By M. V. Singer, D. Brenner

ISBN-10: 3805580304

ISBN-13: 9783805580304

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Carcinogenesis 1988;9:2093–2098. 53 Seitz HK, Czygan P, Simanowski U, Waldherr R, Veith S, Raedsch R, Kommerell B: Stimulation of chemically induced rectal carcinogenesis by chronic ethanol ingestion. Alcohol Alcohol 1985;20:427–433. 54 Hakkak R, Korourian S, Ronis MJ, IngelmanSundberg M, Badger TM: Effects of diet and ethanol on the expression and localization of cytochromes P450 2E1 and P450 2C7 in the colon of male rats. Biochem Pharmacol 1996; 51:61–69. 55 Choi SW, Stickel F, Baik HW, Kim YI, Seitz HK, Mason JB: Chronic alcohol consumption induces genomic but not p53-specific DNA hypomethylation in rat colon.

However, these injuries were reversible after ethibloc decomposition. Further prolonged alcohol administration with an intragastric cannulae inhibited the recovery, and resulted frequently in parenchymal calcifications. Pancreatic regeneration was less pronounced in ethanol-fed animals, and calcifications remained in some animals [81]. Hyperstimulation of the pancreas with supramaximal doses of CCK increases exocrine pancreatic secretion and induces acute edematous pancreatitis. Rats received an ethanol diet for 2 or 6 weeks according to the TsukamotoFrench model [82].

Surprisingly, 30% of the baboons developed cirrhosis after a time period of 5 years. Histologically perivenular fibrosis was demonstrated whereas no signs of inflammation were detected. The application of a non-human primate animal model is self-evident, but the long duration and the low outcome of major histological liver changes including cirrhosis represent a major disadvantage to this model. Furthermore, these results could not yet be reproduced by other investigators. Tsukamoto-French Model In 1984, Tsukamoto et al.

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Alcohol And the Gastrointestinal Tract: Special Issue: Digestive Diseases 2005 by M. V. Singer, D. Brenner


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