Search

Your search keyword '"Shields DC"' showing total 5 results
Start Over Author "Shields DC" Database OAIster
5 results on '"Shields DC"'

1. Meta-analysis of genome-wide association studies of HDL cholesterol response to statins

Author

Postmus, I, Warren, HR, Trompet, S, Arsenault, BJ, Avery, CL, Bis, JC, Chasman, DI, de Keyser, Toke, Deshmukh, HA, Evans, DS, Feng, Q, Li, X, Smit, RAJ, Smith, AV, Sun, F, Taylor, KD, Arnold, AM, Barnes, MR, Barratt, BJ, Betteridge, J, Boekholdt, SM, Boerwinkle, E, Buckley, BM, Chen, YDI, de Craen, AJM, Cummings, SR, Denny, JC, Dube, MP, Durrington, PN, Eiriksdottir, G, Ford, I, Guo, X, Harris, TB, Heckbert, SR, Hofman, Bert, Hovingh, GK, Kastelein, JJP, Launer, LJ, Liu, C-T, Liu, Y, Lumley, T, Mckeigue, PM, Munroe, PB, Neil, A, Nickerson, DA, Nyberg, F, O'Brien, E, O'Donnell, CJ, Post, W, Poulter, N, Vasan, RS, Rice, K, Rich, SS, Rivadeneira, Fernando, Sattar, N, Sever, P, Shaw-Hawkins, S, Shields, DC, Slagboom, PE (Eline), Smith, NL, Smith, JD, Sotoodehnia, N, Stanton, A, Stott, DJ, Stricker, Bruno, Sturmer, T, Uitterlinden, André, Wei, W-Q, Westendorp, RGJ, Whitsel, EA, Wiggins, KL, Wilke, RA, Ballantyne, CM, Colhoun, HM, Cupples, LA, Franco Duran, OH, Gudnason, V, Hitman, G, Palmer, CNA, Psaty, BM, Ridker, PM, Stafford, JM, Stein, CM, Tardif, J-C, Caulfield, MJ, Jukema, JW, Rotter, JI, Krauss, RM, Postmus, I, Warren, HR, Trompet, S, Arsenault, BJ, Avery, CL, Bis, JC, Chasman, DI, de Keyser, Toke, Deshmukh, HA, Evans, DS, Feng, Q, Li, X, Smit, RAJ, Smith, AV, Sun, F, Taylor, KD, Arnold, AM, Barnes, MR, Barratt, BJ, Betteridge, J, Boekholdt, SM, Boerwinkle, E, Buckley, BM, Chen, YDI, de Craen, AJM, Cummings, SR, Denny, JC, Dube, MP, Durrington, PN, Eiriksdottir, G, Ford, I, Guo, X, Harris, TB, Heckbert, SR, Hofman, Bert, Hovingh, GK, Kastelein, JJP, Launer, LJ, Liu, C-T, Liu, Y, Lumley, T, Mckeigue, PM, Munroe, PB, Neil, A, Nickerson, DA, Nyberg, F, O'Brien, E, O'Donnell, CJ, Post, W, Poulter, N, Vasan, RS, Rice, K, Rich, SS, Rivadeneira, Fernando, Sattar, N, Sever, P, Shaw-Hawkins, S, Shields, DC, Slagboom, PE (Eline), Smith, NL, Smith, JD, Sotoodehnia, N, Stanton, A, Stott, DJ, Stricker, Bruno, Sturmer, T, Uitterlinden, André, Wei, W-Q, Westendorp, RGJ, Whitsel, EA, Wiggins, KL, Wilke, RA, Ballantyne, CM, Colhoun, HM, Cupples, LA, Franco Duran, OH, Gudnason, V, Hitman, G, Palmer, CNA, Psaty, BM, Ridker, PM, Stafford, JM, Stein, CM, Tardif, J-C, Caulfield, MJ, Jukema, JW, Rotter, JI, and Krauss, RM

Published
2016

2. Pharmacogenetic meta-analysis of genome-wide association studies of LDL cholesterol response to statins

Author

Postmus, I, Trompet, S, Deshmukh, HA, Barnes, MR, Li, XH, Warren, HR, Chasman, DI, Zhou, KX, Arsenault, BJ, Donnelly, LA, Wiggins, KL, Avery, CL, Griffin, P, Feng, QP, Taylor, KD, Li, G, Evans, DS, Smith, AV, de Keyser, Toke, Johnson, AD, de Craen, AJM, Stott, DJ, Buckley, BM, Ford, I, Westendorp, RGJ, Slagboom, PE (Eline), Sattar, N, Munroe, PB, Sever, P, Poulter, N, Stanton, A, Shields, DC, O'Brien, E, Shaw-Hawkins, S, Chen, YDI, Nickerson, DA, Smith, JD, Dube, MP, Boekholdt, SM, Hovingh, GK, Kastelein, JJP, Mckeigue, PM, Betteridge, J, Neil, A, Durrington, PN, Doney, A, Carr, F, Morris, A, McCarthy, MI, Groop, L, Ahlqvist, E, Bis, JC, Rice, K, Smith, NL, Lumley, T, Whitsel, EA, Sturmer, T, Boerwinkle, E, Ngwa, JS, O'Donnell, CJ, Vasan, RS, Wei, WQ, Wilke, RA, Liu, CT, Sun, FG, Guo, XQ, Heckbert, SR, Post, W, Sotoodehnia, N, Arnold, AM, Stafford, JM, Ding, JZ (Jing Zhong), Herrington, DM, Kritchevsky, SB, Eiriksdottir, G, Launer, LJ (Lenore), Harris, TB, Chu, AY, Giulianini, F, MacFadyen, JG, Barratt, BJ, Nyberg, F, Stricker, Bruno, Uitterlinden, André, Hofman, Bert, Rivadeneira, Fernando, Emilsson, V, Franco Duran, OH, Ridker, PM, Gudnason, V, Liu, YM, Denny, JC, Ballantyne, CM, Rotter, JI, Cupples, LA, Psaty, BM, Palmer, CNA, Tardif, JC, Colhoun, HM, Hitman, G, Krauss, RM, Jukema, JW, Caulfield, MJ, Postmus, I, Trompet, S, Deshmukh, HA, Barnes, MR, Li, XH, Warren, HR, Chasman, DI, Zhou, KX, Arsenault, BJ, Donnelly, LA, Wiggins, KL, Avery, CL, Griffin, P, Feng, QP, Taylor, KD, Li, G, Evans, DS, Smith, AV, de Keyser, Toke, Johnson, AD, de Craen, AJM, Stott, DJ, Buckley, BM, Ford, I, Westendorp, RGJ, Slagboom, PE (Eline), Sattar, N, Munroe, PB, Sever, P, Poulter, N, Stanton, A, Shields, DC, O'Brien, E, Shaw-Hawkins, S, Chen, YDI, Nickerson, DA, Smith, JD, Dube, MP, Boekholdt, SM, Hovingh, GK, Kastelein, JJP, Mckeigue, PM, Betteridge, J, Neil, A, Durrington, PN, Doney, A, Carr, F, Morris, A, McCarthy, MI, Groop, L, Ahlqvist, E, Bis, JC, Rice, K, Smith, NL, Lumley, T, Whitsel, EA, Sturmer, T, Boerwinkle, E, Ngwa, JS, O'Donnell, CJ, Vasan, RS, Wei, WQ, Wilke, RA, Liu, CT, Sun, FG, Guo, XQ, Heckbert, SR, Post, W, Sotoodehnia, N, Arnold, AM, Stafford, JM, Ding, JZ (Jing Zhong), Herrington, DM, Kritchevsky, SB, Eiriksdottir, G, Launer, LJ (Lenore), Harris, TB, Chu, AY, Giulianini, F, MacFadyen, JG, Barratt, BJ, Nyberg, F, Stricker, Bruno, Uitterlinden, André, Hofman, Bert, Rivadeneira, Fernando, Emilsson, V, Franco Duran, OH, Ridker, PM, Gudnason, V, Liu, YM, Denny, JC, Ballantyne, CM, Rotter, JI, Cupples, LA, Psaty, BM, Palmer, CNA, Tardif, JC, Colhoun, HM, Hitman, G, Krauss, RM, Jukema, JW, and Caulfield, MJ

Abstract

Statins effectively lower LDL cholesterol levels in large studies and the observed interindividual response variability may be partially explained by genetic variation. Here we perform a pharmacogenetic meta-analysis of genome-wide association studies (GWAS) in studies addressing the LDL cholesterol response to statins, including up to 18,596 statin-treated subjects. We validate the most promising signals in a further 22,318 statin recipients and identify two loci, SORT1/CELSR2/PSRC1 and SLCO1B1, not previously identified in GWAS. Moreover, we confirm the previously described associations with APOE and LPA. Our findings advance the understanding of the pharmacogenetic architecture of statin response.

Published
2014

3. Genome-wide analysis of blood pressure variability and ischemic stroke

Author

Yadav, S, Cotlarciuc, I, Munroe, PB, Khan, MS, Nalls, MA, Bevan, S, Cheng, YC, Chen, WM, Malik, R, Mccarthy, NS, Holliday, EG, Speed, D, Hasan, N, Pucek, M, Rinne, PE, Sever, P, Stanton, A, Shields, DC, Maguire, JM, Mcevoy, M, Scott, RJ, Ferrucci, L, Macleod, MJ, Attia, J, Markus, HS, Sale, MM, Worrall, BB, Mitchell, BD, Dichgans, M, Sudlow, C, Meschia, JF, Rothwell, PM, Caulfield, M, Sharma, P, Yadav, S, Cotlarciuc, I, Munroe, PB, Khan, MS, Nalls, MA, Bevan, S, Cheng, YC, Chen, WM, Malik, R, Mccarthy, NS, Holliday, EG, Speed, D, Hasan, N, Pucek, M, Rinne, PE, Sever, P, Stanton, A, Shields, DC, Maguire, JM, Mcevoy, M, Scott, RJ, Ferrucci, L, Macleod, MJ, Attia, J, Markus, HS, Sale, MM, Worrall, BB, Mitchell, BD, Dichgans, M, Sudlow, C, Meschia, JF, Rothwell, PM, Caulfield, M, and Sharma, P

Abstract

Background and Purpose-Visit-to-visit variability in blood pressure (vBP) is associated with ischemic stroke. We sought to determine whether such variability has genetic causes and whether genetic variants associated with BP variability are also associated with ischemic stroke. Methods-A Genome Wide Association Study (GWAS) for loci influencing BP variability was undertaken in 3802 individuals from the Anglo-Scandinavian Cardiac Outcome Trial (ASCOT) study, in which long-term visit-to-visit and within-visit BP measures were available. Because BP variability is strongly associated with ischemic stroke, we genotyped the sentinel single nucleotide polymorphism in an independent ischemic stroke population comprising 8624 cases and 12 722 controls and in 3900 additional (Scandinavian) participants from the ASCOT study to replicate our findings. Results-The ASCOT discovery GWAS identified a cluster of 17 correlated single nucleotide polymorphisms within the NLGN1 gene (3q26.31) associated with BP variability. The strongest association was with rs976683 (P=1.4×10-8). Conditional analysis of rs976683 provided no evidence of additional independent associations at the locus. Analysis of rs976683 in patients with ischemic stroke found no association for overall stroke (odds ratio, 1.02; 95% CI, 0.97-1.07; P=0.52) or its subtypes: cardioembolic (odds ratio, 1.07; 95% CI, 0.97-1.16; P=0.17), large vessel disease (odds ratio, 0.98; 95% CI, 0.89-1.07; P=0.60), and small vessel disease (odds ratio, 1.07; 95% CI, 0.97-1.17; P=0.19). No evidence for association was found between rs976683 and BP variability in the additional (Scandinavian) ASCOT participants (P=0.18). Conclusions-We identified a cluster of single nucleotide polymorphisms at the NLGN1 locus showing significant association with BP variability. Follow-up analyses did not support an association with risk of ischemic stroke and its subtypes. © 2013 American Heart Association, Inc.

Published
2013

4. Genome-wide analysis of blood pressure variability and ischemic stroke

Author

Yadav, S, Cotlarciuc, I, Munroe, PB, Khan, MS, Nalls, MA, Bevan, S, Cheng, YC, Chen, WM, Malik, R, Mccarthy, NS, Holliday, EG, Speed, D, Hasan, N, Pucek, M, Rinne, PE, Sever, P, Stanton, A, Shields, DC, Maguire, JM, Mcevoy, M, Scott, RJ, Ferrucci, L, Macleod, MJ, Attia, J, Markus, HS, Sale, MM, Worrall, BB, Mitchell, BD, Dichgans, M, Sudlow, C, Meschia, JF, Rothwell, PM, Caulfield, M, Sharma, P, Yadav, S, Cotlarciuc, I, Munroe, PB, Khan, MS, Nalls, MA, Bevan, S, Cheng, YC, Chen, WM, Malik, R, Mccarthy, NS, Holliday, EG, Speed, D, Hasan, N, Pucek, M, Rinne, PE, Sever, P, Stanton, A, Shields, DC, Maguire, JM, Mcevoy, M, Scott, RJ, Ferrucci, L, Macleod, MJ, Attia, J, Markus, HS, Sale, MM, Worrall, BB, Mitchell, BD, Dichgans, M, Sudlow, C, Meschia, JF, Rothwell, PM, Caulfield, M, and Sharma, P

Abstract

Background and Purpose-Visit-to-visit variability in blood pressure (vBP) is associated with ischemic stroke. We sought to determine whether such variability has genetic causes and whether genetic variants associated with BP variability are also associated with ischemic stroke. Methods-A Genome Wide Association Study (GWAS) for loci influencing BP variability was undertaken in 3802 individuals from the Anglo-Scandinavian Cardiac Outcome Trial (ASCOT) study, in which long-term visit-to-visit and within-visit BP measures were available. Because BP variability is strongly associated with ischemic stroke, we genotyped the sentinel single nucleotide polymorphism in an independent ischemic stroke population comprising 8624 cases and 12 722 controls and in 3900 additional (Scandinavian) participants from the ASCOT study to replicate our findings. Results-The ASCOT discovery GWAS identified a cluster of 17 correlated single nucleotide polymorphisms within the NLGN1 gene (3q26.31) associated with BP variability. The strongest association was with rs976683 (P=1.4×10-8). Conditional analysis of rs976683 provided no evidence of additional independent associations at the locus. Analysis of rs976683 in patients with ischemic stroke found no association for overall stroke (odds ratio, 1.02; 95% CI, 0.97-1.07; P=0.52) or its subtypes: cardioembolic (odds ratio, 1.07; 95% CI, 0.97-1.16; P=0.17), large vessel disease (odds ratio, 0.98; 95% CI, 0.89-1.07; P=0.60), and small vessel disease (odds ratio, 1.07; 95% CI, 0.97-1.17; P=0.19). No evidence for association was found between rs976683 and BP variability in the additional (Scandinavian) ASCOT participants (P=0.18). Conclusions-We identified a cluster of single nucleotide polymorphisms at the NLGN1 locus showing significant association with BP variability. Follow-up analyses did not support an association with risk of ischemic stroke and its subtypes. © 2013 American Heart Association, Inc.

Published
2013

5. Genome-wide association study of blood pressure extremes identifies variant near UMOD associated with hypertension

Author

Padmanabhan, S, Melander, O, Johnson, T, Di Blasio, A, Lee, W, Gentilini, D, Hastie, C, Menni, C, Monti, M, Delles, C, Laing, S, Corso, B, Navis, G, Kwakernaak, A, van der Harst, P, Bochud, M, Maillard, M, Burnier, M, Hedner, T, Kjeldsen, S, Wahlstrand, B, Sjögren, M, Fava, C, Montagnana, M, Danese, E, Torffvit, O, Hedblad, B, Snieder, H, Connell, J, Brown, M, Samani, N, Farrall, M, Cesana, G, Mancia, G, Signorini, S, Grassi, G, Eyheramendy, S, Wichmann, H, Laan, M, Strachan, D, Sever, P, Shields, D, Stanton, A, Vollenweider, P, Teumer, A, Völzke, H, Rettig, R, Newton Cheh, C, Arora, P, Zhang, F, Soranzo, N, Spector, T, Lucas, G, Kathiresan, S, Siscovick, D, Luan, J, Loos, R, Wareham, N, Penninx, B, Nolte, I, Mcbride, M, Miller, W, Nicklin, S, Baker, A, Graham, D, Mcdonald, R, Pell, J, Sattar, N, Welsh, P, Munroe, P, Caulfield, M, Zanchetti, A, Dominiczak, A, Di Blasio, AM, Lee, WK, Hastie, CE, Monti, MC, Kwakernaak, AJ, Connell, JMC, Samani, NJ, CESANA, GIANCARLO, Wichmann, HE, Strachan, DP, Shields, DC, Spector, TD, Siscovick, DS, Loos, RJF, Wareham, NJ, Penninx, BW, Nolte, IM, McBride, M, Miller, WH, Nicklin, SA, Baker, AH, McDonald, RA, Pell, JP, Caulfield, MJ, Dominiczak, AF, GRASSI, GUIDO, Padmanabhan, S, Melander, O, Johnson, T, Di Blasio, A, Lee, W, Gentilini, D, Hastie, C, Menni, C, Monti, M, Delles, C, Laing, S, Corso, B, Navis, G, Kwakernaak, A, van der Harst, P, Bochud, M, Maillard, M, Burnier, M, Hedner, T, Kjeldsen, S, Wahlstrand, B, Sjögren, M, Fava, C, Montagnana, M, Danese, E, Torffvit, O, Hedblad, B, Snieder, H, Connell, J, Brown, M, Samani, N, Farrall, M, Cesana, G, Mancia, G, Signorini, S, Grassi, G, Eyheramendy, S, Wichmann, H, Laan, M, Strachan, D, Sever, P, Shields, D, Stanton, A, Vollenweider, P, Teumer, A, Völzke, H, Rettig, R, Newton Cheh, C, Arora, P, Zhang, F, Soranzo, N, Spector, T, Lucas, G, Kathiresan, S, Siscovick, D, Luan, J, Loos, R, Wareham, N, Penninx, B, Nolte, I, Mcbride, M, Miller, W, Nicklin, S, Baker, A, Graham, D, Mcdonald, R, Pell, J, Sattar, N, Welsh, P, Munroe, P, Caulfield, M, Zanchetti, A, Dominiczak, A, Di Blasio, AM, Lee, WK, Hastie, CE, Monti, MC, Kwakernaak, AJ, Connell, JMC, Samani, NJ, CESANA, GIANCARLO, Wichmann, HE, Strachan, DP, Shields, DC, Spector, TD, Siscovick, DS, Loos, RJF, Wareham, NJ, Penninx, BW, Nolte, IM, McBride, M, Miller, WH, Nicklin, SA, Baker, AH, McDonald, RA, Pell, JP, Caulfield, MJ, Dominiczak, AF, and GRASSI, GUIDO

Abstract

Hypertension is a heritable and major contributor to the global burden of disease. The sum of rare and common genetic variants robustly identified so far explain only 1%-2% of the population variation in BP and hypertension. This suggests the existence of more undiscovered common variants. We conducted a genome-wide association study in 1,621 hypertensive cases and 1,699 controls and follow-up validation analyses in 19,845 cases and 16,541 controls using an extreme case-control design. We identified a locus on chromosome 16 in the 5' region of Uromodulin (UMOD; rs13333226, combined P value of 3.6 × 10−11). The minor G allele is associated with a lower risk of hypertension (OR [95%CI]: 0.87 [0.84-0.91]), reduced urinary uromodulin excretion, better renal function; and each copy of the G allele is associated with a 7.7% reduction in risk of CVD events after adjusting for age, sex, BMI, and smoking status (H.R. = 0.923, 95% CI 0.860-0.991; p = 0.027). In a subset of 13,446 individuals with estimated glomerular filtration rate (eGFR) measurements, we show that rs13333226 is independently associated with hypertension (unadjusted for eGFR: 0.89 [0.83-0.96], p = 0.004; after eGFR adjustment: 0.89 [0.83-0.96], p = 0.003). In clinical functional studies, we also consistently show the minor G allele is associated with lower urinary uromodulin excretion. The exclusive expression of uromodulin in the thick portion of the ascending limb of Henle suggests a putative role of this variant in hypertension through an effect on sodium homeostasis. The newly discovered UMOD locus for hypertension has the potential to give new insights into the role of uromodulin in BP regulation and to identify novel drugable targets for reducing cardiovascular risk.

Published
2010

Catalog

Books, media, physical & digital resources
See catalog results