J G DeLamatre, J T Schilleci, L H Hanson – 1 September 1996 – This study investigates the effects of either a high‐fat diet or endotoxin on peroxisome metabolism as assessed by measuring catalase activity, catalase mass, and peroxisomal β‐oxidation. Three mouse strains C3H/HeJ, BALB/c, and C57BL/6J were fed either a low‐fat or a high‐fat diet and injected intraperitoneally with 1 microg Escherichia coli lipopolysaccharide. These parameters were not different in C3H/HeJ mice fed a high‐fat diet compared with controls fed a low‐fat diet.

Michael Burt, Elizabeth Jazwinska, Stephen Lynch, Paul Kerlin, Devinder Gill, Charles Steadman, Julie Jonsson, Russell Strong, Elizabeth Powell – 1 September 1996 – The diagnosis of graft‐versus‐host disease following liver transplantation may be delayed because the clinical and pathological features are nonspecific. We report the use of microsatellites to support a diagnosis of GVHD in a patient who developed fever and a skin rash 28 days after liver transplantation.

J Cocjin, P Rosenthal, V Buslon, L Luk, L Barajas, S A Geller, B Ruebner, S French – 1 September 1996 – The cell of origin of intrahepatic bile ducts during fetal development remains a subject of controversy, although there has been recent evidence that they form from hepatocytes. However, the origin of neoductules and ducts in the setting of liver disease has not been extensively investigated in humans.

I Chemin, S Takahashi, C Belloc, M A Lang, K Ando, L G Guidotti, F V Chisari, C P Wild – 1 September 1996 – The objective of this work is to examine the possible modulation of carcinogen metabolism (activation by cytochrome P450s and detoxification by conjugation via glutathione S‐transferases [GST]) in relation to hepatitis B virus (HBV)‐associated liver injury.

Chandrashekhar R. Gandhi, Yoogoo Kang, Andre De Wolf, Juan Madariaga, Shushma Aggarwal, Victor Scott, John Fung – 1 September 1996 – The liver is a major site of synthesis, clearance, and actions of the powerful vasoactive peptide endothelin‐1 (ET‐1).

E Hildt, S Urban, C Eckerskorn, P H Hofschneider – 1 September 1996 – Carboxy‐terminally truncated hepatitis B virus (HBV) middle surface proteins (MHBst) show a transcriptional activator function. Two different subtypes of MHBst activators can be distinguished: an ER‐localized type, represented here by MHBst76 (truncated at amino acid 76), and a cytosol‐localized type, represented here by MHBst63.

M Lindh, P Horal, A P Dhillon, Y Furuta, G Norkrans – 1 September 1996 – Hepatitis B e antigen (HBeAg) is considered to be a major target for the immune response in chronic hepatitis B. The G → A mutation at nucleotide 1896 may mediate viral escape by creating a TAG stop codon in the precore region, thus preventing HBeAg production. This mutation frequently evolves during HBe seroconversion if thymine, but rarely if cytosine, is present in position 1858.

M Sasaki, Y Nakanuma – 1 September 1996 – MUC1 apomucin is proposed as an “oncofetal” antigen in the biliary system. We surveyed the biliary expression of MUC1 apomucin and mature MUC1 mucin (highly‐glycosylated MUC1 apomucin) in hepatic cysts, biliary microhamartomas, and intrahepatic bile ducts in various cystic liver diseases and clarified the relationship between the expression of these mucins and cystogenesis in the liver. The expression of MUC1 apomucin and mature MUC1 mucin were detected immunohistochemically using the monoclonal antibodies DF3 and SM3, and HMFG1, respectively.

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).

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.