Sodium-Calcium Exchanger
Calcium
Antiporters
Aflatoxin M1
Zeolites
Aluminum Silicates
Sodium
Drug Residues
Thiourea
Calcium Signaling
Sodium-Hydrogen Antiporter
Calcium-Transporting ATPases
Myocytes, Cardiac
Mercury
Access to Information
Journal Impact Factor
Bibliometrics
Publishing
Peer Review, Research
Long QT Syndrome
Electrocardiography
Congenital Disorders of Glycosylation
Ether-A-Go-Go Potassium Channels
Syncope
The sarcoplasmic reticulum and the Na+/Ca2+ exchanger both contribute to the Ca2+ transient of failing human ventricular myocytes. (1/1416)
Our objective was to determine the respective roles of the sarcoplasmic reticulum (SR) and the Na+/Ca2+ exchanger in the small, slowly decaying Ca2+ transients of failing human ventricular myocytes. Left ventricular myocytes were isolated from explanted hearts of patients with severe heart failure (n=18). Cytosolic Ca2+, contraction, and action potentials were measured by using indo-1, edge detection, and patch pipettes, respectively. Selective inhibitors of SR Ca2+ transport (thapsigargin) and reverse-mode Na+/Ca2+ exchange activity (No. 7943, Kanebo Ltd) were used to define the respective contribution of these processes to the Ca2+ transient. Ca2+ transients and contractions induced by action potentials (AP transients) at 0.5 Hz exhibited phasic and tonic components. The duration of the tonic component was determined by the action potential duration. Ca2+ transients induced by caffeine (Caf transients) exhibited only a phasic component with a rapid rate of decay that was dependent on extracellular Na+. The SR Ca2+-ATPase inhibitor thapsigargin abolished the phasic component of the AP Ca2+ transient and of the Caf transient but had no significant effect on the tonic component of the AP transient. The Na+/Ca2+ exchange inhibitor No. 7943 eliminated the tonic component of the AP transient and reduced the magnitude of the phasic component. In failing human myocytes, Ca2+ transients and contractions exhibit an SR-related, phasic component and a slow, reverse-mode Na+/Ca2+ exchange-related tonic component. These findings suggest that Ca2+ influx via reverse-mode Na+/Ca2+ exchange during the action potential may contribute to the slow decay of the Ca2+ transient in failing human myocytes. (+info)Effects of impaired Ca2+ homeostasis on contraction in postinfarction myocytes. (2/1416)
The significance of altered Ca2+ influx and efflux pathways on contractile abnormalities of myocytes isolated from rat hearts 3 wk after myocardial infarction (MI) was investigated by varying extracellular Ca2+ concentration ([Ca2+]o, 0.6-5.0 mM) and pacing frequency (0.1-5.0 Hz). Myocytes isolated from 3-wk MI hearts were significantly longer than those from sham-treated (Sham) hearts (125 +/- 1 vs. 114 +/- 1 micrometer, P < 0.0001). At high [Ca2+]o and low pacing frequency, conditions that preferentially favored Ca2+ influx over efflux, Sham myocytes shortened to a greater extent than 3-wk MI myocytes. Conversely, under conditions that favored Ca2+ efflux (low [Ca2+]o and high pacing frequency), MI myocytes shortened more than Sham myocytes. At intermediate [Ca2+]o and pacing frequencies, differences in steady-state contraction amplitudes between Sham and MI myocytes were no longer significant. Collectively, the interpretation of these data was that Ca2+ influx and efflux pathways were subnormal in MI myocytes and that they contributed to abnormal cellular contractile behavior. Because Na+/Ca2+ exchange activity, but not whole cell Ca2+ current, was depressed in 3-wk MI rat myocytes, our results on steady-state contraction are consistent with, but not proof of, the hypothesis that depressed Na+/Ca2+ exchange accounted for abnormal contractility in MI myocytes. The effects of depressed Na+/Ca2+ exchange on MI myocyte mechanical activity were further evaluated in relaxation from caffeine-induced contractures. Because Ca2+ uptake by sarcoplasmic reticulum was inhibited by caffeine and with the assumption that intracellular Na+ and membrane potential were similar between Sham and MI myocytes, myocyte relaxation from caffeine-induced contracture can be taken as an estimate of Ca2+ extrusion by Na+/Ca2+ exchange. In MI myocytes, in which Na+/Ca2+ exchange activity was depressed, the half time of relaxation (1.54 +/- 0.14 s) was significantly (P < 0.02) prolonged compared with that measured in Sham myocytes (1.10 +/- 0.10 s). (+info)Direct evidence of Na+/Ca2+ exchange in squid rhabdomeric membranes. (3/1416)
Na+/Ca2+ exchange has been investigated in squid (Loligo pealei) rhabdomeric membranes. Ca2+-containing vesicles have been prepared from purified rhabdomeric membranes by extrusion through polycarbonate filters of 1-micrometer pore size. After removal of external Ca2+, up to 90% of the entrapped Ca2+ could be specifically released by the addition of Na+; this finding indicates that most of the vesicles contained Na+/Ca2+ exchanger. The Na+-induced Ca2+ efflux had a half-maximum value (K1/2) of approximately 44 mM and a Hill coefficient of approximately 1.7. The maximal Na+-induced Ca2+ efflux was approximately 0.6 nmol Ca2+. s-1. mg protein-1. Similar Na+-induced Ca2+ effluxes were measured if K+ was replaced with Li+ or Cs+. Vesicles loaded with Ca2+ by Na+/Ca2+ exchange also released this Ca2+ by Na+/Ca2+ exchange, suggesting that Na+/Ca2+ exchange operated in both forward and reverse modes. Limited proteolysis by trypsin resulted in a rate of Ca2+ efflux enhanced by approximately fivefold when efflux was activated with 95 mM NaCl. For vesicles subjected to limited proteolysis by trypsin, Na+/Ca2+ exchange was characterized by a K1/2 of approximately 25 mM and a Hill coefficient of 1.6. For these vesicles, the maximal Na+-induced Ca2+ efflux was about twice as great as in control vesicles. We conclude that Na+/Ca2+ exchange proteins localized in rhabdomeric membranes mediate Ca2+ extrusion in squid photoreceptors. (+info)Developmental expression of sodium entry pathways in rat nephron. (4/1416)
During the past several years, sites of expression of ion transport proteins in tubules from adult kidneys have been described and correlated with functional properties. Less information is available concerning sites of expression during tubule morphogenesis, although such expression patterns may be crucial to renal development. In the current studies, patterns of renal axial differentiation were defined by mapping the expression of sodium transport pathways during nephrogenesis in the rat. Combined in situ hybridization and immunohistochemistry were used to localize the Na-Pi cotransporter type 2 (NaPi2), the bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2), the thiazide-sensitive Na-Cl cotransporter (NCC), the Na/Ca exchanger (NaCa), the epithelial sodium channel (rENaC), and 11beta-hydroxysteroid dehydrogenase (11HSD). The onset of expression of these proteins began in post-S-shape stages. NKCC2 was initially expressed at the macula densa region and later extended into the nascent ascending limb of the loop of Henle (TAL), whereas differentiation of the proximal tubular part of the loop of Henle showed a comparatively retarded onset when probed for NaPi2. The NCC was initially found at the distal end of the nascent distal convoluted tubule (DCT) and later extended toward the junction with the TAL. After a period of changing proportions, subsegmentation of the DCT into a proximal part expressing NCC alone and a distal part expressing NCC together with NaCa was evident. Strong coexpression of rENaC and 11HSD was observed in early nascent connecting tubule (CNT) and collecting ducts and later also in the distal portion of the DCT. Ontogeny of the expression of NCC, NaCa, 11HSD, and rENaC in the late distal convolutions indicates a heterogenous origin of the CNT. These data present a detailed analysis of the relations between the anatomic differentiation of the developing renal tubule and the expression of tubular transport proteins. (+info)A circularized sodium-calcium exchanger exon 2 transcript. (5/1416)
Previous reports of Na/Ca exchanger gene 1 (NCX1) expression have revealed a major RNA transcript of 7 kilobase pairs (kb), minor transcripts of approximately 13 and approximately 4 kb, and a relatively abundant 1.8-kb RNA band. In the present report we demonstrate that the 1.8-kb message, which has a tissue and subcellular distribution matching that of full-length NCX1 but is not polyadenylated, corresponds to a perfectly circularized exon 2 species. The circular transcript contained the normal NCX1 start codon, a new stop codon introduced as a consequence of circularization, and encoded a protein corresponding to the NH2-terminal portion of NCX1, terminating just after amino acid 600 in the cytoplasmic loop. A linear version of the circular transcript was prepared and transfected into HEK-293 cells. A protein, matching the predicted size of approximately 70 kDa, was expressed, and the transfected cells possessed Na/Ca exchange activity. Although in native tissue we could not detect a protein corresponding exactly to that predicted from the circular transcript, a prominent band of slightly shorter size, possibly representing further proteolytic processing of circular transcript protein, was observed in membranes from LLC-MK2 cells and rat kidney. (+info)Mechanisms of altered excitation-contraction coupling in canine tachycardia-induced heart failure, I: experimental studies. (6/1416)
Pacing-induced heart failure in the dog recapitulates many of the electrophysiological and hemodynamic abnormalities of the human disease; however, the mechanisms underlying altered Ca2+ handling have not been investigated in this model. We now show that left ventricular midmyocardial myocytes isolated from dogs subjected to 3 to 4 weeks of rapid pacing have prolonged action potentials and Ca2+ transients with reduced peaks, but durations approximately 3-fold longer than controls. To discriminate between action potential effects on Ca2+ kinetics and direct changes in Ca2+ regulatory processes, voltage-clamp steps were used to examine the time constant for cytosolic Ca2+ removal (tauCa). tauCa was prolonged by just 35% in myocytes from failing hearts after fixed voltage steps in physiological solutions (tauCa control, 216+/-25 ms, n=17; tauCa failing, 292+/-23 ms, n=22; P<0.05), but this difference was markedly accentuated when Na+/Ca2+ exchange was eliminated (tauCa control, 282+/-30 ms, n=13; tauCa failing, 576+/-83 ms, n=11; P<0. 005). Impaired sarcoplasmic reticular (SR) Ca2+ uptake and a greater dependence on Na+/Ca2+ exchange for cytosolic Ca2+ removal was confirmed by inhibiting SR Ca2+ ATPase with cyclopiazonic acid, which slowed Ca2+ removal more in control than in failing myocytes. beta-Adrenergic stimulation of SR Ca2+ uptake in cells from failing hearts sufficed only to accelerate tauCa to the range of unstimulated controls. Protein levels of SERCA2a, phospholamban, and Na+/Ca2+ exchanger revealed a pattern of changes qualitatively similar to the functional measurements; SERCA2a and phospholamban were both reduced in failing hearts by 28%, and Na+/Ca2+ exchange protein was increased 104% relative to controls. Thus, SR Ca2+ uptake is markedly downregulated in failing hearts, but this defect is partially compensated by enhanced Na+/Ca2+ exchange. The alterations are similar to those reported in human heart failure, which reinforces the utility of the pacing-induced dog model as a surrogate for the human disease. (+info)Mechanisms of altered excitation-contraction coupling in canine tachycardia-induced heart failure, II: model studies. (7/1416)
Ca2+ transients measured in failing human ventricular myocytes exhibit reduced amplitude, slowed relaxation, and blunted frequency dependence. In the companion article (O'Rourke B, Kass DA, Tomaselli GF, Kaab S, Tunin R, Marban E. Mechanisms of altered excitation-contraction coupling in canine tachycardia-induced heart, I: experimental studies. Circ Res. 1999;84:562-570), O'Rourke et al show that Ca2+ transients recorded in myocytes isolated from canine hearts subjected to the tachycardia pacing protocol exhibit similar responses. Analyses of protein levels in these failing hearts reveal that both SR Ca2+ ATPase and phospholamban are decreased on average by 28% and that Na+/Ca2+ exchanger (NCX) protein is increased on average by 104%. In this article, we present a model of the canine midmyocardial ventricular action potential and Ca2+ transient. The model is used to estimate the degree of functional upregulation and downregulation of NCX and SR Ca2+ ATPase in heart failure using data obtained from 2 different experimental protocols. Model estimates of average SR Ca2+ ATPase functional downregulation obtained using these experimental protocols are 49% and 62%. Model estimates of average NCX functional upregulation range are 38% and 75%. Simulation of voltage-clamp Ca2+ transients indicates that such changes are sufficient to account for the reduced amplitude, altered shape, and slowed relaxation of Ca2+ transients in the failing canine heart. Model analyses also suggest that altered expression of Ca2+ handling proteins plays a significant role in prolongation of action potential duration in failing canine myocytes. (+info)Significance of Na/Ca exchange for Ca2+ buffering and electrical activity in mouse pancreatic beta-cells. (8/1416)
We have combined the patch-clamp technique with microfluorimetry of the cytoplasmic Ca2+ concentration ([Ca2+]i) to characterize Na/Ca exchange in mouse beta-cells and to determine its importance for [Ca2+]i buffering and shaping of glucose-induced electrical activity. The exchanger contributes to Ca2+ removal at [Ca2+]i above 1 microM, where it accounts for >35% of the total removal rate. At lower [Ca2+]i, thapsigargin-sensitive Ca2+-ATPases constitute a major (70% at 0.8 microM [Ca2+]i) mechanism for Ca2+ removal. The beta-cell Na/Ca exchanger is electrogenic and has a stoichiometry of three Na+ for one Ca2+. The current arising from its operation reverses at approximately -20 mV (current inward at more negative voltages), has a conductance of 53 pS/pF (14 microM [Ca2+]i), and is abolished by removal of external Na+ or by intracellularly applied XIP (exchange inhibitory peptide). Inhibition of the exchanger results in shortening (50%) of the bursts of action potentials of glucose-stimulated beta-cells in intact islets and a slight (5 mV) hyperpolarization. Mathematical simulations suggest that the stimulatory action of glucose on beta-cell electrical activity may be accounted for in part by glucose-induced reduction of the cytoplasmic Na+ concentration with resultant activation of the exchanger. (+info)A sodium-calcium exchanger (NCX) is a type of ion transport protein found in the membranes of cells, including those of the heart and brain. It plays a crucial role in regulating intracellular calcium concentrations by facilitating the exchange of sodium ions for calcium ions across the cell membrane.
During each heartbeat, calcium ions enter the cardiac muscle cells to trigger contraction. After the contraction, the sodium-calcium exchanger helps remove excess calcium from the cell by exchanging it for sodium ions. This process is essential for maintaining normal calcium levels within the cell and allowing the heart muscle to relax between beats.
There are three main isoforms of the sodium-calcium exchanger (NCX1, NCX2, and NCX3) with different tissue distributions and functions. Dysfunction in sodium-calcium exchangers has been implicated in various pathological conditions such as heart failure, hypertension, and neurological disorders.
Calcium is an essential mineral that is vital for various physiological processes in the human body. The medical definition of calcium is as follows:
Calcium (Ca2+) is a crucial cation and the most abundant mineral in the human body, with approximately 99% of it found in bones and teeth. It plays a vital role in maintaining structural integrity, nerve impulse transmission, muscle contraction, hormonal secretion, blood coagulation, and enzyme activation.
Calcium homeostasis is tightly regulated through the interplay of several hormones, including parathyroid hormone (PTH), calcitonin, and vitamin D. Dietary calcium intake, absorption, and excretion are also critical factors in maintaining optimal calcium levels in the body.
Hypocalcemia refers to low serum calcium levels, while hypercalcemia indicates high serum calcium levels. Both conditions can have detrimental effects on various organ systems and require medical intervention to correct.
Antiporters, also known as exchange transporters, are a type of membrane transport protein that facilitate the exchange of two or more ions or molecules across a biological membrane in opposite directions. They allow for the movement of one type of ion or molecule into a cell while simultaneously moving another type out of the cell. This process is driven by the concentration gradient of one or both of the substances being transported. Antiporters play important roles in various physiological processes, including maintaining electrochemical balance and regulating pH levels within cells.
Aflatoxin M1 is a type of mycotoxin, which is a toxic compound that is produced by certain types of molds or fungi. Aflatoxin M1 is produced by the mold Aspergillus flavus and Aspergillus parasiticus, and it can contaminate a variety of agricultural products, including grains, nuts, and milk.
Aflatoxin M1 is a metabolite of aflatoxin B1, which is the most potent naturally occurring carcinogen known. Aflatoxin M1 is formed in the liver of dairy animals after they consume feed contaminated with aflatoxin B1 and then passes into their milk. It can also be found in other tissues of dairy animals, such as meat and organs.
Exposure to aflatoxin M1 has been linked to various health effects, including liver damage, immune suppression, and increased risk of liver cancer. For this reason, regulatory agencies around the world have set limits on the amount of aflatoxin M1 that is allowed in milk and other dairy products.
Zeolites are not typically a subject of medical definition, as they are naturally occurring or synthetically produced minerals used in various industrial applications. They are microporous, aluminosilicate minerals with a crystal-like structure, composed of aluminum, silicon, and oxygen tetrahedra. These minerals have a negative charge and can exchange positively charged ions, making them useful for water purification, odor control, and as catalysts in chemical reactions.
However, there is some research into the potential use of zeolites in medical applications, such as drug delivery systems or as adsorbents to remove toxins from the body. In these contexts, the definition of zeolites would be similar to their industrial definition.
Aluminum silicates are a type of mineral compound that consist of aluminum, silicon, and oxygen in their chemical structure. They are often found in nature and can be categorized into several groups, including kaolinite, illite, montmorillonite, and bentonite. These minerals have various industrial and commercial uses, including as fillers and extenders in products like paper, paint, and rubber. In the medical field, certain types of aluminum silicates (like bentonite) have been used in some medicinal and therapeutic applications, such as detoxification and gastrointestinal disorders. However, it's important to note that the use of these minerals in medical treatments is not widely accepted or supported by extensive scientific evidence.
Sodium is an essential mineral and electrolyte that is necessary for human health. In a medical context, sodium is often discussed in terms of its concentration in the blood, as measured by serum sodium levels. The normal range for serum sodium is typically between 135 and 145 milliequivalents per liter (mEq/L).
Sodium plays a number of important roles in the body, including:
* Regulating fluid balance: Sodium helps to regulate the amount of water in and around your cells, which is important for maintaining normal blood pressure and preventing dehydration.
* Facilitating nerve impulse transmission: Sodium is involved in the generation and transmission of electrical signals in the nervous system, which is necessary for proper muscle function and coordination.
* Assisting with muscle contraction: Sodium helps to regulate muscle contractions by interacting with other minerals such as calcium and potassium.
Low sodium levels (hyponatremia) can cause symptoms such as confusion, seizures, and coma, while high sodium levels (hypernatremia) can lead to symptoms such as weakness, muscle cramps, and seizures. Both conditions require medical treatment to correct.
Mycotoxicosis is not a specific medical condition itself, but rather a term that refers to the toxic effects on livestock or human health due to the consumption of food or feed contaminated with mycotoxins. Mycotoxins are toxic compounds produced by certain types of mold (fungi) that can grow on various agricultural products before and after harvest, during storage, or in contaminated animal feeds.
Mycotoxicosis can cause a wide range of symptoms depending on the specific mycotoxin involved, the amount and duration of exposure, and the overall health of the individual. These symptoms may include acute gastrointestinal distress, immunosuppression, neurological disorders, reproductive issues, and even cancer in severe cases.
Some common mycotoxins that can lead to mycotoxicosis include aflatoxins, ochratoxins, fumonisins, trichothecenes, zearalenone, and patulin. Preventing mold growth and mycotoxin production in food and feed through proper agricultural practices, storage conditions, and monitoring is crucial to prevent mycotoxicosis.
Drug residues refer to the remaining amount of a medication or drug that remains in an animal or its products after the treatment period has ended. This can occur when drugs are not properly metabolized and eliminated by the animal's body, or when withdrawal times (the recommended length of time to wait before consuming or selling the animal or its products) are not followed.
Drug residues in animals can pose a risk to human health if consumed through the consumption of animal products such as meat, milk, or eggs. For this reason, regulatory bodies set maximum residue limits (MRLs) for drug residues in animal products to ensure that they do not exceed safe levels for human consumption.
It is important for farmers and veterinarians to follow label instructions and recommended withdrawal times to prevent the accumulation of drug residues in animals and their products, and to protect public health.
Thiourea is not a medical term, but a chemical compound. It's a colorless crystalline solid with the formula SC(NH2)2. Thiourea is used in some industrial processes and can be found in some laboratory reagents. It has been studied for its potential effects on certain medical conditions, such as its ability to protect against radiation damage, but it is not a medication or a treatment that is currently in clinical use.
Calcium signaling is the process by which cells regulate various functions through changes in intracellular calcium ion concentrations. Calcium ions (Ca^2+^) are crucial second messengers that play a critical role in many cellular processes, including muscle contraction, neurotransmitter release, gene expression, and programmed cell death (apoptosis).
Intracellular calcium levels are tightly regulated by a complex network of channels, pumps, and exchangers located on the plasma membrane and intracellular organelles such as the endoplasmic reticulum (ER) and mitochondria. These proteins control the influx, efflux, and storage of calcium ions within the cell.
Calcium signaling is initiated when an external signal, such as a hormone or neurotransmitter, binds to a specific receptor on the plasma membrane. This interaction triggers the opening of ion channels, allowing extracellular Ca^2+^ to flow into the cytoplasm. In some cases, this influx of calcium ions is sufficient to activate downstream targets directly. However, in most instances, the increase in intracellular Ca^2+^ serves as a trigger for the release of additional calcium from internal stores, such as the ER.
The release of calcium from the ER is mediated by ryanodine receptors (RyRs) and inositol trisphosphate receptors (IP3Rs), which are activated by specific second messengers generated in response to the initial external signal. The activation of these channels leads to a rapid increase in cytoplasmic Ca^2+^, creating a transient intracellular calcium signal known as a "calcium spark" or "calcium puff."
These localized increases in calcium concentration can then propagate throughout the cell as waves of elevated calcium, allowing for the spatial and temporal coordination of various cellular responses. The duration and amplitude of these calcium signals are finely tuned by the interplay between calcium-binding proteins, pumps, and exchangers, ensuring that appropriate responses are elicited in a controlled manner.
Dysregulation of intracellular calcium signaling has been implicated in numerous pathological conditions, including neurodegenerative diseases, cardiovascular disorders, and cancer. Therefore, understanding the molecular mechanisms governing calcium homeostasis and signaling is crucial for the development of novel therapeutic strategies targeting these diseases.
A Sodium-Hydrogen Antiporter (NHA) is a type of membrane transport protein that exchanges sodium ions (Na+) and protons (H+) across a biological membrane. It is also known as a Na+/H+ antiporter or exchanger. This exchange mechanism plays a crucial role in regulating pH, cell volume, and intracellular sodium concentration within various cells and organelles, including the kidney, brain, heart, and mitochondria.
In general, NHA transporters utilize the energy generated by the electrochemical gradient of sodium ions across a membrane to drive the uphill transport of protons from inside to outside the cell or organelle. This process helps maintain an optimal intracellular pH and volume, which is essential for proper cellular function and homeostasis.
There are several isoforms of Sodium-Hydrogen Antiporters found in different tissues and organelles, each with distinct physiological roles and regulatory mechanisms. Dysfunction or alterations in NHA activity have been implicated in various pathophysiological conditions, such as hypertension, heart failure, neurological disorders, and cancer.
Calcium-transporting ATPases, also known as calcium pumps, are a type of enzyme that use the energy from ATP (adenosine triphosphate) hydrolysis to transport calcium ions across membranes against their concentration gradient. This process helps maintain low intracellular calcium concentrations and is essential for various cellular functions, including muscle contraction, neurotransmitter release, and gene expression.
There are two main types of calcium-transporting ATPases: the sarcoplasmic/endoplasmic reticulum Ca^2+^-ATPase (SERCA) and the plasma membrane Ca^2+^-ATPase (PMCA). SERCA is found in the sarcoplasmic reticulum of muscle cells and endoplasmic reticulum of other cell types, where it pumps calcium ions into these organelles to initiate muscle relaxation or signal transduction. PMCA, on the other hand, is located in the plasma membrane and extrudes calcium ions from the cell to maintain low cytosolic calcium concentrations.
Calcium-transporting ATPases play a crucial role in maintaining calcium homeostasis in cells and are important targets for drug development in various diseases, including heart failure, hypertension, and neurological disorders.
Cardiac myocytes are the muscle cells that make up the heart muscle, also known as the myocardium. These specialized cells are responsible for contracting and relaxing in a coordinated manner to pump blood throughout the body. They differ from skeletal muscle cells in several ways, including their ability to generate their own electrical impulses, which allows the heart to function as an independent rhythmical pump. Cardiac myocytes contain sarcomeres, the contractile units of the muscle, and are connected to each other by intercalated discs that help coordinate contraction and ensure the synchronous beating of the heart.
In the context of medicine, Mercury does not have a specific medical definition. However, it may refer to:
1. A heavy, silvery-white metal that is liquid at room temperature. It has been used in various medical and dental applications, such as therapeutic remedies (now largely discontinued) and dental amalgam fillings. Its use in dental fillings has become controversial due to concerns about its potential toxicity.
2. In microbiology, Mercury is the name of a bacterial genus that includes the pathogenic species Mercury deserti and Mercury avium. These bacteria can cause infections in humans and animals.
It's important to note that when referring to the planet or the use of mercury in astrology, these are not related to medical definitions.
A "periodical" in the context of medicine typically refers to a type of publication that is issued regularly, such as on a monthly or quarterly basis. These publications include peer-reviewed journals, magazines, and newsletters that focus on medical research, education, and practice. They may contain original research articles, review articles, case reports, editorials, letters to the editor, and other types of content related to medical science and clinical practice.
As a "Topic," periodicals in medicine encompass various aspects such as their role in disseminating new knowledge, their impact on clinical decision-making, their quality control measures, and their ethical considerations. Medical periodicals serve as a crucial resource for healthcare professionals, researchers, students, and other stakeholders to stay updated on the latest developments in their field and to share their findings with others.
"Access to information," in a medical context, refers to the ability of individuals, patients, healthcare providers, and researchers to obtain, request, and disseminate health-related data, records, research findings, and other important information. This includes access to personal medical records, clinical trial results, evidence-based practices, and public health statistics.
Promoting access to information is crucial for informed decision-making, ensuring transparency, advancing medical research, improving patient care, and enhancing overall healthcare system performance. Various laws, regulations, and policies at the local, national, and international levels aim to protect and facilitate access to information while balancing privacy concerns, data security, and intellectual property rights.
The Journal Impact Factor (JIF) is a measure of the frequency with which the "average article" in a journal has been cited in a particular year. It is calculated by dividing the number of current year citations to the source items published in that journal during the previous two years. For example, if a journal has an Impact Factor of 3 in 2020, that means articles published in 2018 and 2019 were cited 3 times on average in 2020. It is used to gauge the importance or rank of a journal by comparing the times it's articles are cited relative to other journals in the field. However, it has been criticized for various limitations such as being manipulated by editors and not reflecting the quality of individual articles.
Bibliometrics is the use of statistical methods to analyze books, articles, and other publications. In the field of information science, bibliometrics is often used to measure the impact of scholarly works or authors by counting the number of times that a work has been cited in other publications. This can help researchers identify trends and patterns in research output and collaboration, as well as assess the influence of individual researchers or institutions.
Bibliometric analyses may involve a variety of statistical measures, such as citation counts, author productivity, journal impact factors, and collaborative networks. These measures can be used to evaluate the performance of individual researchers, departments, or institutions, as well as to identify areas of research strength or weakness.
It is important to note that while bibliometrics can provide useful insights into research trends and impact, they should not be the sole basis for evaluating the quality or significance of scholarly work. Other factors, such as the rigor of the research design, the clarity of the writing, and the relevance of the findings to the field, are also important considerations.
I'm sorry for any confusion, but "publishing" is not a term that has a medical definition. Publishing typically refers to the process of preparing and disseminating information, such as books, journals, or articles, to the public or a specific audience. It could involve both print and digital media. If you have any questions related to medicine or healthcare, I'd be happy to try to help answer those!
Peer review in the context of research refers to the evaluation of scientific, academic, or professional work by others working in the same field. The purpose of peer review is to ensure that the research is rigorous, valid, and relevant to the field. In a peer-review process, experts in the relevant field assess the research article, report, or other type of scholarly work for its accuracy, quality, and significance before it is published or presented at a conference.
The peer-review process typically involves several stages:
1. Submission: The author(s) submit their manuscript to a journal, conference, or other publication venue.
2. Assignment: The editor of the publication assigns the manuscript to one or more reviewers who are experts in the field.
3. Review: The reviewers evaluate the manuscript based on criteria such as originality, methodology, data analysis, interpretation of results, and contribution to the field. They provide feedback and recommendations to the editor.
4. Decision: Based on the feedback from the reviewers, the editor makes a decision about whether to accept, reject, or request revisions to the manuscript.
5. Revision: If the manuscript is rejected or requires revisions, the author(s) may have an opportunity to revise and resubmit the manuscript for further consideration.
Peer review is a critical component of the scientific process, as it helps ensure that research is held to high standards of quality and integrity. It also provides a mechanism for identifying and correcting errors or weaknesses in research before it is published or disseminated widely.
Long QT syndrome (LQTS) is a cardiac electrical disorder characterized by a prolonged QT interval on the electrocardiogram (ECG), which can potentially trigger rapid, chaotic heartbeats known as ventricular tachyarrhythmias, such as torsades de pointes. These arrhythmias can be life-threatening and lead to syncope (fainting) or sudden cardiac death. LQTS is often congenital but may also be acquired due to certain medications, medical conditions, or electrolyte imbalances. It's essential to identify and manage LQTS promptly to reduce the risk of severe complications.
Electrocardiography (ECG or EKG) is a medical procedure that records the electrical activity of the heart. It provides a graphic representation of the electrical changes that occur during each heartbeat. The resulting tracing, called an electrocardiogram, can reveal information about the heart's rate and rhythm, as well as any damage to its cells or abnormalities in its conduction system.
During an ECG, small electrodes are placed on the skin of the chest, arms, and legs. These electrodes detect the electrical signals produced by the heart and transmit them to a machine that amplifies and records them. The procedure is non-invasive, painless, and quick, usually taking only a few minutes.
ECGs are commonly used to diagnose and monitor various heart conditions, including arrhythmias, coronary artery disease, heart attacks, and electrolyte imbalances. They can also be used to evaluate the effectiveness of certain medications or treatments.
The KCNQ1 potassium channel, also known as the Kv7.1 channel, is a voltage-gated potassium ion channel that plays a crucial role in the regulation of electrical excitability in cardiac myocytes and inner ear epithelial cells. In the heart, it helps to control the duration and frequency of action potentials, thereby contributing to the maintenance of normal cardiac rhythm. Mutations in the KCNQ1 gene can lead to various cardiac disorders, such as long QT syndrome type 1 and familial atrial fibrillation. In the inner ear, it helps regulate potassium homeostasis and is essential for hearing and balance functions. Dysfunction of this channel has been linked to deafness and balance disorders.
Congenital Disorders of Glycosylation (CDG) are a group of genetic disorders that affect the body's ability to add sugar molecules (glycans) to proteins and lipids. This process, known as glycosylation, is essential for the proper functioning of many cellular processes, including protein folding, trafficking, and signaling.
CDG can be caused by mutations in genes that are involved in the synthesis or transport of glycans. These genetic defects can lead to abnormal glycosylation patterns, which can result in a wide range of clinical manifestations, including developmental delay, intellectual disability, seizures, movement disorders, hypotonia, coagulation abnormalities, and multi-organ involvement.
CDG are typically classified into two main types: type I CDG, which involves defects in the synthesis of the lipid-linked oligosaccharide precursor used for N-glycosylation, and type II CDG, which involves defects in the processing and transfer of glycans to proteins.
The diagnosis of CDG is often based on clinical features, laboratory tests, and genetic analysis. Treatment is typically supportive and multidisciplinary, focusing on addressing specific symptoms and improving quality of life. In some cases, dietary modifications or supplementation with mannose or other sugars may be beneficial.
Ether-à-go-go (EAG) potassium channels are a type of voltage-gated potassium channel that are widely expressed in the heart, brain, and other tissues. They are named after the ethereal dance movements observed in fruit flies with mutations in these channels.
EAG potassium channels play important roles in regulating electrical excitability and signaling in excitable cells. In the heart, they help to control the duration of the action potential and the refractory period, which is critical for maintaining normal heart rhythm. In the brain, they are involved in regulating neuronal excitability and neurotransmitter release.
Mutations in EAG potassium channels have been associated with various human diseases, including cardiac arrhythmias, epilepsy, and bipolar disorder. The medical definition of "Ether-A-Go-Go Potassium Channels" refers to the genetic components that make up these channels and their role in physiological processes and disease states.
Syncope is a medical term defined as a transient, temporary loss of consciousness and postural tone due to reduced blood flow to the brain. It's often caused by a drop in blood pressure, which can be brought on by various factors such as dehydration, emotional stress, prolonged standing, or certain medical conditions like heart diseases, arrhythmias, or neurological disorders.
During a syncope episode, an individual may experience warning signs such as lightheadedness, dizziness, blurred vision, or nausea before losing consciousness. These episodes usually last only a few minutes and are followed by a rapid, full recovery. However, if left untreated or undiagnosed, recurrent syncope can lead to severe injuries from falls or even life-threatening conditions related to the underlying cause.
Cardiac arrhythmias are abnormal heart rhythms that result from disturbances in the electrical conduction system of the heart. The heart's normal rhythm is controlled by an electrical signal that originates in the sinoatrial (SA) node, located in the right atrium. This signal travels through the atrioventricular (AV) node and into the ventricles, causing them to contract and pump blood throughout the body.
An arrhythmia occurs when there is a disruption in this electrical pathway or when the heart's natural pacemaker produces an abnormal rhythm. This can cause the heart to beat too fast (tachycardia), too slow (bradycardia), or irregularly.
There are several types of cardiac arrhythmias, including:
1. Atrial fibrillation: A rapid and irregular heartbeat that starts in the atria (the upper chambers of the heart).
2. Atrial flutter: A rapid but regular heartbeat that starts in the atria.
3. Supraventricular tachycardia (SVT): A rapid heartbeat that starts above the ventricles, usually in the atria or AV node.
4. Ventricular tachycardia: A rapid and potentially life-threatening heart rhythm that originates in the ventricles.
5. Ventricular fibrillation: A chaotic and disorganized electrical activity in the ventricles, which can be fatal if not treated immediately.
6. Heart block: A delay or interruption in the conduction of electrical signals from the atria to the ventricles.
Cardiac arrhythmias can cause various symptoms, such as palpitations, dizziness, shortness of breath, chest pain, and fatigue. In some cases, they may not cause any symptoms and go unnoticed. However, if left untreated, certain types of arrhythmias can lead to serious complications, including stroke, heart failure, or even sudden cardiac death.
Treatment for cardiac arrhythmias depends on the type, severity, and underlying causes. Options may include lifestyle changes, medications, cardioversion (electrical shock therapy), catheter ablation, implantable devices such as pacemakers or defibrillators, and surgery. It is essential to consult a healthcare professional for proper evaluation and management of cardiac arrhythmias.
Sodium-calcium exchanger
Potassium-dependent sodium-calcium exchanger
AKAP6
Magnesium transporter
Sense of smell
Caveolin 3
Calcium:cation antiporter
Novel Therapeutic Targets for Antiarrhythmic Drugs
Mitochondrial calcium uniporter
SLC8B1
Solute carrier family
Drosophila melanogaster
Hodgkin-Huxley model
Calcium ATPase
Plasma membrane Ca2+ ATPase
Amelogenesis imperfecta
Kohlschütter-Tönz syndrome
ATP2B3
Cardiac pacemaker
Neuropathix
KLS-13019
Cerberin
Andersen-Tawil syndrome
Active transport
Anrep effect
Acid-sensing ion channel
Tiger eye
Calcium pump
Calotropin
Cotransporter
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Mitochondrial2
- The paper, titled " Knockdown siRNA Targeting the Mitochondrial Sodium-Calcium Exchanger-1 Inhibits the Protective Effects of Two Cannabinoids Against Acute Paclitaxel Toxicity ," compares cannabidiol (CBD) and Kannalife's proprietary CBD-like molecule KLS-13019 and its effects on the mitochondrial sodium-calcium exchanger-1. (biospace.com)
- CGP 37157 is a benzothiazepine that acts as a selective inhibitor of the mitochondrial sodium-calcium exchanger (IC50 = 0.36 μM in isolated mitochondria). (adooq.com)
Inhibitors1
- Inhibitors may appear to be more effective when the exchanger is operating in net calcium entry mode than in calcium exit mode. (ox.ac.uk)
Protein3
- The sodium-calcium exchanger (often denoted Na+/Ca2+ exchanger, exchange protein, or NCX) is an antiporter membrane protein that removes calcium from cells. (wikipedia.org)
- Protein deficiency is an important cause of deranged calcium metabolism. (raypeat.com)
- As you can see, the calcium ion is highly represented, and in fact, this messenger is recycled for many different purposes to mediate the actions (for example) of G protein-coupled receptors, receptor tyrosine kinases, voltage-operated calcium channels, among others. (hstalks.com)
Extracellular6
- This fact can be protective because increases in intracellular Ca2+ concentration that occur in excitotoxicity may activate the exchanger in the forward direction even in the presence of a lowered extracellular Na+ concentration. (wikipedia.org)
- During the resting potential, the Na+/Ca2+ exchanger takes advantage of the large extracellular Na+ concentration gradient to help pump Ca2+ out of the cell. (wikipedia.org)
- The sodium/calcium exchangers (NCX) use the extracellular sodium concentration to facilitate the extrusion of calcium out of the cell. (guidetopharmacology.org)
- Magnesium and potassium are mainly intracellular ions, sodium and calcium are mainly extracellular ions. (raypeat.com)
- Welcome to this lecture on extracellular calcium signaling. (hstalks.com)
- However, an interesting corollary of these plasma membrane fluxes is that they can potentially lead to significant alterations in local calcium concentration at the extracellular face of the cell. (hstalks.com)
Potassium6
- Alongside the plasma membrane Ca 2+ -ATPase ( PMCA ) and sarcoplasmic/endoplasmic reticulum Ca 2+ -ATPase ( SERCA ), as well as the sodium/potassium/calcium exchangers (NKCX, SLC24 family ), NCX allow recovery of intracellular calcium back to basal levels after cellular stimulation. (guidetopharmacology.org)
- Expression of Potassium-Dependent Sodium-Calcium Exchanger in the Murine Lens. (wustl.edu)
- When cells are excited, stressed, or de-energized, they lose magnesium and potassium, and take up sodium and calcium. (raypeat.com)
- We sought to directly monitor cAMP in a microdomain formed around sodium-potassium ATPase (NKA) in healthy and failing cardiomyocytes and to better understand alterations of cAMP compartmentation in heart failure. (dundee.ac.uk)
- These bind to a site on the cell membrane, producing reversible inhibition of the sodium (Na + )-potassium (K + )-adenosine triphosphatase (ATPase) pump. (medscape.com)
- This increases intracellular sodium and decreases intracellular potassium. (medscape.com)
Cardiac4
- The ability for the Na+/Ca2+ exchanger to reverse direction of flow manifests itself during the cardiac action potential. (wikipedia.org)
- As a result of this excessive intracellular calcium, enhanced cardiac contractions, which are delayed after depolarizations, occur. (medscape.com)
- Functional states of the sodium channel (closed, open, and inactivated) and their structure help to understand the cardiac regulation processes. (bvsalud.org)
- Finally, it seems appropriate to consider the "sodium channel syndrome" (mutations in the gene of the α subunit of the sodium channel, SCN5A gene) as a single clinical entity that may manifest in a wide range of phenotypes, to thus have a better insight on these cardiac syndromes and potential outcomes for their clinical treatment. (bvsalud.org)
Myocytes3
- The role of the Na+/Ca2+ exchangers in Ca2+ dynamics in ventricular myocytes. (ox.ac.uk)
- The role of the Na+/Ca2+ exchanger (NCX) as the main pathway for Ca2+ extrusion from ventricular myocytes is well established. (ox.ac.uk)
- In myocytes, elevated intracellular sodium concentrations produce increased intracellular calcium concentrations via an Na + -calcium (Ca ++ )-exchanger. (medscape.com)
Intracellular calcium2
- All of this transport activity is, of course, exceedingly important in shaping the intracellular calcium signal. (hstalks.com)
- In response to the increased intracellular calcium, the sarcoplasmic reticulum releases additional calcium intracellularly, resulting in depolarization of the cell. (medscape.com)
Characterization1
- 6] "Molecular cloning and characterization of two novel truncated isoforms of human Na+/Ca2+ exchanger 3, expressed in fetal brain. (tcdb.org)
Inhibits1
- When cells are stressed or dying, they take up calcium, which tends to excite the cells at the same time that it inhibits their energy production, intensifying their stress. (raypeat.com)
Important in regulat1
- Vitamins K, E, and A are important in regulating calcium metabolism, and preventing osteoporosis. (raypeat.com)
Endoplasmic reticulum1
- The exchanger is usually found in the plasma membranes and the mitochondria and endoplasmic reticulum of excitable cells. (wikipedia.org)
Inhibitor3
- SEA0400 is a novel and selective inhibitor of the Na+-Ca2+ exchanger with IC50 of 5-33 nM (inhibiting Na+-dependent Ca2+ uptake in cultured neurons, astrocytes, and microglia). (adooq.com)
- ORM-10103 is a specific inhibitor of the Na+/Ca2+ exchanger (NCX), which decreases the NCX current with estimated IC50s of 55 and 67 nM at -80 and at 20 mV, respectively. (adooq.com)
- ORM-10962 is a potent, highly selective sodium-calcium exchanger (NCX) inhibitor, with IC50 values of 67 and 55 nM for the reverse and forward mode inhibition, respectively. (adooq.com)
Reversal3
- This causes the reversal of the Na+/Ca2+ exchanger to pump Na+ ions out of the cell and Ca2+ ions into the cell. (wikipedia.org)
- However, this reversal of the exchanger lasts only momentarily due to the internal rise in [Ca2+] as a result of the influx of Ca2+ through the L-type calcium channel, and the exchanger returns to its forward direction of flow, pumping Ca2+ out of the cell. (wikipedia.org)
- If such agents are necessary, reversal with sugammadex sodium may make postoperative ventilator support less likely to be required. (medscape.com)
Concentration2
- The sodium-calcium exchanger is only one of the systems by which the cytoplasmic concentration of calcium ions in the cell is kept low. (wikipedia.org)
- Thus, the plasma sodium concentration is typically normal, and hypervolemia is infrequent unless dietary intake of sodium or water is very restricted or excessive. (msdmanuals.com)
SLC8A31
- 1] "The human SLC8A3 gene and the tissue-specific Na+/Ca2+ exchanger 3 isoforms. (tcdb.org)
Efflux3
- In fact, the Na+/Ca2+ exchanger is in the Ca2+ efflux position most of the time. (wikipedia.org)
- While the exchanger normally works in the Ca2+ efflux position (with the exception of early in the action potential), certain conditions can abnormally switch the exchanger to the reverse (Ca2+ influx, Na+ efflux) position. (wikipedia.org)
- When intracellular sodium ion levels rise, for example, following depolarisation, these transporters can operate in the reverse direction to allow calcium influx and sodium efflux, as an electrogenic mechanism. (guidetopharmacology.org)
ATPase2
- Another, more ubiquitous transmembrane pump that exports calcium from the cell is the plasma membrane Ca2+ ATPase (PMCA), which has a much higher affinity but a much lower capacity. (wikipedia.org)
- Calcium moves across the plasma membrane through pathways such as the plasma membrane calcium ATPase (PMCA), or the sodium calcium exchanger, these are important in expelling calcium from the cell. (hstalks.com)
Metabolism1
- But there are ways of looking at the organism, focusing on energy metabolism, that dont involve the ad hoc theory of calcium pumps, and that make it easy to keep things in context. (raypeat.com)
Tissue-specific1
- Khananshvili D. (2014) Sodium-calcium exchangers (NCX): molecular hallmarks underlying the tissue-specific and systemic functions. (guidetopharmacology.org)
Gene2
- Khananshvili D. (2013) The SLC8 gene family of sodium-calcium exchangers (NCX) - structure, function, and regulation in health and disease. (guidetopharmacology.org)
- Lytton J. (2007) Na+/Ca2+ exchangers: three mammalian gene families control Ca2+ transport. (guidetopharmacology.org)
Pharmacology1
- 2004) Pharmacology of brain Na+/Ca2+ exchanger: from molecular biology to therapeutic perspectives. (guidetopharmacology.org)
Molecules2
- Calcium is the most studied of all regulatory molecules, so it isnt surprising that there is more than one calcium paradox. (raypeat.com)
- The paper details the protective action of both molecules against this exchanger, known to increase calcium levels in patients taking the chemotherapy drug paclitaxel. (biospace.com)
Demyelinating diseases1
- The Na + /Ca 2+ exchangers in demyelinating diseases. (nih.gov)
Signaling2
- So it's powerful signaling actions can only be controlled by moving the calcium ion about in different locations inside and outside the cell, or by temporarily buffering it. (hstalks.com)
- The acetate enhancement of calcium signaling was abolished by memantine. (bvsalud.org)
Cytosolic1
- Here, we investigated the effect of acetate on CeA neurons with the axon projecting to the rostral ventrolateral medulla (CeA-RVLM), as well as quantified cytosolic calcium responses in primary neuronal cultures. (bvsalud.org)
Abnormality1
- Persons suffering from arthritis, bursitis, scleroderma, hardening of the arteries and any abnormality where calcium deposits or spurs may cause pain are often afraid to eat foods rich in calcium. (raypeat.com)
Concentrations2
- Thus, the exchanger also likely plays an important role in regaining the cell's normal calcium concentrations after an excitotoxic insult. (wikipedia.org)
- Since the PMCA is capable of effectively binding to Ca2+ even when its concentrations are quite low, it is better suited to the task of maintaining the very low concentrations of calcium that are normally within a cell. (wikipedia.org)
Regulation1
- Gabellini N. (2004) Transcriptional regulation by cAMP and Ca2+ links the Na+/Ca2+ exchanger 3 to memory and sensory pathways. (guidetopharmacology.org)
Barium1
- 1973. The determination of trace amounts of barium in calcium carbonate by atomic- absorption spectrophotometry. (cdc.gov)
Neuronal1
- This effect may prolong calcium transients following bursts of neuronal activity, thus influencing neuronal information processing. (wikipedia.org)
Uptake1
- Inflammation leads to excessive uptake of calcium by cells, and is a factor in obesity, depression, and the degenerative diseases. (raypeat.com)
Depolarization1
- Furthermore, as measured by multiple electrode arrays and calcium imaging, mild depolarization acutely subdues subsequent spontaneous and bicuculline-evoked activity via calcium- and N-methyl-d-aspartate receptor-dependent mechanisms. (bvsalud.org)
Bind2
- The exchanger does not bind very tightly to Ca2+ (has a low affinity), but it can transport the ions rapidly (has a high capacity), transporting up to five thousand Ca2+ ions per second. (wikipedia.org)
- The mitochondria can bind a certain amount of calcium during stress, but accumulating calcium can reach a point at which it inactivates the mitochondria, forcing cells to increase their inefficient glycolytic energy production, producing an excess of lactic acid. (raypeat.com)
Pathways2
- Most of the other pathways in this list rely on metabolic reactions for their initiation and termination, calcium differs in an important way from these other pathways in that as an inorganic cation, calcium can be neither created nor destroyed. (hstalks.com)
- Calcium can enter through pathways such as store-operated, voltage-operated, or receptor-operated calcium channels. (hstalks.com)
Plasma membrane2
- It uses the energy that is stored in the electrochemical gradient of sodium (Na+) by allowing Na+ to flow down its gradient across the plasma membrane in exchange for the countertransport of calcium ions (Ca2+). (wikipedia.org)
- Such a primary transporter of calcium ions is present in the plasma membrane of most animal cells. (wikipedia.org)
Symptoms1
- Magnesium deficiency and calcium deficiency have some similar symptoms (such as cramping), but magnesium is antagonistic to calcium in many systems. (raypeat.com)
Protective1
- It is the basic protective calcium blocker. (raypeat.com)
Occur1
- Such calcium deposits can also occur when vitamin E is undersupplied. (raypeat.com)
Cell5
- The exchanger exists in many different cell types and animal species. (wikipedia.org)
- Cell Calcium. (nih.gov)
- Furthermore, under conditions favoring reverse operation of the Na + -Ca 2+ exchanger, Zn 2+ application induced a slow increase in [Zn 2+ ] i and outward whole-cell current sensitive to benzamil-amiloride. (jneurosci.org)
- In today's talk, I'm going to discuss the emerging idea that these calcium fluctuations outside the cell may serve as signals in their own right. (hstalks.com)
- A drug that inhibited calcium entry, while still allowing transport of calcium out of the cell would then seem attractive. (ox.ac.uk)
Transport1
- Giladi M, Shor R, Lisnyansky M, Khananshvili D. (2016) Structure-Functional Basis of Ion Transport in Sodium-Calcium Exchanger (NCX) Proteins. (guidetopharmacology.org)
Role1
- Heart relaxation also stands out as an active process, dependent on the energetic output and on specific ion and enzymatic actions, with the role of sodium channel being outstanding in the functional process. (bvsalud.org)
Function1
- From a physiological and pathophysiological point of view, the conformational states of the sodium channel during heart function constitute a significant aspect for the diagnosis and treatment of heart diseases. (bvsalud.org)