Andre L. Weigert, Pierre‐Yves Martin, Michel Niederberger, Elisa M. S. Higa, Ivan F. McMurtry, Pere Gines, Robert W. Schrier – 1 December 1995 – The present experiments were designed to test if induction of nitric oxide synthase (NOS) plays a role in the systemic vasodilation observed in hepatic cirrhosis. Because endotoxin levels are elevated in cirrhosis, and endotoxin stimulates inducible nitric oxide synthase (iNOS) expression in several cell lines, aortas of carbon tetrachloride‐induced cirrhotic rats with ascites were evaluated for iNOS expression.

Ignazio Roberto Marino, Howard R. Doyle, Luca Aldrighetti, Cataldo Doria, John McMichael, Timothy Gayowski, John J. Fung, Andreas G. Tzakis, Thomas E. Starzl – 1 December 1995 – We correlated donor and recipient factors with graft outcome in 436 adult patients who underwent 462 liver transplants. Donor variables analyzed were age, gender, ABO blood group, cause of death, length of stay in the intensive care unit, use of pressors or pitressin, need for cardiopulmonary resuscitation, terminal serum transaminases, and ischemia time.

Peter Karayiannis, Alexandra Alexopoulou, Stephanos Hadziyannis, Mark Thursz, Richard Watts, Seiji Seito, Howard C. Thomas – 1 December 1995 – The precore stop‐codon variant of hepatitis B virus (HBV) has been implicated in fulminant hepatitis. The precore/core regions of such variants from two sets of patients with interpartner transmission resulting in fulminant hepatitis in the contact, were sequenced to establish whether further sequence variations in the core region are specifically associated with the fulminant disease.

Andres T. Blei – 1 December 1995

Hiroshi Hayashi, Kenji Sugio, Takashi Matsumata, Eisuke Adachi, Kenji Takenaka, Keizo Sugimachi – 1 December 1995 – To clarify the clinical significance of the mutation of p53 gene in hepatocellular carcinoma (HCC), 90 resected specimens from Japanese patients were assayed using a polymerase chain reaction‐single strand conformation polymorphism (PCR‐SSCP) analysis. p53 mutations were detected in 25 cases (27.8%) at exons 4, 5, 6, 7, and 8, and the most frequent region of the mutation was at exons 5 and 7.

Juan Antonio Quiroga, Jan van Binsbergen, Chang Yi Wang, Margarita Pardo, Sonia Navas, Chantal Trines, Montserrat Herrero, Vicente Carreno – 1 December 1995 – Immunoglobulin M (IgM) antibody to hepatitis C core antigen (anti‐HCV‐core) was tested by enzyme immunoassay against a synthetic peptide representing amino acids 1 to 62 of the core protein. Of 214 patients with different categories of histological activity, 193 (90%) showed positive results for IgM anti‐HCV‐core, and 207 (97%) had HCV RNA; most cases (186, 87%) had both markers detectable simultaneously.

1 December 1995

Sook Ping Lim, Fiona Jane Andrews, Paul Edmond O'Brien – 1 December 1995 – Studies into the mechanism of acetaminophen (APAP)‐induced hepatotoxicity have focused mainly at the hepatocellular level. This study aimed to investigate the effect of acetaminophen on the hepatic microvasculature using a vascular casting technique. Acetaminophen was administered at a dose of 650 mg/kg body weight (intraperitoneally) to fasted male Long Evans rats. Microvascular casting was performed at various points after drug administration.

Geoffrey M. Dusheiko, Jennifer A. Roberts – 1 December 1995 – The aim of this study is to assess the long‐term economic impact of treatment of chronic hepatitis B and C with interferon alfa. Estimates were made of the progression of the disease over a 30‐year period using a transitional probability model. Cohorts of 1,000 hypothetical patients with either chronic hepatitis B or C treated with interferon alfa were compared with an untreated cohort. The costs were estimated for therapy, monitoring, and treatment of the disease, including transplantation.

Irmin Sternlieb, Nelson Quintana, Irene Volenberg, Michael L. Schilsky – 1 December 1995 – In an attempt to identify the cellular targets of copper toxicity, we studied the ultrastructure of hepatocytes in the livers of 23 Long‐Evans Cinnamon (LEC) rats ranging in age from 10 to 89 weeks. The hepatic copper concentration ranged from 325 to 2,126 (mean, 930) μg/g dry weight. Thirteen rats displayed varying degrees of jaundice at the time of killing. Numerous nuclei were indented by cytoplasmic invaginations. Conspicuous abnormalities were displayed by mitochondria.