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Titlebook: Hepatic Encephalopathy, Hyperammonemia, and Ammonia Toxicity; Vicente Felipo,Santiago Grisolia Book 1994 The Editor(s) (if applicable) and

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书目名称Hepatic Encephalopathy, Hyperammonemia, and Ammonia Toxicity
编辑Vicente Felipo,Santiago Grisolia
视频video
丛书名称Advances in Experimental Medicine and Biology
图书封面Titlebook: Hepatic Encephalopathy, Hyperammonemia, and Ammonia Toxicity;  Vicente Felipo,Santiago Grisolia Book 1994 The Editor(s) (if applicable) and
描述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 bo
出版日期Book 1994
关键词Pathogene; brain; death; enzymes; liver; toxicity; hepatology
版次1
doihttps://doi.org/10.1007/978-1-4615-1989-8
isbn_softcover978-1-4613-5820-6
isbn_ebook978-1-4615-1989-8Series ISSN 0065-2598 Series E-ISSN 2214-8019
issn_series 0065-2598
copyrightThe Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Science+Busines
The information of publication is updating

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S-Adenosyl-L-Methionine Synthetase and Methionine Metabolism Deficiencies in Cirrhosis,toxics and an attenuation of the morfological alteration produced in the liver, including fiber production. This findings might have pharmacological implications in the treatment of liver diseases, since the possible beneficial effect of long term administration of SAM could include a reduction of fiber production.
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Use of Hepatocyte Cultures for Liver Support Bioreactors,ies are not sufficient to give statements about a clinical improvement of therapy of acute liver failure. Although important progress has been made in the development of the systems, multiple different hepatocyte culture models and bioreactor constructions are discussed in the literature, indicating competition in this field of medical research.
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