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Books on the topic 'Cystic fibrosis transmembrane'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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1

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

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

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3

Emili, Alia Qureshi. Expression and purification of transmembrane segments 3 and 4 of the cystic fibrosis transmembrane conductance regulator. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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4

Seibert, Fabian S. Structure-function relationships of the cytoplasmic domains of the cystic fibrosis transmembrane conductance regulator. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1997.

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5

Wong, Melanie Hoi-Lee. The role of the C-terminus in the cellular physiology of cystic fibrosis transmembrane-conductance regulator (CTFR). Ottawa: National Library of Canada, 2000.

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6

Grondin, Ronald Thomas. Expression, purification, refolding, and ATP binding of the first nucleotide binding domain of the cystic fibrosis transmembrane conductance regulator. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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7

Li, Xiaobin. Characterization of multiple copies of a DNA segment containing cystic fibrosis transmembrane conductance regulator gene exon 9 in the human genome. Ottawa: National Library of Canada, 1999.

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8

Beattie, R. Mark, Anil Dhawan, and John W.L. Puntis. Cystic fibrosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0021.

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Gastrointestinal manifestations 156Management of gastrointestinal symptoms in children with CF 158Nutrition in CF 158Nutritional management 159Vitamins 160The incidence of cystic fibrosis (CF) is around 1 in 2500. Cases are diagnosed as a consequence of population screening or high-risk screening, or following presentation with clinical symptoms typical of the disorder. The basic defect is in the CFTR (cystic fibrosis transmembrane conductance regulator) protein which codes for a cyclic adenosine monophosphate-regulated chloride transporter in epithelial cells of exocrine organs. This is involved in salt and water balance across epithelial surfaces. The gene is on chromosome 7. There are multiple known mutations, the most common being ...

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9

Snell, Jamey, and Thomas J. Mancuso. Cystic Fibrosis. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0023.

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Cystic fibrosis (CF) is an inherited, autosomal recessive, multisystem disease. Dysfunction of the cystic fibrosis transmembrane conductance regulator protein (CFTR) in epithelial cells is the primary defect in CF. Defects in CFTR are the cause for lung disease, exocrine pancreatic insufficiency and failure, male infertility, and liver disease. CF can present with a variety of respiratory and gastrointestinal signs, including meconium ileus in the newborn period, hypernatremic dehydration, pulmonary insufficiency, nasal polyps, and insulin-dependent diabetes mellitus. As affected children grow, dysfunction in CFTR leads to chronic and progressive lung disease, characterized by suppurative infection and the development of bronchiectasis. CFTR dysfunction also affects exocrine function, leading to pancreatic insufficiency, malabsorption, and growth failure. In the past, history and physical exam with sweat chloride testing were the cornerstones of diagnosis. Diagnosis is now made with the newborn screening test for immunoreactive trypsinogen.

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10

Beattie, R. Mark, Anil Dhawan, and 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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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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11

William, Skach, ed. Cystic fibrosis methods and protocols. Totowa, N.J: Humana Press, 2002.

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12

William, Skach, ed. Cystic fibrosis methods and protocols. Totowa, N.J: Humana Press, 2002.

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13

Choi, Mei Yee. Interactions between the transmembrane helices of the cystic fibrosis transmembrane conductance regulator (CFTR). 2004.

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14

(Editor), Kevin L. Kirk, and David C. Dawson (Editor), eds. The Cystic Fibrosis Transmembrane Conductance Regulator (Molecular Biology Intelligence Unit). Springer, 2003.

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15

Bush, Andrew, 1954 Apr. 24-, ed. Cystic fibrosis in the 21st century. Basel: Karger, 2006.

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16

Carsten, Schultz, ed. Defects of secretion in cystic fibrosis. New York: Springer, 2005.

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17

Chen, Gong. Interhelical interactions of transmembrane segments 9 and 10 in the cystic fibrosis transmembrane conductance regulator. 2007.

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18

Kogan, Ilana. Regulation and function of the cystic fibrosis transmembrane conductance regulator (CFTR). 2003.

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19

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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20

Skach, William R. Cystic Fibrosis: Methods and Protocols (Methods in Molecular Medicine). Humana Press, 2002.

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21

Cuppens, Harry. Genetic Studies of the Cystic Fibrosis Transmembrane Conductance Regulator Gene in Belgian Cf Patients. Coronet Books Inc, 1995.

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22

Reynaert, Ingrid. Study of the Cystic Fibrosis Transmembrane Conductance Regulator (Cftr) Protein in Human and Mouse Vas Deferens. Leuven Univ Pr, 1998.

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