D J Tuma, G M Thiele, D Xu, L W Klassen, M F Sorrell – 1 April 1996 – Acetaldehyde and the lipid peroxidation‐derived aldehyde malondialdehyde (MDA), are reactive compounds that are generated during ethanol metabolism in the liver, and both aldehydes have been shown to be capable of binding to proteins and forming stable adducts. Because similar concentrations of MDA and acetaldehyde can coexist in the liver during ethanol oxidation, protein adduct formation in the presence of both of these aldehydes was studied under both in vitro and in vivo conditions.

E Levy, C Garofalo, T Rouleau, V Gavino, M Bendayan – 1 April 1996 – The major aim of the current investigation was to define whether essential fatty acid (EFA) deficiency modifies the intrahepatic metabolism and biliary output of sterols in rats. EFA‐deficient diet caused an impoverishment in linoleic, arachidonic, and docosahexaenoic acids, and a marked enrichment in the eicosatrienoic acid of the plasma, liver, and hepatic microsomes.

F V Schiødt, S Bondesen, I Petersen, K Dalhoff, P Ott, N Tygstrup – 1 April 1996 – Gc‐globulin scavenges actin released from necrotic hepatocytes to the extracellular space. In 77 patients with fulminant hepatic failure (FHF) (excluding patients treated with liver transplantation), admission levels of serum Gc‐globulin and degree of complexing with monomeric actin (complex ratio) were determined to evaluate their predictive values in relation to survival/nonsurvival. Gc‐globulin levels were significantly reduced in 47 nonsurvivors, compared with 30 survivors (96 +/‐ 71 mg/L vs.

S Strasberg, T K Howard – 1 April 1996

A D Cooper – 1 April 1996

J Deleuze, E Jacquemin, C Dubuisson, D Cresteil, M Dumont, S Erlinger, O Bernard, M Hadchouel – 1 April 1996 – Disruption of the murine mdr2 (multidrug‐resistance) gene, which encodes a phosphatidylcholine flippase, leads to a hepatic disorder because of loss of biliary phospholipid secretion. Among the hereditary human cholestasis, a subtype of progressive familial intrahepatic cholestasis with high gamma‐glutamyltranspeptidase (GGT) serum activity shares histological, biochemical, and genetic features with mice lacking mdr2 gene expression (mdr2 ‐/‐ mice).

K P Rioux, K A Sharkey, J L Wallace, M G Swain – 1 April 1996 – Mast cells have been shown to play a role in many chronic inflammatory and fibrotic disorders. However, their possible contribution to the pathological changes that occur in liver cirrhosis is unknown. To explore this, we examined whether changes in hepatic mast cell number and mediator content were associated with fibrotic changes in experimental biliary cirrhosis. Rats were studied 7, 14, or 21 days after bile duct resection (BDR). Hepatic mast cells were identified by histochemical and immunohistochemical stains.

N Chalasani, C M Wilcox – 1 April 1996 – Although liver test abnormalities are frequently identified in patients with acquired immunodeficiency syndrome (AIDS), the causes, evaluation, and outcome of jaundice in these patients have not been systematically evaluated. From August 1, 1990 through September 1, 1994, all human immunodeficiency virus (HIV)‐infected patients with liver test abnormalities seen by the gastroenterology service at a large, inner‐city hospital were prospectively identified. Jaundice was defined as a serum bilirubin concentration ≥ 3 mg/dL.

P C Adams, S Agnew – 1 April 1996 – The relationship between alcoholism and hereditary hemochromatosis remains controversial. Previous studies have included patients with alcoholic siderosis rather than hereditary hemochromatosis. In this retrospective study, the clinical features, iron status, alcohol history, liver histology, and long‐term survival were reviewed in 105 homozygotes for hemochromatosis using rigid diagnostic criteria including an HLA identical sibling with iron overload. Heavy alcohol consumption (>80 g ethanol/day) was found in 15% of hemochromatosis patients.

C L Booth, G M Pollack, K L Brouwer – 1 April 1996 – Previous work in this laboratory has suggested that the nonlinear disposition of valproic acid (VPA) in the rat may be due to nonlinear distribution of VPA into the liver. The present study was undertaken to elucidate further the hepatobiliary disposition of VPA. VPA (0.1‐2 mmol/L) was incubated with isolated rat hepatocytes in vitro. Uptake of [3H]‐VPA was linear from 10 to 50 seconds, with minimal (<7 percent) biotransformation.