Expression of E‐selectin and E‐selectin ligands in human liver inflammation

D H Adams, S G Hubscher, N C Fisher, A Williams, M Robinson – 1 September 1996 – Lymphocyte recruitment to tissue is regulated by homing molecules expressed on subsets of leukocytes that bind to endothelial adhesion molecules termed addressins in target tissues. The addressins and homing molecules involved in recruiting lymphocytes to inflamed human liver are not known.

Concanavalin A induces perforin‐mediated but not Fas‐mediated hepatic injury

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.

A percutaneous technique for venovenous bypass in orthotopic cadaver liver transplantation and comparison with the open technique

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.

Inhibition of anaphylatoxin C3a‐ and C5a‐ but not nerve stimulation‐ or Noradrenaline‐dependent increase in glucose output and reduction of flow in Kupffer cell‐depleted perfused rat livers

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.

Antifibrogenic effect of a deletion variant of hepatocyte growth factor on liver fibrosis in rats

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.

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