Hitoshi Kondo, Kainosuke Saito, Joseph P. Grasso, Philip Aisen – 1 January 1988 – Like the peritoneal macrophage, the isolated Kupffer cell is capable of processing and releasing iron acquired by phagocytosis of immunosensitized homologous red blood cells. When erythrophagocytosis is restrained to levels which do not affect cell viability, or less than 1.5 red cells/macrophage (phagocytic index of 150%), over 40% of iron acquired from red cells is released within 24 hr. More active erythrophagocytosis results in greater release of iron but progressive deterioration in cell viability.

Kei Miyamoto, Samuel W. French – 1 January 1988 – Rats fed a diet high in fat and low in protein continuously infused by intragastric cannula were given ethanol for 2 to 6 months in order to examine the response of liver adenine nucleotides to changes in systemic PO2. Hepatic adenine nucleotides were measured in vivo monthly using liver obtained by biopsy from rats while a high blood alcohol level was maintained. Ethanol decreased hepatic ATP and the total adenylate pool, but did not change the levels of ADP and AMP. Adenylate energy charge showed only a tendency to be decreased.

Peter J. Kniskern, Arpi Hagopian, Pamela Burke, Nancy Dunn, Emilio A. Emini, William J. Miller, Shigeko Yamazaki, Ronald W. Ellis – 1 January 1988 – The entire surface protein of hepatitis B virus sero‐type ayw containing the preS (preS1+preS2) and S domains has been expressed in the yeast Saccharomyces cerevisiae. Yeast containing a recombinant plasmid utilizing a constitutive promoter did not express this gene successfully due to the toxicity of the protein.

Charles H. Firth – 1 January 1988

Llúcia Titó, Antoni Rimola, Pere Ginès, Josep Llach, Vicente Arroyo, Joan Rodés – 1 January 1988 – We investigated whether spontaneous bacterial peritonitis in cirrhosis is a recurrent process and attempted to identify possible predictors of recurrence in 75 consecutive cirrhotics who had recovered from a first episode of spontaneous bacterial peritonitis between January, 1981 and December, 1984 and who were followed closely throughout their illness (follow‐up period 10 ± 13 months; mean ± S.D.).

Lennox J. Jeffers, Richard A. Dubow, Leslie Zieve, K. Rajender Reddy, Alan S. Livingstone, Sidney Neimark, Manuel Viamonte, Eugene R. Schiff – 1 January 1988 – A 40‐yr‐old man presented with encephalopathy and was found to have hepatocellular carcinoma without cirrhosis. A large vascular hepatic mass was defined by CT scan and angiography; laparoscopy with biopsy confirmed the absence of chronic liver disease. A definitive tissue diagnosis of hepatocellular carcinoma was made at laparotomy; the tumor was unresectable.

Ian R. Wanless – 1 January 1988 – Twenty‐six patients with the clinical and histologic diagnosis of primary biliary cirrhosis were reviewed. Nodular hyperplasia of the liver without fibrous rims, not reported hitherto in patients with primary biliary cirrhosis, was found in several patients with early histological stages. These changes resembled “nodular regenerative hyperplasia of the liver” and were usually present as multicellular thickness in zones 1 and 2 of the hepatic lobules.

M. G. Courtney, D. G. Weir, G. S. A. McDonald, Alain G. Lachaux, Bruno P. Descos, Irene C. Loras‐Duclaux, Michel R. Hermier, G. Fattovich, A. Alberti, G. Realdi, G. Hoffman – 1 January 1988

William G. Rector, John C. Hoefs, Kenneth F. Hossack, Gregory T. Everson – 1 January 1988 – Six of 85 patients (7%) with alcoholic liver disease undergoing transhepatic portal pressure measurement had either stagnant (3 patients) or reversed (3 patients) portal blood flow documented by gentle hand injection of 1 to 2 ml of angiographic contrast. Portal blood flow was uniformly hepatopetal in 24 patients with nonalcoholic liver disease.

Peter Ferenci, Josef Ebner, Christof Zimmermann, Christian Kikuta, Erich Roth, Dieter Häussinger – 1 January 1988 – Sera of patients with hepatic encephalopathy strongly inhibit the specific binding of γ‐aminobutyric acid to synaptic membranes. In a previous study, this inhibition of specific γ‐aminobutyric acid binding was attributed to γ‐aminobutyric acid itself, and it was assumed that serum γ‐aminobutyric acid is increased 5‐ to 30‐fold in patients with hepatic encephalopathy. The findings of that study, however, were not confirmed by other analytical methods.