Hepatitis B vaccines in clinical practice. Edited by Ronald W. Ellis, 418 pp. New York: Marcel Dekker, 1993. $155
Raymond S. Koff – 1 January 1994
Androgen receptor in human liver: Characterization and quantitation in normal and diseased liver
Patricia K. Eagon, Mary S. Elm, Elizabeth A. Stafford, Lynne E. Porter – 1 January 1994 – Liver is responsive to sex hormones. The role of androgens in normal human liver function is not well understood, although androgens have been implicated in several liver diseases. Because the human hepatic androgen receptor has not been adequately characterized, we analyzed cytosolic and nuclear fractions from normal human liver of both sexes for androgenbinding activity using multipoint saturation analysis with the androgenic radioligand methyltrienelone (R1881).
Vasoactive effect of endothelin‐1 on rat liver in vivo
Shigetoshi Okumura, Yoshiyuki Takei, Sunao Kawano, Kouichi Nagano, Eiji Masuda, Moritaka Goto, Shingo Tsuji, Tomoki Michida, Sheng‐Song Chen, Toru Kashiwagi, Hideyuki Fusamoto, Takenobu Kamada, Nobuhiro Sato – 1 January 1994 – The purpose of this study was to evaluate the role of endothelin‐1 in modulating hepatic microcirculation and liver damage. Rats were infused with endothelin‐1 at doses ranging from 30 to 1,000 pmol/kg over 1 min through an indwelling cannula placed in the portal vein. In control rats, saline solution was infused at the same rate.
The search for the ultimate screening test for hepatocellular carcinoma continues
Andrea Ewing Reid, T. Jake Liang – 1 January 1994
Preneoplastic significance of hepatic iron–free foci in genetic hemochromatosis: A study of 185 patients
Yves M. Deugnier, Paul Charalambous, Daniéle Le Quilleuc, Bruno Turlin, Jeffrey Searle, Pierre Brissot, Lawrie W. Powell, June W. Halliday – 1 December 1993 – Sublobular nodules of hepatocytes free of iron or exhibiting much less iron than the surrounding parenchyma, referred to in this study as iron‐free‐foci, are frequently found in the livers of patients with genetic hemochromatosis complicated by hepatocellular carcinoma.
Histological evidence for recurrence of primary biliary cirrhosis after liver transplantation
Vijayan Balan, Kennetii P. Batts, Michael K. Porayko, Ruud A. F. Krom, Jurgen Ludwig, Russell H. Wiesner – 1 December 1993 – Whether primary biliary cirrhosis recurs after orthotopic liver transplantation remains a controversial issue. Sixty consecutive patients with primary biliary cirrhosis with at least 1 yr of follow‐up after liver transplantation were studied. All patients were treated with triple‐drug immunosuppression (cyclospoine, prednisone, azathioprine).
Normal increase in glucose output by portal noradrenaline and glucagon but not nerve stimulation with enhanced portal resistance, not only in micronodular but also in intermediate thioacetamide cirrhotic livers
Andreas Gardemann, Thomas Zimmermann, Georg Machnik, Rolf Dargel, Kurt Jungermann – 1 December 1993
The pathology of hepatitis C as a function of mode of transmission: Blood transfusion vs. Intravenous drug use
Stuart C. Gordon, Richard S. Elloway, John C. Long, Carl F. Dmuchowski – 1 December 1993 – We reviewed the clinical records of 140 consecutively evaluated patients with chronic hepatitis C infection. One hundred twenty‐four patients (89%) contracted infection through blood transfusion or intravenous drug use. The liver biopsy specimens of 83 patients (43 blood transfusion cases and 40 intravenous drug abuse cases) were examined without knowledge of the mode of disease transmission.
Degradation and intracellular accumulation of a residualizing hyaluronan derivative by liver endothelial cells
Carl T. McGary, Judith Yannariello‐Brown, Dennis W. Kim, Tami C. Stinson, Paul H. Weige – 1 December 1993 – The release and intracellular accumulation of 125I‐hyaluronan degradation products was studied in cultured liver endothelial cells with hyaluronan oligosaccharides (relative molecular mass = approximately 44,000) uniquely modified and radiolabeled at the terminal reducing sugar. Two methods were combined to measure 125I‐hyaluronan degradation by liver endothelial cells.