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Articles by M Cushman
Total Records ( 4 ) for M Cushman
  N. L Smith , M. H Chen , A Dehghan , D. P Strachan , S Basu , N Soranzo , C Hayward , I Rudan , M Sabater Lleal , J. C Bis , M. P. M de Maat , A Rumley , X Kong , Q Yang , F. M. K Williams , V Vitart , H Campbell , A Malarstig , K. L Wiggins , C. M Van Duijn , W. L McArdle , J. S Pankow , A. D Johnson , A Silveira , B McKnight , A. G Uitterlinden , Aleksic Wellcome Trust Case Control Consortium; , J. B Meigs , A Peters , W Koenig , M Cushman , S Kathiresan , J. I Rotter , E. G Bovill , A Hofman , E Boerwinkle , G. H Tofler , J. F Peden , B. M Psaty , F Leebeek , A. R Folsom , M. G Larson , T. D Spector , A. F Wright , J. F Wilson , A Hamsten , T Lumley , J. C. M Witteman , W Tang and C. J. O'Donnell
 

Background— Plasma levels of coagulation factors VII (FVII), VIII (FVIII), and von Willebrand factor (vWF) influence risk of hemorrhage and thrombosis. We conducted genome-wide association studies to identify new loci associated with plasma levels.

Methods and Results— The setting of the study included 5 community-based studies for discovery comprising 23 608 European-ancestry participants: Atherosclerosis Risk In Communities Study, Cardiovascular Health Study, British 1958 Birth Cohort, Framingham Heart Study, and Rotterdam Study. All subjects had genome-wide single-nucleotide polymorphism (SNP) scans and at least 1 phenotype measured: FVII activity/antigen, FVIII activity, and vWF antigen. Each study used its genotype data to impute to HapMap SNPs and independently conducted association analyses of hemostasis measures using an additive genetic model. Study findings were combined by meta-analysis. Replication was conducted in 7604 participants not in the discovery cohort. For FVII, 305 SNPs exceeded the genome-wide significance threshold of 5.0x10–8 and comprised 5 loci on 5 chromosomes: 2p23 (smallest P value 6.2x10–24), 4q25 (3.6x10–12), 11q12 (2.0x10–10), 13q34 (9.0x10–259), and 20q11.2 (5.7x10–37). Loci were within or near genes, including 4 new candidate genes and F7 (13q34). For vWF, 400 SNPs exceeded the threshold and marked 8 loci on 6 chromosomes: 6q24 (1.2x10–22), 8p21 (1.3x10–16), 9q34 (<5.0x10–324), 12p13 (1.7x10–32), 12q23 (7.3x10–10), 12q24.3 (3.8x10–11), 14q32 (2.3x10–10), and 19p13.2 (1.3x10–9). All loci were within genes, including 6 new candidate genes, as well as ABO (9q34) and VWF (12p13). For FVIII, 5 loci were identified and overlapped vWF findings. Nine of the 10 new findings were replicated.

Conclusions— New genetic associations were discovered outside previously known biological pathways and may point to novel prevention and treatment targets of hemostasis disorders.

  M Cushman , L. A McClure , V. J Howard , N. S Jenny , S. G Lakoski and G. Howard
 

Background: We evaluated prevalence and correlates of increased high-sensitivity C-reactive protein (hsCRP) in a large population of blacks and whites, and the impact of hsCRP measurement on coronary heart disease risk reclassification.

Methods: We studied 19 080 participants of the REGARDS (REasons for Geographic And Racial Differences in Stroke) study (age >45 years, without vascular diagnoses, and living dispersed across the US). A total of 8309 nondiabetic participants not using lipid-lowering medications were classified into 4 risk categories based on the Framingham vascular disease risk score. Participants with hsCRP <1 mg/L were reclassified to the next lower risk group, and those with hsCRP >3 mg/L to the next higher risk group. We also assessed reclassification of risk based on the Reynolds vascular risk score, incorporating hsCRP and family history.

Results: Overall, 40% of participants had hsCRP >3 mg/L. Blacks, women, and obese people were at highest risk for increased hsCRP. Among nondiabetic women at 5%–20% Framingham vascular predicted risk, hsCRP data led to reclassification of 48% to a higher risk group and 19% to a lower risk group. For men, these percentages were 24% and 40%. Blacks were more often reclassified to a higher risk group than whites. Reynolds vascular risk score data led to reclassification of 85% of women and 67% of men, almost exclusively to a lower risk group than the Framingham vascular score.

Conclusions: In this national study, a majority of participants, especially blacks and women, were reclassified to a different 10-year vascular risk category on the basis of hsCRP testing after risk assessment. With the inclusion of hsCRP testing data, the Reynolds risk score classified the population differently than the new Framingham vascular score. .

  L. A Colangelo , P Ouyang , K Liu , P Kopp , S. H Golden , A. S Dobs , M Szklo , D Vaidya , M Cushman and S. M. Gapstur
  OBJECTIVE

To assess associations of sex hormones with impaired fasting glucose (IFG) and type 2 diabetes in men.

RESEARCH DESIGN AND METHODS

A total of 3,156 African American, Non-Hispanic white, Hispanic, and Chinese-American men aged 45–84 years who participated in the baseline visit of the Multi-Ethnic Study of Atherosclerosis (MESA) were included. Oddsratios and95% CIs for type 2 diabetes and IFG compared with normal fasting glucose for quartiles of hormones were estimated.

RESULTS

After adjusting for age, ethnicity, BMI, and waist circumference, IFG and diabetes were associated inversely with total testosterone and sex hormone–binding globulin (SHBG) and positively with estradiol (E2). Dehydroepiandrosterone was positively associated with IFG but not with diabetes. Associations did not differ across ethnic groups.

CONCLUSIONS

Regardless of obesity, total testosterone and SHBG were associated inversely and E2 was associated positively with IFG and diabetes in men. Further research is warranted to better understand the underlying biological mechanisms.

  G. Y. F Ho , X Xue , M Cushman , G McKeown Eyssen , R. S Sandler , D. J Ahnen , E. L Barry , F Saibil , R. S Bresalier , T. E Rohan and J. A. Baron
 

The Aspirin/Folate Polyp Prevention Trial found that aspirin, but not folic acid, reduced recurrence of colorectal adenomas. This study examined whether treatment effects on inflammation markers explained the trial results. The trial had a factorial design with three aspirin (placebo, 81, and 325 mg/d) and two folic acid (placebo and 1 mg/d) groups. There were 884 subjects who had colonoscopic evaluation for adenomas at year 3 and plasma levels of C-reactive protein (CRP), interleukin 6 (IL-6), tumor necrosis factor (TNF-), soluble TNF receptor type II (sTNF-R2), and IL-1 receptor antagonist (IL-1Ra) measured at baseline and year 3. Among individuals not receiving folic acid, there was a 4% decrease (mean ratio of year 3 to baseline levels = 0.96, 95% confidence interval [CI] = 0.82 to 1.14) in CRP for a period of 3 years in the 325 mg of aspirin group vs a 20% increase (mean ratio = 1.20, 95% CI = 1.03 to 1.41) in the placebo group (P = .027). By contrast, the reverse was observed among individuals who also received folic acid (Pinteraction = .013). Changes in inflammation markers were not associated with adenoma recurrence. Low-dose aspirin (325 mg/d) is beneficial in stabilizing CRP levels, which may be abrogated by folate. Nevertheless, inflammation markers do not mediate the chemopreventive effect of aspirin on colorectal adenomas.

 
 
 
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