle isoform of troponin T (cTnT). Human cTnT is an ~36-kDa protein consisting of 297 amino acids including the first methionine with an isoelectric point (pI) of 4.88.
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Nonmuscle tropomyosin isoforms function in all cells, both muscle and nonmuscle cells, and are involved in a range of cellular pathways that control and regulate the cell's cytoskeleton and other key cellular functions. The actin filament system that is involved in regulating these cellular pathways is more complex than the actin filament systems that regulates muscle contraction. The contractile system relies upon 4 actin filament isoforms and 5 tropomyosin isoforms, whereas the actin filament system of the cytoskeleton uses two actin filament isoforms and over 40 tropomyosin isoforms.
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In a number of cases, brain areas are organized into topographic maps, where adjoining bits of the cortex correspond to adjoining parts of the body, or of some more abstract entity. A simple example of this type of correspondence is the primary motor cortex, a strip of tissue running along the anterior edge of the central sulcus. Motor areas innervating each part of the body arise from a distinct zone, with neighboring body parts represented by neighboring zones. Electrical stimulation of the cortex at any point causes a muscle-contraction in the represented body part.
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Because the intracellular calcium ion concentration is extremely low (see above) the entry of minute quantities of calcium ions from the endoplasmic reticulum or from the extracellular fluids, cause rapid, very marked, and readily reversible changes in the relative concentration of these ions in the cytosol. This can therefore serve as a very effective intracellular signal (or "second messenger") in a variety of circumstances, including muscle contraction, the release of hormones (e.g. insulin from the beta cells in the pancreatic islets) or neurotransmitters (e.g. acetylcholine from pre-synaptic terminals of nerves) and other functions.
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This may be followed by a tonic–clonic seizure consisting of two phases: intense muscle contraction occurs for several seconds (tonic phase); followed by rapid spasms of alternate muscle relaxation and contraction producing convulsive jerking (clonic phase). The seizure ends with a period of unconsciousness (the postictal state). The onset of seizure depends upon the partial pressure of oxygen in the breathing gas and exposure duration. However, exposure time before onset is unpredictable, as tests have shown a wide variation, both amongst individuals, and in the same individual from day to day.
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A representation of glucose molecules linked by α-1,4-glycosidic bonds, with a single α-1,6-glycosidic bond leading to a branch off of the chain. Glycogen is a molecular polymer of glucose (a polysaccharide) used to store energy, and is important for maintaining glucose homeostasis in the blood, as well as for providing energy for skeletal muscle and cardiac muscle contraction. Molecules of glucose are linked into linear chains by α-1,4-glycosidic bonds. Additionally, branches of glucose are formed off of the chain by α-1,6-glycosidic bonds.
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In 1961, Shimomura and Johnson isolated the protein aequorin, and its small molecule cofactor, coelenterazine, from large numbers of Aequorea jellyfish at Friday Harbor Laboratories. They discovered, after initially finding bright luminescence on adding seawater to a purified sample, that calcium ions (Ca2+) were required to trigger bioluminescence. This research also marked the beginning of research into green fluorescent protein which was summarized by Shimomura. In 1967, Ridgeway and Ashley microinjected aequorin into single muscle fibers of barnacles, and observed transient calcium ion-dependent signals during muscle contraction.
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The function of liver glycogen is to maintain glucose homeostasis, generating glucose via glycogenolysis to compensate for the decrease of glucose levels that can occur between meals. Thanks to the presence of the glucose-6-phosphatase enzyme, the hepatocytes are capable of turning glycogen to glucose, releasing it into blood to prevent hypoglycemia. In skeletal muscle, glycogen is used as an energy source for muscle contraction during exercise. The different functions of glycogen in muscle or liver make the regulation mechanisms of its metabolism differ in each tissue.
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In addition to the actin and myosin components that constitute the sarcomere, skeletal muscle fibers also contain two other important regulatory proteins, troponin and tropomyosin, that are necessary for muscle contraction to occur. These proteins are associated with actin and cooperate to prevent its interaction with myosin. Skeletal muscle cells are excitable and are subject to depolarization by the neurotransmitter acetylcholine, released at the neuromuscular junction by motor neurons. Once a cell is sufficiently stimulated, the cell's sarcoplasmic reticulum releases ionic calcium (Ca2+), which then interacts with the regulatory protein troponin.
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Therefore, in cardiac muscle, activation of PKA, through the cyclic AMP pathway, results in increased muscle contraction (via RyR2 phosphorylation) and increased relaxation (via phospholamban phosphorylation), which increases heart rate. The mechanism behind the termination of calcium release through the RyR is still not fully understood. Some researchers believe it is due to the random closing of ryanodine receptors (known as stochastic attrition), or the ryanodine receptors becoming inactive after a calcium spark, while others believe that a decrease in SR calcium, triggers the receptors to close (see calcium sparks for more details).
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As the space within the lumen of the T-tubule is continuous with the space that surrounds the cell (the extracellular space), ion concentrations between the two are very similar. However, due to the importance of the ions within the T-tubules (particularly calcium in cardiac muscle), it is very important that these concentrations remain relatively constant. As the T-tubules are very thin, they essentially trap the ions. This is important as, regardless of the ion concentrations elsewhere in the cell, T-tubules still have enough calcium ions to permit muscle contraction.
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Neuromuscular blocking agents exert its effect by modulating the signal transmission in skeletal muscles. An action potential is, in other words, a depolarisation in neurone membrane due to a change in membrane potential greater than the threshold potential leads to an electrical impulse generation. The electrical impulse travels along the pre-synaptic neurone axon to synapse with the muscle at the neuromuscular junction (NMJ) to cause muscle contraction. When the action potential reaches the axon terminal, it triggers the opening of the calcium ion gated channels, which causes the influx of Ca2+.
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Potassium voltage-gated channel, shaker-related subfamily, member 3, also known as KCNA3 or Kv1.3, is a protein that in humans is encoded by the KCNA3 gene. Potassium channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. Four sequence-related potassium channel genes – shaker, shaw, shab, and shal – have been identified in Drosophila, and each has been shown to have human homolog(s).
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Kavain has anticonvulsive properties, attenuating vascular smooth muscle contraction through interactions with voltage-dependent Na+ and Ca2+ channels. How this effect is mediated and to what extent this mechanism is involved in the anxiolytic and analgesic effects of kavalactones on the central nervous system is unknown. Kavain's pharmacological activities have not been sufficiently investigated, and neither its effect as a serotonin reuptake inhibitor nor its monoamine (norepinephrine) uptake inhibitions and activation of NMDA receptors have been confirmed. The mechanism behind the psychotropic, sedative, and anxiolytic actions of kavain and related kavalactones is still debated.
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Due to a short half-life, propofol, is a quick-acting medication whose administration and removal is well tolerated, with hypotension being the limiting factor in its continued use. Additionally, the use of nondepolarizing neuromusclar blocking agents (NMBA), such as doxacurium or atracurium, have been indicated to facilitate ventilation and manage brain injuries but there are no controlled studies on the use of NMBAs in the management of increased intracranial pressure. Depolarizing neuromuscular blocking agents, most notably succinylcholine, can worsen increased ICP due to induction of muscle contraction within the body.
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Its effects, depending on dosage, include an increase in sodium excretion by the kidneys, an increase in urine output, an increase in heart rate, and an increase in blood pressure. At low doses it acts through the sympathetic nervous system to increase heart muscle contraction force and heart rate, thereby increasing cardiac output and blood pressure. Higher doses also cause vasoconstriction that further increases blood pressure. While some effects result from stimulation of dopamine receptors, the prominent cardiovascular effects result from dopamine acting at α1, β1, and β2 adrenergic receptors.
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In 1914 he was elected to the Chair of Biochemistry at Cambridge University, thus becoming the first Professor in that discipline at Cambridge. His Cambridge students included neurochemistry pioneer Judah Hirsch Quastel and pioneer embryologist Joseph Needham. Hopkins had for a long time studied how cells obtain energy via a complex metabolic process of oxidation and reduction reactions. His study in 1907 with Sir Walter Morley Fletcher of the connection between lactic acid and muscle contraction was one of the central achievements of his work on the biochemistry of the cell.
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When a motor unit is activated, all of its fibers contract. In vertebrates, the force of a muscle contraction is controlled by the number of activated motor units. The number of muscle fibers within each unit can vary within a particular muscle and even more from muscle to muscle; the muscles that act on the largest body masses have motor units that contain more muscle fibers, whereas smaller muscles contain fewer muscle fibers in each motor unit. For instance, thigh muscles can have a thousand fibers in each unit, while extraocular muscles might have ten.
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Typically, this protein is broken into three domains, domains AB, CD and EF, each individually containing a helix-loop-helix motif. The AB domain houses a two amino-acid deletion in the loop region, whereas domains CD and EF contain the N-terminal and C-terminal, respectively. Calcium binding proteins like parvalbumin play a role in many physiological processes, namely cell-cycle regulation, second messenger production, muscle contraction, organization of microtubules and phototransduction. Therefore, calcium-binding proteins must distinguish calcium in the presence of high concentrations of other metal ions.
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Glycogenolysis takes place in the cells of the muscle and liver tissues in response to hormonal and neural signals. In particular, glycogenolysis plays an important role in the fight- or-flight response and the regulation of glucose levels in the blood. In myocytes (muscle cells), glycogen degradation serves to provide an immediate source of glucose-6-phosphate for glycolysis, to provide energy for muscle contraction. In hepatocytes (liver cells), the main purpose of the breakdown of glycogen is for the release of glucose into the bloodstream for uptake by other cells.
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Whytt's theories on the nervous system and its role on movement opposed many of the teachings that were in place in the 18th century. During that time, many physiologists still supported Descartes' theory of movement which hypothesized that muscle contraction was due to the activation of a fluid in the nervous system called animal spirits. Physiologists, such as Whytt's colleague, Albrecht von Haller, also believed that muscles were capable of action independent of the nerves. Whytt strongly advocated against Descartes' theory, and explicitly denied the concept of animal spirits.
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Potassium voltage-gated channel subfamily H member 1 is a protein that in humans is encoded by the KCNH1 gene. Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. This gene encodes a member of the potassium channel, voltage- gated, subfamily H. This member is a pore-forming (alpha) subunit of a voltage-gated non-inactivating delayed rectifier potassium channel.
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In mice, NADA was shown to induce the tetrad of physiological paradigms associated with cannabinoids: hypothermia, hypo-locomotion, catalepsy, and analgesia. NADA has been found to play a regulatory role in both the peripheral and central nervous systems, and displays antioxidant and neuroprotectant properties. NADA has also been implicated in smooth muscle contraction and vasorelaxation in blood vessels. Additionally, NADA has been observed to suppress inflammatory activation of human Jurkat T cells and to inhibit the release of prostaglandin E2 (PGE2) from lipopolysaccharide (LPS)-activated astrocytes, microglia and mouse brain ECs (MEC-Brain).
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Myoclonus is defined as a sequence of repeated, often nonrhythmic, brief, shock-like jerks due to sudden involuntary contraction or relaxation of one or more muscles. These movements may be asynchronous, in which several muscles contract variably in time, synchronous, in which muscles contract simultaneously, or spreading, in which several muscles contract sequentially. It is characterized by a sudden, unidirectional movement due to muscle contraction, followed by a relaxation period in which the muscle is no longer contracted. However, when this relaxation phase is decreased, as when muscle contractions become faster, a myoclonic tremor results.
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Some key roles of TPCs include calcium dependent responses in muscle contraction(s), hormone secretion, fertilization, and differentiation. Disorders linked to TPCs include membrane trafficking, Parkinson’s disease, Ebola, and fatty liver. As implied by their name, TPC channels possess two pores and were named for their two Shaker-like repeats, which each have a pore domain. This contrasts with two-pore-domain potassium channels, which confusingly have only one pore and were named for the fact that each subunit has two P (pore) domains in its primary sequence.
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Muscle contraction as a means of moving spermatozoa through the reproductive system into and out of the storage structures has been examined in Diptera, Orthoptera, and Lepidoptera as well as in the species Rhodnius prolixus and the boll weevil. In R. prolixus, rhythmic peristaltic contractions of the oviduct cause contractions of the bursa copulatrix and spermatheca movement. This movement of the spermatheca results in spermatozoa migration into the spermathecal duct and into the spermatheca reservoir. In the boll weevil, contractions are also used to move sperm from the spermathecae so they can fertilize the egg.
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The presence of these rods is not itself causing muscle weakness; rather they appear as a result of something going wrong within the muscle fiber. There is no connection between the number of rods found in the muscle cells and the amount of weakness a person has. All of the different gene mutations leading to the condition called nemaline myopathy that have been found so far are in genes that encode different components of the sarcomere. In normal muscle cells, the various parts of the muscle fibers that make up the sarcomere are distributed evenly in a pattern for effective muscle contraction.
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Andrew Huxley and Niedergerke introduced it as a "very attractive" hypothesis. Before the 1950s there were several competing theories on muscle contraction, including electrical attraction, protein folding, and protein modification. The novel theory directly introduced a new concept called cross-bridge theory (classically swinging cross-bridge, now mostly referred to as cross-bridge cycle) which explains the molecular mechanism of sliding filament. Cross-bridge theory states that actin and myosin form a protein complex (classically called actomyosin) by attachment of myosin head on the actin filament, thereby forming a sort of cross-bridge between the two filaments.
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The first muscle protein discovered was myosin by a German scientist Willy Kühne, who extracted and named it in 1864. In 1939 a Russian husband and wife team Vladimir Alexandrovich Engelhardt and Militsa Nikolaevna Lyubimova discovered that myosin had an enzymatic (called ATPase) property that can breakdown ATP to release energy. Albert Szent-Györgyi, a Hungarian physiologist, turned his focus on muscle physiology after winning the Nobel Prize in Physiology or Medicine in 1937 for his works on vitamin C and fumaric acid. He demonstrated in 1942 that ATP was the source of energy for muscle contraction.
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In muscle cells, actomyosin myofibrils make up much of the cytoplasmic material. These myofibrils are made of thin filaments of actin (typically around 7 nm in diameter), and thick filaments of the motor-protein myosin (typically around 15 nm in diameter). These myofibrils use energy derived from ATP to create movements of cells, such as muscle contraction. Using the hydrolysis of ATP for energy, myosin heads undergo a cycle during which they attach to thin filaments, exert a tension, and then, depending on the load, perform a power stroke that causes the thin filaments to slide past, shortening the muscle.
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In addition to his administrative and teaching duties, he continued to work actively on muscle contraction, and also made theoretical contributions to other work in the department, such as that on animal reflectors. In 1963, he was jointly awarded the Nobel Prize in Physiology or Medicine for his part in discoveries concerning the ionic mechanisms of the nerve cell. In 1969 he was appointed to a Royal Society Research Professorship, which he held in the Department of Physiology at University College London. In 1980, Huxley was elected as President of the Royal Society, a post he held until 1985.
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The mechanism of action of Cardiac contractility modulation has been subject to continuous research since its initial discovery. Based on animal testing and experiments on human myocardial tissue obtained by biopsies, essential parts of the mechanism of action have been identified. According to current understanding (as of February 2015), the mechanism of action of Cardiac contractility modulation may be summarized in the following manner: The signals applied during the electrical non-excitatory state of the cardiac muscle cells (the absolute refractory period) cause an increase in myocyte calcium in the cytosol during systole. This increases the muscle contraction strength.
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Myoclonic dystonia or Myoclonus dystonia syndrome is a rare movement disorder that induces spontaneous muscle contraction causing abnormal posture. The prevalence of myoclonus dystonia has not been reported, however, this disorder falls under the umbrella of movement disorders which affect thousands worldwide. Myoclonus dystonia results from mutations in the SGCE gene coding for an integral membrane protein found in both neurons and muscle fibers. Those suffering from this disease exhibit symptoms of rapid, jerky movements of the upper limbs (myoclonus), as well as distortion of the body's orientation due to simultaneous activation of agonist and antagonist muscles (dystonia).
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In a large proportion (50–70%) of cases, the propensity for malignant hyperthermia is due to a mutation of the ryanodine receptor (type 1), located on the sarcoplasmic reticulum (SR), the organelle within skeletal muscle cells that stores calcium. RYR1 opens in response to increases in intracellular level mediated by L-type calcium channels, thereby resulting in a drastic increase in intracellular calcium levels and muscle contraction. RYR1 has two sites believed to be important for reacting to changing concentrations: the A-site and the I-site. The A-site is a high affinity binding site that mediates RYR1 opening.
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Muscle contraction results from an attachment–detachment cycle between the myosin heads extending from myosin filaments and the sites on actin filaments. The myosin head first attaches to actin together with the products of ATP hydrolysis, performs a power stroke associated with release of hydrolysis products, and detaches from actin upon binding with new ATP. The detached myosin head then hydrolyses ATP, and performs a recovery stroke to restore its initial position. The strokes have been suggested to result from rotation of the lever arm domain around the converter domain, while the catalytic domain remains rigid.
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Initially, the visual stimuli is first received by the visual thalamus and relayed to the amygdala for potential danger. The visual thalamus also relays the information to the visual cortex and is processed to see if the stimuli poses a potential threat. If so, this information is relayed to the amygdala and the muscle contraction, increased heart rate and blood pressure begins, thus activating the sympathetic neuronal pathway. A presentation of a neutral visual stimuli has been shown to intensify the percept of fear or suspense induced by a different channel of information, such as audition.
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Since that time almost all rehabilitation involving muscle contraction has been done with a symmetrical rectangular biphasic waveform. During the 1940s, however, the U.S. War Department, investigating the application of electrical stimulation not just to retard and prevent atrophy but to restore muscle mass and strength, employed what was termed galvanic exercise on the atrophied hands of patients who had an ulnar nerve lesion from surgery upon a wound.Licht, "History of Electrotherapy" These galvanic exercises employed a monophasic waveform, direct current. The American Physical Therapy Association, a professional organization representing physical therapists, accepts the use of electrotherapy in the field of physical therapy.
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A calcium spark is the microscopic release of calcium (Ca2+) from a store known as the sarcoplasmic reticulum (SR), located within muscle cells. This release occurs through an ion channel within the membrane of the SR, known as a ryanodine receptor (RyR), which opens upon activation.Lanner, J.T., Georgiou, D.K., Joshi, A.D. and Hamilton, S.L. (2010) 'Ryanodine receptors: Structure, expression, molecular details, and function in calcium release', 2(11) This process is important as it helps to maintain Ca2+ concentration within the cell. It also initiates muscle contraction in skeletal and cardiac muscles and muscle relaxation in smooth muscles.
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This period is approximately equal to the absolute refractory period (ARP), it occurs because the fast sodium channels remain closed until the cell fully repolarizes. During this period, depolarization on adjacent cardiac muscles does not produce a new depolarization in the current cell as it has to refract back to phase 4 of the action potential before a new action potential can activate it. ERP acts as a protective mechanism and keeps the heart rate in check and prevents arrhythmias, and it helps coordinates muscle contraction. Anti-arrhythmic agents used for arrhythmias usually prolong the ERP.
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In 1951 they were joined by James Watson. 1953 was an annus mirabilis: Watson and Crick discovered the double-helical structure of DNA, which revealed that biological information was encoded in a linear structure and how this information could be duplicated during cell division. Perutz discovered that the detailed three-dimensional structures of proteins, such as myoglobin and hemoglobin could, in principle, be solved by X-ray analysis using a heavy metal atom labeling technique. Hugh Huxley discovered that muscle contraction works by a sliding filament mechanism. In 1957 the group's name was changed to the “MRC Unit for Molecular Biology”.
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The epinephrine and norepinephrine strike the beta receptors of the heart, which feeds the heart's sympathetic nerve fibres to increase the strength of heart muscle contraction; as a result, more blood gets circulated, increasing the heart rate and respiratory rate. The sympathetic nervous system also stimulates the skeletal system and muscular system to pump more blood to those areas to handle the acute stress. Simultaneously, the sympathetic nervous system inhibits the digestive system and the urinary system to optimise blood flow to the heart, lungs, and skeletal muscles. This plays a role in the alarm reaction stage.
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In the human Enteric Nervous System, the slow-wave threshold is the potential which must be reached before a slow wave can be propagated in gut wall smooth muscle. Slow waves themselves seldom cause any smooth muscle contraction (Except for, probably in the stomach). When the amplitude of slow waves in smooth muscle cells reaches a certain threshold—the slow-wave threshold—the L-type Ca2+ channels are activated, resulting in calcium influx and initiation of motility. Slow waves are generated at unique intrinsic frequencies by the interstitial cells of Cajal, even within the same organ.
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Engelmann's major contribution to the field of physiology emerged from a study lasting from 1873 to 1897, in which he observed the contractions of striated muscles. Focusing on the visible bands of fibers in the muscles, he noted that the volume of the anisotropic band increased during contraction, whereas the volume of the isotropic band decreased. He theorized that it was this interaction between the two bands which allowed for muscle contraction. He also demonstrated, after experiments with dissected frogs in 1875, that contractions of the heart were caused by the heart muscle itself, not an external nerve stimulus, as was previously believed.
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PLA1's are present in numerous species including humans, and have a variety of cellular functions that include regulation and facilitation of the production of lysophospholipid mediators, and acting as digestive enzymes. These enzymes are responsible for fast turnover rates of cellular phospholipids. In addition to this, the products of the reaction catalyzed by PLA1 which are a fatty acid and a lysophospholipid are important in various biological functions such as platelet aggregation and smooth muscle contraction. In addition, lysophospholipids can be found as surfactants in food techniques and cosmetics, and can be used in drug delivery.
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Potassium voltage-gated channel, subfamily H (eag-related), member 5, also known as KCNH5, is a human gene encoding the Kv10.2 protein. Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. This gene encodes a member of the potassium channel, voltage-gated, subfamily H. This member is a pore-forming (alpha) subunit of a voltage-gated non-inactivating delayed rectifier potassium channel.
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One exception was a paper in 1844 that reported on a series of experiments on dogs and established the importance of bile in digestion. In examining processes such as muscle contraction, fermentation, digestion, and putrefaction, Schwann sought to show that living phenomena were the result of physical causes rather than "some immaterial vital force". Nonetheless, he still sought to reconcile "an organic nature" with "a divine plan." Some writers have suggested that Schwann's move in 1838, and his decreased scientific productivity after that, reflect religious concerns and perhaps even a crisis relating to the theoretical implications of his work on cell theory.
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Given the proposed manner of action of the muscle pump to increase arterial blood flow, it would seem impossible for a muscle contraction and skeletal muscle hyperemia to be uncoupled. Another experiment recently was only able to find evidence that vasodilation, not the skeletal muscle pump was responsible for maintaining proper pressure and blood return. However, this might have to do with the lack of rigorous physiological tests thus far used to be able to prove the pump. Experiments have shown the use of passive leg exercises where only vasodilation was responsible for increased blood return.
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In the 1950s he was one of the first to use electron microscopy to study biological specimens. During his postdoctoral at Massachusetts Institute of Technology, he, with fellow researcher Jean Hanson, discovered the underlying principle of muscle movement, popularised as the sliding filament theory in 1954. After 15 years of research, he proposed the "swinging cross-bridge hypothesis" in 1969, which became modern understanding of the molecular basis of muscle contraction, and much of other cellular motility. Huxley worked at University College London for seven years, and at Laboratory of Molecular Biology for fifteen years, where he was its Deputy Director from 1979.
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Physical therapists might use neuromuscular/sensory stimulation techniques such as quick stretch, resistance, joint approximation, and tapping to increase tone by facilitating or enhancing muscle contraction in patients with hypotonia. For patients who demonstrate muscle weakness in addition to hypotonia strengthening exercises that do not overload the muscles are indicated. Electrical Muscle Stimulation, also known as Neuromuscular Electrical Stimulation (NMES) can also be used to “activate hypotonic muscles, improve strength, and generate movement in paralyzed limbs while preventing disuse atrophy (p.498).” When using NMES it is important to have the patient focus on attempting to contract the muscle(s) being stimulated.
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Electromyography (EMG) recordings of demonstrate the triphasic muscle activation begins with a brief agonist motor unit activation signal with firing rates of 60 to 120 Hz that may last for 100ms and occurs 50 to 100ms before movement begins. The firing rates of ballistic movements are much higher than that of slow ramp movements (5–15 Hz). The brief agonist muscle contraction is thus followed by antagonist muscle unit activation. The degree of antagonist muscle unit activation is dependent on the task at hand unlike the first agonist muscle activation which is independent to environmental stimuli.
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Mutations altering the usual structure and function of this sodium channel therefore disrupt regulation of muscle contraction, leading to episodes of severe muscle weakness or paralysis. Mutations have been identified in residues between transmembrane domains III and IV which make up the fast inactivation gate of Nav1.4. Mutations have been found on the cytoplasmic loops between the S4 and S5 helices of domains II, III and IV, which are the binding sites of the inactivation gate. The pathological mechanism of SCN4A mutations in hyperkalemic periodic paralysis is complex, but explains the autosomal dominant and hyperkalemia-related aspects of the disease.
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In biochemistry, a cholinesterase or choline esterase is a family of esterases that lyses choline-based esters, several of which serve as neurotransmitters. Thus, it is either of two enzymes that catalyze the hydrolysis of these cholinergic neurotransmitters, such as breaking acetylcholine into choline and acetic acid. These reactions are necessary to allow a cholinergic neuron to return to its resting state after activation. For example, in muscle contraction, acetylcholine at a neuromuscular junction triggers a contraction; but for the muscle to relax afterward, rather than remaining locked in a tense state, the acetylcholine must be broken down by a choline esterase.
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This is in conflict with the suggested unitary nature of stroke as a relatively simple shape. In the research field of handwriting motor control, the term ballistic stroke is used. It is defined as the trajectory segment between two consecutive minima in the absolute velocity of the pen tip. The time delay between the cortical brain command and a muscle contraction is so large that the 100 millisecond ballistic strokes need to be planned in advance by the brain, as feedback by hand-eye coordination requires a much slower movement than is the case in the normal handwriting process.
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Force spectroscopy measures the behavior of a molecule under stretching or torsional mechanical force. In this way a great deal has been learned in recent years about the mechanochemical coupling in the enzymes responsible for muscle contraction, transport in the cell, energy generation (F1-ATPase), DNA replication and transcription (polymerases), DNA unknotting and unwinding (topoisomerases and helicases). As a single-molecule technique, as opposed to typical ensemble spectroscopies, it allows a researcher to determine properties of the particular molecule under study. In particular, rare events such as conformational change, which are masked in an ensemble, may be observed.
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Later his research focussed on the role of the endothelium- derived hyperpolarizing factor (EDHF) and in particular on the role of gap junctions. He conducted research in three areas: endothelial control of arterial tone by nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF;,"Using nitrosomonas bacteria to enhance vascular, sexual and skin health". US Patent 7820420 B2, David R. Whitlock. applications of “Chaos Theory” and nonlinear mathematics in the analysis of microcirculatory perfusion and modelling of the cellular mechanisms that underpin smooth muscle contraction, and applications of computational fluid dynamics and magnetic resonance angiography in large artery haemodynamics.
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February 1986 He discovered that venous blood flow is pulsatile which, prior to Rai's discovery, was described only as linear flow. He is best known for his discovery of the mechanical function of atrial chambers of the heart. With experimental evidence on the canine heart, he discovered that atrial diastole is the key force that creates a negative pressure that brings blood back to the heart. Diastole is an - active expansion of the muscle on which the cardiac return depends. This is an addition to Starling’s law of muscle contraction that muscle not only actively contracts but expands as well.
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A transthoracic echocardiogram (TTE) is the most common type of echocardiogram, which is a still or moving image of the internal parts of the heart using ultrasound. In this case, the probe (or ultrasonic transducer) is placed on the chest or abdomen of the subject to get various views of the heart. It is used as a non-invasive assessment of the overall health of the heart, including a patient's heart valves and degree of heart muscle contraction (an indicator of the ejection fraction). The images are displayed on a monitor for real-time viewing and then recorded.
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In invertebrates, depending on the neurotransmitter released and the type of receptor it binds, the response in the muscle fiber could be either excitatory or inhibitory. For vertebrates, however, the response of a muscle fiber to a neurotransmitter can only be excitatory, in other words, contractile. Muscle relaxation and inhibition of muscle contraction in vertebrates is obtained only by inhibition of the motor neuron itself. This is how muscle relaxants work by acting on the motor neurons that innervate muscles (by decreasing their electrophysiological activity) or on cholinergic neuromuscular junctions, rather than on the muscles themselves.
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During quiet breathing, there is little or no muscle contraction involved in exhalation; this process is simply driven by the elastic recoil of the lungs. When forceful exhalation is required, or when the elasticity of the lungs is reduced (as in emphysema), active exhalation can be achieved by contraction of the abdominal wall muscles (rectus abdominis, transverse abdominis, external oblique muscle and internal oblique muscle). These press the abdominal organs cranially (upward) into the diaphragm, reducing the volume of the thoracic cavity. The internal intercostal muscles have fibres that are angled obliquely downward and backward from rib to rib.
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Stimulation of a motor neuron causes it to release acetylcholine, which is stored up in vesicles at the axon terminal. The acetylcholine binds to nicotinic receptors on the muscle fiber, which open sodium channels and depolarizes the muscle cell. As nerve stimulation is rapidly repeated, the acetylcholine stored in the nerve terminal is gradually depleted, and there is a slight weakening of the acetylcholine signal sent to the muscle fiber, resulting in smaller endplate potentials (EPPs). In normal muscle, although the EPPs become smaller with repetitive stimulation, they remain above the threshold needed to trigger muscle contraction.
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Brenner was born in Stuttgart, capital of Baden-Württenberg state in Germany. He studied Medicine at the University of Tübingen between the years of 1969-1975. In 1980, Bernhard Brenner became associate researcher visitor at National Institute of Health (NIH) where he clarified that, when the muscle is in its relaxed state, the complex tropomyosin-troponin does not block cross-bridge bounds to actin. Due to this revelation, the pathway of muscle contraction was decoded, and then he correlated a rate of force for muscle redevelopment under calcium regulation called KTR to the number of cross-bridges turnover kinetics.
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A diagram of the structure of a myofibril (consisting of many myofilaments in parallel, and sarcomeres in series Sliding filament model of muscle contraction A myofibril (also known as a muscle fibril) is a basic rod-like unit of a muscle cell. Muscles are composed of tubular cells called myocytes, known as muscle fibres in striated muscle, and these cells in turn contain many chains of myofibrils. They are created during embryonic development in a process known as myogenesis. Myofibrils are composed of long proteins including actin, myosin, and titin, and other proteins that hold them together.
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This influx of sodium ions generates the EPP (depolarization), and triggers an action potential which travels along the sarcolemma and into the muscle fiber via the T-tubules (transverse tubules) by means of voltage- gated sodium channels. The conduction of action potentials along the T-tubules stimulates the opening of voltage-gated Ca2+ channels which are mechanically coupled to Ca2+ release channels in the sarcoplasmic reticulum. The Ca2+ then diffuses out of the sarcoplasmic reticulum to the myofibrils so it can stimulate contraction. The endplate potential is thus responsible for setting up an action potential in the muscle fiber which triggers muscle contraction.
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Central nervous system oxygen toxicity manifests as symptoms such as visual changes (especially tunnel vision), ringing in the ears (tinnitus), nausea, twitching (especially of the face), behavioural changes (irritability, anxiety, confusion), and dizziness. This may be followed by a tonic–clonic seizure consisting of two phases: intense muscle contraction occurs for several seconds (tonic phase); followed by rapid spasms of alternate muscle relaxation and contraction producing convulsive jerking (clonic phase). The seizure ends with a period of unconsciousness (the postictal state). The onset of seizure depends upon the partial pressure of oxygen in the breathing gas and exposure duration.
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MLC-2v plays a key role in the regulation of cardiac muscle contraction, through its interactions with myosin. Loss of MLC-2v in mice is associated with ultrastructural defects in sarcomere assembly and results in dilated cardiomyopathy and heart failure with reduced ejection fraction, leading to embryonic lethality at E12.5. More recently, a mutation in zebrafish tell tale heart (telm225) that encodes MLC-2, demonstrated that cardiac MLC-2 is required for thick filament stabilization and contractility in the embryonic zebrafish heart. The role of Myl2 mutations in pathogenesis has been determined through the generation of a number of mouse models.
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The columella, the central pillar within the shell, serves as the attachment point for the white columellar muscle. Contraction of this strong muscle allows the animal's soft parts to shelter in the shell in response to undesirable stimuli. Aliger gigas has an unusual means of locomotion, first described in 1922 by George Howard Parker (1864–1955). The animal first fixes the posterior end of the foot by thrusting the point of the sickle-shaped operculum into the substrate, then it extends the foot in a forward direction, lifting and throwing the shell forward in a so-called leaping motion.
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The extensor muscle contraction is quite slow (almost isometric), which allows it to develop high force (up to 14 N in the desert locust), but because it is slow only low power is needed. The third stage of the jump is the trigger relaxation of the flexor muscle, which releases the tibia from the flexed position. The subsequent rapid tibial extension is driven mainly by the relaxation of the elastic structures, rather than by further shortening of the extensor muscle. In this way the stiff cuticle acts like the elastic of a catapult, or the bow of a bow-and-arrow.
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Hyperglycemia-induced involuntary movements, which, in this case, did not consist of typical hemiballismus but rather of hemichorea (dance-like movements of one side of the body; initial movements of the right arm in the video) and bilateral dystonia (slow muscle contraction in legs, chest, and right arm) in a 62-year-old Japanese woman with type 1 diabetes. Symptoms vary according to the kind of dystonia involved. In most cases, dystonia tends to lead to abnormal posturing, in particular on movement. Many sufferers have continuous pain, cramping, and relentless muscle spasms due to involuntary muscle movements.
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In the 1940s, neurosurgeon Wilder Penfield and his neurologist colleague Herbert Jasper developed a technique of brain mapping to help reduce side effects caused by surgery to treat epilepsy. They stimulated motor and somatosensory cortices of the brain with small electrical currents to activate discrete brain regions. They found that stimulation of one hemisphere's motor cortex produces muscle contraction on the opposite side of the body. Furthermore, the functional map of the motor and sensory cortices is fairly consistent from person to person; Penfield and Jasper's famous pictures of the motor and sensory homunculi were the result.
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Like skeletal muscle, depolarization causes the opening of voltage-gated calcium channels and release of Ca2+ from the t-tubules. This influx of calcium causes calcium-induced calcium release from the sarcoplasmic reticulum, and free Ca2+ causes muscle contraction. After a delay, potassium channels reopen, and the resulting flow of K+ out of the cell causes repolarization to the resting state. There are important physiological differences between nodal cells and ventricular cells; the specific differences in ion channels and mechanisms of polarization give rise to unique properties of SA node cells, most importantly the spontaneous depolarizations necessary for the SA node's pacemaker activity.
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Adrenergic receptor autoantibodies The adrenergic receptors (or adrenoreceptors) are a class of cell membrane-bound protein receptors throughout the body that are targets of the catecholamines, especially norepinephrine (or noradrenaline) and epinephrine (or adrenaline). The binding to these receptors by catecholamines will generally stimulate the sympathetic nervous system, the arm of the autonomic nervous system responsible for the fight-or-flight response. The mechanism of adrenergic receptors. Adrenaline or noradrenaline are receptor ligands to either α1, α2 or β-adrenergic receptors. α1 couples to Gq, which results in increased intracellular Ca2+ and subsequent smooth muscle contraction.
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In the SAN cAMP binds to an ion channel involved in action potential initiation, speeding up the production of the action potential (see sinoatrial node for more detail). cAMP also, activates a protein called protein kinase A (PKA). PKA affects both the DHPR and RyR, increasing the rise in Ca 2+ within the contractile cells and therefore increasing rate of muscle contraction. PKA also affects the myofilaments as well as a protein called phospholamban (PLB; see sarcoplasmic reticulum for more details), speeding up the rate of Ca2+decline in the cell and so speeding up muscle relaxation.
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The distinction between the two Hill equations is whether they measure occupancy or response. The Hill–Langmuir equation reflects the occupancy of macromolecules: the fraction that is saturated or bound by the ligand.For clarity, this article will use the International Union of Basic and Clinical Pharmacology convention of distinguishing between the Hill-Langmuir equation (for receptor saturation) and Hill equation (for tissue response) This equation is formally equivalent to the Langmuir isotherm. Conversely, the Hill equation proper reflects the cellular or tissue response to the ligand: the physiological output of the system, such as muscle contraction.
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These neurotransmitters bind and activate receptors on the post-synaptic neuron thereby transmitting the signal to the target cell. Thus, a post-synaptic membrane belongs to the membrane receiving the signal, while a pre-synaptic membrane is the source of the neurotransmitter. In a neuromuscular junction, a synapse is formed between a motor neuron and muscle fibers. In vertebrates, acetylcholine released from the motor neuron acts as a neurotransmitter which depolarizes the muscle fiber and causes muscle contraction. A neuron’s ability to receive and integrate simultaneous signals from the environment and other neurons allows for complex animal behavior.
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The size principle has important functional benefits. Primarily, this system frees higher centers of the CNS from having to signal specific contraction patterns for distinct levels of muscle contraction. The level of synaptic input that higher centers provide to a given motor pool must determine the contraction strength, and this simplifies the process of contraction strength modulation. This system allows for very precise and consistent modulation of contraction strength from just increased or decreased levels of synaptic input: with additional motor units of increasing size, there will be a consistent and precise effect on the force of contraction.
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Electromyographic feedback includes visual EMG signals (coming from facial muscle sites displayed to the patient from a computer in the form of waveform traces) or auditory signals that indicate strength of muscle contraction. The subsequent role of the patient is to control the movement of undesired muscle during volitional movement by incorporating the information perceived through the EMG. While mirror feedback is a much more basic way of providing the patient feedback on muscle movement, studies have shown that both are very effective options for synkinesis/paresis reduction. Biofeedback is commonly coupled to facial retraining techniques to achieve maximal effectiveness.
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They roost inside the rolled leaves of the traveller's tree, using their suckers to attach themselves to the smooth surface. Despite the name, it is now known that the bats do not use suction to attach themselves to roost sites, but instead use a form of wet adhesion by secreting a body fluid at their pads.Brown University News, December 2009, Bats Don’t Use Suction After All The ankle and wrist pads of the bat are controlled by muscle contraction and allow the bat to separate the pads to reduce the adhesive effect. This allows the bats to climb with ease and to remove themselves from surfaces after sticking.
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Type 1 HRS is characterized by rapidly progressive kidney failure, with a doubling of serum creatinine to a level greater than 221 μmol/L (2.5 mg/dL) or a halving of the creatinine clearance to less than 20 mL/min over a period of less than two weeks. The prognosis of individuals with type 1 HRS is particularly grim, with a mortality rate exceeding 50% after one month. Patients with type 1 HRS are usually ill, may have low blood pressure, and may require therapy with drugs to improve the strength of heart muscle contraction (inotropes) or other drugs to maintain blood pressure (vasopressors).Mukherjee, S. Hepatorenal syndrome. emedicine.com.
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The abundance of minerals and trace elements is also of note as deficiencies in macro minerals and micro trace elements can lead to premature aging, immune dysfunction and susceptibility to cardiovascular related diseases. The minerals and trace elements (DOM) present in DOW have three important functions: #Provide the structure to our organs, tissues and bones – calcium, phosphorus, magnesium, fluorine and sulfur. #The electrolyte form facilitates body fluid activity in tissues to maintain fluid balance, acid-base balance, membrane permeability, tissue irritability (including nerve transmission and muscle contraction) - sodium, potassium, chloride, calcium and magnesium in blood, all present in DOMs. #Magnesium alone, potentially catalyses up to 600 enzyme and hormone reactions.
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Together, these abnormalities lead to the decrease in muscle contractility. Repeated stimuli over a period of about 10 seconds eventually lead to sufficient delivery of calcium, and an increase in muscle contraction to normal levels, which can be demonstrated using an electrodiagnostic medicine study called needle electromyography by increasing amplitude of repeated compound muscle action potentials. The antibodies found in LEMS associated with lung cancer also bind to calcium channels in the cancer cells, and it is presumed that the antibodies originally develop as a reaction to these cells. It has been suggested that the immune reaction to the cancer cells suppresses their growth and improves the prognosis from the cancer.
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Ilona Banga (1906–1998) was a Hungarian biochemist known for co-discovering actomyosin and working to characterize how actin and myosin interact to produce muscle contraction. She and her husband József Mátyás Baló discovered the first elastase – an enzyme capable of degrading the protein elastin which gives tissues like veins their flexibility. She also contributed to work that earned Albert Szent-Györgyi the Nobel Prize in Physiology or Medicine in 1937, including by developing methods for the purification and characterization of large quantities of vitamin C. During World War II she saved the equipment of the Institute of Chemistry of the University of Szeged.
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Banga's initial work as Szent-Györgyi's associate involved studying carbohydrate metabolism. She developed methods for the large-scale purification of ascorbic acid (vitamin C) from Hungarian paprika – work that entailed extracting the vitamin from close to a metric ton of paprika. After winning the Nobel Prize in Physiology or Medicine in 1937 (for work to which Banga contributed), Albert Szent-Györgyi switched his lab's focus to researching muscle contraction, motivated by the findings of Engelhardt and Ljubimova that the muscle protein myosin wasn't merely a structural protein – it had phosphatase (ATPase) activity. Banga confirmed these findings and further characterized myosin's ability to split ATP.
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Normally, muscle contraction is a result of electrical signals sent from the central nervous system to muscle fibers via nerve impulses. At the neuromuscular junction, this electrical message is converted into a chemical message as acetylcholine is released from nerve fibers and attaches to corresponding receptors on the muscle fiber. In MG, antibodies are produced that block acetylcholine receptors, preventing the molecule from binding to the receptor and leading to a breakdown in communication between the nervous system and the muscle, resulting in muscle fatigue, and sometimes paralysis. Autoantibodies against acetylcholine receptors are detectable in 70–90% of patients with generalized MG, but only 50% in ocular MG.
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One of the best-understood roles for bioelectric gradients is at the tissue-level endogenous electric fields utilized during wound healing. It is challenging to study wound-associated electric fields, because these fields are weak, less fluctuating, and do not have immediate biological responses when compared to nerve pulses and muscle contraction. The development of the vibrating and glass microelectrodes, demonstrated that wounds indeed produced and, importantly, sustained measurable electric currents and electric fields. These techniques allow further characterization of the wound electric fields/currents at cornea and skin wounds, which show active spatial and temporal features, suggesting active regulation of these electrical phenomena.
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This is because, the Ca2+ that enters the cell via the DHPR in response to the action potential, stimulates both muscle contraction and calcium release from the SR. The Ca2+ released during the spark, then activates two other ion channels on the membrane. One channel allows potassium ions to enter the cell, whereas the other allows chloride ions to leave the cell. The result of this movement of ions, is that the membrane voltage becomes more negative. This deactivates the DHPR (which was activated by the positive membrane potential produced by the action potential), causing it to close and stopping the flow of Ca2+into the cell, leading to relaxation.
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Fimasartan acts on the kidney's rennin-angiotensin cascade, which begins when renin release from the kidney causes the breakdown of angiotensinogen into angiotensin I. Angiotensin-converting enzyme (ACE) then catalyzes the reaction that forms angiotensin II, which acts on AT1 receptors on the blood vessels, heart, and kidneys. On blood vessels, the AT1 receptor is coupled to an intracellular pathway that causes smooth muscle contraction (vasoconstriction) of blood vessels. In blocking the AT1 receptor, fimasartan inhibits vasoconstriction, favouring vasodilation. At the kidney and adrenal gland, AT1 blockage and prevention of aldosterone formation increase excretion of water and salt by the kidneys, which decreases overall blood volume.
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In 1948, he predicted the phenomenon that is known as Davydov splitting or factor-group splitting, "the splitting of bands in the electronic or vibrational spectra of crystals due to the presence of more than one (interacting) equivalent molecular entity in the unit cell." In the period 1958–1960 he developed the theory of collective excited states in spherical and non-spherical nuclei, known as Davydov-Filippov Model and Davydov-Chaban Model. In 1973, Davydov applied the concept of molecular solitons in order to explain the mechanism of muscle contraction in animals. He studied theoretically the interaction of intramolecular excitations or excess electrons with autolocal breaking of the translational symmetry.
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The study stated that 2 in every 100,000 children under the age of 18 in Australia were considered diabetic. The findings further suggested that Indigenous children were at a much higher risk, as 16 in every 100,000 children were considered to be diabetic. The condition is one where the body cells are unable to absorb sufficient amounts of insulin, due to tissue resistance, thus being unable to reduce blood sugar levels after eating. The body requires insulin produced by the pancreas, in order to uptake glucose within the cells for the production of energy (ATP) and to perform active processes within the body, such as digestion, muscle contraction and brain stimulation.
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Moyle's first major research, in collaboration with Dorothy L. Foster, focused on the interconversion of lactic acid and glycogen in muscle, recapitulating the work of Otto Fritz Meyerhof. After that, she studied the roles of succinic acid, fumaric acid, and malic acid in muscle metabolism, as well as the biochemical differences and relationships between aerobic and anaerobic pathways.Teich, p. 354-355 She subsequently worked on cyclic phosphate transfer in muscle contraction and, with collaborators, established for the first time a direct correlation of structure and function in muscle by confirming in 1939 that myosin, the contractile protein of muscle, behaves as the enzyme ATPase (adenosine triphosphatase).
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The respiratory center sends a signal along the phrenic nerve, excites the diaphragm muscle cells, leading to muscle contraction and descent of the diaphragm dome. As a result, the pressure in the airway drops, causing an inflow of air into the lungs. With NAVA, the electrical activity of the diaphragm (Edi) is captured, fed to the ventilator and used to assist the patient's breathing in synchrony with and in proportion to the patients own efforts, regardless of patient category or size. As the work of the ventilator and the diaphragm is controlled by the same signal, coupling between the diaphragm and the SERVO-i ventilator is synchronized simultaneously.
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Presynaptic parasympathetic signals that originate in the Edinger-Westphal nucleus are carried by cranial nerve III (the oculomotor nerve) and travel through the ciliary ganglion via the postganglionic parasympathetic fibers which travel in the short ciliary nerves and supply the ciliary body and iris. Parasympathetic activation of the M3 muscarinic receptors causes ciliary muscle contraction. The effect of contraction is to decrease the diameter of the ring of ciliary muscle causing relaxation of the zonule fibers, the lens becomes more spherical, increasing its power to refract light for near vision. The parasympathetic tone is dominant when a higher degree of accommodation of the lens is required, such as reading a book.
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Ribbon representation of the human cardiac troponin core complex (52 kDa core) in the calcium-saturated form. Blue = troponin C; green = troponin I; magenta = troponin T.; ; rendered with PyMOL Troponin, or the troponin complex, is a complex of three regulatory proteins (troponin C, troponin I, and troponin T) that are integral to muscle contraction in skeletal muscle and cardiac muscle, but not smooth muscle. Measurements of cardiac-specific troponins I and T are extensively used as diagnostic and prognostic indicators in the management of myocardial infarction and acute coronary syndrome. Blood troponin levels may be used as a diagnostic marker for stroke, although the sensitivity of this measurement is low.
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TnT is a tropomyosin-binding subunit which regulates the interaction of troponin complex with thin filaments; TnI inhibits ATP-ase activity of acto-myosin; TnC is a Ca2+-binding subunit, playing the main role in Ca2+ dependent regulation of muscle contraction. TnT and TnI in cardiac muscle are presented by forms different from those in skeletal muscles. Two isoforms of TnI and two isoforms of TnT are expressed in human skeletal muscle tissue (skTnI and skTnT). Only one tissue-specific isoform of TnI is described for cardiac muscle tissue (cTnI), whereas the existence of several cardiac specific isoforms of TnT (cTnT) are described in the literature.
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Bressler's research program in skeletal muscle biophysics received support from the Medical Research Council of Canada and the Canadian Institutes for Health Research for 29 years. His research focuses on providing new information about the fundamental mechanisms for force production in skeletal muscle. Experiments are designed to test some fundamental assumptions of the cross-bridge model as well as the role of the protein troponin C (TnC) in the regulation of calcium sensitivity in striated muscle. Part of the research is designed to explore how the level of activation of skeletal muscle is controlled by the calcium binding properties of troponin C – the protein responsible for the initiation of muscle contraction.
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2004 There is scientific support for the concept of a temperature set point; that is, maintenance of an optimal temperature for the metabolic processes that life depends on. Nervous activity in the preoptic-anterior hypothalamus of the brain triggers heat losing (sweating, etc.) or heat generating (shivering and muscle contraction, etc.) activities through stimulation of the autonomic nervous system. The pre-optic anterior hypothalamus has been shown to contain warm sensitive, cool sensitive, and temperature insensitive neurons, to determine the body's temperature setpoint. As the temperature that these neurons are exposed to rises above , the rate of electrical discharge of the warm-sensitive neurons increases progressively.
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Acute, or central nervous system oxygen toxicity is a time variable response to the partial pressure exposure history of the diver and is both complex and not fully understood. Central nervous system oxygen toxicity manifests as symptoms such as visual changes (especially tunnel vision), ringing in the ears (tinnitus), nausea, twitching (especially of the face), behavioural changes (irritability, anxiety, confusion), and dizziness. This may be followed by a tonic–clonic seizure consisting of two phases: intense muscle contraction occurs for several seconds (tonic phase); followed by rapid spasms of alternate muscle relaxation and contraction producing convulsive jerking (clonic phase). The seizure ends with a period of unconsciousness (the postictal state).
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Chills is a feeling of coldness occurring during a high fever, but sometimes is also a common symptom which occurs alone in specific people. It occurs during fever due to the release of cytokines and prostaglandins as part of the inflammatory response, which increases the set point for body temperature in the hypothalamus. The increased set point causes the body temperature to rise (pyrexia), but also makes the patient feel cold or chills until the new set point is reached. Shivering also occurs along with chills because the patient's body produces heat during muscle contraction in a physiological attempt to increase body temperature to the new set point.
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Glutamate functions as a neurotransmitter in every type of animal that has a nervous system, including ctenophores (comb jellies), which branched off from other phyla at an early stage in evolution and lack the other neurotransmitters found ubiquitously among animals, including serotonin and acetylcholine. Rather, ctenophores have functionally distinct types of ionotropic glutamate receptors, such that activation of these receptors may trigger muscle contraction and other responses. Sponges do not have a nervous system, but also make use of glutamate for cell-to-cell signalling. Sponges possess metabotropic glutamate receptors, and application of glutamate to a sponge can trigger a whole-body response that sponges use to rid themselves of contaminants.
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Choline acetyltransferase was first described by David Nachmansohn and A. L. Machado in 1943. A German biochemist, Nachmansohn had been studying the process of nerve impulse conduction and utilization of energy-yielding chemical reactions in cells, expanding upon the works of Nobel laureates Otto Warburg and Otto Meyerhof on fermentation, glycolysis, and muscle contraction. Based on prior research showing that "acetylcholine's actions on structural proteins" were responsible for nerve impulses, Nachmansohn and Machado investigated the origin of acetylcholine. The acetyl transferase mode of action was unknown at the time of this discovery, however Nachmansohn hypothesized the possibility of acetylphosphate or phosphorylcholine exchanging the phosphate (from ATP) for choline or acetate ion.
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Contact or absorption of poisons can cause rapid death or impairment. Agents that act on the nervous system can paralyze in seconds or less, and include both biologically derived neurotoxins and so- called nerve gases, which may be synthesized for warfare or industry. Inhaled or ingested cyanide, used as a method of execution in gas chambers, almost instantly starves the body of energy by inhibiting the enzymes in mitochondria that make ATP. Intravenous injection of an unnaturally high concentration of potassium chloride, such as in the execution of prisoners in parts of the United States, quickly stops the heart by eliminating the cell potential necessary for muscle contraction.
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Glycogen phosphorylase is found in muscle and is responsible for mobilising the energy store of glycogen to provide fuel to sustain muscle contraction. In resting muscle the enzyme is switched off to prevent wasteful degradation of the fuel but in response to nervous or hormonal signals the enzyme is switched on almost simultaneously to generate the energy supply. Her research was directed towards understanding the molecular basis of the biological properties of control and catalytic mechanism. Her team used the bright x-ray source generated at the Synchrotron Radiation Source at Daresbury, which provided data that could not be obtained with the home source.
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Functional electrical stimulation (FES) is a technique that uses low-energy electrical pulses to artificially generate body movements in individuals who have been paralyzed due to injury to the central nervous system. More specifically, FES can be used to generate muscle contraction in otherwise paralyzed limbs to produce functions such as grasping, walking, bladder voiding and standing. This technology was originally used to develop neuroprostheses that were implemented to permanently substitute impaired functions in individuals with spinal cord injury (SCI), head injury, stroke and other neurological disorders. In other words, a person would use the device each time he or she wanted to generate a desired function.
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Fly spray contains chemicals (including many organophosphate compounds) that bind to and permanently block the action of an enzyme called acetylcholinesterase. Acetyl choline (ACh) is the nerve transmitter substance released by motor neurones (at a site called the neuromuscular junction) to stimulate muscle contraction. The muscles relax (stop contracting) when the ACh is removed from the neuromuscular junction (NMJ) by the action of acetylcholinesterase. By inhibiting the cholinesterase the insect can no longer break down ACh in the NMJ and so its muscles lock up in a state of tetany (continuous contraction) making flying and respiration impossible, and the insect then dies of asphyxiation.
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At this point the hip extends and the hip flexors are elongated. Muscle spindles within the hip flexors detect this stretch and trigger muscle contraction of the hip flexors required for the initiation of the swing phase of gait. However, Golgi tendon organs in the extensor muscles also send signals related to the amount of weight being supported through the stance leg to ensure that limb flexion does not occur until the leg is adequately unweighted and the majority of weight has been transferred to the opposite leg. Information from the spinal cord is transmitted for higher order processing to supraspinal structures via spinothalamic, spinoreticular, and spinocerebellar tracts.
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Inflammation, in the biological sense, refers to the cellular response of the body to disturbances, be they internal or external. In the case of asthma or chronic bronchitis the human body responds to allergens or pollutants by flooding the bronchial tree and airway walls with mononuclear cells. The layers of the airway wall, including the inner epithelial tissue lining thickens and expands anywhere from 10% to 300% of healthy individuals, and obstructs air flow. Enduring the disease long term coupled with airway hyperresponsiveness (smooth muscle contraction or Bronchial hyperresponsiveness) leads to chronic continuous inflammation and thickening, and noticeable airway remodeling consisting of stiffer airways and lost elasticity.
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Smooth muscle is a type of non-striated muscle, and, unlike striated muscle, contraction of smooth muscle is not under conscious control. Smooth muscle may contract spontaneously or rhythmically and be induced by a number of physiochemical agents (hormones, drugs, neurotransmitters). Smooth muscle is found within the walls of various organs and tubes in the body such as the esophagus, stomach, intestines, bronchi, urethra, bladder, and blood vessels. Although smooth muscles do not form regular arrays of thick and thin filaments like the sarcomeres of striated muscles, contraction is still due to the same sliding filament mechanism controlled by myosin crossbridges interacting with actin filaments.
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A stimulus, in the form of positively charged current, is transmitted from the neuromuscular junction down the length of the T tubules, activating dihydropyridine receptors (DHPRs). Their activation causes 1) a negligible influx of calcium and 2) a mechanical interaction with calcium- conducting ryanodine receptors (RyRs) on the adjacent SR membrane. Activation of RyRs causes the release of calcium from the SR, which subsequently initiates a cascade of events leading to muscle contraction. These muscle contractions are caused by calcium's bonding to troponin and unmasking the binding sites covered by the troponin-tropomyosin complex on the actin myofilament and allowing the myosin cross-bridges to connect with the actin.
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In addition, Neanderthal genes have also been implicated in the structure and function of the brain, keratin filaments, sugar metabolism, muscle contraction, body fat distribution, enamel thickness, and oocyte meiosis. Nonetheless, a large portion of surviving introgression appears to be non-coding ("junk") DNA with few biological functions. Due to the absence of Neanderthal-derived mtDNA (which is passed on from mother to child) in modern populations, it has been suggested that the progeny of Neanderthal females who mated with modern human males were either rare, absent, or sterile—that is to say, admixture stems from the progeny of Neanderthal males with modern human females.
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The calcium sensitivity of the sarcomere, that is, the calcium concentration at which muscle contraction occurs, is directly determined by the calcium binding affinity of cNTnC. To date, there are no known post-translational modifications of cTnC that impact its calcium binding affinity. However, calcium binding by cNTnC is a dynamic process that can be impacted by the closed-to-open conformational equilibrium of cNTnC, the domain positioning of cNTnC, or the relative availability of cTnI148-159, the physiologic binding partner of cNTnC. The closed-to-open equilibrium of cNTnC can be shifted towards the open state by small compounds (see section below on troponin-binding drugs).
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Voltage- gated potassium (Kv) channels represent the most complex class of voltage- gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. Four sequence-related potassium channel genes - shaker, shaw, shab, and shal - have been identified in Drosophila, and each has been shown to have human homolog(s). This gene encodes a member of the potassium channel, voltage-gated, shal-related subfamily, members of which form voltage-activated A-type potassium ion channels and are prominent in the repolarization phase of the action potential.
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Structure of a skeletal muscle. A key component in lateral force transmission in skeletal muscle is the extracellular matrix (ECM). Skeletal muscle is a complex biological material that is composed of muscle fibers and an ECM consisting of the epimysium, perimysium, and endomysium. It can be described as a collagen fiber-reinforced composite. The ECM has at least three functions: (1) to provide a framework binding muscle fibers together and ensure their proper alignment, (2) to transmit the forces, either from active muscle contraction or ones passively imposed on it, and (3) providing lubricated surfaces between muscle fibers and bundles enabling the muscle to change shape.
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These sites were hypothesized to be a focal region for delivery of tension during muscle contraction. To test the possibility of tensile force transmission via the perimysium, it was experimentally shown that cutting of the aponeurosis in a pennate muscle did not prevent tension generation further along towards the tendon. Also, in a separate study it was clearly demonstrated that the perimysium could transmit force if tendons normally transmitting force from distinct parts of the extensor digitorum longus muscle were cut. Although a lot of evidence may seem to point to lateral force transmission via the perimysium in tension, the experiments were conducted at very high loads.
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Butanolic and ethyl acetate extract of rhizome of C. comosa had a stimulative effect on bile secretion and a decrease in blood cholesterol was reported. Separation of the active ingredients from diarylheptanoids and phloracetophenone glucoside compounds were carried out and some active compounds, such as 1,7-diphenyl-5-hydroxy-(1E)-1-heptene and 4,6-dihydroxy-2-o-(b-D- glucopyranosyl) acetophenone, were found to have a stimulative effect on bile secretion in rats. A 95% ethanol extract of C. comosa decreased uterine smooth muscle contraction in rats. An ethyl acetate extract of the rhizome was orally administered to male sheep and hamsters and a decrease in cholesterol and triglyceride were reported.
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Some elements of the cholinergic crisis can be treated with antimuscarinic drugs like atropine or diphenhydramine, but the most important element, respiratory arrest, cannot. The neuromuscular junction, where the brain communicates with muscles (like the diaphragm, the main breathing muscle), works by acetylcholine activating nicotinic acetylcholine receptors and leading to muscle contraction. Atropine only blocks muscarinic acetylcholine receptors (a different subtype than the nicotinic receptors at the neuromuscular junction), so atropine will not improve the muscle strength and ability to breathe in someone with cholinergic crisis. Such a patient will require neuromuscular blocking drugs and mechanical ventilation support via endotracheal intubation until the crisis resolves on its own.
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He and Fletcher showed that oxygen depletion causes an accumulation of lactic acid in the muscle. Their work paved the way for the later discovery by Archibald Hill and Otto Fritz Meyerhof that a carbohydrate metabolic cycle supplies the energy used for muscle contraction. In 1912 Hopkins published the work for which he is best known, demonstrating in a series of animal feeding experiments that diets consisting of pure proteins, carbohydrates, fats, minerals, and water fail to support animal growth. This led him to suggest the existence in normal diets of tiny quantities of as yet unidentified substances that are essential for animal growth and survival.
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A voltage applied to a human body causes an electric current through the tissues, and although the relationship is non-linear, the greater the voltage, the greater the current. The threshold for perception varies with the supply frequency and with the path of the current, but is about 0.1 mA to 1 mA for mains-frequency electricity, though a current as low as a microamp can be detected as an electrovibration effect under certain conditions. If the current is sufficiently high, it will cause muscle contraction, fibrillation of the heart, and tissue burns. The lack of any visible sign that a conductor is electrified makes electricity a particular hazard.
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Patrick Obyedkov, a respected pianist, suffers a painful involuntary muscle contraction in his left hand during a piano concert. The case attracts the attention of House, who learns from Patrick's father that Patrick suffered severe brain damage from a bus accident that also killed his mother. House is intrigued as to why Patrick, who had no musical training at the time of the accident, could suddenly play the piano flawlessly after suffering a severe injury. While trying to deduce the origin of the brain rewiring responsible for Patrick's mysterious gift of music, House and his team must stop the deadly bleeding that is quickly threatening his life.
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Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. Four sequence-related potassium channel genes – shaker, shaw, shab, and shal – have been identified in Drosophila, and each has been shown to have human homolog(s). Kv4.3 is a member of the potassium channel, voltage-gated, shal- related subfamily, members of which form voltage-activated A-type potassium ion channels and are prominent in the repolarization phase of the action potential.
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The somatic nervous system (SNS or voluntary nervous system) is the part of the peripheral nervous system associated with the voluntary control of body movements via skeletal muscles. The somatic nervous system consists of afferent nerves or sensory nerves, and efferent nerves or motor nerves. Afferent nerves are responsible for relaying sensation from the body to the central nervous system; efferent nerves are responsible for sending out commands from the CNS to the body, stimulating muscle contraction; they include all the non-sensory neurons connected with skeletal muscles and skin. The a- of afferent and the e- of efferent correspond to the prefixes ad- (to, toward) and ex- (out of).
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Six decades later, in 1849, Emil du Bois-Reymond discovered that it was also possible to record electrical activity during a voluntary muscle contraction. The first actual recording of this activity was made by Marey in 1890, who also introduced the term electromyography. In 1922, Gasser and Erlanger used an oscilloscope to show the electrical signals from muscles. Because of the stochastic nature of the myoelectric signal, only rough information could be obtained from its observation. The capability of detecting electromyographic signals improved steadily from the 1930s through the 1950s, and researchers began to use improved electrodes more widely for the study of muscles.
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A 50% solution of DMSO had the potential to create irreversible muscle contraction. However, a lesser solution of 25% was found to be reversible. Long-term use of DMSO is questionable, as its mechanism of action is not fully understood though DMSO is thought to inhibit mast cells and may have anti-inflammatory, muscle- relaxing, and analgesic effects. Other agents used for bladder instillations to treat interstitial cystitis include: heparin, lidocaine, chondroitin sulfate, hyaluronic acid, pentosan polysulfate, oxybutynin, and botulinum toxin A. Preliminary evidence suggests these agents are efficacious in reducing symptoms of interstitial cystitis, but further study with larger, randomized, controlled clinical trials is needed.
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Because channels underlie the nerve impulse and because "transmitter-activated" channels mediate conduction across the synapses, channels are especially prominent components of the nervous system. Indeed, numerous toxins that organisms have evolved for shutting down the nervous systems of predators and prey (e.g., the venoms produced by spiders, scorpions, snakes, fish, bees, sea snails, and others) work by modulating ion channel conductance and/or kinetics. In addition, ion channels are key components in a wide variety of biological processes that involve rapid changes in cells, such as cardiac, skeletal, and smooth muscle contraction, epithelial transport of nutrients and ions, T-cell activation and pancreatic beta-cell insulin release.
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From his experimental work with Hodgkin, Huxley developed a set of differential equations that provided a mathematical explanation for nerve impulses—the "action potential". This work provided the foundation for all of the current work on voltage-sensitive membrane channels, which are responsible for the functioning of animal nervous systems. Quite separately, he developed the mathematical equations for the operation of myosin "cross-bridges" that generate the sliding forces between actin and myosin filaments, which cause the contraction of skeletal muscles. These equations presented an entirely new paradigm for understanding muscle contraction, which has been extended to provide understanding of almost all of the movements produced by cells above the level of bacteria.
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Voltage-dependent calcium channels mediate the entry of calcium ions into excitable cells, and are also involved in a variety of calcium- dependent processes, including muscle contraction, hormone or neurotransmitter release, and gene expression. Calcium channels are multisubunit complexes composed of alpha-1, beta, alpha-2/delta, and gamma subunits. The channel activity is directed by the pore-forming alpha-1 subunit, whereas, the others act as auxiliary subunits regulating this activity. The distinctive properties of the calcium channel types are related primarily to the expression of a variety of alpha-1 isoforms, alpha-1A, B, C, D, E, and S. This gene encodes the alpha-1A subunit, which is predominantly expressed in neuronal tissue.
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Muscle contraction is caused by the sliding action of thick filaments over thin filaments of the myofibril. Myosin is a major component of thick filaments and most myosin molecules are composed of a head, neck, and tail domain; the myosin head binds to thin filamentous actin, and uses ATP hydrolysis to generate force and "walk" along the thin filament. Myosin exists as a hexamer of two heavy chains, two alkali light chains, and two regulatory light chains. The heavy chain can be subdivided into the globular head at the N-terminal and the coiled-coil rod-like tail at the C-terminal, although some forms have a globular region in their C-terminal.
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Tongue projection occurs at extremely high performance, reaching the prey in as little as 0.07 seconds, having been launched at accelerations exceeding 41 g. The power with which the tongue is launched, known to exceed 3000 W kg−1, exceeds that which muscle is able to produce, indicating the presence of an elastic power amplifier to power tongue projection. The recoil of elastic elements in the tongue apparatus is thus responsible for large percentages of the overall tongue projection performance. One consequence of the incorporation of an elastic recoil mechanism to the tongue projection mechanism is relative thermal insensitivity of tongue projection relative to tongue retraction, which is powered by muscle contraction alone, and is heavily thermally sensitive.
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Presynaptic neurons traveling from the spinal cord terminate in the paravertebral ganglia (cervical, thoracic, lumbar, sacral) or the prevertebral ganglia. They synapse with either the postsynaptic neuron of the corresponding level of the spinal cord or ascend and descend to synapse at the lower or upper paravertebral ganglia, respectively. Neurotransmitters are released in the paravertebral ganglia to activate the postganglionic neurons to send efferent sympathetic output to the lower extremities to prepare the body for the “fight or flight” responses. These responses include dilating pupils, constricting blood vessels, and stimulating the secretion of acetylcholine, which causes smooth muscle contraction that leads to an increase in heart rate, blood sugar level, and blood pressure.
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This 'low' level of contraction is a protective mechanism to prevent avulsion of the tendon--the force generated by a 95% contraction of all fibers is sufficient to damage the body. In multiple fiber summation, if the central nervous system sends a weak signal to contract a muscle, the smaller motor units, being more excitable than the larger ones, are stimulated first. As the strength of the signal increases, more motor units are excited in addition to larger ones, with the largest motor units having as much as 50 times the contractile strength as the smaller ones. As more and larger motor units are activated, the force of muscle contraction becomes progressively stronger.
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Nishikawa is the principal investigator leading the Muscle and Motor Control Laboratory at Northern Arizona University (NAU), where her laboratory investigates muscle contraction, including the role of titin and creating motorized prostheses for lower limbs. Previously, Nishikawa's lab acquired an atomic force microscope in order to test how change in a single muscle fibre impacts the overall muscle (referred to as the winding filament hypothesis). Nishikawa's laboratory has also developed prosthetic software, called BiOM T2, and are studying whether this provides additional advantages compared to currently available commercial software. Nishikawa holds the position of Regents' Professor of Biological Sciences at NAU, and is also the director of the NAU's Center of Bioengineering Innovation.
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A ribosome is a biological machine that utilizes protein dynamics on nanoscales Proteins are not however strictly static objects, but rather populate ensembles of conformational states. Transitions between these states typically occur on nanoscales, and have been linked to functionally relevant phenomena such as allosteric signaling and enzyme catalysis. Protein dynamics and conformational changes allow proteins to function as nanoscale biological machines within cells, often in the form of multi-protein complexes. Examples include motor proteins, such as myosin, which is responsible for muscle contraction, kinesin, which moves cargo inside cells away from the nucleus along microtubules, and dynein, which moves cargo inside cells towards the nucleus and produces the axonemal beating of motile cilia and flagella.
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Upon activation by its ligand agrin, MuSK signals via the proteins called casein kinase 2 (CK2), Dok-7 and rapsyn, to induce "clustering" of acetylcholine receptors (AChR). Both CK2 and Dok-7 are required for MuSK-induced formation of the neuromuscular junction, since mice lacking Dok-7 failed to form AChR clusters or neuromuscular synapses, and since downregulation of CK2 also impedes recruitment of AChR to the primary MuSK scaffold. In addition to the proteins mentioned, other proteins are then gathered, to form the endplate to the neuromuscular junction. The nerve terminates onto the endplate, forming the neuromuscular junction - a structure required to transmit nerve impulses to the muscle, and thus initiating muscle contraction.
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He wanted the characters to portray realistic motion, which begins with an abrupt twitch for a muscle contraction and must also account for momentum and mass. For example, Landreth stated that an individual's arm should be slightly in front of the body, at 30 degrees with respect to the "scapular plane of the skeleton". Cords are used to animate coloured threads that wrap themselves around the character's heads, and are used metaphorically in the film to represent Landreth's fear of failure and Larkin's loss of creativity. The use of coloured threads is explained by Landreth's character in first-person narrative at the beginning of the film as metaphorically representing emotional scars and frustrations.
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Windhorst's research has revolved around the control of skeletal muscle contraction based on sensory signal arising in muscles and skin and on neuronal networks predominantly in the spinal cord and brainstem. In this wider context, one line of research strived to elucidate the dynamic signal processing of the participating neurons, such as muscle spindles, motoneurons and interneurons (particularly Renshaw cells) and their importance for oscillatory process such as tremor. Related issues were the plastic properties of such networks and their modulation by signals arising in the peripheral and central nervous system, specifically in the context of muscle fatigue. A related aspect of research concerned the origin of muscle pain and its effects on spinal neurons.
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In his most famous experiment, Loewi took fluid from one frog heart and applied it to another, slowing the second heart and showing that synaptic signaling used chemical messengers. The Nobel Prize diploma of Otto Loewi, housed at the University of Graz Before Loewi's experiments, it was unclear whether signaling across the synapse was bioelectrical or chemical. While pharmacology experiments had established that physiological responses such as muscle contraction could be induced by chemical application, there was no evidence that cells released chemical substances to cause these responses. On the contrary, researchers had shown that physiological responses could be caused by applying an electrical impulse, which suggested that electrical transmission may be the only mode of endogenous signaling.
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Excessive vasoconstriction can cause cardiac output reduction or even fatal heart complication particularly in those with weak myocardial function. In those whose vasodilatory shock is caused by hypocalcemic cardiomyopathy in the context of dilated cardiomyopathy with documented both reduced heart ejection fraction and contractile performance, the uses of calcium and active vitamin D or recombinant human parathyroid hormone treatment are viable since there were many successful cases reported while given the physiological role of calcium on muscle contraction. A successful treatment requires leveraging the respective unique contributions of a multi-disciplinary team not only critical care doctors and often, infectious disease specialists but also respiratory therapy, nursing, pharmacy and others in collaboration.
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Structure of ATP Structure of ADP Four possible resonance structures for orthophosphate ATP hydrolysis is the catabolic reaction process by which chemical energy that has been stored in the high-energy phosphoanhydride bonds in adenosine triphosphate (ATP) is released by splitting these bonds, for example in muscles, by producing work in the form of mechanical energy. The product is adenosine diphosphate (ADP) and an inorganic phosphate, orthophosphate (Pi). ADP can be further hydrolyzed to give energy, adenosine monophosphate (AMP), and another orthophosphate (Pi). ATP hydrolysis is the final link between the energy derived from food or sunlight and useful work such as muscle contraction, the establishment of electrochemical gradients across membranes, and biosynthetic processes necessary to maintain life.
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Following his undergraduate studies, Peter Caldwell worked with Professor Cyril Hinshelwood, completing his PhD on the influences on the growth rate of bacteria, which led to important ideas about the ways in which cells synthesized proteins. The key new idea was that a coded sequence of nucleic acids specified the sequence of amino acids in a protein. In 1950 he moved to University College London to work with the Nobel prize winning Archibald Hill, where he developed new methods for measuring pH. In 1955 he joined the Marine Biological Association's Laboratory in Plymouth, working with squid nerves and crab muscles to study the energy sources for the complex processes involved in the neuronal communication and muscle contraction.
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Electrolytes enter and leave cells through proteins in the cell membrane called ion channels. For example, muscle contraction depends upon the movement of calcium, sodium and potassium through ion channels in the cell membrane and T-tubules. Transition metals are usually present as trace elements in organisms, with zinc and iron being most abundant of those. These metals are used in some proteins as cofactors and are essential for the activity of enzymes such as catalase and oxygen-carrier proteins such as hemoglobin Metal cofactors are bound tightly to specific sites in proteins; although enzyme cofactors can be modified during catalysis, they always return to their original state by the end of the reaction catalyzed.
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For these obliquely oriented fibers the strain in the longitudinal direction is greater than the strain in the muscle fiber direction leading to an architectural gear ratio greater than 1. A higher initial angle of orientation and more dorsoventral bulging produces a faster muscle contraction but results in a lower amount of force production. It is hypothesized that animals employ a variable gearing mechanism that allows self-regulation of force and velocity to meet the mechanical demands of the contraction. When a pennate muscle is subjected to a low force, resistance to width changes in the muscle cause it to rotate which consequently produce a higher architectural gear ratio (AGR) (high velocity).
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The IgE-coated cells, at this stage, are sensitized to the allergen. If later exposure to the same allergen occurs, the allergen can bind to the IgE molecules held on the surface of the mast cells or basophils. Cross-linking of the IgE and Fc receptors occurs when more than one IgE-receptor complex interacts with the same allergenic molecule, and activates the sensitized cell. Activated mast cells and basophils undergo a process called degranulation, during which they release histamine and other inflammatory chemical mediators (cytokines, interleukins, leukotrienes, and prostaglandins) from their granules into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve stimulation, and smooth-muscle contraction.
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Proposed creatine kinase/phosphocreatine (CK/PCr) energy shuttle. CRT = creatine transporter; ANT = adenine nucleotide translocator; ATP = adenine triphosphate; ADP = adenine diphosphate; OP = oxidative phosphorylation; mtCK = mitochondrial creatine kinase; G = glycolysis; CK-g = creatine kinase associated with glycolytic enzymes; CK-c = cytosolic creatine kinase; CK-a = creatine kinase associated with subcellular sites of ATP utilization; 1 – 4 sites of CK/ATP interaction. Creatine is transported through the blood and taken up by tissues with high energy demands, such as the brain and skeletal muscle, through an active transport system. The concentration of ATP in skeletal muscle is usually 2–5 mM, which would result in a muscle contraction of only a few seconds.
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Although the exact mechanism is unclear, p11 protein has shown to be essential in the regulation of serotonin signaling in the brain. Serotonin (5-hydroxytryptamine or 5-HT), is a neurotransmitter found in the central and peripheral nervous systems. It is involved in mechanisms responsible for memory formation and learning, but is most known for its role in the regulation muscle contraction, appetite, sleep, and mood. Varying levels of serotonin found in the brain are associated with the development of mood disorders, such as clinical depression. P11 interacts with the serotonin receptor proteins, 5-HT receptors such as 5-HT1B, modulating the receptor signal transduction pathways activated by the binding of serotonin.
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In cases when an abrupt acoustic, tactile or visual stimulus elicits a single action potential in one M-cell, it always correlates with a contralateral C-start escape. An extremely quick mutual feedback inhibitory circuit then assures that only one M-cell reaches spiking threshold—as the C-start has to be unilateral by definition—and that only one action potential is fired. The Mauthner cell- mediated C-start reflex is very quick, with about 5-10 ms latency between the acoustic/tactile stimulus and the Mauthner cell discharge, and only about 2 ms between the discharge and the unilateral muscle contraction. Mauthner cells are thus the quickest motor neuron to respond to the stimulus.
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Those who think that the major part of the respiratory changes are pre-programmed in the brain, which would imply that neurons from locomotion centers of the brain connect to respiratory centers in anticipation of movements. 2\. Those who think that the major part of the respiratory changes result from the detection of muscle contraction, and that respiration is adapted as a consequence of muscular contraction and oxygen consumption. This would imply that the brain possesses some kind of detection mechanisms that would trigger a respiratory response when muscular contraction occurs. Many now agree that both mechanisms are probably present and complementary, or working alongside a mechanism that can detect changes in oxygen and/or carbon dioxide blood saturation.
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The curriculum for exercise physiology includes biology, chemistry, and applied sciences. The purpose of the classes selected for this major is to have a proficient understanding of human anatomy, human physiology, and exercise physiology. Includes instruction in muscular and skeletal anatomy; molecular and cellular basis of muscle contraction; fuel utilization; neurophysiology of motor mechanics; systemic physiological responses (respiration, blood flow, endocrine secretions, and others); fatigue and exhaustion; muscle and body training; physiology of specific exercises and activities; physiology of injury; and the effects of disabilities and disease. Not only is a full class schedule needed to complete a degree in Exercise Physiology, but a minimum amount of practicum experience is required and internships are recommended.
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PCr generated by mtCK in mitochondria is shuttled to cytosolic CK that is coupled to ATP-dependent processes, e.g. ATPases, such as acto-myosin ATPase and calcium ATPase involved in muscle contraction, and sodium/potassium ATPase involved in sodium retention in the kidney. The bound cytosolic CK accepts the PCr shuttled through the cell and uses ADP to regenerate ATP, which can then be used as energy source by the ATPases (CK is associated intimately with the ATPases, forming a functionally coupled microcompartment). PCr is not only an energy buffer but also a cellular transport form of energy between subcellular sites of energy (ATP) production (mitochondria and glycolysis) and those of energy utilization (ATPases).
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Scott and Fredericson describe that agonistic behaviour is displayed in a variety of different circumstances in response to different stimuli. Scott and Fredericson studied mice and rats, and classified three main categories of agonistic behaviour these animals display, which include preliminary behaviour, attack, and defensive and escape behaviour. Preliminary behaviour describes the behaviours displayed by these rodents if fighting does not immediately begin. These may include involuntary behaviours such as hair-fluffing, where the rodent's hair stands up on end with no prominence on a particular region of the body, or tail-rattling where the rodent's tail experiences muscle contraction and twitches from side to side, making a loud sound if struck against a hard object.
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Around that time, Hugh Huxley and Jean Hanson came to a similar observation. Authored in pairs, their papers were simultaneously published in the 22 May 1954 issue of Nature. Thus the four people introduced what is called the sliding filament theory of muscle contractions. Huxley synthesized his findings, and the work of colleagues, into a detailed description of muscle structure and how muscle contraction occurs and generates force that he published in 1957. In 1966 his team provided the proof of the theory, and has remained the basis of modern understanding of muscle physiology. In 1953, Huxley worked at Woods Hole, Massachusetts, as a Lalor Scholar. He gave the Herter Lectures at Johns Hopkins Medical School in 1959 and the Jesup Lectures at Columbia University in 1964.
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The greatest adjustment of focus (relatively more ocular muscle contraction) is required to view shorter distances, such as the gun's rear sight. In the modern technique, the shooter is taught to focus on the front sight of the pistol and align it against the target, ignoring the rear sight for quicker aiming and minimal physical requirements. This prevents the focus of the eye from hunting between rear sight, front sight and target, wasting vital time in refocusing. The technique is called "flash" sight picture because the cognition is best able to perform this function when the target and front sight are presented quickly as a single image, in a 'flash', as if the shooter had just turned around to face a threat appearing from close by.
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A 3D representation of PP1 (shown in red) and a portion of MYPT1 (shown in blue), with the manganese ion catalysts shown in white. The yellow lines mark the grooves that are critical for enzyme binding and catalysis. Myosin phosphatase is made of three subunits. The catalytic subunit, PP1, is one of the more important Ser/Thr phosphatases in eukaryotic cells, as it plays a role in glycogen metabolism, intracellular transport, protein synthesis, and cell division as well as smooth muscle contraction. Because it is so important to basic cellular functions, and because there are far fewer protein phosphatases than kinases in cells, PP1’s structure and function is highly conserved (though the specific isoform used in myosin phosphatase is the δ isoform, PP1δ).
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A gain-of- function mutation in SGK1, or serum and glucocorticoid-inducible kinase 1, can lead to a shortening of the QT interval, which represents the repolarization time of the cardiac cells after a cardiac muscle contraction action potential. SGK1 does this by interacting with the KvLQT1 channel in cardiac cells, stimulating this channel when it is complex with KCNE1. SGK1 stimulates the slow delayed rectifier potassium current through this channel by phosphorylating PIKfyve, which then makes PI(3,5)P2, which goes on to increase the RAB11-dependent insertion of the KvLQT1/KCNE1 channels into the plasma membrane of cardiac neurons. SGK1 phosphorylates PIKfyve, which results in regulated channel activity through RAB11-dependent exocytosis of these KvLQT1/KCNE1-containing vesicles.
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Shortly after his graduation in 1921, he began assisting Nobel laureate A. V. Hill in his work on the biophysics of muscle contraction. After working for two years at University College London, Long sailed on 4 September 1925 on the RMS Aurania from Liverpool to Quebec, to work in Montreal with Jonathan Meakins at McGill University; he received his M.D. there in 1928. He served as director of the George S. Cox Medical Research Institute, a diabetes research center at the University of Pennsylvania. In 1936, Long moved to the School of Medicine. At Yale, he was Director of the Division of Biological Sciences (1939–42), Dean of the School of Medicine (1947–52), and Chair of Physiology (1951–64).
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In the early stages of acute allergic reaction, lymphocytes previously sensitized to a specific protein or protein fraction react by quickly producing a particular type of antibody known as secreted IgE (sIgE), which circulates in the blood and binds to IgE-specific receptors on the surface of other kinds of immune cells called mast cells and basophils. Both of these are involved in the acute inflammatory response. Activated mast cells and basophils undergo a process called degranulation, during which they release histamine and other inflammatory chemical mediators (cytokines, interleukins, leukotrienes, and prostaglandins) into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve stimulation, and smooth muscle contraction. This results in runny nose, itchiness, shortness of breath, and potentially anaphylaxis.
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The differential diagnosis for LUTS is broad and includes various medical conditions, neurologic disorders, and other diseases of the bladder, urethra, and prostate such as bladder cancer, urinary tract infection, urethral stricture, urethral calculi (stones), chronic prostatitis, and prostate cancer. Neurogenic bladder can cause urinary retention and cause symptoms similar to those of BPH. This may occur as a result of uncoordinated contraction of the bladder muscle or impairment in the timing of bladder muscle contraction and urethral sphincter relaxation. Notable causes of neurogenic bladder include disorders of the central nervous system such as Parkinson's disease, multiple sclerosis, and spinal cord injuries as well as disorders of the peripheral nervous system such as diabetes mellitus, vitamin B12 deficiency, and alcohol-induced nerve damage.
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At the start of Stamler's research career, nitric oxide (NO) gas recently had been identified as a signaling molecule that mediated control of blood pressure. NO gas released from blood vessel endothelial cells travels into surrounding vascular smooth muscle cells to vasodilate arteries (thereby decreasing blood pressure) by binding to the heme cofactor in the enzyme soluble guanylyl cyclase to produce cyclic guanosine monophosphate (cGMP) that activates the cGMP-dependent protein kinase to phosphorylate proteins regulating muscle contraction, among other targets. NO gas is unsuited to widespread signaling throughout the body. Its actions cannot be controlled and it exhibits high affinity binding to the hemes in red blood cell hemoglobin, whose vast quantity should prevent NO activity from traversing the bloodstream.
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Cardiac glycosides have long served as the main medical treatment to congestive heart failure and cardiac arrhythmia, due to their effects of increasing the force of muscle contraction while reducing heart rate. Heart failure is characterized by an inability to pump enough blood to support the body, possibly due to a decrease in the volume of the blood or its contractile force. Treatments for the condition thus focus on lowering blood pressure, so that the heart does not have to exert as much force to pump the blood, or directly increasing the heart's contractile force, so that the heart can overcome the higher blood pressure. Cardiac glycosides, such as the commonly used digoxin and digitoxin, deal with the latter, due to their positive inotropic activity.
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The presumable effect that emodepside interaction with these channels would exert on the neuron would be to activate the channel causing potassium ion efflux, hyper-polarization and subsequent inhibition of excitatory neurotransmitter effect (acetylcholine if acting at the neuromuscular junction), having an inhibitory effect on synaptic transmission, the production of postsynaptic action potentials and ultimately muscle contraction (manifesting itself as paralysis or reduced pharyngeal pumping). Which out of Latrophilin receptors and BK-potassium channels is emodepside's primary site of action remains to be completely deduced. Both LAT-1/LAT-2 and slo-1 mutants (reduction/loss of function) show significant resistance to emodepside with it being conceivable that the presence of both is required for emodepside to induce its full effect.
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Poisoning can be caused by excessive consumption of generally safe substances, as in the case of water intoxication. Agents that act on the nervous system can paralyze in seconds or less, and include both biologically derived neurotoxins and so- called nerve gases, which may be synthesized for warfare or industry. Inhaled or ingested cyanide, used as a method of execution in gas chambers, or as a suicide method, almost instantly starves the body of energy by inhibiting the enzymes in mitochondria that make ATP. Intravenous injection of an unnaturally high concentration of potassium chloride, such as in the execution of prisoners in parts of the United States, quickly stops the heart by eliminating the cell potential necessary for muscle contraction.
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Since his thesis, Alain Chédotal has been interested in the development of neurons (called commissuraux) whose axons interconnect the right and left halves of the brain. These neurons allow 3D vision, the localization of sounds in space, the coordination of muscle contraction during movement, especially during walking. Their abnormal development is at the origin of neurological diseases such as mirror movements or HGPPS, a rare disease (mutation of the ROBO3 gene) that combines severe scoliosis and strabismus In a series of articles published over the past 20 years, Alain Chédotal has identified some of the molecular and cellular mechanisms controlling axon guidance and neuron migration in several brain regions. His team is also studying the evolution of axonal guidance mechanisms.
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The famous philosopher René Descartes (1596–1650) speculated that every activity of an animal was a necessary reaction to some external stimulus; the connection between the stimulus and the response was made through a definite nervous path. Luigi Galvani (1737–1798) demonstrated that electrical stimulation of nerve produced muscle contraction, and the competing work of Charles Bell (1774–1842) and Francois Magendie (1783–1855 ) led to the view that the ventral horns of the spinal cord were motor and the dorsal horns sensory. Only when cells were identified microscopically was it possible to progress beyond the crudest anatomical notion. J.E. Purkinje (1787–1869) in 1837 gave the first description of neurones, indeed a very early description of cells of any kind.
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IL-6 is also considered a myokine, a cytokine produced from muscle, which is elevated in response to muscle contraction. It is significantly elevated with exercise, and precedes the appearance of other cytokines in the circulation. During exercise, it is thought to act in a hormone-like manner to mobilize extracellular substrates and/or augment substrate delivery.. Like in humans, there seems to be an increase in IL-6 expression in working muscle and plasma IL-6 concentration during exercise in rodents. Studies in mice with IL-6 gene knockout indicate that lack of IL-6 in mice affect exercise function. It has been shown that the reduction of abdominally obesity by exercise in human adults can be reversed by the IL-6 receptor blocking antibody tocilizumab.
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EC coupling results in the sequential contraction of the heart muscles that allows blood to be pumped, first to the lungs (pulmonary circulation) and then around the rest of the body (systemic circulation) at a rate between 60 and 100 beats every minute, when the body is at rest.Gordan, R., Gwathmey, J.K. and Xie, L.-H. (2015) ‘Autonomic and endocrine control of cardiovascular function’, 7(4). This rate can be altered, however, by nerves that work to either increase heart rate (sympathetic nerves) or decrease it (parasympathetic nerves), as the body's oxygen demands change. Ultimately, muscle contraction revolves around a charged atom (ion), calcium (Ca2+),Marks, A.R. (2003) ‘Calcium and the heart: A question of life and death’, 111(5).
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The myogenic mechanism is how arteries and arterioles react to an increase or decrease of blood pressure to keep the blood flow within the blood vessel constant. Myogenic response refers to a contraction initiated by the myocyte itself instead of an outside occurrence or stimulus such as nerve innervation. Most often observed in (although not necessarily restricted to) smaller resistance arteries, this 'basal' tone may be useful in the regulation of organ blood flow and peripheral resistance, as it positions a vessel in a preconstricted state that allows other factors to induce additional constriction or dilation to increase or decrease blood flow. The smooth muscle of the blood vessels reacts to the stretching of the muscle by opening ion channels, which cause the muscle to depolarize, leading to muscle contraction.
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The helical F-actin filament found in muscles also contains a tropomyosin molecule, a 40-nanometre protein that is wrapped around the F-actin helix. During the resting phase the tropomyosin covers the actin's active sites so that the actin-myosin interaction cannot take place and produce muscular contraction (the interaction gives rise to a movement between the two proteins that, because it is repeated many times, produces a contraction). There are other protein molecules bound to the tropomyosin thread, these include the troponins that have three polymers: troponin I, troponin T, and troponin C. Tropomyosin's regulatory function depends on its interaction with troponin in the presence of Ca2+ ions. Both actin and myosin are involved in muscle contraction and relaxation and they make up 90% of muscle protein.
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Further work by another lab member, Brunó Straub, showed that Banga had extracted a combination of actin and myosin, which they called actinomyosin. Straub was able to isolate the actin and he, Banga, and other members of the lab carried out extensive characterization of actin, myosin, and actinomyosin, showing that it is responsible for muscle contraction. The widespread distribution of their findings was hampered by World War II – Szent-Györgyi was wanted for anti-Nazi activities and went into hiding, and other male colleagues left the lab to escape drafting. Banga remained behind and saved the Department of Medicinal Chemistry and its equipment by posting signs on the door in German, Hungarian, and Russian identifying the facilities as an infectious disease laboratory and reporting hours for the drop-off of infectious materials.
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Myosin light-chain phosphatase, more commonly called myosin phosphatase (), is an enzyme (specifically a serine/threonine-specific protein phosphatase) that dephosphorylates the regulatory light chain of myosin II. This dephosphorylation reaction occurs in smooth muscle tissue and initiates the relaxation process of the muscle cells. Thus, myosin phosphatase undoes the muscle contraction process initiated by myosin light-chain kinase. The enzyme is composed of three subunits: the catalytic region (protein phosphatase 1, or PP1), the myosin binding subunit (MYPT1), and a third subunit (M20) of unknown function. The catalytic region uses two manganese ions as catalysts to dephosphorylate the light-chains on myosin, which causes a conformational change in the myosin and relaxes the muscle. The enzyme is highly conserved and is found in all organisms’ smooth muscle tissue.
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Activated mast cells and basophils undergo a process called degranulation, during which they release histamine and other inflammatory chemical mediators called (cytokines, interleukins, leukotrienes, and prostaglandins) into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve stimulation, and smooth-muscle contraction. This results in runny nose, itchiness, shortness of breath, and potentially anaphylaxis. Depending on the individual, the allergen, and the mode of introduction, the symptoms can be system-wide (classical anaphylaxis), or localized to particular body systems; asthma is localized to the respiratory system while eczema is localized to the skin. After the chemical mediators of the acute response subside, late-phase responses can often occur due to the migration of other white blood cells such as neutrophils, lymphocytes, eosinophils, and macrophages to the initial reaction sites.
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Inositol trisphosphate (IP3) functions as an intracellular second messenger, which initiates the intracellular release of calcium ions (which activates intracellular enzymes, causes the release of hormones and neurotransmitters from the cells in which they are stored, and causes smooth muscle contraction when released by IP3), and the activation of protein kinase C (PKC), which is then translocated from the cell cytoplasm to the cell membrane. Although inositol trisphosphate, (IP3), diffuses into the cytosol, diacylglycerol (DAG) remains within the plasma membrane, due to its hydrophobic properties. IP3 stimulates the release of calcium ions from the smooth endoplasmic reticulum, whereas DAG is a physiological activator of protein kinase C (PKC), promoting its translocation from the cytosol to the plasma membrane. PKC is a multifunctional protein kinase which phosphorylates serine and threonine residues in many target proteins.
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A8V is point mutation on Troponin C (cTNC) that leads to a hypertrophic cardiomyopathy. The coordinated cardiac muscle contraction is regulated by the troponin complex on thin filament (troponin C which is calcium binding, troponin T that plays the role with tropomyosin, and troponin I which has an inhibitory action annulating the S1 ATPase activity in the presence of tropomyosin and troponin and absence of Ca2+). This mutation is determined by the change of Alanine to Valine at nucleotide 23 from C to T. Patients with this type of mutation shows thickness on the left ventricle wall of around 18 mm, compared to the normal this thickness would be 12 mm. Also, A8V affects the Ca2+ binding affinity compared to normal genotype and increased sensitivity on force development.
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Waldrop, Iwamoto and Haouzi, 2006 The authors can be classified in 2 schools: #Those who think that the major part of the respiratory changes are pre-programmed in the brain, which would imply that neurons from locomotion centers of the brain connect to respiratory centers in anticipation of movements. #Those who think that the major part of the respiratory changes result from the detection of muscle contraction, and that respiration is adapted as a consequence of muscular contraction and oxygen consumption. This would imply that the brain possesses some kind of detection mechanisms that would trigger a respiratory response when muscular contraction occurs. Many now agree that both mechanisms are probably present and complementary, or working alongside a mechanism that can detect changes in oxygen and/or carbon dioxide blood saturation.
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John E. Heuser (born August 29, 1942) is an American Professor of Biophysics in the department of Cell Biology and Physiology at the Washington University School of Medicine as well as a Professor at the Institute for Integrated Cell-Matieral Sciences (iCeMS) at Kyoto University. Heuser created quick- freeze deep-etch electron microscopy (a variant of cell unroofing), a pioneering technique that lets biologists take detailed pictures of fleeting events inside living cells. For decades, Heuser has used this technique to capture details of the molecular mechanisms that underlie many basic biological activities, including nerve cell signal transmission, muscle contraction, and most recently, the fusion of viruses with cells during the spread of infection. He compares quick-freeze deep-etch electron microscopy to using a stroboscopic flash to freeze the action in a photograph.
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In the miniseries Toxin: The Devil You Know, the King Cobra himself says: Piet Voorhees possesses certain unusual physical powers derived from his mutagenically altered physiology which, among other things, help him simulate the movement of a snake by using his great degree of independent control over every muscle in his body, enabling him to slither across the ground (at up to 50 miles per hour) without using his arms and legs, simply by muscle contraction. All of the bones in his body, including his skull, are malleable and his muscle tissue is exceedingly resilient, making his body very flexible and pliant. It is nearly impossible for him to break a bone or tear a muscle.F.B.I. Agent Coville revealed in White Tiger #1 that Piet has all of the same superpowers that his uncle possesses.
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The high voltage radio frequency (RF) discharges from the output terminal of a Tesla coil pose a unique hazard not found in other high voltage equipment: when passed through the body they often do not cause the painful sensation and muscle contraction of electric shock, as lower frequency AC or DC currents do. The nervous system is insensitive to currents with frequencies over 10 – 20 kHz. It is thought that the reason for this is that a certain minimum number of ions must be driven across a nerve cell's membrane by the imposed voltage to trigger the nerve cell to depolarize and transmit an impulse. At radio frequencies, there is insufficient time during a half-cycle for enough ions to cross the membrane before the alternating voltage reverses.
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A coup-contra-coup injury occurs as the brain is accelerated into the cranium as the head and neck hyperextend, and is then accelerated into the other side as the head and neck rebound to hyper-flexion or neutral position. "Volunteer studies of experimental, low-velocity rear-end collisions have shown a percentage of subjects to report short-lived symptoms", From this type of research it has been inferred that whiplash symptoms might not always have any pathological (injury) explanation. However, over the last decade, academic surgeons in the UK and US have sought to unravel the whiplash enigma. A 1000-case, four-year observational study published in 2012 said that the "missing link" in whiplash injuries is the trapezius muscle which may be damaged through eccentric muscle contraction during the whiplash mechanism described above and below.
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The acoustic reflex (also known as the stapedius reflex, stapedial reflex, auditory reflex, middle-ear-muscle reflex (MEM reflex, MEMR), attenuation reflex, cochleostapedial reflex or intra-aural reflex) is an involuntary muscle contraction that occurs in the middle ear in response to loud sound stimuli or when the person starts to vocalize. When presented with an intense sound stimulus, the stapedius and tensor tympani muscles of the ossicles contract. The stapedius stiffens the ossicular chain by pulling the stapes (stirrup) of the middle ear away from the oval window of the cochlea and the tensor tympani muscle stiffens the ossicular chain by loading the tympanic membrane when it pulls the malleus (hammer) in toward the middle ear. The reflex decreases the transmission of vibrational energy to the cochlea, where it is converted into electrical impulses to be processed by the brain.
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In this conception, neural processing begins with stimuli that activate sensory neurons, producing signals that propagate through chains of connections in the spinal cord and brain, giving rise eventually to activation of motor neurons and thereby to muscle contraction, i.e., to overt responses. Descartes believed that all of the behaviors of animals, and most of the behaviors of humans, could be explained in terms of stimulus-response circuits, although he also believed that higher cognitive functions such as language were not capable of being explained mechanistically. Charles Sherrington, in his influential 1906 book The Integrative Action of the Nervous System, developed the concept of stimulus- response mechanisms in much more detail, and Behaviorism, the school of thought that dominated Psychology through the middle of the 20th century, attempted to explain every aspect of human behavior in stimulus-response terms.
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When a motor neuron generates an action potential, it travels rapidly along the nerve until it reaches the neuromuscular junction, where it initiates an electrochemical process that causes acetylcholine to be released into the space between the presynaptic terminal and the muscle fiber. The acetylcholine molecules then bind to nicotinic ion-channel receptors on the muscle cell membrane, causing the ion channels to open. Sodium ions then flow into the muscle cell, initiating a sequence of steps that finally produce muscle contraction. Factors that decrease release of acetylcholine (and thereby affecting P-type calcium channels): 1) Antibiotics (clindamycin, polymyxin) 2) Magnesium: antagonizes P-type calcium channels 3) Hypocalcemia 4) Anticonvulsants 5) Diuretics (furosemide) 6) Eaton-Lambert syndrome: inhibits P-type calcium channels 7) Botulinum toxin: inhibits SNARE proteins Calcium channel blockers (nifedipine, diltiazem) do not affect P-channels.
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The alanine aminotransferase reaction takes place in reverse in the liver, where the regenerated pyruvate is used in gluconeogenesis, forming glucose which returns to the muscles through the circulation system. Glutamate in the liver enters mitochondria and is broken down by glutamate dehydrogenase into α-ketoglutarate and ammonium, which in turn participates in the urea cycle to form urea which is excreted through the kidneys.. The glucose–alanine cycle enables pyruvate and glutamate to be removed from muscle and safely transported to the liver. Once there, pyruvate is used to regenerate glucose, after which the glucose returns to muscle to be metabolized for energy: this moves the energetic burden of gluconeogenesis to the liver instead of the muscle, and all available ATP in the muscle can be devoted to muscle contraction. It is a catabolic pathway, and relies upon protein breakdown in the muscle tissue.
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With this design (marketed by E. Leitz) 60 mm beam separation was achieved in microscopy but here the new difficulty has arisen of balancing optical thicknesses of two separate microscope slide preparations (sample and dummy) and maintaining this critical balance during longer observations (e.g. time-lapse studies of living cells maintained at 37 °C), otherwise a gradual change in background interference colour occurs over time. The main advantage offered by interference microscopy measurements is the possibility of measuring the projected dry mass of living cells, which was first effectively exploited by Andrew Huxley in studies of striated muscle cell structure and function, leading to the sliding filament model of muscle contraction. Interference microscopy became relatively popular in the 1940–1970 decades but fell into disuse because of the complexity of the instrument and difficulties in both its use and in the interpretation of image data.
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A variety of different ions, including Calcium (Ca2+), play a vital role in the regulation of cellular functions. Calmodulin (CaM), a Calcium-binding protein, that mediates Ca2+ signaling is involved in all types of cellular mechanisms, including metabolism, synaptic plasticity, nerve growth, smooth muscle contraction, etc. Calmodulin allows for a number of proteins to aid in the progression of these pathways using their interactions with CaM in its Ca2+ bound conformation (Ca2+ -CaM) or as its Ca2+ -free state (ApoCaM). Proteins each have their own unique affinities for CaM, that can be manipulated by the presence or absence of Ca2+ concentrations to allow for the desired release or binding to CaM that determines its ability to carry out its cellular function. Proteins that get activated upon binding to Ca2+ -CaM, include Myosin light- chain kinase, Phosphatase, Ca2+/calmodulin-dependent protein kinase II(CaMKs), etc.
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It does this by binding to the SERCA and decreasing its attraction (affinity) to calcium, therefore preventing calcium uptake into the SR. Failure to remove Ca2+ from the cytosol, prevents muscle relaxation and therefore means that there is a decrease in muscle contraction too. However, molecules such as adrenaline and noradrenaline, can prevent PLB from inhibiting SERCA. When these hormones bind to a receptor, called a beta 1 adrenoceptor, located on the cell membrane, they produce a series of reactions (known as a cyclic AMP pathway) that produces an enzyme called protein kinase A (PKA). PKA can add a phosphate to PLB (this is known as phosphorylation), preventing it from inhibiting SERCA and allowing for muscle relaxation.Akin, B., Hurley, T., Chen, Z. and Jones, L. (2013) ‘The structural basis for phospholamban inhibition of the calcium pump in sarcoplasmic reticulum’, The Journal of Biological Chemistry.
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Subsequently, from 1894 Frank worked as an assistant in Carl von Voit's Physiological Institute in München where he studied cardiac function using approaches derived from earlier thermodynamic analyses of skeletal muscle contraction. His work on the behaviour of heart muscle was the topic of his post doctoral work. In 1902 he became an Extraordinary Professor and from 1905 to 1908 he undertook further work on this topic before becoming a full professor (Ordinariat). Then he returned to München to continue this work. Carl J. Wiggers visited Frank’s laboratory in 1912 and found Frank a ‘‘brilliant analyst, a skillful systematist, a talented mathematician, and a creative thinker...’’, but secretive and difficult to work with. Wiggers returned to the US in the fall of 1912 having ‘smuggled’ copies of some of Frank’s equipment out with him, despite this Wiggers and Frank seem to have maintained cordial relations subsequently.
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David Herman MacLennan, (July 3, 1937 - June 24, 2020) was a Canadian biochemist and geneticist known for his basic work on proteins that regulate calcium flux through the sarcoplasmic reticulum (SR), thereby regulating muscle contraction and relaxation, and for his discoveries in the field of muscle diseases caused by genetic defects in calcium regulatory proteins. Born in Swan River, Manitoba to Douglas MacLennan and Sigriður Sigurðardóttir, he received a BSA from the University of Manitoba in 1959 and a DSc (hc) in 2001. He received MS (1961) and PhD (1963) degrees from Purdue University under Harry Beevers, and was then a Postdoctoral Fellow (1963-1964) under David E. Green and an Assistant Professor (1964-1968) at the University of Wisconsin–Madison. In 1969, he was appointed Associate Professor in the Banting and Best Department of Medical Research and, later, Professor (1974), Chair (1978-1990), J. W. Billes Professor of Medical Research (1987-2007) and University Professor (1993-2015).
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A ribosome translating a protein The most complex macromolecular machines are found within cells, often in the form of multi-protein complexes. Some biological machines are motor proteins, such as myosin, which is responsible for muscle contraction, kinesin, which moves cargo inside cells away from the nucleus along microtubules, and dynein, which moves cargo inside cells towards the nucleus and produces the axonemal beating of motile cilia and flagella. "[I]n effect, the [motile cilium] is a nanomachine composed of perhaps over 600 proteins in molecular complexes, many of which also function independently as nanomachines ... Flexible linkers allow the mobile protein domains connected by them to recruit their binding partners and induce long-range allostery via protein domain dynamics." Other biological machines are responsible for energy production, for example ATP synthase which harnesses energy from proton gradients across membranes to drive a turbine-like motion used to synthesise ATP, the energy currency of a cell.
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Indeed, in C.elegans DAG regulates UNC-13, a plasma-membrane associated protein critical for vesicle-mediated neurotransmitter release and mutational studies have shown that two UNC-13 reduction of function mutants show resistance to emodepside, observations supporting this hypothesized mechanism of action. The mechanism by which activation of UNC-13 results in neurotransmitter release (the ultimate result of latrophilin activation) is through interaction with the synaptosomal membrane protein syntaxin, with UNC-13 binding to the N-terminus of syntaxin and promoting the switch from the closed form of syntaxin (which is incompatible with SNARE complex synaptobrevin, SNAP-25 and syntaxin formation) to its open formation so that SNARE complex formation can be achieved, thereby allowing vesicle fusion and release to take place. At a molecular level, the net result of the activation of this pathway, is the spontaneous stimulation of inhibitory PF1-like neuropeptide release (this is suspected due to Emodepside's inhibition of acetylcholine-elicited muscle contraction requiring both calcium ions and extracellular potassium ions, similar to the action of PF1/PF2).
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This different distribution of secondary chains accounts for the difference distribution of completed receptors, being IL-4RI prevalently expressed in lymphocyte, and IL-4RII prevalently in non-hematopoietic cells. Consequently, only IL-4, through IL-4R1, is able to modulate the function of lymphocytes inducing Th2 polarisation and B cells IgG1/IgE class switching, while IL-13 is mainly acting on myeloid cells and non-hematopoietic cells, having strong effects on mucus production, smooth muscle contraction, epithelium permeabilisation (e.g. allergic asthma). After the complete assemblage, the conformational changes in IL-4RI or IL-4RII tails leads to the intracellular signaling, starting with the auto and cross-phosphorylation of associated Jak kinases (Jak3 for IL-2Rγc, Jak1 for IL-4Rα, Jak2 and Tyk2 for IL-13Rα1), and followed by phosphorylation of intracellular domains of IL-4Rα in critical Y residues which are therefore activated to form the docking sites for downstream signalling molecules endowed with SH domains. While the docking sites in IL-4R1 (and consequently IL-4) are able to efficiently activate both STAT6 and IRS2 signalling molecules, IL-4RII (and consequently IL-13) only activates effectively STAT6.
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From these observations it is apparent that the myofibrillar fraction, which is a key component of the muscle, is targeted for net degradation (as noted above) for two reasons: # degradation of this fraction allows smaller-diameter fibers to become manifest to meet the reduced requirements for force generation, and # the unraveling of the myofibrillar system allows faster MHC isoforms to become incorporated into the contractile machinery to replace the slower ones so that the muscle is able to function more effectively under a reduced state of gravitational loading. Providing further insight is the observation that the unloading state of spaceflight and of HS also increases the expression of fast type II sarcoplasmic reticulum (SR) ATPase-driven calcium pumps (SERCA II) while repressing the slower type I SERCA calcium pump. Since calcium cycling is used to regulate fiber activation and relaxation, the SR component of the muscle fiber controls the synchrony of contraction-relaxation processes. Since calcium cycling and crossbridge cycling are the two major systems that account for the vast majority of the energy expended during muscle contraction to support movement, when this property of the muscle is switched to a faster system the muscle can function more effectively in the unloaded environment.
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Their existence was initially combated but is now established, for example by the demonstration of their messenger RNA in noradrenergic neurones.Ralf Gilsbach, Lutz Hein: Presynaptic metabotropic receptors for acetylcholine and adrenaline/noradrenaline. In: Thomas C. Südhoff, Klaus Starke (Eds.): Pharmacology of Neurotransmitter Release. Handbook of Experimental Pharmacology 184. Springer, Berlin 2008, pp. 261–288. . They differed from α-receptors on effector cells and in 1974 became the prototype α2-receptors, the long-known smooth muscle contraction-mediating receptors becoming α1. Even before dopamine was identified as the third catecholamine transmitter, Blaschko suspected it might possess receptors of its own, since Peter Holtz and his group in 1942 had found that small doses of dopamine lowered the blood pressure of rabbits and guinea pigs, whereas adrenaline always increased the blood pressure. Holtz erred in his interpretation, but Blaschko had ″no doubt that his observations are of the greatest historical importance, as the first indication of an action of dopamine that characteristically and specifically differs from those of the two other catecholamines″. A re-investigation of the blood pressure-lowering effect in dogs in 1964 proposed ″specific dopamine receptors for dilation″, and at the same time evidence for dopamine receptors distinct from α- and β-adrenoceptors accrued from other experimental approaches.
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Early researches by Friedrich Wilhelm Bessel (1784–1846) in Königsberg and Adolf Hirsch led to the development of a highly precise chronoscope by Matthäus Hipp that, in turn, was based on a design by Charles Wheatstone for a device that measured the speed of artillery shells (Edgell & Symes, 1906). Other timing instruments were borrowed from physiology (e.g., Carl Ludwig's kymograph) and adapted for use by the Utrecht ophthalmologist Franciscus Donders (1818–1899) and his student Johan Jacob de Jaager in measuring the duration of simple mental decisions. The 19th century was also the period in which physiology, including neurophysiology, professionalized and saw some of its most significant discoveries. Among its leaders were Charles Bell (1774–1843) and François Magendie (1783–1855) who independently discovered the distinction between sensory and motor nerves in the spinal column, Johannes Müller (1801–1855) who proposed the doctrine of specific nerve energies, Emil du Bois-Reymond (1818–1896) who studied the electrical basis of muscle contraction, Pierre Paul Broca (1824–1880) and Carl Wernicke (1848–1905) who identified areas of the brain responsible for different aspects of language, as well as Gustav Fritsch (1837–1927), Eduard Hitzig (1839–1907), and David Ferrier (1843–1924) who localized sensory and motor areas of the brain.
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