Cell death, inflammation, and repair in rabbits' aortas and pulmonary arteries were observed at 3-, 7-, and 10-day periods after the intravenous injection of oxygenated sterols. Thus, oxygenated sterols, not cholesterol, may play the primary role in arterial wall injury and lesion development.
The effect of dimethylarsenics on the pulmonary tumorigenesis initiated by 4-nitroquinoline 1-oxide (4NQO) in mice was examined. The exposure of mice to dimethylarsinic acid (DMAA), a major metabolite of inorganic arsenics in mammals, resulted in not only promotion but also progression of the tumorigenic process in the lungs of mice administered 4NQO. Furthermore, dimethylarsenics influenced the differentiation process in lung tumorigenesis by 4NQO. These results may pave the way for the elucidation of lung carcinogenesis caused by arsenics.
Background. There is a hypothesis explaining the pathogenesis of carcinoma that increased proliferation of tissue cells correlates with the development of carcinoma, presumably by increased rate of random muta‐tions and by promotion. In this study, the significance of hepatocellular proliferation in the development of human hepatocellular carcinoma (HCC) from anti‐hepatitis C virus (HCV)‐positive cirrhotic patients was studied.
Method. Twenty‐eight Child A cirrhotic patients who were anti‐HCV (C‐100 antibody) positive were studied. At the beginning of the study, the in vitro uptake of bromodeoxyuridine (BrdU, a thymidine analogue) by he‐patocytes in biopsied liver specimens was investigated as labeling indices (LIs), and they were divided into high‐DNA synthetic (BrdU LI 2 1.5%) and low‐DNA synthetic (BrdU LI < 1.5%) groups. The patients were then surveyed prospectively with frequent ultrasonography (every 3 months) for the development of HCC for 3 years.
Result. The mean BrdU LI plus or minus standard deviation for 14 cirrhotic patients with high‐DNA synthesis activity (BrdU LI 2 1.5%) was 2.7 kO.8%, and this was significantly (P < 0.001) higher than that for 14 cirrhotic patients with low‐DNA synthesis activity (BrdU LI < 1.5%, 0.5 k 0.3%). Nine of 14 (64.3%) of the cirrhotic patients with high‐DNA synthesis activity developed HCC in the 3‐year period, in contrast to only 2 of 14 (14.3%) of the cirrhotic patients with low‐DNA synthesis activity (P < 0.05).
Conclusions. Proliferation of hepatocytes is important in HCC development from anti‐HCV‐positive cir‐rhotic patients.
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