{"created":"2023-07-27T06:31:57.169273+00:00","id":17572,"links":{},"metadata":{"_buckets":{"deposit":"7ec5e9e8-a59b-4376-b370-296691fa7075"},"_deposit":{"created_by":3,"id":"17572","owners":[3],"pid":{"revision_id":0,"type":"depid","value":"17572"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00017572","sets":["1132:1137:1270:1360"]},"author_link":["31159"],"item_7_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"1995-08-01","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"4","bibliographicPageEnd":"504","bibliographicPageStart":"492","bibliographicVolumeNumber":"104","bibliographic_titles":[{"bibliographic_title":"金沢大学十全医学会雑誌"}]}]},"item_7_description_16":{"attribute_name":"その他の識別子","attribute_value_mlt":[{"subitem_description":"1996125670","subitem_description_type":"Other"}]},"item_7_description_21":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"1)マウスのテレピン油刺激により急性期炎症蛋白の一つであるハプトグロビンが誘導,産生された.それに先駆けてIL-1αとIL-6の産生が認められ,これらにより急性期炎症蛋白が誘導されることが明らかとなった.遅れてIL-1raの産生も認められ,急性炎症の進展に影響を与えていると考えられた.以上から急性炎症における炎症性サイトカインと急性期炎症蛋白との関わり,及びIL-1raによる炎症の制御が示唆された. 2)大腸菌から遺伝子組み換え型IL-1raが発現,精製された.マイトゲン刺激胸腺細胞を用いたIL-1測定法において遺伝子組み換え型IL-1raはIL-1のもつ生物学的活性を抑制したが,マウスにおいてテレピン油によるハプトグロビンの産生は抑制しなかった.すなわちIL-1のみをブロックしてもハプトグロビンの産生は抑制されず,IL-6など他の介在物質の関与が示唆された","subitem_description_type":"Abstract"}]},"item_7_description_5":{"attribute_name":"提供者所属","attribute_value_mlt":[{"subitem_description":"金沢大学 医 整形外科","subitem_description_type":"Other"}]},"item_7_publisher_17":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"金沢大学十全医学会"}]},"item_7_source_id_11":{"attribute_name":"NCID","attribute_value_mlt":[{"subitem_source_identifier":"AN00044397","subitem_source_identifier_type":"NCID"}]},"item_7_source_id_9":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"0022-7226","subitem_source_identifier_type":"ISSN"}]},"item_7_version_type_25":{"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":"本荘, 茂"}],"nameIdentifiers":[{"nameIdentifier":"31159","nameIdentifierScheme":"WEKO"}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2017-10-04"}],"displaytype":"detail","filename":"AN00044397-104-047.pdf","filesize":[{"value":"2.4 MB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"AN00044397-104-047.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/17572/files/AN00044397-104-047.pdf"},"version_id":"83e0c82f-a1a2-403b-8483-d452aa8b25cc"}]},"item_keyword":{"attribute_name":"キーワード","attribute_value_mlt":[{"subitem_subject":"炎症","subitem_subject_scheme":"Other"},{"subitem_subject":"蛋白質","subitem_subject_scheme":"Other"},{"subitem_subject":"Interleukin 1 Receptor Antagonist Protein","subitem_subject_scheme":"Other"},{"subitem_subject":"マウス","subitem_subject_scheme":"Other"},{"subitem_subject":"動物","subitem_subject_scheme":"Other"}]},"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":"departmental bulletin paper","resourceuri":"http://purl.org/coar/resource_type/c_6501"}]},"item_title":"急性期炎症蛋白産生調節におけるインターロイキン1リセプターアンタゴニストの役割に関する研究","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"急性期炎症蛋白産生調節におけるインターロイキン1リセプターアンタゴニストの役割に関する研究"}]},"item_type_id":"7","owner":"3","path":["1360"],"pubdate":{"attribute_name":"公開日","attribute_value":"2017-10-04"},"publish_date":"2017-10-04","publish_status":"0","recid":"17572","relation_version_is_last":true,"title":["急性期炎症蛋白産生調節におけるインターロイキン1リセプターアンタゴニストの役割に関する研究"],"weko_creator_id":"3","weko_shared_id":-1},"updated":"2023-07-28T00:01:22.861274+00:00"}