David Siegel, Miriam J. Alter, Stephen Morse – 1 July 1995 – To examine the extent of hepatitis B virus infection (HBV) in an inner‐city community, we determined the prevalence, incidence, and correlates of HBV seroreactivity in a representative sample of unmarried whites, African‐Americans, and Hispanics living in San Francisco during 1988 to 1989 and again 1 year later in 1989 to 1990. Unmarried men and women aged 20 to 44 years were surveyed in a random household sample drawn from three neighborhoods of varying geographic and cultural characteristics.

T Maeka, M Eto, T Lin, Y Nishimura, YY Kong, K Nomoto, J Immunol – 1 July 1995 – We investigated whether tolerance can be reestablished in mice with graft‐versus‐host disease (GVHD) by using a short‐term, T‐celldepleting treatment with an anti‐TCR‐αβ mAb. GVHD was induced in 950‐rad—irradiated AKR mice (H‐2k, Mls‐1a) by injecting 5 × 106 T celldepleted bone marrow cells together with either 107 or 2 × 106 lymph node (LN) cells from BALB/c mice (H‐2d, and Mls‐1b). AKR mice that received 107 LN cells exhibited a severe form of acute GVHD, in which all mice died by day 60.

Maher Daas, David J. Plevak, Eelco F. M. Wijdicks, Jorge Rakela, Russell H. Wiesner, David G. Piepgras, William F. Dunn, Jeffery L. Steers – 1 July 1995 – This investigation summarizes and evaluates the results of a clinical protocol that we designed to care for patients with acute liver failure (ALF). Adult patients with ALF were enrolled in the protocol. Grade II portal‐systemic encephalopathy prompted admission to the intensive care unit (ICU). Patients who met the clinical criterion were activated for liver transplantation.

Jürgen G. Pauletzki, Qi‐Wei Xu, Eldon A. Shaffer – 1 July 1995 – Impaired gallbladder emptying is frequent in cholesterol gallstone disease as well as in predisposing conditions like pregnancy and obesity. Gallbladder hypomotility is considered a pathogenic factor for gallstone formation, providing the residence time for cholesterol crystal nucleation, but any effect on the enterohepatic circulation of bile acids and subsequently on biliary lipid composition is unknown.

Richard A. Rippe, Ghamen Almounajed, David A. Brenner – 1 July 1995 – Ito cells are the primary cell type in the liver responsible for increased type I collagen production observed during fibrogenesis. After a fibrogenic stimulus, Ito cells change from their normal quiescent state to an activated state. In this study, we examined the expression of the α1(I) collagen gene in Ito cells that were freshly isolated from normal rat liver (quiescent) and Ito cells that were activated by culture on plastic.

Debra L. Laskin, Marina Rodriguez Del Valle, Diane E. Heck, Shaw‐Min Hwang, S. Tsuyoshi Ohnishi, Stephen K. Durham, Nancy L. Goller, Jeffrey D. Laskin – 1 July 1995 – In the present studies, we analyzed the effects of acute endotoxemia on hepatocyte nitric oxide production and functional activity. Treatment of rats with 5 mg/kg of lipopolysaccharide (LPS), which induces acute endotoxemia, caused an increase in nitric oxide production in the liver, as measured by electron paramagnetic spin trapping, which was evident within 6 hours.

Didier Samuel, Graeme Alexander – 1 July 1995

Kris V. Kowdley, Tarek Hassanein, Sumanjit Kaur, Frank J. Farrell, David H. van Thiel, Emmet B. Keeffe, Michael F. Sorrell, Bruce R. Bacon, Frederick L. Weber, Anthony S. Tavill – 1 July 1995 – Cirrhotic patients with hereditary hemochromatosis (HHC) have an increased risk of primary liver cancer (PLC). The purpose of this study was to determine the prevalence of primary liver cancer in patients with HHC undergoing orthotopic liver transplantation (OLT).

Hanns F. Löhr, Wolfgang Weber, Jörg Schlaak, Bernd Goergen, Karl‐Hermann Meyer Zum Büschenfelde, Guido Gerken – 1 July 1995 – To assess the significance of cell‐mediated immunity, T cells were derived from the peripheral blood and liver tissue of hepatitis B virus (HBV)‐infected patients and controls.

Hau‐Tim Chung, Ching‐Lung Lai, Anna S. F. Lok – 1 July 1995 – This study was conducted to determine the rate of detection of serum hepatitis B virus (HBV) DNA in hepatitis B surface antigen (HBsAg)‐negative decompensated cirrhotic patients who had hepatitis B core and/or surface antibodies (anti‐HBc and/or anti‐HBs), and to compare the outcome of HBsAg‐positive cirrhotic patients who did or did not clear HBsAg during follow‐up. Six (5%) of 121 HBsAg‐positive cirrhotic patients lost HBsAg after 0.2 to 17.1 years (mean, 9.1 ± 6.2 yr) of follow‐up.