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        <identifier>oai:ipsj.ixsq.nii.ac.jp:00211729</identifier>
        <datestamp>2025-01-19T17:42:06Z</datestamp>
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          <dc:title>Estimation of Metabolic Effects of Cadmium Exposure during Pregnancy by Tensor Decomposition</dc:title>
          <dc:title xml:lang="en">Estimation of Metabolic Effects of Cadmium Exposure during Pregnancy by Tensor Decomposition</dc:title>
          <jpcoar:creator>
            <jpcoar:creatorName>Yuki, Amakura</jpcoar:creatorName>
          </jpcoar:creator>
          <jpcoar:creator>
            <jpcoar:creatorName>Y-H, Taguchi</jpcoar:creatorName>
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          <jpcoar:creator>
            <jpcoar:creatorName xml:lang="en">Yuki, Amakura</jpcoar:creatorName>
          </jpcoar:creator>
          <jpcoar:creator>
            <jpcoar:creatorName xml:lang="en">Y-H, Taguchi</jpcoar:creatorName>
          </jpcoar:creator>
          <jpcoar:subject subjectScheme="Other">バイオ情報学 (2)</jpcoar:subject>
          <datacite:description descriptionType="Other">studies have shown that exposure to cadmium during maternal pregnancy disrupts insulin metabolism in the unborn child. The purpose of this study is to estimate the genes actually affecting by the data obtained in this report using tensor decomposition and to speculate on the possible mechanisms of insulin metabolism disruption by these genes. By identifying genes with high expression levels, we were able to speculate on a pathway in which the effects of endoplasmic reticulum stress induced by cadmium might somehow promote increased expression of TNF-α, and the effects of intracellular oxidative stress via TNF-α-induced ceramide accumulation might lead to phosphorylation of IRS1, which plays an important role in insulin signaling. We hypothesized a pathway in which insulin resistance is acquired by phosphorylation of a protein, IRS1.</datacite:description>
          <datacite:description descriptionType="Other">studies have shown that exposure to cadmium during maternal pregnancy disrupts insulin metabolism in the unborn child. The purpose of this study is to estimate the genes actually affecting by the data obtained in this report using tensor decomposition and to speculate on the possible mechanisms of insulin metabolism disruption by these genes. By identifying genes with high expression levels, we were able to speculate on a pathway in which the effects of endoplasmic reticulum stress induced by cadmium might somehow promote increased expression of TNF-α, and the effects of intracellular oxidative stress via TNF-α-induced ceramide accumulation might lead to phosphorylation of IRS1, which plays an important role in insulin signaling. We hypothesized a pathway in which insulin resistance is acquired by phosphorylation of a protein, IRS1.</datacite:description>
          <dc:publisher xml:lang="ja">情報処理学会</dc:publisher>
          <datacite:date dateType="Issued">2021-06-21</datacite:date>
          <dc:language>eng</dc:language>
          <dc:type rdf:resource="http://purl.org/coar/resource_type/c_18gh">technical report</dc:type>
          <jpcoar:identifier identifierType="URI">https://ipsj.ixsq.nii.ac.jp/records/211729</jpcoar:identifier>
          <jpcoar:sourceIdentifier identifierType="ISSN">2188-8590</jpcoar:sourceIdentifier>
          <jpcoar:sourceIdentifier identifierType="NCID">AA12055912</jpcoar:sourceIdentifier>
          <jpcoar:sourceTitle>研究報告バイオ情報学（BIO）</jpcoar:sourceTitle>
          <jpcoar:volume>2021-BIO-66</jpcoar:volume>
          <jpcoar:issue>26</jpcoar:issue>
          <jpcoar:pageStart>1</jpcoar:pageStart>
          <jpcoar:pageEnd>5</jpcoar:pageEnd>
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            <datacite:date dateType="Available">2023-06-21</datacite:date>
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