45 research outputs found

    Type II diabetes mellitus and cardiovascular markers in humans: a prospective study in hellenic homogeneous population

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    Approximately 200 million people, worldwide, are currently having Type 2 diabetes mellitus (T2DM), a prevalence that has been predicted to increase to 366 million by 2030. Atherosclerotic coronary heart disease (CHD) and other forms of cardiovascular disease (CYD) are the major cause of mortality in T2DM as well as a major contributor to morbidity and lifetime costs. A number of unfavorable conditions predisposing to CVD coexist with diabetic status including hyperglycaemia, dyslipidaemia, inflammation and coagulation, many of which may be closely associated with insulin resistance. In addition, mutations and polymorphisms in a number of genes have also been linked with monogenic and polygenic forms of T2DM. In this respect, the possible relationship between these disorders and a number of biochemical factors in a selection of different age groups of diabetic patients was studied. The purpose of the present work was the identification of biochemical parameters in plasma, which may serve as predisposition factors to CVD in T2DM patients of different age. The variability of hyperglycaemia, dyslipidaemia, and inflammation with age progression were studied. Four different diabetic groups allocated based on the subjects age (Group A:15-25 years old; Group 13:26-40 years old; Group C:40-60 years old; Group D:60-80 years old) and consisting of ten patients each, in parallel with ten matched for age, sex and ethnic origin healthy controls, were screened for glucose, insulin, lipid profile (total cholesterol, triglycerides, LDL and HDL) and inflammatory mediators (Homocysteine, CRP, IL-6, TNF-a). Significant differences were observed between the expression of biochemical markers among different age groups. Hyperglycaemia showed no variability with age whereas dyslipidaemia correlated positively with age progression, as well as obesity, low physical activity and family history of heart disease or diabetes. Marked inflammation was prominent only in Groups C and D. The present study indicates that different biochemical parameters may be used for assessment of CVD risk in T2DM patients of variable age

    Overview of MS 6q23 interactions.

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    <p>Tracks are labelled as follows: A–LD regions targeted in ‘region’ Capture Hi-C; B–Gene regions targeted in ‘promoter’ Capture Hi-C; C–RefSeq genes (packed for clarity); D–MS index SNPs; E–MS LD regions; F–Interactions observed in the GM12878 B-cell line and G–Interactions observed in the Jurkat T-cell line. Promoter and region Capture Hi-C experiments have been merged for clarity. The genomic region chr6:136,650,000–137,280,000 has been omitted for clarity. All co-ordinates are based on GRCh37. Generated using the WashU EpiGenome Browser (<a href="http://epigenomegateway.wustl.edu/browser/" target="_blank">http://epigenomegateway.wustl.edu/browser/</a>).</p

    Summary data of the interaction analysis for <i>HLA-DRB1</i> SE allelic groups and SNP rs3087456 for the Swedish cohort.

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    <p>Additive interaction is presented as attributable proportion (AP) with 95% confidence interval (CI). For additional analysis see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0032861#pone.0032861.s005" target="_blank">Table S5</a>. SE = shared epitope; ACPA+ = anti citrullinated protein antibody positive RA patients.</p

    Risk of developing RA for combinations of the <i>HLA-DRB1</i> SE and rs3087456 alleles in Swedish.

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    <p>British. Dutch and Norwegian cohorts.</p><p>Results for additive (add.) and multiplicative (mult.) interaction is displayed as significance (P value) of deviation from expected risk given no interaction. AP = attributable proportion; SE = shared epitope; OR = odds ratio; ACPA+ = anti citrullinated protein antibody positive RA patients; CI = confidence interval.</p

    Summary data for interaction analysis between <i>CIITA</i> rs4781019 and <i>HLA-DRB1</i> SE.

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    <p>The table presents the best result after analysis of interaction between the <i>CIITA</i> locus and <i>HLA-DRB1</i>. Dominant and recessive (for the risk allele) genetic models were tested for each SNP, see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0032861#pone.0032861.s004" target="_blank">Table S4</a> for complete results. AP = attributable proportion; SE = shared epitope; ACPA+ = anti citrullinated protein antibody positive RA patients.</p

    Heritability of genome-wide SNPs for nine complex traits.

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    <p>Components of heritability for typed markers (blue) over nine traits and imputed markers (green) over seven WTCCC1 traits shown. Light bars correspond to estimates from the standard variance-component and dark bars correspond to estimate from LD-adjusted variance-component. Two control sub-groups (NBS and 58C) tested against each other as negative control; diseases tested are Bipolar Disorder (BD), Coronary Artery Disease (CAD), Crohn's Disease (CD), Hypertension (HT), Rheumatoid Arthritis (RA), Type 1 Diabetes (T1D), Type 2 Diabetes (T2D), Multiple Sclerosis (MS), Ulcerative Colitis (UC). Autoimmune traits (CD, RA, T1D, UC, and MS) excluded the well-studied MHC region. All traits exhibit an increase after LD adjustment, indicative of a genetic architecture that is shifted towards low-frequency causal variants. Error bars show analytical standard error of estimate.</p
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