J Sastre, F V Pallardó, R Plá, A Pellín, G Juan, J E O'Connor, J M Estrela, J Miquel, J Viña – 1 November 1996 – Mitochondrial damage may be a major cause of cellular aging. So far, this hypothesis had only been tested using isolated mitochondria. The aim of this study was to investigate the involvement of mitochondria in aging using whole liver cells and not isolated mitochondria only.
I Wéry, M Kaouass, P Deloyer, J Buts, H Barbason, G Dandrifosse – 1 November 1996 – In the present study, we investigated the effects of spermine on postnatal liver maturation in suckling rats. The animals were given spermine either per os (8 μmol) or by intraperitoneal injection (1 μmol), once daily for three or five days. The percentage of liver cells in different cell cycle phases and of diploid cells in the parenchyma was estimated.
A A Demetriou – 1 November 1996
Gian Luca Grazi, Alighieri Mazziotti, Claudia Sama, Elio Jovine, Francesco Stefanini, Rolando Paladini, Roberto Rossi, Antonino Cavallari – 1 November 1996 – The presence of a positive hepatitis B surface antigen (HBsAg) has been considered a highly questionable indication for orthotopic liver transplantation. We report our experience in the treatment of HBsAg‐positive HBV‐DNA—negative cirrhotics with liver transplantation, whether or not followed by passive prophylaxis with specific immunoglobulins.
J Napoli, G A Bishop, P H McGuinness, D M Painter, G W McCaughan – 1 October 1996 – An imbalance between T helper cell (Th)1 and Th2‐like cytokines has been described in several chronic infectious diseases. We therefore analyzed the intrahepatic messenger RNA (mRNA) expression of Th1‐like (interleukin [IL]‐2, interferon [IFN]‐gamma) and Th2‐like (IL‐4, IL‐10) cytokines in chronic hepatitis C patients (n = 17) and controls (n = 6) and correlated the results with liver histology and intrahepatic viral load.
I P Hällström, D Liao, Y Assefaw‐Redda, L C Ohlson, L Sahlin, P Eneroth, L Eriksson, J Gustafsson, A Blanck – 1 October 1996 – Synthetic estrogens act as tumor promoters in rat liver. Because estrogen treatment markedly increases the secretion of pituitary prolactin, also shown to be a tumor promoter in rat liver, the possibility of a pituitary influence in estrogen promotion was investigated in Wistar rats.
T Kimura, K Suzuki, S Inada, A Hayashi, M Isobe, Y Matsuzaki, N Tanaka, T Osuga, M Fujiwara – 1 October 1996 – Interaction between intercellular adhesion molecule 1 (ICAM‐1) and lymphocyte function‐associated antigen 1 (LFA‐1) might be involved in the pathogenesis of liver diseases. We investigated whether monoclonal antibodies (mAbs) against these two adhesion molecules could inhibit the formation of primary biliary cirrhosis (PBC)‐like lesions in an animal model using graft‐versus‐host reaction (GVHR) with major histocompatibility complex class II disparity.
R Mastai, S Laganiere, I R Wanless, L Giroux, B Rocheleau, P Huet – 1 October 1996 – We assessed hepatic functions and systemic and splanchnic hemodynamics in a new model of hepatic sinusoidal fibrosis. Fibrosis was induced by the simultaneous administration for 8 weeks of diethyl‐stilbestrol (DES) (10 mg twice weekly, subcutaneously) and cholesterol‐supplemented diet (1%) in rabbits.
L Krahenbuhl, C Talos, J Reichen, S Krahenbuhl – 1 October 1996 – Liver and skeletal muscle glycogen metabolism were investigated in rats 1 and 4 weeks after bile duct ligation (BDL) and in pair‐fed, sham‐ operated control rats. Livers were subjected to morphometric analysis to express glycogen content and enzyme activities per mL hepatocytes. One week after BDL, the hepatic glycogen content was 28.8 ± 13.8 versus 38.6 ± 16.4 mg/mL hepatocyte in BDL and control rats, respectively. Total activity of glycogen synthase (50.2 ± 7.0 vs.
M G Swain, M Maric – 1 October 1996 – Both interleukin (IL)‐1β and psychological stress activate the hypothalamic‐pituitary‐adrenal (HPA) axis by stimulating neuronal activity within the paraventricular nucleus of the hypothalamus via different pathways. Because it has been shown previously that cholestatic rats show defective cytokine‐and stress‐induced HPA axis activation, neuronal activation in the paraventricular nucleus of rats with cholestasis caused by bile duct resection and in noncholestatic sham‐resected (sham) controls was examined.