Biomedical subjects
Publications and source records attributed to H Miyake.
We report a case of successful percutaneous retrieval of a broken Kirschner's wire that had entered the venous system and the right atrium and later migrated to the left pulmonary artery. The management of a long, rigid, nail-like foreign body within the heart and/or the pulmonary artery is discussed.
An appendiceal abscess with intestinal malrotation can occur anywhere in the abdomen, not only in the right lower quadrant. We report a case presenting a midline mass of the lower abdomen whose computed tomography (CT) and ultrasonography (US) findings mimicked a urachal abscess. A retrospective review of CT findings led to the correct diagnosis by showing malposition of the ascending colon.
BACKGROUND: Drug resistance is a major problem in tumor chemotherapy, and recent studies have suggested that the differential sensitivity of cancer cells to chemotherapy is associated with different susceptibilities to undergoing apoptosis. The aim of this study was to evaluate the effects of introduction of wild-type p53 or p21WAF1/CIP1 (p21) on chemosensitivity of bladder cancer cells. MATERIALS AND METHODS: The human bladder cancer cell line HT1376, which contains mutant p53 and p21 genes, was used in this study. The effects of adenoviral-mediated p53 or p21 gene transfer on sensitivity of HT1376 cells to cisplatin were analyzed both in vitro and in vivo. RESULTS: The introduction of wild-type p53 gene into HT1376 markedly enhanced the sensitivity to cisplatin in vitro. Direct injection of the p53-adenoviral vector into subcutaneous HT1376 tumors established in nude mice, followed by intraperitoneally administration of cisplatin, induced massive apoptotic destruction of the tumors. In contrast, the sensitivity of HT1376 to cisplatin was not increased by the introduction of the p21 gene either in vitro or in vivo. CONCLUSIONS: These findings suggest that the combined regimen of adenoviral-mediated p53 gene transfer and cisplatin may become an efficient and powerful tool for treatment of bladder cancer.
BACKGROUND/AIMS: A great number of hepatocellular carcinoma (HCC) develop from chronic liver disease. Among a total of 23,000 deaths of HCC in 1988 in Japan, 82% had positive antibodies against HBV and/or HCV. In the present study we investigated the etiological factors involved in this process, employing patients with chronic hepatitis as controls. METHODOLOGY: In this study, alcohol consumption and cigarette smoking were investigated in 104 male patients with HCC which developed from chronic liver disease and 104 male controls with chronic liver disease without HCC (one for each case) matched for age. RESULTS: When compared with non-drinkers and non-smokers, the relative risk (RR) for developing HCC rose to 17.9 among those with both drinking and smoking habits. The risk was greater than for those in whom either habit existed alone. The RR decreased among ex-smokers who were non-drinkers or ex-drinkers, but it was still as high as 9.4. For current smokers, even if they were non- or ex-drinkers, the RR was 15.4. CONCLUSIONS: Drinking and the cigarette smoking were both risk factors, but the existence of synergism between them was also suggested. Therefore, patients with chronic liver disease should be thoroughly counseled to refrain from both drinking and smoking.