Cornel C. Sieber – 1 November 1995 – Background/Aims: Because the vasodilator nitric oxide is overproduced in cirrhosis, this substance may decrease pressor responses to the vasoconstrictor endothelin 1. This study aimed to examine the effects of a NO synthesis inhibitor (NG‐nitro‐L‐arginine methyl ester; L‐NAME) on vascular responsiveness to endothelin 1 in normal and cirrhotic rats. Methods: Pressor dose‐response curves to endothelin 1 (0.5, 1, 3, 6, and 10 μg/kg intravenously) were obtained in animals with or without pretreatment with L‐NAME.

Philip Rosenthal, Luis Podesta, Robert Grier, Jonathan W. Said, Linda Sher, Jose Cocjin, Frederick Watanabe, Eric Vasiliauskas, Robert Van De Velde, Leonard Makowka – 1 November 1995 – Orthotopic liver transplantation has been used to treat glycogen storage disease type IV. Most long‐term surviving patients who have undergone liver transplantation have been free of neuromuscular and cardiac morbidity, and regression of cardiac amylopectin infiltration has been reported after liver transplantation. Leukocyte inclusions in glycogen storage disease type IV have also been reported.

David H. van Thiel – 1 November 1995

Shinichi Kiso, Sumio Kawata, Shinji Tamura, Shigeki Higashiyama, Nobuyuki Ito, Hirofumi Tsushima, Naoyuki Taniguchi, Yuji Matsuzawa – 1 November 1995 – Several growth factors including hepatocyte growth factor (HGF) have been implicated in the regulation of liver regeneration. Recently, we reported that heparinbinding epidermal growth factor (EGF)‐like growth factor (HB‐EGF) has hepatotrophic effects in vitro. We investigated the role of HB‐EGF as a hepatotrophic factor in regenerating rat liver after 70% partial hepatectomy.

Koichi Tsuneyama, Judy van de Water, David van Thiel, Ross Coppel, Boris Ruebner, Yasuni Nakanuma, E. Rolland Dickson, M. Eric Gershwin – 1 November 1995 – The presence of antimitochondrial antibodies (AMA) is a major criterion for the diagnosis of primary biliary cirrhosis (PBC). Although it is not clear that AMA are involved in the pathogenesis of the disease, the study of these autoantibodies has enabled much information to be accumulated about the specificity of this response.

Giovanna Fattovich, Graham McIntyre, Mark Thursz, Kathryn Colman, Giustina Giuliano, Alfredo Alberti, Howard C. Thomas, William F. Carman – 1 November 1995 – Precore/core genes from hepatitis B e antigen (HBeAg)‐positive and antibody to HBeAg (anti‐HBe) positive individuals with active hepatitis have been analyzed to search for correlations with response to interferon before and after treatment. Pretreatment, no precore stop codon mutants were detected, even at the 3% level, in HBeAg‐positive responders or nonresponders.

Mohammed Al Edreesi, Gilles Caillé, Claire Dupuis, Yves Théoret, Khazal Paradis – 1 November 1995 – Thirty‐two children who had undergone liver transplantation were paired according to their post‐transplantation duration, renal function, and diagnoses when possible and randomized either to continue nifedipine (NIF group) or switch to diltiazem (DIL group), in addition to continuing their usual immunosuppressive medications.

Micheal D. Apstein – 1 November 1995

Joseph Wagstaff, Maureen M. Jonas – 1 November 1995 – It is now feasible to map disease genes by screening the genome for linkage disequilibrium between the disease and marker alleles. This report presents the first application of this approach for a previously unmapped locus. A gene for benign recurrent intrahepatic cholestasis (BRIC) was mapped to chromosome 18 by searching for chromosome segments shared by only three distantly related patients. The screening results were confirmed by identifying an extended haplotype conserved between the patients.

Thomas S. Helling, Brent M. Wogahn, Steve A. Olson, Laurie S. Evans, Bokka R. Reddy, Charles Vanway – 1 November 1995 – The liver has been judged relatively resistant to ischemia, but prolonged inflow occlusion at normothermic conditions can produce evidence of reversible or irreversible hepatocellular damage. Cytoprotective agents have been used both experimentally and clinically to afford extended viability of hepatocytes under reduced perfusion. One agent, prostaglandin E1, has been described clinically as effective in sustaining liver function under ischemic conditions.