Frederick K. Askari – 1 June 1995 – Liver injury in PiZZ α1‐antitrypsin (α1‐AT) deficiency probably results from toxic effects of the abnormal α1‐AT molecule accumulating within the ER of liver cells. However, only 12–15% of individuals with this same genotype develops liver disease. Therefore, we predicted that other genetic traits that determine the net intracellular accumulation of the mutant α1‐AT molecule would also determine susceptibility to liver disease.

Bruce A. Runyon, Mauro Borzio, Sharon Young, Susan U. Squier, Carlos Guarner, Michelle A. Runyon – 1 June 1995 – Selective bowel decontamination with the orally administered quinolone antibiotic, norfloxacin, has been shown to suppress gut gram‐negative bacteria and help prevent gram‐negative infections in cirrhotic patients who are at high risk of bacterial infection. Because this drug does not eradicate gram‐positive organisms, it is conceivable that gram‐positives could replace the suppressed gram‐negatives in the gut and lead to subsequent infection.

Dianzhong Luo, Karin Vanderkerken, Luc Bouwens, Peter J. K. Kuppen, Evelyne Crabbé, Eddie Wisse – 1 June 1995 – Pit cells are a unique population of cells in sinusoids and peripheral blood, which can be considered natural killer (NK) cells with large granular lymphocyte (LGL) morphology. The aim of this study was to investigate the use of the monoclonal antibody (MAb) 3.2.3 as a specific marker of rat pit cells to detect their number and distribution in the liver.

Han Roelofsen, Conny T. M. Bakker, Berry Schoemaker, Marc Heijn, Peter L. M. Jansen, Ronald P. J. Oude Elferink – 1 June 1995 – The hepatocanalicular transport of a large number of organic anions, such as bilirubin glucuronides and glutathione conjugates in the rat, is mediated by an adenosine triphosphate (ATP)‐dependent transport system, which is termed canalicular multispecific organic anion transporter (cMOAT). This system is mainly defined by its deficiency in mutant TR− rats.

Maureen S. Thorniley, Sandra Simpkin, Barry Fuller, Mandana Z. Jenabzadeh, Colin J. Green – 1 June 1995 – Ischemia‐reperfusion injury is a major cause of transplant dysfunction. One feature of this damage is mitochondrial dysfunction.

Sabine Angermüller, Marcus Schunk, Klaus Kusterer – 1 June 1995 – In the model of the perfused rat liver, we investigated the alterations of sinusoidal cells in the pathogenesis of liver injury caused by hypoxia and reperfusion. In sinusoidal endothelial cells, the activity of xanthine oxidase (XOX), a cytoplasmic marker enzyme, was located cytochemically and determined biochemically. Kupffer cells, identified by their endogenous peroxidase staining, were studied with regard to changes in their ultrastructure.

Albrecht Guhlmann, Katja Krauss, Franz Oberdorfer, Thilo Siegel, Peter H. Scheuber, Juliane Müller, Brigitte Csuk‐Glänzer, Sibylle Ziegler, Hermann Ostertag, Dietrich Keppler – 1 June 1995 – N‐Acetyl‐leukotriene E4 has been identified as an endogenous, biologically less active cysteinyl leukotriene metabolite in rodents and humans. To evaluate the ratio of hepatobiliary to renal elimination of leukotrienes noninvasively by positron emission tomography (PET), we synthesized N‐[11C]acetyl‐leukotriene E4 by chemical N‐acetylation of leukotriene E4.

Shu Fukushima, Kazuo Honda, Masaaki Awane, Eiji Yamamoto, Ryouji Takeda, Ichiro Kaneko, Akira Tanaka, Taisuke Morimoto, Koichi Tanaka, Yoshio Yamaoka – 1 June 1995 – Using a polymerase chain reaction (PCR) method, we tested for the hepatic mitochondrial DNA (mtDNA) deletion in 40 hepatic tumors (28 hepatocellular carcinomas [HCCs], 9 other malignant tumors, and 3 benign tumors) and in the livers of 71 patients, including 16 pediatric patients with end‐stage liver disease who underwent living related donor liver transplantation and 16 liver donors.

Gloria Taliani, Franca Duca, Rosina Lecce, Donatella Livoli, Caterina Pasquazzi, Carlo De Bac, Andrea Fabbri, Giampaolo P. Bianchi, Guilio Marchesini – 1 June 1995

Christine A. Wanke – 1 June 1995