Lack of increase in heterozygous α1‐antitrypsin deficiency phenotypes among patients with hepatocellular and bile duct carcinoma

Mordechai Rabinovitz, Judith S. Gavaler, Robert H. Kelly, Martin Prieto, David H. Van Thiel – 1 March 1992 – Homozygous α1‐antitrypsin deficiency (PiZZ phenotype) is known to be associated with increased risk of cirrhosis and primary liver cancer. Although a relationship between heterozygous α1‐antitrypsin deficiency and chronic liver disease was suggested recently, it is still a matter of controversy whether such patients are at increased risk of liver cancer.

Differences in the abundance of variably spliced transcripts for the second asialoglycoprotein receptor polypeptide, H2, in normal and transformed human liver

Elisabeth Paietta, Richard J. Stockert, Janis Racevskis – 1 March 1992 – The human hepatic asialoglycoprotein receptor comprises two homologous polypeptides designated H1 and H2. Two distinct complementary DNA clones encoding these receptor subunits have been previously isolated from the human hepatoblastoma cell line HepG2. We discovered that multiple variants of H2 transcripts exist both in HepG2 cells and in the normal human liver that, at least in part, appear to be the result of alternative splicing events.

Inhibition by noradrenaline and adrenaline of the increase in glucose and lactate output and decrease in flow after sympathetic nerve stimulation in perfused rat liver: Possible involvement of protein kinase C

Hisayuki Miura, Andreas Gardemann, Josip Rosa, Kurt Jungermann – 1 March 1992 – In perfused rat liver stimulation of the hepatic nerve plexuses increased via α1‐receptors glucose and lactate output decreased flow and caused an overflow of noradrenaline into the hepatic vein. Infusion of noradrenaline and adrenaline also elicited similar metabolic and hemodynamic alterations via α1‐receptors, whereas infusion of isoproterenol via β2‐receptors enhanced glucose output and slightly reduced lactate release without affecting flow.

Ethanol enhances ADP‐ribosylation of protein in rat hepatocytes

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.

Liver plasma membrane–associated fibroblast growth: Stimulatory and inhibitory activities during experimental cirrhosis

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.

Improved serodiagnosis of non‐A, non‐B hepatitis by an assay detecting antibody to hepatitis C virus core antigen

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.

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