Patterns of Pain Descriptor Usage in African Americans and European Americans With Chronic Pain.

2004 ◽  
Vol 10 (1) ◽  
pp. 81-89 ◽  
Author(s):  
Jeffrey E. Cassisi ◽  
Masataka Umeda ◽  
Julie A. Deisinger ◽  
Christine Sheffer ◽  
Kenneth R. Lofland ◽  
...  
2008 ◽  
Vol 39 (4) ◽  
pp. 589-610 ◽  
Author(s):  
Leslie Gordon Simons ◽  
Ellen Granberg ◽  
Yi-Fu Chen ◽  
Ronald L. Simons ◽  
Rand D. Conger ◽  
...  

2008 ◽  
Vol 39 (2) ◽  
pp. 207-228
Author(s):  
Leslie Gordon Simons ◽  
Gene R. Brody ◽  
Velma M. Murry ◽  
Ellen Granberg ◽  
Yi-Fu Chen ◽  
...  

Author(s):  
David W. Stowe

Religious music functions both to create group identities and to dissolve social boundaries. Historically, American music has been characterized by racial and religious crossover. While many ethnic groups have participated in constituting American music, the most seminal crossovers have occurred between African and European Americans. Jazz was shaped largely by the interactions of Jews and African Americans. Gospel music developed from the interaction of vernacular slave spirituals, Protestant hymns, and the secular blues. Christian hymns have been thoroughly indigenized by many Native American groups. Compared to Buddhists and Jews, American Hindus and Muslims have made few musical adaptations of their worship music, but their music has been widely sampled in American popular styles. In recent decades, mainline Protestant hymnals have come to reflect the deeply multicultural reality of American sacred song.


Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Lu-Chen Weng ◽  
Weihong Tang ◽  
Mary Cushman ◽  
James S Pankow ◽  
Saonli Basu ◽  
...  

Introduction: Activated partial thromboplastin time (aPTT) is commonly used to screen for coagulation factor deficiencies. Shorter aPTT is also a risk marker for incident and recurrent venous thromboembolism (VTE). Genetic factors influencing aPTT are not well understood. aPTT was associated with common genetic variants of coagulation factors V (F5), XI (F11), XII (F12), KNG1, HRG, and ABO in previously reported genome-wide association studies (GWAS) that were conducted in individuals of European ancestry; no data have been reported in other race groups. Hypothesis: The present study aimed to identify aPTT-related gene variants in European Americans (EAs) and African Americans (AAs). Methods: We conducted a large-scale candidate gene study for aPTT in 9,719 EAs and 2,799 AAs from the Atherosclerosis Risk in Communities (ARIC) study. Subjects on anticoagulants were excluded. Nearly 50,000 single nucleotide polymorphisms (SNPs) located in 2,100 candidate genes were genotyped by the Candidate gene Association Resource (CARe) gene chip. The association between each SNP and aPTT was assessed with an additive genetic model using linear regression adjusted for age, sex, and field center. We additionally adjusted for principal components in AAs to account for potential population stratification. P-value for significant threshold was set at 2x10-6 after accounting for multiple testing. Results: In EAs, fifty-five SNPs from F5, HRG, KNG1, F11, F12, and ABO genes exceeded the significant p-value threshold. The signals in HRG, KNG1, F11, F12, and ABO genes replicated the previously reported GWAS findings. The top variant in F5 identified in EAs was only weakly associated with the previously reported GWAS variant (rs2239852, p=1.89x10-08 and r2=0.02 with rs9332701 reported in the previously reported GWAS). In AAs, twenty-seven SNPs from the HRG, KNG1, F12, and ABO genes were significantly associated with aPTT. The top signals from the HRG (rs9898, p=1.19x10-27) and KNG1 genes ( rs710446 , p=8.41x10-42) replicated the previously reported signals in EAs with similar effect size and direction of association, but the top signals in the F12 and ABO genes were weakly associated with the previously reported variants in EAs (rs1801020 in F12: p=1.01x10-84 and r2=0.12 with rs2545801, and rs8176722 in ABO: p=1.62x10-29 and r2=0.26 with rs687621 , respectively). Conclusions: Our study replicated the previously reported associations of aPTT with HRG, KNG1, F11, F12, and ABO genes in EAs and with HRG and KNG1 in AAs. The signals from F5 identified in EAs and from F12 and ABO identified in AAs may represent new genetic variants for aPTT.


Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Jaclyn Ellis ◽  
Jeremy Walston ◽  
Josee Dupuis ◽  
Emma Larkin ◽  
Maja Barbalic ◽  
...  

INTRODUCTION: C-reactive protein (CRP) is a heritable biomarker of systemic inflammation and a predictor of cardiovascular disease (CVD). Cigarette smoking is a major risk factor in the development of CVD and has been shown to affect circulating levels of CRP. Therefore, we sought to determine how this important environmental exposure may influence genetic associations with CRP in a multi-ethnic setting. METHODS: Using the ITMAT Broad-CARe (IBC) SNP array, a custom 50,000 SNP gene-centric array having dense coverage of over 2,000 candidate genes for CVD pathways, we performed a meta-analysis of up to 26,065 participants of European descent and 7,584 participants of African descent for association with log-CRP level within smoking status stratum. The 2 smoking strata were: never smokers and ever smokers (comprising of current and former smokers). We conducted IBC-wide association scans for CRP within cohort-, race- and smoking-stratum and meta-analyzed by race. Samples were from the Candidate gene Association Resource (CARe) cohorts (Atherosclerosis Risk in Communities Study, Framingham Heart Study, Cardiovascular Health Study, Cleveland Family Study , Coronary Artery Risk Development in Young Adults Study, Jackson Heart Study, and Multi-Ethnic Study of Atherosclerosis Study). Results were considered to be panel wide statistically significant if p<2.2×10−6. RESULTS: The overall sample size for ever smokers (never smokers) was 11,698 (10,344) in European Americans and 3,448 (4,330) in African Americans. The per-allele beta coefficients for genes previously established to be associated with CRP and present on the IBC chip ( CRP, APOE, GCKR, IL6R, LEPR, HNF1A, NLRP3 ) were very similar in magnitude between smoking strata in European Americans. However, in the African Americans, the estimated per-allele CRP and IL6R betas were 2-times larger for the ever smokers as compared to the never smokers. In the European American analysis, one gene not previously reported for association with CRP reached IBC-wide significance for a CRP-lowering effect in the never smokers ( GSTT1 , p=4.8E-07 for SNP rs405597 ), but not in the ever smokers (p=0.078). CONCLUSION: This large scale candidate gene based meta-analysis identified one novel locus for CRP ( GSTT1 ) associated with serum CRP levels in those reporting having never regularly smoked. Polymorphisms in GSTT1 , which plays a role in detoxification, have previously been reported to interact with smoking for other phenotypes including birth weight and colorectal cancer. We also observed evidence that smoking modifies the effects for previously established loci CRP and IL6R in African Americans. These results may identify important context genetic specific effects that influence chronic inflammation.


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