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Books on the topic 'Skeletal muscle satellite cells'

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Author: Grafiati

Published: 11 March 2023

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1

Greg, Molnar, and United States. National Aeronautics and Space Administration., eds. Skeletal muscle satellite cells cultured in simulated microgravity. [Washington, DC: National Aeronautics and Space Administration, 1993.

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2

Vandenburgh, Herman H. Computer aided mechanogenesis of skeletal muscle organs from single cells in vitro. [Washington, DC]: National Aeronautics and Space Administration, 1990.

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3

Herman, Vandenburgh, and United States. National Aeronautics and Space Administration., eds. Tissue-engineered skeletal muscle organoids for reversible gene therapy: Brief report. [Washington, DC: National Aeronautics and Space Administration, 1996.

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4

Sarabia, Vivian E. Calcium homeostasis and regulation of glucose uptake in human skeletal muscle cells in culture. Ottawa: National Library of Canada, 1990.

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5

Prud'homme, Renée. The Role of calmodulin and nuclear factor of activated T-cells in growth of mature skeletal muscle after injury or overload. Sudbury, Ont: Laurentian University, 2002.

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6

Skeletal muscle satellite cells cultured in simulated microgravity. [Washington, DC: National Aeronautics and Space Administration, 1993.

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7

Molnar, Greg. Properties of satellite cells isolated from sheep skeletal muscle. 1993.

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8

Skeletal Muscle Muscular Dystrophy A Visual Approach. Morgan & Claypool Publishers, 2011.

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9

Pinheiro, Carlos Hermano J., and Lucas Guimarães-Ferreira, eds. Frontiers in Skeletal Muscle Wasting, Regeneration and Stem Cells. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-832-0.

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10

Fibre Types in Skeletal Muscles (Advances in Anatomy, Embryology and Cell Biology). Springer, 2002.

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11

Tissue-engineered skeletal muscle organoids for reversible gene therapy: Brief report. [Washington, DC: National Aeronautics and Space Administration, 1996.

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12

Muñoz-Cánoves, Pura, Jaime J. Carvajal, Adolfo Lopez de Munain, and Ander Zeta, eds. Role of Stem Cells in Skeletal Muscle Development, Regeneration, Repair, Aging and Disease. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-866-5.

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13

Khayat, Zayna A. Multiple mechanisms of regulating glucose transporters and glucose transport in skeletal muscle cells. 2001.

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14

Sassoon, D. A. Stem Cells and Cell Signalling in Skeletal Myogenesis (Advances in Developmental Biology and Biochemistry, V. 11). Elsevier Science, 2002.

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15

Ueda, Yoji. Effects of selenium on differentiation and degeneration of cultured L8 rat skeletal muscle cells. 1997.

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16

Marco, Crescenzi, ed. Reactivation of the cell cycle in terminally differentiated cells. Georgetown, Tex: Landes Bioscience, 2002.

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17

Crescenzi, Marco. Reactivation of the Cell Cycle in Terminally Differentiated Cells (Molecular Biology Intelligence Unit, 17). Springer, 2003.

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18

Hopkins, Philip M. Neuromuscular physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0007.

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The pharmacological interventions that constitute general anaesthesia are targeted at producing unconsciousness and an immobile patient even in response to noxious stimuli. Surgical anaesthesia also requires skeletal muscle relaxation, the degree of which depends on the site and nature of the surgical procedure. The anaesthetist therefore needs an advanced level of knowledge and understanding of the function of nerves, synapses, and muscle in order to understand, from first principles, how the drugs they use every day mediate their effects. Nerves and muscle cells are termed excitable cells because the electrical potential across their cell membranes (membrane potential) can be rapidly and profoundly altered because of the presence of specialized ion channels. Some drugs, such as local anaesthetics, act on ion channels involved in nerve conduction while many others act on synaptic transmission, the neurochemical communication between neurons or between a neuron and its effector organ. The neuromuscular junction is a synapse of specific interest to anaesthetists because it is the site of action of neuromuscular blocking drugs. This chapter covers the fundamentals of cellular electrophysiology, structure and function of key ion channels, and the physiology of nerves, synapses, and skeletal muscle.

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19

Rich, Mark M. Critical Illness Neuropathy, Myopathy, and Sodium Channelopathy. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0033.

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Skeletal muscle weakness is a common problem that complicates recovery from critical illness. The primary causes of weakness include neuropathic disorders, myopathic disorders, and mixed disorders. Recent studies have demonstrated that reduced excitability of the nerve and muscle cell membranes might contribute to weakness during the acute stages of the polyneuropathy and myopathy encountered in critically ill patients. In both tissues, an acquired sodium channelopathy can lead to increased inactivation of channels, leading to inexcitability an paralysis. Experimental sepsis models have demonstrated a similar reduction in excitability in myocardial cells as well as in motor neurons within the spinal cord. The presence of a channelopathy in multiple tissues raises the possibility that reduced excitability of neurons within the CNS might contribute to septic encephalopathy. If this is the case, a single therapy to improve excitability might treat failure of a number of electrically active tissues.

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20

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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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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21

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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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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