Experimental Mallory body formation is accompanied by modulation of the expression of multidrug‐resistance genes and their products

K Preisegger, C Stumptner, D Riegelnegg, P C Brown, J A Silverman, S S Thorgeirsson, H Denk – 1 July 1996 – Mallory bodies (MBs) are characteristic morphological features of alcoholic hepatitis and are also found in other chronic liver disorders and hepatocellular neoplasms. MBs can be produced in mouse liver by chronic administration of the porphyrinogenic drugs griseofulvin (GF) and 3,5‐diethoxy‐carbonyl‐1,4‐dihydrocollidine (DDC). The mechanisms causing the formation of MBs are poorly understood, and the significance of MB formation during the course of liver disease remains unclear.

The polymeric immunoglobulin receptor is the major calmodulin‐binding protein in an endosome fraction from rat liver enriched in recycling receptors

C Enrich, S Jäckle, R J Havel – 1 July 1996 – Rat liver endosomes contain one major high‐affinity calmodulin‐binding protein (CaMBP) that now has been identified as the polymeric immunoglobulin receptor (pIgR). In isolated endosomes pIgR was enriched in the receptor‐recycling compartment (RRC); lesser enrichment was found in ‘early’ endosome (CURL) and much less in ‘late’ endosome fractions (multivesicular bodies, MVB).

Effects of polyamine imbalance on the induction of stress genes in hepatocarcinoma cells exposed to heat shock

M A Desiderio, L Tacchini, E Anzon, G Pogliaghi, L Radice, A Bernelli‐Zazzera – 1 July 1996 – The expression of hsp70–the inducible member of the corresponding heat shock gene family‐of the oxidative stress marker gene heme oxygenase (HOx), and of the immediate early response genes c‐fos and c‐jun has been studied in FAO hepatocarcinoma cells depleted of polyamines and exposed to heat shock.

Role in nitric oxide in Kupffer cell–mediated hepatoma cell cytotoxicity in vitro and ex vivo

D Fukumura, Y Yonei, I Kurose, H Saito, T Ohishi, H Higuchi, S Miura, S Kato, H Kimura, H Ebinuma, H Ishi – 1 July 1996 – The metabolic change in tumor cells (AH70, a rat hepatoma cell line) cocultured with isolated rat Kupffer cells were visualized and analyzed by a laser scanning confocal imaging system. When AH70 cells were cocultured with Kupffer cells, fluorescence intensity of rhodamine 123 (Rh123) decreased, indicating the reduction of mitochondrial function.

Liver hepatocyte growth factor does not always correlate with hepatocellular proliferation in human liver lesions: Its specific receptor c‐met does

A D'Errico, M Fiorentino, A Ponzetto, Y Daikuhara, H Tsubouchi, C Brechot, J Scoazec, W F Grigioni – 1 July 1996 – Increased levels of expression of hepatocyte growth factor (HGF) and its specific receptor c‐met have been shown in the liver of several benign and malignant pathologies, both in experimental models and humans. We investigated by immunohistochemistry the presence of both HGF and c‐met protoocogene product (c‐met pp) in 20 hepatocellular carcinomas (HCCs), 5 focal nodular hyperplasias (FNHs), 4 cases of fulminant hepatitis (FH), and 1 case of regenerated liver.

Endothelin induced contractility of stellate cells from normal and cirrhotic rat liver: implications for regulation of portal pressure and resistance

D C Rockey, R A Weisiger – 1 July 1996 – Hepatic stellate cells are similar to tissue pericytes and have been shown to be contractile. In this study, we examined the effects of known mediators of stellate cell contraction on portal pressure in rat livers after carbon tetrachloride induced injury (including cirrhosis) and investigated the contractility of stellate cells as a function of liver injury.

Glycohydrolases as markers of hepatic ischemia‐reperfusion injury and recovery

W Liu, O Schöb, J E Pugmire, D Jackson, K A Zucker, D E Fry, R H Glew – 1 July 1996 – Advances in liver surgery and transplantation have lead to a steady increase in the number of these interventions. Prompt quantitative assessment of hepatic of hepatic function and a patient's subsequent morbidity and mortality following surgery remain difficult despite the currently utilized historic markers of hepatic parenchymal injury (e.g., aspartate transaminase [AST], lactate dehydrogenase [LDH] γ‐glutamyl transpeptidase [GGT]).

Variable gene expression within human tyrosinemia type 1 liver may reflect region‐specific dysplasia

B A Haber, E Chuang, W Lee, R Taub – 1 July 1996 – Patients with hereditary tyrosinemia type 1 have a deficiency of fumarylacetoacetate hydrolase (FAH) and develop progressive hepatocellular dysfunction with a high risk of malignant transformation. Serum alpha‐fetoprotein levels are frequently elevated in these patients; therefore, this commonly used marker of tumorigenesis is inadequate. To date, no literature exists describing the hepatic gene alterations in patients with this disease.

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