Alexander E. S. Gimson, John O'Grady, Roland J. Ede, Bernard Portmann, Roger Williams – 1 March 1986 – The clinical, laboratory and histological features of 47 patients with what is defined as late onset hepatic failure are reviewed. Twenty‐five of the patients werefemale and 22 male with a median age of 45 years. Hepatic dysfunction was severe as evidenced by the prolongation of prothrombin time (median = 32 sec, range = 17 to 120 sec).

B. Leggett, R. Collins, R. Prentice, L. W. Powell, Lawrence E. Gurian, Thomas M. Rogoff, Athol J. Ware, Burton Combes – 1 March 1986

Reginald G. Hanson, Marion G. Peters, Jay H. Hoofnagle – 1 March 1986 – B and T lymphocyte function was studied in 10 patients with chronic type B hepatitis before, during and after a 28‐day course of prednisolone therapy. Lymphocyte function was assessed by measuring the in vitro synthesis of immunoglobulin by peripheral blood mononuclear cells stimulated with pokeweed mitogen and by assaying lymphocyte proliferation in response to B and T cell mitogens.

Richard A. Weisiger, Denis J. Morgan, D. Brian Jones, Michael S. Ching, Richard A. Smallwood – 1 March 1986

Marsha Y. Morgan – 1 March 1986

Richard B. Sewell, Catherine Dillon, Susan Grinpukel, Neville D. Yeomans, Richard A. Smallwood – 1 March 1986 – Lysosomes constitute a small proportion of hepatocyte volume, but they play a key degradative role, particularly during catabolic states such as nutritional deprivation. Our preliminary observations in hepatocytes suggested that fasting may alter the distribution of lysosomes, which are thought to congregate about the biliary canaliculus.

Lorenz Theilmann, Mo‐Quen Klinkert, Karl Gmelin, Jochen Salfeld, Heinz Schaller, Eberhard Pfaff – 1 March 1986 – The presence of pre‐S1 proteins in serum and liver of individuals with acuteand chronic hepatitis B virus infection was investigated in Western blots using antibodies against a fusion protein, containing amino acids 20—120 of the pre‐S region. Pre‐S1 proteins were present in 20 of 38 HBsAg‐positive sera.

Harold O. Conn, L. Siw Eriksson – 1 March 1986 – Elevated plasma ammonia level in hepatic cirrhosis has been attributed to a lack ofconversion of enteric ammonia into urea or to its entry into systemic circulation via portasystemic shunting, or to both. It is exaggerated by excessive protein intake. Because hyperglucagonemia is well documented in cirrhosis and a protein meal is an effective glucagon secretogogue, plasma glucose, insulin, glucagon, and ammonia levels were determined in 50 cirrhotic patients after an overnight fast.

Teri J. Mauch, Terrence M. Donohue, Rowen K. Zetterman, Michael F. Sorrell, Dean J. Tuma – 1 March 1986 – Hepatic ethanol metabolism generates the reactive intermediate, acetaldehyde, whichbinds to proteins. The binding of acetaldehyde to purified enzymes was determined in order to ascertain whether such binding altered their catalytic functions. [14C]Acetaldehyde was incubated with alcohol dehydrogenase, glucose‐6‐phosphate dehydrogenase, lactate dehydrogenase and RNase A, each at 37°C(pH 7.4).

Giovambattista Pinzello, Roberto Virdone, Francesca Lojacono, Maddalena Ciambra, Gabriella Dardanoni, Germana Fiorentino, Loredana Riccobono, Luigi Pagliaro – 1 March 1986 – Ascitic fluid pH and arterial‐ascitic fluid pH gradient were compared to ascitic fluid polymorphonuclear cell count in 84 patients with cirrhotic ascites and in 12 with malignant ascites to assess their role as diagnostic tests for spontaneous bacterial peritonitis and to clarify the relationship between ascitic fluid pH and lactate.