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  <Article>
    <Journal>
      <PublisherName>VM Media SP. zo.o VM Group SK</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1898-018X</Issn>
      <Volume>29</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2021</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>The number of circulating CD34-positive cells is an independent predictor of coronary artery calcification progression: Sub-analysis of a prospective multicenter study</ArticleTitle>
    <FirstPage LZero="delete">423</FirstPage>
    <LastPage>431</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Keishi</FirstName>
        <LastName>Ichikawa</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toru</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuhiro</FirstName>
        <LastName>Osawa</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Japanese Red Cross Okayama Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Miki</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kunihisa</FirstName>
        <LastName>Kohno</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazufumi</FirstName>
        <LastName>Nakamura</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasushi</FirstName>
        <LastName>Koyama</LastName>
        <Affiliation>Department of Cardiology, Sakurabashi Watanabe Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Ito</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Background: Decreases in circulating CD34-positive cells are associated with increases in cardiovascular events. We investigated the association between the number of CD34-positive cells and the progression of coronary artery calcification (CAC), a marker of atherosclerosis, in patients with hypercholesteremia under statin therapy in a sub-analysis of a multicenter study.&lt;br&gt;
Methods: In the principal study, patients with CAC scores of 1–999 were treated with pitavastatin. Measurement of CAC by non-enhanced computed tomography and a blood test were performed at baseline and at 1-year follow-up. Patients were divided into two groups: CAC progression (change in CAC score &gt; 0) and non-progression. The number of circulating CD34-positive cells was counted using flow cytometry.&lt;br&gt;
Results: A total of 156 patients (mean age 67 years, 55% men) were included in this sub-analysis. CD34 positive cell numbers at baseline as a continuous variable was inversely correlated with annual change in the log-transformed CAC score (r = –0.19, p = 0.02). When patients were divided into high and low CD34 groups based on the median value of 0.8 cells/μL, the adjusted change in CAC score in the low-CD34 group was significantly greater than that in the high-CD34 group (54.2% vs. 20.8%, respectively, p = 0.04). In multiple logistic analysis, a low CD34-positive cell number was an independent predictor of CAC progression, with an odds ratio of 2.88 (95% confidence interval 1.28–6.49, p = 0.01).&lt;br&gt;
Conclusions: Low numbers of CD34-positive cells are associated with CAC progression in patients with hypercholesterolemia under statin therapy. The number of CD34-positive cells may help to identify patients at increased cardiovascular risk.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">coronary artery calcification</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">computed tomography</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">endothelial progenitor cells</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">hypercholesterolemia</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>75</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2021</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Possible Protective Effect of Remote Ischemic Preconditioning on Acute Kidney Injury Following Elective Percutaneous Coronary Intervention: Secondary Analysis of a Multicenter, Randomized Study</ArticleTitle>
    <FirstPage LZero="delete">45</FirstPage>
    <LastPage>53</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Hiroaki</FirstName>
        <LastName>Otsuka</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toru</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kentaro</FirstName>
        <LastName>Ejiri</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kunihisa</FirstName>
        <LastName>Kohno</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Makoto</FirstName>
        <LastName>Nakahama</LastName>
        <Affiliation>Department of Cardiology, Fukuyama City Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masayuki</FirstName>
        <LastName>Doi</LastName>
        <Affiliation>Department of Cardiology, Kagawa Prefectural Central Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mitsuru</FirstName>
        <LastName>Munemasa</LastName>
        <Affiliation>Department of Cardiology, Okayama Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masaaki</FirstName>
        <LastName>Murakami</LastName>
        <Affiliation>Department of Cardiology, Okayama Heart Clinic</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazufumi</FirstName>
        <LastName>Nakamura</LastName>
        <Affiliation>Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Density 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, Density and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/61433</ArticleId>
    </ArticleIdList>
    <Abstract>Remote ischemic preconditioning (RIPC) is a promising strategy for protecting against ischemic reperfusion injury. This study is a secondary analysis of a randomized study that aimed to evaluate the effect of RIPC on the early increase in serum creatinine (SCr) following percutaneous coronary intervention (PCI), which is associ-ated with contrast-induced acute kidney injury. Patients with stable angina undergoing elective PCI were assigned to control, RIPC, and continuous infusion of nicorandil (nicorandil) groups. The endpoint of this study was the incidence of the early increase in SCr, a predictor of contrast-induced acute kidney injury, which was defined as either a &gt; 20% or absolute increase by 0.3 mg/dl of SCr levels after 24 h of PCI. This study included 220 patients for whom a dataset of SCr values was available. The incidence of the early increase in SCr was significantly lower in the RIPC than in the control (1.3% vs 10.8%, p = 0.03) group, but was not significantly different between the nicorandil and control groups. In multivariate analysis, RIPC remained a significant fac-tor associated with a reduction in the incidence of early increase in SCr. RIPC reduces the incidence of early increase in SCr in patients with stable angina following elective PCI.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">remote ischemic preconditioning</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">stable angina</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">serum creatinine</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">acute kidney injury</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName/>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn/>
      <Volume>19</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2013</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Serum cystatin C as a biomarker of cardiac diastolic dysfunction in patients with cardiac disease and preserved ejection fraction</ArticleTitle>
    <FirstPage LZero="delete">E35</FirstPage>
    <LastPage>E39</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Kazumasa</FirstName>
        <LastName>Nosaka</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazufumi</FirstName>
        <LastName>Nakamura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kengo</FirstName>
        <LastName>Kusano</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norihisa</FirstName>
        <LastName>Toh</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takeshi</FirstName>
        <LastName>Tada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toru</FirstName>
        <LastName>Miyoshi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masayuki</FirstName>
        <LastName>Doi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kunihisa</FirstName>
        <LastName>Kohno</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Morita</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Ito</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Diastolic dysfunction of the heart is correlated with cardiac mortality. Serum cystatin C (CysC) is an endogenous marker of kidney function. It is not clear whether serum CysC is associated with diastolic dysfunction in patients with varying cardiac conditions with concomitant diastolic abnormalities and preserved ejection fraction (EF). The authors measured serum CysC levels in patients with cardiac diseases and examined the relationships between serum CysC levels and diastolic function. Serum CysC was measured and echocardiography was performed in 124 consecutive patients with cardiac diseases. Transmitral flow (TMF) patterns surrogating diastolic function were categorized into two groups: a normal group and an abnormal group. Serum CysC and BNP showed a significant positive correlation. There were no significant differences in serum CysC among those cardiac diseases. Seventy-eight patients with cardiac disease and preserved EF (left ventricular EF ≥50%) and without renal dysfunction (estimated glomerular filtration rate ≥60 mL/minute/1.73 m(2) ) were examined. Multivariate linear regression analysis demonstrated that left atrium diameter and abnormal TMF patterns were independent determinants of serum CysC. Furthermore, patients with elevated serum CysC levels had poor prognosis. Serum CysC is associated with diastolic dysfunction in patients with various cardiac diseases and preserved EF. Serum CysC might be a biomarker of cardiac diastolic dysfunction in patients with preserved EF.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList/>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName/>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn/>
      <Volume/>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>1997</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Effects of intracoronary fentanyl on left ventricular mechanoenergetics in the excised cross-circulated canine heart.</ArticleTitle>
    <FirstPage LZero="delete"/>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N"/>
        <LastName/>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList/>
    <ReferenceList/>
  </Article>
</ArticleSet>
