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Libri sul tema "Chloride channels"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 6 luglio 2024

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1

Roland, Kozlowski, a cura di. Chloride channels. Oxford: Isis Medical Media, 1999.

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2

J, Alvarez-Leefmans F., Russell John M. 1942- e International Brain Research Organization. Congress, a cura di. Chloride channels and carriers in nerve, muscle, and glial cells. New York: Plenum Press, 1990.

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3

Giovanni, Biggio, Costa Erminio e Capo Boi Conference on Neuroscience (5th : 1987 : Villasimius, Italy), a cura di. Chloride channels and their modulation by neurotransmitters and drugs. New York: Raven Press, 1988.

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4

W, Olsen Richard, e Venter J. Craig, a cura di. Benzodiazepine/GABA receptors and chloride channels: Structural and functional properties. New York: A.R. Liss, 1986.

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5

H, Durham John, Hardy Marcos A e New York Academy of Sciences., a cura di. Bicarbonate, chloride, and proton transport systems. New York, N.Y: New York Academy of Sciences, 1989.

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6

Alvarez-Leefmans, Francisco J., e John M. Russell, a cura di. Chloride Channels and Carriers in Nerve, Muscle, and Glial Cells. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4757-9685-8.

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7

Michael, Pusch, a cura di. Chloride movements across cellular membranes. Amsterdam: Boston, 2007.

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8

Kirk, Kevin L. The cystic fibrosis transmembrane conductance regulator. Georgetown, Tex: Landes Bioscience / Eurekah.com, 2003.

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9

Kirk, Kevin L. The cystic fibrosis transmembrane conductance regulator. Georgetown, TX: Landes Bioscience : Eurekah.com, 2004.

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10

Wong, Simeon. Regulation of Clc-2 chloride channel by protein kinase C phosphorylation. Ottawa: National Library of Canada, 2000.

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11

Ahmed, Najma Nusarat. Proteins which interact with and regulate the chloride channel, CIC-2. Ottawa: National Library of Canada, 2001.

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12

Kleinzeller, Arnost, Douglas M. Fambrough e William B. Guggino. Chloride Channels. Elsevier Science & Technology Books, 1994.

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13

Kozlowski, Ronald. Chloride Channels. Informa Healthcare, 2000.

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14

(Editor), William B. Guggino, Arnost Kleinzeller (Series Editor) e Douglas M. Fambrough (Series Editor), a cura di. Chloride Channels, Volume 42 (Current Topics in Membranes). Academic Press, 1994.

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15

Fuller, Catherine Mary. Calcium-Activated Chloride Channels. Elsevier Science & Technology Books, 2002.

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16

Mary, Fuller Catherine, a cura di. Calcium-activated chloride channels. San Diego, Calif: Academic Press, 2002.

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17

Alvarez-Leefmans, F. J., e Russell John M. Chloride Channels and Carriers in Nerve, Muscle, and Glial Cells. Springer London, Limited, 2013.

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18

Alvarez-Leefmans, F. J. "Chloride Channels and Carriers in Nerve, Muscle, and Glial Cells". Springer, 2013.

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19

Physiology And Pathology Of Chloride Transporters And Channels In The Nervous System From Molecules To Diseases. Academic Press, 2009.

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20

Pusch, Michael. Chloride Movements Across Cellular Membranes. Elsevier Science & Technology Books, 2011.

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21

Physiology and Pathology of Chloride Transporters and Channels in the Nervous System. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-374373-2.x0001-5.

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22

Ischemic preconditioning of the myocardium: Role of chloride and inward-rectifier potassium channels. Ottawa: National Library of Canada, 2001.

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23

Chang, Martin Chung-San. On the regulation and function of potassium and chloride channels in human T lymphocytes. 1999.

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24

Fuller, Catherine Mary. Calcium-Activated Chloride Channels (Current Topics in Membranes, Volume 53) (Current Topics in Membranes). Academic Press, 2002.

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25

Pahapill, Peter Ain. Regulation of potassium and chloride channels in normal human T lymphocytes: a patch-clamp study. 1990.

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26

Olsen, Richard W. Benzodiazepine/Gaba Receptors and Chloride Channels: Structural and Functional Properties (Receptor Biochemistry and Methodology, Vol 5). Wiley-Liss, 1986.

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27

Delpire, Eric, e F. Javier Alvarez-Leefmans. Physiology and Pathology of Chloride Transporters and Channels in the Nervous System: From Molecules to Diseases. Elsevier Science & Technology Books, 2009.

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28

(Editor), Kevin L. Kirk, e David C. Dawson (Editor), a cura di. The Cystic Fibrosis Transmembrane Conductance Regulator (Molecular Biology Intelligence Unit). Springer, 2003.

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29

Wei, Lin. Electrophysiological Studies of Cftr Function: Effects of Cftr Mutations and Interactions With Other Chloride Channels (Acta Biomedica Lovaniensia, 236). Leuven Univ Pr, 2001.

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30

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

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Abstract (sommario):

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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31

Shaibani, Aziz. Myotonia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0021.

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Myotonia is a slow relaxation phase of a muscle after normal contraction. Patients report myotonia as muscle stiffness and sometimes pain. They usually adapt to it well. Falls due to myotonia may lead to accidents. Checking for percussion and action myotonia should be part of neuromuscular examination. Electrically silent myotonia is a sign of Brody’s syndrome. Myotonia may be incidentally discovered during EMG. The most important task is to differentiate between myotonia and paramyotonia clinically and electromyographically. Most myotonic disorders are caused by mutations of sodium, and chloride channels. There has been a significant understanding of the underlying channelopathies recently. Severe myotonia respond well to Mexiletine.

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32

O’Riordan, Stephen MP, e Antoinette Moran. Cystic fibrosis-related diabetes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0008.

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Abstract (sommario):

This chapter on CFRD reviews the ever-evolving topic and provides up-to-date information on how to diagnose and manage cystic fibrosis-related diabetes CFRD in the acute and chronic setting. The treatments necessary to treat and prolong life in CF, including their unique dietary requirements, must always be followed as a first priority, with diabetes care adjusted accordingly. Early intervention with insulin has been shown to reverse clinical deterioration, even in those with mild diabetes. Newly emerging treatments for CF which have the potential to restore defective chloride channels may have implications for the development and treatment of CFRD. Whilst CFRD shares features of both type 1 and type 2 diabetes, there are important differences which necessitate a unique approach to diagnosis and management. Factors specific to CF that variably affect glucose metabolism include chronic respiratory infection and inflammation, increased energy expenditure, malnutrition, glucagon deficiency, and gastrointestinal abnormalities.

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33

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

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34

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

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35

Pitt, Matthew. Investigation of channelopathies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198754596.003.0008.

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The chapter begins with a general description of the clinical findings in conditions where hyperexcitability occurs. These are divided into the dystrophic conditions, such as myotonia dystrophy, and the non-dystrophic conditions, which include myotonia congenita, paramyotonia congenita, and potassium-aggravated myotonia. Conditions where hypoexcitability occurs such as periodic paralysis are next discussed. The associated disorders of sodium, calcium, chloride, and potassium channels are described. Next, the protocols for the neurophysiological tests that are used in myotonia, and the short exercise test either at room temperature or after cooling are introduced. The different patterns seen in these tests are outlined and the algorithms allowing precise targeting of genetic testing explained. The inter-discharge interval calculation that can be used in delineating the causes of myotonia is discussed. Other conditions where prominent spontaneous activity occurs such as Schwartz–Jampel syndrome and Pompe’s disease are described. The chapter concludes with details of the long exercise test used in diagnosis of periodic paralysis.

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36

Andrews, Leslie K. Nucleotide interaction regulates the chloride channel, ClC-4. 2004.

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37

Dhani, Sonja Urmilla. An investigation of the endosomal trafficking of the ClC-2 chloride channel. 2006.

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38

Cheung, Min Rex. A view of the cystic fibrosis transmembrane conductance regulator chloride channel from the sixth transmembrane domain. 1997.

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39

Beattie, R. Mark, Anil Dhawan e John W.L. Puntis. Cystic fibrosis-associated liver disease. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0022.

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Abstract (sommario):

Pathophysiology 162Clinical features 162Diagnosis 163Management 164Cystic fibrosis (CF) is an autosomal recessive disease resulting from mutations in the gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) (see Chapter 21). CFTR functions as a transmembrane chloride channel in the apical membrane of most secretory epithelia and the disease thus affects lungs, pancreas, exocrine glands, gut, and liver. In CF-associated liver disease the biliary tract is most commonly involved in a spectrum from asymptomatic to biliary cirrhosis. The liver disease runs from mild and subclinical to severe cirrhosis and portal hypertension. Clinical disease is seen in 4–6% of cases, but there are biochemical abnormalities in 20–50%. At autopsy, fibrosis is present in 20% and steatosis in 50%....

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40

Ducharme, Guillaume. The small conductance swelling-activated chloride channel in primary rat microglia: Biophysical characterization and its contribution to volume regulation and phagocytosis. 2007.

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41

Kriemler, Susi. Exercise, physical activity, and cystic fibrosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199232482.003.0033.

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Cystic fibrosis (CF) is the most common genetic autosomal recessive disease of the Caucasian race, generally leading to death in early adulthood.1 The frequency of the gene carrier (heterozygote) is 1:20–25 in Caucasian populations, 1:2000 in African-Americans, and practically non-existent in Asian populations. The disease occurs in about 1 in every 2500 life births of the white population. Mean survival has risen from 8.4 years in 1969 to 32 years in 2000 due to improvements in treatment. The genetic defect causes a pathological electrolyte transport through the cell membranes by a defective chloride channel membrane transport protein [cystic fibrosis transmembrane conductance regulator (CFTR)]. With respect to the function, this affects mainly the exocrine glands of secretory cells, sinuses, lungs, pancreas, liver, and the reproductive tract of the human body leading to a highly viscous, water-depleted secretion. The secretion cannot leave the glands and in consequence causes local inflammation and destruction of various organs. The main symptoms include chronic inflammatory pulmonary disease with a progressive loss of lung function, exocrine and sometimes endocrine pancreas insufficiency, and an excessive salt loss through the sweat glands.1 A summary of the signs and symptoms of CF will be given with a special emphasis on the effect of exercise performance and capacity.

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