Liver‐associated lymphocytes expressing NK1.1 are essential for oral immune tolerance induction in a murine model

Shivti Trop, Dimitri Samsonov, Israel Gotsman, Ruslana Alper, Judith Diment, Yaron Ilan – 30 December 2003 – Oral tolerance is the induction of immunological hyporesponsiveness towards orally administered antigens. Tolerance initiation involves induction of anti‐inflammatory (Th2) lymphocytes, with downregulation of pro‐inflammatory (Th1) lymphocytes. The liver was previously shown to play a critical role in oral tolerance induction.

Twelve‐year follow‐up of a prospective randomized trial of hepatitis b recombinant DNA yeast vaccine versus plasma‐derived vaccine without booster doses in children

Man‐Fung Yuen, Wei‐Ling Lim, Chi‐Chung Cheng, Shiu‐Kam Lam, Ching‐Lung Lai – 30 December 2003 – A total of 318 children were prospectively randomized in group 1 with two 5‐μg doses of recombinant vaccine given at 0 and 1 month; in group 2 with three 5‐μg doses of recombinant vaccine given at 0, 1, and 6 months; or in group 3 with three doses of plasma‐derived vaccine given at 0, 1, and 6 months. Eleven subjects with a hepatitis B surface antigen antibody (anti‐HBs) titer of less than 10 mIU/mL at 12 months were given an extra dose of vaccine and were excluded from analysis.

Carbohydrate‐deficient transferrin, a sensitive marker of chronic alcohol abuse, is highly influenced by body iron

Tullia Maria De Feo, Silvia Fargion, Lorena Duca, Michela Mattioli, Maria Domenica Cappellini, Maurizio Sampietro, Bruno Mario Cesana, Gemino Fiorelli – 30 December 2003 – Carbohydrate‐deficient transferrin(CDT) a microheterogeneous form of serum transferrin (Tf) has been proposed as the most reliable marker of chronic alcohol consumption, although unexplained false‐positive and ‐negative results have been reported.We investigated whether body iron influenced CDT serum levels by studying alcohol abusers with or without iron overload and nonabusers with iron deficiency or iron overload cause

Persistence of viremia and the importance of long‐term follow‐up after acute hepatitis C infection

Stephen A. Villano, David Vlahov, Kenrad E. Nelson, Sylvia Cohn, David L. Thomas – 30 December 2003 – The purpose of this investigation was to prospectively characterize acute hepatitis C virus (HCV) infections and to evaluate the hypothesis that the outcome is affected by identifiable clinical or viral factors. One hundred forty‐two people with a history of illicit drug use who were HCV antibody–negative in 1988 were followed semiannually through 1996.

The human p53 gene mutated at position 249 per se is not sufficient to immortalize human liver cells

Claudia Schleger, Roger Becker, Franz Oesch, Pablo Steinberg – 30 December 2003 – A particular point mutation of the tumor suppressor gene p53, namely a G→T transversion at the third base of codon 249, is frequently detected in primary hepatocellular carcinomas from patients living in areas where the levels of dietary exposure to aflatoxin B1 and the rates of infection with the hepatitis B virus are very high.

Long‐term ursodeoxycholic acid delays histological progression in primary biliary cirrhosis

Paul Angulo, Kenneth P. Batts, Terry M. Therneau, Roberta A. Jorgensen, E. Rolland Dickson, Keith D. Lindor – 30 December 2003 – Primary biliary cirrhosis (PBC) is a progressive cholestatic liver disease frequently leading to development of cirrhosis and its complications. Ursodeoxycholic acid (UDCA) is a beneficial medical therapy for patients with PBC. Improvement in some histological features, but not in histological stage, has been reported after 2 years of UDCA therapy.

Glutathione peroxidase–deficient mice are more susceptible to neutrophil‐mediated hepatic parenchymal cell injury during endotoxemia: importance of an intracellular oxidant stress

Hartmut Jaeschke, Ye‐Shih Ho, Michael A. Fisher, Judy A. Lawson, Anwar Farhood – 30 December 2003 – Neutrophils contribute to hepatocellular injury in a number of acuteinflammatory reactions. However, the molecular mechanism of parenchymal cell injury remains controversial. To address the issue of whether or not reactive oxygen species (ROS) are important in the injury process, we used the galactosamine/endotoxin (Gal/ET) model of acute liver failure, which involves a neutrophil‐mediated parenchymal cell injury.

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