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.

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).

A D Cooper – 1 April 1996

S Strasberg, T K Howard – 1 April 1996

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.

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.

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.

M Kobayashi, E Tanaka, T Sodeyama, A Urushihara, A Matsumoto, K Kiyosawa – 1 April 1996 – This study was conducted to clarify if the long‐term histological outcome among patients with chronic hepatitis C differs according to whether they are infected with genotype 1 or 2 hepatitis C virus (HCV). We examined 140 patients with chronic hepatitis C. The HCV genotype was determined by the enzyme‐linked immunosorbent assay (ELISA) based on genotypes 1 and 2 specific recombinant proteins; genotype 1 was found in 100 patients (96 were 1b and 4 were indeterminate) and genotype 2 in 36.

Y Gong, L Cui, G Y Minuk – 1 April 1996 – The gene responsible for transcribing glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH) is commonly used as a reporter gene to estimate the amount of RNA present in Northern analyses. However, recent data suggest that GAPDH gene expression may vary with the extent of cell proliferation and differentiation. 28S‐ribosomal RNA (28S‐rRNA) has also been employed to normalize Northern blots prepared with total RNA.

E Bhunchet, Y Eishi, K Wake – 1 April 1996 – To investigate whether hepatic fibrosis induced by porcine serum in rats is caused by an immune reaction to porcine serum, rats that were immunologically tolerant exclusively to porcine serum were subjected to the repeated injection of porcine serum over a long period. This porcine serum‐tolerant group consisted of 15 Wistar rats that had been injected intraperitoneally with porcine serum twice a week from the first postnatal day for 18 weeks.