G A Tipples, M M Ma, K P Fischer, V G Bain, N M Kneteman, D L Tyrrell – 1 September 1996 – The (‐) enantiomer of 3′‐thiacytidine (lamivudine) has been found to be a potent inhibitor of hepatitis B virus (HBV) and human immunodeficiency virus (HIV) replication. Mutation of methionine to valine or isoleucine at the YMDD (tyrosine, methionine, aspartate, aspartate) motif of the HIV reverse transcriptase has been shown to be responsible for lamivudine resistance in HIV. The hepadnaviruses also have the YMDD motif in their DNA polymerase.

Zhi Zhong, Henry Connor, Ronald P. Mason, Wei Qu, Robert F. Stachlewitz, Wenshi Gao, John J. Lemasters, Ronald G. Thurman – 1 September 1996 – This study investigated the role of Kupffer cells on survival and graft injury in transplanted fatty livers from rats treated acutely with ethanol. Donor rats were given ethanol (5 g/kg, by mouth) 20 hours before explantation, and liver grafts were preserved in University of Wisconsin cold storage solution for 24 to 42 hours prior to implantation. Blood samples were taken from the inferior vena cava for 3 hours after implantation.

H M El‐Newihi, M E Alamy, T B Reynolds – 1 September 1996 – The liver is commonly involved in patients with typhoid fever. However, severe hepatic derangement simulating acute viral hepatitis is rare. Our aim was to characterize the clinical picture, biochemical features, and prognosis of Salmonella hepatitis. Retrospective case‐control analysis of medical records included 27 patients with Salmonella hepatitis and 27 inpatients with acute viral hepatitis from 1973 to 1993.

M W Fried, D G Connaghan, S Sharma, L G Martin, S Devine, K Holland, A Zuckerman, S Kaufman, J Wingard, T D Boyer – 1 September 1996 – Hepatic venoocclusive disease (VOD) is a common, life‐threatening complication of bone marrow transplantation (BMT). Portal hypertension is usually present and accounts for many of the clinical manifestations of this syndrome. We describe the results of transjugular intrahepatic portosystemic shunt (TIPS) for the management of VOD after BMT TIPS was performed in six patients with histologically confirmed VOD who had progressive jaundice and ascites.

H Yasuda, E Imai, A Shiota, N Fujise, T Morinaga, K Higashio – 1 September 1996 – Hepatic fibrosis, which may lead to cirrhosis, is associated with most chronic liver diseases. Current therapies for hepatic fibrosis are, however, generally ineffective. In this report we assessed the efficacy of the treatment of hepatic fibrosis with a naturally occurring deletion variant of hepatocyte growth factor (dHGF). The administration of dHGF increased liver weight and suppressed the increase of hepatic collagen content in rats treated with dimethylnitrosamine (DMN) to induce hepatic fibrosis.

G P Puschel, A Nolte, H L Schieferdecker, E Rothermel, O Gotze, K Jungermann – 1 September 1996 – In isolated in situ perfused rat livers, infusion of anaphylatoxins C3a and C5a, activation peptides of the complement system, as well as stimulation of sympathetic hepatic nerves have been shown to increase hepatic glucose output and to reduce hepatic flow. These effects were mediated via an at least partially prostanoid‐dependent intercellular signalling chain between nonparenchymal cells and hepatocytes.

A K Burroughs, D Patch – 1 September 1996

1 September 1996

Scott R. Johnson, William F. Marterre, Maria H. Alonso, Douglas W. Hanto – 1 September 1996 – Venovenous bypass minimizes the hemodynamic alterations during the anhepatic phase of liver transplantation. A new technique for the percutaneous placement of the bypass cannulae is described and compared to the cut‐down (“open”) technique.

Y Watanabe, M Morita, T Akaike – 1 September 1996 – Concanavalin A (Con A) induces T‐cell‐mediated hepatic injury in vivo, although Con A‐stimulated lymphocytes are not cytotoxic to normal hepatocytes in vitro. This contradiction makes the mechanism of Con A‐induced hepatitis elusive. In this study, we demonstrate that Con A but not tumor necrosis factor α (TNF‐α), interferon γ (IFN‐γ), or actinomycin D (ActD) induced the susceptibility of hepatocytes to activated autologous lymphocyte cytotoxicity.