{"_buckets": {"deposit": "4f67f38e-f942-4580-b5a8-de86e7323da4"}, "_deposit": {"id": "21777", "owners": [], "pid": {"revision_id": 0, "type": "depid", "value": "21777"}, "status": "published"}, "_oai": {"id": "oai:soar-ir.repo.nii.ac.jp:00021777", "sets": ["461:462"]}, "author_link": ["110338", "110339", "110340", "110341", "110342", "110343", "110344", "110345", "110346", "110347"], "item_1628147817048": {"attribute_name": "\u51fa\u7248\u30bf\u30a4\u30d7", "attribute_value_mlt": [{"subitem_version_resource": "http://purl.org/coar/version/c_970fb48d4fbd8a85", "subitem_version_type": "VoR"}]}, "item_6_biblio_info_6": {"attribute_name": "\u66f8\u8a8c\u60c5\u5831", "attribute_value_mlt": [{"bibliographicIssueDates": {"bibliographicIssueDate": "2018-04-04", "bibliographicIssueDateType": "Issued"}, "bibliographicPageStart": "5620", "bibliographicVolumeNumber": "8", "bibliographic_titles": [{"bibliographic_title": "SCIENTIFIC REPORTS"}]}]}, "item_6_description_20": {"attribute_name": "\u6284\u9332", "attribute_value_mlt": [{"subitem_description": "During acute-phase response (APR), there is a dramatic increase in serum amyloid A (SAA) in plasma high density lipoproteins (HDL). Elevated SAA leads to reactive AA amyloidosis in animals and humans. Herein, we employed apolipoprotein A-II (ApoA-II) deficient (Apoa2(-/-)) and transgenic (Apoa2Tg) mice to investigate the potential roles of ApoA-II in lipoprotein particle formation and progression of AA amyloidosis during APR. AA amyloid deposition was suppressed in Apoa2(-/-) mice compared with wild type (WT) mice. During APR, Apoa2(-/-) mice exhibited significant suppression of serum SAA levels and hepatic Saa1 and Saa2 mRNA levels. Pathological investigation showed Apoa2(-/-) mice had less tissue damage and less inflammatory cell infiltration during APR. Total lipoproteins were markedly decreased in Apoa2(-/-) mice, while the ratio of HDL to low density lipoprotein (LDL) was also decreased. Both WT and Apoa2(-/-) mice showed increases in LDL and very large HDL during APR. SAA was distributed more widely in lipoprotein particles ranging from chylomicrons to very small HDL in Apoa2(-/-) mice. Our observations uncovered the critical roles of ApoA-II in inflammation, serum lipoprotein stability and AA amyloidosis morbidity, and prompt consideration of therapies for AA and other amyloidoses, whose precursor proteins are associated with circulating HDL particles.", "subitem_description_type": "Abstract"}]}, "item_6_description_30": {"attribute_name": "\u8cc7\u6e90\u30bf\u30a4\u30d7\uff08\u30b3\u30f3\u30c6\u30f3\u30c4\u306e\u7a2e\u985e\uff09", "attribute_value_mlt": [{"subitem_description": "Article", "subitem_description_type": "Other"}]}, "item_6_description_5": {"attribute_name": "\u5f15\u7528", "attribute_value_mlt": [{"subitem_description": "SCIENTIFIC REPORTS.8:5620(2018)", "subitem_description_type": "Other"}]}, "item_6_link_3": {"attribute_name": "\u4fe1\u5dde\u5927\u5b66\u7814\u7a76\u8005\u7dcf\u89a7\u3078\u306e\u30ea\u30f3\u30af", "attribute_value_mlt": [{"subitem_link_text": "Dai, Jian", "subitem_link_url": "https://soar-rd.shinshu-u.ac.jp/profile/ja.ZacNuhkh.html"}, {"subitem_link_text": "Mori, Masayuki", "subitem_link_url": "https://soar-rd.shinshu-u.ac.jp/profile/ja.OpSCZafV.html"}, {"subitem_link_text": "Miyahara, Hiroki", "subitem_link_url": "https://soar-rd.shinshu-u.ac.jp/profile/ja.OhLmPNym.html"}, {"subitem_link_text": "Higuchi, Keiichi", "subitem_link_url": "https://soar-rd.shinshu-u.ac.jp/profile/ja.gCfUPmAh.html"}]}, "item_6_link_67": {"attribute_name": "WoS", "attribute_value_mlt": [{"subitem_link_text": "Web of Science", "subitem_link_url": "http://gateway.isiknowledge.com/gateway/Gateway.cgi?\u0026GWVersion=2\u0026SrcAuth=ShinshuUniv\u0026SrcApp=ShinshuUniv\u0026DestLinkType=FullRecord\u0026DestApp=WOS\u0026KeyUT=000429095600029"}]}, "item_6_publisher_4": {"attribute_name": "\u51fa\u7248\u8005", "attribute_value_mlt": [{"subitem_publisher": "NATURE PUBLISHING GROUP"}]}, "item_6_relation_47": {"attribute_name": "PubMed", "attribute_value_mlt": [{"subitem_relation_name": [{"subitem_relation_name_text": "29618729"}], "subitem_relation_type_id": {"subitem_relation_type_id_text": "https://www.ncbi.nlm.nih.gov/pubmed/29618729", "subitem_relation_type_select": "PMID"}}]}, "item_6_relation_48": {"attribute_name": "DOI", "attribute_value_mlt": [{"subitem_relation_name": [{"subitem_relation_name_text": "10.1038/s41598-018-23755-y"}], "subitem_relation_type_id": {"subitem_relation_type_id_text": "https://doi.org/10.1038/s41598-018-23755-y", "subitem_relation_type_select": "DOI"}}]}, "item_6_rights_62": {"attribute_name": "\u6a29\u5229", "attribute_value_mlt": [{"subitem_rights": "This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article\u2019s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article\u2019s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/."}]}, "item_6_select_64": {"attribute_name": "\u8457\u8005\u7248\u30d5\u30e9\u30b0", "attribute_value_mlt": [{"subitem_select_item": "publisher"}]}, "item_6_source_id_35": {"attribute_name": "ISSN", "attribute_value_mlt": [{"subitem_source_identifier": "2045-2322", "subitem_source_identifier_type": "EISSN"}]}, "item_6_source_id_39": {"attribute_name": "NII ISSN", "attribute_value_mlt": [{"subitem_source_identifier": "2045-2322", "subitem_source_identifier_type": "EISSN"}]}, "item_6_text_69": {"attribute_name": "wosonly authkey", "attribute_value_mlt": [{"subitem_text_value": "HIGH-DENSITY-LIPOPROTEIN; SENESCENCE-ACCELERATED MOUSE; TRANSGENIC MICE; APOA-II; SENILE AMYLOIDOSIS; PROTEIN SAA; EXPERIMENTAL INDUCTION; SERUM; METABOLISM; HDL"}]}, "item_6_text_70": {"attribute_name": "wosonly keywords", "attribute_value_mlt": [{"subitem_text_value": "During acute-phase response (APR), there is a dramatic increase in serum amyloid A (SAA) in plasma high density lipoproteins (HDL). Elevated SAA leads to reactive AA amyloidosis in animals and humans. Herein, we employed apolipoprotein A-II (ApoA-II) deficient (Apoa2(-/-)) and transgenic (Apoa2Tg) mice to investigate the potential roles of ApoA-II in lipoprotein particle formation and progression of AA amyloidosis during APR. AA amyloid deposition was suppressed in Apoa2(-/-) mice compared with wild type (WT) mice. During APR, Apoa2(-/-) mice exhibited significant suppression of serum SAA levels and hepatic Saa1 and Saa2 mRNA levels. Pathological investigation showed Apoa2(-/-) mice had less tissue damage and less inflammatory cell infiltration during APR. Total lipoproteins were markedly decreased in Apoa2(-/-) mice, while the ratio of HDL to low density lipoprotein (LDL) was also decreased. Both WT and Apoa2(-/-) mice showed increases in LDL and very large HDL during APR. SAA was distributed more widely in lipoprotein particles ranging from chylomicrons to very small HDL in Apoa2(-/-) mice. Our observations uncovered the critical roles of ApoA-II in inflammation, serum lipoprotein stability and AA amyloidosis morbidity, and prompt consideration of therapies for AA and other amyloidoses, whose precursor proteins are associated with circulating HDL particles."}]}, "item_creator": {"attribute_name": "\u8457\u8005", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "Yang, Mu", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "110338", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Liu, Yingye", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "110339", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Dai, Jian", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "110340", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Li, Lin", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "110341", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Ding, Xin", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "110342", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Xu, Zhe", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "110343", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Mori, Masayuki", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "110344", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Miyahara, Hiroki", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "110345", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Sawashita, Jinko", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "110346", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Higuchi, Keiichi", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "110347", "nameIdentifierScheme": "WEKO"}]}]}, "item_files": {"attribute_name": "\u30d5\u30a1\u30a4\u30eb\u60c5\u5831", "attribute_type": "file", "attribute_value_mlt": [{"accessrole": "open_date", "date": [{"dateType": "Available", "dateValue": "2021-02-16"}], "displaytype": "detail", "download_preview_message": "", "file_order": 0, "filename": "16K07086_04.pdf", "filesize": [{"value": "2.6 MB"}], "format": "application/pdf", "future_date_message": "", "is_thumbnail": false, "licensefree": "This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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