Roger F. Butterworth, Gilles Pomier Layrargues – 1 March 1990

Marcos Rojking – 1 March 1990 – It has not yet been established whether serum proline and blood lactate levels are increased in alcoholic liver disease. We measured serum proline and blood lactate in controls and in patients with different stages of alcoholic liver disease in the absence of hepatic failure. Samplings were done in both abstinent and drinking alcoholics. Compared to controls, there was a striking increase in serum proline levels in 52 abstinent alcoholics with little or no hepatic fibrosis by histological assessment (0.10 ± 0.01 vs. 0.155 ± 0.008; p < 0.005).

1 March 1990

Sergio H. Gammal, Anthony S. Basile, David Geller, Phil Skolnick, E. Anthony Jones – 1 March 1990 – Behavioral and electrophysiological evidence implicating the GABA‐benzodiazepine receptor complex in the pathogenesis of hepatic encephalopathy was obtained using an improved rat model of hepatic encephalopathy caused by thioacetamide‐induced fulminant hepatic failure. After the administration of thioacetamide together with supportive therapy, acute hepatocellular failure developed in rats as a result of massive hepatocellular necrosis without evidence of renal failure or hypoglycemia.

Prakash N. Rao, Thomas R. Walsh, Leonard Makowka, Randy S. Rubin, Thomas Weber, James T. Snyder, Thomas E. Starzl – 1 February 1990 – The effect of ischemia and reperfusion on purine nucleoside phosphorylase was studied in an isolated perfused rat liver model. This enzyme is localized primarily in the cytoplasm of the endothelial and Kupffer cells; some activity is associated with the parenchymal cells. Levels of this enzyme accurately predicted the extent of ischemia and reperfusion damage to the microvascular endothelial cell of the liver.

Ramesh A. Bhat, Paul P. Ulrich, Girish N. Vyas – 1 February 1990 – Based on the diversity of nucleotide sequences of cloned hepatitis B virus DNA genomes, we have predicted possible replication of genetic variants of human hepatitis B virus. This prediction is exemplified by studies of a chronic carrier of HBsAg/adw2, who lacked anti‐HBc but carried exceedingly high levels of hepatitis B virus DNA in serum.

Masaki Matsuoka, Martin Y. Zhang, Hidekazu Tsukamoto – 1 February 1990 – A high‐fat diet has previously been shown to be a key factor for induction of alcoholic liver fibrosis in a rat model of intragastric ethanol infusion. To explore a possible mechanism by which the high‐fat diet facilitated such an effect, the present study examined how the high‐fat diet with or without ethanol affected proliferation and collagen formation of hepatic lipocytes, perisinusoidal cells that have been suggested to be involved in liver fibrogenesis.

Fernando Corrales, Carmen Cabrero, Maria A. Pajares, Pablo Ortiz, Antonio Martin‐Duce, Jose M. Mato – 1 February 1990 – Catalytically active human and rat liver S‐adenosylmethionine synthetase exists mainly in tetramer and dimer form. In liver biopsy samples from cirrhotic patients a marked reduction in total S‐adenosylmethionine synthetase activity and a specific loss of the tetrameric form of the enzyme exist. We have investigated the possible role of sulfhydryl groups in maintaining the structure and activity of S‐adenosylmethionine synthetase.

Arie J. Zuckerman – 1 February 1990 – A random‐primed complementary DNA library was constructed from plasma containing the uncharacterized non‐A, non‐B hepatitis (NANBH) agent and screened with serum from a patient diagnosed with NANBH. A complementary DNA clone was isolated that was shown to encode an antigen associated specifically with NANBH infections. This clone is not derived from host DNA but from an RNA molecule present in NANBH infections that consists of at least 10,000 nucleotides and that is positive‐stranded with respect to the encoded NANBH antigen.

Shashi Kumar, Rudolf E. Stauber, Judith S. Gavaler, Michael H. Basista, Vincents J. Dindzans, Robert R. Schade, Mordechai Rabinovitz, Ralph E. Tarter, Robert Gordon, Thomas E. Starzl, David H. Van Thiel – 1 February 1990 – Alcohol abuse is the most common cause of end‐stage liver disease in the United States, but many transplant centers are unwilling to accept alcoholic patients because of their supposed potential for recidivism, poor compliance with the required immunosuppression regimen and resulting failure of the allograft.