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Biological late effects for secondary radiations from carbon ions simulating clinical heavy-ion radiotherapy

https://repo.qst.go.jp/records/71500
https://repo.qst.go.jp/records/71500
c2fa1e1f-55d4-4c17-b235-c85d0970bcb8
Item type 会議発表用資料 / Presentation(1)
公開日 2014-09-29
タイトル
タイトル Biological late effects for secondary radiations from carbon ions simulating clinical heavy-ion radiotherapy
言語
言語 jpn
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_c94f
資源タイプ conference object
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 鈴木, 雅雄

× 鈴木, 雅雄

WEKO 703055

鈴木, 雅雄

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鈴木 雅雄

× 鈴木 雅雄

WEKO 703056

en 鈴木 雅雄

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内容記述タイプ Abstract
内容記述 Radiation-induced cancer is growing as one of the major concerns with the increasing number of patents surviving long time. Most current-particle radiotherapy is spread out the beams to cover the cancer using scattering and collimation systems, resulting in an extra whole-body irradiation from low dose secondary radiations, such as neutrons, protons and gamma rays. It is indeed observed in many secondary radiations from a carbon-ion track simulated by the Monte Carlo methods. We examined gene mutation at the HPRT locus as one of the indicators for late biological effects in normal human cells irradiated with low-fluence neutrons from an 241Am-Be source. The mutation frequency in the cells induced by 200kV X-ray challenging dose was reduced at 0.15 times in the cells pretreated with low-dose-rate neutrons (1mGy/8h) compared to non-pretreated cells, but the reduced mutation frequency was returned to the control level, when using a specific inhibitor of gap-junction mediated cell-cell communication. The result suggested that neutron-induced adaptive response was induced by gap-junction mediated bystander effect. (This is the co-operative study with Drs. T. Konishi and H. Kitamura.)
会議概要(会議名, 開催地, 会期, 主催者等)
内容記述タイプ Other
内容記述 第73回日本癌学会学術総会
発表年月日
日付 2014-09-25
日付タイプ Issued
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