Grace H. Elta, Frederic E. Eckhauser – 1 March 1992 – Objective. – To determine the effectiveness of the Palmaz balloon expandable stent for the creation of a transjugular intrahepatic portosystemic shunt. The device is designed to achieve portal decompression in patients with variceal hemorrhage secondary to portal hypertension.
1 March 1992
Thomas Zimmermann, Andreas Gardemann, Georg Machnik, Rolf Dargel, Kurt Jungermann – 1 March 1992 – Thioacetamide‐induced rat cirrhosis was characterized by single‐cell necroses, fibrosis, nodular parenchyma, decrease in parenchymal volume density and an increase in liver weight per body weight so that the total amount of parenchyma was not altered. The glycogen content was normal, and signs of decompensation were not found.
Scott L. Friedman – 1 March 1992
M. Victoria Marx, David Williams – 1 March 1992
1 March 1992
Tohru Katayama, Toshio Mazda, Shu Kikuchi, Shizuko Harada, Yoshiharu Matsuura, Joe Chiba, Hiroyoshi Ohba, Izumu Saito, Tatsuo Miyamura – 1 March 1992 – We examined sequential serum samples from 12 patients with well‐characterized posttransfusion non‐A, non‐B hepatitis who had an acute, resolving self‐limited type of clinical course for the presence of antibody to the hepatitis C virus nucleocapsid (core) protein (p22) expressed by a recombinant baculovirus.
Nickolay D. Belyaev, Vladimir G. Budker, Ludmila V. Deriy, Irina A. Smolenskaya, Vladimir M. Subbotin – 1 March 1992 – During experimental CCl4 cirrhosis, an increase of membrane‐associated factor stimulating 3T3 cell proliferation in vitro was observed. This stimulator is a 150‐kD protein similar to one previously described. In situ perfusion released growth stimulatory activity, suggesting a peripheral plasma membrane protein localizing on basolateral surfaces. The activity increased with increasing number of CCl4 treatments, reaching a maximum at the 14th intoxication.
1 March 1992
B. Emmanuel Akinshola, Savitri Sharma, James J. Potter, Esteban Mezey – 1 March 1992 – Decreases in hepatocyte NAD+ produced by ethanol are only partially explained by the increased conversion of NAD+ to NADH and NADP+. The purpose of this study was to determine whether a mechanism for the ethanol‐induced decrease in NAD+ is its increased use in ADP‐ribosylation. Exposure of hepatocytes in culture for 2 hr to 100 mmol/L ethanol increased the incorporation of 14C‐ribose from prelabeled NAD+ into 14C‐ribosylated proteins.