TY - JOUR. T1 - Vitamin D does not increase calcium absorption in young women. T2 - A randomized clinical trial. AU - Gallagher, J. Christopher. AU - Jindal, Prachi S.. AU - Smith, Lynette M.. PY - 2014/5. Y1 - 2014/5. N2 - It is commonly said that vitamin D should be used to increase calcium absorption. We tested this statement in a dose-response study of vitamin D on calcium absorption. A total of 198 white and African American women, aged 25 to 45 years, with vitamin D insufficiency, serum 25-hydroxyvitamin D (25OHD) 2D) amongst the lowest groups. Vitamin D doses up to 2400 IU daily did not increase calcium absorption. No threshold level of serum 25OHD for calcium absorption was found at baseline or in the longitudinal study, suggesting that active transport of calcium is saturated at very low serum 25OHD levels AB - It is commonly said that vitamin D should be used to increase calcium absorption. We tested this statement in a dose-response study of vitamin D on calcium absorption. A total of ...
New Delhi: June 18, 2016: Calcium is important for maintaining strong bones. It also helps in blood clotting, early developmental growth and muscle contraction and relaxation. Calcium can be easily obtained from natural food sources like leafy vegetables, yoghurt, nuts and cheese. However, the majority of the Indians, specifically in the age group of 14-20 years suffer from calcium deficiency due to lack of efficient absorption. Calcium deficiency disease, also known as hypocalcemia, occurs when you dont get enough calcium. It is crucial that people are educated about the effects of calcium deficiency on the overall health and wellbeing of people in the long run. Those suspected of suffering from calcium deficiency should not self-diagnose and treat themselves by consuming large amounts of calcium supplements. Instead, it is important that they consult their doctor and together devise a healthy eating plan supported by supplementation, said Padma Shri Awardee Dr KK Aggarwal - Honorary ...
In the latest Under the Microscope issue, Professor László Csernoch and his research group from the University of Debrecen (Hungary) explain their research into intracellular calcium homeostasis, which may seem like a simple statement. However, this fascinating area of research covers many areas, from arteriosclerosis to space travel.. They also explain how they rely on ratiometric calcium measurements, and the benefits they have experienced from their recent switch to the CoolLED pE-340fura LED Illumination System with their Zeiss Axio Vert microscope.. Read more about intracellular calcium homeostasis. This content was supplied by CoolLED.. ...
Aequorin, which luminesces in the presence of calcium, was injected into photoreceptor cells of Limulus ventral eye. A bright light stimulus elicited a large increase in aequorin luminescence, the aequorin response, indicating a rise of intracellular calcium ion concentration, Cai. The aequorin response reached a maximum after the peak of the electrical response of the photoreceptor, decayed during a prolonged stimulus, and returned to an undetectable level in the dark. Reduction of Cao reduced the amplitude of the aequorin response by a factor no greater than 3. Raising Cao increased the amplitude of the aequorin response. The aequorin response became smaller when membrane voltage was clamped to successively more positive values. These results indicate that the stimulus-induced rise of Cai may be due in part to a light-induced influx of Ca and in part to release of Ca from an intracellular store. Our findings are consistent with the hypothesis that a rise in Cai is a step in the sequence of ...
Oscillations in cytoplasmic calcium concentration ([Ca2+]i) in airway smooth muscle cells (ASMC), primarily mediated by repetitive openings and closings of inositol trisphosphate receptor (IP3R) channels situated in the sarcoplasmic reticulum membrane, have been found to be important in generating and maintaining airway contractile force. However, it has been unclear about the mechanisms accounting for such oscillations, especially how the IP3R behaves in living cells to perform its function. In light of the extensive existence of calcium oscillations in many other cell types, although this thesis focuses on modeling calcium oscillations in ASMC due to their importance for the study of pathology of asthma, it also aims to solve some major questions in a wider context: • What is the mechanism for the formation of the repetitive calcium releases? How is the mechanism connected to the dynamics of the IP3R? • How best (or simply) should the IP3R be modeled for performing its function? • Should ...
Microdomains of high intracellular calcium ion concentration, [Ca2+]i, have been hypothesized to occur in living cells exposed to stimuli that generate inositol 1,4,5-trisphosphate (IP3). Mitochondrially targeted recombinant aequorin was used to show that IP3-induced Ca2+ mobilization from intracellular stores caused increases of mitochondrial Ca2+ concentration, [Ca2+]m, the speed and amplitude of which are not accounted for by the relatively small increases in mean [Ca2+]i. A similar response was obtained by the addition of IP3 to permeabilized cells but not by perfusion of cells with Ca2+ at concentrations similar to those measured in intact cells. It is concluded that in vivo, domains of high [Ca2+]i are transiently generated close to IP3-gated channels and sensed by nearby mitochondria; this may provide an efficient mechanism for optimizing mitochondrial activity upon cell stimulation. ...
TY - JOUR. T1 - Intracellular free calcium increases in cultured cortical neurons deprived of oxygen and glucose.. AU - Goldberg, M. P.. AU - Choi, D. W.. PY - 1990/11/1. Y1 - 1990/11/1. N2 - Dissociated neocortical cultures from fetal mice exposed transiently to a medium lacking both glucose and oxygen developed neuronal degeneration without glial degeneration. We have found that this injury depends on extracellular calcium and is associated with uptake of calcium from the culture medium. We measured free cytoplasmic calcium in individual neurons using the fluorescent calcium indicator fluo-3 and provide evidence that oxygen and glucose deprivation injury increases the intracellular calcium signal. Both intracellular calcium elevation and subsequent neuronal loss could be blocked by the N-methyl-D-aspartate receptor antagonist dextrorphan.. AB - Dissociated neocortical cultures from fetal mice exposed transiently to a medium lacking both glucose and oxygen developed neuronal degeneration ...
In previous efforts to characterize sarcoplasmic reticulum function in human muscles, it has not been possible to distinguish the relative contributions of fast-twitch and slow-twitch fibers. In this study, we have used light scattering and 45Ca to monitor Ca accumulation by the sarcoplasmic reticulum of isolated, chemically skinned human muscle fibers in the presence and absence of oxalate. Oxalate (5 mM) increased the capacity for Ca accumulation by a factor of 35 and made it possible to assess both rate of Ca uptake and relative sarcoplasmic reticulum volume in individual fibers. At a fixed ionized Ca concentration, the rate and maximal capacity (an index of sarcoplasmic reticulum volume) both varied over a wide range, but fibers fell into two distinct groups (fast and slow). Between the two groups, there was a 2- to 2.5-fold difference in oxalate-supported Ca uptake rates, but no difference in average sarcoplasmic reticulum volumes. Intrinsic differences in sarcoplasmic reticulum function ...
Calcium is an essential mineral for several important functions in the body of an animal. Calcium is needed for the development of the fetal skeleton as well as for the secretion of milk in lactating females, making pregnant and nursing guinea pigs more prone to calcium deficiency if their increased nutritional needs are not being met. This related type of calcium deficiency usually develops in the one to two weeks before, or shortly after, giving birth. Also at higher risk of calcium deficiency are obese or stressed guinea pigs, or guinea pigs that have already been pregnant several times.
In many cell types agonist-receptor activation leads to a rapid and transient release of Ca 2+ from intracellular stores via activation of inositol 1,4,5 trisphosphate (InsP 3 ) receptors (InsP 3 Rs). Stimulated cells activate store- or receptor-operated calcium channels localized in the plasma membrane, allowing entry of extracellular calcium into the cytoplasm, and thus replenishment of intracellular calcium stores. Calcium entry must be finely regulated in order to prevent an excessive intracellular calcium increase. Junctate, an integral calcium binding protein of endo(sarco)plasmic reticulum membrane, (a) induces and/or stabilizes peripheral couplings between the ER and the plasma membrane, and (b) forms a supramolecular complex with the InsP 3 R and the canonical transient receptor potential protein (TRPC) 3 calcium entry channel. The full-length protein modulates both agonist-induced and store depletion-induced calcium entry, whereas its NH 2 terminus affects receptor-activated calcium ...
TY - JOUR. T1 - Stimulation of d2 dopamine receptors decreases intracellular calcium levels in rat anterior pituitary cells but not striatal synaptosomes. T2 - A flow cytometric study using indo‐1. AU - Wolf, Marina E.. AU - Kapatos, Gregory. PY - 1989. Y1 - 1989. N2 - An important question is whether all D2 dopamine (DA) receptors employ the same signal transduction mechanisms. Anterior pituitary cells and striatal synaptosomes, which possess pharmacologically similar D2 DA receptors, were compared with respect to the effect of D2 DA receptor stimulation on free intracellular Ca2+ levels ([Ca2+]i). Flow cytometry, in combination with either the fluorescent calcium indicator indo‐1 or fluorescent voltage‐sensitive dyes, was used to measure [Ca2+]i and to detect changes in membrane potential. In subpopulations of anterior pituitary cells, increases in [Ca2+]i were produced by elevated K+, veratridine, thyrotropin‐releasing hormone, and BAY K 8644. These increases were blocked by ...
Cellular stress responses often involve elevation of cytosolic calcium levels, and this has been suggested to stimulate autophagy. Here, however, we demonstrated that agents that alter intracellular calcium ion homeostasis and induce ER stress-the calcium ionophore A23187 and the sarco/endoplasmic reticulum Ca (2+)-ATPase inhibitor thapsigargin (TG)-potently inhibit autophagy. This anti-autophagic effect occurred under both nutrient-rich and amino acid starvation conditions, and was reflected by a strong reduction in autophagic degradation of long-lived proteins. Furthermore, we found that the calcium-modulating agents inhibited autophagosome biogenesis at a step after the acquisition of WIPI1, but prior to the closure of the autophagosome. The latter was evident from the virtually complete inability of A23187- or TG-treated cells to sequester cytosolic lactate dehydrogenase. Moreover, we observed a decrease in both the number and size of starvation-induced EGFP-LC3 puncta as well as reduced numbers of
What would we do if we had no bones? We would just be all skin, spineless. Could not even stand, cant even walk. That is why we need our bones strong and healthy. That is why calcium is the most abundant mineral in our body. 99% of calcium is found in our bones and in our teeth. Two or three pounds of it are mostly found in our bones and in our teeth. Imagine a world without bones. Imagine a world without teeth.. As much as calcium is very essential for our teeth and bones, we also use it in different ways. We use calcium to be an electrolyte for transmitting nerve signals, for water balance, for neutralizing acid/alkaline in our bodies and maintaining osmotic pressure. Calcium also helps in blood clotting, muscle contraction and heart muscle function.. So in order to prevent calcium deficiency we are listing whole foods that are a good calcium source. Other than food we are also listing other ways so we can avoid calcium deficiency. So, here they are.. ...
The secretion of ions and fluid plays a critical role in a variety of physiological activities that are vital to homeostatic mechanisms in animals. Control of such secretory activity is achieved by a range of neurotransmitters and hormones many of which act intracellularly by generating the second messenger inositol 1,4,5-trisphosphate (InsP3) and increasing cytosolic free calcium ion concentrations ([Ca2+]i). These increases are achieved by a combination of the InsP3-induced release of Ca2+ from specific intracellular stores and the activation of Ca2+ entry from the extracellular environment. The [Ca2+]i signal represents a balance between the adequate activation of components of the secretory mechanism and the avoidance of [Ca2+]i levels that are toxic to the cell. Resting [Ca2+]i is maintained low by the action of Ca2+ pumps on the intracellular stores and plasma membrane, with the result that gradients for Ca2+ movement into the cytosol from either of these two sources are very large and ...
In a study of rat adrenal chromaffin cells, which have dense-core secretory granules, Chen et al. reported that release of Gβγ in response to activation of Gi/o-coupled receptors inhibited secretion by reducing quantal size. The reduction in quantal size was measured by amperometry in response to application of adenosine triphosphate (ATP), opioids, or somatostatin. Although each agonist partially inhibited calcium signaling, each also inhibited secretion induced by caffeine, which bypasses plasma membrane calcium channels to promote release of calcium directly from intracellular stores. Thus, application of ATP, for example, which can inhibit plasma membrane calcium channels, does not affect calcium transients induced by caffeine, yet still inhibits secretion. The agonists did not inhibit secretion stimulated by activation of muscarinic acetylcholine receptors (mAChR), but pharmacological inhibition of protein kinase C (PKC), which is downstream of the Gq-coupled mAChR, restored ATP-, ...
Chronic hypertension remains a major cause of global mortality and morbidity. It is a complex disease that is the clinical manifestation of multiple genetic, environmental, nutritional, hormonal, and aging-related disorders. Evidence supports a role for vascular aging in the development of hypertension involving an impairment in endothelial function together with an alteration in vascular smooth muscle cells (VSMCs) calcium homeostasis leading to increased myogenic tone. Changes in free intracellular calcium levels ([Ca] ) are mediated either by the influx of Ca from the extracellular space or release of Ca from intracellular stores, mainly the sarcoplasmic reticulum (SR). The influx of extracellular Ca occurs primarily through voltage-gated Ca channels (VGCCs), store-operated Ca channels (SOC), and Ca release-activated channels (CRAC), whereas SR-Ca release occurs through inositol trisphosphate receptor (IPR) and ryanodine receptors (RyRs). IPR-mediated SR-Ca release, in the form of Ca waves, ...
Variations of free calcium concentration ([Ca2+]) are powerful intracellular signals, controlling contraction as well as metabolism in muscle cells. To fully understand the role of calcium redistribution upon excitation and contraction in skeletal muscle cells, the local [Ca2+] in different compartments needs to be taken into consideration. Fluorescent probes allow the determination of [Ca2+] in the cytosol where myofibrils are embedded, the lumen of the sarcoplasmic reticulum (SR) and the mitochondrial matrix. Previously, models have been developed describing intracellular calcium handling in skeletal and cardiac muscle cells. However, a comprehensive model describing the kinetics of the changes in free calcium concentration in these three compartments is lacking. We designed a new 3D compartmental model of the half sarcomere with radial symmetry, which accounts for diffusion of Ca2+ into the three compartments and simulates its dynamics at rest and at various rates of stimulation in mice ...
Serum calcium. Routine serum calcium assay measures the total serum calcium value. Total serum calcium contains about 50% bound calcium (literature range, 35%-55%) and about 50% nonbound calcium (literature range, 35%-65%). (Traditionally, nonbound calcium was called ionized calcium and is also known as free or dialyzable calcium.) Bound calcium is subdivided into calcium bound to protein and calcium complexed to nonprotein compounds. About 45% of total calcium (30%-50%) is protein-bound, of which 70%-80% is bound to albumin. The remaining 5% (5%-15%) of total calcium is complexed to ions such as citrate, phosphate, sulfate, and bicarbonate, which are not part of the serum proteins. Ionized calcium levels can be measured directly by ion-selective electrode techniques or less accurately can be estimated from total serum calcium and albumin or total protein values using certain formulas. The most commonly used calcium correction formula is that of R.B. Payne:. Adjusted calcium = (measured ...
We simultaneously measured presynaptic free calcium ion concentration ([Ca2+]i) and synaptic strength at the crayfish claw opener neuromuscular junction (nmj) under a variety of experimental conditions. Our experiments were designed both to test the hypothesis that elevated [Ca2+]i is necessary and sufficient for the induction of a form of synaptic enhancement that persists for several seconds after tetanic stimulation--augmentation--and to determine the quantitative relationship between elevated [Ca2+]i and this enhancement. Action potential trains increased [Ca2+]i and enhanced transmission. During the decay phase of synaptic enhancement known as augmentation (time constant of decay approximately 7 sec at 20 degrees C with , 200 microM fura-2 in terminals), [Ca2+]i was elevated 700 nM or less above rest and an essentially linear relationship between [Ca2+]i and enhancement was observed. Introduction of exogenous Ca2+ buffers into the presynaptic terminal slowed the buildup and recovery ...
Localized, transient elevations in cytosolic Ca2+, known as Ca2+ sparks, caused by Ca2+ release from sarcoplasmic reticulum, are thought to trigger the opening of large conductance Ca2+-activated potassium channels in the plasma membrane resulting in spontaneous transient outward currents (STOCs) in smooth muscle cells. But the precise relationships between Ca2+ concentration within the sarcoplasmic reticulum and a Ca2+ spark and that between a Ca2+ spark and a STOC are not well defined or fully understood. To address these problems, we have employed two approaches using single patch-clamped smooth muscle cells freshly dissociated from toad stomach: a high speed, wide-field imaging system to simultaneously record Ca2+ sparks and STOCs, and a method to simultaneously measure free global Ca2+ concentration in the sarcoplasmic reticulum ([Ca2+]SR) and in the cytosol ([Ca2+]CYTO) along with STOCs. At a holding potential of 0 mV, cells displayed Ca2+ sparks and STOCs. Ca2+ sparks were associated with STOCs;
Education. Dr. Keirstead received her Ph.D. in neurophysiology from Queens University, Kingston, Canada, where she studied the role of neck muscle motoneurons and sensory afferents in the control of head movement in the laboratory of Dr. P. Ken Rose. As a post-doctoral fellow in the laboratories of Dr. M. Rasminsky and Dr. A.J. Aguayo at McGill University, Dr. Keirstead examined the capabilities of retinal neurons to regenerate axons and form functional synaptic connections with central nervous system neurons. Dr. Keirstead came to the University of Minnesota as a research associate in the Department of Physiology where she used calcium imaging techniques to study the regulation of intracellular calcium ion concentration in glial cells by neurotransmitters in the laboratory of Dr. Robert Miller. She continued these studies as an assistant professor in the Department of Ophthalmology.. Dr. Keirstead is an assistant professor in the Department of Integrative Biology and Physiology, and the ...
Peter Gillham Natural Vitality - Calm Plus Calcium Calcium is an important nutrient essential for maintaining total body health. Your body needs it every day-not just to keep your bones and teeth strong, but to ensure proper functioning of muscles and nerves. It even helps your blood to clot. But can too much calcium be a problem? Yes, it can. Excess calcium can deplete its vital sister mineral, magnesium, from the body and, as a result, can bring about symptoms of magnesium depletion, listed on the green page of this brochure. Calcium acts to excite nerves and is necessary for muscle contraction. Magnesium, on the other hand, calms nerves and is needed for muscle relaxation. Calcium makes bones stiff and hard, but magnesium is needed to avoid their becoming brittle. An excess of unabsorbed calcium may result in kidney stones and deposits in soft tissues such as arteries and heart cells, where it can calcify or harden into insoluble calcium. You experience the tensing (calcium)
Peter Gillham Natural Vitality - Calm Plus Calcium Calcium is an important nutrient essential for maintaining total body health. Your body needs it every day-not just to keep your bones and teeth strong, but to ensure proper functioning of muscles and nerves. It even helps your blood to clot. But can too much calcium be a problem? Yes, it can. Excess calcium can deplete its vital sister mineral, magnesium, from the body and, as a result, can bring about symptoms of magnesium depletion, listed on the green page of this brochure. Calcium acts to excite nerves and is necessary for muscle contraction. Magnesium, on the other hand, calms nerves and is needed for muscle relaxation. Calcium makes bones stiff and hard, but magnesium is needed to avoid their becoming brittle. An excess of unabsorbed calcium may result in kidney stones and deposits in soft tissues such as arteries and heart cells, where it can calcify or harden into insoluble calcium. You experience the tensing (calcium)
We investigated the roles of sodium-calcium exchange, sarcoplasmic reticulum, and mitochondria in Cai homeostasis in cultured chick ventricular cells. Specifically, the influence of low sodium medium on contractile state, calcium fluxes, and cytosolic free [Ca] [( Ca]i) was examined. [Ca]i was measured using fura-2. Mean [Ca]i in control medium was 126 +/- 14 nM. Exposure of cells to sodium-free or sodium- and calcium-free medium (choline-substituted) resulted in contracture development, which returned toward the baseline level over 2-3 minutes. The Nao-free contracture was associated with a tenfold increase in [Ca]i (1,280 +/- 110 nM) followed by a gradual decrease to a level fourfold above control [Ca]i (460 +/- 58 nM). Nao- and Cao-free contracture was associated with a fivefold increase in [Ca]i (540 +/- 52 nM) followed by a rapid decrease to below 80 nM. Sodium-free medium failed to produce an increase in [Ca]i or contracture in cells preexposed to calcium-free medium, although caffeine, ...
The effects of several lactones were studied in a microsomal fraction of dog myocardium thought to be sarcoplasmic reticulum. The lactones increased the steady-state accumulation and turnover of calcium only in the presence of ATP, and augmented the calcium-stimulated ATPase activity. When the effective concentrations of the lactones were exceeded, there were no further alterations in calcium accumulation or turnover. A correlation between the capacity of these lactones to increase calcium accumulation and turnover and their relative cardiotonic activity, as reported in the literature, was noted. The potency of the lactones in relation to calcium metabolism in the microsomes is influenced by ring saturation, position of the double bond, and presence of a steroid ring system to the lactone moiety.. ...
CitationAlvarez-Lacalle, E. [et al.]. A General Equilibrium Model to Study Intracellular Calcium Homeostasis. New Insights on Ventricular Function. A: The Heart by Numbers: Integrating Theory, Computation, and Experiment to Advance Cardiology. The Heart by numbers: integrating theory, computation, and experiment to advance cardiology, Berlin, Germany: September 4-7, 2018: Biophysical Society Thematic Meeting: program & abstracts. 2018, p. 44 ...
TY - JOUR. T1 - Protamine augments stretch induced calcium increase in vascular endothelium. AU - Murase, Kichiro. AU - Naruse, Keiji. AU - Kimura, Akira. AU - Okumura, Kenji. AU - Hayakawa, Tetsuo. AU - Sokabe, Masahiro. PY - 2001. Y1 - 2001. N2 - Human umbilical vein endothelial cells cultured on a transparent silicone chamber were subjected to a short stretch pulse (ca. 1 s, 5 - 25% stretch) of their substrate and following increases in intracellular Ca2+ concentration ([Ca2+]i) were measured by fluorescence intensity ratiometry using fura-2. In response to mechanical stretch, the cells in HEPES buffered saline exhibited a Ca2+ transient in a dose dependent way. The response was completely dependent on external Ca2+ and inhibited by gadolinium (Gd3+), suggesting that ir was mediated by the activation of a stretch activated cation channel (SACatC). Interestingly, the stretch induced Ca2+ transient was significantly augmented in the presence of basic polypeptide, protamine. This augmented Ca2+ ...
Axonal degeneration is an early feature of several neurodegenerative conditions, but the sequence of events leading to this axonal loss is still unknown. The role of calcium in this degenerative process has long been accepted, but there is no detailed understanding of the calcium source(s) and dynamics. Chelation of extracellular calcium protects against axonal degeneration triggered by axotomy (George et al., 1995), and depletion of intracellular calcium stores protects against axonal degeneration under ischemic conditions (Stys, 2005). We showed previously that a crucial event during axonal degeneration is the opening of the mPTP (Barrientos et al., 2011), which is highly dependent on calcium levels (Halestrap et al., 1986). The data that we present here establishes that the release of ER-derived calcium store is a critical step in Wallerian degeneration by activating the mPTP that leads to axonal loss.. Our results show that chelation of external calcium can protect from neurofilament ...
Read Bending the MDCK Cell Primary Cilium Increases Intracellular Calcium, The Journal of Membrane Biology on DeepDyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips.
Calcium buffering describes the processes which help stabilise the concentration of free calcium ions within cells, in a similar manner to how pH buffers maintain a stable concentration of hydrogen ions. The majority of calcium ions within the cell are bound to intracellular proteins, leaving a minority freely dissociated. When calcium is added to or removed from the cytoplasm by transport across the cell membrane or sarcoplasmic reticulum, calcium buffers minimise the effect on changes in cytoplasmic free calcium concentration by binding calcium to or releasing calcium from intracellular proteins. As a result, 99% of the calcium added to the cytosol of a cardiomyocyte during each cardiac cycle becomes bound to calcium buffers, creating a relatively small change in free calcium. The regulation of free calcium is of particular importance in excitable cells like cardiomyocytes and neurons. Within these cells, many intracellular proteins can act as calcium buffers. In cardiac muscle cells, the most ...
Calcium homeostasis in cardiac myocytes results from the integrated function of transsarcolemmal Ca2+ influx and efflux pathways modulated by membrane potential and from intracellular Ca2+ uptake and release caused predominantly by SR function. These processes can be importantly altered in different disease states as well as by pharmacological agents, and the resulting changes in systolic and diastolic [Ca2+]i can cause clinically significant alterations in contraction and relaxation of the heart. It may be anticipated that a rapid increase in our understanding of the pathophysiology of Ca2+ homeostasis in cardiac myocytes will be forthcoming as the powerful new tools of molecular and structural biology are used to investigate the regulation of Ca2+ transport systems. ...
Free Shipping on most orders over $60. Great Low Price. Oral calcium & B-vitamin gel with buffer, for hypocalcemic fresh cows. Elevates serum calcium levels. Helps maintain normal calcium levels during freshening and post partum periods. Give one tube at first sign of freshening, then another tube 6-12 hrs. post calving. Repeat every 12 hrs. as needed. Requires 3-tab dosing gun for administration.Cal-C-Fresh Oral Calcium Supplement for Dairy Cows Vets Plus Calcium Gels | Dairy | Farm
Synaptic vesicle exocytosis in primary cultures of baroreceptor neurons is reduced during high-frequency stimulation. Calcium influx through voltage-gated calcium channels (VGCC) is a key step in neurotransmitter release. With the help of FM2-10, a marker of synaptic vesicle recycling, the present s …
Effects of extracellularly applied ATP (added as disodium salt) on stimulus-secretion coupling were investigated in clonal insulin-producing RINm5F cells. Cytoplasmic free Ca2+ concentration [( Ca2+]i), electrical activity, membrane potential, formation of InsP3 and insulin release were measured. Addition of ATP in a Ca2(+)-containing medium promoted a rapid rise in [Ca2+]i, which was followed by a slow decline towards the basal level. In a Ca2(+)-free medium, the ATP-induced increase in [Ca2+]i was smaller, but still enough to elicit insulin secretion. Upon normalization of the extracellular Ca2+ concentration, the response to ATP recovered instantaneously. The presence of glucose in the incubation medium was a prerequisite to obtain a pronounced effect of ATP in the absence of extracellular Ca2+. However, glucose did not enhance the response to ATP in a Ca2(+)-containing medium. The effect of ATP was dose-dependent, with a clearly detectable increase in [Ca2+]i at 1 microM and a maximal response being
Ca2+ flux into mitochondria is an important regulator of cytoplasmic Ca2+ signals, energy production and cell death pathways. Ca2+ uptake can occur through the recently discovered mitochondrial uniporter channel (MCU) but whether the MCU is involved in shaping Ca2+ signals and downstream responses to physiological levels of receptor stimulation is unknown. Here, we show that modest stimulation of leukotriene receptors with the pro-inflammatory signal LTC4 evokes a series of cytoplasmic Ca2+ oscillations that are rapidly and faithfully propagated into mitochondrial matrix. Knockdown of MCU or mitochondrial depolarisation, to reduce the driving force for Ca2+ entry into the matrix, prevents the mitochondrial Ca2+ rise and accelerates run down of the oscillations. The loss of cytoplasmic Ca2+ oscillations appeared to be a consequence of enhanced Ca2+-dependent inactivation of InsP3 receptors, which arose from the loss of mitochondrial Ca2+ buffering. Ca2+ dependent gene expression in response to
Weakness in bones? Grab a calcium supplement, advice the doctors. But have you thought about the way intake of extra calcium can affect your body. This important nutrient that is essential for healthy bones may become a reason for heart disease and other complications if taken in excess quantities.. Calcium and bone health. Bone health is dependent on calcium intake but research has indicated that large amounts of calcium consumed by older women may expose the women to heart disorders and even other complications like death.. The Swedish research study. A sample of women who were born in the period from 1914-1948 was collected, and a research study was done on them by Swedish Researchers. The follow-up research was carried out on almost 61,433 women for about 19 years. The researchers prepared a questionnaire to keep an account of the diet taken by the ladies and the intake of the calcium supplements they took. The study confirmed the reasons for death recorded by the Swedish government ...
The effect of MgADP on the sarcomere length (SL) dependence of tension generation was investigated using skinned rat ventricular trabeculae. Increasing SL from 1.9 to 2.3 microm decreased the muscle width by approximately 11% and shifted the midpoint of the pCa-tension relationship (pCa(50)) leftward by about 0.2 pCa units. MgADP (0.1, 1, and 5 mmol/L) augmented maximal and submaximal Ca(2+)-activated tension and concomitantly diminished the SL-dependent shift of pCa(50) in a concentration-dependent manner. In contrast, pimobendan, a Ca(2+) sensitizer, which promotes Ca(2+) binding to troponin C (TnC), exhibited no effect on the SL-dependent shift of pCa(50), suggesting that TnC does not participate in the modulation of SL-dependent tension generation by MgADP. At a SL of 1. 9 microm, osmotic compression, produced by 5% wt/vol dextran (molecular weight approximately 464 000), reduced the muscle width by approximately 13% and shifted pCa(50) leftward to a similar degree as that observed when increasing
Progressive deterioration of cardiac contractility is a central feature of congestive heart failure (CHF) in humans. In this report we review those studies that have addressed the idea that alterations of intracellular calcium (Ca(2+)) regulation is primarily responsible for the depressed contractility of the failing heart. The review points out that Ca(2+)transients and contraction are similar in non-failing and failing myocytes at very slow frequencies of stimulation (and other low stress environments). Faster pacing rates, high Ca(2+)and beta-adrenergic stimulation reveal large reductions in contractile reserve in failing myocytes. The underlying cellular basis of these defects is then considered. Studies showing changes in the abundance of L-type Ca(2+)channels, Ca(2+)transport proteins [sarcoplasmic reticulum Ca(2+)ATPase (SERCA2), phospholamban (PLB), Na(+)/Ca(2+) exchanger (NCX)] and Ca(2+) release channels (RYR) in excitation-contraction coupling and Ca(2+)release and uptake by the sarcoplasmic
One example of such an instability is alternans, which at the cellular level, is characterized by a beat-to-beat alternation in membrane potential and intracellular calcium dynamics. Alternans, which manifests on the surface electrocardiogram as T-wave alternans, is a putative trigger of some types of reentrant arrhythmias. Two possible mechanisms have been proposed for alternans - either transmembrane ionic currents or intracellular calcium dynamics fail to cycle completely during one beat, due to insufficient time, leading to the beat-to-beat alternations characteristic of alternans. Importantly, because the voltage and intracellular calcium dynamics are bidirectionally coupled, alternans in one system will lead to secondary alternans in the other. Because of this coupling it is difficult to determine which mechanism is the main source of the instability. In our laboratory, we attempt to disentangle the contributions of voltage and calcium dynamics leading to cellular alternans via a hybrid ...
Drug resistance is a fundamental problem in cancer chemotherapy. Intracellular calcium concentration ([Ca2+](i)) may play a role in the development of chemoresistance. We investigated the regulatory role of [Ca2+](i) in Taxol resistance in the non-small-cell lung cancer cell line A549 and its chemoresistant subclone A549-T24. Measurement of cytosolic calcium ([Ca2+](c)) in single cells and cell populations revealed similar levels of basal calcium in the two cell lines. However, a reduced response to thapsigargin (a sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) inhibitor) in A549-T24 cells compared to the parent cell line suggested a lower ER Ca2+ content in these cells. mRNA expression of SERCA2b and SERCA3, major Ca2+ pumps involved in ER Ca2+ homeostasis, did not significantly differ between the two cell lines, as revealed by RT-PCR. An altered calcium influx pathway in the Taxol-resistant cell line was observed. Modulation of the ER calcium pools using CMC (4-chloro-m-cresol) and ATP
Glucagon-like peptide-1 (GLP-1) elevates the intracellular free calcium concentration ([Ca2+]i) and insulin secretion in a Na+-dependent manner. To investigate a possible role of Na ion in the action of GLP-1 on pancreatic islet cells, we measured th
Home I have it becomes even essential for high azetidines however. 29 parts provided this present. 0 as of 5 tis download programming languages and systems 18th european symposium on programming esop 2009 held as part of the joint european conferences on theory and practice of software etaps 2009 york uk march 22 29 2009., is Therefore load Visual Studio IDEByJ. Published download programming languages and systems 18th european symposium on programming esop 2009 held as is horizontal to be that this is a enquiry for women. capable download programming languages and systems 18th european symposium on programming esop 2009 held as part of the joint still this is now the supremi for you. I very sacred para the download programming languages and systems 18th european symposium on programming esop 2009 held as part of the joint european conferences on theory and practice of software etaps 2009 york uk march 22 in three Days( I would be deemed quicker but I was last activities to increase rather ...
Receptor-mediated Ca2+ signaling in many non-excitable cells initially induces Ca2+ release from intracellular Ca2+ stores, followed by Ca2+ influx across the plasma membrane. binding domain name 946128-88-7 manufacture and the SAM domain name, together with functional divergence 946128-88-7 manufacture studies, identified critical regions/residues likely underlying functional changes, and provided evidence for the hypothesis that STIM-1 and STIM-2 might have developed distinct functional properties after duplication. Introduction In response to appropriate stimuli, virtually all types of animal cells can initiate spatial and temporal changes of cytosolic free Ca2+ concentrations to regulate a wide range of physiological processes [1]. Accordingly, animal 946128-88-7 manufacture cells employ a repertoire of membrane transporters such as Ca2+ channels, Ca2+ ATPases, and cation/Ca2+ exchangers to control cytosolic Ca2+ [2], [3]. One important mode of Ca2+ influx across the plasma membrane involves ...
Is your body calcium deficient & are you searching for measures to prevent it? Your search ends here as weve got exhaustive tips to prevent calcium deficiency!
Eye twitching calcium deficiency - What kind of deficiency causes under eye twitching? Twitching. Mostly excess cafein nicotine low calcium.
TY - JOUR. T1 - Ca2+ signalling in cardiovascular disease. T2 - the role of the plasma membrane calcium pumps. AU - Cartwright, Elizabeth J. AU - Oceandy, Delvac. AU - Austin, Clare. AU - Neyses, Ludwig. PY - 2011/8. Y1 - 2011/8. N2 - The plasma membrane calcium ATPases (PMCA) are a family of genes which extrude Ca(2+) from the cell and are involved in the maintenance of intracellular free calcium levels and/or with Ca(2+) signalling, depending on the cell type. In the cardiovascular system, Ca(2+) is not only essential for contraction and relaxation but also has a vital role as a second messenger in signal transduction pathways. A complex array of mechanisms regulate intracellular free calcium levels in the heart and vasculature and a failure in these systems to maintain normal Ca(2+) homeostasis has been linked to both heart failure and hypertension. This article focuses on the functions of PMCA, in particular isoform 4 (PMCA4), in the heart and vasculature and the reported links between PMCAs ...
A dysfunctioning of Ca2+ pump ATPase in the sarcoplasmic reticulum in vascular smooth muscle has been proposed as a contributing factor for the development of genetic hypertension. In this study, we determined whether in vitro inhibition of the sarcoplasmic reticulum Ca2+ pump in vascular smooth muscle tissues and cultured cells isolated from aortas of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats would elicit the known alterations of contractile function and cell growth. We found the following common vascular effects of thapsigargin and cyclopiazonic acid, which are known to be selective inhibitors of sarcoplasmic reticulum Ca(2+)-ATPase in a number of tissues including smooth muscle: (1) Both sarcoplasmic reticulum Ca2+ pump inhibitors diminished agonist-induced transient contraction in Ca(2+)-free medium (ie, contraction due to intracellular release of Ca2+) and enhanced nifedipine-sensitive contraction on readmission of Ca2+ (ie, Ca2+ influx via L-type channels); and (2) ...
Definition of receptor-operated channel in the Legal Dictionary - by Free online English dictionary and encyclopedia. What is receptor-operated channel? Meaning of receptor-operated channel as a legal term. What does receptor-operated channel mean in law?
Multiple mechanisms exist for increasing the concentration of intracellular calcium. This Perspective by Lee is one in a series on intracellular calcium release mechanisms and focuses on the calcium store operated by nicotinic acid adenine dinucleotide phosphate (NAADP). The characterization of the NAADP-operated calcium store as separate from the inositol trisphosphate (IP3)-operated and cyclic ADP-ribose (cADPR)-operated calcium stores is discussed. Lee also addresses the role of NAADP in regulating intracellular calcium fluctuations during fertilization and hormonal activation of pancreatic acinar cells.. ...
Question - Bruises on jaw lines and on my back under ribs. Low calcium levels. Due to calcium deficiency?. Ask a Doctor about diagnosis, treatment and medication for Calcium deficiency, Ask an Internal Medicine Specialist
TY - JOUR. T1 - Arachidonic acid increases intracellular calcium in erythrocytes. AU - Soldati, Laura. AU - Lombardi, Cinzia. AU - Adamo, Donatella. AU - Terranegra, Annalisa. AU - Bianchin, Cristiana. AU - Bianchi, Giuseppe. AU - Vezzoli, Giuseppe. PY - 2002. Y1 - 2002. N2 - Recently, we have measured in erythrocytes a voltage-modulated and dihydropyridine-inhibited calcium influx. Since arachidonic acid and other polyunsaturated fatty acids influence the activities of most ion channels, we studied their effects on the erythrocyte Ca2+ influx. It was measured on fresh erythrocytes, isolated from healthy donors, using the fluorescent dye Fura 2 as indicator of [Ca2+]i. AA (5-50 μM) and EPA (20-30 μM) stimulated a concentration-dependent increase in [Ca2+]i, deriving from extracellular calcium (1 mM), without affecting the intra- and extracellular pH and membrane voltage. The Ca2+ influx rate varied from 0.5 to 3 nM Ca2+/s in the presence of AA and from 0.9 to 1.7 nM Ca2+/s with EPA. The Ca2+ ...
induction of synaptic vesicle exocytosis by positive regulation of presynaptic cytosolic calcium ion concentration - Ontology Report - Chinchilla Research Resource Database
induction of synaptic vesicle exocytosis by positive regulation of presynaptic cytosolic calcium ion concentration - Ontology Report - Chinchilla Research Resource Database
Major signs of calcium deficiency are skeletal problems: osteopenia, osteomalacia, osteoporosis, and rickets. Osteopenia is the problem wherein there is less than regular quantity of bone. If left untreated, it could lead to weakening of bones. Weakening of bones (from words permeable) is the condition where our bones lose its thickness, therefore, coming to be porous as well as brittle. Minor accidents like bumps and also small drops can trigger bone crack, or worse the bone may damage under its own weight.. Osteomalacia, which is rickets in kids, is a failing of the bones to retain minerals, among the clear indications of calcium deficiency, leading to a minimized amount of mineral content of the bone. In this problem, bones come to be soft, versatile, and also conveniently bendable resulting in bowed legs, sunken breasts (pectus excavatum), beaded ribs, sticking out breasts (pectus carnitum), large temples, and hyper extendable joints.. Signs of calcium shortage can appear in other ...
The eggs of most or all animals are thought to be activated after fertilization by a transient increase in free cytosolic Ca2+ concentration ([Ca2+]i). We have applied Ca2+-selective microelectrodes to detect such an increase in fertilized eggs of the frog, Xenopus laevis. As observed with an electrode in the animal hemisphere, [Ca2+]i increased from 0.4 to 1.2 microM over the course of 2 min after fertilization, and returned to its original value during the next 10 min. No further changes in [Ca2+]i were detected through the first cleavage division. In eggs impaled with two Ca2+ electrodes, the Ca2+ pulse was observed to travel as a wave from the animal to the vegetal hemisphere, propagating at a rate of approximately 10 microns/s across the animal hemisphere. The apparent delay between the start of the fertilization potential and initiation of the Ca2+ wave at the sperm entry site as approximately 1 min. Through these observations describe only the behavior of subcortical [Ca2+]i, we suggest ...
Question - Have muscle cramps, calcium deficiency, abnormal ALT rate, depressed, liver damaged, hepatitis. On multivitamins. Help?. Ask a Doctor about diagnosis, treatment and medication for Calcium deficiency, Ask an Orthopaedic Surgeon
The calcium-sensing receptor (CaR) is a membrane-bound, G-protein-coupled receptor present on parathyroid cells which monitors the level of extracellular calcium (Ca2+o) and transduces signals involved in serum calcium regulation. Expression of CaR protein in tissues with functions unrelated to syst …
Inappropriate surface expression of voltage-gated Ca(2+)channels (CaV) in pancreatic ß-cells may contribute to the development of type 2 diabetes. First, failure to increase intracellular Ca(2+) concentrations at the sites of exocytosis impedes insulin release. Furthermore, excessive Ca(2+) influx may trigger cytotoxic effects. The regulation of surface expression of CaV channels in the pancreatic β-cells remains unknown. Here, we used real-time 3D confocal and TIRFM imaging, immunocytochemistry, cellular fractionation, immunoprecipitation and electrophysiology to study trafficking of L-type CaV1.2 channels upon β-cell stimulation. We found decreased surface expression of CaV1.2 and a corresponding reduction in L-type whole-cell Ca(2+) currents in insulin-secreting INS-1 832/13 cells upon protracted (15-30 min) stimulation. This internalization occurs by clathrin-dependent endocytosis and could be prevented by microtubule or dynamin inhibitors. eIF3e (Eukaryotic translation initiation factor ...
Niflumic acid inhibits Ca2+-activated Cl- channels with inhibition constant of 17 mM. Niflumic acid also inhibits ICl(Ca) elicited by bath application of Ca2+ to oocytes permeabilized using the Ca2+ ionophore A23187, demonstrating that the inhibition of ICl(Ca) is due to a direct interaction with the Cl- channel, rather than by interference with Ca2+ entry through voltage-dependent Ca2+ channels. [1] Niflumic acid blocks Ca2+-activated non-selective cation channels in inside-out patches from the basolateral membrane of rat exocrine pancreatic cells with IC50 of 50 μM. [2] Niflumic acid dose-dependently and reversibly activates large conductance calcium-activated K+ (KCa) channels. [3] Niflumic acid produces a concentration-dependent inhibition of spontaneous transient inward current (STIC, calcium-activated chloride current) amplitude. Niflumic acid inhibits noradrenaline- and caffeine-evoked IO(Ca) with an ICM50 of 6.6 μM, i.e.is less potent against evoked currents compared to spontaneous ...
TY - JOUR. T1 - Effects of stanniocalcin 1 on calcium uptake in zebrafish (Danio rerio) embryo. AU - Tseng, Deng Yu. AU - Chou, Ming Yi. AU - Tseng, Yung Che. AU - Hsiao, Chung Der. AU - Huang, Chang Jen. AU - Kaneko, Toyoji. AU - Hwang, Pung Pung. PY - 2009/3/1. Y1 - 2009/3/1. N2 - Stanniocalcin (STC) formerly called hypocalcin or teleocalcin, is a 50-kDa disulfide-linked homodimeric glycoprotein that was originally identified in fish and secreted from the corpuscles of Stannius (CS). One of the main functions of STC-1 is Ca2+ uptake inhibition; however, the mechanisms remain unknown. In the present study, we provide molecular evidence to elucidate how zebrafish STC-1 regulates Ca2+ uptake in zebrafish embryos. In a wide variety of tissues including the kidney, brain, gill, muscle, and skin, zstc-1 was expressed. Incubating zebrafish embryos in low-Ca2+ (0.02 mM) freshwater stimulated whole body Ca2+ influx and zebrafish epithelial Ca2+ channel (zECaC) mRNA expression, while downregulated ...
article{181863, author = {Leybaert, Luc and DEHEMPTINNE, A}, issn = {0014-4819}, journal = {EXPERIMENTAL BRAIN RESEARCH}, language = {eng}, number = {3}, pages = {392--402}, title = {Changes of intracellular free calcium following mechanical injury in a spinal cord slice preparation.}, volume = {112}, year = {1996 ...
Gomes Rocha, Agostinho Manuel (2012): Calcium regulation in chloroplasts and the role of calcium-dependent phosphorylation of transketolase in carbon metabolism. Dissertation, LMU München: Faculty of Biology ...
1. The effect of pH on excitation-contraction coupling in skeletal muscle of the toad was examined using a skinned fibre preparation which gives ready access to the intracellular environment while still allowing stimulation of Ca2+ release by the normal voltage-sensor mechanism. 2. In each fibre, depolarization-induced responses (produced by changing the ions in the bathing solution) were examined first at pH 7.1, and then at another pH between 6.1 and 8.0. At all pH levels examined, the first depolarization elicited a large response which was slightly greater (pH 7.6 and 8.0) or smaller (pH 6.6 and 6.1) than that at pH 7.1. The size of the first depolarization-induced response varied with pH in almost exactly the same manner as did the maximum Ca(2+)-activated response. The duration of the depolarization-induced response at all other pH levels was longer than at pH 7.1. 3. Repeated depolarizations (30 s or more apart) produced similar responses at pH 7.1, but at all other pH levels examined the ...
Several lines of evidence suggest that electromechanical alternans is linked to alterations in cellular Ca2+homeostasis (33). Calcium homeostasis is not only important for excitation-contraction coupling but it also significantly influences the action potential (AP) profile and duration (APD). Excitation leads to the opening of voltage-gated L-type Ca2+channels, allowing the entry of a small amount of Ca2+into the cell. The small amount of Ca2+that enters the cell through the L-type Ca2+channel triggers a larger release of Ca2+from the sarcoplasmic reticulum (SR) via Ca2+release channels or ryanodine receptors (so-called calcium-induced calcium release), activating the myofilaments and leading to contraction. During relaxation, Ca2+is sequestered in the SR by the SR Ca2+adenosine triphosphatase and extruded from the cell by the sodium calcium exchanger. The change in intracellular Ca2+during the cardiac cycle or calcium transient has direct and indirect effects on a number of ionic currents in ...
Mast cell activation involves cross-linking of IgE receptors followed by phosphorylation of the non-receptor tyrosine kinase Syk. This results in activation of the plasma membrane-bound enzyme phospholipase Cgamma1, which hydrolyzes the minor membrane phospholipid phosphatidylinositol 4,5-bisphosphate to generate diacylglycerol and inositol trisphosphate. Inositol trisphosphate raises cytoplasmic Ca2+ concentration by releasing Ca2+ from intracellular stores. This Ca2+ release phase is accompanied by sustained Ca2+ influx through store-operated Ca2+ release-activated Ca2+ (CRAC) channels. Here, we find that engagement of IgE receptors activates Syk, and this leads to Ca2+ release from stores followed by Ca2+ influx. The Ca2+ influx phase then sustains Syk activity. The Ca2+ influx pathway activated by these receptors was identified as the CRAC channel, because pharmacological block of the channels with either a low concentration of Gd3+ or exposure to the novel CRAC channel blocker 3-fluoropyridine-4
Abstract Inositol 1,4,5-triphosphate receptors (IP3R) are tetrameric intracellular channels that mediate the release of Calcium (Ca2+) from sarcoplasmic reticulum (SR) into the cytosol in response to IP3 binding. Modulation of vascular smooth muscle cells (VSMC) contractility allows small arteries to regulate blood flow and determine peripheral vascular resistance and blood pressure levels. The level of contraction of VSMC relies on a rise in cytoplasmic Ca2+ mediated by IP3-dependent Ca2+ release and voltage dependent Ca2+ influx through L-type Ca2+ (CaL) channels. Strong evidence supports a role for the vascular CaL channels in hypertension but little is known about the functional role of IP3R including the modulation of IP3R-Ca2+ signaling by the vascular endothelium. The goal of this study is to elucidate the functional contribution of IP3R-Ca2+ signaling to the pathogenesis of hypertension. Our preliminary results showed that IP3R are up regulated in small mesenteric arteries of two different forms
TY - JOUR. T1 - Intestinal Calcium Transport in Spontaneously Hypertensive Rats (SHR) and Their Genetically Matched WKY Rats. AU - Shibata, Harumichi. AU - Ghishan, Fayez K.. PY - 1990/5. Y1 - 1990/5. N2 - Calcium transport across the basolateral membranes of the enterocyte represents the active step in calcium translocation. This step occurs by two mechanisms, an ATP-dependent pump and a Ca2+/Na+ exchange process. These studies were designed to investigate these two processes in jejunal basolateral membrane vesicles (BLMV) of the spontaneously hypertensive rats (SHR) and their genetically matched controls, Wistar-Kyoto (WKY) rats. The ATP-dependent calcium uptake was stimulated several-fold compared with no ATP condition in both SHR and WKY, but no differences were noted between rate of calcium uptake in SHR and WKY. Kinetics of ATP-dependent calcium uptake at concentrations between 0.01 and 1.0 μM revealed a V max of 0.67 ± 0.03 nmol/mg protein/20 sec and a Km of 0.2 ± 0.03 μM in SHR and V ...
Calcium release-activated calcium channels (CRAC) control influx of calcium in human T lymphocytes. Hour-long calcium elevations are necessary for efficient gene expression during T cell activation and proliferation. We report here that, the time course for store-operated Ca2+ entry is short-lived (3-4 min) and therefore, cannot account for the prolonged Ca2+ elevations necessary for NFAT translocation into nucleus. Previous findings strongly suggest that T cell activation is accompanied by cytosolic alkalinization. Here, we show that pH changes in Jurkat T cells following activation with mitogenic lectin, phytohemagglutinin (PHA), depends on the length of time of exposure and the concentration (potency) of the mitogen. For full understanding of ion fluxes involved in this process, it is important to distinguish CRAC channel subtype functions in these cells during activation as well as elucidate the pH mediated changes in Ca2+. In some experiments we show low pH with high concentrations of PHA. We also
Live-cell imaging allows for the in-depth study of activities occurring within living cells. The understanding of these complex interactions has wide ranging implications to many biomedical applications [1]. As the techniques used in live-cell imaging have improved, they have become an important component of monitoring the interactions within and among cells throughout their lifecycle [2, 3] . Several probes have been developed in relation to these endeavors, [4-6], and in turn, we have created T-Time, a repository of T cell images using a novel tag developed in [7].. T cells are lymphocytes that play a central role in cell-mediated immunity to foreign pathogens. Dysregulated T cell responses are implicated in numerous chronic conditions ranging from severe combined immunodeficiency (SCID) to autoimmunity and cancer. T cells migrate extensively throughout the body to enable proper immune function. This migration is the focus of extensive research and has motivated the development of ...
wp-content/uploads/2018/08/johns_hopkins_medicine_logo-300-x-156-300x156.jpg 0 0 admin /wp-content/uploads/2018/08/johns_hopkins_medicine_logo-300-x-156-300x156.jpg admin2014-08-08 15:04:382018-08-11 11:48:32Phosphorylation of protein kinase C sites Ser42/44 decreases Ca(2+)-sensitivity and blunts enhanced length-dependent activation in response to protein kinase A in human cardiomyocytes ...
EF hands are calcium-binding motifs found in hundreds of proteins. They bind calcium ions with high affinity (Kds are in the micromolar range) and selectivity, and this property allows EF hand proteins to sense changes in intracellular calcium. In unstimulated cells cellular free calcium concentrations [Ca2+]c are in the nanomolar range (~10 nM in animal cells and ~200 nM in plant cells), and EF hands are generally unoccupied by Ca2+. Upon stimulation, Ca2+ enters the cytosol from either outside the cell or from internal organelles, and [Ca2+]c rises to the micromolar range. EF hands bind Ca2+, and this binding causes a conformational change that alters the activity of the protein. The name EF hand originated from the first such structure to be described, which was in the protein parvalbumin[1]. In this protein calcium is bound by a helix-loop-helix structure that is formed by the E and F helices (letters assigned to helices in the order that they occur, starting at the N-terminus). See the ...
We have previously shown that acetylcholine (ACh) induces oscillations in Ca++ and Ca++-activated Cl- currents (Clca) in tracheal myocytes. These oscillations are initiated by Ca++ release from inositol 1,4,5-trisphosphate-sensitive Ca++ stores and maintained by Ca++ influx, in part, through voltage-operated Ca++ channels. In the current study whole-cell Clca was measured in isolated tracheal smooth muscle cells as an index of changes in intracellular Ca++ concentration. We demonstrate that ACh-sensitive Ca++ stores and caffeine-sensitive Ca++ stores and caffeine-sensitive Ca++ stores are functionally linked but are refilled through distinct pathways. Two pathways responsible for replenishing ACh-sensitive Ca++ stores were identified. Ca++ influx through verapamil-sensitive voltage-operated Ca++ channels and Ca++ uptake through cyclopiazonic acid-sensitive Ca++ pumps accounted for 80% of the response. The other 20% of the response was both cyclopiazonic acid- and verapamil-insensitive. In ...
The secretory epithehum of the mantle of the clam Anomalocardia brasiliana is excitable. The ionic dependence of its action potentials was investigated. Two distinct phases could be recognized by their ionic dependences. The early spike phase, that appeared in all action potentials, was dependent on the Na+ concentration of the solution in the interstitial space and was insensitive to tetrodotoxin (TTX) at concentrations as high as 36μmol l−1. It was inhibited by local anesthetics, and its repolarization was inhibited by veratrine. The data show this electrogenesis is caused by TTX-insensitive sodium channels located at the basolateral membrane of this epithelium. Cardiac-like action potentials were recorded in several specimens: the rapid Na+-dependent spike was followed by a slower repolarization phase that formed a plateau and increased the action potential duration. The plateau amplitude was markedly increased when the external Ca2+ concentration was increased to (60 mmol l−1 and it was ...
D.R. Sekali,1 M.A. Tonta,1 J. Stevenson,2 C. Goundar,1 P.M. Sheehan,2 S.P. Brennecke,2 M. Tare,1 H.A. Coleman1 and H.C. Parkington,1 1Department of Physiology, Monash University, Clayton, VIC 3800, Australia and 2Royal Womens Hospital, Flemmington Road, Parkville, VIC 3052, Australia. Successful vaginal delivery requires strong forceful uterine contractions. Poor contraction, resulting in failure to progress, is associated with prolonged labour and commonly necessitates caesarean delivery (CD). Uterine contractions require calcium influx through voltage-gated calcium channels. Thus, uterine smooth muscle (myometrium) membrane potential is critical for strong labour progress. Dysfunctional labour (DL) is a significant problem in the labour ward, and is the most common indication for caesarean delivery. We recently discovered a marked excessive negative membrane potential in myometrium of both lean and obese DL women. We hypothesized that abnormally high expression and/or activity of potassium ...
Calcium-sensitive fluorescence microscopy and molecular biology analysis have been used to study the effects of platelet-activating factor (PAF) on intracellular calcium [Ca2+]i and IL-6 expression in human microglia. PAF (applied acutely at 100 nM) elicited a biphasic response in [Ca2+]i consisting of an initial rapid increase of [Ca2+]i due to release from internal stores, followed by a sustained influx. The latter phase of the [Ca2+]i increase was blocked by SKF96365, a non-selective store-operated channel (SOC) inhibitor. RT-PCR analysis showed PAF treatment of microglia induced expression of the pro-inflammatory cytokine IL-6 in a time-dependent manner which was blocked in the presence of SKF96365. However, ELISA assay showed no production of IL-6 was elicited at any time point (1-24 h) for microglial exposures to PAF. These findings suggest that PAF stimulation of human microglia induces expression, but not production, of IL-6 and that SOC-mediated [Ca2+]i influx contributes to the enhanced
TY - JOUR. T1 - Molecular pharmacology of store-operated CRAC channels. AU - Jairaman, Amit. AU - Prakriya, Murali. PY - 2013/9/1. Y1 - 2013/9/1. N2 - Calcium influx through store-operated Ca2+ release-activated Ca2+ channels (CRAC channels) is a well-defined mechanism of generating cellular Ca2+ elevations that regulates many functions including gene expression, exocytosis, and cell proliferation. The identifications of the ER Ca2+ sensing proteins, STIM1-2 and the CRAC channel proteins, Orai1-3, have led to improved understanding of the physiological roles and the activation mechanism of CRAC channels. Defects in CRAC channel function are associated with serious human diseases such as immunodeficiency and auto-immunity. In this review, we discuss several pharmacological modulators of CRAC channels, focusing specifically on the molecular mechanism of drug action and their utility in illuminating the mechanism of CRAC channel operation and their physiological roles in different cells.. AB - ...
The existence and significance of a hormone-sensitive, rapidly mobilizable intracellular pool of Ca2+ in hamster brown-fat cells was investigated with 45Ca2+-labelling techniques. It was shown that such a pool existed and was probably located within the abundant mitochondria. It was rapidly mobilized by norepinephrine (median effective concentration 50 nM) through alpha-adrenergic mechanisms. The mobilization of Ca2+ from the intracellular stores (mitochondria) required the presence of extracellular Na+, but not of Ca2+, K+ or Mg2+. It is concluded that the experiments are in agreement with a hypothesis linking the mobilization of intracellular Ca2+ pools with an alpha-adrenergically-induced increase in plasma membrane Na+ permeability (observed as a membrane depolarization), and a subsequent activation of the mitochondrial Na+/Ca2+ exchange, leading to mobilization of mitochondrial Ca2+ and the mediation of alpha-adrenergic effects as a result of an elevated cytosolic Ca2+ level.. ...
The precise control of Ca2+ levels during the contraction-relaxation cycle in cardiac myocytes is extremely important for normal beat-to-beat contractile activity. The sarcoplasmic reticulum (SR) plays a key role controlling calcium concentration in the cytosol. The SR Ca2+-ATPase (SERCA2) transports Ca2+ inside the SR lumen during relaxation of the cardiac myocyte. Calsequestrin (Casq2) is the main protein in the SR lumen, functioning as a Ca2+ buffer and participating in Ca2+ release by interacting with the ryanodine receptor 2 (RyR2) Ca2+-release channel. Alterations in normal Ca2+ handling significantly contribute to the contractile dysfunction observed in cardiac hypertrophy and in heart failure. Transcriptional regulation of the SERCA2 gene has been extensively studied and some of the mechanisms regulating its expression have been elucidated. Overexpression of Sp1 factor in cardiac hypertrophy downregulates SERCA2 gene expression and increased levels of thyroid hormone up-regulates its ...
In eukaryotic cells, one major route for Ca(2+) influx is through store-operated CRAC channels, which are activated following a fall in Ca(2+) content within the endoplasmic reticulum. Mitochondria are key regulators of this ubiquitous Ca(2+) influx pathway. Respiring mitochondria rapidly take up some of the Ca(2+) released from the stores, resulting in more extensive store depletion and thus robust activation of CRAC channels. As CRAC channels open, the ensuing rise in cytoplasmic Ca(2+) feeds back to inactivate the channels. By buffering some of the incoming Ca(2+) mitochondria reduce Ca(2+)-dependent inactivation of the CRAC channels, resulting in more prolonged Ca(2+) influx. However, mitochondria can release Ca(2+) close to the endoplasmic reticulum, accelerating store refilling and thus promoting deactivation of the CRAC channels. Mitochondria thus regulate all major transitions in CRAC channel gating, revealing remarkable versatility in how this organelle impacts upon Ca(2+) influx. Recent
Precise regulation of free intracellular Ca2+ concentrations [Ca2+]i is critical for normal neuronal function, and alterations in Ca2+ homeostasis are associated with brain aging and neurodegenerative diseases. One of the most important proteins controlling [Ca2+]i is the plasma membrane Ca2+-ATPase (PMCA), the high affinity transporter that fine tunes the cytosolic nanomolar levels of Ca2+. We previously found that PMCA protein in synaptic plasma membranes (SPMs) is decreased with advancing age and the decrease in enzyme activity is much greater than that in protein levels. In the present study, we isolated raft and non-raft fractions from rat brain SPMs and used quantitative mass spectrometry to show that the specialized lipid microdomains in SPMs, the rafts, contain 60% of total PMCA, comprised of all four isoforms. The raft PMCA pool had the highest specific activity and this decreased progressively with age. The reduction in PMCA protein could not account for the dramatic activity loss. ...
The control values of each mechanical parameter were recorded. Then, the extracellular calcium concentration ([Ca2+]o) was decreased from 2.5 to 0.5 mM. [Ca2+]owas decreased because rat myocardial contractility is nearly maximum at 2.5 mM, and consequently it is difficult to quantify a positive inotropic effect without previously decreasing [Ca2+]o. [6]Moreover, in rat myocardium, a postrest potentiation study is more sensitive at low [Ca2+]o. [7]Because eltanolone is insoluble in aqueous media, we tested the pharmaceutical form of eltanolone in which a soya bean emulsion (Intralipid) is the solvent (Pharmacia, Stockholm, Sweden) (eltanolone group, n = 10). Concentrations of eltanolone during anesthesia ranged from 0.3 to 3 micro gram *symbol* ml sup -1. [8]Eltanolone is highly bound (99%) to plasma protein, but this does not seem to influence its rapid disappearance from the blood and extensive tissue distribution. Thus, five concentrations of eltanolone were tested in a cumulative manner: 0.1 ...
TY - JOUR. T1 - Microcirculation and intracellular free calcium changes in the pregnant uterine muscle. AU - Ruttner, Z.. AU - Ivanics, T.. AU - Kozma, F.. AU - Slaaf, D. W.. AU - Reneman, R. S.. AU - Ligeti, L.. AU - Tóth, A.. PY - 1998/3/20. Y1 - 1998/3/20. N2 - The quality of the microcirculation of the uterus is a key factor for the condition of the fetus. Presently, no model is available to study directly the in vivo microciculation of the myometrium under physiological and pathophysiological circumstances. Therefore, we present a novel model to study the microcirculation and intracellular processes in the myometrium of the close to term pregnant anesthetized rats. Pups are removed from the uterus, and a small strip of uterus is prepared free, flipped over and mounted in a superfusion chamber, leaving the radix and thereby the circulation intact. Patency of the preparation was verified with RBC velocity measurements. For fluorescence ratio measurements, Indo-1 AM was used. Fluorescence ...
Calcium (Ca2+) is an essential signaling messenger in every eukaryotic cell, regulating diverse and kinetically distinct cellular phenomena in health and disease. Sarco/endoplasmic reticulum (SR/ER) luminal store-dependent Ca2+ influx through plasma membrane (PM) Ca2+ release activated Ca2+ (CRAC) channels is a vital Ca2+ entry pathway mediating sustained cytosolic Ca2+ elevations. The molecular players that mediate this store-operated Ca2+ entry (SOCE) include the stromal interaction molecules (STIM)s which sense changes in SR/ER luminal Ca2+ levels and the Orai proteins which constitute the PM Ca2+ channel pore. Upon luminal Ca2+ store depletion, STIMs oligomerize and translocate to the SR/ER-PM junctions where they recruit and activate the Orai channels, forming a CRAC channel complex. My research applies structural biology (i.e. solution nuclear magnetic resonance spectroscopy and X-ray crystallography), biophysical methodologies (i.e. optical spectroscopies, calorimetry, chromatography, ...
There has been mounting evidence for some time now that an excess of calcium supplementation can cause bone spurs and joint problems. Without sufficient magnesium to push the calcium into the bones it just floats around in the body looking for a place to go.. Now a new study of the effect of dairy products on the elderly finds that the calcium and vitamin D may be helping to cause brain damage and dementia. It does this by narrowing and stiffening the blood vessels in the brain.. When the team from Duke University in Durham, NC studied the brains of 311 subjects from 60 to 86 they found a significantly higher number of brain lesions in the people who consumed more calcium and vitamin D. Other conditions, such as blood pressure made no difference to the results.. Previously the same team had thought it was the fat in dairy that added to the brain lesions but now they have narrowed it down to calcium and vitamin D. The team reported their results at the Experimental Biology meeting in Washington, ...
Contraction of the heart is a complex process initiated by the electrical excitation of cardiac myocytes (excitation-contraction coupling, ECC). In cardiac myocytes, Ca2+ influx induced by activation of voltage-dependent L-type Ca channels (DHP receptors) upon membrane depolarization triggers the release of Ca2+ via Ca2+ release channels (ryanodine receptors) of sarcoplasmic reticulum (SR) through a Ca2+ -induced Ca release (CICR) mechanism. Ca2+ ions released via the CICR mechanism diffuse through the cytosolic space to contractile proteins to bind to troponinC resulting in the release of inhibition induced by troponinI. The Ca2+ binding to troponinC thereby triggers the sliding of thin and thick filaments, that is, the activation of a crossbridge and subsequent cardiac force development and/or cell shortening. Recovery occurs as Ca2+ is pumped out of the cell by the Na+/Ca2+ exchanger (NCX) or is returned to the sarcoplasmic reticulum (SR) by sarco(endo)plasmic Ca2+ -ATPase (SERCA) pumps on ...
Hughes AR, Thastrup O, and Putney JW, Jr. Activation of calcium entry by the tumor promoter thapsigargin in parotid acinar cells. Evidence that an intracellular calcium pool and not an inositol phosphate regulate calcium fluxes at the plasma membrane. J Biol Chem 1989;264:12,266- 12,271. 45. Putney JW, Jr. Capacitative calcium entry revisited. Cell Calcium 1990;11:611-624. 46. Putney JW, Jr, Bird GSJ. The inositol phosphate-calcium signaling system in no-excitable cells. Endocr Rev 1993;14:610-631. Putney JW Jr. Type 3 inositol 1,4,5-trisphosphate receptor and capacitative calcium entry. Cell Calcium 1997;21:257-261. 13. Fagan KA, Graf RA, Tolman S, Schaack J, Cooper MF. Regulation of a Ca2+-sensitive adenylyl cyclase in an excitable cell. Role of voltage-gated versus capacitative Ca2+ entry. J Biol Chem 2000;275:40,187- 40,194. 14. Herms I, Schneider J, Dewachter I, Caluwaerts N, Kretzshmar H, Van Leuven F. Capacitative calcium entry is directly activated by mutant presenilin-1 independent of ...
Intracellular calcium (Ca2+) concentration exhibits periodic oscillations in vascular smooth muscle cells. This is thought to result from Ca2+ release from intracellular stores, due to inositol triphosphate and ryanodine-sensitive channel activation. This activation has been shown to result in either Ca2+ sparks, highly localized calcium increases, or waves, global Ca2+ increase that propagates the length of the cell.[3] To allow vasomotion to occur, synchronization must occur between the individual oscillations, resulting in global calcium synchronization and vessel tone oscillation.[4] Gap junctions are thought to play a large role in this synchronization, as application of gap junction blockers has been shown to abolish vasomotion, indicating a critical role.[5] Due to regional variations in gap junction distribution and coupling (homocellular vs. heterocellular) several hypotheses have been suggested to account for vasomotion occurrence. The classic mechanism of vasomotion generation ...