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Книги з теми "Potassium Ion Cells"

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Автор: Grafiati
Опубліковано: 6 вересня 2023

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1

Yoshihisa, Kurachi, Jan Lily Yeh, and Lazdunski Michel, eds. Potassium ion channels: Molecular structure, function, and diseases. San Diego: Academic Press, 1999.

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2

Ian, Glynn, Ellory J. C, and Company of Biologists, eds. The sodium pump: Proceedings of the Fourth International Conference on Na, K-ATPase, held at the Physiological Laboratory, Cambridge, in August 1984. Cambridge, U.K: Company of Biologists, 1985.

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3

E, Vance Dennis, and Vance Jean E, eds. Biochemistry of lipids, lipoproteins, and membranes. Amsterdam: Elsevier, 1991.

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4

Adragna, Norma, and Peter Lauf. Cell Volume and Signaling. Springer, 2014.

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5

Cell Volume and Signaling (Advances in Experimental Medicine and Biology). Springer, 2005.

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6

Benos, Dale J., Arnost Kleinzeller, Lily Yeh Jan, Douglas M. Fambrough, and Yoshihisa Kurachi. Potassium Ion Channels: Molecular Structure, Function, and Diseases. Elsevier Science & Technology Books, 1999.

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7

Doucet, Alain, and Gilles Crambert. Potassium homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0023.

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Анотація:
The equilibrium between the concentration of K+ in the extracellular space (low) and the intracellular compartment (high) is crucial for maintaining the electrical properties of excitable and non-excitable cells, because it determines the membrane resting potential. The high intracellular concentration of K+ (120–140 mmol/L) also contributes to the intracellular osmolarity, a determinant of cell volume. It is therefore crucial to finely tune both extracellular and intracellular K+ concentrations. There is a coordinated regulation between processes/mechanisms that store/release K+ from internal stores (internal balance) and those that retain/excrete K+ (external balance).
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8

(Editor), Yoshihisa Kurachi, Lily Yeh Jan (Editor), Michel Lazdunski (Editor), Arnost Kleinzeller (Series Editor), Douglas M. Fambrough (Series Editor), and Dale J. Benos (Series Editor), eds. Current Topics in Membrances, Volume 46: Potassium Ion Channels: Molecular Structure, Function and Disease (Current Topics in Membranes). Academic Press, 1999.

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9

Potassium malate transport into plant cell vacuoles: The characterization of ion channels. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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10

Frise, Matthew C., and Jonathan B. Salmon. Disorders of potassium in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0251.

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Анотація:
Plasma potassium levels are maintained in health between 3.5 and 5.0 mmol/L, and reflect total body potassium only in stable states at normal pH. Most true hyperkalaemia results from renal insufficiency. The goals of therapy are myocardial protection and return of plasma potassium to a safe level. Measures are commonly initiated above 5.5 mmol/L; above 6.5 mmol/L, aggressive measures should be adopted and calcium salts given if there are cardiac dysrhythmias or QRS-broadening. Glucose-insulin infusions and beta-2-agonists promote potassium shifts into cells. Diuretics and sodium bicarbonate may be helpful, but persistent hyperkalaemia is an indication for renal replacement therapy. Hypokalaemia may lead to dangerous arrhythmias, skeletal muscle weakness, ileus, and reduced vascular smooth muscle contractility. Rapid replacement should only be undertaken for severe hypokalaemia or in the context of arrhythmias. Once the extracellular deficit is corrected, there will usually be a continuing need for potassium supplementation to replenish intracellular stores.
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11

Esen, Figen. Disorders of magnesium in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0252.

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Анотація:
Plasma potassium levels are maintained in health between 3.5 and 5.0 mmol/L, and reflect total body potassium only in stable states at normal pH. Most true hyperkalaemia results from renal insufficiency. The goals of therapy are myocardial protection and return of plasma potassium to a safe level. Measures are commonly initiated above 5.5 mmol/L; above 6.5 mmol/L, aggressive measures should be adopted and calcium salts given if there are cardiac dysrhythmias or QRS-broadening. Glucose-insulin infusions and beta-2-agonists promote potassium shifts into cells. Diuretics and sodium bicarbonate may be helpful, but persistent hyperkalaemia is an indication for renal replacement therapy. Hypokalaemia may lead to dangerous arrhythmias, skeletal muscle weakness, ileus, and reduced vascular smooth muscle contractility. Rapid replacement should only be undertaken for severe hypokalaemia or in the context of arrhythmias. Once the extracellular deficit is corrected, there will usually be a continuing need for potassium supplementation to replenish intracellular stores.
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12

Na+-H+ exchange, intracellular pH, and cell function. Orlando: Academic Press, 1986.

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13

Slimp, Jefferson C. Neurophysiology of Multiple Sclerosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199341016.003.0003.

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Анотація:
Any discussion of the pathomechanisms and treatments of MS benefits from an understanding of the physiology of the neuronal membrane and the action potential. Neurons and glia, are important for signal propagation, synaptic function, and neural development. The neuronal cell membrane, maintains different ionic environments inside and outside the cell, separating charge across the membrane and facilitating electrical excitability. Ion channels allow flow of sodium, potassium, and calcium ions across the membrane at selected times. At rest, potassium ion efflux across the membrane establishes the nerve membrane resting potential. When activated by a voltage change to threshold, sodium influx generates an action potential, or a sudden alteration in membrane potentials, that can be conducted along an axon. The myelin sheaths around an axon, increase the speed of conduction and conserve energy. The pathology of MS disrupts the myelin structures, disturbs conduction, and leads to neurodegeneration. Ion channels have been the target of investigation for both restoration of conduction and neuroprotection.
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14

The Na, K-pump: Proceedings of the 5th International Conference on Na, K-ATPase held at Fuglso Conference Center, Denmark, June 14-19, 1987 (Progress in clinical and biological research). A.R. Liss, 1988.

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15

The Na, K-pump: Proceedings of the 5th International Conference on Na, K-ATPase held at Fuglso Conference Center, Denmark, June 14-19, 1987 (Progress in clinical and biological research). A.R. Liss, 1988.

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16

Kleinzeller, Arnost. Current Topics in Membranes and Transport: Na+ - H+ Exchange, Intracellular Ph, and Cell Function (Current Topics in Membranes). Academic Pr, 1986.

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17

Kleinzeller, Arnost. Current Topics in Membranes and Transport: Na+ - H+ Exchange, Intracellular Ph, and Cell Function (Current Topics in Membranes). Academic Pr, 1986.

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18

Mason, Peggy. The Neuron at Rest. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0009.

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Анотація:
Neuronal membrane potential depends on the distribution of ions across the plasma membrane and the permeability of the membrane to those ions afforded by transmembrane proteins. Ions cannot pass through a lipid bilayer but enter or exit neurons through ion channels. When activated by voltage or a ligand, ion channels open to form a pore through which selective ions can pass. The ion channels that support a resting membrane potential are critical to setting a cell’s excitability. From the distribution of an ionic species, the Nernst potential can be used to predict the steady-state potential for that one ion. Neurons are permeable to potassium, sodium, and chloride ions at rest. The Goldman-Hodgkin-Katz equation takes into consideration the influence of multiple ionic species and can be used to predict neuronal membrane potential. Finally, how synaptic inputs affect neurons through synaptic currents and changes in membrane resistance is described.
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19

Koch, Christof. Biophysics of Computation. Oxford University Press, 1998. http://dx.doi.org/10.1093/oso/9780195104912.001.0001.

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Анотація:
Neural network research often builds on the fiction that neurons are simple linear threshold units, completely neglecting the highly dynamic and complex nature of synapses, dendrites, and voltage-dependent ionic currents. Biophysics of Computation: Information Processing in Single Neurons challenges this notion, using richly detailed experimental and theoretical findings from cellular biophysics to explain the repertoire of computational functions available to single neurons. The author shows how individual nerve cells can multiply, integrate, or delay synaptic inputs and how information can be encoded in the voltage across the membrane, in the intracellular calcium concentration, or in the timing of individual spikes. Key topics covered include the linear cable equation; cable theory as applied to passive dendritic trees and dendritic spines; chemical and electrical synapses and how to treat them from a computational point of view; nonlinear interactions of synaptic input in passive and active dendritic trees; the Hodgkin-Huxley model of action potential generation and propagation; phase space analysis; linking stochastic ionic channels to membrane-dependent currents; calcium and potassium currents and their role in information processing; the role of diffusion, buffering and binding of calcium, and other messenger systems in information processing and storage; short- and long-term models of synaptic plasticity; simplified models of single cells; stochastic aspects of neuronal firing; the nature of the neuronal code; and unconventional models of sub-cellular computation. Biophysics of Computation: Information Processing in Single Neurons serves as an ideal text for advanced undergraduate and graduate courses in cellular biophysics, computational neuroscience, and neural networks, and will appeal to students and professionals in neuroscience, electrical and computer engineering, and physics.
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20

Kleinzeller, Arnost. Current Topics in Membranes and Transport. Elsevier Science & Technology Books, 1988.

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21

Kleinzeller, Arnost. Current Topics in Membranes and Transport. Elsevier Science & Technology Books, 1990.

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22

Kleinzeller, Arnost. Current Topics in Membranes and Transport. Elsevier Science & Technology Books, 1987.

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23

Kleinzeller, Arnost. Current Topics in Membranes and Transport. Elsevier Science & Technology Books, 1986.

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24

Bronner, Felix, and Arnost Kleinzeller. Current Topics in Membranes and Transport. Elsevier Science & Technology Books, 1986.

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25

Daudon, Michel, and Paul Jungers. Cystine stones. Edited by Mark E. De Broe. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0203_update_001.

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Cystinuria, an autosomal recessive disease (estimated at 1:7000 births worldwide), results from the defective reabsorption of cystine and dibasic amino acids (also ornithine, arginine, lysine, COAL) by epithelial cells of renal proximal tubules, leading to an abnormally high urinary excretion of these amino acids. Due to the poor solubility of cystine at the usual urine pH, formation of cystine crystals and stones ensues. Incidence of homozygotes is estimated at 1 in 7000 births worldwide, but is lower in European countries and much higher in populations with frequent consanguinity. Cystine stones represent 1–2% of all stones in adults and 5–8% in paediatric patients, with an equal distribution between males and females.Cystinuria is caused by inactivating mutations in the gene SLC3A1 or SLC7A9, both encoding proteins contributing to the function of the heterodimeric transport system of cystine.Cystine nephrolithiasis may present in infants, most frequently in adolescents or young adults, sometimes later. Cystine calculi are weakly radio-opaque. Stone analysis using infrared spectroscopy (or X-ray diffraction) allows immediate and accurate diagnosis. Urinary amino acid chromatography quantifies urinary cystine excretion, needed to define the therapeutic strategy.Urological treatment of cystine stones currently uses extracorporeal stone wave lithotripsy or flexible ureterorenoscopy with Holmium laser, that is, minimally invasive techniques. However, as cystine stones are highly recurrent, preventive therapy is essential.Medical treatment combines reduced methionine and sodium intake, to lower cystine excretion; hyperdiuresis (> 3 L/day) to reduce cystine concentration; and active alkalinization preferably using potassium citrate (40–80 mEq/day) to increase cystine solubility by rising urine pH up to 7.5–8. If these measures are insufficient to prevent recurrent stone formation, a thiol derivative (D-penicillamine or tiopronin), which converts cystine into a more soluble disulphide, should be added. Close monitoring and adherence of the patient to the therapeutic programme are needed to ensure life-long compliance, the key for successful prevention in the long term.
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