Jianye Xu, David Brown, Tim Harrison, Yue Lin, Geoffrey Dusheiko – 1 June 1992 – Precore defective HBV mutants may gradually prevail because of immune selection and explain spontaneous seroconversion from HBeAg to anti‐HBe in HBV carriers. We have analyzed whether the presence of precore HBV mutants is a determinant of responsiveness to interferon‐α therapy. Fifteen carriers (nine responders and six nonresponders)who were treated with interferon‐α were examined. Serum samples were collected before and after therapy.

M. Sawkat Anwer – 1 June 1992 – The Ca2+ signal observed in individual fura‐2‐loaded hepatocytes stimulated with the α1‐adrenergic agonist phenylephrine consisted of a variable latency period, a rapid biphasic increase in the cytosolic free Ca2+, followed by a period of maintained elevated cytosolic Ca2+ (plateau phase) that depended on the continued presence of both agonist and external Ca2+, Microinjection of guanosine‐5′‐O‐(3‐thiophosphate) elicited a Ca2+ transient with the same basic features.

Ji‐Feng Wang, Pavel Komarov, Helmut Sies, Herbert de Groot – 1 June 1992 – Luminol chemiluminescence in phorbolesteractivated cultured rat liver Kupffer cells was strongly inhibited by the selenoorganic compound ebselen (IC50 = 2 μmol/L). Ebselen (2‐phenyl‐1,2‐benzisoselenazol‐3[2H]one) also diminished reduction of ferricytochrome c (IC50 = 10μmol/L), indicating a suppression of superoxide anion formation.

Lidia L. Ignatenko, Guranda D. Mataradze, Victor B. Rozen – 1 June 1992 – The use of a modified, adequate method of quantification of estrogen receptors has permitted us to prove the existence of sex‐specific peculiarities in rat liver estrogen reception and their significance for the realization of sex‐dependent changes in angiotensinogen plasma level after estrogenization. Endocrine mechanisms for the formation of sex‐related differences in hepatic estrogen receptor content in rats were investigated in detail.

Julia A. Wendon, Phillip M. Harrison, Richard Keays, Alexander E. Gimsson, Graeme J. M. Alexander, Roger Williams – 1 June 1992 – Hypotension is a serious complication in patients with fulminant hepatic failure, because it is associated with tissue hypoxia and a further compromise to end‐organ function. In this study we investigated the effects of epinephrine and norepinephrine on hemodynamics and oxygen transport variables in 30 patients with fulminant hepatic failure. All had a mean arterial pressure of less than 60 mm Hg, despite adequate intravascular filling pressures.

Michiko Shindo, Adrian M. di Bisceglie, Jay H. Hoofnagle – 1 June 1992 – We reanalyzed the results of a pilot study of recombinant α‐interferon therapy for chronic non‐A, non‐B hepatitis in light of the recent discovery of the hepatitis C virus and the development of diagnostic assays for this agent. Stored serum samples from 10 patients treated between 1984 and 1986 were tested for antibody to hepatitis C virus and hepatitis C virus RNA before, during and after therapy.

1 June 1992

Antoine Hadengue, Richard Moreau, Christophe Gaudin, Yannick Bacq, Bruno Champigneulle, Didier Lebrec – 1 May 1992 – Although arterial vasodilation is a well‐known feature in patients with cirrhosis, the venous system remains unexplored. To measure total effective vascular compliance, a reflection of the properties of the venous system, rapid volume expansion (300 ml of a gelatin solution in 3 min) was performed in 23 patients. Eleven patients had compensated cirrhosis (Child‐Pugh grade A or B), and eight had decompensated cirrhosis (Child‐Pugh grade C).

Dieter Jüngst, Thomas Lang, Christoph von Ritter, Ekkehard Pratschke, Gustav Paumgartner – 1 May 1992 – Patients with multiple cholesterol gallbladder stones have been found to be at a higher risk for the recurrence of gallstones after successful nonsurgical treatment than those with a solitary stone. Cholesterol gallstone recurrence, like primary gallstone formation, probably involves a triple defect with supersaturation, abnormally rapid nucleation of cholesterol in bile and altered gallbladder motor function.

Piter J. Bosma, Namita Roy Chowdhury, Bart G. Goldhoorn, Martin H. Hofker, Ronald P. J. Oude Elferink, Peter L. M. Jansen, Jayanta Roy Chowdhury – 1 May 1992 – Crigler‐Najjar syndrome, type I is a heterogeneous disorder that may result from mutations of various regions of the bilirubin‐UDP‐glucuronosyltransferase gene complex that encodes two bilirubin‐UDP‐glucuronosyltransferase isoforms and a phenol‐UDP‐glucuronosyltransferase isoform in the human liver.