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  1. 学位論文
  2. 博士論文(医学)
  3. 本文

Suprabasin-null mice retain skin barrier function and show high contact hypersensitivity to nickel upon oral nickel loading

http://hdl.handle.net/10271/00003856
http://hdl.handle.net/10271/00003856
82a9a1c5-8f0c-4beb-aa2f-7eef4fa56829
名前 / ファイル ライセンス アクション
DT_848ronbun.pdf 論文本文 (3.0 MB)
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Item type 学位論文 / Thesis or Dissertation(1)
公開日 2021-07-01
タイトル
タイトル Suprabasin-null mice retain skin barrier function and show high contact hypersensitivity to nickel upon oral nickel loading
言語 en
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_db06
資源タイプ doctoral thesis
アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
その他のタイトル
その他のタイトル スプラバシンノックアウトマウスは皮膚バリア機能を保持し経口ニッケル負荷でニッケル接触過敏症が亢進する
著者 中澤, 慎介

× 中澤, 慎介

ja 中澤, 慎介

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書誌情報 en : Scientific Reports

巻 10, p. 14559, 発行日 2020
出版者
出版者 Springer Nature
言語 en
権利
言語 en
権利情報 Copyright The Author(s) 2020. 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creat iveco mmons .org/licen ses/by/4.0/.
抄録
内容記述タイプ Abstract
内容記述 Suprabasin (SBSN) is expressed not only in epidermis but also in epithelial cells of the upper digestive tract where metals such as nickel are absorbed. We have recently shown that SBSN level is decreased in the stratum corneum and serum of atopic dermatitis (AD) patients, especially in intrinsic AD, which is characterized by metal allergy. By using SBSN-null (Sbsn-/-) mice, this study was conducted to investigate the outcome of SBSN deficiency in relation to AD. Sbsn-/- mice exhibited skin barrier dysfunction on embryonic day 16.5, but after birth, their barrier function was not perturbed despite the presence of ultrastructural changes in stratum corneum and keratohyalin granules. Sbsn-/- mice showed a comparable ovalbumin-specific skin immune response to wild type (WT) mice and rather lower contact hypersensitivity (CHS) responses to haptens than did WT mice. The blood nickel level after oral feeding of nickel was significantly higher in Sbsn-/- mice than in WT mice, and CHS to nickel was elevated in Sbsn-/- mice under nickel-loading condition. Our study suggests that the completely SBSN deficient mice retain normal barrier function, but harbor abnormal upper digestive tract epithelium that promotes nickel absorption and high CHS to nickel, sharing the features of intrinsic AD.
言語 en
学位名
学位名 博士(医学)
学位の区分
内容記述 doctoral
学位の分野
内容記述 医学系研究科
学位授与機関
学位授与機関識別子Scheme kakenhi
学位授与機関識別子 13802
学位授与機関名 浜松医科大学
学位授与年月日
学位授与年月日 2020-11-20
学位授与番号
学位授与番号 甲第848号
ISSN
収録物識別子タイプ PISSN
収録物識別子 2045-2322
PubMed番号
識別子タイプ PMID
関連識別子 32884021
出版社DOI
識別子タイプ DOI
関連識別子 https://doi.org/10.1038/s41598-020-71536-3
著者版フラグ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
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