Inhibition of rat hepatic lipocyte activation in culture by interferon‐γ

Don C. Rockey, Jacquelyn J. Maher, William R. Jarnagin, Giulio Gabbiani, Scott L. Friedman – 1 September 1992 – Hepatic lipocytes (perisinusoidal, Ito cells) are the primary matrix‐producing cells in liver fibrosis. During liver injury they undergo activation, a process characterized by cell proliferation and increased fibrogenesis. We and others have established a culture model in which in vivo features of lipocyte activation can be mimicked by cells grown on plastic.

Ursodeoxycholic acid for treatment of primary sclerosing cholangitis: A placebo‐controlled trial

Ulrich Beuers, Ulrich Spengler, Wolfgang Kruis, ülker Aydemir, Baldur Wiebecke, Walter Heldwein, Marlene Weinzierl, Gerd R. Pape, Tilman Sauerbruch, Gustav Paumgartner – 1 September 1992 – The efficacy and safety of ursodeoxycholic acid for the treatment of primary sclerosing cholangitis were evaluated in a prospective, randomized, double‐blind, placebo‐controlled trial. Fourteen patients with primary sclerosing cholangitis documented by cholestatic serum enzyme pattern, liver histological appearance and endoscopic retrograde cholangiography were included in the trial.

Flow‐limited tracer oxygen distribution in the isolated perfused rat liver: Effects of temperature and hematocrit

Ibrahim Kassissia, Colin P. Rose, Carl A. Goresky, Andreas J. Schwab, Glen G. Bach, Suzette Guirguis – 1 September 1992 – We used the multiple‐indicator dilution technique to examine the kinetics of tracer oxygen distribution and uptake in the rat liver perfused in a nonrecirculating fashion with blood. 51Cr‐labeled 18O2‐saturated erythrocytes, labeled albumin, sucrose and water (the tracers for oxygen and vascular, interstitial and cellular references) were injected simultaneously into the portal vein.

Hepatitis B and C viral infections in patients with hepatocellular carcinoma

Juan Ruiz, Bruno Sangro, José I. Cuende, Oscar Beloqui, JosBé I. Riezu‐Boj, JOSé I. Herrero, Jesús Prieto – 1 September 1992 – The prevalence of hepatitis B and C virus infections was studied in 70 patients diagnosed as having hepatocellular carcinoma. In addition to viral serological markers, serum hepatitis B virus DNA and hepatitis C virus RNA were determined with a nested polymerase chain reaction assay. Twelve patients (17%) were HBsAg positive, 26 (37%) had antibodies to HBs, HBc or both and 32 (46%) were negative for all hepatitis B virus serological markers.

Aflatoxin and hepatocellular carcinoma: A useful paradigm for environmentally induced carcinogenesis

Joseph C. Kolars – 1 September 1992 – Aflatoxin is believed to be a major causative agent in the high incidence of primary liver cancer seen in certain regions of the world. In Fujian Province, an aflatoxin‐endemic region of China, we compared the cigarette smoking habits of 200 primary hepatoma patients with those of 200 matched nonhepatoma controls. We excluded from our study all individuals with evidence of hepatitis B virus serum antigen and/or alcoholic cirrhosis. Interestingly, two groups of hepatoma patients could be discerned.

Cell‐cell interactions: Clues to hepatocyte heterogeneity and beyond?

Jorge J. Gumucio, Rolf Gebhardt – 1 September 1992 – We previously demonstrated that glutamine synthetase (GS) and ornithine aminotransferase (OAT) mRNAs are expressed in the mouse liver acinus preferentially in pericentral hepatocytes, that is, those immediately surrounding terminal central veins (A. L. Bennett, K. E. Paulson, R. E. Miller, and J. E. Darnell, Jr., J. Cell Biol. 105:1073–1085, 1987, and F. C. Kuo, W. L. Hwu, D. Valle, and J. E. Darnell, Jr., Proc. Natl. Acad. Sci. USA, (in press).

Fraternal concordance of types of abnormal hepatocellular mitochondria in Wilson's disease

Irmin Sternlieb – 1 September 1992 – Three distinct patterns of structural abnormalities of mitochondria, indicated as types I, II and III and associated with steatosis, were identified in the hepatocytes of 40 of 42 asymptomatic and 8 of 22 symptomatic patients with documented Wilson's disease before treatment. No correlation was seen between the type of mitochondrial abnormality and the patient's age, hepatic copper concentration, degree of hepatic steatosis or serum aminotransferase level.

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