G K Lau, G L Davis, S P Wu, R G Gish, L A Balart, J Y Lau – 1 June 1996 – Hepatitis C virus (HCV) replicates at a low rate and this makes its detection and intrahepatic localization difficult. To evaluate the clinical implications and effect of interferon alfa (IFN‐α) therapy on hepatic expression of HCV RNA, HCV RNA was detected by in situ reverse‐transcription polymerase chain reaction (IS‐RT‐PCR) in formalin‐fixed paraffin‐embedded liver sections from 26 patients with chronic hepatitis C. Results were compared with RT‐PCR of HCV RNA extracted from liver sections/tissue.

L J Born, K K Kharbanda, D L McVicker, R K Zetterman, T M Donohue – 1 June 1996 – Hepatic protein accumulation during ethanol administration may result partly from an ethanol‐elicited decline in hepatic protein degradation, which we have previously shown. We conducted the current studies to examine the effects of ethanol administration on the levels of hepatic ubiquitin, an 8.5‐kd protein which is an important mediator of extralysosomal protein catabolism. Rats were pair‐fed liquid diets containing either ethanol (36% of calories) or isocaloric maltose‐dextrin for 1 to 5 weeks.

H Mizuhara, M Uno, N Seki, M Yamashita, M Yamaoka, T Ogawa, K Kaneda, T Fujii, H Senoh, H Fujiwara – 1 June 1996 – A single intravenous injection of concanavalin A (Con A) induces T‐cell activation and an acute hepatitis in mice. This study investigated the role of interferon γ (IFN‐γ) in the pathogenesis of this hepatitis model. Striking increases in the plasma levels of various cytokines, including tumor necrosis factor (TNF), interleukin‐2 (IL‐2), and IFN‐γ, were detected before the increase in plasma aminotransferase levels induced by Con A injection.

1 June 1996

J N Ijzermans, D J Bac, B G Niesters – 1 June 1996

N Funaki, S Arii, K Monden, H Higashitsuji, M Furutani, M Mise, J Tanaka, M Imamura – 1 June 1996 – To elucidate the possible role of chemical mediators in modulating the host‐defense activity of patients with cirrhosis, primary‐cultured human hepatic macrophages (HHMΦ) were obtained from cirrhotic and noncirrhotic patients who received liver resections because of the presence of malignant liver tumors. The cirrhotic and noncirrhotic groups consisted of patients with similar malignancies: noncirrhotic patients had normal liver function and normal liver histology for nontumorous portions.

Y Niwa, M Matsumura, Y Shiratori, M Imamura, N Kato, S Shiina, T Okudaira, Y Ikeda, T Inoue, M Omata – 1 June 1996 – To analyze gene expression of α‐fetoprotein (AFP) and albumin in hepatocellular carcinoma (HCC), messenger RNAs (mRNAs) of these proteins in six human hepatoma cell lines and in 30 cases of HCC were quantitatively analyzed by competitive reverse transcription (RT) followed by polymerase chain reaction (PCR).

F Farinati, R Cardin, A D'Errico, N De Maria, R Naccarato, A Cecchetto, W Grigioni – 1 June 1996 – Hepatitis B virus (HBV)‐ and hepatitis C virus (HCV)‐related liver damage is linked to an increased risk of hepatocellular carcinoma, but the mechanisms underlying hepatitis C viral activity are not known. We therefore compared hepatocellular proliferative activity in chronic C virus‐related hepatitis and in liver damage of other etiology. Hepatocyte proliferation rate was investigated in 56 patients with chronic hepatitis using the Ki67 MIB1 monoclonal antibody in archival material.

H Schlossberg, Y Zhang, L Dudus, J F Engelhardt – 1 June 1996 – The expression of the immediate early genes (IEGs) c‐fos and e‐jun have been hypothesized to potentially play key roles in mediating cellular responses following injury to the liver. In this study, we sought to evaluate the potential involvement of c‐jun and c‐fos as determinants either of cellular regeneration or programmed cell death following ischemia/reperfusion (I/R) in mouse liver. To this end, we have analyzed the in situ messenger RNA (mRNA) expression patterns of c‐jun and c‐fos following lobar I/R in mouse liver.

H Shinozuka, T Ohmura, S L Katyal, A I Zedda, G M Ledda‐Columbano, A Columbano – 1 June 1996 – A single intravenous injection of lead nitrate (LN) to rats induces liver cell proliferation without causing cell necrosis (direct hyperplasia). We suggested that liver cell proliferation in this model may be triggered by the induction of liver tumor necrosis factor α (TNF‐α).