42 research outputs found

    Common CRP haplotypes, risk of CHD, and relative effects of haplotypes on plasma CRP levels

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    *<p>Cutoff set as ≥5.0%, based on 744 women and 781 men.</p>†<p>Haplotype-specific ORs (multiplicative increase in odds per copy of haplotype) using unconditional logistic regression, adjusted for matching factors</p>‡<p>Log-transformed CRP adjusted for matching factors</p>§<p>All other haplotypes</p>¥<p>Globally-adjusted likelihood ratio test</p

    Pairwise linkage disequilibrium (D') and correlation coefficients (r<sup>2</sup>) between CRP polymorphisms and control women and men

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    <p>Pairwise linkage disequilibrium (D') and correlation coefficients (r<sup>2</sup>) between CRP polymorphisms and control women and men</p

    Baseline characteristics of participants with incident CHD (cases) and matched* controls among women (Nurses' Health Study) and men (Health Professionals Follow-up Study)<sup>†</sup>

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    *<p>Matched on age, smoking status, date of blood drawing, and fasting status (women only)</p>†<p>Values are least square mean ± standard error for continuous variables and proportions for categorical variables, except for CRP, which is shown as log-transformed geometric mean and 95% confidence interval</p>‡<p>P for difference between cases and controls by matching factor-adjusted t-Test for rows with means, and by Chi-Square Test for rows with proportions</p>§<p>Race unknown in 10 cases and 21 controls (HPFS); 18 cases and 16 controls (NHS)</p

    Association of CRP SNPs with risk of coronary heart disease, and with plasma CRP levels among women and men

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    *<p>Conditional logistic regression under the additive genetic model</p>†<p>Matching factor-adjusted, log-transformed, multiplicative change per copy of the allele among controls</p>‡<p>P for change in CRP levels</p

    Quantile-Quantile(QQ) plots on SNP set enrichment.

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    <p>QQ-plots of SNP set enrichment test. Solid line represents normal distribution and black dots represent data distribution of p-values for eSNPs representing genes within the gene set of interest. Deviation of the data from the solid line indicates a non-normal distribution. Plots are shown for the top ranking gene sets A: published mRNA profiling signatures from infarcted tissue and B: implicated causal genes from the Global Lipid Genetics GWAS Consortium.</p

    Distribution of population characteristics by stress level at work and at home.

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    a<p>P-value from ANOVA for continuous variables, from Chi Square for categorical variables (P-values significant at alpha = 0.05 shown in bold). Distribution of characteristics similar to smaller sample of men with data on sICAM-1/sVCAM-1. Abbreviations: aHEI, alternative healthy eating index; BMI, body mass index; mets, metabolic equivalents; SD, standard deviation.</p

    Linear Regression models for stress at work and at home and inflammation, sVCAM-1, and sICAM-1 among healthy men.

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    a<p>Model A is adjusted for age and self-reported race.</p>b<p>Model B is additionally adjusted for health behaviors (smoking, diet, exercise, and BMI-continuous).</p><p>Beta coefficients (SE) and P-values significant at alpha ≤0.05 shown in bold.</p

    Average and maximum pair CVs for standardized values of 61 miRNAs measured in 15 duplicate (split) samples.

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    <p>Bold indicates acceptable results and italics indicates unacceptable results. Avg CV = average CV; Max CV = maximum CV; % Detected = % samples with detectable levels; NC = not calculated.</p><p>Average and maximum pair CVs for standardized values of 61 miRNAs measured in 15 duplicate (split) samples.</p
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