SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Hamsten Anders) "

Sökning: WFRF:(Hamsten Anders)

  • Resultat 1-10 av 93
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Peden, John F., et al. (författare)
  • A genome-wide association study in Europeans and South Asians identifies five new loci for coronary artery disease
  • 2011
  • Ingår i: Nature genetics. - 1546-1718. ; 43:4, s. 339-U89
  • Tidskriftsartikel (refereegranskat)abstract
    • Genome-wide association studies have identified 11 common variants convincingly associated with coronary artery disease (CAD)(1-7), a modest number considering the apparent heritability of CAD(8). All of these variants have been discovered in European populations. We report a meta-analysis of four large genome-wide association studies of CAD, with similar to 575,000 genotyped SNPs in a discovery dataset comprising 15,420 individuals with CAD (cases) (8,424 Europeans and 6,996 South Asians) and 15,062 controls. There was little evidence for ancestry-specific associations, supporting the use of combined analyses. Replication in an independent sample of 21,408 cases and 19,185 controls identified five loci newly associated with CAD (P < 5 x 10(-8) in the combined discovery and replication analysis): LIPA on 10q23, PDGFD on 11q22, ADAMTS7-MORF4L1 on 15q25, a gene rich locus on 7q22 and KIAA1462 on 10p11. The CAD-associated SNP in the PDGFD locus showed tissue-specific cis expression quantitative trait locus effects. These findings implicate new pathways for CAD susceptibility.
  •  
2.
  • Bruzelius, Maria, et al. (författare)
  • Influence of coronary artery disease-associated genetic variants on risk of venous thromboembolism
  • 2014
  • Ingår i: Thrombosis Research. - 0049-3848. ; 134:2, s. 426-432
  • Tidskriftsartikel (refereegranskat)abstract
    • INTRODUCTION:We investigated whether genetic variations robustly associated with coronary artery disease are also associated with risk of venous thromboembolism in a well-defined, female case-control study (n=2753) from Sweden.MATERIALS AND METHODS:39 single nucleotide polymorphisms in 32 loci associated with coronary artery disease in genome-wide association studies were identified in a literature search and genotyped in the ThromboEmbolism Hormone Study (TEHS). Association with venous thromboembolism was assessed by logistic regression.RESULTS:Only rs579459 in the ABO locus demonstrated a significant association with VTE. A tentative association between ANRIL and VTE in the discovery analysis failed to replicate in a meta-analysis of 4 independent cohorts (total n=7181).CONCLUSIONS:It appears that only the ABO locus is a shared risk factor for coronary artery disease and VTE.
  •  
3.
  • Chernogubova, Ekaterina, et al. (författare)
  • Common and Low-Frequency Genetic Variants in the PCSK9 Locus Influence Circulating PCSK9 Levels
  • 2012
  • Ingår i: Arteriosclerosis, Thrombosis and Vascular Biology. - 1079-5642. ; 32:6, s. 1526-1534
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective- Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a circulating protein that influences plasma low-density lipoprotein concentration and susceptibility to coronary heart disease. Circulating PCSK9 levels show considerable interindividual differences, but the factors responsible for this variation are largely unknown.Methods and Results- We analyzed circulating PCSK9 levels in 4 cohorts of healthy, middle-aged Swedes (n=5722) and found that PCSK9 levels varied over approximate to 50-fold range, showed a positive relationship with plasma low-density lipoprotein-cholesterol concentration, and were associated with plasma triglyceride, fibrinogen, insulin, and glucose concentrations. A genome-wide association study conducted in 2 cohorts (n=1215) failed to uncover common genetic variants robustly associated with variation in circulating PCSK9 level. As expected, the minor allele of the PCSK9 R46L variant was in all cohorts associated with reduced PCSK9 levels and decreased plasma low-density lipoprotein-cholesterol concentrations, but no relationship was observed with the plasma triglyceride concentration. Further mapping of the PCSK9 locus revealed a common polymorphism (rs2479415, minor allele frequency 43.9%), located approximate to 6 kb upstream from PCSK9, which is independently associated with increased circulating PCSK9 levels.Conclusion- Common and low-frequency genetic variants in the PCSK9 locus influence the pronounced interindividual variation in circulating PCSK9 levels in healthy, middle-aged white (predominantly Swedish) subjects.
  •  
4.
  • Deloukas, Panos, et al. (författare)
  • Large-scale association analysis identifies new risk loci for coronary artery disease
  • 2013
  • Ingår i: Nature Genetics. - Nature Publishing Group. - 1546-1718. ; 45:1, s. 25-33
  • Tidskriftsartikel (refereegranskat)abstract
    • Coronary artery disease (CAD) is the commonest cause of death. Here, we report an association analysis in 63,746 CAD cases and 130,681 controls identifying 15 loci reaching genome-wide significance, taking the number of susceptibility loci for CAD to 46, and a further 104 independent variants (r(2) < 0.2) strongly associated with CAD at a 5% false discovery rate (FDR). Together, these variants explain approximately 10.6% of CAD heritability. Of the 46 genome-wide significant lead SNPs, 12 show a significant association with a lipid trait, and 5 show a significant association with blood pressure, but none is significantly associated with diabetes. Network analysis with 233 candidate genes (loci at 10% FDR) generated 5 interaction networks comprising 85% of these putative genes involved in CAD. The four most significant pathways mapping to these networks are linked to lipid metabolism and inflammation, underscoring the causal role of these activities in the genetic etiology of CAD. Our study provides insights into the genetic basis of CAD and identifies key biological pathways.
  •  
5.
  • Folkersen, Lasse, et al. (författare)
  • Association of genetic risk variants with expression of proximal genes identifies novel susceptibility genes for cardiovascular disease
  • 2010
  • Ingår i: Circulation : Cardiovascular Genetics. - 1942-325X. ; 3:4, s. 365-373
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND:Population-based genome-wide association studies have identified several single nucleotide polymorphisms (SNPs) associated with cardiovascular disease or its risk factors. Genes in close proximity to these risk-SNPs are often thought to be pathogenetically important based on their location alone. However, the actual connections between SNPs and disease mechanisms remain largely unknown.METHODS AND RESULTS: To identify novel susceptibility genes, we investigated how 166 SNPs previously found to be associated with increased cardiovascular risk and/or predisposing metabolic traits relate to the expression of nearby genes. Gene expression in 577 samples of aorta, liver, mammary artery, and carotid atherosclerotic plaque was measured using expression arrays. For 47 SNPs, the expression levels of proximal genes (located within 200 kb) were affected (P&lt;0.005). More than 20 of these genes had not previously been identified as candidate genes for cardiovascular or related metabolic traits. SNP-associated gene effects were tissue-specific and the tissue specificity was phenotype-dependent.CONCLUSIONS: This study demonstrates several instances of association between risk-SNPs and genes immediately adjacent to them. It also demonstrates instances in which the associated gene is not the immediately proximal and obvious candidate gene for disease. This shows the necessity of careful studies of genetic marker data as a first step toward application of genome-wide association studies findings in a clinical setting.
  •  
6.
  • Folkersen, Lasse, et al. (författare)
  • Mapping of 79 loci for 83 plasma protein biomarkers in cardiovascular disease
  • 2017
  • Ingår i: PLoS Genetics. - PUBLIC LIBRARY SCIENCE. - 1553-7390 .- 1553-7404. ; 13:4
  • Tidskriftsartikel (refereegranskat)abstract
    • Recent advances in highly multiplexed immunoassays have allowed systematic large-scale measurement of hundreds of plasma proteins in large cohort studies. In combination with genotyping, such studies offer the prospect to 1) identify mechanisms involved with regulation of protein expression in plasma, and 2) determine whether the plasma proteins are likely to be causally implicated in disease. We report here the results of genome-wide association (GWA) studies of 83 proteins considered relevant to cardiovascular disease (CVD), measured in 3,394 individuals with multiple CVD risk factors. We identified 79 genome-wide significant (p&lt;5e-8) association signals, 55 of which replicated at P&lt;0.0007 in separate validation studies (n = 2,639 individuals). Using automated text mining, manual curation, and network-based methods incorporating information on expression quantitative trait loci (eQTL), we propose plausible causal mechanisms for 25 trans-acting loci, including a potential post-translational regulation of stem cell factor by matrix metalloproteinase 9 and receptor-ligand pairs such as RANK-RANK ligand. Using public GWA study data, we further evaluate all 79 loci for their causal effect on coronary artery disease, and highlight several potentially causal associations. Overall, a majority of the plasma proteins studied showed evidence of regulation at the genetic level. Our results enable future studies of the causal architecture of human disease, which in turn should aid discovery of new drug targets.
7.
  • Gertow, Karl, et al. (författare)
  • Identification of the BCAR1-CFDP1-TMEM170A Locus as a Determinant of Carotid Intima-Media Thickness and Coronary Artery Disease Risk
  • 2012
  • Ingår i: Circulation: Cardiovascular Genetics. - American Heart Association. - 1942-325X. ; 5:6, s. 656-665
  • Tidskriftsartikel (refereegranskat)abstract
    • Background-Carotid intima-media thickness (cIMT) is a widely accepted marker of subclinical atherosclerosis. To date, large-scale investigations of genetic determinants of cIMT are sparse. Methods and Results-To identify cIMT-associated genes and genetic variants, a discovery analysis using the Illumina 200K CardioMetabochip was conducted in 3430 subjects with detailed ultrasonographic determinations of cIMT from the IMPROVE (Carotid Intima Media Thickness [IMT] and IMT-Progression as Predictors of Vascular Events in a High Risk European Population) study. Segment-specific IMT measurements of common carotid, bifurcation, and internal carotid arteries, and composite IMT variables considering the whole carotid tree (IMTmean, IMTmax, and IMTmean-max), were analyzed. A replication stage investigating 42 single-nucleotide polymorphisms for association with common carotid IMT was undertaken in 5 independent European cohorts (total n=11 590). A locus on chromosome 16 (lead single-nucleotide polymorphism rs4888378, intronic in CFDP1) was associated with cIMT at significance levels passing multiple testing correction at both stages (array-wide significant discovery P=6.75x10(-7) for IMTmax; replication P=7.24x10(-6) for common cIMT; adjustments for sex, age, and population substructure where applicable; minor allele frequency 0.43 and 0.41, respectively). The protective minor allele was associated with lower carotid plaque score in a replication cohort (P=0.04, n=2120) and lower coronary artery disease risk in 2 case-control studies of subjects with European ancestry (odds ratio [95% confidence interval] 0.83 [0.77-0.90], P=6.53x10(-6), n=13 591; and 0.95 [0.92-0.98], P=1.83x10(-4), n= 82 297, respectively). Queries of human biobank data sets revealed associations of rs4888378 with nearby gene expression in vascular tissues (n=126-138). Conclusions-This study identified rs4888378 in the BCAR1-CFDP1-TMEM170A locus as a novel genetic determinant of cIMT and coronary artery disease risk in individuals of European descent. (Circ Cardiovasc Genet. 2012;5:656-665.)
  •  
8.
  •  
9.
  • Meisgen, Sabrina, et al. (författare)
  • The HLA locus contains novel foetal susceptibility alleles for congenital heart block with significant paternal influence
  • 2014
  • Ingår i: Journal of Internal Medicine. - 0954-6820. ; 275:6, s. 640-651
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: The main aim of this study was to identify foetal susceptibility genes on chromosome six for Ro/SSA autoantibody-mediated congenital heart block.SUBJECTS AND DESIGN: Single nucleotide polymorphism (SNP) genotyping of individuals in the Swedish Congenital Heart Block (CHB) study population was performed. Low-resolution HLA-A, -Cw and -DRB1 allele typing was carried out in 86 families comprising 339 individuals (86 Ro/SSA autoantibody-positive mothers, 71 fathers, 87 CHB index cases, and 95 unaffected siblings).RESULTS: A case-control comparison between index cases and population-based out-of-study controls (n=1710) revealed association of CHB with 15 SNPs in the 6p21.3 MHC locus at a chromosome-wide significance of p&lt;2.59×10(-6) (OR 2.21-3.12). In a family-based analysis of association of SNP markers as well as distinct MHC class I and II alleles with CHB, HLA-DRB1*04 and HLA-Cw*05 variants were significantly more frequently transmitted to affected individuals (p&lt;0.03 and p&lt;0.05, respectively), while HLA-DRB1*13 and HLA-Cw*06 variants were significantly less often transmitted to affected children (p&lt;0.04 and p&lt;0.03). We further observed marked association of increased paternal (but not maternal) HLA-DRB1*04 transmission to affected offspring (p&lt;0.02).CONCLUSIONS: HLA-DRB1*04 and HLA-Cw*05 were identified as novel foetal HLA allele variants that confer susceptibility to CHB in response to Ro/SSA autoantibody exposure, while DRB1*13 and Cw*06 emerged as protective alleles. Additionally, we demonstrated a paternal contribution to foetal susceptibility to CHB for the first time.
  •  
10.
  • Sandling, Johanna K., et al. (författare)
  • A candidate gene study of the type I interferon pathway implicates IKBKE and IL8 as risk loci for SLE
  • 2011
  • Ingår i: European Journal of Human Genetics. - Nature Publishing Group. - 1476-5438. ; 19:4, s. 479-484
  • Tidskriftsartikel (refereegranskat)abstract
    • Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease in which the type I interferon pathway has a crucial role. We have previously shown that three genes in this pathway, IRF5, TYK2 and STAT4, are strongly associated with risk for SLE. Here, we investigated 78 genes involved in the type I interferon pathway to identify additional SLE susceptibility loci. First, we genotyped 896 single-nucleotide polymorphisms in these 78 genes and 14 other candidate genes in 482 Swedish SLE patients and 536 controls. Genes with P < 0.01 in the initial screen were then followed up in 344 additional Swedish patients and 1299 controls. SNPs in the IKBKE, TANK, STAT1, IL8 and TRAF6 genes gave nominal signals of association with SLE in this extended Swedish cohort. To replicate these findings we extracted data from a genomewide association study on SLE performed in a US cohort. Combined analysis of the Swedish and US data, comprising a total of 2136 cases and 9694 controls, implicates IKBKE and IL8 as SLE susceptibility loci (P-meta=0.00010 and P-meta=0.00040, respectively). STAT1 was also associated with SLE in this cohort (P-meta=3.3 x 10(-5)), but this association signal appears to be dependent of that previously reported for the neighbouring STAT4 gene. Our study suggests additional genes from the type I interferon system in SLE, and highlights genes in this pathway for further functional analysis. European Journal of Human Genetics (2011) 19, 479-484; doi:10.1038/ejhg.2010.197; published online 22 December 2010
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-10 av 93
Åtkomst
fritt online (18)
Typ av publikation
tidskriftsartikel (89)
annan publikation (3)
konferensbidrag (1)
Typ av innehåll
refereegranskat (87)
övrigt vetenskapligt (5)
populärvet., debatt m.m. (1)
Författare/redaktör
Hamsten, Anders (86)
Strawbridge, Rona J. (34)
de Faire, Ulf (30)
Ingelsson, Erik, (29)
Silveira, Angela (28)
Salomaa, Veikko (26)
visa fler...
Lind, Lars, (25)
Syvänen, Ann-Christi ... (25)
Esko, Tonu (25)
Metspalu, Andres (25)
Boehnke, Michael (23)
Hofman, Albert, (22)
Wareham, Nicholas J. (22)
Deloukas, Panos (21)
Laakso, Markku, (21)
Jackson, Anne U. (21)
Luan, Jian'an (21)
Loos, Ruth J. F. (21)
Sennblad, Bengt, (21)
McCarthy, Mark I (20)
Gieger, Christian (20)
Collins, Francis S. (20)
Watkins, Hugh (20)
Eriksson, Per, (20)
Gigante, Bruna, (20)
Syvanen, AC (20)
Uitterlinden, Andre ... (19)
Kuusisto, Johanna, (19)
Langenberg, Claudia (19)
Pedersen, Nancy L. (19)
Samani, Nilesh J. (19)
Boerwinkle, Eric (19)
Wilson, James F. (19)
Lindgren, Cecilia M. (19)
Humphries, Steve E. (19)
Kanoni, Stavroula, (19)
Melander, Olle, (18)
Gudnason, Vilmundur, (18)
Chasman, Daniel I. (18)
Thorleifsson, Gudmar (18)
Hayward, Caroline (18)
Morris, Andrew P. (18)
Ripatti, Samuli (18)
Kathiresan, Sekar (18)
Tuomilehto, Jaakko (18)
Harris, Tamara B. (18)
Goel, Anuj (18)
Tremoli, Elena (18)
Boomsma, Dorret I., (17)
Van Duijn, Cornelia ... (17)
visa färre...
Lärosäte
Karolinska Institutet (76)
Uppsala universitet (72)
Lunds universitet (41)
Umeå universitet (20)
Göteborgs universitet (14)
Kungliga Tekniska Högskolan (10)
visa fler...
Linköpings universitet (5)
Högskolan Dalarna (3)
Stockholms universitet (3)
Högskolan i Borås (2)
Högskolan Kristianstad (1)
Sveriges Lantbruksuniversitet (1)
visa färre...
Språk
Engelska (88)
Svenska (1)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (79)
Naturvetenskap (11)
Teknik (1)
Samhällsvetenskap (1)

År

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy