{"_buckets": {"deposit": "4a731740-a861-4289-9c41-61e054aad08a"}, "_deposit": {"created_by": 24, "id": "5649", "owners": [24], "pid": {"revision_id": 0, "type": "depid", "value": "5649"}, "status": "published"}, "_oai": {"id": "oai:ir.soken.ac.jp:00005649", "sets": ["34"]}, "author_link": ["8195", "8194"], "item_2_creator_3": {"attribute_name": "著者名(英)", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "オカダ, ヤスノブ", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "8195", "nameIdentifierScheme": "WEKO"}]}]}, "item_2_date_4": {"attribute_name": "発行日", "attribute_value_mlt": [{"subitem_date_issued_datetime": "2015-06-23", "subitem_date_issued_type": "Created"}]}, "item_2_description_13": {"attribute_name": "研究課題番号", "attribute_value_mlt": [{"subitem_description": "25670112", "subitem_description_type": "Other"}]}, "item_2_description_14": {"attribute_name": "フォーマット", "attribute_value_mlt": [{"subitem_description": "application/pdf", "subitem_description_type": "Other"}]}, "item_2_description_16": {"attribute_name": "研究期間", "attribute_value_mlt": [{"subitem_description": "2013～2014", "subitem_description_type": "Other"}]}, "item_2_description_17": {"attribute_name": "抄録", "attribute_value_mlt": [{"subitem_description": "研究成果の概要（和文）:\n脳内は虚血条件、テンカン、脳外傷および過血糖症において強度に酸性化し、ニューロンやグリアは酸毒性死に至る。一方、強酸条件下では、外向整流性アニオンチャネルASOR が活性化され、酸毒性死誘導に関与することが、他の細胞種において知られている。今回、私達はマウス大脳皮質ニューロンにもASORが発現し、酸毒性ネクローシス死の誘導に関与すること、そしてこのASORは高い温度感受性を示し、25℃以下の低温で酸毒性死が救済され、脳障害低体温療法の一部の成因となることを明らかにした。また、これまで考えられてきた多くの候補分子が、ASOR分子実体から排除されること示した。\n研究成果の概要（英文）:\nIn the brain, strong acidosis is a common feature of ischemia, seizure, trauma and hyperglycemia, and it contributes to neuronal injury. On the other hand, the acid-sensitive outwardly rectifying anion channel (ASOR) has been found in non-neuronal cell types and to be involved in acidotoxic cell death. In the present study, we found that ASOR is expressed in mouse cortical neurons and involved in acidotoxic neuronal cell death. Also, it was found that the neuronal ASOR exhibits strong sensitiviry to temperature and that acidotoxic neuronal necrosis is largely protected by reduction of temperature to 25℃. Thus, it is suggested that this high temperature sensitivity provides a basis for hypothermic neuroprotection under acidotoxic conditions. Furthermore, we tried to identify the ASOR molecule. 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