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.

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.

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.

Marsha Y. Morgan – 1 March 1986

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

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

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).

Shou‐Dong Lee, Jaw‐Ching Wu, Jiin‐Yu Wang, Yang‐Te Tsai, Kwang‐Juei Lo, Benjamin N. Chiang – 1 March 1986

Lawrence Lumeng – 1 March 1986 – Markedly increased circulating concentrations of pyridoxal‐5′‐phosphate (PLP) were found in each of 14 patients representing all clinical forms of hypophosphatasia, an inborn error characterized by deficient activity of the tissue‐nonspecific (bone/liver/kidney) isoenzyme of alkaline phosphatase (AP). The mean PLP concentration in plasma was 1,174 nM (range, 214 to 3,839 nM) in the patients and 57 ± 26 nM (mean ± S.D.) in 38 control subjects.