John T. Galambos – 1 March 1986

Kenichi Kitani – 1 March 1986

Michael M. Thaler – 1 March 1986 – A general impairment of liver mitochondrial enzymes is central to Reye's syndrome (RS). The respiration of isolated liver mitochondria was measured after the addition of concentrated normal serum or RS serum derived from 12 patients. RS serum stimulates oxygen consumption in isolated rat liver mitochondria. This effect is due to (a) the oxidation of uric acid by peroxisomes contaminating the preparation and (b) a stimulation of mitochondrial respiration (1.05 ± 0.14 nmole of O2/ min · mg of protein; control 0.30 ± 0.08 nmole O2/min · mg).

Alan G. Maloney, Douglas L. Schmucker, Donald S. Vessey, Rose K. Wang – 1 March 1986 – Studies were conducted to determine the effects of aging on certain biochemical andbiophysical properties of the hepatic microsomes and on the kinetic properties of a constituent drug‐metabolizing enzyme and a heme protein in a nonhuman primate. Outbred male and female rhesus monkeys (Macaque mulatta) ranging in age from 1 to 25 years were employed as animal models.

I. A. Rajkovic, Roger Williams – 1 March 1986 – Neutrophil functions of phagocytosis and intracellular killing of bacteria were examined in 40 patients with alcoholic cirrhosis of whom 18 had a superimposed acute alcoholic hepatitis. In 65% of these, defective neutrophil phagocytosis was demonstrable, and in 62.5% there was a defect of intracellular killing of either Staphylococcus aureus or Escherichia coli. Studies of the patients' serum failed to reveal inhibitors of neutrophil function.

Francis J. Dudley, Gary C. Kanel, Laurence J. Wood, Telfer B. Reynolds – 1 March 1986 – A urinary sodium concentration [U(Na)] of <10 mmoles per liter is considered important in differentiating hepatorenal syndrome from other causes of progressive renal impairment in patients with liver disease. However, occasionally, patients with hepatorenal syndrome have been recognized in whom the U(Na) is consistently >10 mmoles per liter. Eight such patients, in all of whom there was no clinical or laboratory evidence to implicate other causes of progressive renal impairment, were identified.

Mario Mondelli, Richard S. Tedder, Bridget Ferns, Patrizia Pontisso, Giuseppe Realdi, Alfredo Alberti – 1 March 1986 – Current knowledge on the expression of HBeAg in hepatocytes is incomplete because of difficulties in obtaining monospecific antisera devoid of anti‐HBc reactivity. In this study, we have examined by immunofluorescence the expression of HBcAg and HBeAgin cryostat liver sections from 25 chronic carriers of HBsAg using monoclonal antibodies.

Giovanna Fattovich, Massimo Rugge, Lucio Brollo, Patrizia Pontisso, Franco Noventa, Maria Guido, Alfredo Alberti, Professor Giuseppe Realdi – 1 March 1986 – Seventy consecutive HBsAg‐ and HBeAg‐positive patients with biopsy‐proven chronic hepatitis were followed prospectively with serial determinations of SGPT levels and hepatitis B virus serum markers including HBsAg, HBeAg, anti‐HBeand hepatitis B virus DNA.

Ghanshyam Lohiya, Sunita Lohiya, Vinh Trong Ngo, Ramona Crinella – 1 March 1986 – Screening for HBeAg and anti‐HBe was performed on 133 carriers of HBsAg in aninstitution for the mentally retarded. By radioimmunoassay, the prevalences of HBeAg and anti‐HBe were determined to be 16 and 78%, respectively. HBeAg prevalence was significantly different in the following pairs of carriers: 70% in blacks, 10% in whites, and 35% incarriers with Down's syndrome, 8% in carriers without Down's syndrome.

Howard Rosenblate – 1 March 1986