{"created":"2023-05-15T15:16:58.653543+00:00","id":2971,"links":{},"metadata":{"_buckets":{"deposit":"886029d7-a916-47a4-b3af-cf97f862b66d"},"_deposit":{"created_by":12,"id":"2971","owners":[12],"pid":{"revision_id":0,"type":"depid","value":"2971"},"status":"published"},"_oai":{"id":"oai:obihiro.repo.nii.ac.jp:00002971","sets":["242:243"]},"author_link":["227","178"],"item_6_alternative_title_1":{"attribute_name":"その他（別言語等）の研究課題名","attribute_value_mlt":[{"subitem_alternative_title":"Analytical study of the myasthenic syndrome by chemical agents","subitem_alternative_title_language":"en"}]},"item_6_contributor_5":{"attribute_name":"研究分担者","attribute_value_mlt":[{"contributorNames":[{"contributorName":"佐藤, 栄輝","lang":"ja"}],"nameIdentifiers":[{"nameIdentifier":"227","nameIdentifierScheme":"WEKO"},{"nameIdentifier":"9000006582679","nameIdentifierScheme":"CiNii ID","nameIdentifierURI":"http://ci.nii.ac.jp/nrid/9000006582679"},{"nameIdentifier":"50178711","nameIdentifierScheme":"e-Rad","nameIdentifierURI":"https://kaken.nii.ac.jp/ja/search/?qm=50178711"},{"nameIdentifier":"read0167490","nameIdentifierScheme":"researchmap","nameIdentifierURI":"https://researchmap.jp/read0167490"}]}]},"item_6_description_10":{"attribute_name":"研究代表者番号","attribute_value_mlt":[{"subitem_description":"50011995","subitem_description_type":"Other"}]},"item_6_description_11":{"attribute_name":"研究機関","attribute_value_mlt":[{"subitem_description":"帯広畜産大学","subitem_description_type":"Other"}]},"item_6_description_13":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"化学物質による自己免疫疾患としての筋無力症の発症に内因性因子が関与する可能性を調べた成績からその発症機作を考察することを目的とした.この目的で,運動神経筋間の興奮伝達におよぼすD-ペニシラミン(DPN),ジチオスレイトール(DTT),およびN-エチルマレイミド(NEM)などの慢性投与の影響を調べた.筋無力症が胸腺肥大と関連する可能性が提案されているので,胸腺肥大を誘起する方法の一つであるチロキシン(TRX)の慢性投与がこれら薬物の作用を修飾する可能性についても検討した.その結果,DPNおよびTRXの慢性投与は共にクラ-レ(dTc)のLD_<50>値を下げ,TRXの作用はDPNの同時投与により抑制された.この作用には性依存性を認めなかった.よってDPNによる筋無力症の発症に胸腺肥大が関与するとしても,dTcのLD_<50>値を指標とした場合,TRXの過剰分泌が因子となる可能性は乏しかった.TRXは雌性マウスの胸腺重量を選択的に増加した.しかしdTc感受性に対する作用は性依存性を示さなかったので,その影響が胸腺の肥大を介した可能性は乏しい.DTTおよびNEMはdTc感受性に影響した.これらは横隔膜神経筋系に選択的に影響したが,その影響は自己免疫疾患の特性を示さなかった.雌性マウスにおいて,TRXあるいはDPNとTRXの複合投与は筋力低下,胸腺重量の増加および腹水の貯留等を生じた.TRXはLD_<50>値および摘出運動神経筋標本のdTc感受性を亢進した.しかし,DPNはこれら全てのTRXの作用を亢進しなかった.また,DPNはLD_<50>値としてのdTc感受性を亢進したが,TRXはこの作用を増強しなかった.ただし,DPNは摘出運動神経筋標本のdTc感受性には影響しなかった.従って,仮にDPNが筋麻痺作用を持つとしても,その作用がTRXの過剰分泌ないし胸腺肥大の影響を受ける可能性を示唆できなかった.演繹するに,DPN投与によるヒトの筋無力症が胸腺肥大と関連するとしても,その肥大がDPN筋無力症を誘発ないし増強する過程では,胸腺の質的な因子,例えば癌および腫瘍などの病的因子が重要であると考えられる.","subitem_description_language":"ja","subitem_description_type":"Abstract"},{"subitem_description":"The purpose of this research was to analyze and discuss the mechanism by which the myathenic syndrome appears in mice chronically administered some chemicals including d-penicillamine (DPN), dithiothreitol (DTT). N-ethylmaleimide (NEM). This trial examined a possible role of hypertrophy of the thymus on the incidence of this syndrome. Thyroxine (TRX) was administered to test this possibility. Both DPN and TRX elevated the sensitivity of the mouse to d-tubocurarine (dTc) measured as LD_<50>. This effect did not depend on the sex. TRX was more potent in this effect than DPN.DPN administered simultaneously with TRX reduced the effect of TRX alone. Thus, an excess amount of TRX secreted may have a poor possibility to accelerate the effect of DPN even if it may cause the thymokesis. TRX actually increased the weight of thymus in female mice. However, the sensitization to dTc did not depend on the sex. Chronic treatment of the mouse with DTT or NEM accelerated selectively the sensitivity of neuromuscular transmission in the diaphragm in vitro, showing that the change did not derive from characteristic autoimmune disease. Female mice administered TRX alone or combined with DPN showed the muscle weakness, increased the weight of thymus, accumulated abdominal dropsy, and increased the sensitivity to dTc both in vivo and in vitro. However, DPN never accelerated all of these effects of TRX.Chronic treatment with DPN alone did not affect the sensitivity of nerve-muscle preparations to dTc in vitro while it sensitized to dTc in vivo.Thus, the present observations did not support both ideas that DPN may be causal in the incidence of myathenic syndrome and that TRX may accelerate the effect of DPN via making hypertrophic the thymus in the mouse. It was speculative that the hypertrophic diseases of the thymus as thymoma may be important to incidence of the myathenic syndrome on the process that the thymokesis accelerates the effect of DPN inducing the syndrome even if the induction of the myathenia gravis by DPN in man relates to the thymokesis.","subitem_description_language":"en","subitem_description_type":"Abstract"}]},"item_6_description_14":{"attribute_name":"内容記述","attribute_value_mlt":[{"subitem_description":"平成4・5・6年度科学研究費補助金(一般研究(B))研究成果報告書","subitem_description_language":"ja","subitem_description_type":"Other"}]},"item_6_description_19":{"attribute_name":"フォーマット","attribute_value_mlt":[{"subitem_description":"application/pdf","subitem_description_type":"Other"}]},"item_6_description_9":{"attribute_name":"研究課題番号","attribute_value_mlt":[{"subitem_description":"04454118","subitem_description_type":"Other"}]},"item_6_text_12":{"attribute_name":"助成元","attribute_value_mlt":[{"subitem_text_language":"ja","subitem_text_value":"科学研究費助成事業"}]},"item_6_version_type_20":{"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_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2018-01-30"}],"displaytype":"detail","filename":"H7nisimura.pdf","filesize":[{"value":"24.1 MB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"H7nisimura.pdf","url":"https://obihiro.repo.nii.ac.jp/record/2971/files/H7nisimura.pdf"},"version_id":"2a20385e-0e13-4797-8c65-608f72264ae9"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"jpn"}]},"item_researcher":{"attribute_name":"研究代表者","attribute_type":"creator","attribute_value_mlt":[{"creatorAffiliations":[{"affiliationNameIdentifiers":[{"affiliationNameIdentifier":"","affiliationNameIdentifierScheme":"ISNI","affiliationNameIdentifierURI":"http://www.isni.org/isni/"}],"affiliationNames":[{"affiliationName":"","affiliationNameLang":"ja"}]}],"creatorNames":[{"creatorName":"Nishimura, Masakazu","creatorNameLang":"en"},{"creatorName":"西村, 昌数","creatorNameLang":"ja"}],"familyNames":[{},{}],"givenNames":[{},{}],"nameIdentifiers":[{},{},{},{}]}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"research report","resourceuri":"http://purl.org/coar/resource_type/c_18ws"}]},"item_title":"化学物質による自己免疫疾患としての筋無力症の発症機作の解析","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"化学物質による自己免疫疾患としての筋無力症の発症機作の解析","subitem_title_language":"ja"}]},"item_type_id":"6","owner":"12","path":["243"],"pubdate":{"attribute_name":"PubDate","attribute_value":"2007-02-15"},"publish_date":"2007-02-15","publish_status":"0","recid":"2971","relation_version_is_last":true,"title":["化学物質による自己免疫疾患としての筋無力症の発症機作の解析"],"weko_creator_id":"12","weko_shared_id":-1},"updated":"2024-05-20T01:11:22.616416+00:00"}