Z Spolarics, D S Stein, Z C Garcia – 1 September 1996 – The study aimed to assess the effect of lipopolysaccharide (LPS) in vivo (from Escherichia coli, 2 mg/kg body weight intraperitoneally) on the production and elimination of hydrogen peroxide (H2O2) in rat hepatic endothelial and Kupffer cells. Twenty‐two hours after the injection of LPS, hepatic cells were isolated by collagenase and pronase digestion followed by centrifugal elutriation, and cell‐ associated H2O2 was determined by flow cytometry analysis using 2′,7′‐ dichloroflorescin diacetate (DCF‐diacetate).

C Hellerbrand, S C Wang, H Tsukamoto, D A Brenner, R A Rippe – 1 September 1996 – The hepatic stellate cell (HSC), following a fibrogenic stimulus, is transformed from a quiescent to an activated cell. HSC activation results in numerous changes in cellular morphology, cellular metabolism, and in the pattern of gene expression. Many of the changes that are observed in activated HSCs in animal models of hepatic fibrosis are also seen when these cells are activated by culturing on plastic.

J Inadomi, J P Cello, J Koch – 1 September 1996 – The purpose of this study was to develop a method by which ascitic volume can be calculated using transcorporeal ultrasonography, and to determine the accuracy of this method by comparison with the volume of distribution of a radiolabeled tracer (indicator dilution technique [IDT]). Subjects with ascites confirmed by ultrasonography were recruited from the San Francisco General Hospital Gastroenterology and Liver Clinics.

K R Huber, C Sebesta, K Bauer – 1 September 1996 – The causal agent of most posttransfusion non‐A and non‐B hepatitis infections was characterized in 1989 by molecular biological techniques as a positive‐stranded, enveloped RNA virus, designated hepatitis C virus (HCV). Only since 1990 has it been possible to screen for an infection with antibody tests or direct amplification assays for the nucleic acid (i.e., reverse‐transcription polymerase chain reaction [PCR]). However, these nucleic acid based tests are time consuming and rather expensive.

Erck B. Edwards, William P. Boyd – 1 September 1996

Fin Stolze Larsen, Ellen Ejlersen, Jens Otto Clemmesen, Preben Kirkegaard, Bent Adel Hansen – 1 September 1996 – Under normal conditions cerebral blood flow (CBF) is regulated to secure oxidative brain metabolism, but in patients with fulminant hepatic failure (FHF), insufficient CBF has been suggested to precede cerebral edema and intracranial hypertension. In order to determine if insufficient CBF and hypoxia are present in patients with FHF we increased the mean arterial pressure and measured cerebral metabolism.

1 September 1996

G M Thiele, J A Miller, L W Klassen, D J Tuma – 1 September 1996 – Previous reports have shown that long‐term ethanol administration alters receptor‐mediated endocytosis (RME) of a variety of macromolecules by liver endothelial cells (LEC). Acetaldehyde is the major metabolic product of ethanol metabolism and has been shown to bind to proteins to form adducts. In this study, the level of protein modification by acetaldehyde necessary for the uptake and degradation of acetaldehyde‐modified proteins by LEC was investigated.

Q X Yuan, N Marceau, B A French, P Fu, S W French – 1 September 1996 – The aim of this study was to determine the various factors that are involved in the induction of Mallory body (MB) formation. A model was developed where MB formation was induced by refeeding either of the drugs griseofulvin or diethyl 1,4‐dihydro‐1,4,6‐trimethyl‐3,5‐ pyridinedicarboxylate (DDC). Mice were fed the drugs for 5 months, followed by withdrawal of the drugs for 1 month (drug‐primed livers). The drugs were refed for 1,3,5,7, or 11 days.

L S Miller, T D Schiano, A Adrain, M Cassidy, J Liu, H Ter, S V Bellary, M A Dabezies, M Black – 1 September 1996 – High‐resolution endoluminal sonography (HRES) was used to image and measure esophageal varices in control subjects and patients with portal hypertension and compared with endoscopic findings. Nine control patients and 68 patients with known cirrhosis or noncirrhotic portal hypertension underwent videotaped HRES and videotaped esophagoscopy (EGD).