Stefan Post, Alberto P. Gonzalez, Pablo Palma, Markus Rentsch, Adolf Stiehl, Michael D. Menger – 1 September 1992 – Phagocytic activity of sinusoidal lining cells was studied in 32 livers of male Lewis rats by in vivo fluorescence microscopy with epiillumination. Normal livers (group 1, n = 8) were compared with orthotopic syngeneic liver grafts 90 min after reperfusion after a period of cold storage in University of Wisconsin solution for 17 hr (group 2, n = 10) or 24 hr (group 3. n = 14).

Seon‐Kyeong Kim, Folkert O. Belzer, James H. Southard – 1 September 1992 – Preservation of the liver involves a period of cold (0° to 4°C) ischemia; the longer the ischemic period, the greater the injury to the liver. The mechanisms for cold‐induced ischemic injury are not known, but it is clear that after preservation the liver has a reduced capacity to regenerate high‐energy phosphate compounds (ATP). One cause for the delayed rate of ATP synthesis could be injury to the mitochondria.

Keith S. Henley, Michael R. Lucey, Henry D. Appelman, Prabhakar Baliga, Kimberly A. Brown, Gordon D. Burtch, Darrell A. Campbell, John M. Ham, Robert M. Merion, Jeremiah G. Turcotte – 1 September 1992 – It is not known whether the histopathology of the liver allograft can be predicted from biochemical measurements in serum with the same confidence as in the native liver.

Stefan Schwögler, Margarete Odenthal, Thomas Knittel, Karl‐Hermann Meyer zum Büschenfelde, Giuliano Ramadori – 1 September 1992 – During liver fibrogenesis, fat‐storing cells transform into myofibroblast‐like cells and produce increasing amounts of extracellular matrix proteins. Because fat‐storing cells produce α2‐macroglobulin, an important serine protease inhibitor (serpin), we investigated whether fat‐storing cells also synthesize C1‐esterase inhibitor, another important serpin.

David H. Adams, Elizabeth Mainolfi, Patrizia Burra, James M. Neuberger, Reuben Ayres, Elwyn Elias, Robert Rothlein – 1 September 1992 – The leucocyte adhesion molecule intercellular adhesion molecule–1 is induced on bile ducts in patients with primary biliary cirrhosis and primary sclerosing cholangitis and may be involved in targeting immune damage to these structures. It has recently been reported that, when activated, in vitro lymphocytes release a soluble form of intercellular adhesion molecule–1 that can also be detected in human serum.

Oliviero Riggio, Manuela Merli, Livio Capocaccia, Massimo Caschera, Angelo Zullo, Giorgio Pinto, Eugenio Gaudio, Antonio Franchitto, Roberta Spagnoli, Elvira D'aquilino, Siro Seri, Renzo Moretti, Alfredo Cantafora – 1 September 1992 – Zinc deficiency is common in cirrhosis and may be involved in the alteration of ammonia metabolism. Rats with carbon tetrachloride–induced cirrhosis have high plasma ammonia and low serum and tissue zinc levels.

Peter W. J. Kowalski‐Saunders, Paul J. Winwood, Michael J. P. Arthur, Ralph Wright – 1 September 1992 – Decreased albumin synthesis by hepatocytes in liver injury is thought to occur in response to Kupffer cell–derived acute‐phase cytokines. In this study we used hepatocytes maintained in a differentiated phenotype, by culture on a laminin‐rich gel substratum (Engelbreth‐Holm‐Swarm matrix), to investigate the effects of Kupffer cell–conditioned medium and purified cytokines (interleukin‐1, interleukin‐6 and tumor necrosis factor–a) on albumin synthesis.

Yvon Calmus, Jerome Guechot, Philippe Podevin, Marie‐Therese Bonnefis, Jacqueline Giboudeau, Raoul Poupon – 1 September 1992 – Cell‐mediated immunity and macrophage activity, especially that of Kupffer cells, are impaired during cholestasis. Some evidence exists that bile acids play a role in these immune defects. The purpose of this study was to evaluate the effects of individual bile acids on immunity and to determine whether monocytes could be a target.

Steven M. Strasberg, Pierre‐Alain Clavien – 1 September 1992

Patrick N. Gilles, Deborah L. Guerrette, Richard J. Ulevitch, Robert D. Schreiber, Francis V. Chisari – 1 September 1992 – The role that inflammatory cytokines may play in the life cycle of the hepatitis B virus and in the pathogenesis of its associated liver disease has not been carefully delineated.