The demography of primary biliary cirrhosis in ontario, canada

Helga Witt‐Sullivan, Jenny Heathcote, Karen Cauch, Laurence Blendis, Cameron Ghent, Allen Katz, Ruth Milner, S. Chris Pappas, James Rankin, Ian R. Wanless – 1 July 1990 – The demographics of primary biliary cirrhosis in Ontario, Canada, are described. Two hundred and twenty‐five primary biliary cirrhosis patients were identified by 85 of 502 gastroenterologists (or internists) practicing in Ontario acute care hospitals that have 150 or more beds.

Prevention of hepatocyte injury and lipid peroxidation by iron chelators and α‐tocopherol in isolated iron‐loaded rat hepatocytes

Bipin K. Sharma, Bruce R. Bacon, Robert S. Britton, Chanho H. Park, Christopher J. Magiera, Rosemary O'Neill, Nicholas Dalton, Patricia Smanik, Theodore Speroff – 1 July 1990 – These experiments were performed to characterize the relationship between lipid peroxidation and hepatocyte viability in iron overload. Hepatocytes were isolated from rats with chronic dietary iron overload and the effects of in vitro iron chelation on lipid peroxidation, cell viability and ultrastructure were studied over a 4‐hr incubation period.

Renal and systemic hemodynamics in experimental cirrhosis in rats: Relation to hepatic function

Georg Wensing, Ramzi Sabra, Robert A. Branch – 1 July 1990 – The onset of sodium retention in the phenobarbital and carbon tetrachloride model of cirrhosis in the rat is preceded by a linear decrease in hepatic function as measured by the aminopyrine breath test. Sodium retention occurs when liver function decreases below a critical threshold. Changes in systemic hemodynamics may be responsible for initiating the development of renal sodium retention.

Depressed liver regeneration after partial hepatectomy of germ‐free, athymic and lipopolysaccharide‐resistant mice

Robert P. Cornell, Barbara L. Liljequist, Kenneth F. Bartizal – 1 June 1990 – A hypothesis has been proposed by this laboratory that endogenous gut‐derived lipopolysaccharide is responsible for systemic endotoxemia in animals with acute liver injury particularly after partial (67%) hepatectomy. Systemic lipopolysaccharide and possibly fibrin aggregates or tissue debris then elicit release of cytokines from phagocytizing macrophages and/or monocytes that may be essential for normal liver regeneration.

Prevention of ursodeoxycholate hepatotoxicity in the rabbit by conjugation with N‐methyl amino acids

Adrian Schmassmann, Alan F. Hofmann, M. Antonietta Angellotti, Huong‐Thu Ton‐Nu, Claudio D. Schteingart, Carlo Clerici, Steven S. Rossi, Marcus A. Rothschild, Bertram I. Cohen, Richard J. Stenger, Erwin H. Mosbach – 1 June 1990 – The effect of dietary administration of four different amino acid (N‐acyl) conjugates of ursodeoxycholic acid on biliary bile acid composition, liver tests and hepatic morphology by light microscopy was examined in the rabbit.

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