| Project/Area Number |
14570838
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Radiation science
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| Research Institution | Chiba University |
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Principal Investigator |
KAWATA Tetsuya Chiba University, Graduate School of Medicine, Lecture, 大学院・医学研究院, 講師 (60234077)
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| Co-Investigator(Kenkyū-buntansha) |
ISOBE Koichi Chiba University, University Hospital, Assistant, 医学部附属病院, 助手 (80334184)
UNO Takashi Chiba University, Graduate School of Medicine, Associate Professor, 大学院・医学研究院, 助教授 (30302540)
ITO Hisao Chiba University, Graduate School of Medicine, Professor, 大学院・医学研究院, 教授 (20095574)
有賀 隆 千葉大学, 医学部附属病院, 助手 (20261901)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2002: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | FISH / Chromosomal aberration / Radiosensitivity / Radiotherapy |
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| Research Abstract |
We have studied the relationship between individual radiosensitivity and chromosome aberration using Fluorescence in situ hybridization (FISH). To achieve this purpose, homozygous ataxia telangiectasia cells and normal human fibroblast cells were used. Confluent cultures of normal fibroblast cells (AG1522, AG1523, AG1518) and fibroblast cells derived from an individual with A-T (GM02052, GM01823) were exposed to gamma-rays and allowed to repair at 37 ℃ for 24-hr. At 10 % survival doses, GM02052 cells were approximately 5 times more sensitive to γ-rays than AG1522 cells. For a given dose, GM02052 cells contained a much higher frequency of deletions and misrejoining than AG1522 cells. For both cell types, good correlation was found between the percentage of aberrant cells and cell survival. These results indicate that both repair deficiency and misrepair may be involved in A-T hyper radiosensitivity. Similar studies are underway using human lymphocytes.
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