L D DeLeve – 1 October 1996 – Hepatic venoocclusive disease (HVOD) is caused by the disruption of the microcirculation by an as‐yet unknown mechanism. Previous in vitro studies with azathioprine, monocrotaline, and dacarbazine suggested that toxins that cause HVOD initially causing HVOD target sinusoidal endothelial cells (SEC) perhaps via profound glutathione (GSH) depletion. The current study examines cyclophosphamide toxicity in SEC and hepatocytes, as well as the interplay between the two cell types.

P A Knolle, G Gerken, E Löser, H P Dienes, F Gantner, G Tiegs, K Meyer zum Büschenfelde, A W Lohse – 1 October 1996 – CD4+ T lymphocytes have been identified as being responsible for organ damage in the murine model of experimental liver injury induced by intravenous injection of concanavalin A (Con A). Liver sinusoidal endothelial cells (SEC) and Kupffer's cells (KC) are among the first cells that come into contact with lymphocytes in the liver sinusoid.

A Michalak, C Rose, J Butterworth, R F Butterworth – 1 October 1996 – It has been proposed that alterations of excitatory and inhibitory amino acids play a role in the pathogenesis of hepatic encephalopathy in acute liver failure. To evaluate this possibility, in vivo cerebral microdialysis was used to sample extracellular concentrations of amino acids in the frontal cortex of unanesthetized rats at various times during the progression of encephalopathy resulting from acute liver failure.

J Córdoba, J Gottstein, A T Blei – 1 October 1996 – Brain myo‐inositol, an organic osmolyte, is decreased in cirrhotic patients with hepatic encephalopathy but appears unchanged in fulminant hepatic failure. An osmoregulatory response to the increase in brain glutamine may explain the decrease in brain myo‐inositol; if this is the case, organic osmolytes may account for differences in the development of brain edema seen in acute or chronic liver failure.

R H Moseley – 1 October 1996

P J Meier‐Abt – 1 October 1996

C Luscombe, J Pedersen, E Uren, S Locarnini – 1 October 1996 – Long‐term antiviral chemotherapy using the nucleoside analogue ganciclovir was undertaken with the aim of eliminating hepadnaviral covalently closed circular (CCC) DNA from the livers of ducks that were congenitally infected with the duck hepatitis B virus (DHBV). Twenty‐ four weeks of ganciclovir therapy caused a substantial reduction in viremia, intrahepatic viral DNA replicative intermediates, and viral core proteins.

M F Fromm, D Busse, H K Kroemer, M Eichelbaum – 1 October 1996 – Cytochrome P450 (CYP) enzymes, which metabolize numerous drugs, are expressed both in liver and in extrahepatic tissues. CYP3A4 for example is present and inducible by rifampin in epithelial cells of the gastrointestinal tract. It has been shown that such prehepatic metabolism contributes substantially to total clearance of CYP3A4 substrates (e.g., cyclosporine) before and even more pronounced during enzyme induction.

B Gil, M Casado, M A Pajares, L Bosca, J M Mato, P Martin‐Sanz, L Alvarez – 1 October 1996 – The pattern of expression of liver‐specific and extrahepatic S‐adenosylmethionine (SAM) synthetase in developing rat liver was established by determining steady‐state levels of the respective messenger RNAs (mRNAs) and protein content. Levels of liver‐specific SAM synthetase mRNA increased progressively from day 20 of gestation, increased 10‐fold immediately after birth, and reached a peak at 10 days of age, decreasing slightly by adulthood.

T Poynard, V Leroy, M Cohard, T Thevenot, P Mathurin, P Opolon, J P Zarski – 1 October 1996 – The aims of this study were to evaluate the benefits of higher doses or of longer duration in comparison with a standard interferon regimen (3 MU three times per week for 6 months) in chronic hepatitis C, and to assess the efficacy of interferon in acute hepatitis C. Meta‐analysis made use of the Peto et al. and the Der Simonian and Laird methods, with heterogeneity and sensitivity analyses.