Hun‐Taek Kim, George Stoica, Fuller W. Bazer, Troy L. Ott – 30 December 2003 – Clinical applications of Type I interferon (IFN) are limited by adverse side effects mediated largely by unknown mechanisms. This study examined the mechanisms of acute hepatic injury in lambs treated with systemic administration of IFN‐τ, a Type I IFN. Liver tissues were collected at 24, 48, or 96 hours after treatment with either IFN‐τ or saline.
Alexander Y. Lee, William C. Manning, Christopher L. Arian, Noelle K. Polakos, Jose L. Barajas, Jeffrey B. Ulmer, Michael Houghton, Xavier Paliard – 30 December 2003 – The immunology of hepatitis C virus (HCV) infection should be studied in the context of HCV antigen expression in the liver, because HCV primarily infects this organ.
Emmet B. Keeffe – 30 December 2003
Nobuaki Kawarabayashi, Shuhji Seki, Kazuo Hatsuse, Takashi Ohkawa, Yuji Koike, Tsukasa Aihara, Yoshiko Habu, Ryusuke Nakagawa, Katsunori Ami, Hoshio Hiraide, Hidetaka Mochizuki – 30 December 2003 – CD56+T cells and CD56+natural killer (NK) cells are abundant in the human liver. The aim of this study was the further characterization of these cells in the liver with or without hepatitis C virus (HCV) infection. Liver mononuclear cells (MNC) were isolated from liver specimens obtained from the patients during abdominal surgery.
Eric Barriere, Khalid A. Tazi, Jean‐Pierre Rona, Fabienne Pessione, Jörg Heller, Didier Lebrec, Richard Moreau – 30 December 2003 – In cirrhosis, in splanchnic arteries, endothelium‐dependent relaxation may persist even if overactive nitric oxide synthase (NOS) and cyclooxygenase (COX) are inhibited. In normal arteries, a significant endothelium‐dependent relaxation to acetylcholine persists after NOS/COX inhibition.
Evangelista Sagnelli, Nicola Coppola, Carlo Scolastico, Pietro Filippini, Teresa Santantonio, Tommaso Stroffolini, Felice Piccinino – 30 December 2003 – We studied 648 hepatitis B surface antigen (HBsAg)‐ and/or anti–hepatitis C virus (HCV)‐positive patients to evaluate the virologic and clinical characteristics of multiple hepatitis viral infection. We defined as Case B‐C an HBsAg/anti‐HCV positive patient and as Case b‐C an anti‐HCV/anti‐HBc‐positive, HBsAg/anti‐HBs–negative patient.
Shin‐Han Yu, Kazuyoshi Nagayama, Nobuyuki Enomoto, Namiki Izumi, Fumiaki Marumo, Chifumi Sato – 30 December 2003 – As a part of the defense mechanism of the host to viral infection, interferons induce the transcription of several genes. These interferon‐inducible genes contribute to the eradication of the viruses. Whereas some studies suggested the participation of a dsRNA‐dependent protein kinase in the host reaction to hepatitis C virus infection, the involvement of other interferon‐inducible genes has not been evaluated.
Olivier Chazouilléres, Annie Robert – 30 December 2003
Stephan F. Schlosser, Francesco Azzaroli, Tao Dao, Ravi Hingorani, I. Nicholas Crispe, James L. Boyer – 30 December 2003 – Hepatocytes constitutively express CD95 (also called Fas/APO‐1) and are therefore potential targets for CD95‐ligand (CD95L)‐mediated injury. To study this mechanism of cell death in hepatocytes we developed an in vitro model of liver cell apoptosis using membrane‐bound CD95L as the inducing agent. Primary mouse hepatocytes were cocultured with NIH 3T3 fibroblasts, stably transfected with mouse CD95L (FCD95L+).
Young‐Myeong Kim, Tae‐Hyoung Kim, Hun‐Taeg Chung, Robert V. Talanian, Xiao‐Ming Yin, Timothy R. Billiar – 30 December 2003 – Mitochondrial cytochrome c release plays a critical role in apoptotic signal cascade after the activation of cell surface death receptors. We investigated the role played by nitric oxide (NO) in mitochondrial apoptotic signaling in tumor necrosis factor α (TNF‐α) plus actinomycin D (TNF‐α/ActD)‐induced apoptosis.