198 research outputs found

    Clinical characteristics of the study cohort.

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    <p>Data are medians (interquartile range).</p><p>BAI, body adiposity index; BMI, body mass index; Carotid IMT, carotid intima-media thickness; CRP, C-reactive protein; DBP, diastolic blood pressure; HDL-C, high density lipoprotein cholesterol; LDL-C, low density lipoprotein cholesterol; MCRI, metabolic clearance rate of insulin; M/I, insulin sensitivity index from the euglycemic-hyperinsulinemic clamp; PAI-1, plasminogen activator inhibitor-1; PBF, percent total body fat; SBP, systolic blood pressure; TG, triglycerides.</p

    Relationship of percent body fat (PBF) with body adiposity index (BAI) and body mass index (BMI) in men and women.

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    <p>A. BAI versus PBF. B. BMI versus PBF. The graphs are generated on untransformed data for the BAI and BMI variables, while the main analyses in our study are based on log transformations of these variables. Therefore, the correlation coefficients (r) here are slightly different than those reported elsewhere in the text.</p

    Comparison of correlation coefficients between cardiometabolic risk factors and BMI versus BAI.

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    <p>Correlation coefficients that are significantly greater are highlighted in bold.</p>a<p><i>P</i> values from Hotelling’s T-test.</p

    Clinical Characteristics of PCOS and control subjects.

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    <p>*P<0.001 compared to control group. Data are median (interquartile range). In the replication cohort, androgen measurements were available only in the cases and controls recruited by R. S. Legro.</p><p>Abbreviations: BMI: body mass index; mFG: modified Ferriman-Gallwey hirsutism score; NA: Data not Available; HOMA-IR, homeostasis model assessment of insulin resistance; HOMA-%B, homeostasis model assessment of beta-cell function (insulin secretion).</p

    Gene structure and linkage disequilibrium plot for <i>DKK1</i> and <i>DNAJB1</i>.

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    <p>The gene structure is shown at top, with exons shown as filled boxes, untranslated regions as unfilled boxes and introns as connecting lines. The locations of the genotyped SNPs relative to the exons are indicated. The linkage disequilibrium (LD) plot at the bottom displays D' values (%) for each pair of SNPs in the box at the intersection of the diagonals from each SNP. The solid blocks indicate D' = 1 for the corresponding pair of variants. The darker solid blocks indicate a logarithm of the odds (LOD) score ≥2 for the corresponding pair of variants; lighter solid blocks indicate a LOD score <2. Within each gene, SNPs were considered together in one haplotype block as indicated.</p

    Top Associations with Additional SNPs.

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    <p>Associations with pvalues <5×10<sup>−5</sup> are listed here. Of the ∼115,000 SNPs tested for this table, ∼20,000 SNPs are not in linkage disequilibrium. Since 3 phenotypes were tested, the Bonferroni correction for multiple comparisons is 0.05/(20,000×3) = 8×10<sup>−7</sup>.</p><p>Top Associations with Additional SNPs.</p

    Association of known IBD SNPs.

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    <p>“Previously reported SNPs” are those IBD snps added to the design of the ImmunoChip; one per locus is shown here. Since 2 phenotypes were tested for this table (CD and UC) and 100 of the SNPs were not in linkage disequilibrium in Puerto Rico controls, the Bonferroni correction for multiple comparisons is 0.05/(2*100) = 0.00025.</p><p>Association of known IBD SNPs.</p

    “Global” continental ancestry in Puerto Rican subjects.

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    <p>A. Principal components analysis of the combined Puerto Rican and HGDP subjects. B. “Global” continental ancestry was estimated using Admixture 1.2 in an analysis supervised by data from HGDP populations as described in Methods (AFR, sub-Saharan African continent, dark blue; EUR, European continent, red; and AMR, Mexico, Central and South America continents, green). HGDP subjects not originating from these three continents are black. Puerto Rican subjects were sorted left-to-right based on ancestry from the African continent.</p
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