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Libros sobre el tema "Epithelialer Transport"

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Publicado: 4 de junio de 2021
Última modificación: 1 de febrero de 2022

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1

Wills, Nancy K., Luis Reuss y Simon A. Lewis, eds. Epithelial Transport. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-1495-7.

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2

Gerencser, George A. Epithelial transport physiology. New York: Humana Press, 2010.

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3

Gerencser, George A., ed. Epithelial Transport Physiology. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-229-2.

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4

Symposium on Epithelial Anion Transport in Health and Disease: the Role of the SLC26 Transporters Family (2005 Novartis Foundation). Epithelial Anion Transport in Health and Disease. New York: John Wiley & Sons, Ltd., 2006.

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5

Hamilton, Kirk L. y Daniel C. Devor, eds. Ion Transport Across Epithelial Tissues and Disease. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-55310-4.

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6

Hamilton, Kirk L. y Daniel C. Devor, eds. Basic Epithelial Ion Transport Principles and Function. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-52780-8.

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7

Harris, Michael Stephen Henry. Pulmonary edema's effect on epithelial ion and fluid transport. Ottawa: National Library of Canada, 2003.

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8

Greger, Rainer. Von der Rektaldrüse des Haies (Squalus acanthias) zum epithelialen NaCl-Transport beim Menschen. Berlin: Springer, 1998.

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9

Greger, Rainer. Von der Rektaldrüse des Haies (Squalus acanthias) zum epithelialen NaCl-Transport beim Menschen. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-58795-5.

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10

Dickie, A. John. Mechanisms by which endotoxin-stimulated alveolar macrophages impair lung epithelial sodium transport. Ottawa: National Library of Canada, 1997.

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11

Compeau, Christopher Gary. Endotoxin-stimulated alveolar macrophages impair distal lung epithelial permeability and ion transport. Ottawa: National Library of Canada, 1994.

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12

Tari, Shahryar Rafi. Characterization of AZT transport properties in a continuous renal epithelial cell line. Ottawa: National Library of Canada, 1995.

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13

Epithelial anion transport in health and disease: The role of the SLC26 transporters family. Chichester, U.K: John Wiley & Sons, 2006.

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14

Chadwick, Derek J. y Jamie Goode, eds. Epithelial Anion Transport in Health and Disease: The Role of the SLC26 Transporters Family. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/0470029579.

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15

Epithelial Transport. Springer My Copy UK, 1996.

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16

Gerencser, George A. Epithelial Transport Physiology. Humana Press, 2011.

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17

Wills, N. K., L. Reuss y S. A. Lewis. Epithelial Transport: A Guide to Methods and Experimental Analysis. Springer, 1996.

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18

K, Wills Nancy, Reuss Luis 1940- y Lewis Simon A, eds. Epithelial transport: A guide to methods and experimental analysis. London: Chapman & Hall, 1996.

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19

W, Read N., ed. The relationships between intestinal motility and epithelial transport. [s.l.]: [s.n.], 1987.

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20

Wills, Nancy K. Epithelial Transport: A guide to Methods and Experimental Analysis. Brand: Springer, 2011.

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21

Servais, Aude y Bertrand Knebelmann. Cystinuria. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0024.

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Cystinuria (OMIM #220100) is an autosomal recessive disorder of a dibasic amino acid transport in the apical membrane of epithelial cells of the renal proximal tubule and small intestine. It leads to increased urinary cystine excretion and recurrent urolithiasis. The cystine transporter is an heterodimeric transporter which is composed of a heavy subunit, rBAT, linked to a light subunit, b0,+AT. Two genes, SLC3A1 (solute carrier family 3 member 1) and SLC7A9, coding for rBAT and b0,+AT, account for the genetic basis of cystinuria. Cystinuria may lead to obstruction, infections, and ultimately to renal insufficiency. The diagnosis of cystinuria mainly relies on stone analysis, urinary cystine measurement, or urinary cystine crystal identification. Medical treatment is based upon a stepwise strategy using hydration and alkalinization as basic measures, with the addition of thiol derivatives in refractory cases. Urological interventions are often indicated for the management of cystine stones >5 mm in diameter.
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22

A, Young J. y Wong, P. Y. D., 1946-, eds. Epithelial secretion of water and electrolytes. Berlin: Springer-Verlag, 1990.

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23

Sebastio, Gianfranco, Manuel Schiff y Hélène Ogier de Baulny. Lysinuric Protein Intolerance and Hartnup Disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0025.

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Lysinuric protein intolerance (LPI) is an inherited aminoaciduria caused by defective cationic amino acid transport at the basolateral membrane of epithelial cells in intestine and kidney. LPI is caused by mutations in the SLC7A7 gene, which encodes the y+LAT-1 protein, the catalytic light chain subunit of a complex belonging to the heterodimeric amino acid transporter family. Symptoms usually begin after weaning with refusal of feeding, vomiting, and consequent failure to thrive. Hepatosplenomegaly, hematological anomalies, and neurological involvement including hyperammonemic coma will progressively appear. Lung involvement (specifically pulmonary alveolar proteinosis), chronic renal disease that may lead to end stage renal disease, and hemophagocytic lymphohistiocytosis with macrophage activation all represent complications of LPI that may appear at any time from childhood to adulthood. The great variability of the clinical presentation frequently causes misdiagnosis or delayed diagnosis. The basic therapy of LPI consist of a low-protein diet, low-dose citrulline supplementation, nitrogen-scavenging compounds to prevent hyperammonemia, lysine, and carnitine supplements.
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24

(Editor), John N. Abelson, Melvin I. Simon (Editor), Sidney Fleischer (Editor) y Becca Fleischer (Editor), eds. Biomembranes, Part W: Cellular and Subcellular Transport: Epithelial Cells, Volume 192: Volume 192: Biomembranes Part W (Methods in Enzymology). Academic Press, 1990.

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25

Beattie, R. Mark, Anil Dhawan y 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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26

Gandhi, Shephali G. The effect of pulmonary edema fluid on ion transport by adult alveolar type II epithelial cells. 2007.

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27

Bronner, Felix y Sandy I. Helman. Current Topics in Membranes and Transport: Channels and Noise in Epithelial Tissue (Current Topics in Membranes). Academic Press, 1990.

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28

Bronner, Felix y Sandy I. Helman. Current Topics in Membranes and Transport: Channels and Noise in Epithelial Tissue (Current Topics in Membranes). Academic Press, 1990.

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29

Ware, Lorraine B. Pathophysiology of acute respiratory distress syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0108.

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The acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure characterized by the acute onset of non-cardiogenic pulmonary oedema due to increased lung endothelial and alveolar epithelial permeability. Common predisposing clinical conditions include sepsis, pneumonia, severe traumatic injury, and aspiration of gastric contents. Environmental factors, such as alcohol abuse and cigarette smoke exposure may increase the risk of developing ARDS in those at risk. Pathologically, ARDS is characterized by diffuse alveolar damage with neutrophilic alveolitis, haemorrhage, hyaline membrane formation, and pulmonary oedema. A variety of cellular and molecular mechanisms contribute to the pathophysiology of ARDS, including exuberant inflammation, neutrophil recruitment and activation, oxidant injury, endothelial activation and injury, lung epithelial injury and/or necrosis, and activation of coagulation in the airspace. Mechanical ventilation can exacerbate lung inflammation and injury, particularly if delivered with high tidal volumes and/or pressures. Resolution of ARDS is complex and requires coordinated activation of multiple resolution pathways that include alveolar epithelial repair, clearance of pulmonary oedema through active ion transport, apoptosis, and clearance of intra-alveolar neutrophils, resolution of inflammation and fibrinolysis of fibrin-rich hyaline membranes. In some patients, activation of profibrotic pathways leads to significant lung fibrosis with resultant prolonged respiratory failure and failure of resolution.
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30

(Editor), Jorg-Dieter Schulzke, Michael Fromm (Editor), Ernst-Otto Riecken (Editor) y Henry J. Binder (Editor), eds. Epithelial Transport and Barrier Function: Pathomechanisms in Gastrointestinal Disorders (Annals of the New York Academy of Sciences). New York Academy of Sciences, 2001.

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31

Foundation, Novartis. Epithelial Anion Transport in Health and Disease: The Role of the SLC26 Transporters Family (Novartis Foundation Symposia). Wiley, 2006.

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32

Schulzke, Jorg-Dieter. Epithelial Transport and Barrier Function: Pathomechanisms in Gastrointestinal Disorders (Annals of the New York Academy of Sciences, V. 915). New York Academy of Sciences, 2000.

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33

(Editor), John N. Abelson, Melvin I. Simon (Editor), Sidney Fleischer (Editor) y Becca Fleischer (Editor), eds. Biomembranes, Part V: Cellular and Subcellular Transport: Epithelial Cells, Volume 191: Volume 191: Biomembranes Part V (Methods in Enzymology). Academic Press, 1990.

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34

1961-, Lehr Claus-Michael, ed. Cell culture models of biological barriers: In vitro test systems for drug absorption and delivery. London: Taylor & Francis, 2002.

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35

Greger, Rainer. Von der Rektaldrüse des Haies (Squalus acanthias) zum epithelialen NaCI-Transport beim Menschen: vorgetragen am 19.04.1997 (Schriften der Mathematisch-naturwissenschaftlichen ... Heidelberger Akademie der Wissenschaften). Springer, 1997.

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36

Daudon, Michel y Paul Jungers. Cystine stones. Editado por 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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