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42 results on '"Iakoubova, Olga A"'

10. Identification of four gene variants associated with myocardial infarction

Author

Shiffman, Dov, Ellis, Stephen G., Rowland, Charles M., Malloy, Mary J., Luke, May M., Iakoubova, Olga A., Pullinger, Clive R., Cassano, June, Aouizerat, Bradley E., Fenwick, Raymond G., Reitz, Richard E., Catanese, Joseph J., Leong, Diane U., Zellner, Christian, Sninsky, John J., Topol, Eric J., Devlin, James J., and Kane, John P.

Subjects
Heart attack -- Genetic aspects, Heart attack -- Research, Heart attack -- Statistics, Biological sciences
Published
2005

11. Genetic variation in PCAF, a key mediator in epigenetics, is associated with reduced vascular morbidity and mortality: evidence for a new concept from three independent prospective studies

Author

Pons, Douwe, Trompet, Stella, de Craen, Anton J M, Thijssen, Peter E, Quax, Paul H A, de Vries, Margreet R, Wierda, Rutger J, van den Elsen, Peter J, Monraats, Pascalle S, Ewing, Mark M, Heijmans, Bastiaan T, Slagboom, P Eline, Zwinderman, Aeilko H, Doevendans, Pieter A F M, Tio, René A, de Winter, Robbert J, de Maat, Moniek P M, Iakoubova, Olga A, Sattar, Naveed, Shepherd, Jim, Westendorp, Rudi G J, and Jukema, J Wouter

Published
2011
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14. Genome-Tagged Mice (GTM): Two Sets of Genome-wide Congenic Strains

Author

Iakoubova, Olga A., Olsson, Christine L., Dains, Katherine M., Ross, David A., Andalibi, Ali, Lau, Kit, Choi, Jim, Kalcheva, Iveta, Cunanan, Madalyne, Louie, Judi, Nimon, Vitaly, Machrus, Migdad, Bentley, L.Gordon, Beauheim, Catherine, Silvey, Scott, Cavalcoli, James, Lusis, Aldons J., and West, David B.

Published
2001
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16. Genetic Variants in FBN-1 and Risk for Thoracic Aortic Aneurysm and Dissection

Author

Iakoubova, Olga A., primary, Tong, Carmen H., additional, Rowland, Charles M., additional, Luke, May M., additional, Garcia, Veronica E., additional, Catanese, Joseph J., additional, Moomiaie, Remo M., additional, Sotonyi, Peter, additional, Ascady, Gyorgy, additional, Nikas, Demitrios, additional, Dedelias, Panagiotis, additional, Tranquilli, Maryann, additional, and Elefteriades, John A., additional

Published
2014
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17. Genome-Wide Study of Gene Variants Associated with Differential Cardiovascular Event Reduction by Pravastatin Therapy

Author

Shiffman, Dov, primary, Trompet, Stella, additional, Louie, Judy Z., additional, Rowland, Charles M., additional, Catanese, Joseph J., additional, Iakoubova, Olga A., additional, Kirchgessner, Todd G., additional, Westendorp, Rudi G. J., additional, de Craen, Anton J. M., additional, Slagboom, P. Eline, additional, Buckley, Brendan M., additional, Stott, David J., additional, Sattar, Naveed, additional, Devlin, James J., additional, Packard, Christopher J., additional, Ford, Ian, additional, Sacks, Frank M., additional, and Jukema, J. Wouter, additional

Published
2012
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18. Abstract P103: Genome-Wide Study of Gene Variants Associated with Differential Event Reduction by Pravastatin Therapy

Author

Shiffman, Dov, primary, Trompet, Stella, additional, Louie, Judy Z, additional, Rowland, Charles M, additional, Catanese, Joseph J, additional, Iakoubova, Olga A, additional, Kirchgessner, Todd G, additional, Scott, David J, additional, Sattar, Naveed, additional, Devlin, James J, additional, Packard, Christopher J, additional, Ford, Ian, additional, Sacks, Frank M, additional, and Jukema, J W, additional

Published
2011
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19. Genetic variants in the KIF6 region and coronary event reduction from statin therapy

Author

Li, Yonghong, primary, Sabatine, Marc S., additional, Tong, Carmen H., additional, Ford, Ian, additional, Kirchgessner, Todd G., additional, Packard, Christopher J., additional, Robertson, Michele, additional, Rowland, Charles M., additional, Bare, Lance A., additional, Shepherd, James, additional, Devlin, James J., additional, and Iakoubova, Olga A., additional

Published
2010
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24. Association Between ADAMTS1 Matrix Metalloproteinase Gene Variation, Coronary Heart Disease, and Benefit of Statin Therapy

Author

Sabatine, Marc S., primary, Ploughman, Lynn, additional, Simonsen, Katy L., additional, Iakoubova, Olga A., additional, Kirchgessner, Todd G., additional, Ranade, Koustubh, additional, Tsuchihashi, Zenta, additional, Zerba, Kim E., additional, Long, Diane U., additional, Tong, Carmen H., additional, Packard, Christopher J., additional, Pfeffer, Marc A., additional, Devlin, James J., additional, Shepherd, James, additional, Campos, Hannia, additional, Sacks, Frank M., additional, and Braunwald, Eugene, additional

Published
2008
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26. Association of Gene Variants With Incident Myocardial Infarction in the Cardiovascular Health Study

Author

Shiffman, Dov, primary, O’Meara, Ellen S., additional, Bare, Lance A., additional, Rowland, Charles M., additional, Louie, Judy Z., additional, Arellano, Andre R., additional, Lumley, Thomas, additional, Rice, Kenneth, additional, Iakoubova, Olga, additional, Luke, May M., additional, Young, Bradford A., additional, Malloy, Mary J., additional, Kane, John P., additional, Ellis, Stephen G., additional, Tracy, Russell P., additional, Devlin, James J., additional, and Psaty, Bruce M., additional

Published
2008
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28. Gene Expression Signature in Peripheral Blood Detects Thoracic Aortic Aneurysm

Author

Wang, Yulei, primary, Barbacioru, Catalin C., additional, Shiffman, Dov, additional, Balasubramanian, Sriram, additional, Iakoubova, Olga, additional, Tranquilli, Maryann, additional, Albornoz, Gonzalo, additional, Blake, Julie, additional, Mehmet, Necip N., additional, Ngadimo, Dewi, additional, Poulter, Karen, additional, Chan, Frances, additional, Samaha, Raymond R., additional, and Elefteriades, John A., additional

Published
2007
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29. Asp92Asn Polymorphism in the Myeloid IgA Fc Receptor Is Associated With Myocardial Infarction in Two Disparate Populations

Author

Iakoubova, Olga A., primary, Tong, Carmen H., additional, Chokkalingam, Anand P., additional, Rowland, Charles M., additional, Kirchgessner, Todd G., additional, Louie, Judy Z., additional, Ploughman, Lynn M., additional, Sabatine, Marc S., additional, Campos, Hannia, additional, Catanese, Joseph J., additional, Leong, Diane U., additional, Young, Bradford A., additional, Lew, David, additional, Tsuchihashi, Zenta, additional, Luke, May M., additional, Packard, Christopher J., additional, Zerba, Kim E., additional, Shaw, Peter M., additional, Shepherd, James, additional, Devlin, James J., additional, and Sacks, Frank M., additional

Published
2006
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31. Genetic Variants in FBN-1 and Risk for Thoracic Aortic Aneurysm and Dissection.

Author

Iakoubova, Olga A., Tong, Carmen H., Rowland, Charles M., Luke, May M., Garcia, Veronica E., Catanese, Joseph J., Moomiaie, Remo M., Sotonyi, Peter, Ascady, Gyorgy, Nikas, Demitrios, Dedelias, Panagiotis, Tranquilli, Maryann, and Elefteriades, John A.

Subjects
*THORACIC aneurysms, *SINGLE nucleotide polymorphisms, *HYPERTENSION, *ALLELES, *LOGISTIC regression analysis, *MOLECULAR genetics
Abstract

Objectives: A recent genome wide association study (GWAS) by LeMaire et al. found that two single nucleotide polymorphisms (SNPs), rs2118181 and rs10519177 in the FBN-1 gene (encoding Fibrillin-1), were associated with thoracic aortic dissection (TAD), non-dissecting thoracic aortic aneurysm (TAA), and thoracic aortic aneurysm or dissection (TAAD); the largest effect was observed for the association of rs2118181 with TAD. We investigated whether rs2118181 and rs10519177 were associated with TAD, TAA, and TAAD in the Yale study. Methods: The genotypes of rs2118181 and rs10519177 were determined for participants in the Yale study: 637 TAAD cases (140 TAD, 497 TAA) and 275 controls from the United States, Hungary, and Greece. The association of the genotypes with TAD, TAA and TAAD were assessed using logistic regression models adjusted for sex, age, study center and hypertension. Results and Conclusions: In the Yale study, rs2118181 was associated with TAD: compared with non-carriers, carriers of the risk allele had an unadjusted odds ratio for TAD of 1.80 (95% CI 1.15–2.80) and they had odds ratio for TAD of 1.87 (95% CI 1.09–3.20) after adjusting for sex, age, study center and hypertension. We did not find significant differences in aortic size, a potential confounder for TAD, between rs2118181 risk variant carriers and non-carriers: mean aortic size was 5.56 (95% CI: 5.37–5.73) for risk variant carriers (CC+CT) and was 5.48 (95% CI: 5.36–5.61) for noncarriers (TT) (p = 0.56). rs2118181 was not associated with TAA or TAAD. rs10519177 was not associated with TAD, TAA, or TAAD in the Yale study. Thus, the Yale study provided further support for the association of the FBN-1 rs2118181SNP with TAD. [ABSTRACT FROM AUTHOR]

Published
2014
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35. Genetic variants in the KIF6 region and coronary event reduction from statin therapy.

Author

Yonghong Li, Sabatine, Marc S., Tong, Carmen H., Ford, Ian, Kirchgessner, Todd G., Packard, Christopher J., Robertson, Michele, Rowland, Charles M., Bare, Lance A., Shepherd, James, Devlin, James J., and Iakoubova, Olga A.

Subjects
NUCLEOTIDE sequence, GENETIC polymorphisms, STATINS (Cardiovascular agents), RANDOMIZED controlled trials, CHOLESTEROL, THROMBOLYTIC therapy, MYOCARDIAL infarction
Abstract

single nucleotide polymorphism (SNP) in KIF6, a member of the KIF9 family of kinesins, is associated with differential coronary event reduction from statin therapy in four randomized controlled trials; this SNP (rs20455) is also associated with the risk for coronary heart disease (CHD) in multiple prospective studies. We investigated whether other common SNPs in the KIF6 region were associated with event reduction from statin therapy. Of the 170 SNPs in the KIF6 region investigated in the Cholesterol and Recurrent Events trial (CARE), 28 were associated with differential event reduction from statin therapy ( P < 0.1 in Caucasians, adjusted for age and sex) and were further investigated in the Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction 22 (PROVE IT-TIMI22) and West of Scotland Coronary Prevention Study (WOSCOPS). These analyses revealed that two SNPs (rs9462535 and rs9471077), in addition to rs20455, were associated with event reduction from statin therapy ( P < 0.1 in each of the three studies). The relative risk reduction ranged from 37 to 50% ( P < 0.01) in carriers of the minor alleles of these SNPs and from −4 to 13% ( P > 0.4) in non-carriers. These three SNPs are in high linkage disequilibrium with one another ( r > 0.84). Functional studies of these variants may help to understand the role of KIF6 in the pathogenesis of CHD and differential response to statin therapy. [ABSTRACT FROM AUTHOR]

Published
2011
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36. Association of the Trp719Arg Polymorphism in Kinesin-Like Protein 6 With Myocardial Infarction and Coronary Heart Disease in 2 Prospective Trials: The CARE and WOSCOPS Trials

Author

Iakoubova, Olga A., Tong, Carmen H., Rowland, Charles M., Kirchgessner, Todd G., Young, Bradford A., Arellano, Andre R., Shiffman, Dov, Sabatine, Marc S., Campos, Hannia, Packard, Christopher J., Pfeffer, Marc A., White, Thomas J., Braunwald, Eugene, Shepherd, James, Devlin, James J., and Sacks, Frank M.

Subjects
*GENETIC polymorphisms, *CHROMOSOME polymorphism, *POPULATION genetics, *MYOCARDIAL infarction
Abstract

Objectives: We asked whether 35 genetic polymorphisms, previously found to be associated with cardiovascular disease, were associated with myocardial infarction (MI) in the CARE (Cholesterol and Recurrent Events) trial and with coronary heart disease (CHD) in the WOSCOPS (West of Scotland Coronary Prevention Study) trial and whether the risk associated with these polymorphisms could be reduced by pravastatin treatment. Background: Identification of genetic polymorphisms associated with CHD may improve assessment of CHD risk and understanding of disease pathophysiology. Methods: We tested the association between genotype and recurrent MI in the CARE study and between genotype and primary CHD in the WOSCOPS trial using regression models that adjusted for conventional risk factors: Cox proportional hazards models for the CARE study and conditional logistic regression models for a nested case-control study of the WOSCOPS trial. Results: We found that Trp719Arg (rs20455) in KIF6 was associated with coronary events. KIF6 encodes kinesin-like protein 6, a member of the molecular motor superfamily. In placebo-treated patients, carriers of the KIF6 719Arg allele (59.4% of the CARE trial cohort) had a hazard ratio of 1.50 (95% confidence interval [CI] 1.05 to 2.15) in the CARE trial and an odds ratio of 1.55 (95% CI 1.14 to 2.09) in the WOSCOPS trial. Among carriers, the absolute risk reduction by pravastatin was 4.89% (95% CI 1.81% to 7.97%) in the CARE trial and 5.49% (95% CI 3.52% to 7.46%) in the WOSCOPS trial. Conclusions: In both the CARE and the WOSCOPS trials, carriers of the KIF6 719Arg allele had an increased risk of coronary events, and pravastatin treatment substantially reduced that risk. [Copyright &y& Elsevier]

Published
2008
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37. KIF6 Trp719Arg polymorphism and the effect of statin therapy in elderly patients: results from the PROSPER study

Author

Iakoubova, Olga, Robertson, Michele, Tong, Carmen, Rowland, Charles, Catanese, Joseph, Blauw, Gerard, Jukema, J.W., Murphy, Michael, Devlin, James, Ford, Ian, and Shepherd, James

Abstract

Background Statin therapy has been found to substantially and significantly reduce coronary events in carriers of the KIF6 719Arg variant (rs20455) but not in noncarriers. We investigated whether, among the elderly, statin therapy also significantly reduced coronary events in carriers but not in noncarriers.Design and methods Among 5752 patients of the PROspective Study of Pravastatin in the Elderly at Risk (PROSPER) study, we assessed the effect of pravastatin, compared with placebo, on coronary events according to 719Arg carrier status using proportional hazards models.Results Since benefit from statin therapy in elderly patients has been primarily shown among those with prior vascular disease, we performed analyses in PROSPER patients with prior disease and found that pravastatin therapy significantly reduced events in 719Arg carriers [hazards ratio (HR): 0.66, 95% confidence interval (CI): 0.52–0.86] but not in noncarriers (HR: 0.94, 95% CI: 0.69–1.28), P= 0.09 for interaction between treatment and carrier status. Among those without prior disease, no significant benefit was observed in either carriers or noncarriers. Among those with prior vascular disease in the placebo arm, Trp719Arg heterozygotes were at significantly greater risk, compared with noncarriers (HR: 1.36, 95% CI: 1.03–1.81, P = 0.03); the HR of 719Arg carriers, compared with noncarriers, was 1.28 (95% CI: 0.98–1.69, P =0.07).Conclusion Elderly carriers of the KIF6 719Arg variant with prior vascular disease received significant benefit from pravastatin therapy; no benefit was observed in noncarriers with prior disease or in those without prior disease (carriers or noncarriers).

Published
2010
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40. Abstract 11923: Annual Screening and Digital Behavioral Counseling in a Workplace Setting Reduce 10-year Cardiovascular Risk

Author

Iakoubova, Olga, Lagier, Robert J, Fragala, Maren S, McNamara, Kelsey, Castro Sweet, Cynthia M, and Birse, Charles E

Abstract

Background:Behavioral counseling has been shown to improve modifiable cardiovascular risk factors. We asked whether the 10-year risk for ASCVD events could be reduced within the first year of a digital (on-line) counseling program.Methods:Individuals were included in the study if they (i) participated in an annual employer-sponsored wellness program with year-end biometric screening for 3 years (2016, 2017, and 2018), (ii) had metabolic syndrome at the end of 2017, and (iii) completed at least 9 lessons in a digital behavioral counseling program initiated at the beginning of 2018. Paired t-Tests and McNemar tests were used to assess changes in ASCVD risk before and after intervention.Results:The baseline characteristics of the 144 participants are shown in the table. Participants engaged in the counseling program for a mean of 8.9 months (SD, 1.3) and completed a mean of 24 lessons (SD, 12). In the year before participation in counseling (2016-2017), mean 10-year ASCVD risk increased from 3.5% to 4.4%, P=0.0002 for difference in the annual ASCVD risk change before and after the program. In the year after participation in the counseling program (2017-2018), mean 10-year ASCVD risk decreased from 4.4% to 3.6%, and the fraction of participants with 10-year ASCVD risk ?5% decreased from 30% to 22%: P=0.04. Metabolic syndrome was substantially reduced (p<0.0001), and CVD risk factors were shifted in a favorable direction (Table).Conclusions:In participants with metabolic syndrome digital behavioral counseling reduced 10-year ASCVD risk after the first year on the program.

Published
2019
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41. 1103-194 Identification of novel genetic markers associated with risk of myocardial infarction from a genomic scale scan of putative functional polmorphisms.

Author

Shiffman, Dov, Luke, May, Iakoubova, Olga, Aouizerat, Bradley E, Zellner, Christian A, Pullinger, Clive R, Drew, Denis W, Catanese, Joseph J, Leong, Diane U, Liu, Dongming, Louie, Judy Z, Lew, David, Tong, Carmen H, Ross, David A, McAllister, Linda B, Rowland, Charles M, Lau, Kit F, Devlin, James J, Malloy, Mary J, and Kane, John P

Subjects
*MYOCARDIAL infarction risk factors, *GENETIC markers, *GENETIC polymorphisms, *APOLIPOPROTEINS, *PEOPLE with diabetes
Published
2004
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42. Novel genetic markers for structural coronary artery disease, myocardial infarction, and familial combined hyperlipidemia: candidate and genome scans of functional SNPs

Author

Kane, John P., Aouizerat, Bradley E., Luke, May M., Shiffman, Dov, Iakoubova, Olga, Liu, Dongming, Rowland, Charlie M., Catanese, Joseph J., Leong, Diane U., Lau, Kit F., Louie, Judy Z., Tong, Carmen H., McAllister, Linda B., Dabby, Lisa F., Ports, Thomas A., Michaels, Andrew D., Zellner, Christian, Pullinger, Clive R., Malloy, Mary J., and Devlin, James J.

Subjects
*GENETIC markers, *BIOMARKERS, *CORONARY disease, *HEART diseases, *HYPERLIPIDEMIA
Abstract

Association studies were conducted on a large number of single nucleotide polymorphisms (SNPs) in pooled screening for association with angiographically determined coronary artery disease (CAD) and myocardial infarction (MI), followed by individual genotyping of those showing association. Forty-seven SNPs showed association with severity of CAD in a replication study applying individual genotyping in 1250 patients. Case control analysis of 340 patients with MI and 300 controls revealed significant associations of three novel genes: an immune cell receptor on chromosome 20p (p=0.02), a zinc finger protein on chromosome 3 (p=0.04), and an unknown gene on chromosome 3 (p=0.01). Associations of polymorphisms in three genes with the phenotype of familial combined hyperlipidemia (FCH), Apo A-V, PPAR alpha and microsomal triglyceride transfer protein (MTP) were established, supporting a metabolic model for the disorder based on misdirection of fatty acid metabolism. Congruence of SNP associations in non-alcoholic steatohepatitis suggests overlap of this syndrome with FCH. [Copyright &y& Elsevier]

Published
2004
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