query: where is ca + + stored in the muscle

pos: Sarcoplasmic reticulum Sarcoplasmic reticulum The sarcoplasmic reticulum (SR) is a membrane-bound structure found within muscle cells that is similar to the endoplasmic reticulum in other cells. The main function of the SR is to store calcium ions (Ca). Calcium ion levels are kept relatively constant, with the concentration of calcium ions within a cell being 100,000 times smaller than the concentration of calcium ions outside the cell. This means that small increases in calcium ions within the cell are easily detected and can bring about important cellular changes (the calcium is said to be a second messenger; see calcium in biology for

pos: Micropeptide posterior, notochord. Although it is annotated as a lncRNA in zebrafish, mouse, and human, the 58 aa sORF was found to be highly conserved in vertebrates. Myoregulin (Mln) is encoded by a gene originally annotated as a lncRNA. Mln is expressed in all 3 types of skeletal muscle, and works similarly to the micropeptides phospholamban (Pln) in the cardiac muscle and sarcolipin (Sln) in slow (Type I) skeletal muscle. These micropeptides interact with sarcoplasmic reticulum Ca-ATPase (SERCA), a membrane pump responsible for regulating Ca uptake into the sarcoplasmic reticulum (SR). By inhibiting Ca uptake into the SR, they cause muscle

pos: Calcium sparks Calcium sparks A calcium spark is the microscopic release of calcium (Ca) 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. This process is important as it helps to maintain Ca concentration within the cell. It also initiates muscle contraction in skeletal and cardiac muscles and muscle relaxation in smooth muscles. Ca sparks are important in physiology as they show how Ca can be used at a subcellular level, to signal both local

pos: Calcium sparks all Ca spark events, their true properties can finally help us to answer the unsolved mystery of spark termination. Software Calcium sparks A calcium spark is the microscopic release of calcium (Ca) 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. This process is important as it helps to maintain Ca concentration within the cell. It also initiates muscle contraction in skeletal and cardiac muscles and muscle relaxation in smooth muscles. Ca sparks

pos: Inositol trisphosphate through the cytoplasm to the ER, or the sarcoplasmic reticulum (SR) in the case of muscle cells, once it has been produced by the action of PLC. Once at the ER, IP is able to bind to the Ins3P receptor (Ins3PR) on a ligand-gated Ca channel that is found on the surface of the ER. The binding of IP3 (the ligand in this case) to InsP3R triggers the opening of the Ca channel, and thus release of Ca into the cytoplasm. In heart muscle cells this increase in Ca activates the ryanodine receptor-operated channel on the SR, results in further

pos: Mydicar increase in cytosolic Ca during diastole by increasing reuptake into the SR. Mydicar Mydicar is a genetically targeted enzyme replacement therapy being studied for use in patients with severe heart failure. It is designed to increase the level of SERCA2a, a sarcoplasmic endoplasmic reticulum calcium (Ca) ATPase found in the membrane of the sarcoplasmic reticulum (SR). The SERCA2a gene is delivered to the heart via an adeno-associated viral vector. Using the α-myosin heavy chain gene promoter in the cardiac muscle cells, also called cardiomyocytes, Mydicar is able to direct the gene expression only to the heart muscle. Mydicar is being

pos: SERCA increasing the overall complexity of the Ca signaling mechanism. SERCA SERCA, or sarco/endoplasmic reticulum Ca-ATPase, or SR Ca-ATPase, is a calcium ATPase-type P-ATPase. SERCA resides in the sarcoplasmic reticulum (SR) within myocytes. It is a Ca ATPase that transfers Ca from the cytosol of the cell to the lumen of the SR at the expense of ATP hydrolysis during muscle relaxation. There are 3 major domains on the cytoplasmic face of SERCA: the phosphorylation and nucleotide-binding domains, which form the catalytic site, and the actuator domain, which is involved in the transmission of major conformational changes. It seems that, in

pos: SERCA SERCA SERCA, or sarco/endoplasmic reticulum Ca-ATPase, or SR Ca-ATPase, is a calcium ATPase-type P-ATPase. SERCA resides in the sarcoplasmic reticulum (SR) within myocytes. It is a Ca ATPase that transfers Ca from the cytosol of the cell to the lumen of the SR at the expense of ATP hydrolysis during muscle relaxation. There are 3 major domains on the cytoplasmic face of SERCA: the phosphorylation and nucleotide-binding domains, which form the catalytic site, and the actuator domain, which is involved in the transmission of major conformational changes. It seems that, in addition to the calcium-transporting properties, SERCA1 generates heat in

neg: Sarcoplasmic reticulum decreases the amount of free Ca within the SR (as more is bound to calsequestrin). Therefore, more calcium can be stored (the calsequestrin is said to be a buffer). It is primarily located within the junctional SR/terminal cisternae, in close association with the calcium release channel (described below). Calcium ion release from the SR, occurs in the junctional SR/terminal cisternae through a ryanodine receptor (RyR) and is known as a calcium spark. There are three types of ryanodine receptor, RyR1 (in skeletal muscle), RyR2 (in cardiac muscle) and RyR3 (in the brain). Calcium release through ryanodine receptors in the SR

neg: Calcium ATPase muscle cells. It is a Ca ATPase that transfers Ca from the cytosol of the cell to the lumen of the SR at the expense of ATP hydrolysis during muscle relaxation. Calcium ATPase Ca ATPase is a form of P-ATPase that transfers calcium after a muscle has contracted. The two kinds of calcium ATPase are: Plasma membrane Ca ATPase (PMCA) is a transport protein in the plasma membrane of cells that serves to remove calcium (Ca) from the cell. It is vital for regulating the amount of Ca within cells. In fact, the PMCA is involved in removing Ca from

neg: Brody myopathy rule out other similar disorders. There is no cure for BD, although treatment options are available for reducing the negative symptoms of BD. The drugs dantrolene and verapamil are used in BD treatment due to their effects on Ca. Dantrolene is a muscle relaxer that decreases the symptoms of BD by inhibiting Ca release channels in the sarcoplasmic reticulum, while verapamil sequesters Ca in the sarcoplasmic reticulum of muscle cells by functioning as a Ca channel blocker. These drugs act by limiting the amount of Ca from being released from the sarcoplasmic reticulum. When a muscle is stimulated, Ca is

neg: Calcium sparks the cell. During evoked Ca sparks, all clusters of ryanodine receptors, throughout the cell are activated at almost exactly the same time. This produces an increase in Ca concentration across the whole cell (not just locally) and is known as a whole cell Ca transient. This Ca then binds to a protein, called troponin, initiating contraction, through a group of proteins known as myofilaments. In smooth muscle cells, the Ca released during a spark is used for muscle relaxation. This is because, the Ca that enters the cell via the DHPR in response to the action potential, stimulates both muscle

neg: Ballistic movement 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. The second agonist muscle activation is suggested to terminate the negative acceleration of the antagonist muscle contraction and thus the ballistic movement. Ballistic movements are often powered through elastic energy storage and subsequent recovery mechanisms. The power required to produce the extremely rapid velocities of ballistic movements is made possible through muscle work being stored in elastic elements (such as tendons, aponeuroses, or even

neg: Phospholamban Phospholamban Phospholamban, also known as PLN or PLB, is a protein that in humans is encoded by the "PLN" gene. Phospholamban is a 52-amino acid integral membrane protein that regulates the Calcium (Ca) pump in cardiac muscle cells. This protein is found as a pentamer and is a major substrate for the cAMP-dependent protein kinase (PKA) in cardiac muscle. In the unphosphorylated state, phospholamban is an inhibitor of cardiac muscle sarcoplasmic reticulum Ca-ATPase (SERCA2) which transports calcium from cytosol into the sarcoplasmic reticulum. When phosphorylated (by PKA) - disinhibition of Ca-ATPase of SR leads to faster Ca uptake into the

neg: Brody myopathy released from the sarcoplasmic reticulum into the cytoplasm where it binds to a protein called troponin. This event allows the muscle fibers to overlap, causing a contraction. In BD, Ca levels are high in the cytoplasm, which means Ca can readily bind troponin, leading to muscles that are in an extended state of contraction. Brody myopathy Brody myopathy, also known as Brody disease (BD), is a rare disorder that affects skeletal muscle function. BD was first characterized in 1969 by Dr. Irwin A. Brody at Duke University Medical Center. Individuals with BD have difficulty relaxing their muscles after exercise. This

neg: Tropomyosin 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. The contraction of skeletal muscle is triggered by nerve impulses that in turn stimulate the release of Ca. The release of Ca from the sarcoplasmic reticulum causes an increase in the concentration of Ca in the cytosol. Calcium ions then bind to troponin, which is associated with tropomyosin. Binding causes changes in the

neg: Brody myopathy The gene involved in BD encodes the fast-twitch skeletal muscle ATPase, SERCA1. SERCA1 is a protein pump that uses ATP to pump Ca ions from the cytosol to the sarcoplasmic reticulum in skeletal muscle. In those with BD, SERCA1 pumps are unable to effectively move Ca across the membrane, leading to increased levels of cytoplasmic Ca. Increases in cytoplasmic Ca 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.

neg: Ballistic movement muscle). Muscle work is applied to these elastic elements over a relatively slow period of time, and is released very rapidly. Higher power output is produced because the energy is released in a much shorter amount of time than it is stored. 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

neg: Troponin vivo "and" in vitro". Individual subunits serve different functions: Smooth muscle does not have troponin. 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 Ca-binding subunit, playing the main role in Ca 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),

neg: Discovery and development of beta2 agonists muscles. cAMP levels are regulated through the activity of phosphodiesterase isozymes/isoforms, which degrades it to 5′-AMP. The mechanism by which cAMP induces relaxation in airway smooth muscle cells is not fully understood. It is believed that cAMP catalyzes the activation of PKA, which in turn phosphorylates key regulatory proteins involved in the control of muscle tone. cAMP also has a role in inhibition of calcium ion (Ca) release from intracellular stores, sequestration of intracellular Ca, and reduction of membrane Ca entry, leading to relaxation of the airway smooth muscle. The binding of norephinephrine to the binding site consists of one

neg: STIM2 (Ca) sensors which participate in a mechanism of Ca entry into the cell referred to as store-operated Ca entry (SOCE). Many cellular processes and signaling pathways are started by previous release of Ca stored in subcellular organelles, which needs of a continuous refilling. SOCE is considered the mechanism of store refilling and an essential mechanism of Ca signaling in non-electrically excitable cells. While STIM1 triggers SOCE, research on STIM2 function suggests a major role as feedback regulator that stabilizes basal cytosolic and S/ER Ca concentration [Ca]. STIM2 detects small decreases in Ca content stored in the S/ER, switches to the

neg: Parve101q Parve101q ParvE101Q is an experimental modification of parvalbumin, designed to delay calcium sequestration in heart muscles to enhance contraction. The protein parvalbumin has EF hand motifs used for calcium binding. EF hands are structural helix-loop-helix protein subunits that have a high affinity for calcium ions, and a moderate affinity for magnesium ions. In muscle, the binding of Ca by parvalbumin efficiently sequesters it following contraction. This increases the speed of muscle relaxation, allowing the muscle to contract again sooner. Although parvalbumin is classified as a delayed calcium buffer, it quickly sequesters Ca, usually before the muscle is done fully contracting.

neg: Calciseptine at low subjected amounts of 0.1 till 1 µM calciseptine. In mouse myotube the Ca currents show higher amplitude after incubation in calciseptine (1 μM). This effect of calciseptine on the Ca current develops relatively fast. Calciseptine changes the reversal potential of the Ca current in mouse myotubes. In adult frog skeletal muscle fibers calciseptine also causes an increased Ca current. This increase is comparable to the increase which was found in mouse myotubes. In contrast to the mouse myotubes calciseptine did not change the reversal potential of the Ca current. In rat muscle fibers after applying calciseptine there were

neg: Inositol trisphosphate increases in Ca through a process known as calcium-induced calcium release. IP may also activate Ca channels on the cell membrane indirectly, by increasing the intracellular Ca concentration. IP's main functions are to mobilize Ca from storage organelles and to regulate cell proliferation and other cellular reactions that require free calcium. In smooth muscle cells, for example, an increase in concentration of cytoplasmic Ca results in the contraction of the muscle cell. In the nervous system, IP serves as a second messenger, with the cerebellum containing the highest concentration of IP receptors. There is evidence that IP receptors play an

neg: Frank–Starling law by increasing the calcium sensitivity of the myofibrils, causing a greater number of actin-myosin cross-bridges to form within the muscle fibers. Specifically, the sensitivity of troponin for binding Ca increases and there is an increased release of Ca from the sarcoplasmic reticulum. In addition, there is a decrease in the spacing between thick and thin filaments, when a cardiac muscle fiber is stretched, allowing an increased number of cross-bridges to form. The force that any single cardiac muscle fiber generates is related to the sarcomere length at the time of muscle cell activation by calcium. The stretch on the individual

neg: Glaucine binds to the benzothiazepine site on L-type Ca-channels, thereby blocking calcium ion channels in smooth muscle like the human bronchus. Glaucine has no effect on intracellular calcium stores, but rather, does not allow the entry of Ca after intracellular stores have been depleted. Ca influx is a vital component in the process of muscular contraction, and the blocking of this influx therefore reduces the ability of the muscle to contract. In this way, glaucine can prevent smooth muscle from contracting, allowing it to relax. Glaucine has also been demonstrated to be a dopamine receptor antagonist, favoring D1 and D1-like receptors.

neg: Urinary system wastes (in the form of urine) exit the kidney via the ureters, tubes made of smooth muscle fibres that propel urine towards the urinary bladder, where it is stored and subsequently expelled from the body by urination (voiding). The female and male urinary system are very similar, differing only in the length of the urethra. Urine is formed in the kidneys through a filtration of blood. The urine is then passed through the ureters to the bladder, where it is stored. During urination, the urine is passed from the bladder through the urethra to the outside of the body. 8002,000

neg: Muscle fatigue The change in membrane potential causes a decrease in the release of calcium (Ca) from the sarcoplasmic reticulum. It was once believed that lactic acid build-up was the cause of muscle fatigue. The assumption was lactic acid had a "pickling" effect on muscles, inhibiting their ability to contract. Though the impact of lactic acid on performance is now uncertain, it may assist or hinder muscle fatigue. Produced as a by-product of fermentation, lactic acid can increase intracellular acidity of muscles. This can lower the sensitivity of contractile apparatus to Ca but also has the effect of increasing cytoplasmic Ca concentration

neg: Haemodynamic response which may interfere with astrocytes' constriction pathways and lead to vasodilation. It has also been proposed that NO may amplify astrocyte Ca influx and activate Ca-dependent potassium channels, releasing K into the interstitial space and inducing hyperpolarization of smooth muscle cells. 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

neg: Repetitive nerve stimulation response (a smaller and smaller muscle response with each repetitive stimulus) is abnormal and indicates NMJ dysfunction. This can be further confirmed if the response normalizes after administration of edrophonium or neostigmine. 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

neg: Troponin C type 1 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 (cTnI) and C-terminal (cTnI) regions. This prevents actin-myosin cross-bridging and effectively shuts off muscle contraction. As the cytoplasmic Ca concentration rises to ~1 μM during systole, Ca binding to the regulatory domain of cardiac troponin C (cNTnC) is the key event that leads to muscle contraction. Hydrophobic binding of cNTnC to the "switch" region of troponin I, cTnI, stabilizes the Ca-bound open conformation of cNTnC (increasing the Ca

neg: Intramyocellular lipids Intramyocellular lipids Intramyocellular lipids are fats stored in droplets in muscle cells. They provide an important energy source for working muscle. During exercise, a large amount of circulating free fatty acids are directed into muscle cells for energy; during rest, incoming fatty acids are instead stored in the muscle cell as triglycerides for later burning. However, an increase in muscle insulin resistance, caused by obesity, diabetes mellitus type 2, and metabolic syndrome, will result in an excess accumulation of intramyocellular lipids. Other expert opinions and researchers argue the exact opposite: that accumulation of intramyocellular lipids would, in fact, be the

neg: Ryanodine-Inositol 1,4,5-triphosphate receptor calcium channels have been identified in heart mitochondria where they provide the main pathway for Ca entry. Sun et al. (2011) have demonstrated oxygen-coupled redox regulation of the skeletal muscle ryanodine receptor-Ca release channel (RyR1;TC# 1.A.3.1.2) by NADPH oxidase 4. Ryanodine (Ry)-sensitive and inositol 1,4,5-triphosphate (IP)-sensitive Ca-release channels function in the release of Ca from intracellular storage sites in animal cells and thereby regulate various Ca-dependent physiological processes. The Ry receptors are activated as a result of the activity of dihydropyridine-sensitive Ca channels. Ry receptors, IP receptors, and dihydropyridine-sensitive Ca channels (TC#1.A.1.11.2) are members of the voltage-sensitive ion channel (VIC) superfamily (TC#

neg: Intramyocellular lipids cause of the insulin resistance that leads to type II diabetes. Insulin glargine Intramyocellular lipids Intramyocellular lipids are fats stored in droplets in muscle cells. They provide an important energy source for working muscle. During exercise, a large amount of circulating free fatty acids are directed into muscle cells for energy; during rest, incoming fatty acids are instead stored in the muscle cell as triglycerides for later burning. However, an increase in muscle insulin resistance, caused by obesity, diabetes mellitus type 2, and metabolic syndrome, will result in an excess accumulation of intramyocellular lipids. Other expert opinions and researchers argue

neg: Calcium-induced calcium release of CICR across the cell causes the significant increase in cytosolic Ca that is important in activating muscle contraction. Calcium-induced calcium release Calcium-induced calcium release (CICR) describes a biological process whereby calcium is able to activate calcium release from intracellular Ca stores (e.g., endoplasmic reticulum or sarcoplasmic reticulum). Although CICR was first proposed for skeletal muscle in the 1970s, it is now known that CICR is unlikely to be its primary mechanism for activating SR calcium release. Instead, CICR is thought to be crucial for excitation-contraction coupling in cardiac muscle and it is now obvious that CICR is a widely

neg: PPP1R14A smooth muscle enhances CPI-17 phosphorylation mainly through PKC and ROCK. Myosin phosphatase inhibition increases myosin phosphorylation and smooth muscle contraction in the absence of increased intracellular Ca concentration. This phenomenon is known as Ca sensitization, which occurs in response to agonist stimulation of smooth muscle. In Purkinje neuron, CPI-17 is involved in long-term synaptic depression. There are three homologues of CPI-17: CPI-17 is up-regulated some cancer cells, and causes hyperphosphorylation of tumor suppressor merlin/NF2. PPP1R14A Protein phosphatase 1 regulatory subunit 14A also known as CPI-17 (C-kinase potentiated Protein phosphatase-1 Inhibitor Mr = 17 kDa) is a protein that in humans

neg: Myometrium are caused by changes in the distribution of Ca, Na, K and Cl ions between the intracellular and extracellular spaces, which, in turn, reflects the permeability of the plasma membrane to each of those ions. K is the major ion responsible for such changes in ion flux, reflecting changes in various K channels. The excitation-contraction coupling of uterine smooth muscle is also very similar to that of other smooth muscle in general, with intracellular increase in calcium (Ca) leading to contraction. However, the stimulating factors for uterine smooth muscle differs from other types of muscles in the body. Removal of

neg: Glucose Some glucose is converted to lactic acid by astrocytes, which is then utilized as an energy source by brain cells; some glucose is used by intestinal cells and red blood cells, while the rest reaches the liver, adipose tissue and muscle cells, where it is absorbed and stored as glycogen (under the influence of insulin). Liver cell glycogen can be converted to glucose and returned to the blood when insulin is low or absent; muscle cell glycogen is not returned to the blood because of a lack of enzymes. In fat cells, glucose is used to power reactions that synthesize

neg: Calcium pump important roles as an intracellular messenger. The release of a large amount of free Ca can trigger a fertilized egg to develop, skeletal muscle cells to contract, secretion by secretory cells and interactions with Ca -responsive proteins like calmodulin. To maintain low concentrations of free Ca in the cytosol, cells use membrane pumps like calcium ATPase found in the membranes of sarcoplasmic reticulum of skeletal muscle. These pumps are needed to provide the steep electrochemical gradient that allows Ca to rush into the cytosol when a stimulus signal opens the Ca channels in the membrane. The pumps are also necessary

neg: Ripping (bodybuilding) Too much cardiovascular exercise can directly affect muscle tissue if it is used excessively and without eating the correct food. The reason for this is because if the human body doesn't have sufficient energy stored in the form of glucose, then it will begin using energy from other sources, i.e., muscles. For example, eating a little extra carbohydrates (which eventually transforms into glucose) will help the body to divert away from muscle tissue and extract energy from the glucose supplies. The time in which one eats is an important factor in ripping where cardiovascular training is concerned. Particular foods take

neg: Absorptive state Absorptive state Absorptive state is the period in which the gastrointestinal tract is full and the anabolic processes exceed catabolism. The fuel used for this process is glucose. Carbohydrates - Simple sugars are sent to the liver where they are converted to glucose. The glucose then travels to the blood or is converted to glycogen and fat (triglyceride). The glycogen and fat will be stored in the liver and adipose tissue, respectively, as reserves for the post-absorptive state. The remaining glucose is taken in for use by body cells or stored in skeletal muscle as glycogen. Triglycerides - Chylomicrons, the

neg: Bodybuilding and other slowly digesting carbohydrates, which release energy in a more stable fashion than high-glycemic sugars and starches. This is important as high-glycemic carbohydrates cause a sharp insulin response, which places the body in a state where it is likely to store additional food energy as fat. However, bodybuilders frequently do ingest some quickly digesting sugars (often in form of pure dextrose or maltodextrin) after a workout. This may help to replenish glycogen stored within the muscle, and to stimulate muscle protein synthesis. The motor proteins actin and myosin generate the forces exerted by contracting muscles. Current advice says that

neg: Myocyte junction, each muscle fiber receives input from just one somatic efferent neuron. Action potential in a somatic efferent neuron causes the release of the neurotransmitter acetylcholine. When the acetylcholine is released it diffuses across the synapse and binds to a receptor on the sarcolemma, a term unique to muscle cells that refers to the cell membrane. This initiates an impulse that travels across the sarcolemma. When the action potential reaches the sarcoplasmic reticulum it triggers the release of Ca from the Ca channels. The Ca flows from the sarcoplasmic reticulum into the sarcomere with both of its filaments. This causes

neg: Calciseptine the breakdown of the protein by proteases. Calciseptine has been shown to block L-type calcium channels, thus inhibiting smooth muscle contraction and cardiac function. Voltage-dependent calcium channels are important for generating electrical signals in excitable cells like neurons and cardiac or smooth muscle cells. N-type Ca 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 Ca-channels include T-type and P-type channels. Because the presence of calcium in the cytosol

neg: MYL2 MYL2 Myosin regulatory light chain 2, ventricular/cardiac muscle isoform (MLC-2) also known as the regulatory light chain of myosin (RLC) is a protein that in humans is encoded by the "MYL2" gene. This cardiac ventricular RLC isoform is distinct from that expressed in skeletal muscle (MYLPF), smooth muscle (MYL12B) and cardiac atrial muscle (MYL7). Ventricular myosin light chain-2 (MLC-2v) refers to the ventricular cardiac muscle form of myosin light chain 2 (Myl2). MLC-2v is a 19-KDa protein composed of 166 amino acids, that belongs to the EF-hand Ca binding superfamily. MLC-2v interacts with the neck/tail region of the muscle thick

neg: Calcium ATPase Calcium ATPase Ca ATPase is a form of P-ATPase that transfers calcium after a muscle has contracted. The two kinds of calcium ATPase are: Plasma membrane Ca ATPase (PMCA) is a transport protein in the plasma membrane of cells that serves to remove calcium (Ca) from the cell. It is vital for regulating the amount of Ca within cells. In fact, the PMCA is involved in removing Ca from all eukaryotic cells. There is a very large transmembrane electrochemical gradient of Ca driving the entry of the ion into cells, yet it is very important for cells to maintain low

neg: Asynchronous muscles In comparison, synchronous muscles in "Schistocerca americana" are composed of 65% myofibril, 23.5% mitochondria and 9.6% sarcoplasmic reticulum. Although synchronous muscle has a higher percentage of myofibril, the cross-sectional area of asynchronous myofibril is 3.7 µm as opposed to 0.82 µm in synchronous muscle for the previously described species. The defining characteristic of asynchronous muscles is that there is no direct relationship between neural activation and muscle contraction. Typically, the number of muscle contractions is an order of magnitude greater than the number of action potentials sent to the muscle. Instead of directly controlling force generation, neural signals maintain [Ca]

neg: Physiology of marathons maintained. The Phosphogenic (ATP-PC) anaerobic energy pathway restores ATP after its breakdown via Creatine Phosphate stored in skeletal muscle. This pathway is anaerobic because it does not require oxygen to synthesize or utilize ATP. ATP restoration only lasts for approximately the first 30 seconds of exercise. This rapid rate of ATP production is essential at the onset of exercise. The amount of creatine phosphate and ATP stored in the muscle is small, readily available, and is utilized quickly due these two factors. An example of exercise that would primarily use this energy pathway could be weight lifting or performing sprints.

neg: Toom's rule lattice by taking the spin value of current site plus that of the 4 neighboring sites and makes this spin +1 in the next time step if the sum is positive and -1 if the sum is negative. Just as for Toom's rule we can construct a probabilistic version of the majority vote CA where the output can be changed with probability q from spin +1 to spin -1 and with probability p from spin -1 to a spin +1. Instead of ground states information is stored in stable states of the CA. These are states such that the spins

neg: Triadin Ca receptors. Triadin is also able to sense luminal Ca concentrations by mediating interactions between RYR2 and CASQ2. Triadin has several different forms; Trisk 95 and Trisk 51, which are expressed in skeletal muscle, and Trisk 32 (CT1), which is mainly expressed in cardiac muscle. TRDN has been shown to interact with RYR1. Triadin is required to physically link the RYR2 and CASQ2 proteins, so that RYR2 channel activity can be regulated by CASQ2. The linkage of RYR2 with CASQ2 occurs via highly charged luminal sections of Triadin that are characterized as alternating positively and negatively charged amino acids, known

neg: Lipid signaling different second messengers, inositol triphosphate (IP) and Diacylglycerol (DAG). IP is soluble and diffuses freely into the cytoplasm. As a second messenger, it is recognized by the inositol triphosphate receptor (IP3R), a Ca channel in the endoplasmic reticulum (ER) membrane, which stores intracellular Ca. The binding of IP to IP3R releases Ca from the ER into the normally Ca-poor cytoplasm, which then triggers various events of Ca signaling. Specifically in blood vessels, the increase in Ca concentration from IP releases nitric oxide, which then diffuses into the smooth muscle tissue and causes relaxation. DAG remains bound to the membrane by

neg: Myophosphorylase Myophosphorylase Myophosphorylase or glycogen phosphorylase, muscle associated (PYGM) is the muscle isoform of the enzyme "glycogen phosphorylase" and is encoded by the "PYGM" gene. This enzyme helps break down glycogen (a form of stored carbohydrate) into glucose-1-phosphate (not glucose), so it can be used within the muscle cell. Mutations in this gene are associated with McArdle disease (myophosphorylase deficiency), a glycogen storage disease of muscle. "PYGM" is located on the q arm of chromosome 11 in position 13.1 and has 20 exons. PYGM, the protein encoded by this gene, is a member of the glycogen phosphorylase family and is a

neg: Ryanodine-Inositol 1,4,5-triphosphate receptor calcium channels Ryanodine-Inositol 1,4,5-triphosphate receptor calcium channels The ryanodine-inositol 1,4,5-triphosphate receptor Ca channel (RIR-CaC) family includes Ryanodine receptors and Inositol trisphosphate receptors. Members of this family are large proteins, some exceeding 5000 amino acyl residues in length. This family belongs to the Voltage-gated ion channel (VIC) superfamily. Ry receptors occur primarily in muscle cell sarcoplasmic reticular (SR) membranes, and IP receptors occur primarily in brain cell endoplasmic reticular (ER) membranes where they effect release of Ca into the cytoplasm upon activation (opening) of the channel. They are redox sensors, possibly providing a partial explanation for how they control cytoplasmic Ca. Ry receptors

neg: Cardiac excitation-contraction coupling into the cell. Secondly Ca indirectly activates proteins, called myofilaments, resulting in muscle contraction. The two main myofilaments in cardiac (and skeletal) muscle are actin and myosin. Ca binds to a protein called troponin, which is bound to the actin filament. This binding causes a shape change in the troponin which exposes areas on the actin, to which the head of the myosin filament binds. The binding of the myosin head to actin is known as a cross-bridge. A molecule, called adenosine triphosphate (ATP) which is produced by an intracellular structure called a mitochondrion, is then used, as a source

neg: Calcium sparks cardiac muscle cells, however, these receptors are located within structures known as T-tubules, that are extensions of the plasma membrane penetrating deep into the cell (see figure 1). These DHPRs are located directly opposite to the ryanodine receptors, located on the sarcoplasmic reticulum and activation, by the action potential causes the DHPRs to change shape. In cardiac and smooth muscle, activation of the DHPR results in it forming an ion channel. This allows Ca to pass into the cell, increasing the local Ca concentration, around the RyR. When four Ca molecules bind to the RyR, it opens, resulting in a

neg: Calcium sparks changes, known as local control, as well as whole cell changes. As mentioned above, Ca sparks depend on the opening of ryanodine receptors, of which there are three types: Opening of the channel allows Ca to pass from the SR, into the cell. This increases the local Ca concentration around the RyR, by a factor of 10. Calcium sparks can either be evoked or spontaneous, as described below. Electrical impulses, known as action potentials, travel along the cell membrane (sarcolemma) of muscle cells. Located in the sarcolemma of smooth muscle cells are receptors, called dihydropyridine receptors (DHPR). In skeletal and

neg: Canadian health claims for food functions as a calcium-binding protein thereby enhancing calcium absorption. As a result of the body scavenging for calcium from bones; the bones may become fragile, brittle and weak, which in prolonged states can lead to osteoporosis and or bone fractures. Conversely, if there is an adequate level of Ca in the blood, PTH will be inhibited. Similarly, in the case where there is an excess of Ca in the blood, it will be stored in bones as this is the nutritional reserve for Calcium and Phosphorus Bone depends upon dietary intake to supply the bulk materials needed for synthesis of

neg: Sarcoplasmic reticulum binds to the pump, causing the pump to change shape. This shape change causes the cytosolic side of the pump to open, allowing the two Ca to enter. The cytosolic side of the pump then closes and the sarcoplasmic reticulum side opens, releasing the Ca into the SR. A protein found in cardiac muscle, called phospholamban (PLB) has been shown to prevent SERCA from working. 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 Ca from the cytosol, prevents muscle relaxation and therefore means

neg: Sarcolipin beta-adrenergic responses in atria. Recently it has been shown that SLN is an important mediator of muscle based thermogenesis and loss of sarcolipin predisposes mice to diet-induced obesity thus suggesting its role in energy metabolism and regulation of weight gain SLN (gene) has been shown to interact with PLN and ATP2A1. Sarcolipin Sarcolipin is a protein that in humans is encoded by the "SLN" gene. Sarcoplasmic reticulum Ca-ATPases are transmembrane proteins that catalyze the ATP-dependent transport of Ca from the cytosol into the lumen of the sarcoplasmic reticulum in muscle cells. The SLN gene encodes a small transmembrane proteolipid that

neg: Muscle weakness if there were no lactic acid to remove the chloride ions. Ultimately, it is uncertain if lactic acid reduces fatigue through increased intracellular calcium or increases fatigue through reduced sensitivity of contractile proteins to Ca. Muscle cells work by detecting a flow of electrical impulses from the brain which signals them to contract through the release of calcium by the sarcoplasmic reticulum. Fatigue (reduced ability to generate force) may occur due to the nerve, or within the muscle cells themselves. New research from scientists at Columbia University suggests that muscle fatigue is caused by calcium leaking out of the muscle

neg: Amifampridine The dose-limiting side effects include tingling or numbness, difficulty sleeping, fatigue, and loss of muscle strength. Interactions via the liver's cytochrome P450 enzyme system are considered unlikely. In Lambert–Eaton myasthenic syndrome, acetylcholine release is inhibited as antibodies involved in the host response against certain cancers cross-react with Ca channels on the prejunctional membrane. Amifampridine works by blocking potassium channel efflux in nerve terminals so that action potential duration is increased. Ca channels can then be open for a longer time and allow greater acetylcholine release to stimulate muscle at the end plate. Amifampridine is quickly and almost completely (93–100%) absorbed

neg: Biological functions of nitric oxide by deactivating them. Guanylate cyclase is a key component of the famous smooth-muscle relaxing properties of NO. It is a heme-containing enzyme that is acted on by NO, which binds to the heme. Cyclic-GMP activates protein kinase G, which causes reuptake of Ca and the opening of calcium-activated potassium channels. The fall in concentration of Ca ensures that the myosin light-chain kinase (MLCK) can no longer phosphorylate the myosin molecule, thereby stopping the crossbridge cycle and leading to relaxation of the smooth muscle cell. Nitric oxide dilates blood vessels, raising blood supply and lowering blood pressure. Conversely, it helps protect

neg: Calcium-induced calcium release other cells. Since CICR is a positive-feedback system, it has been of great interest to elucidate the mechanism(s) responsible for its termination. Excitation-contraction coupling in myocardium relies on sarcolemma depolarization and subsequent Ca entry to trigger Ca release from the sarcoplasmic reticulum. When an action potential depolarizes the cell membrane, voltage-gated Ca channels (e.g., L-type calcium channels) are activated. CICR occurs when the resulting Ca influx activates ryanodine receptors on the SR membrane, which causes more Ca to be released into the cytosol. In cardiac muscle, the result of CICR is observed as a spatio-temporally restricted Ca spark. The result

neg: Troponin C type 1 cNTnC enters into a rapid equilibrium between closed and open forms, however, the closed form still predominates. The structural domain, cCTnC, exists as a "molten globule" in the apo state, but forms a well structured open conformation in the Ca-bound state. These structural differences change the relative stabilities of the apo- and Ca-bound states, accounting for the divergent Ca-binding affinities between the two domains. In cardiac muscle, cTnC binds to cardiac troponin I (cTnI) and cardiac troponin T (cTnT), whereas cTnC binds to slow skeletal troponin I (ssTnI) and troponin T (ssTnT) in slow-twitch skeletal muscle. The structural domain of

neg: Goniopora toxin in response to an unusually small depolarizing stimulus. The 19 kDa GPT stimulates Ca influx and its activity can be prevented in the presence of a calcium channel blocker. This suggests that GPT directly activates Ca channels or indirectly activates Ca by influencing sodium currents. Frequency-dependent effects of GPT were studied on bullfrog atrial muscle. Application of GPT on the muscle showed broadening of action potential duration and showed a positive inotropic effect. When the stimulus frequency was increased, the effects of GPT were considerably suppressed as opposed to low-frequency stimulation. Also, the action potential was prolonged when long intervals

neg: Malignant hyperthermia a person's parents in an autosomal dominant manner. The condition may also occur as a new mutation or be associated with a number of inherited muscle diseases, such as central core disease. In susceptible individuals, the medications induce the release of stored calcium ions within muscle cells. The resulting increase in calcium concentrations within the cells cause the muscle fibers to contract. This generates excessive heat and results in metabolic acidosis. Diagnosis is based on symptoms in the appropriate situation. Family members may be tested to see if they are susceptible by muscle biopsy or genetic testing. Treatment is with

neg: Calcium sparks larger release of Ca, from the SR . This process, of using Ca to activate release of Ca from the SR is known as calcium-induced calcium release. However, in skeletal muscle the DHPR touches the RyR. Therefore, the shape change of the DHPR activates the RyR directly, without the need for Ca to flood into the cell first. This causes the RyR to open, allowing Ca to be released from the SR. Ca sparks can also occur in cells at rest (i.e. cells that have not been stimulated by an action potential). This occurs roughly 100 times every second in

neg: Cardiac excitation-contraction coupling of energy, to help move the myosin head, carrying the actin. As a result, the actin slides across the myosin filament shortening the muscle. This is called a power stroke. Myosin then detaches from the actin and resets itself back to its original position, binding to another part of the actin and producing another power stroke, shortening the muscle further. This process continues, with the myosin head moving in a motion similar to that of an oar rowing a boat, until the Ca level within the cell decreases (see figure 1). Contraction ends when the Ca is removed from the

neg: Asynchronous muscles is sufficient Ca. This can be achieved in one of two ways. First, two antagonistic muscles can be configured with elastic structures such that the contraction of one muscle stretches the other, causing it to activate and vice versa. This configuration is found in the power muscles of flying insects. Second, a single asynchronous muscle can deform an elastic element which then stretches the muscle and causes the muscle to contract again. This setup is used by "Drosophila" to oscillate mechanosensory organs known as halteres. As long as neural stimulus turn the muscles "on," both systems will continue to oscillate.

neg: Weakness myocytes. This can occur through a simple lack of energy to fuel contraction, or through interference with the ability of Ca to stimulate actin and myosin to contract. Weakness Weakness or asthenia is a symptom of a number of different conditions. The causes are many and can be divided into conditions that have true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in neuromuscular junction disorders, such as myasthenia gravis. Muscle cells work by detecting a flow of electrical impulses from the

neg: Sarcolipin Sarcolipin Sarcolipin is a protein that in humans is encoded by the "SLN" gene. Sarcoplasmic reticulum Ca-ATPases are transmembrane proteins that catalyze the ATP-dependent transport of Ca from the cytosol into the lumen of the sarcoplasmic reticulum in muscle cells. The SLN gene encodes a small transmembrane proteolipid that regulates several sarcoplasmic reticulum Ca-ATPases by reducing the accumulation of Ca in the sarcoplasmic reticulum without affecting the rate of ATP hydrolysis. Ablation of sarcolipin increases atrial Ca transient amplitudes and enhanced atrial contractility. Furthermore, atria from sarcolipin-null mice have blunted response to isoproterenol stimulation, implicating sarcolipin as a mediator of

neg: Key ring file certificate to the entity. This certificate received from the CA has to be stored in the key ring. Key ring file A key ring is a file which contains multiple public keys of certificate authority (CA). A key ring is a file which is necessary for Secure Sockets Layer (SSL) connection over the web. It is securely stored on the server which hosts the website. It contains the public/private key pair for the particular website. It also contains the public/private key pairs from various certificate authorities and the trusted root certificate for the various certification authorities. An entity or website

neg: Pressure–volume loop analysis in cardiology be explained on the basis of preload. As the heart fills with more blood than usual, there is an increase in the load experienced by each myocyte. This stretches the muscle fibers, increasing the affinity of troponin C to Ca ions, causing a greater number of cross-bridges to form within the muscle fibers. This increases the contractile force of the cardiac muscle, resulting in increased stroke volume. Frank–Starling curves can be used as an indicator of muscle contractility (inotropy). However, there is no single Frank–Starling curve on which the ventricle operates but rather a family of curves, each of which

neg: Glucose pancreatic β-cells. GLUT3 is highly expressed in nerve cells. Glucose from the bloodstream is taken up by GLUT4 from muscle cells (of the skeletal muscle and heart muscle) and fat cells. GLUT14 is formed exclusively in testes. Excess glucose is broken down and converted into fatty acids, which are stored as triacylglycerides. In the kidneys, glucose in the urine is absorbed via SGLT1 and SGLT2 in the apical cell membranes and transmitted via GLUT2 in the basolateral cell membranes. About 90% of kidney glucose reabsorption is via SGLT2 and about 3% via SGLT1. In plants and some prokaryotes, glucose is

neg: Vasoconstriction calcium (Ca ions) within vascular smooth muscle cells. However, the specific mechanisms for generating an increased intracellular concentration of calcium depends on the vasoconstrictor. Smooth muscle cells are capable of generating action potentials, but this mechanism is rarely utilized for contraction in the vasculature. Hormonal or pharmacokinetic components are more physiologically relevant. 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

neg: Myofibril into ADP and phosphate. Energy is released and stored in the myosin head to utilize for later movement. The myosin heads now return to their upright relaxed position. If calcium is present, the process is repeated. When a muscle contracts, the actin is pulled along myosin toward the center of the sarcomere until the actin and myosin filaments are completely overlapped. The H zone becomes smaller and smaller due to the increasing overlap of actin and myosin filaments, and the muscle shortens. Thus when the muscle is fully contracted, the H zone is no longer visible. Note that the actin

neg: Vasomotion Vasomotion Vasomotion is the spontaneous oscillation in tone of blood vessel walls, independent of heart beat, innervation or respiration. While vasomotion was first observed by Jones in 1852, the complete mechanisms responsible for its generation and its physiological importance remain to be elucidated, however several hypotheses have been put forth. Intracellular calcium (Ca) concentration exhibits periodic oscillations in vascular smooth muscle cells. This is thought to result from Ca release from intracellular stores, due to inositol triphosphate and ryanodine-sensitive channel activation. This activation has been shown to result in either Ca "sparks", highly localized calcium increases, or "waves", global Ca

neg: Muscle weakness reduction in contractile force due to the direct or indirect effects of the reduction of substrates or accumulation of metabolites within the muscle fiber. This can occur through a simple lack of energy to fuel contraction, or through interference with the ability of Ca to stimulate actin and myosin to contract. It was once believed that lactic acid build-up was the cause of muscle fatigue. The assumption was lactic acid had a "pickling" effect on muscles, inhibiting their ability to contract. The impact of lactic acid on performance is now uncertain, it may assist or hinder muscle fatigue. Produced as

neg: Exercise physiology loss of integrity to the blood brain barrier. Hyperthermia also can lower cerebral blood flow, and raise brain temperature. 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 Ca ions from the muscle fibre’s sarcoplasmic reticulum. The

neg: Sarcoplasm inside the cell membrane (sarcolemma), and a smooth endoplasmic reticulum (specialized for muscle function and called the sarcoplasmic reticulum). While "sarcoplasm" and "myoplasm," viewed etymologically, might seem to be synonyms, they are not. Whereas sarcoplasm is a type of cytoplasm, myoplasm is the entire contractile portion of muscle tissue. Sarcoplasm Sarcoplasm is the cytoplasm of a myocyte (muscle fiber). It is comparable to the cytoplasm of other cells, but it contains unusually large amounts of "glycosomes" (granules of stored glycogen) and significant amounts of myoglobin, an oxygen-binding protein. The calcium ion concentration in sarcoplasma is also a special element of

neg: Ryanodine receptor a function of Ca concentration is a bell-curve. Furthermore, RyR can sense the Ca concentration inside the ER/SR and spontaneously open in a process known as store overload-induced calcium release (SOICR). RyRs are especially important in neurons and muscle cells. In heart and pancreas cells, another second messenger (cyclic ADP-ribose) takes part in the receptor activation. The localized and time-limited activity of Ca in the cytosol is also called a "Ca wave". The building of the wave is done by RyRs form docking platforms for a multitude of proteins and small molecule ligands. The cardiac-specific isoform of the receptor (RyR2)

neg: Sarcoplasm Sarcoplasm Sarcoplasm is the cytoplasm of a myocyte (muscle fiber). It is comparable to the cytoplasm of other cells, but it contains unusually large amounts of "glycosomes" (granules of stored glycogen) and significant amounts of myoglobin, an oxygen-binding protein. The calcium ion concentration in sarcoplasma is also a special element of the muscle fiber; it is the means by which muscle contractions take place and are regulated. It contains mostly myofibrils (which are composed of sarcomeres), but its contents are otherwise comparable to those of the cytoplasm of other cells. It has a Golgi apparatus near the nucleus, mitochondria just

neg: Calcium cycle bone growth, cellular signalling, blood clotting, muscle contraction and neuron function. Calcium is one of the essential components of bone, contributing to its strength and structure in addition to being the main site at which it is stored within the body. Within the muscles, its primary use is to enable contractions. Muscle cells draw calcium from the blood, allowing it to bind with troponin, a component of the muscle fibre that signals for a contraction by moving actin and myosin. After a contraction, calcium dissipates and the filaments move back to a resting state before the release of more calcium

neg: Electrolyte channels". For example, muscle contraction is dependent upon the presence of calcium (Ca), sodium (Na), and potassium (K). Without sufficient levels of these key electrolytes, muscle weakness or severe muscle contractions may occur. Electrolyte balance is maintained by oral, or in emergencies, intravenous (IV) intake of electrolyte-containing substances, and is regulated by hormones, in general with the kidneys flushing out excess levels. In humans, electrolyte homeostasis is regulated by hormones such as antidiuretic hormones, aldosterone and parathyroid hormones. Serious electrolyte disturbances, such as dehydration and overhydration, may lead to cardiac and neurological complications and, unless they are rapidly resolved, will

neg: Muscular system since muscles store little ATP, they must continuously replace the discharged ADP with ATP. Muscle tissue also contains a stored supply of a fast acting recharge chemical, creatine phosphate, which when necessary can assist with the rapid regeneration of ADP into ATP. Calcium ions are required for each cycle of the sarcomere. Calcium is released from the sarcoplasmic reticulum into the sarcomere when a muscle is stimulated to contract. This calcium uncovers the actin binding sites. When the muscle no longer needs to contract, the calcium ions are pumped from the sarcomere and back into storage in the sarcoplasmic reticulum.

neg: Calcium pump Calcium pump Calcium pumps are a family of ion transporters found in the cell membrane of all animal cells. They are responsible for the active transport of calcium out of the cell for the maintenance of the steep Ca electrochemical gradient across the cell membrane. Calcium pumps play a crucial role in proper cell signalling by keeping the intracellular calcium concentration roughly 10,000 times lower than the extracellular concentration. Failure to do so is one cause of muscle cramps. The plasma membrane Ca ATPase and the sodium-calcium exchanger are together the main regulators of intracellular Ca concentrations. Ca has many

neg: Reduced muscle mass, strength and performance in space of different muscle types to oxidize the long-chain fatty acid, palmitate, was observed. This latter finding is in agreement with the observation that muscles exposed to spaceflight increase the level of stored lipid within their myofibers. Additionally, use of the metabolic pathway for glucose uptake is increased in muscles undergoing HS. Thus, while the enzyme data are equivocal, it appears that in response to states of unloading, some shift in substrate preference may occur whereby carbohydrates are preferentially utilized based on utilization capability. If this is indeed the case, it could result in a greater tendency for muscle fatigue, should

neg: Elastic mechanisms in animals their intrinsic enzymatic processes. The process of amplification begins when a muscle contracts steadily, storing elastic strain energy in the tendon. Once the energy is completely stored, the tendon releases it in a much shorter time span than was required to create it within the muscle. The tendon is actually producing energy at a level slightly below the work done by the contracting muscle, but because power is equivalent to work over time, the considerably shorter time increases the power significantly. This phenomenon has been observed in numerous vertebrate behaviors, one of the most notable being jumping. Observed in kangaroos,

neg: Elastic mechanisms in animals of muscle fibers results in both an accumulation and loss of energy. Even though energy is briefly stored in stretched elastic elements are also released, there is an overall net gain. This shows that muscle fibers are effective in both power production and for energy consumption utilized by the body or individual body segments with muscle-tendon units. Tendons, connective tissues, and molecular structures within a skeletal system can act as power amplifiers by storing energy gradually and releasing it rapidly. This amplification process is possible because spring-like tendons are not limited by the same rate limits imposed upon muscles by

neg: Calcium-induced calcium release Calcium-induced calcium release Calcium-induced calcium release (CICR) describes a biological process whereby calcium is able to activate calcium release from intracellular Ca stores (e.g., endoplasmic reticulum or sarcoplasmic reticulum). Although CICR was first proposed for skeletal muscle in the 1970s, it is now known that CICR is unlikely to be its primary mechanism for activating SR calcium release. Instead, CICR is thought to be crucial for excitation-contraction coupling in cardiac muscle and it is now obvious that CICR is a widely occurring cellular signaling process present even in many non-muscle cells, e.g. in the insulin-secreting pancreatic beta cells and many

neg: Larynx the only muscle capable of separating the vocal cords for normal breathing is the posterior cricoarytenoid. If this muscle is incapacitated on both sides, the inability to pull the vocal folds apart (abduct) will cause difficulty breathing. Bilateral injury to the recurrent laryngeal nerve would cause this condition. It is also worth noting that all muscles are innervated by the recurrent laryngeal branch of the vagus except the cricothyroid muscle, which is innervated by the external laryngeal branch of the superior laryngeal nerve (a branch of the vagus). Additionally, intrinsic laryngeal muscles present a constitutive Ca-buffering profile that predicts their

neg: Telokin is higher than MLCK concentration. Telokin has been shown to bind to unphosphorylated myosin filaments and to stimulate myosin mini-filament assembly in vitro. The major mechanism for initiating smooth muscle (SM)2 contraction is the rise in Ca concentration resulting in an increase in 20-kDa myosin regulatory light chain (MLC20) phosphorylation at Ser-19. KRP presence in different tissues has been assessed by immunoblots using anti-KRP antibodies, and by analyses of its mRNA in Northern blot. KRP is an abundant smooth muscles-pecific protein. So far it has not been detected in non-muscle tissues and striated muscles. Its concentration in gizzard muscle is

neg: Dantrolene Dantrolene Dantrolene sodium is a postsynaptic muscle relaxant that lessens excitation-contraction coupling in muscle cells. It achieves this by inhibiting Ca ions release from sarcoplasmic reticulum stores by antagonizing ryanodine receptors. It is the primary drug used for the treatment and prevention of malignant hyperthermia, a rare, life-threatening disorder triggered by general anesthesia. It is also used in the management of neuroleptic malignant syndrome, muscle spasticity (e.g. after strokes, in paraplegia, cerebral palsy, or patients with multiple sclerosis), and 2,4-dinitrophenol poisoning, and the related compounds dinoseb and dinoterb. It is marketed by Par Pharmaceuticals LLC as Dantrium (in North America)

neg: Cardiac excitation-contraction coupling body is at rest. 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 (Ca), which is responsible for converting the electrical energy of the action potential into mechanical energy (contraction) of the muscle. This is achieved in a region of the muscle cell, called the transverse-tubule during a process known as calcium induced calcium release. Located in the wall of the right atrium is a group of specialised cells, called the

neg: Muscle weakness a by-product of fermentation, lactic acid can increase intracellular acidity of muscles. This can lower the sensitivity of contractile apparatus to calcium ions (Ca) but also has the effect of increasing cytoplasmic Ca concentration through an inhibition of the chemical pump that actively transports calcium out of the cell. This counters inhibiting effects of potassium ions (K) on muscular action potentials. Lactic acid also has a negating effect on the chloride ions in the muscles, reducing their inhibition of contraction and leaving K as the only restricting influence on muscle contractions, though the effects of potassium are much less than

neg: Vsevolod Tkachuk in vessel cells. It was demonstrated that when a single smooth muscle cell is rhythmically stretched, it shows increased expression of a number of genes (caldesmon, calpomin, α-actine, smooth muscle myosin), along with increased proliferation ability. Discovery and research of T-Cadherin functions In the early of the 90s, while studying blood cells, V. A. Tkachuk and his colleagues discovered that calcium ions get mobilized in platelets under the influence of lipoproteins, which leads to their aggregation. This effect is more pronounced under the influence of adrenaline. Around the same time it was discovered that Ca is mobilized in smooth muscle

neg: Calcium in biology 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. In the endothelial cells which line the inside of blood vessels, Ca ions can regulate several signaling pathways which cause the smooth muscle surrounding blood vessels to relax. Some of these Ca-activated pathways include the stimulation of eNOS to produce nitric oxide, as well as the stimulation of K channels to efflux K and cause hyperpolarization of the cell membrane. Both nitric oxide and hyperpolarization cause the smooth

neg: CA Workload Automation AE default user interface for AutoSys is Workload Control Centre (WCC). It consists of a number of applets that provide job management: eTrust Embedded Entitlements Manager allows user and group access to AutoSys and WCC resources via an ACL administered GUI, access can be granted or denied based upon filters and groups or managed explicitly. Several components used by AutoSys are shared with other CA products (e.g. CA NSM or CA Audit) and are stored in a common folder. Following are the classification of autosys job types. The command job is used to execute a command. Box job contains one or

neg: Vasomotion displaying altered flow patterns as compared to normotensive vessels. Vasomotion Vasomotion is the spontaneous oscillation in tone of blood vessel walls, independent of heart beat, innervation or respiration. While vasomotion was first observed by Jones in 1852, the complete mechanisms responsible for its generation and its physiological importance remain to be elucidated, however several hypotheses have been put forth. Intracellular calcium (Ca) concentration exhibits periodic oscillations in vascular smooth muscle cells. This is thought to result from Ca release from intracellular stores, due to inositol triphosphate and ryanodine-sensitive channel activation. This activation has been shown to result in either Ca

neg: Electrical conduction system of the heart characteristic of an action potential. Like skeletal muscle, depolarization causes the opening of voltage-gated calcium channels and release of Ca from the t-tubules. This influx of calcium causes calcium-induced calcium release from the sarcoplasmic reticulum, and free Ca 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 important, the spontaneous depolarizations necessary for

neg: Calciseptine 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. The average tetanic tension after applying calciseptine was slightly higher than the control value. Though calciseptine gives an increase in charge movement and increase in influx of Ca through L-type channels this has no major effects on contraction of the muscle, even in tetanus. Research on rats and guinea pigs