Imad Abou Hashieh, Lionel Rémy, Sylvie Mathieu, André Gérolami – 1 July 1989 – A kinetic study of horseradish peroxidase transport was carried out on short‐term cultured adult rat hepatocytes. After 4 hr of plating, cells were preincubated with monensin (1 μM) for 1 hr before their incubation with horseradish peroxidase for different times. Monensin treatment resulted in the dilatation of the Golgi apparatus and caused the appearance of numerous intracellular lumina lined with microvilli in associated as well as isolated hepatocytes but did not modify newly formed bile canaliculi.

Sugantha Govindarajan, Sanjeev Gupta, Boontar Valinluck, Allan G. Redeker – 1 July 1989 – One hundred forty‐four serum samples from 52 patients with chronic hepatitis D virus infection were analyzed for hepatitis D virus RNA by dot‐blot hybridization using hepatitis D virus cDNA probe labeled with 32p. The results were correlated with the presence of serum IgM anti‐hepatitis D virus and hepatitis D antigen in liver biopsy specimens when available.

Shuhei Nishiguchi, Tetsuo Kuroki, Shuzo Otani, Tadashi Takeda, Satoshi Hirota, Yutaka Shimizu, Shinya Nakajima, Shinobu Saito, Susumu Shiomi, Kenzo Kobayashi – 1 July 1989 – Two years or more after 35 patients (29 men and six women) with chronic hepatitis B were treated by interferon, we studied relationships of age, ALT activity, activity of serum DNA polymerase associated with the hepatitis B virus, serum levels of hepatitis B e antigen and activity of 2′, 5′‐oligoadenylate synthetase in peripheral blood mononuclear cells when treatment started in comparison with treatment results.

Basil Rigas – 1 July 1989 – Amiodarone is believed to have caused acute hepatitis 24 hours after intravenous administration in two patients in whom no other alternative cause of hepatitis was found.

Charles L. Witte, Marlys H. Witte – 1 July 1989 – Plasma immunoreactive alpha‐human atrial natriuretic peptide (ANP) was measured in six cirrhotic patients with massive refractory ascites, under strict metabolic conditions, while they were receiving a 20‐meq sodium diet, both before and at two‐hour intervals for eight hours following peritoneovenous shunting (PVS). The mean preoperative level of ANP was 75±18pg/ml, which was found to be significantly higher than the normal range for this laboratory *8 to 24pg/ml) (p<0.05).

Justine Meehan Carr – 1 July 1989 – Hemorrhagic sequelae of liver disease were recognized and described over a century ago (1). Bleeding has been a common complication and a leading cause of death in patients with cirrhosis (2, 3). The coincidence of low clotting factor levels, hypofibrinogenemia and thrombo‐cytopenia has prompted many investigators to ask whether disseminated intravascular coagulation (DIC) plays a role in the pathogenesis of hemorrhage in these patients (4–16).

Caroline A. Riely – 1 July 1989

Wilfried Bursch, Hendryk S. Taper, Marie P. Somer, Stefan Meyer, Barbara Putz, Rolf Schulte‐Hermann – 1 June 1989 – In the present study, it was investigated whether the prostacyclin derivative Iloprost would protect hepatocytes against CCl4‐induced liver injury and which mechanism(s) of hepatocellular pathogenesis might be affected by it. Rats were treated with a single oral dose of CC14 (2 ml per kg); Iloprost was infused continuously from 2 to 4 hr before intoxication until killing. The following results were obtained.

Olivier Chazouillères, François Ballet, Yves Chrétien, Philippe Marteau, Colette Rey, Dominique Maillard, Raoul Poupon – 1 June 1989 – The effects of two vasodilators, papaverine and pentoxifylline (a methylxanthine derivative), on liver function after 19 hr hypothermic preservation were investigated. Hypothermic preservation was performed according to the standard technique, and liver hemodynamics and function were studied during 70 min immediately after reperfusion in an isolated perfused rat liver system. No significant changes occurred after hypothermic storage for 5 hr.

Richard A. Galbraith, Attallah Kappas – 1 June 1989 – Tin‐mesoporphyrin shares many of the properties of its parent compound, tin‐protoporphyrin. These include competitive inhibition of heme oxygenase, amelioration of jaundice and suppression of chemically induced hepatic porphyria. Tin‐mesoporphyrin is cleared from the plasma of normal subjects with dose‐dependent pharmacokinetics (T1/2 = 3.8 hr following i.v. administration of 1 μmole per kg body weight), and small amounts (<1% of administered dose) are excreted into the urine and feces.