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Academic literature on the topic 'Sodium Ion Cells'
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Journal articles on the topic "Sodium Ion Cells"
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Ban, Yue, Benjamin E. Smith, and Michael R. Markham. "A highly polarized excitable cell separates sodium channels from sodium-activated potassium channels by more than a millimeter." Journal of Neurophysiology 114, no. 1 (2015): 520–30. http://dx.doi.org/10.1152/jn.00475.2014.
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The bioelectrical properties and resulting metabolic demands of electrogenic cells are determined by their morphology and the subcellular localization of ion channels. The electric organ cells (electrocytes) of the electric fish Eigenmannia virescens generate action potentials (APs) with Na+ currents >10 μA and repolarize the AP with Na+-activated K+ (KNa) channels. To better understand the role of morphology and ion channel localization in determining the metabolic cost of electrocyte APs, we used two-photon three-dimensional imaging to determine the fine cellular morphology and immunohistochemistry to localize the electrocytes' ion channels, ionotropic receptors, and Na+-K+-ATPases. We found that electrocytes are highly polarized cells ∼1.5 mm in anterior-posterior length and ∼0.6 mm in diameter, containing ∼30,000 nuclei along the cell periphery. The cell's innervated posterior region is deeply invaginated and vascularized with complex ultrastructural features, whereas the anterior region is relatively smooth. Cholinergic receptors and Na+ channels are restricted to the innervated posterior region, whereas inward rectifier K+ channels and the KNa channels that terminate the electrocyte AP are localized to the anterior region, separated by >1 mm from the only sources of Na+ influx. In other systems, submicrometer spatial coupling of Na+ and KNa channels is necessary for KNa channel activation. However, our computational simulations showed that KNa channels at a great distance from Na+ influx can still terminate the AP, suggesting that KNa channels can be activated by distant sources of Na+ influx and overturning a long-standing assumption that AP-generating ion channels are restricted to the electrocyte's posterior face.
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Li, Xianji, Andrew L. Hector, John R. Owen, and S. Imran U. Shah. "Evaluation of nanocrystalline Sn3N4derived from ammonolysis of Sn(NEt2)4as a negative electrode material for Li-ion and Na-ion batteries." Journal of Materials Chemistry A 4, no. 14 (2016): 5081–87. http://dx.doi.org/10.1039/c5ta08287k.
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Bulk nanocrystalline Sn<sub>3</sub>N<sub>4</sub>powders were synthesised by a two step ammonolysis route. These provided good capacities in sodium and lithium cells, and good stability in sodium cells.
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Sabzpoushan, S. H., and A. Faghani Ghodrat. "Role of Sodium Channel on Cardiac Action Potential." Engineering, Technology & Applied Science Research 2, no. 3 (2012): 232–36. http://dx.doi.org/10.48084/etasr.174.
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Sudden cardiac death is a major cause of death worldwide. In most cases, it's caused by abnormal action potential propagation that leads to cardiac arrhythmia. The aim of this article is to study the abnormal action potential propagation through sodium ion concentration variations. We use a new electrophysiological model that is both detailed and computationally efficient. This efficient model is based on the partial differential equation method. The central finite difference method is used for numerical solving of the two-dimensional (2D) wave propagation equation. Simulations are implemented in two stages, as a single cardiac cell and as a two-dimensional grid of cells. In both stages, the normal action potential formation in case of a single cell and it's normal propagation in case of a two-dimensional grid of cells were simulated with nominal sodium ion conductance. Then, the effect of sodium ion concentration on the action potential signal was studied by reducing the sodium ion conductance. It is concluded that reducing the sodium ion conductance, decreases both passing ability and conduction velocity of the action potential wave front.
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Niu, Yu‐Bin, Ya‐Xia Yin, and Yu‐Guo Guo. "Nonaqueous Sodium‐Ion Full Cells: Status, Strategies, and Prospects." Small 15, no. 32 (2019): 1900233. http://dx.doi.org/10.1002/smll.201900233.
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Stanton, B. A., and B. Kaissling. "Regulation of renal ion transport and cell growth by sodium." American Journal of Physiology-Renal Physiology 257, no. 1 (1989): F1—F10. http://dx.doi.org/10.1152/ajprenal.1989.257.1.f1.
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Intracellular sodium has been implicated in a variety of cellular processes including regulation of Na+-K+-ATPase activity, mitogen-induced cell growth, and proliferation and stimulation of Na+-K+-ATPase by aldosterone. In renal epithelial cells a rise in sodium uptake across the apical membrane increases intracellular sodium concentration, which in turn stimulates the turnover rate of Na+-K+-ATPase and thereby enhances sodium efflux across the basolateral membrane. A prolonged increase in sodium uptake causes dramatic hypertrophy and hyperplasia and a rise in the quantity of Na+-K+-ATPase in the basolateral membrane. These structural and functional changes occur in the kidney in the absence of alterations in plasma aldosterone and vasopressin levels. Several mitogens induce growth and proliferation by initiating a cascade of events, which include a rise in intracellular sodium. Accordingly, an increase in the sodium concentration within renal epithelial cells may elicit a “mitogen-like” effect by initiating the cascade at the sodium step, even in the absence of a mitogen. A rise in cell sodium may also stimulate the production of autocrine growth factors that directly or indirectly regulate cell growth and proliferation, by modifying the response to mitogens or to changes in the ionic composition of the extracellular fluid. In this review we will examine the evidence that supports a role for intracellular sodium in regulating these cellular events in renal epithelial cells.
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Karasawa, Akira, Haijiao Liu, Matthias Quick, Wayne A. Hendrickson, and Qun Liu. "Crystallographic Characterization of Sodium Ions in a Bacterial Leucine/Sodium Symporter." Crystals 13, no. 2 (2023): 183. http://dx.doi.org/10.3390/cryst13020183.
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Na+ is the most abundant ion in living organisms and plays essential roles in regulating nutrient uptake, muscle contraction, and neurotransmission. The identification of Na+ in protein structures is crucial for gaining a deeper understanding of protein function in a physiological context. LeuT, a bacterial homolog of the neurotransmitter:sodium symporter family, uses the Na+ gradient to power the uptake of amino acids into cells and has been used as a paradigm for the study of Na+-dependent transport systems. We have devised a low-energy multi-crystal approach for characterizing low-Z (Z ≤ 20) anomalous scattering ions such as Na+, Mg2+, K+, and Ca2+ by combining Bijvoet-difference Fourier syntheses for ion detection and f” refinements for ion speciation. Using the approach, we experimentally identify two Na+ bound near the central leucine binding site in LeuT. Using LeuT microcrystals, we also demonstrate that Na+ may be depleted to study conformational changes in the LeuT transport cycle.
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Berkowitz, L. R., and E. P. Orringer. "Passive sodium and potassium movements in sickle erythrocytes." American Journal of Physiology-Cell Physiology 249, no. 3 (1985): C208—C214. http://dx.doi.org/10.1152/ajpcell.1985.249.3.c208.
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Deoxygenation causes an increase in passive Na and K movements across the membrane of the sickle erythrocyte. Some investigators find that these ion movements are accompanied by cell dehydration, while others find no evidence for cell water loss with sickling. Because gelation of hemoglobin S would be enhanced by cell water loss, we reinvestigated Na and K movements in sickle cells to define further the role that ion movements might play in the pathogenesis of sickling. With deoxygenation, we found that sickle cells gained Na and lost K without losing cell water. These net ion movements were not seen in control red blood cells. For sickle cells, deoxygenation also increased passive unidirectional influxes of Na and K, effects not observed when control red blood cells were deoxygenated. The deoxygenation-induced passive influxes of Na and K in sickle cells were not diminished by anion substitution or by the addition of the diuretic furosemide. We also found differences in passive Na and K fluxes between oxygenated sickle cells and normal red blood cells. The addition of furosemide or replacement of Cl with NO3 or SCN, maneuvers that largely reduced passive Na and K movements in oxygenated normal cells, had no effect on Na and K movements in oxygenated sickle cells. These findings militate against the idea that solute and water loss occur as a consequence of deoxygenation but do indicate that there are acquired membrane abnormalities in sickle red blood cells.
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Peters, Jens, Alexandra Peña Cruz, and Marcel Weil. "Exploring the Economic Potential of Sodium-Ion Batteries." Batteries 5, no. 1 (2019): 10. http://dx.doi.org/10.3390/batteries5010010.
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Sodium-ion batteries (SIBs) are a recent development being promoted repeatedly as an economically promising alternative to lithium-ion batteries (LIBs). However, only one detailed study about material costs has yet been published for this battery type. This paper presents the first detailed economic assessment of 18,650-type SIB cells with a layered oxide cathode and a hard carbon anode, based on existing datasheets for pre-commercial battery cells. The results are compared with those of competing LIB cells, that is, with lithium-nickel-manganese-cobalt-oxide cathodes (NMC) and with lithium-iron-phosphate cathodes (LFP). A sensitivity analysis further evaluates the influence of varying raw material prices on the results. For the SIB, a cell price of 223 €/kWh is obtained, compared to 229 €/kWh for the LFP and 168 €/kWh for the NMC batteries. The main contributor to the price of the SIB cells are the material costs, above all the cathode and anode active materials. For this reason, the amount of cathode active material (e.g., coating thickness) in addition to potential fluctuations in the raw material prices have a considerable effect on the price per kWh of storage capacity. Regarding the anode, the precursor material costs have a significant influence on the hard carbon cost, and thus on the final price of the SIB cell. Organic wastes and fossil coke precursor materials have the potential of yielding hard carbon at very competitive costs. In addition, cost reductions in comparison with LIBs are achieved for the current collectors, since SIBs also allow the use of aluminum instead of copper on the anode side. For the electrolyte, the substitution of lithium with sodium leads to only a marginal cost decrease from 16.1 to 15.8 €/L, hardly noticeable in the final cell price. On the other hand, the achievable energy density is fundamental. While it seems difficult to achieve the same price per kWh as high energy density NMC LIBs, the SIB could be a promising substitute for LFP cells in stationary applications, if it also becomes competitive with LFP cells in terms of safety and cycle life.
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Cragg, Peter J. "Artificial Transmembrane Channels for Sodium and Potassium." Science Progress 85, no. 3 (2002): 219–41. http://dx.doi.org/10.3184/003685002783238780.
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Transport of alkali metals, particularly sodium and potassium, across cell membranes is an essential function performed by special proteins that enable cells to regulate inter- and extracellular ion concentrations with exceptional selectivity. The importance of these channel-forming proteins has led to researchers emulating of their structural features: an ion-specific filter and conduction at rates up to 108 ions per second. Synthetic helical and cyclic polypeptides form channels, however, the specificity of ion transport is often low. Ion-specific macrocycles have been used as filters from which membrane-spanning derivatives have been prepared. Success has been limited as many compounds act as ion carriers rather than forming transmembrane channels. Surfactant compounds also allow ions to cross membranes but any specificity is serendipitous. Overall it seems possible to mimic either ion specificity or efficient transmembrane ion transport. The goal for the future will be to combine both characteristics in one artificial system.
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Van Mil, H. G. J. "Analysis of a Model Describing the Dynamics of Intracellular Ion Composition in Biological Cells." International Journal of Bifurcation and Chaos 08, no. 05 (1998): 1043–47. http://dx.doi.org/10.1142/s0218127498000851.
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An electrophysiological model describing the dynamics of the intracellular ion concentration and the membrane potential (Vm) in biological cells is presented. The model links passive ion fluxes through channels of sodium, potassium and chloride to active ion fluxes generated by the sodium potassium pump. To model the interaction of Vm to the ionic fluxes Kirchhoff current law is used. Only one Vm-dependent permeability as represented by an inwardly rectifying potassium channel (IKR) is incorporated. It is shown that the resulting system of ordinary differential equations is degenerate. Decomposition of the system into noninteracting subsystems allows a dynamically independent description of the currents of sodium and potassium in relation to Vm. Physical and mathematical arguments for the decomposition into subsystems are presented. Analysis of the model show hysteresis properties that can account for the experimentally-observed bistability in skeletal and heart muscles fibers.