By M. V. Singer, D. Brenner
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Pharmaceutical businesses are spending expanding quantities of cash on drug discovery and improvement. however, attrition premiums in medical improvement are nonetheless very excessive, and as much as ninety% of latest compounds fail in scientific part I - III trials, that is partly because of loss of scientific efficacy. this means a powerful want for hugely predictive in vitro and in vivo versions.
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Extra resources for Alcohol And the Gastrointestinal Tract: Special Issue: Digestive Diseases 2005
60 Sarles H: Chronic calcifying pancreatitis – chronic alcoholic pancreatitis. Gastroenterology 1974;66:604–616. 61 Siech M, Heinrich P, Letko G: Development of acute pancreatitis in rats after single ethanol administration and induction of a pancreatic juice edema. Int J Pancreatol 1991; 8: 169– 175. 62 Foitzik T, Lewandrowski KB, Fernandez-del Castillo C, Rattner DW, Klar E, Warshaw AL: Exocrine hyperstimulation but not pancreatic duct obstruction increases the susceptibility to alcohol-related pancreatic injury.
33 Tarnawski A, Lu SY, Stachura J, Sarfeh IJ: Adaptation of gastric mucosa to chronic alcohol administration is associated with increased mucosal expression of growth factors and their receptor. Scand J Gastroenterol Suppl 1992; 193:59–63. 34 Hernandez-Munoz R, Montiel-Ruiz C, Vazquez-Martinez O: Gastric mucosal cell proliferation in ethanol-induced chronic mucosal injury is related to oxidative stress and lipid peroxidation in rats. Lab Invest 2000; 80: 1161–1169. 35 Jedrzejewska A, Staff-Zielinska E: Neuropathology of intramural autonomic innervation of mice stomach in chronic ethanol intoxication.
Interestingly, the generation of hydroxyethyl radicals was attenuated by the prior intraperitoneal administration of the antioxidant vitamins C and E. These results represent a startling but yet undeﬁned link between carcinogenesis and acute ethanol effects possibly accumulating after frequent recurrence of binge drinking. Furthermore, acute ethanol administration caused mitochondrial lipid hydroperoxide formation in rats in conjunction with a marked impairment in mitochondrial oxidative function due to glutathione depletion, which entailed deterioration of liver protection against oxidative stress .