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Articles by T Nishimura
Total Records ( 3 ) for T Nishimura
  J Xu , M Futakuchi , M Iigo , K Fukamachi , D. B Alexander , H Shimizu , Y Sakai , S Tamano , F Furukawa , T Uchino , H Tokunaga , T Nishimura , A Hirose , J Kanno and H. Tsuda

Titanium dioxide (TiO2) is evaluated by World Health Organization/International Agency for Research on Cancer as a Group 2B carcinogen. The present study was conducted to detect carcinogenic activity of nanoscale TiO2 administered by a novel intrapulmonary spraying (IPS)-initiation–promotion protocol in the rat lung. Female human c-Ha-ras proto-oncogene transgenic rat (Hras128) transgenic rats were treated first with N-nitrosobis(2-hydroxypropyl)amine (DHPN) in the drinking water and then with TiO2 (rutile type, mean diameter 20 nm, without coating) by IPS. TiO2 treatment significantly increased the multiplicity of DHPN-induced alveolar cell hyperplasias and adenomas in the lung, and the multiplicity of mammary adenocarcinomas, confirming the effectiveness of the IPS-initiation–promotion protocol. TiO2 aggregates were localized exclusively in alveolar macrophages and had a mean diameter of 107.4 nm. To investigate the underlying mechanism of its carcinogenic effects, TiO2 was administered to wild-type rats by IPS five times over 9 days. TiO2 treatment significantly increased 8-hydroxydeoxy guanosine level, superoxide dismutase activity and macrophage inflammatory protein 1 (MIP1) expression in the lung. MIP1, detected in the cytoplasm of TiO2-laden alveolar macrophages in vivo and in the media of rat primary alveolar macrophages treated with TiO2 in vitro, enhanced proliferation of human lung cancer cells. Furthermore, MIP1, also detected in the sera and mammary adenocarcinomas of TiO2-treated Hras128 rats, enhanced proliferation of rat mammary carcinoma cells. These data indicate that secreted MIP1 from TiO2-laden alveolar macrophages can cause cell proliferation in the alveoli and mammary gland and suggest that TiO2 tumor promotion is mediated by MIP1 acting locally in the alveoli and distantly in the mammary gland after transport via the circulation.

  S. C Leary , F Sasarman , T Nishimura and E. A. Shoubridge

Human SCO1 and SCO2 code for essential metallochaperones with ill-defined functions in the biogenesis of the CuA site of cytochrome c oxidase subunit II (CO II). Here, we have used patient cell lines to investigate the specific roles of each SCO protein in this pathway. By pulse-labeling mitochondrial translation products, we demonstrate that the synthesis of CO II is reduced in SCO2, but not in SCO1, cells. Despite this biosynthetic defect, newly synthesized CO II is more stable in SCO2 cells than in control cells. RNAi-mediated knockdown of mutant SCO2 abolishes CO II labeling in the translation assay, whereas knockdown of mutant SCO1 does not affect CO II synthesis. These results indicate that SCO2 acts upstream of SCO1, and that it is indispensable for CO II synthesis. The subsequent maturation of CO II is contingent upon the formation of a complex that includes both SCO proteins, each with a functional CxxxC copper-coordinating motif. In control cells, the cysteines in this motif in SCO1 exist as a mixed population comprised of oxidized disulphides and reduced thiols; however, the relative ratio of oxidized to reduced cysteines in SCO1 is perturbed in cells from both SCO backgrounds. Overexpression of wild-type SCO2, or knockdown of mutant SCO2, in SCO2 cells alters the ratio of oxidized to reduced cysteines in SCO1, suggesting that SCO2 acts as a thiol-disulphide oxidoreductase to oxidize the copper-coordinating cysteines in SCO1 during CO II maturation. Based on these data we present a model in which each SCO protein fulfills distinct, stage-specific functions during CO II synthesis and CuA site maturation.

  Y Okuchi , S Nagayama , Y Mori , J Kawamura , S Matsumoto , T Nishimura , A Yoshizawa and Y. Sakai

We present a case of pseudo-meigs’ syndrome caused by a metastatic ovarian tumor of rectal cancer origin, and examine the possible involvement of vascular endothelial growth factor (VEGF) in the pathogenesis of refractory fluid retention. A 42-year-old woman with advanced rectal cancer underwent a laparoscopic anterior resection of the rectum. During systemic chemotherapy treatment, she complained of severe abdominal distension 16 months following the operation. We failed to improve massive ascites by diuretics and repeated abdominocenteses. Without any definite evidence of carcinomatous peritonitis, we chose to extirpate an enlarged ovarian tumor on the presumptive diagnosis of pseudo-meigs’ syndrome. Ascites disappeared promptly after resecting the ovarian tumors and the subject resumed systemic chemotherapy. Preoperative high levels of serum VEGF were normalized promptly after the operation. Levels of VEGF expression in metastatic ovarian tumors were as weak as in the primary tumor upon immunohistochemical staining. In contrast, increased VEGF expression was evident in epithelial cells of oviducts. For patients with massive and refractory ascites, we need to keep in mind the disease entity of pseudo-meigs’ syndrome, since surgical intervention possibly improves conditions. Furthermore, the hypersecretion of VEGF from oviducts may play a role in the pathogenesis of clinical manifestations of pseudo-meigs’ syndrome.

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