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Hepatic Encephalopathy, Hyperammonemia, and Ammonia Toxicity (Paperback, Softcover reprint of the original 1st ed. 1994)
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Hepatic Encephalopathy, Hyperammonemia, and Ammonia Toxicity (Paperback, Softcover reprint of the original 1st ed. 1994)
Series: Advances in Experimental Medicine and Biology, 368
Expected to ship within 10 - 15 working days
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This volume contains the papers presented at the International
Symposium on "Cirrhosis, Hyperammonemia and Hepatic
Encephalopathy," held in Valencia, Spain, January 24th-27th, 1994.
Liver cirrhosis and other hepatic dysfunctions such as fulminant
hepatic failure and congenital defects of urea cycle enzymes can
lead to hepatic encephalopathy, coma and death. Hepatic
encephalopathy is one of the main causes of death in western
countries. The ability to detoxify ammonia by its incorporation
into urea is diminished by impaired liver function, resulting in
increased ammonia levels in blood and brain. Hyperammonemia is
considered one of the main factors in the mediation of hepatic
encephalopathy and the classical clinical treatments are directed
towards reducing blood ammonia levels. However, the molecular bases
of the pathogenesis of hepatic encephalopathy and the role of
hyperammonemia in this process remain unclear and several
hypotheses have been proposed. To clarify the mechanisms involved
in hepatic encephalopathy and hyperammonemia suitable animal models
are necessary. The animal models available and the ideal features
of an animal model are presented in the initial part of the book.
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