| Project/Area Number |
24592677
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | Dokkyo Medical University (2014)
Iwate Medical University (2012-2013) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
FUJIWARA Takamitsu 岩手医科大学, 医学部, 講師 (30405766)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥130,000 (Direct Cost: ¥100,000、Indirect Cost: ¥30,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2012: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
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| Keywords | 網膜電図 / 網膜 / 視細胞変性 / 網膜変性 / 緑内障 / 黄斑円孔 / 網膜内層 / ERG / 網膜神経節細胞 / 網膜疾患 / 黄斑疾患 |
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| Outline of Final Research Achievements |
We investigated functional changes of the inner retina in animal models and clinical cases. In the animal research, we isolated electrical responses from each retinal layer by intravitreally injecting drugs that blocks synaptic transmission. In early stage of photoreceptor degeneration, responses of the ON-bipolar cells were enhanced. In addition, sensitivity of amacrine cells to NMDA increased. In clinical research, we found that the photopic negative response (PhNR) driven by the inner retina were irreversibly deteriorated in macular hole patients treated by vitrectomy using indocyanine green. In glaucoma patients, in the macular region the PhNR amplitude severely declined with loss of the inner retinal thickness while in the extra-macular region it deteriorated gradually. This suggested that glaucoma should be categorized into macular disease.
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