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300 results on '"Beaty, T. H."'

13. Genome-wide scan of bipolar disorder in 65 pedigrees: supportive evidence for linkage at 8q24, 18q22, 4q32, 2p12, and 13q12

Author

McInnis, M G, Lan, T-H, Willour, V L, McMahon, F J, Simpson, S G, Addington, A M, MacKinnon, D F, Potash, J B, Mahoney, A T, Chellis, J, Huo, Y, Swift-Scanlan, T, Chen, H, Koskela, R, Colin Stine, O, Jamison, K R, Holmans, P, Folstein, S E, Ranade, K, Friddle, C, Botstein, D, Marr, T, Beaty, T H, Zandi, P, and Raymond DePaulo, J

Published
2003
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18. TSLP polymorphisms are associated with asthma in a sex-specific fashion

Author

Hunninghake, G. M., Soto-Quirós, M. E., Avila, L., Kim, H. P., Lasky-Su, J., Rafaels, N., Ruczinski, I., Beaty, T. H., Mathias, R. A., Barnes, K. C., Wilk, J. B., OʼConnor, G. T., James Gauderman, W., Vora, H., Baurley, J. W., Gilliland, F., Liang, C., Sylvia, J. S., Klanderman, B. J., Sharma, S. S., Himes, B. E., Bossley, C. J., Israel, E., Raby, B. A., Bush, A., Choi, A. M., Weiss, S. T., and Celedón, J. C.

Published
2010
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23. New genetic signals for lung function highlight pathways and chronic obstructive pulmonary disease associations across multiple ancestries

Author

Shrine, N. (Nick), Guyatt, A. L. (Anna L.), Erzurumluoglu, A. M. (A. Mesut), Jackson, V. E. (Victoria E.), Hobbs, B. D. (Brian D.), Melbourne, C. A. (Carl A.), Batini, C. (Chiara), Fawcett, K. A. (Katherine A.), Song, K. (Kijoung), Sakornsakolpat, P. (Phuwanat), Li, X. (Xingnan), Boxall, R. (Ruth), Reeve, N. F. (Nicola F.), Obeidat, M. (Ma'en), Zhao, J. H. (Jing Hua), Wielscher, M. (Matthias), Weiss, S. (Stefan), Kentistou, K. A. (Katherine A.), Cook, J. P. (James P.), Sun, B. B. (Benjamin B.), Zhou, J. (Jian), Hui, J. (Jennie), Karrasch, S. (Stefan), Imboden, M. (Medea), Harris, S. E. (Sarah E.), Marten, J. (Jonathan), Enroth, S. (Stefan), Kerr, S. M. (Shona M.), Surakka, I. (Ida), Vitart, V. (Veronique), Lehtimäki, T. (Terho), Allen, R. J. (Richard J.), Bakke, P. S. (Per S.), Beaty, T. H. (Terri H.), Bleecker, E. R. (Eugene R.), Bosse, Y. (Yohan), Brandsma, C.-A. (Corry-Anke), Chen, Z. (Zhengming), Crapo, J. D. (James D.), Danesh, J. (John), DeMeo, D. L. (Dawn L.), Dudbridge, F. (Frank), Ewert, R. (Ralf), Gieger, C. (Christian), Gulsvik, A. (Amund), Hansell, A. L. (Anna L.), Hao, K. (Ke), Hoffman, J. D. (Joshua D.), Hokanson, J. E. (John E.), Homuth, G. (Georg), Joshi, P. K. (Peter K.), Joubert, P. (Philippe), Langenberg, C. (Claudia), Li, X. (Xuan), Li, L. (Liming), Lin, K. (Kuang), Lind, L. (Lars), Locantore, N. (Nicholas), Luan, J. (Jian'an), Mahajan, A. (Anubha), Maranville, J. C. (Joseph C.), Murray, A. (Alison), Nickle, D. C. (David C.), Packer, R. (Richard), Parker, M. M. (Margaret M.), Paynton, M. L. (Megan L.), Porteous, D. J. (David J.), Prokopenko, D. (Dmitry), Qiao, D. (Dandi), Rawal, R. (Rajesh), Runz, H. (Heiko), Sayers, I. (Ian), Sin, D. D. (Don D.), Smith, B. H. (Blair H.), Artigas, M. S. (Maria Soler), Sparrow, D. (David), Tal-Singer, R. (Ruth), Timmers, P. R. (Paul R. H. J.), Van den Berge, M. (Maarten), Whittaker, J. C. (John C.), Woodruff, P. G. (Prescott G.), Verges-Armstrong, L. M. (Laura M.), Troyanskaya, O. G. (Olga G.), Raitakari, O. T. (Olli T.), Kähönen, M. (Mika), Polasek, O. (Ozren), Gyllensten, U. (Ulf), Rudan, I. (Igor), Deary, I. J. (Ian J.), Probst-Hensch, N. M. (Nicole M.), Schulz, H. (Holger), James, A. L. (Alan L.), Wilson, J. F. (James F.), Stubbe, B. (Beate), Zeggini, E. (Eleftheria), Järvelin, M.-R. (Marjo-Riitta), Wareham, N. (Nick), Silverman, E. K. (Edwin K.), Hayward, C. (Caroline), Morris, A. P. (Andrew P.), Butterworth, A. S. (Adam S.), Scott, R. A. (Robert A.), Walters, R. G. (Robin G.), Meyers, D. A. (Deborah A.), Cho, M. H. (Michael H.), Strachan, D. P. (David P.), Hall, I. P. (Ian P.), Tobin, M. D. (Martin D.), Wain, L. V. (Louise, V), Shrine, N. (Nick), Guyatt, A. L. (Anna L.), Erzurumluoglu, A. M. (A. Mesut), Jackson, V. E. (Victoria E.), Hobbs, B. D. (Brian D.), Melbourne, C. A. (Carl A.), Batini, C. (Chiara), Fawcett, K. A. (Katherine A.), Song, K. (Kijoung), Sakornsakolpat, P. (Phuwanat), Li, X. (Xingnan), Boxall, R. (Ruth), Reeve, N. F. (Nicola F.), Obeidat, M. (Ma'en), Zhao, J. H. (Jing Hua), Wielscher, M. (Matthias), Weiss, S. (Stefan), Kentistou, K. A. (Katherine A.), Cook, J. P. (James P.), Sun, B. B. (Benjamin B.), Zhou, J. (Jian), Hui, J. (Jennie), Karrasch, S. (Stefan), Imboden, M. (Medea), Harris, S. E. (Sarah E.), Marten, J. (Jonathan), Enroth, S. (Stefan), Kerr, S. M. (Shona M.), Surakka, I. (Ida), Vitart, V. (Veronique), Lehtimäki, T. (Terho), Allen, R. J. (Richard J.), Bakke, P. S. (Per S.), Beaty, T. H. (Terri H.), Bleecker, E. R. (Eugene R.), Bosse, Y. (Yohan), Brandsma, C.-A. (Corry-Anke), Chen, Z. (Zhengming), Crapo, J. D. (James D.), Danesh, J. (John), DeMeo, D. L. (Dawn L.), Dudbridge, F. (Frank), Ewert, R. (Ralf), Gieger, C. (Christian), Gulsvik, A. (Amund), Hansell, A. L. (Anna L.), Hao, K. (Ke), Hoffman, J. D. (Joshua D.), Hokanson, J. E. (John E.), Homuth, G. (Georg), Joshi, P. K. (Peter K.), Joubert, P. (Philippe), Langenberg, C. (Claudia), Li, X. (Xuan), Li, L. (Liming), Lin, K. (Kuang), Lind, L. (Lars), Locantore, N. (Nicholas), Luan, J. (Jian'an), Mahajan, A. (Anubha), Maranville, J. C. (Joseph C.), Murray, A. (Alison), Nickle, D. C. (David C.), Packer, R. (Richard), Parker, M. M. (Margaret M.), Paynton, M. L. (Megan L.), Porteous, D. J. (David J.), Prokopenko, D. (Dmitry), Qiao, D. (Dandi), Rawal, R. (Rajesh), Runz, H. (Heiko), Sayers, I. (Ian), Sin, D. D. (Don D.), Smith, B. H. (Blair H.), Artigas, M. S. (Maria Soler), Sparrow, D. (David), Tal-Singer, R. (Ruth), Timmers, P. R. (Paul R. H. J.), Van den Berge, M. (Maarten), Whittaker, J. C. (John C.), Woodruff, P. G. (Prescott G.), Verges-Armstrong, L. M. (Laura M.), Troyanskaya, O. G. (Olga G.), Raitakari, O. T. (Olli T.), Kähönen, M. (Mika), Polasek, O. (Ozren), Gyllensten, U. (Ulf), Rudan, I. (Igor), Deary, I. J. (Ian J.), Probst-Hensch, N. M. (Nicole M.), Schulz, H. (Holger), James, A. L. (Alan L.), Wilson, J. F. (James F.), Stubbe, B. (Beate), Zeggini, E. (Eleftheria), Järvelin, M.-R. (Marjo-Riitta), Wareham, N. (Nick), Silverman, E. K. (Edwin K.), Hayward, C. (Caroline), Morris, A. P. (Andrew P.), Butterworth, A. S. (Adam S.), Scott, R. A. (Robert A.), Walters, R. G. (Robin G.), Meyers, D. A. (Deborah A.), Cho, M. H. (Michael H.), Strachan, D. P. (David P.), Hall, I. P. (Ian P.), Tobin, M. D. (Martin D.), and Wain, L. V. (Louise, V)

Abstract

Reduced lung function predicts mortality and is key to the diagnosis of chronic obstructive pulmonary disease (COPD). In a genome-wide association study in 400,102 individuals of European ancestry, we define 279 lung function signals, 139 of which are new. In combination, these variants strongly predict COPD in independent populations. Furthermore, the combined effect of these variants showed generalizability across smokers and never smokers, and across ancestral groups. We highlight biological pathways, known and potential drug targets for COPD and, in phenome-wide association studies, autoimmune-related and other pleiotropic effects of lung function–associated variants. This new genetic evidence has potential to improve future preventive and therapeutic strategies for COPD.

Published
2019

28. Gene-Gene Interactions among SPRYs for Nonsyndromic Cleft Lip/Palate.

Author

Zhou, R., Wang, M., Li, W., Wang, S., Zhou, Z., Li, J., Wu, T., Zhu, H., and Beaty, T. H.

Subjects
CLEFT lip, CLEFT palate, SINGLE nucleotide polymorphisms, X chromosome, BIOLOGICAL tags, COMPARATIVE studies, DISEASE susceptibility, GENES, GENETIC polymorphisms, RESEARCH methodology, MEDICAL cooperation, MEMBRANE proteins, PHOSPHOPROTEINS, RESEARCH, WHITE people, EVALUATION research, CASE-control method, SIGNAL peptides, SEQUENCE analysis
Abstract

Nonsyndromic cleft lip with or without cleft palate (NSCL/P) is a common birth defect with a complex genetic architecture. Gene-gene interactions have been increasingly regarded as contributing to the etiology of NSCL/P. A recent genome-wide association study revealed that a novel single-nucleotide polymorphism at SPRY1 in 4q28.1 showed a significant association with NSCL/P. In the current study, we explored the role of 3 SPRY genes in the etiology of NSCL/P by detecting gene-gene interactions: SPRY1, SPRY2, and SPRY4-with SPRY3 excluded due to its special location on the X chromosome. We selected markers in 3 SPRY genes to test for gene-gene interactions using 1,908 case-parent trios recruited from an international consortium established for a genome-wide association study of nonsyndromic oral clefts. As the trios came from populations with different ancestries, subgroup analyses were conducted among Europeans and Asians. Cordell's method based on conditional logistic regression models was applied to test for potential gene-gene interactions via the statistical package TRIO in R software. Gene-gene interaction analyses yielded 10 pairs of SNPs in Europeans and 6 pairs in Asians that achieved significance after Bonferroni correction. The significant interactions were confirmed in the 10,000-permutation tests (empirical P = 0.003 for the most significant interaction). The study identified gene-gene interactions among SPRY genes among 1,908 NSCL/P trios, which revealed the importance of potential gene-gene interactions for understanding the genetic architecture of NSCL/P. The evidence of gene-gene interactions in this study also provided clues for future biological studies to further investigate the mechanism of how SPRY genes participate in the development of NSCL/P. [ABSTRACT FROM AUTHOR]

Published
2019
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30. Evidence of interaction between genes in the folate/homocysteine metabolic pathway in controlling risk of non‐syndromic oral cleft.

Author

Wang, P., Wu, T., Schwender, H., Wang, H., Shi, B., Wang, Z. Q., Yuan, Y., Liu, D. J., Wang, M. Y., Li, J., Zhou, Z. B., Zhu, H. P., and Beaty, T. H.

Subjects
CLEFT lip, CLEFT palate, CLEFT lip -- Risk factors, FOLIC acid metabolism, ASIANS, GENE expression, METABOLISM, OXIDOREDUCTASES, TRANSFERASES, HOMOCYSTEINE, GENETIC markers, CASE-control method, BETAINE, PREVENTION, GENETICS, DISEASE risk factors
Abstract

Objective: Little consistent evidence is available for the association between the risk of non‐syndromic cleft lip with or without cleft palate (NSCL/P) and any of the individual genes in the folate/homocysteine metabolic pathway. We investigated the genes in the folate pathway to further clarify its potential influence on the risk of NSCL/P considering gene–gene (G×G) interaction. Subjects and methods: We selected markers in 18 genes from the pathway and applied Cordell's method to test for G×G interaction using 1,908 NSCL/P case–parent trios ascertained in an international consortium where a genomewide association study (GWAS) of oral clefts was conducted. Results: We found intriguing signals among Asian and European ancestry groups for G×G interaction between markers in betaine‐homocysteine methyltransferase gene (BHMT/BHMT2) and dimethylglycine dehydrogenase gene (DMGDH) attaining genomewide significance. In the pooled data, the top significant interaction was found between rs13158309 (BHMT) and rs10514154 (DMGDH, p = 1.45 × 10−12). Conclusions: Our study illustrated the importance of taking into account potential G×G interaction for genetic association analysis in NSCL/P, and this study suggested both BHMT/BHMT2 and DMGDH should be considered as candidate genes for NSCL/P in future studies. [ABSTRACT FROM AUTHOR]

Published
2018
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32. Genetic association between human chitinases and lung function in COPD

Author

Aminuddin, F., primary, Akhabir, L., additional, Stefanowicz, D., additional, Paré, P. D., additional, Connett, J. E., additional, Anthonisen, N. R., additional, Fahy, J. V., additional, Seibold, M. A., additional, Burchard, E. G., additional, Eng, C., additional, Gulsvik, A., additional, Bakke, P., additional, Cho, M. H., additional, Litonjua, A., additional, Lomas, D. A., additional, Anderson, W. H., additional, Beaty, T. H., additional, Crapo, J. D., additional, Silverman, E. K., additional, and Sandford, A. J., additional

Published
2011
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33. The PhenX Toolkit: Get the Most From Your Measures

Author

Hamilton, C. M., primary, Strader, L. C., additional, Pratt, J. G., additional, Maiese, D., additional, Hendershot, T., additional, Kwok, R. K., additional, Hammond, J. A., additional, Huggins, W., additional, Jackman, D., additional, Pan, H., additional, Nettles, D. S., additional, Beaty, T. H., additional, Farrer, L. A., additional, Kraft, P., additional, Marazita, M. L., additional, Ordovas, J. M., additional, Pato, C. N., additional, Spitz, M. R., additional, Wagener, D., additional, Williams, M., additional, Junkins, H. A., additional, Harlan, W. R., additional, Ramos, E. M., additional, and Haines, J., additional

Published
2011
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34. Hamilton et al. Respond to "Consolidating Data Harmonization"

Author

Hamilton, C. M., primary, Strader, L. C., additional, Pratt, J. G., additional, Maiese, D., additional, Hendershot, T., additional, Kwok, R. K., additional, Hammond, J. A., additional, Huggins, W., additional, Jackman, D., additional, Pan, H., additional, Nettles, D. S., additional, Beaty, T. H., additional, Farrer, L. A., additional, Kraft, P., additional, Marazita, M. L., additional, Ordovas, J. M., additional, Pato, C. N., additional, Spitz, M. R., additional, Wagener, D., additional, Williams, M., additional, Junkins, H. A., additional, Harlan, W. R., additional, Ramos, E. M., additional, and Haines, J., additional

Published
2011
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36. Leptin receptor polymorphisms and lung function decline in COPD

Author

Hansel, N. N., primary, Gao, L., additional, Rafaels, N. M., additional, Mathias, R. A., additional, Neptune, E. R., additional, Tankersley, C., additional, Grant, A. V., additional, Connett, J., additional, Beaty, T. H., additional, Wise, R. A., additional, and Barnes, K. C., additional

Published
2009
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37. Association Between IRF6 and Nonsyndromic Oral Clefts In 4 Populations

Author

Park, J W, primary, Hetmanski, J B, additional, Jabs, E W, additional, VanderKolk, C, additional, Wu-Chou, Y, additional, Chen, K T, additional, Chong, S S, additional, Jee, S H, additional, Mcintosh, I, additional, Fallin, M D, additional, Ingersoll, R, additional, Scott, A F, additional, and Beaty, T H, additional

Published
2006
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38. Variants in the gene encoding C3 are associated with asthma and related phenotypes among African Caribbean families

Author

Barnes, K C, primary, Grant, A V, additional, Baltadzhieva, D, additional, Zhang, S, additional, Berg, T, additional, Shao, L, additional, Zambelli-Weiner, A, additional, Anderson, W, additional, Nelsen, A, additional, Pillai, S, additional, Yarnall, D P, additional, Dienger, K, additional, Ingersoll, R G, additional, Scott, A F, additional, Fallin, M D, additional, Mathias, R A, additional, Beaty, T H, additional, Garcia, J G N, additional, and Wills-Karp, M, additional

Published
2005
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42. A genome-wide analysis of the response to inhaled ß2-agonists in chronic obstructive pulmonary disease

Author

Hardin, M, Cho, M H, McDonald, M-L, Wan, E, Lomas, D A, Coxson, H O, MacNee, W, Vestbo, J, Yates, J C, Agusti, A, Calverley, P M A, Celli, B, Crim, C, Rennard, S, Wouters, E, Bakke, P, Bhatt, S P, Kim, V, Ramsdell, J, Regan, E A, Make, B J, Hokanson, J E, Crapo, J D, Beaty, T H, and Hersh, C P

Abstract

Short-acting ß2-agonist bronchodilators are the most common medications used in treating chronic obstructive pulmonary disease (COPD). Genetic variants determining bronchodilator responsiveness (BDR) in COPD have not been identified. We performed a genome-wide association study (GWAS) of BDR in 5789 current or former smokers with COPD in one African-American and four white populations. BDR was defined as the quantitative spirometric response to inhaled ß2-agonists. We combined results in a meta-analysis. In the meta-analysis, single-nucleotide polymorphisms (SNPs) in the genes KCNK1(P=2.02 × 10-7) and KCNJ2(P=1.79 × 10-7) were the top associations with BDR. Among African Americans, SNPs in CDH13were significantly associated with BDR (P=5.1 × 10-9). A nominal association with CDH13was identified in a gene-based analysis in all subjects. We identified suggestive association with BDR among COPD subjects for variants near two potassium channel genes (KCNK1and KCNJ2). SNPs in CDH13were significantly associated with BDR in African Americans.

Published
2016
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