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.
Masthead
1 July 1990
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.
Modern concepts of acute and chronic hepatitis. Edited by G. Gitnick, 334 pp. New York: Plenum Publishing Corporation, 1989. $52.75
Jonathan A. Leighton, Thomas E. Whigham – 1 July 1990
Notices
1 July 1990
Correction
1 July 1990
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.
Does the hepatic iron index differentiate hereditary hemochromatosis from secondary hemochromatosis?
C. Th. B. M. van Deursen, M. M. F. Fickers, P. J. Brombacher, Mark Bassett – 1 July 1990
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.