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  <Article>
    <Journal>
      <PublisherName>Wiley Periodicals, Inc</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>2055-5822</Issn>
      <Volume/>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2022</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>High platelet reactivity is a predictor of left ventricular remodelling in patients with acute myocardial infarction</ArticleTitle>
    <FirstPage LZero="delete"/>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Masahiro</FirstName>
        <LastName>Tsuji</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yusuke</FirstName>
        <LastName>Kawai</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama City Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toru</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Eisuke</FirstName>
        <LastName>Saito</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama City Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kohei</FirstName>
        <LastName>Kawamura</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama City Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tamaki</FirstName>
        <LastName>Ono</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama City Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Tokioka</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama City Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tohru</FirstName>
        <LastName>Ohe</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama City Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazufumi</FirstName>
        <LastName>Nakamura</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences </Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Ito</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences </Affiliation>
      </Author>
    </AuthorList>
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      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Aims Acute myocardial infarction (AMI) is associated with left ventricular remodelling (LVR), which leads to progressive heart failure. Platelets play a pivotal role in promoting systemic and cardiac inflammatory responses during the complex process of myocardial wound healing or repair following AMI. This study aimed to investigate the impact of platelet reactivity immediately after primary percutaneous coronary intervention (PCI) on LVR in AMI patients with ST-segment (STEMI) and nonST-segment elevation (NSTEMI). &lt;br&gt;
Methods and results This prospective, single-centre, observational study included 182 patients with AMI who underwent primary PCI (107 patient with STEMI and 75 patients with NSTEMI). Patients were administered a loading dose of aspirin plus prasugrel before the procedure, and platelet reactivity was assessed using the VerifyNow P2Y12 assay immediately after PCI. Echocardiography was performed before discharge and during the chronic phase (8 +/- 3 months after discharge). LVR was defined as a relative &gt;= 20% increase in left ventricular end-diastolic volume index (LVEDVI). LVR in chronic phase was found in 34 patients (18.7%) whose platelet reactivity was significantly higher than those without LVR (259.6 +/- 61.5 and 213.1 +/- 74.8 P2Y12 reaction units [PRU]; P = 0.001). The occurrence of LVR did not differ between patients with STEMI and patients with NSTEMI (21.5% and 14.7%; P = 0.33). The optimal cut-off value of platelet reactivity for discriminating LVR was &gt;= 245 PRU. LVEDVI significantly decreased at chronic phase in patients without high platelet reactivity (&lt;245 PRU) (from 49.2 +/- 13.5 to 45.4 +/- 15.8 ml/m(2); P = 0.02), but not in patients with high platelet reactivity (&gt;= d245 PRU) (P = 0.06). Multivariate logistic analysis showed that high platelet reactivity was an independent predictor of LVR after adjusting for LVEDVI before discharge (odds ratio, 4.13; 95% confidence interval, 1.85-9.79). &lt;br&gt;
Conclusions High platelet reactivity measured immediately after PCI was a predictor of LVR in patients with AMI during the chronic phase. The role of antiplatelet therapy on inflammation in the myocardium is a promising area for further research.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Myocardial infarction</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Left ventricular remodelling</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Platelet reactivity</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Inflammation</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Reverse remodelling</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Prasugrel</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Springer Japan</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0912-3814</Issn>
      <Volume>27</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2012</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Natural genetic variation in fluctuating asymmetry of wing shape in Drosophila melanogaster</ArticleTitle>
    <FirstPage LZero="delete">133</FirstPage>
    <LastPage>143</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Masahiro</FirstName>
        <LastName>Tsujino</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuo H.</FirstName>
        <LastName>Takahashi</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Fluctuating asymmetry (FA), defined as random deviation from perfect symmetry, has been used to assay the inability of individuals to buffer their developmental processes from environmental perturbations (i.e., developmental instability). In this study, we aimed to characterize the natural genetic variation in FA of wing shape in Drosophila melanogaster, collected from across the Japanese archipelago. We quantified wing shapes at whole wing and partial wing component levels and evaluated their mean and FA. We also estimated the heritability of the mean and FA of these traits. We found significant natural genetic variation in all the mean wing traits and in FA of one of the partial wing components. Heritability estimates for mean wing shapes were significant in two and four out of five wing traits in males and females, respectively. On the contrary, heritability estimates for FA were low and not significant. This is a novel study of natural genetic variation in FA of wing shape. Our findings suggest that partial wing components behave as distinct units of selection for FA, and local adaptation of the mechanisms to stabilize developmental processes occur in nature.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">Animal model</Param>
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      <Object Type="keyword">
        <Param Name="value">Geometric morphometrics</Param>
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      <Object Type="keyword">
        <Param Name="value">Heritability</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Natural genetic variation</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Wing shape</Param>
      </Object>
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  </Article>
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