p53 Proteins and aflatoxin B1: The good, the bad, and the ugly
T. Jake Liang – 1 October 1995
T. Jake Liang – 1 October 1995
Hari S. Conjeevaram, James E. Everhart, Jay H. Hoofnagle – 1 October 1995
Gregorio Varela‐Moreiras, Elena Alonso‐Aperte, Mireia Rubio, Marta Gasso, Ramón Deulofeu, Luis Alvarez, Juan Caballería, Juan Rodés, José M. Mato – 1 October 1995 – Carbon tetrachloride (CCl4) administration to rats produces hepatic cirrhosis and supplementation with S‐adenosylmethionine (SAM) can partially prevent CCl4‐induced liver injury. These effects are thought to be caused by oxidative stress and the subsequent formation of free radicals, but the mechanism whereby this occurs and the accurate nature of the mechanisms by which SAM exerts its protective action are not well understood.
Luba Dumenco, Delphine Oguey, Justina Wu, Norma Messier, Nelson Fausto – 1 October 1995 – The p53 gene is frequently mutated in human tumors; in hepatocellular carcinomas, there is a high frequency of a specific mutation at codon 249 in regions with significant aflatoxin exposure. To assess the role of this p53 mutation in the development of hepatocellular carcinoma, a mutant murine p53 gene, p53ser246, which corresponds to human codon 249, was transfected into a differentiated, nontransformed hepatocyte cell line AML12.
Michele Martinot‐Peignoux, Patrick Marcellin, Mièle Pouteau, Corinne Castelnau, Nathalie Boyer, Marc Poliquin, Claude Degott, Isabelle Descombes, Véronique Le Breton, Véronica Milotova, Jean Pierre Benhamou, Serge Erlinger – 1 October 1995 – The aim of the study was to determine the respective influence of pretreatment serum hepatitis C virus (HCV) RNA levels and HCV genotype on the response to interferon (IFN) alfa in patients with chronic hepatitis C. We retrospectively studied 141 patients with chronic hepatitis C included in two consecutive controlled trials of IFN alfa.
Gary L. Davis – 1 October 1995
Ahmet Gurakar, Stefano Fagiuoli, Hawazin Faruki, Nicola De Maria, Mujdat Balkan, David H. Van Thiel, Lois Friedlander – 1 October 1995 – A total of 41 patients with chronic hepatitis C virus (HCV) defined as abnormal liver injury test results for 6 months or more and HCV RNA positivity in plasma were studied to determine if the liver might not be the only focus of HCV infection in individuals treated with interferon alfa (IFN‐α). All patients were examined for the presence of confounding liver disease and tested negatively for such findings.
Yun‐Fan Liaw – 1 October 1995 – Hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis delta virus (HDV) share same transmission routes, thus dual or triple infection may occur and even persist in the same patients. A significant amount of literature has accumulated since the advent of HCV assays. It is pertinent to review and evaluate the clinical and virological significance of HCV in multiple hepatotropic viral infection. The reported series on seroprevalence of HCV indicate that HCV is found in more than 10% of HBV‐ or HDV‐infected patients worldwide.
Luigi Fiume, Giuseppina Di Stefano, Corrado Busi, Alessandro Mattioli, Maria Rapicetta, Roberto Giuseppetti, Anna Rita Ciccaglione, Claudio Argentini – 1 October 1995 – We prepared a hepatotropic conjugate, suitable for intramuscular (IM) injection, of lactosaminated poly‐Llysine with adenine arabinoside monophosphate (ara‐AMP), a drug active against hepatitis B virus (HBV). We studied its organ distribution in mice and its antiviral activity in woodchucks that are carriers of woodchuck hepatitis virus (WHV).
Kazuo Iwata, Takaji Wakita, Akihiko Okumura, Kentaro Yoshioka, Masahiro Takayanagi, Jack R. Wands, Shinichi Kakumu – 1 October 1995 – Evidence suggests that cellular immunity to hepatitis C virus (HCV) core protein may be important in the pathogenesis of viral infection. Therefore, interferon gamma (IFN‐γ) production by peripheral blood mononuclear cells (PBMC) derived from patients with chronic HCV infection (genotype 1b) was examined. The cellular immune response was evaluated with a recombinant HCV core fusion protein derived from a patient with genotype 1b.