Hepatocyte proliferative activity in chronic liver damage as assessed by the monoclonal antibody MIB1 Ki67 in archival material: The role of etiology, disease activity, iron, and lipid peroxidation

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.

Expression of c‐fos and c‐jun during hepatocellular remodeling following ischemia/reperfusion in mouse liver

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.

Possible roles of nonparenchymal cells in hepatocyte proliferation induced by lead nitrate and by tumor necrosis factor α

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).

Involvement of platelet‐activating factor in cytokine production and neutrophil activation after hepatic ischemia‐reperfusion

A Serizawa, S Nakamura, S Suzuki, S Baba, M Nakano – 1 June 1996 – Although platelet‐activating factor (PAF) is implicated as an important mediator in the pathogenesis of hepatic ischemia‐reperfusion (IR) injury, the precise mechanism of its action has not been studied.

Inhibition of hepatitis B virus replication by targeted pretreatment of complexed antisense DNA in vitro

K Nakazono, Y Ito, C H Wu, G Y Wu – 1 June 1996 – We have shown that antisense oligonucleotides can be targeted to hepatitis B virus (HBV)‐infected cells, resulting in specific inhibition of viral protein synthesis and replication in vitro. The targeting system was based on the internalization of DNA complexes by highly selective receptors for galactose‐terminal glycoproteins, asialoglycoproteins, on the surface of hepatocytes. Our objective in this study was to determine whether antisense DNA could be targeted to hepatocytes to prevent subsequent infection by HBV.

The hepatocyte growth factor regulates the synthesis of acute‐phase proteins in human hepatocytes: Divergent effect on interleukin‐6‐stimulated genes

M I Guillen, M J Gomez‐Lechon, T Nakamura, J V Castell – 1 June 1996 – Our study addressed the role of the human hepatocyte growth factor (HGF), a potent mitogen for mature rat and human hepatocytes, in the regulation of specific hepatic genes. The experimental evidence obtained in primary cultured human hepatocytes indicates that HGF regulates the synthesis of plasma proteins in a dose‐response fashion.

Severe recurrent cholestatic hepatitis C following orthotopic liver transplantation

L K Schluger, P A Sheiner, S N Thung, J Y Lau, A Min, D C Wolf, I Fiel, D Zhang, M A Gerber, C M Miller, H C Bodenheimer – 1 May 1996 – Recurrent infection with hepatitis C virus (HCV) is almost universal following orthotopic liver transplantation although clinical severity varies. Data on 135 patients who underwent transplantation for hepatitis C cirrhosis were reviewed. We describe a progressive, severe cholestatic form of hepatitis occurring in a subgroup of patients with recurrent hepatitis C.

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