Factors linked to early recurrence of small hepatocellular carcinoma after hepatectomy: Univariate and multivariate analyses

Ken Shirabe, Takashi Kanematsu, Takashi Matsumata, Eisuke Adachi, Kohhei Akazawa, Keizo Sugimachi – 1 November 1991 – The purpose of this study was to clarify the factors linked to recurrence of small hepatocellular carcinomas, up to 3cm in diameter, after hepatectomy. Fifty patients with small hepatocellular carcinomas who underwent hepatectomy between 1976 and 1988 were observed for possible recurrence for at least 2 yr. These patients were divided into two groups: 20 patients who had recurrence within 2 yr and 30 patients who had no recurrence within 2 yr.

Reduced retinoid content in hepatocellular carcinoma with special reference to alcohol consumption

Sadashi Adachi, Hisataka Moriwaki, Yasutoshi Muto, Yasuhiro Yamada, Yasushi Fukutomi, Makoto Shimazaki, Masataka Okuno, Mitsuo Ninomiya – 1 November 1991 – Although alcohol is known to enhance hepatocarcinogenesis, the mechanism of this action remains to be explained. To test the hypothesis that ethanol depletes the liver of antitumor promoters such as retinoid, we measured the retinoid concentration in hepatocellular carcinoma tissues and noncancerous surrounding liver tissues in humans known to have a history of alcohol consumption.

Hepatotoxicity in a rat model caused by orally administered methotrexate

Pauline de la M. Hall, Mark A. Jenner, Michael J. Ahern – 1 November 1991 – We undertook a dose‐response study in Wistar rats to develop an animal model for methotrexate hepatotoxicity. Rats were given oral methotrexate in 300, 200, 150 and 100 m̈g/kg/day doses for variable lengths of time. The 300 m̈g/kg/day dose produced systemic toxicity; the animals needed to be killed early, and hepatotoxicity was not observed.

Isolation and characterization of a novel liver‐derived immunoinhibitory factor

Shie‐Pon Tzung, Katherine C. Gaines, Mark Henderson, Terry J. Smith, Stefan A. Cohen – 1 November 1991 – Cytosolic extracts prepared from perfused whole liver or purified hepatocytes of C57BL/6 mice inhibited interleukin‐2– and concanavalin A–induced spleen cell proliferation in vitro. In contrast, cytosolic extracts from purified nonparenchymal liver cells had no effect. Arginase and very‐low‐density lipoprotein were previously identified as two immunoinhibitory substances present in liver cytosolic extracts.

The role of capillarization in hepatic failure: Studies in carbon tetrachloride‐induced cirrhosis

Antonio Martinez‐Hernandez, Jose Martinez – 1 November 1991 – During the cirrhotic process, the hepatic microvascular phenotype is transformed from sinusoids (discontinuous capillaries) into continuous capillaries. This transformation has been termed capillarization. Many hepatic functions depend on the rapid, bidirectional exchange of macromolecules between plasma and hepatocytes.

Dexamethasone modulates α2‐macroglobulin and apolipoprotein E gene expression in cultured rat liver fat‐storing (Ito) cells

Giuliano Ramadori, Thomas Knittel, Stefan Schwögler, Florian Bieber, Hartmut Rieder, Karl‐Herrmann Meyer Zum Büschenfelde – 1 November 1991 – Fat‐storing (Ito) cells are perisinusoidal liver cells thought to play a central role in vitamin A metabolism and fibrogenesis. Glucocorticoids have been shown to be beneficial in the treatment of certain types of liver diseases by delaying the development of cirrhosis. To study the regulatory effects of dexamethasone on Ito cell gene expression, Ito cells were isolated from normal rat liver and primary cultures were established.

Effect of propranolol on portosystemic collateral circulation in patients with cirrhosis

Stefano Gaiani, Luigi Bolondi, Daphna Fenyves, Gianni Zironi, Alessandra Rigamonti, Luigi Barbara – 1 November 1991 – Propranolol has been demonstrated to be effective in lowering portal pressure in cirrhotic patients. This effect is mediated by a reduction of splanchnic arterial inflow and a consequent decrease of portal vein and portocollateral blood flow. Although experimental studies suggest a direct effect of the drug on portocollateral circulation, little information exists about relative flow changes occurring in the portal vein and in collateral veins feeding esophageal varices.

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