Expression of the c‐myc protooncogene product in cells infected with the hepatitis delta virus

Gianfranco Tappero, Gioacchino Natoli, Giovanni Anfossi, Floriano Rosina, Francesco Negro, Antonina Smedile, Ferruccio Bonino, Alberto Angeli, Robert H. Purcell, Professor Mario Rizzetto, Massimo Levrero – 1 November 1994 – The intrahepatic accumulation of the c‐myc protooncogene product was observed on immunoflourescence in each of six patients with chronic hepatitis delta virus infection who exhibited the hepatitis D antigen in their livers. The c‐myc product was stained in the same nuclei that contained the hepatitis D antigen.

Hepatitis C in HIV‐infected patients with and without AIDS: Prevalence and relationship to patient survival

Teresa L. Wright, Harry Hollander, Xiang Pu, Michael J. Held, Peter Lipson, Stella Quan, Alan Polito, M. Michael Thaler, Peter Bacchetti, Bruce F. Scharschmidt – 1 November 1994 – Background: Limited information is available about the prevalence of hepatitis C virus in patients with human immunodeficiency virus in relation to specific risk factors or about the influence of hepatitis C virus coinfection on survival. This retrospective study addressed these questions.

Identification of the thromboxane A2 receptor in hepatic sinusoidal endothelial cells and its role in Endotoxin‐induced liver injury in rats

Satoshi Ishiguro, Shigeki Arii, Kazunobu Monden, Yukito Adachi, Naomi Funaki, Hiroaki Higashitsuji, Shin‐Ichi Fujita, Masaharu Furutani, Masahiro Mise, Tadahiro Kitao, Toshio Nakamura, Fumitaka Ushikubi, Ken‐Ichi Nakamura, Shuh Narumiya, Katsuhiko Enomoto, Tousei Ohmura, Michio Mori, Masayuki Imamura – 1 November 1994 – The presence of the thromboxane A2 receptor in sinusoidal endothelial cells was investigated and its pathogenic role in endotoxin‐induced liver injury examined. The receptor was measured with a binding assay using a specific thromboxane A2 receptor antagonist, [3H]S‐145.

Tumor vaccination against hepatoma: How does it work?

Shuichi Hanada, Takaji Wakita, Hiroshi Takahashi – 1 November 1994 – Fusion of BERH‐2 rat hepatocellular carcinoma cells with activated B cells produced hybrid cells that lost their tumorigenicity and became immunogenic. Syngeneic rats injected with BERH‐2‐B hybrid cells became resistant to challenge with parental BERH‐2 cells, and rats with established BERH‐2 hepatomas were cured by subsequent injection of BERH‐2‐B cells. Both CD4 and CD8+ cells were essential for the induction of protective immunity; however, only CD8+ cells were required for the eradication of BERH‐2 tumors.

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