{"_buckets": {"deposit": "646729fe-49b0-4467-966b-49a02b255e44"}, "_deposit": {"created_by": 14, "id": "17816", "owners": [14], "pid": {"revision_id": 0, "type": "depid", "value": "17816"}, "status": "published"}, "_oai": {"id": "oai:sapmed.repo.nii.ac.jp:00017816", "sets": ["2250"]}, "author_link": [], "item_3_biblio_info_6": {"attribute_name": "書誌情報", "attribute_value_mlt": [{"bibliographicIssueDates": {"bibliographicIssueDate": "2023-03-31", "bibliographicIssueDateType": "Issued"}, "bibliographicIssueNumber": "1-6", "bibliographicPageEnd": "43", "bibliographicPageStart": "42", "bibliographicVolumeNumber": "91", "bibliographic_titles": [{"bibliographic_title": "札幌医学雑誌=The Sapporo Medical Journal"}, {"bibliographic_title": "The Sapporo Medical Journal", "bibliographic_titleLang": "en"}]}]}, "item_3_description_4": {"attribute_name": "抄録", "attribute_value_mlt": [{"subitem_description": "神経細胞に対する低酸素-低グルコース(OGD)は,虚血モデルとして用いられる.本研究は,ラット脊髄神経節初代培養細胞および遺伝子工学技法を用いて,OGDが神経軸索のミトコンドリア(Mt)の動態にどのような影響を与えるのかを検討した.結果,OGD暴露の6時間後に停留Mtの長さが有意に減少し,軸索内の球状Mtの割合が増加した.停留Mtの長さが減少したのは,輸送Mtの停止,Mtの分裂および停留Mt自身の短縮であることを明らかにした.これらの現象は軸索変性および細胞死よりも先行して観察されたことから,Mtが治療の対象となることが考えられた.", "subitem_description_type": "Abstract"}]}, "item_3_publisher_32": {"attribute_name": "出版者", "attribute_value_mlt": [{"subitem_publisher": "札幌医科大学"}]}, "item_3_source_id_7": {"attribute_name": "ISSN", "attribute_value_mlt": [{"subitem_source_identifier": "0036-472X", "subitem_source_identifier_type": "ISSN"}]}, "item_3_version_type_15": {"attribute_name": "著者版フラグ", "attribute_value_mlt": [{"subitem_version_resource": "http://purl.org/coar/version/c_970fb48d4fbd8a85", "subitem_version_type": "VoR"}]}, "item_creator": {"attribute_name": "著者", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "Shin, KIKUCHI"}]}, {"creatorNames": [{"creatorName": "Takayuki, KOHNO"}]}, {"creatorNames": [{"creatorName": "Takashi, KOJIMA"}]}, {"creatorNames": [{"creatorName": "Haruyuki, TATSUMI"}]}, {"creatorNames": [{"creatorName": "Yuki, OHSAKI"}]}, {"creatorNames": [{"creatorName": "Takafumi, NINOMIYA"}]}]}, "item_files": {"attribute_name": "ファイル情報", "attribute_type": "file", "attribute_value_mlt": [{"accessrole": "open_date", "date": [{"dateType": "Available", "dateValue": "2023-03-14"}], "displaytype": "detail", "download_preview_message": "", "file_order": 0, "filename": "0036472X91142.pdf", "filesize": [{"value": "2.9 MB"}], "format": "application/pdf", "future_date_message": "", "is_thumbnail": false, "licensetype": "license_11", "mimetype": "application/pdf", "size": 2900000.0, "url": {"label": "0036472X91142.pdf", "url": "https://sapmed.repo.nii.ac.jp/record/17816/files/0036472X91142.pdf"}, "version_id": "2fbcb582-4c9d-4330-96b0-35e6909b67ea"}]}, "item_language": {"attribute_name": "言語", "attribute_value_mlt": [{"subitem_language": "jpn"}]}, "item_resource_type": {"attribute_name": "資源タイプ", "attribute_value_mlt": [{"resourcetype": "other", "resourceuri": "http://purl.org/coar/resource_type/c_1843"}]}, "item_title": "Oxygen-glucose deprivation decreases the motility and length of axonal mitochondria in cultured dorsal root ganglion cells of rats", "item_titles": {"attribute_name": "タイトル", "attribute_value_mlt": [{"subitem_title": "Oxygen-glucose deprivation decreases the motility and length of axonal mitochondria in cultured dorsal root ganglion cells of rats", "subitem_title_language": "en"}]}, "item_type_id": "3", "owner": "14", "path": ["2250"], "permalink_uri": "https://sapmed.repo.nii.ac.jp/records/17816", "pubdate": {"attribute_name": "PubDate", "attribute_value": "2023-03-14"}, "publish_date": "2023-03-14", "publish_status": "0", "recid": "17816", "relation": {}, "relation_version_is_last": true, "title": ["Oxygen-glucose deprivation decreases the motility and length of axonal mitochondria in cultured dorsal root ganglion cells of rats"], "weko_shared_id": -1}
Oxygen-glucose deprivation decreases the motility and length of axonal mitochondria in cultured dorsal root ganglion cells of rats
https://sapmed.repo.nii.ac.jp/records/17816
https://sapmed.repo.nii.ac.jp/records/17816