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Articles by F Rivadeneira
Total Records ( 5 ) for F Rivadeneira
  A Dehghan , Q Yang , A Peters , S Basu , J. C Bis , A. R Rudnicka , M Kavousi , M. H Chen , J Baumert , G. D.O Lowe , B McKnight , W Tang , M de Maat , M. G Larson , S Eyhermendy , W. L McArdle , T Lumley , J. S Pankow , A Hofman , J. M Massaro , F Rivadeneira , M Kolz , K. D Taylor , C. M van Duijn , S Kathiresan , T Illig , Y. S Aulchenko , K. A Volcik , A. D Johnson , A. G Uitterlinden , G. H Tofler , C Gieger , Psaty Wellcome Trust Case Control Consortium , D. J Couper , E Boerwinkle , W Koenig , C. J O`Donnell , J. C Witteman , D. P Strachan , N. L Smith and A. R. Folsom
 

Background— Fibrinogen is both central to blood coagulation and an acute-phase reactant. We aimed to identify common variants influencing circulation fibrinogen levels.

Methods and Results— We conducted a genome-wide association analysis on 6 population-based studies, the Rotterdam Study, the Framingham Heart Study, the Cardiovascular Health Study, the Atherosclerosis Risk in Communities Study, the Monitoring of Trends and Determinants in Cardiovascular Disease/KORA Augsburg Study, and the British 1958 Birth Cohort Study, including 22 096 participants of European ancestry. Four loci were marked by 1 or more single-nucleotide polymorphisms that demonstrated genome-wide significance (P<5.0x10–8). These included a single-nucleotide polymorphism located in the fibrinogen β chain (FGB) gene and 3 single-nucleotide polymorphisms representing newly identified loci. The high-signal single-nucleotide polymorphisms were rs1800789 in exon 7 of FGB (P=1.8x10–30), rs2522056 downstream from the interferon regulatory factor 1 (IRF1) gene (P=1.3x10–15), rs511154 within intron 1 of the propionyl coenzyme A carboxylase (PCCB) gene (P=5.9x10–10), and rs1539019 on the NLR family pyrin domain containing 3 isoforms (NLRP3) gene (P=1.04x10–8).

Conclusions— Our findings highlight biological pathways that may be important in regulation of inflammation underlying cardiovascular disease.

  A. C Morrison , J. F Felix , L. A Cupples , N. L Glazer , L. R Loehr , A Dehghan , S Demissie , J. C Bis , W. D Rosamond , Y. S Aulchenko , Y. A Wang , T Haritunians , A. R Folsom , F Rivadeneira , E. J Benjamin , T Lumley , D Couper , B. H Stricker , C. J O'Donnell , K. M Rice , P. P Chang , A Hofman , D Levy , J. I Rotter , E. R Fox , A. G Uitterlinden , T. J Wang , B. M Psaty , J. T Willerson , C. M van Duijn , E Boerwinkle , J. C. M Witteman , R. S Vasan and N. L. Smith
  Background—

Prognosis and survival are significant concerns for individuals with heart failure (HF). To better understand the pathophysiology of HF prognosis, the association between 2 366 858 single-nucleotide polymorphisms (SNPs) and all-cause mortality was evaluated among individuals with incident HF from 4 community-based prospective cohorts: the Atherosclerosis Risk in Communities Study, the Cardiovascular Health Study, the Framingham Heart Study, and the Rotterdam Study.

Methods and Results—

Participants were 2526 individuals of European ancestry and 466 individuals of African ancestry who experienced an incident HF event during follow-up in the respective cohorts. Within each study, the association between genetic variants and time to mortality among individuals with HF was assessed by Cox proportional hazards models that included adjustment for sex and age at the time of the HF event. Prospective fixed-effect meta-analyses were conducted for the 4 study populations of European ancestry (N=1645 deaths) and for the 2 populations of African ancestry (N=281 deaths). Genome-wide significance was set at P=5.0x10–7. Meta-analytic findings among individuals of European ancestry revealed 1 genome-wide significant locus on chromosome 3p22 in an intron of CKLF-like MARVEL transmembrane domain containing 7 (CMTM7, P=3.2x10–7). Eight additional loci in individuals of European ancestry and 4 loci in individuals of African ancestry were identified by high-signal SNPs (P<1.0x10–5) but did not meet genome-wide significance.

Conclusions—

This study identified a novel locus associated with all-cause mortality among individuals of European ancestry with HF. This finding warrants additional investigation, including replication, in other studies of HF.

  N. L Smith , J. F Felix , A. C Morrison , S Demissie , N. L Glazer , L. R Loehr , L. A Cupples , A Dehghan , T Lumley , W. D Rosamond , W Lieb , F Rivadeneira , J. C Bis , A. R Folsom , E Benjamin , Y. S Aulchenko , T Haritunians , D Couper , J Murabito , Y. A Wang , B. H Stricker , J. S Gottdiener , P. P Chang , T. J Wang , K. M Rice , A Hofman , S. R Heckbert , E. R Fox , C. J O'Donnell , A. G Uitterlinden , J. I Rotter , J. T Willerson , D Levy , C. M van Duijn , B. M Psaty , J. C. M Witteman , E Boerwinkle and R. S. Vasan
  Background—

Although genetic factors contribute to the onset of heart failure (HF), no large-scale genome-wide investigation of HF risk has been published to date. We have investigated the association of 2 478 304 single-nucleotide polymorphisms with incident HF by meta-analyzing data from 4 community-based prospective cohorts: the Atherosclerosis Risk in Communities Study, the Cardiovascular Health Study, the Framingham Heart Study, and the Rotterdam Study.

Methods and Results—

Eligible participants for these analyses were of European or African ancestry and free of clinical HF at baseline. Each study independently conducted genome-wide scans and imputed data to the 2.5 million single-nucleotide polymorphisms in HapMap. Within each study, Cox proportional hazards regression models provided age- and sex-adjusted estimates of the association between each variant and time to incident HF. Fixed-effect meta-analyses combined results for each single-nucleotide polymorphism from the 4 cohorts to produce an overall association estimate and P value. A genome-wide significance P value threshold was set a priori at 5.0x10–7. During a mean follow-up of 11.5 years, 2526 incident HF events (12%) occurred in 20 926 European-ancestry participants. The meta-analysis identified a genome-wide significant locus at chromosomal position 15q22 (1.4x10–8), which was 58.8 kb from USP3. Among 2895 African-ancestry participants, 466 incident HF events (16%) occurred during a mean follow-up of 13.7 years. One genome-wide significant locus was identified at 12q14 (6.7x10–8), which was 6.3 kb from LRIG3.

Conclusions—

We identified 2 loci that were associated with incident HF and exceeded genome-wide significance. The findings merit replication in other community-based settings of incident HF.

  E Grundberg , T Kwan , B Ge , K. C.L Lam , V Koka , A Kindmark , H Mallmin , J Dias , D. J Verlaan , M Ouimet , D Sinnett , F Rivadeneira , K Estrada , A Hofman , J. M van Meurs , A Uitterlinden , P Beaulieu , A Graziani , E Harmsen , O Ljunggren , C Ohlsson , D Mellstrom , M. K Karlsson , O Nilsson and T. Pastinen
 

The common genetic variants associated with complex traits typically lie in noncoding DNA and may alter gene regulation in a cell type-specific manner. Consequently, the choice of tissue or cell model in the dissection of disease associations is important. We carried out an expression quantitative trait loci (eQTL) study of primary human osteoblasts (HOb) derived from 95 unrelated donors of Swedish origin, each represented by two independently derived primary lines to provide biological replication. We combined our data with publicly available information from a genome-wide association study (GWAS) of bone mineral density (BMD). The top 2000 BMD-associated SNPs (P < ~10–3) were tested for cis-association of gene expression in HObs and in lymphoblastoid cell lines (LCLs) using publicly available data and showed that HObs have a significantly greater enrichment (threefold) of converging cis-eQTLs as compared to LCLs. The top 10 BMD loci with SNPs showing strong cis-effects on gene expression in HObs (P = 6 x 10–10 – 7 x 10–16) were selected for further validation using a staged design in two cohorts of Caucasian male subjects. All 10 variants were tested in the Swedish MrOS Cohort (n = 3014), providing evidence for two novel BMD loci (SRR and MSH3). These variants were then tested in the Rotterdam Study (n = 2090), yielding converging evidence for BMD association at the 17p13.3 SRR locus (Pcombined = 5.6 x 10–5). The cis-regulatory effect was further fine-mapped to the proximal promoter of the SRR gene (rs3744270, r2 = 0.5, P = 2.6 x 10–15). Our results suggest that primary cells relevant to disease phenotypes complement traditional approaches for prioritization and validation of GWAS hits for follow-up studies.

  A. D Johnson , M Kavousi , A. V Smith , M. H Chen , A Dehghan , T Aspelund , J. P Lin , C. M van Duijn , T. B Harris , L. A Cupples , A. G Uitterlinden , L Launer , A Hofman , F Rivadeneira , B Stricker , Q Yang , C. J O'Donnell , V Gudnason and J. C. Witteman
 

Variation in serum bilirubin is associated with altered cardiovascular disease risk and drug metabolism. We aimed to identify genetic contributors to variability in serum bilirubin levels by combining results from three genome-wide association studies (Framingham heart study, n = 3424; Rotterdam study, n = 3847; Age, Gene, Environment and Susceptibility-Reykjavik, n = 2193). Meta-analysis showed strong replication for a genetic influence on serum bilirubin levels of the UGT1A1 locus (P < 5 x 10–324) and a 12p12.2 locus. The peak signal in the 12p12.2 region was a non-synonymous SNP in SLCO1B1 (rs4149056, P = 6.7 x 10–13), which gives rise to a valine to alanine amino acid change leading to reduced activity for a hepatic transporter with known affinity for bilirubin. There were also suggestive associations with several other loci. The top variants in UGT1A1 and SLCO1B1 explain ~18.0 and ~1.0% of the variation in total serum bilirubin levels, respectively. In a conditional analysis adjusted for individual genotypes for the top UGT1A1 variant, the top SLCO1B1 variant remained highly significant (P = 7.3 x 10–13), but no other variants achieved genome-wide significance. In one of the largest genetic studies of bilirubin to date (n = 9464), we confirm the substantial genetic influence of UGT1A1 variants, consistent with past linkage and association studies, and additionally provide strong evidence of a role for allelic variation in SLCO1B1. Given the involvement of bilirubin in a number of physiological and disease processes, and the roles for UGT1A1 and SLCO1B1 in drug metabolism, these genetic findings have potential clinical importance. In analyses for association with gallbladder disease or gallstones, top bilirubin SNPs in UGT1A1 and SLCO1B1 were not associated.

 
 
 
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