Gregory J. Gores, S. Breanndan Moore, Lloyd D. Fisher, Frank C. Powell, E. Rolland Dickson – 1 September 1987 – Tissue injury in primary biliary cirrhosis is thought to be mediated by immune mechanisms. Various Class II antigens of the major histocompatibility complex are associated with autoimmune diseases and their differing clinical manifestations. Thus, the aim of this study was to examine the relationship between primary biliary cirrhosis, its clinical manifestations and serologically defined Class II antigens (HLA‐DR and HLA‐DQ).

Michael Manns, Guido Gerken, Apostolos Kyriatsoulis, Christian Trautwein, Konrad Reske, Karl‐Hermann Meyer Zum Büschenfelde – 1 September 1987 – Antimitochondrial antibodies from patients with primary biliary cirrhosis react with different mitochondrial polypeptides as demonstrated by Western blots.

James G. Corasanti – 1 September 1987

Gavino Faa, Carla Liguori, Amedeo Columbano, Giacomo Diaz – 1 September 1987 – The pattern of copper distribution in human newborn liver was investigated by histochemical methods (rhodamine, orcein and rubeanic acid) and by atomic absorption spectroscopy. A significant correlation (p < 0.005) was found between the degree of histochemical positivity and the copper concentration found by atomic absorption spectroscopy.

Hartmut Rieder, Giuliano Ramadori, Hans‐Peter Dienes, Karl‐Hermann Meyer Zum Büschenfelde – 1 September 1987 – Endothelial liver cells were obtained from guinea pig by enzymatic digestion and centrifugal elutriation. Cells were cultured on gelatin and fibronectin pretreated culture vessels. Endothelial cells were characterized by phase‐contrast microscopy, electron microscopy and the presence of Factor VIII‐related antigen. Fibronectin secretion was determined in cell‐free supernatants by a sensitive and specific ELISA and localized on fixed cultured cells by immunofluorescence.

Richard A. Robbins, Rowen K. Zetterman, Todd J. Kendall, Gail L. Gossman, Howard P. Monsour, Stephen I. Rennard – 1 September 1987 – Defective regulation of neutrophil chemotaxis occurs in patients with alcoholic liver disease. One potent mediator of neutrophil chemotaxis is the complement‐derived neutrophil chemoattractant, C5a, which can be inhibited by a serum protein, chemotactic factor inactivator. We hypothesized that chemotactic factor inactivator elevation might, in part, explain the defective neutrophil chemotaxis seen in patients with alcoholic hepatitis.

Antonio Francavilla, Lorenzo Polimeno, David H. Van Thiel, Saturo Todo, Igal Kam, Stephen Lynch, Thomas E. Starzl – 1 September 1987 – Glucose intolerance, hyperinsulinemia, peripheral insulin resistance and hyperglucagonemia are common in patients with advanced liver disease. These abnormalities in the plasma levels of the pancreatic hormones, insulin and glucagon have been thought to be responsible, at least in part, for the abnormal plasma ratio of branched‐chain amino acids to aromatic amino acids.

Gang‐Hong Lee, Tokuichi Kawaguchi, Kimie Nomura, Tomoyuki Kitagawa – 1 September 1987 – Woodchucks free from woodchuck hepatitis virus were treated with diethylnitrosamine in vivo for 2 months, and then hepatocytes obtained by enzymatic perfusion were cultured with the hepatopromoter phenobarbital. This in vivo‐in vitro procedure gave rise to proliferating epithelial cell foci, from one of which the presently described hepatocyte cell line (WLC‐3) was established and characterized.

Thomas H. Maren – 1 September 1987 – 1. In isolated perfused rat liver, urea synthesis is rapid and reversibly inhibited not only by the well‐known carbonic anhydrase inhibitors acetazolamide, methazolamide and ethoxzolamide, but also by diuretics, like xipamide, mefruside, chlortalidone, and chlorothiazide. Furosemide was without effect.

H. C. Thomas, S. A. Jenkins, J. N. Baxter, R. Shields – 1 September 1987