Mortality follow‐up of the 1942 epidemic of hepatitis B in the U.S. Army

James E. Norman, Gilbert W. Beebe, Jay H. Hoofnagle, Leonard B. Seeff – 1 October 1993 – The hypothesis that adult infection with the hepatitis B virus in the United States leads to a carrier state with a high risk of primary liver cancer was tested in two ways: (a) a cohort mortality study of U.S. Army veterans given yellow fever vaccine contaminated with hepatitis B virus in 1942 and controls and (b) a case‐control study comparing veterans with hepatocellular carcinoma in Veterans Affairs hospitals with matched controls with respect to receipt of contaminated vaccine in 1942.

Deletion of the E‐cadherin gene in hepatitis B virus–positive chinese hepatocellular carcinomas

Betty L. Slagle, Yi‐Zhong Zhou, Walter Birchmeier, Kathleen A. Scorsone – 1 October 1993 – Frequent allele loss from chromosome 16q was recently described for human tumors of the breast, prostate gland and liver, indicating the possible presence of a tumor‐suppressor gene on that chromosome arm. In this study, the chromosome 16 allele status of 38 hepatocellular carcinomas in Chinese patients was determined with restriction‐fragmentlength polymorphism analysis.

Contribution of sinusoidal endothelial liver cells to liver fibrosis: Expression of transforming growth factor‐β1 receptors and modulation of plasmin‐generating enzymes by transforming growth factor‐β1

Hartmut Rieder, Thomas Armbrust, Karl‐Hermann Meyer zum Büschenfelde, Giuliano Ramadori – 1 October 1993 – Transforming growth factor‐βH1 is an important cytokine in the pathophysiology of liver fibrosis, stimulating the production of extracellular matrix. Whether this cytokine can also control the degradation of matrix proteins in liver cells has not been investigated.

Halothane hepatitis patients have serum antibodies that react with protein disulfide isomerase

Jackie L. Martin, J. Gerald Kenna, Brian M. Martin, David Thomassen, George F. Reed, Lance R. Pohl – 1 October 1993 – Clinical and laboratory evidence suggests that the fulminant liver failure sometimes associated with the inhalation anesthetic halothane may be an immunemediated toxicity. Most importantly, the vast majority of patients with a clinical diagnosis of halothane hepatitis have serum antibodies, which react with one or more specific liver microsomal proteins that have been covalently altered by the trifluoroacetyl chloride metabolite of halothane.

Fatal neonatal liver failure and mitochondrial cytopathy (oxidative phosphorylation deficiency): A light and electron microscopic study of the liver

Paulette Bioulac‐Sage, Françoise Parrot‐Roulaud, Jean Pierre Mazat, Thierry Lamireau, Michelle Coquet, Boris Sandler, Jean Louis Demarquez, Valérie Cormier, Arnold Munnich, Mireille Carré, Charles Balabaud – 1 October 1993 – Mitochondrial cytopathies are multisystemic disorders of extremely variable expression due to a deficiency in oxidative phosphorylation. Cases have recently been reported in which fatal liver failure with neonatal onset was the major clinical and biochemical syndrome.

The activity of the metabolic form of hepatic phosphatidate phosphohydrolase correlates with the severity of alcoholic fatty liver in human beings

Christopher P. Day, Oliver F. W. James, Ashley St. J. M. Brown, Mark K. Bennett, Ian N. Fleming, Stephen J. Yeaman – 1 October 1993 – Increased esterification of fatty acids to triglyceride is common to most of the mechanisms proposed to explain the causation of alcoholic fatty liver. However, it is unclear whether this is caused by increased substrate supply or whether direct stimulation of the enzymes of the esterification pathway occurs after excessive alcohol intake.

The effect of ethanol on one‐carbon metabolism: Increased methionine catabolism and lipotrope methyl‐group wastage

Kenneth C. Trimble, Anne M. Molloy, John M. Scot, Donald G. Weir – 1 October 1993 – Deficiency of choline and methionine produces hepatic steatosis similar to that seen with ethanol, and supplementation with these lipotropes can prevent ethanol‐induced fatty liver. These effects are thought to occur through alterations in membrane phospholipid metabolism, but the mechanism whereby this occurs and the precise nature of the changes brought about by ethanol in the interactions of choline and methionine metabolism remain unclear.

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