Imperial College London

DrAbbasDehghan

Faculty of MedicineSchool of Public Health

Reader in Cardiometabolic Disease Epidemiology
 
 
 
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Contact

 

+44 (0)20 7594 3347a.dehghan CV

 
 
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Location

 

157Norfolk PlaceSt Mary's Campus

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Summary

 

Publications

Publication Type
Year
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270 results found

O'Donnell CJ, Kavousi M, Smith AV, Kardia SLR, Feitosa MF, Hwang S-J, Sun YV, Province MA, Aspelund T, Dehghan A, Hoffmann U, Bielak LF, Zhang Q, Eiriksdottir G, van Duijn CM, Fox CS, de Andrade M, Kraja AT, Sigurdsson S, Elias-Smale SE, Murabito JM, Launer LJ, van der Lugt A, Kathiresan S, Krestin GP, Herrington DM, Howard TD, Liu Y, Post W, Mitchell BD, O'Connell JR, Shen H, Shuldiner AR, Altshuler D, Elosua R, Salomaa V, Schwartz SM, Siscovick DS, Voight BF, Bis JC, Glazer NL, Psaty BM, Boerwinkle E, Heiss G, Blankenberg S, Zeller T, Wild PS, Schnabel RB, Schillert A, Ziegler A, Muenzel T, White CC, Rotter JI, Nalls M, Oudkerk M, Johnson AD, Newman AB, Uitterlinden AG, Massaro JM, Cunningham J, Harris TB, Hofman A, Peyser PA, Borecki IB, Cupples LA, Gudnason V, Witteman JCMet al., 2011, Genome-Wide Association Study for Coronary Artery Calcification With Follow-Up in Myocardial Infarction, CIRCULATION, Vol: 124, Pages: 2855-U255, ISSN: 0009-7322

Journal article

Herder C, Peeters W, Illig T, Baumert J, de Kleijn DPV, Moll FL, Poschen U, Klopp N, Mueller-Nurasyid M, Roden M, Preuss M, Karakas M, Meisinger C, Thorand B, Pasterkamp G, Koenig Wet al., 2011, RANTES/CCL5 and Risk for Coronary Events: Results from the MONICA/KORA Augsburg Case-Cohort, Athero-Express and CARDIoGRAM Studies, PLOS ONE, Vol: 6, ISSN: 1932-6203

Journal article

Leebeek FWG, Dehghan A, Kruip MJHA, Hofman A, Uitterlinden AG, De Wee EM, Witteman JCM, De Maat MPMet al., 2011, The presumed increased bleeding tendency in red-haired individuals is not associated with von Willebrand factor antigen levels in older individuals, JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Vol: 9, Pages: 2509-2511, ISSN: 1538-7933

Journal article

Kiechl S, Pare G, Barbalic M, Qi L, Dupuis J, Dehghan A, Bis JC, Laxton RC, Xiao Q, Bonora E, Willeit J, Xu Q, Witteman JCM, Chasman D, Tracy RP, Ballantyne CM, Ridker PM, Benjamin EJ, Ye Set al., 2011, Association of Variation at the ABO Locus With Circulating Levels of Soluble Intercellular Adhesion Molecule-1, Soluble P-selectin, and Soluble E-selectin A Meta-Analysis, CIRCULATION-CARDIOVASCULAR GENETICS, Vol: 4, Pages: 681-U436, ISSN: 1942-325X

Journal article

Bown MJ, Jones GT, Harrison SC, Wright BJ, Bumpstead S, Baas AF, Gretarsdottir S, Badger SA, Bradley DT, Burnand K, Child AH, Clough RE, Cockerill G, Hafez H, Scott DJA, Futers S, Johnson A, Sohrabi S, Smith A, Thompson MM, van Bockxmeer FM, Waltham M, Matthiasson SE, Thorleifsson G, Thorsteinsdottir U, Blankensteijn JD, Teijink JAW, Wijmenga C, de Graaf J, Kiemeney LA, Assimes TL, McPherson R, Folkersen L, Franco-Cereceda A, Palmen J, Smith AJ, Sylvius N, Wild JB, Refstrup M, Edkins S, Gwilliam R, Hunt SE, Potter S, Lindholt JS, Frikke-Schmidt R, Tybjaerg-Hansen A, Hughes AE, Golledge J, Norman PE, van Rij A, Powel JT, Eriksson P, Stefansson K, Thompson JR, Humphries SE, Sayers RD, Deloukas P, Samani NJet al., 2011, Abdominal Aortic Aneurysm Is Associated with a Variant in Low-Density Lipoprotein Receptor-Related Protein 1, AMERICAN JOURNAL OF HUMAN GENETICS, Vol: 89, Pages: 619-627, ISSN: 0002-9297

Journal article

Chambers JC, Zhang W, Sehmi J, Li X, Wass MN, Van der Harst P, Holm H, Sanna S, Kavousi M, Baumeister SE, Coin LJ, Deng G, Gieger C, Heard-Costa NL, Hottenga J-J, Kuehnel B, Kumar V, Lagou V, Liang L, Luan J, Vidal PM, Leach IM, O'Reilly PF, Peden JF, Rahmioglu N, Soininen P, Speliotes EK, Yuan X, Thorleifsson G, Alizadeh BZ, Atwood LD, Borecki IB, Brown MJ, Charoen P, Cucca F, Das D, de Geus EJC, Dixon AL, Doering A, Ehret G, Eyjolfsson GI, Farrall M, Forouhi NG, Friedrich N, Goessling W, Gudbjartsson DF, Harris TB, Hartikainen A-L, Heath S, Hirschfield GM, Hofman A, Homuth G, Hyppoenen E, Janssen HLA, Johnson T, Kangas AJ, Kema IP, Kuehn JP, Lai S, Lathrop M, Lerch MM, Li Y, Liang TJ, Lin J-P, Loos RJF, Martin NG, Moffatt MF, Montgomery GW, Munroe PB, Musunuru K, Nakamura Y, O'Donnell CJ, Olafsson I, Penninx BW, Pouta A, Prins BP, Prokopenko I, Puls R, Ruokonen A, Savolainen MJ, Schlessinger D, Schouten JNL, Seedorf U, Sen-Chowdhry S, Siminovitch KA, Smit JH, Spector TD, Tan W, Teslovich TM, Tukiainen T, Uitterlinden AG, Van der Klauw MM, Vasan RS, Wallace C, Wallaschofski H, Wichmann H-E, Willemsen G, Wuertz P, Xu C, Yerges-Armstrong LM, Abecasis GR, Ahmadi KR, Boomsma DI, Caulfield M, Cookson WO, van Duijn CM, Froguel P, Matsuda K, McCarthy MI, Meisinger C, Mooser V, Pietilainen KH, Schumann G, Snieder H, Sternberg MJE, Stolk RP, Thomas HC, Thorsteinsdottir U, Uda M, Waeber G, Wareham NJ, Waterworth DM, Watkins H, Whitfield JB, Witteman JCM, Wolffenbuttel BHR, Fox CS, Ala-Korpela M, Stefansson K, Vollenweider P, Voelzke H, Schadt EE, Scott J, Jarvelin M-R, Elliott P, Kooner JSet al., 2011, Genome-wide association study identifies loci influencing concentrations of liver enzymes in plasma, NATURE GENETICS, Vol: 43, Pages: 1131-1138, ISSN: 1061-4036

Journal article

Ehret GB, Munroe PB, Rice KM, Bochud M, Johnson AD, Chasman DI, Smith AV, Tobin MD, Verwoert GC, Hwang S-J, Pihur V, Vollenweider P, O'Reilly PF, Amin N, Bragg-Gresham JL, Teumer A, Glazer NL, Launer L, Zhao JH, Aulchenko Y, Heath S, Sober S, Parsa A, Luan J, Arora P, Dehghan A, Zhang F, Lucas G, Hicks AA, Jackson AU, Peden JF, Tanaka T, Wild SH, Rudan I, Igl W, Milaneschi Y, Parker AN, Fava C, Chambers JC, Fox ER, Kumari M, Go MJ, van der Harst P, Kao WHL, Sjogren M, Vinay DG, Alexander M, Tabara Y, Shaw-Hawkins S, Whincup PH, Liu Y, Shi G, Kuusisto J, Tayo B, Seielstad M, Sim X, Khanh-Dung HN, Lehtimaki T, Matullo G, Wu Y, Gaunt TR, Onland-Moret NC, Cooper MN, Platou CGP, Org E, Hardy R, Dahgam S, Palmen J, Vitart V, Braund PS, Kuznetsova T, Uiterwaal CSPM, Adeyemo A, Palmas W, Campbell H, Ludwig B, Tomaszewski M, Tzoulaki I, Palmer ND, Aspelund T, Garcia M, Chang Y-PC, O'Connell JR, Steinle NI, Grobbee DE, Arking DE, Kardia SL, Morrison AC, Hernandez D, Najjar S, McArdle WL, Hadley D, Brown MJ, Connell JM, Hingorani AD, Day INM, Lawlor DA, Beilby JP, Lawrence RW, Clarke R, Hopewell JC, Ongen H, Dreisbach AW, Li Y, Young JH, Bis JC, Kahonen M, Viikari J, Adair LS, Lee NR, Chen M-H, Olden M, Pattaro C, Bolton JAH, Koettgen A, Bergmann S, Mooser V, Chaturvedi N, Frayling TM, Islam M, Jafar TH, Erdmann J, Kulkarni SR, Bornstein SR, Graessler J, Groop L, Voight BF, Kettunen J, Howard P, Taylor A, Guarrera S, Ricceri F, Emilsson V, Plump A, Barroso IS, Khaw K-T, Weder AB, Hunt SC, Sun YV, Bergman RN, Collins FS, Bonnycastle LL, Scott LJ, Stringham HM, Peltonen L, Perola M, Vartiainen E, Brand S-M, Staessen JA, Wang TJ, Burton PR, Artigas MS, Dong Y, Snieder H, Wang X, Zhu H, Lohman KK, Rudock ME, Heckbert SR, Smith NL, Wiggins KL, Doumatey A, Shriner D, Veldre G, Viigimaa M, Kinra S, Prabhakaran D, Tripathy V, Langefeld CD, Rosengren A, Thelle DS, Corsi AM, Singleton A, Forrester T, Hilton G, McKenzie CA, Salako T, Iwai N, Kita Y, Ogihara T, Ohkubo T, Okamura T, Ueshimet al., 2011, Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk, NATURE, Vol: 478, Pages: 103-109, ISSN: 0028-0836

Journal article

Strawbridge RJ, Dupuis J, Prokopenko I, Barker A, Ahlqvist E, Rybin D, Petrie JR, Travers ME, Bouatia-Naji N, Dimas AS, Nica A, Wheeler E, Chen H, Voight BF, Taneera J, Kanoni S, Peden JF, Turrini F, Gustafsson S, Zabena C, Almgren P, Barker DJP, Barnes D, Dennison EM, Eriksson JG, Eriksson P, Eury E, Folkersen L, Fox CS, Frayling TM, Goel A, Gu HF, Horikoshi M, Isomaa B, Jackson AU, Jameson KA, Kajantie E, Kerr-Conte J, Kuulasmaa T, Kuusisto J, Loos RJF, Luan J, Makrilakis K, Manning AK, Teresa Martinez-Larrad M, Narisu N, Mannila MN, Ohrvik J, Osmond C, Pascoe L, Payne F, Sayer AA, Sennblad B, Silveira A, Stancakova A, Stirrups K, Swift AJ, Syvanen A-C, Tuomi T, van 't Hooft FM, Walker M, Weedon MN, Xie W, Zethelius B, Ongen H, Malarstig A, Hopewell JC, Saleheen D, Chambers J, Parish S, Danesh J, Kooner J, Ostenson C-G, Lind L, Cooper CC, Serrano-Rios M, Ferrannini E, Forsen TJ, Clarke R, Franzosi MG, Seedorf U, Watkins H, Froguel P, Johnson P, Deloukas P, Collins FS, Laakso M, Dermitzakis ET, Boehnke M, McCarthy MI, Wareham NJ, Groop L, Pattou F, Gloyn AL, Dedoussis GV, Lyssenko V, Meigs JB, Barroso I, Watanabe RM, Ingelsson E, Langenberg C, Hamsten A, Florez JCet al., 2011, Genome-Wide Association Identifies Nine Common Variants Associated With Fasting Proinsulin Levels and Provides New Insights Into the Pathophysiology of Type 2 Diabetes, Diabetes, Vol: 60, Pages: 2624-2634, ISSN: 0012-1797

OBJECTIVE Proinsulin is a precursor of mature insulin and C-peptide. Higher circulating proinsulin levels are associated with impaired β-cell function, raised glucose levels, insulin resistance, and type 2 diabetes (T2D). Studies of the insulin processing pathway could provide new insights about T2D pathophysiology.RESEARCH DESIGN AND METHODS We have conducted a meta-analysis of genome-wide association tests of ∼2.5 million genotyped or imputed single nucleotide polymorphisms (SNPs) and fasting proinsulin levels in 10,701 nondiabetic adults of European ancestry, with follow-up of 23 loci in up to 16,378 individuals, using additive genetic models adjusted for age, sex, fasting insulin, and study-specific covariates.RESULTS Nine SNPs at eight loci were associated with proinsulin levels (P < 5 × 10−8). Two loci (LARP6 and SGSM2) have not been previously related to metabolic traits, one (MADD) has been associated with fasting glucose, one (PCSK1) has been implicated in obesity, and four (TCF7L2, SLC30A8, VPS13C/C2CD4A/B, and ARAP1, formerly CENTD2) increase T2D risk. The proinsulin-raising allele of ARAP1 was associated with a lower fasting glucose (P = 1.7 × 10−4), improved β-cell function (P = 1.1 × 10−5), and lower risk of T2D (odds ratio 0.88; P = 7.8 × 10−6). Notably, PCSK1 encodes the protein prohormone convertase 1/3, the first enzyme in the insulin processing pathway. A genotype score composed of the nine proinsulin-raising alleles was not associated with coronary disease in two large case-control datasets.CONCLUSIONS We have identified nine genetic variants associated with fasting proinsulin. Our findings illuminate the biology underlying glucose homeostasis and T2D development in humans and argue against a direct role of proinsulin in coronary artery disease pathogenesis.

Journal article

Bis JC, Kavousi M, Franceschini N, Isaacs A, Abecasis GR, Schminke U, Post WS, Smith AV, Cupples LA, Markus HS, Schmidt R, Huffman JE, Lehtimaki T, Baumert J, Muenzel T, Heckbert SR, Dehghan A, North K, Oostra B, Bevan S, Stoegerer E-M, Hayward C, Raitakari O, Meisinger C, Schillert A, Sanna S, Voelzke H, Cheng Y-C, Thorsson B, Fox CS, Rice K, Rivadeneira F, Nambi V, Halperin E, Petrovic KE, Peltonen L, Wichmann HE, Schnabel RB, Doerr M, Parsa A, Aspelund T, Demissie S, Kathiresan S, Reilly MP, Taylor K, Uitterlinden A, Couper DJ, Sitzer M, Kahonen M, Illig T, Wild PS, Orru M, Luedemann J, Shuldiner AR, Eiriksdottir G, White CC, Rotter JI, Hofman A, Seissler J, Zeller T, Usala G, Ernst F, Launer LJ, D'Agostino RB, O'Leary DH, Ballantyne C, Thiery J, Ziegler A, Lakatta EG, Chilukoti RK, Harris TB, Wolf PA, Psaty BM, Polak JF, Li X, Rathmann W, Uda M, Boerwinkle E, Klopp N, Schmidt H, Wilson JF, Viikari J, Koenig W, Blankenberg S, Newman AB, Witteman J, Heiss G, van Duijn C, Scuteri A, Homuth G, Mitchell BD, Gudnason V, O'Donnell CJet al., 2011, Meta-analysis of genome-wide association studies from the CHARGE consortium identifies common variants associated with carotid intima media thickness and plaque, NATURE GENETICS, Vol: 43, Pages: 940-U40, ISSN: 1061-4036

Journal article

Wain LV, Verwoert GC, O'Reilly PF, Shi G, Johnson T, Johnson AD, Bochud M, Rice KM, Henneman P, Smith AV, Ehret GB, Amin N, Larson MG, Mooser V, Hadley D, Doerr M, Bis JC, Aspelund T, Esko T, Janssens ACJW, Zhao JH, Heath S, Laan M, Fu J, Pistis G, Luan J, Arora P, Lucas G, Pirastu N, Pichler I, Jackson AU, Webster RJ, Zhang F, Peden JF, Schmidt H, Tanaka T, Campbell H, Igl W, Milaneschi Y, Hottenga J-J, Vitart V, Chasman DI, Trompet S, Bragg-Gresham JL, Alizadeh BZ, Chambers JC, Guo X, Lehtimaki T, Kuehnel B, Lopez LM, Polasek O, Boban M, Nelson CP, Morrison AC, Pihur V, Ganesh SK, Hofman A, Kundu S, Mattace-Raso FUS, Rivadeneira F, Sijbrands EJG, Uitterlinden AG, Hwang S-J, Vasan RS, Wang TJ, Bergmann S, Vollenweider P, Waeber G, Laitinen J, Pouta A, Zitting P, McArdle WL, Kroemer HK, Voelker U, Voelzke H, Glazer NL, Taylor KD, Harris TB, Alavere H, Haller T, Keis A, Tammesoo M-L, Aulchenko Y, Barroso I, Khaw K-T, Galan P, Hercberg S, Lathrop M, Eyheramendy S, Org E, Sober S, Lu X, Nolte IM, Penninx BW, Corre T, Masciullo C, Sala C, Groop L, Voight BF, Melander O, O'Donnell CJ, Salomaa V, d'Adamo AP, Fabretto A, Faletra F, Ulivi S, Del Greco FM, Facheris M, Collins FS, Bergman RN, Beilby JP, Hung J, Musk AW, Mangino M, Shin S-Y, Soranzo N, Watkins H, Goel A, Hamsten A, Gider P, Loitfelder M, Zeginigg M, Hernandez D, Najjar SS, Navarro P, Wild SH, Corsi AM, Singleton A, de Geus EJC, Willemsen G, Parker AN, Rose LM, Buckley B, Stott D, Orru M, Uda M, van der Klauw MM, Zhang W, Li X, Scott J, Chen Y-DI, Burke GL, Kahonen M, Viikari J, Doering A, Meitinger T, Davies G, Starr JM, Emilsson V, Plump A, Lindeman JH, 't Hoen PAC, Koenig IR, Felix JF, Clarke R, Hopewell JC, Ongen H, Breteler M, Debette S, DeStefano AL, Fornage M, Mitchell GF, Smith NL, Holm H, Stefansson K, Thorleifsson G, Thorsteinsdottir U, Samani NJ, Preuss M, Rudan I, Hayward C, Deary IJ, Wichmann H-E, Raitakari OT, Palmas W, Kooner JS, Stolk RP, Jukema JW, Wright AF, Boomsma DI, Bandinelli S, Gyllensteet al., 2011, Genome-wide association study identifies six new loci influencing pulse pressure and mean arterial pressure, NATURE GENETICS, Vol: 43, Pages: 1005-U122, ISSN: 1061-4036

Numerous genetic loci have been associated with systolic blood pressure (SBP) and diastolic blood pressure (DBP) in Europeans1,2,3. We now report genome-wide association studies of pulse pressure (PP) and mean arterial pressure (MAP). In discovery (N = 74,064) and follow-up studies (N = 48,607), we identified at genome-wide significance (P = 2.7 × 10−8 to P = 2.3 × 10−13) four new PP loci (at 4q12 near CHIC2, 7q22.3 near PIK3CG, 8q24.12 in NOV and 11q24.3 near ADAMTS8), two new MAP loci (3p21.31 in MAP4 and 10q25.3 near ADRB1) and one locus associated with both of these traits (2q24.3 near FIGN) that has also recently been associated with SBP in east Asians. For three of the new PP loci, the estimated effect for SBP was opposite of that for DBP, in contrast to the majority of common SBP- and DBP-associated variants, which show concordant effects on both traits. These findings suggest new genetic pathways underlying blood pressure variation, some of which may differentially influence SBP and DBP.

Journal article

Boeger CA, Gorski M, Li M, Hoffmann MM, Huang C, Yang Q, Teumer A, Krane V, O'Seaghdha CM, Kutalik Z, Wichmann H-E, Haak T, Boes E, Coassin S, Coresh J, Kollerits B, Haun M, Paulweber B, Koettgen A, Li G, Shlipak MG, Powe N, Hwang S-J, Dehghan A, Rivadeneira F, Uitterlinden A, Hofman A, Beckmann JS, Kraemer BK, Witteman J, Bochud M, Siscovick D, Rettig R, Kronenberg F, Wanner C, Thadhani RI, Heid IM, Fox CS, Kao WHet al., 2011, Association of eGFR-Related Loci Identified by GWAS with Incident CKD and ESRD, PLOS GENETICS, Vol: 7, ISSN: 1553-7390

Journal article

Butterworth AS, Braund PS, Farrall M, Hardwick RJ, Saleheen D, Peden JF, Soranzo N, Chambers JC, Sivapalaratnam S, Kleber ME, Keating B, Qasim A, Klopp N, Erdmann J, Assimes TL, Ball SG, Balmforth AJ, Barnes TA, Basart H, Baumert J, Bezzina CR, Boerwinkle E, Boehm BO, Brocheton J, Bugert P, Cambien F, Clarke R, Codd V, Collins R, Couper D, Cupples LA, de Jong JS, Diemert P, Ejebe K, Elbers CC, Elliott P, Fornage M, Franzosi M-G, Frossard P, Garner S, Goel A, Goodall AH, Hengstenberg C, Hunt SE, Kastelein JJP, Klungel OH, Klueter H, Koch K, Koenig IR, Kooner AS, Laaksonen R, Lathrop M, Li M, Liu K, McPherson R, Musameh MD, Musani S, Nelson CP, O'Donnell CJ, Ongen H, Papanicolaou G, Peters A, Peters BJM, Potter S, Psaty BM, Qu L, Rader DJ, Rasheed A, Rice C, Scott J, Seedorf U, Sehmi JS, Sotoodehnia N, Stark K, Stephens J, van der Schoot CE, van der Schouw YT, Thorsteinsdottir U, Tomaszewski M, van der Harst P, Vasan RS, Wilde AAM, Willenborg C, Winkelmann BR, Zaidi M, Zhang W, Ziegler A, de Bakker PIW, Koenig W, Maerz W, Trip MD, Reilly MP, Kathiresan S, Schunkert H, Hamsten A, Hall AS, Kooner JS, Thompson SG, Thompson JR, Deloukas P, Ouwehand WH, Watkins H, Danesh J, Samani NJet al., 2011, Large-scale gene-centric analysis identifies novel variants for coronary Artery disease, PLoS Genetics, Vol: 7, ISSN: 1553-7390

Coronary artery disease (CAD) has a significant genetic contribution that is incompletely characterized. To complement genome-wide association (GWA) studies, we conducted a large and systematic candidate gene study of CAD susceptibility, including analysis of many uncommon and functional variants. We examined 49,094 genetic variants in ∼2,100 genes of cardiovascular relevance, using a customised gene array in 15,596 CAD cases and 34,992 controls (11,202 cases and 30,733 controls of European descent; 4,394 cases and 4,259 controls of South Asian origin). We attempted to replicate putative novel associations in an additional 17,121 CAD cases and 40,473 controls. Potential mechanisms through which the novel variants could affect CAD risk were explored through association tests with vascular risk factors and gene expression. We confirmed associations of several previously known CAD susceptibility loci (eg, 9p21.3:p<10−33; LPA:p<10−19; 1p13.3:p<10−17) as well as three recently discovered loci (COL4A1/COL4A2, ZC3HC1, CYP17A1:p<5×10−7). However, we found essentially null results for most previously suggested CAD candidate genes. In our replication study of 24 promising common variants, we identified novel associations of variants in or near LIPA, IL5, TRIB1, and ABCG5/ABCG8, with per-allele odds ratios for CAD risk with each of the novel variants ranging from 1.06–1.09. Associations with variants at LIPA, TRIB1, and ABCG5/ABCG8 were supported by gene expression data or effects on lipid levels. Apart from the previously reported variants in LPA, none of the other ∼4,500 low frequency and functional variants showed a strong effect. Associations in South Asians did not differ appreciably from those in Europeans, except for 9p21.3 (per-allele odds ratio: 1.14 versus 1.27 respectively; P for heterogeneity = 0.003). This large-scale gene-centric analysis has identified several novel genes for CAD that relate to diverse bioc

Journal article

Ricketts SL, Rensing KL, Holly JM, Chen L, Young EH, Luben R, Ashford S, Song K, Yuan X, Dehghan A, Wright BJ, Waterworth DM, Mooser V, Waeber G, Vollenweider P, Epstein SE, Burnett MS, Devaney JM, Hakonarson HH, Rader DJ, Reilly MP, Danesh J, Thompson SG, Dunning AM, van Duijn CM, Samani NJ, McPherson R, Wareham NJ, Khaw KT, Boekholdt SM, Sandhu MSet al., 2011, Prospective study of insulin-like growth factor-I, insulinlike growth factor-binding protein 3, genetic variants in the IGF1 and IGFBP3 genes and risk of coronary artery disease, International Journal of Molecular Epidemiology and Genetics, Vol: 2, Pages: 261-285

Although experimental studies have suggested that insulin-like growth factor I (IGF-I) and its binding protein IGFBP-3 might have a role in the aetiology of coronary artery disease (CAD), the relevance of circulating IGFs and their binding proteins in the development of CAD in human populations is unclear. We conducted a nested case-control study, with a mean follow-up of six years, within the EPIC-Norfolk cohort to assess the association between circulating levels of IGF-I and IGFBP-3 and risk of CAD in up to 1,013 cases and 2,055 controls matched for age, sex and study enrolment date. After adjustment for cardiovascular risk factors, we found no association between circulating levels of IGF-I or IGFBP-3 and risk of CAD (odds ratio: 0.98 (95% CI 0.90-1.06) per 1 SD increase in circulating IGF-I; odds ratio: 1.02 (95% CI 0.94-1.12) for IGFBP-3). We examined associations between tagging single nucleotide polymorphisms (tSNPs) at the IGF1 and IGFBP3 loci and circulating IGF-I and IGFBP-3 levels in up to 1,133 cases and 2,223 controls and identified three tSNPs (rs1520220, rs3730204, rs2132571) that showed independent association with either circulating IGF-I or IGFBP-3 levels. In an assessment of 31 SNPs spanning the IGF1 or IGFBP3 loci, none were associated with risk of CAD in a meta-analysis that included EPIC-Norfolk and eight additional studies comprising up to 9,319 cases and 19,964 controls. Our results indicate that IGF-I and IGFBP-3 are unlikely to be importantly involved in the aetiology of CAD in human populations.

Journal article

Smith NL, Rice KM, Bovill EG, Cushman M, Bis JC, McKnight B, Lumley T, Glazer NL, Vlieg AVH, Tang W, Dehghan A, Strachan DP, O'Donnell CJ, Rotter JI, Heckbert SR, Psaty BM, Rosendaal FRet al., 2011, Genetic variation associated with plasma von Willebrand factor levels and the risk of incident venous thrombosis, BLOOD, Vol: 117, Pages: 6007-6011, ISSN: 0006-4971

Journal article

van Hoek M, van Herpt TW, Dehghan A, Hofman A, Lieverse AG, van Duijn CM, Witteman JCM, Sijbrands EJGet al., 2011, Association of an APOC3 promoter variant with type 2 diabetes risk and need for insulin treatment in lean persons, DIABETOLOGIA, Vol: 54, Pages: 1360-1367, ISSN: 0012-186X

Journal article

Arking DE, Junttila MJ, Goyette P, Huertas-Vazquez A, Eijgelsheim M, Blom MT, Newton-Cheh C, Reinier K, Teodorescu C, Uy-Evanado A, Carter-Monroe N, Kaikkonen KS, Kortelainen M-L, Boucher G, Lagace C, Moes A, Zhao X, Kolodgie F, Rivadeneira F, Hofman A, Witteman JCM, Uitterlinden AG, Marsman RF, Pazoki R, Bardai A, Koster RW, Dehghan A, Hwang S-J, Bhatnagar P, Post W, Hilton G, Prineas RJ, Li M, Koettgen A, Ehret G, Boerwinkle E, Coresh J, Kao WHL, Psaty BM, Tomaselli GF, Sotoodehnia N, Siscovick DS, Burke GL, Marban E, Spooner PM, Cupples LA, Jui J, Gunson K, Kesaniemi YA, Wilde AAM, Tardif J-C, O'Donnell CJ, Bezzina CR, Virmani R, Stricker BHC, Tan HL, Albert CM, Chakravarti A, Rioux JD, Huikuri HV, Chugh SSet al., 2011, Identification of a Sudden Cardiac Death Susceptibility Locus at 2q24.2 through Genome-Wide Association in European Ancestry Individuals, PLOS GENETICS, Vol: 7, ISSN: 1553-7390

Journal article

Nalls MA, Couper DJ, Tanaka T, van Rooij FJA, Chen M-H, Smith AV, Toniolo D, Zakai NA, Yang Q, Greinacher A, Wood AR, Garcia M, Gasparini P, Liu Y, Lumley T, Folsom AR, Reiner AP, Gieger C, Lagou V, Felix JF, Voelzke H, Gouskova NA, Biffi A, Doering A, Voelker U, Chong S, Wiggins KL, Rendon A, Dehghan A, Moore M, Taylor K, Wilson JG, Lettre G, Hofman A, Bis JC, Pirastu N, Fox CS, Meisinger C, Sambrook J, Arepalli S, Nauck M, Prokisch H, Stephens J, Glazer NL, Cupples LA, Okada Y, Takahashi A, Kamatani Y, Matsuda K, Tsunoda T, Tanaka T, Kubo M, Nakamura Y, Yamamoto K, Kamatani N, Stumvoll M, Toenjes A, Prokopenko I, Illig T, Patel KV, Garner SF, Kuhnel B, Mangino M, Oostra BA, Thein SL, Coresh J, Wichmann H-E, Menzel S, Lin J, Pistis G, Uitterlinden AG, Spector TD, Teumer A, Eiriksdottir G, Gudnason V, Bandinelli S, Frayling TM, Chakravarti A, van Duijn CM, Melzer D, Ouwehand WH, Levy D, Boerwinkle E, Singleton AB, Hernandez DG, Longo DL, Soranzo N, Witteman JCM, Psaty BM, Ferrucci L, Harris TB, O'Donnell CJ, Ganesh SKet al., 2011, Multiple Loci Are Associated with White Blood Cell Phenotypes, PLOS GENETICS, Vol: 7, ISSN: 1553-7390

Journal article

Smith NL, Huffman JE, Strachan DP, Huang J, Dehghan A, Trompet S, Lopez LM, Shin S-Y, Baumert J, Vitart V, Bis JC, Wild SH, Rumley A, Yang Q, Uitterlinden AG, Stott DJ, Davies G, Carter AM, Thorand B, Polasek O, McKnight B, Campbell H, Rudnicka AR, Chen M-H, Buckley BM, Harris SE, Peters A, Pulanic D, Lumley T, de Craen AJM, Liewald DC, Gieger C, Campbell S, Ford I, Gow AJ, Luciano M, Porteous DJ, Guo X, Sattar N, Tenesa A, Cushman M, Slagboom PE, Visscher PM, Spector TD, Illig T, Rudan I, Bovill EG, Wright AF, McArdle WL, Tofler G, Hofman A, Westendorp RGJ, Starr JM, Grant PJ, Karakas M, Hastie ND, Psaty BM, Wilson JF, Lowe GDO, O'Donnell CJ, Witteman JCM, Jukema JW, Deary IJ, Soranzo N, Koenig W, Hayward Cet al., 2011, Genetic Predictors of Fibrin D-Dimer Levels in Healthy Adults, CIRCULATION, Vol: 123, Pages: 1864-+, ISSN: 0009-7322

Journal article

Schunkert H, Koenig IR, Kathiresan S, Reilly MP, Assimes TL, Holm H, Preuss M, Stewart AFR, Barbalic M, Gieger C, Absher D, Aherrahrou Z, Allayee H, Altshuler D, Anand SS, Andersen K, Anderson JL, Ardissino D, Ball SG, Balmforth AJ, Barnes TA, Becker DM, Becker LC, Berger K, Bis JC, Boekholdt SM, Boerwinkle E, Braund PS, Brown MJ, Burnett MS, Buysschaert I, Carlquist JF, Chen L, Cichon S, Codd V, Davies RW, Dedoussis G, Dehghan A, Demissie S, Devaney JM, Diemert P, Do R, Doering A, Eifert S, El Mokhtari NE, Ellis SG, Elosua R, Engert JC, Epstein SE, de Faire U, Fischer M, Folsom AR, Freyer J, Gigante B, Girelli D, Gretarsdottir S, Gudnason V, Gulcher JR, Halperin E, Hammond N, Hazen SL, Hofman A, Horne BD, Illig T, Iribarren C, Jones GT, Jukema JW, Kaiser MA, Kaplan LM, Kastelein JJP, Khaw K-T, Knowles JW, Kolovou G, Kong A, Laaksonen R, Lambrechts D, Leander K, Lettre G, Li M, Lieb W, Loley C, Lotery AJ, Mannucci PM, Maouche S, Martinelli N, McKeown PP, Meisinger C, Meitinger T, Melander O, Merlini PA, Mooser V, Morgan T, Muehleisen TW, Muhlestein JB, Muenzel T, Musunuru K, nahrstaedt J, Nelson CP, Noethen MM, Olivieri O, Patel RS, Patterson CC, Peters A, Peyvandi F, Qu L, Quyyumi AA, Rader DJ, Rallidis LS, Rice C, Rosendaal FR, Rubin D, Salomaa V, Sampietro ML, Sandhu MS, Schadt E, Schaefer A, Schillert A, Schreiber S, Schrezenmeir J, Schwartz SM, Siscovick DS, Sivananthan M, Sivapalaratnam S, Smith A, Smith TB, Snoep JD, Soranzo N, Spertus JA, Stark K, Stirrups K, Stoll M, Tang WHW, Tennstedt S, Thorgeirsson G, Thorleifsson G, Tomaszewski M, Uitterlinden AG, van Rij AM, Voight BF, Wareham NJ, Wells GA, Wichmann H-E, Wild PS, Willenborg C, Witteman JCM, Wright BJ, Ye S, Zeller T, Ziegler A, Cambien F, Goodall AH, Cupples LA, Quertermous T, Maerz W, Hengstenberg C, Blankenberg S, Ouwehand WH, Hall AS, Deloukas P, Thompson JR, Stefansson K, Roberts R, Thorsteinsdottir U, O'Donnell CJ, McPherson R, Erdmann J, Samani NJet al., 2011, Large-scale association analysis identifies 13 new susceptibility loci for coronary artery disease, NATURE GENETICS, Vol: 43, Pages: 333-U153, ISSN: 1061-4036

Journal article

Pare G, Ridker PM, Rose L, Barbalic M, Dupuis J, Dehghan A, Bis JC, Benjamin EJ, Shiffman D, Parker AN, Chasman DIet al., 2011, Genome-Wide Association Analysis of Soluble ICAM-1 Concentration Reveals Novel Associations at the NFKBIK, PNPLA3, RELA, and SH2B3 Loci, PLOS GENETICS, Vol: 7, ISSN: 1553-7390

Journal article

Speliotes EK, Yerges-Armstrong LM, Wu J, Hernaez R, Kim LJ, Palmer CD, Gudnason V, Eiriksdottir G, Garcia ME, Launer LJ, Nalls MA, Clark JM, Mitchell BD, Shuldiner AR, Butler JL, Tomas M, Hoffmann U, Hwang SJ, Massaro JM, O'Donnell CJ, Sahani DV, Salomaa V, Schadt EE, Schwartz SM, Siscovick DS, Voight BF, Carr JJ, Feitosa MF, Harris TB, Fox CS, Smith AV, Kao WH, Hirschhorn JN, Borecki IBet al., 2011, Genome-wide association analysis identifies variants associated with nonalcoholic fatty liver disease that have distinct effects on metabolic traits, PLOS Genetics, Vol: 7, ISSN: 1553-7390

Nonalcoholic fatty liver disease (NAFLD) clusters in families, but the only known common genetic variants influencing risk are near PNPLA3. We sought to identify additional genetic variants influencing NAFLD using genome-wide association (GWA) analysis of computed tomography (CT) measured hepatic steatosis, a non-invasive measure of NAFLD, in large population based samples. Using variance components methods, we show that CT hepatic steatosis is heritable ( approximately 26%-27%) in family-based Amish, Family Heart, and Framingham Heart Studies (n = 880 to 3,070). By carrying out a fixed-effects meta-analysis of genome-wide association (GWA) results between CT hepatic steatosis and approximately 2.4 million imputed or genotyped SNPs in 7,176 individuals from the Old Order Amish, Age, Gene/Environment Susceptibility-Reykjavik study (AGES), Family Heart, and Framingham Heart Studies, we identify variants associated at genome-wide significant levels (p<5x10(-8)) in or near PNPLA3, NCAN, and PPP1R3B. We genotype these and 42 other top CT hepatic steatosis-associated SNPs in 592 subjects with biopsy-proven NAFLD from the NASH Clinical Research Network (NASH CRN). In comparisons with 1,405 healthy controls from the Myocardial Genetics Consortium (MIGen), we observe significant associations with histologic NAFLD at variants in or near NCAN, GCKR, LYPLAL1, and PNPLA3, but not PPP1R3B. Variants at these five loci exhibit distinct patterns of association with serum lipids, as well as glycemic and anthropometric traits. We identify common genetic variants influencing CT-assessed steatosis and risk of NAFLD. Hepatic steatosis associated variants are not uniformly associated with NASH/fibrosis or result in abnormalities in serum lipids or glycemic and anthropometric traits, suggesting genetic heterogeneity in the pathways influencing these traits.

Journal article

Dehghan A, Dupuis J, Barbalic M, Bis JC, Eiriksdottir G, Lu C, Pellikka N, Wallaschofski H, Kettunen J, Henneman P, Baumert J, Strachan DP, Fuchsberger C, Vitart V, Wilson JF, Pare G, Naitza S, Rudock ME, Surakka I, de Geus EJC, Alizadeh BZ, Guralnik J, Shuldiner A, Tanaka T, Zee RYL, Schnabel RB, Nambi V, Kavousi M, Ripatti S, Nauck M, Smith NL, Smith AV, Sundvall J, Scheet P, Liu Y, Ruokonen A, Rose LM, Larson MG, Hoogeveen RC, Freimer NB, Teumer A, Tracy RP, Launer LJ, Buring JE, Yamamoto JF, Folsom AR, Sijbrands EJG, Pankow J, Elliott P, Keaney JF, Sun W, Sarin A-P, Fontes JD, Badola S, Astor BC, Hofman A, Pouta A, Werdan K, Greiser KH, Kuss O, Schwabedissen HEMZ, Thiery J, Jamshidi Y, Nolte IM, Soranzo N, Spector TD, Voelzke H, Parker AN, Aspelund T, Bates D, Young L, Tsui K, Siscovick DS, Guo X, Rotter JI, Uda M, Schlessinger D, Rudan I, Hicks AA, Penninx BW, Thorand B, Gieger C, Coresh J, Willemsen G, Harris TB, Uitterlinden AG, Jaervelin M-R, Rice K, Radke D, Salomaa V, van Dijk KW, Boerwinkle E, Vasan RS, Ferrucci L, Gibson QD, Bandinelli S, Snieder H, Boomsma DI, Xiao X, Campbell H, Hayward C, Pramstaller PP, van Duijn CM, Peltonen L, Psaty BM, Gudnason V, Ridker PM, Homuth G, Koenig W, Ballantyne CM, Witteman JCM, Benjamin EJ, Perola M, Chasman DIet al., 2011, Meta-Analysis of Genome-Wide Association Studies in > 80 000 Subjects Identifies Multiple Loci for C-Reactive Protein Levels, CIRCULATION, Vol: 123, Pages: 731-U151, ISSN: 0009-7322

Journal article

Wensley F, Gao P, Burgess S, Kaptoge S, Di Angelantonio E, Shah T, Engert JC, Clarke R, Davey-Smith G, Nordestgaard BG, Saleheen D, Samani NJ, Sandhu M, Anand S, Pepys MB, Smeeth L, Whittaker J, Casas JP, Thompson SG, Hingorani AD, Danesh J, Eiriksdottir G, Harris TB, Launer LJ, Gudnason V, Folsom AR, Andrews G, Ballantyne CM, Samani NJ, Hall AS, Braund PS, Balmforth AJ, Whincup PH, Morris R, Lawlor DA, Lowe GDO, Timpson N, Ebrahim S, Ben-Shlomo Y, Davey-Smith G, Timpson N, Nordestgaard BG, Tybjaerg-Hansen A, Zacho J, Brown M, Sandhu M, Ricketts SL, Ashford S, Lange L, Reiner A, Cushman M, Tracy R, Wu C, Ge J, Zou Y, Sun A, Hung J, McQuillan B, Thompson P, Beilby J, Warrington N, Palmer LJ, Wanner C, Drechsler C, Hoffmann MM, Fowkes FGR, Lowe GDO, Tzoulaki I, Kumari M, Miller M, Marmot M, Onland-Moret C, van der Schouw YT, Boer JM, Wijmenga C, Ricketts SL, Ashford S, Sandhu M, Khaw K-T, Vasan RS, Schnabel RB, Yamamoto JF, Benjamin EJ, Schunkert H, Erdmann J, Koenig IR, Hengstenberg C, Chiodini B, Franzosi MG, Pietri S, Gori F, Rudock M, Liu Y, Lohman K, Harris TB, Humphries SE, Hamsten A, Norman PE, Hankey GJ, Jamrozik K, Palmer LJ, Rimm EB, Pai JK, Psaty BM, Heckbert SR, Bis JC, Yusuf S, Anand S, Engert JC, Xie C, Collins R, Clarke R, Bennett D, Kooner J, Chambers J, Elliott P, Maerz W, Kleber ME, Boehm BO, Winkelmann BR, Melander O, Berglund G, Koenig W, Thorand B, Baumert J, Peters A, Rimm EB, Manson J, Pai JK, Humphries SE, Cooper JA, Talmud PJ, Ladenvall P, Johansson L, Jansson J-H, Hallmans G, Reilly MP, Qu L, Li M, Rader DJ, Watkins H, Clarke R, Hopewell J, Saleheen D, Danesh J, Frossard P, Sattar N, Robertson M, Shepherd J, Schaefer E, Hofman A, Witteman JCM, Kardys I, Dehghan A, de Faire U, Bennet A, Gigante B, Leander K, Ben-Shlomo Y, Davey-Smith G, Timpson N, Peters B, Maitland-van der Zee AH, de Boer A, Klungel O, Reiner A, Manson J, Greenland P, Dai J, Liu S, Kumari M, Brunner E, Kivimaki M, Marmot M, Sattar N, O'Reilly D, Ford I, Packard CJet al., 2011, Association between C reactive protein and coronary heart disease: mendelian randomisation analysis based on individual participant data, British Medical Journal, Vol: 342, ISSN: 1468-5833

Objective To use genetic variants as unconfounded proxies of C reactive protein concentration to study its causal role in coronary heart disease.Design Mendelian randomisation meta-analysis of individual participant data from 47 epidemiological studies in 15 countries.Participants 194 418 participants, including 46 557 patients with prevalent or incident coronary heart disease. Information was available on four CRP gene tagging single nucleotide polymorphisms (rs3093077, rs1205, rs1130864, rs1800947), concentration of C reactive protein, and levels of other risk factors.Main outcome measures Risk ratios for coronary heart disease associated with genetically raised C reactive protein versus risk ratios with equivalent differences in C reactive protein concentration itself, adjusted for conventional risk factors and variability in risk factor levels within individuals.Results CRP variants were each associated with up to 30% per allele difference in concentration of C reactive protein (P<10−34) and were unrelated to other risk factors. Risk ratios for coronary heart disease per additional copy of an allele associated with raised C reactive protein were 0.93 (95% confidence interval 0.87 to 1.00) for rs3093077; 1.00 (0.98 to 1.02) for rs1205; 0.98 (0.96 to 1.00) for rs1130864; and 0.99 (0.94 to 1.03) for rs1800947. In a combined analysis, the risk ratio for coronary heart disease was 1.00 (0.90 to 1.13) per 1 SD higher genetically raised natural log (ln) concentration of C reactive protein. The genetic findings were discordant with the risk ratio observed for coronary heart disease of 1.33 (1.23 to 1.43) per 1 SD higher circulating ln concentration of C reactive protein in prospective studies (P=0.001 for difference).Conclusion Human genetic data indicate that C reactive protein concentration itself is unlikely to be even a modest causal factor in coronary heart disease.

Journal article

el Barzouhi A, Elias-Smale S, Dehghan A, Vliegenthart-Proenca R, Oudkerk M, Hofman A, Witteman JCMet al., 2011, Renal Function Is Related to Severity of Coronary Artery Calcification in Elderly Persons: The Rotterdam Study, PLOS ONE, Vol: 6, ISSN: 1932-6203

Journal article

Versmissen J, Oosterveer DM, Yazdanpanah M, Mulder M, Dehghan A, Defesche JC, Kastelein JJP, Sijbrands EJGet al., 2011, A frequent variant in the ABCA1 gene is associated with increased coronary heart disease risk and a better response to statin treatment in familial hypercholesterolemia patients, EUROPEAN HEART JOURNAL, Vol: 32, Pages: 469-475, ISSN: 0195-668X

Journal article

Yang Q, Koettgen A, Dehghan A, Smith AV, Glazer NL, Chen M-H, Chasman DI, Aspelund T, Eiriksdottir G, Harris TB, Launer L, Nalls M, Hernandez D, Arking DE, Boerwinkle E, Grove ML, Li M, Kao WHL, Chonchol M, Haritunians T, Li G, Lumley T, Psaty BM, Shlipak M, Hwang S-J, Larson MG, O'Donnell CJ, Upadhyay A, van Duijn CM, Hofman A, Rivadeneira F, Stricker B, Uitterlinden AG, Pare G, Parker AN, Ridker PM, Siscovick DS, Gudnason V, Witteman JC, Fox CS, Coresh Jet al., 2010, Multiple Genetic Loci Influence Serum Urate Levels and Their Relationship With Gout and Cardiovascular Disease Risk Factors, CIRCULATION-CARDIOVASCULAR GENETICS, Vol: 3, Pages: 523-530, ISSN: 1942-325X

Journal article

Yang Q, Köttgen A, Dehghan A, Smith AV, Glazer NL, Chen M-H, Chasman DI, Aspelund T, Eiriksdottir G, Harris TB, Launer L, Nalls M, Hernandez D, Arking DE, Boerwinkle E, Grove ML, Li M, Linda Kao WH, Chonchol M, Haritunians T, Li G, Lumley T, Psaty BM, Shlipak M, Hwang S-J, Larson MG, O'Donnell CJ, Upadhyay A, van Duijn CM, Hofman A, Rivadeneira F, Stricker B, Uitterlinden AG, Paré G, Parker AN, Ridker PM, Siscovick DS, Gudnason V, Witteman JC, Fox CS, Coresh Jet al., 2010, Multiple genetic loci influence serum urate levels and their relationship with gout and cardiovascular disease risk factors., Circ Cardiovasc Genet, Vol: 3, Pages: 523-530

BACKGROUND: Elevated serum urate levels can lead to gout and are associated with cardiovascular risk factors. We performed a genome-wide association study to search for genetic susceptibility loci for serum urate and gout and investigated the causal nature of the associations of serum urate with gout and selected cardiovascular risk factors and coronary heart disease (CHD). METHODS AND RESULTS: Meta-analyses of genome-wide association studies (GWAS) were performed in 5 population-based cohorts of the Cohorts for Heart and Aging Research in Genome Epidemiology consortium for serum urate and gout in 28 283 white participants. The effect of the most significant single-nucleotide polymorphism at all genome-wide significant loci on serum urate was added to create a genetic urate score. Findings were replicated in the Women's Genome Health Study (n=22 054). Single-nucleotide polymorphisms at 8 genetic loci achieved genome-wide significance with serum urate levels (P=4×10(-8) to 2×10(-242) in SLC22A11, GCKR, R3HDM2-INHBC region, RREB1, PDZK1, SLC2A9, ABCG2, and SLC17A1). Only 2 loci (SLC2A9, ABCG2) showed genome-wide significant association with gout. The genetic urate score was strongly associated with serum urate and gout (odds ratio, 12.4 per 100 μmol/L; P=3×10(-39)) but not with blood pressure, glucose, estimated glomerular filtration rate, chronic kidney disease, or CHD. The lack of association between the genetic score and the latter phenotypes also was observed in the Women's Genome Health Study. CONCLUSIONS: The genetic urate score analysis suggested a causal relationship between serum urate and gout but did not provide evidence for one between serum urate and cardiovascular risk factors and CHD.

Journal article

O'Seaghdha CM, Yang Q, Glazer NL, Leak TS, Dehghan A, Smith AV, Kao WHL, Lohman K, Hwang S-J, Johnson AD, Hofman A, Uitterlinden AG, Chen Y-DI, Brown EM, Siscovick DS, Harris TB, Psaty BM, Coresh J, Gudnason V, Witteman JC, Liu YM, Kestenbaum BR, Fox CS, Koettgen Aet al., 2010, Common variants in the calcium-sensing receptor gene are associated with total serum calcium levels, HUMAN MOLECULAR GENETICS, Vol: 19, Pages: 4296-4303, ISSN: 0964-6906

Journal article

Struchalin MV, Dehghan A, Witteman JCM, van Duijn C, Aulchenko YSet al., 2010, Variance heterogeneity analysis for detection of potentially interacting genetic loci: method and its limitations, BMC GENETICS, Vol: 11, ISSN: 1471-2156

Journal article

Meyer TE, Verwoert GC, Hwang S-J, Glazer NL, Smith AV, van Rooij FJA, Ehret GB, Boerwinkle E, Felix JF, Leak TS, Harris TB, Yang Q, Dehghan A, Aspelund T, Katz R, Homuth G, Kocher T, Rettig R, Ried JS, Gieger C, Prucha H, Pfeufer A, Meitinger T, Coresh J, Hofman A, Sarnak MJ, Chen Y-DI, Uitterlinden AG, Chakravarti A, Psaty BM, van Duijn CM, Kao WHL, Witteman JCM, Gudnason V, Siscovick DS, Fox CS, Koettgen Aet al., 2010, Genome-Wide Association Studies of Serum Magnesium, Potassium, and Sodium Concentrations Identify Six Loci Influencing Serum Magnesium Levels, PLOS GENETICS, Vol: 6, ISSN: 1553-7404

Journal article

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