57 research outputs found

    Selection of studies for meta-analysis.

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    <p>Literatures search was conducted to identify articles up to April 30, 2012. Abbreviation: GI, glycemic index; GL, glycemic load; CHD, coronary heart disease; MI, myocardial infraction; CVD, cardiovascular disease.</p

    Characteristics of the included studies in this meta-analysis for dietary GI, GL and risk of stroke and related mortality.

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    <p>Abbreviations: GI, glycemic index; GL, glycemic load; FFQ, Food frequency questionnaire.</p>*<p>Study’s quality assessment was the same as the footnote of <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0052182#pone-0052182-t001" target="_blank">Table 1</a>.</p>†<p>Only dietary GI was available in the original article.</p

    Relative risks for the association between dietary GI or GL and risk of stroke.

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    <p>The risk estimate and 95%CI were calculated by comparing the highest category with lowest.</p

    Stratified meta-analyses of association between dietary GI, GL and the risk of CHD by BMI.

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    *<p>Analyses of dietary GI were based on 5 studies (6 data points, because men and women were included separately for the Beulens study <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0052182#pone.0052182-Beulens1" target="_blank">[11]</a>).</p>†<p>Analyses of dietary GL were based on 6 studies (7 data points, because men and women were included separately for the Beulens study <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0052182#pone.0052182-Beulens1" target="_blank">[11]</a>).</p>‡<p><i>P<sub>interaction</sub></i> was for the difference in relative risks between higher and lower BMI overall.</p>§<p>The <i>I</i><sup>2</sup> statistics and the Cochran Q test were used to examine statistical heterogeneity across studies.</p

    Relative risks for the association between dietary GI or GL and risk of CHD among women.

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    <p>The risk estimate and 95%CI were calculated by comparing the highest category with lowest.</p

    Characteristics of included prospective studies in this meta-analysis for dietary GI, GL and risk of CHD.

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    <p>Abbreviation: GI, glycemic index; GL, glycemic load; FFQ, food frequency questionnaire; BMI, body mass index.</p>*<p>Study’s quality assessment was performed by review of study design, including inclusion and exclusion criteria, assessment of exposure, assessment of outcome, control of confounding, and evidence of bias. Each of the 5 quality criteria was evaluated and scored on an integer scale (0 or 1, with 1 being better) and summed; quality scores from 0 to 3 were considered lower and 4 to 5 higher quality.</p

    Relative risks for the association between dietary GI or GL and risk of CHD.

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    <p>The risk estimate and 95%CI were calculated by comparing the highest category with lowest.</p

    Relative risks of CHD and stroke by continuous dietary GL level.

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    <p>The 2-stage generalized least-squares trend estimation (GLST) method <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0052182#pone.0052182-Orsini1" target="_blank">[33]</a> was used to evaluate the relative risks of CHD and stroke by continuous dietary GL level, which allowed combining the GLST-estimated study-specific slopes with the results from studies that only reported effect estimates for continuous associations. The per 50-unit increment in dietary GI level was approximately equivalent to the difference between the medians of the highest and the lowest categories of the included studies.</p

    The <i>myotrophin</i> rs17168525 C/T variant occurs in the let-7/miR-98 binding site.

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    <p>The variant rs17168525 is a C to T change (mRNA sequence as reference) located in the predicted binding site for let-7/miR-98 in the 3′-UTR of the <i>myotrophin</i> gene. C-allele at rs17168525 base-paired with G in Watson—Crick mode (shown with a solid line). However, when the T-allele is present, base-pairing complementarity is interrupted (shown with a dashed line).</p

    Let-7c suppresses the protein expression level of myotrophin <i>in vitro</i> cellular model.

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    <p>Cardiomyocytes were infected with PremiR miRNA precursor or Anti-miR miRNA inhibitor of let-7c (<i>A</i> and <i>B</i>). Myotrophin expression was analyzed by immunoblot 48 h after infection. *p < 0.05.</p
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