@article {8532,
	title = {{Omega-3 Fatty Acids and Genome-Wide Interaction Analyses Reveal DPP10-Pulmonary Function Association},
	journal = {Am J Respir Crit Care Med},
	volume = {199},
	year = {2019},
	month = {03},
	pages = {631{\textendash}642},
	abstract = {Omega-3 polyunsaturated fatty acids (n-3 PUFAs) have anti-inflammatory properties that could benefit adults with comprised pulmonary health.\ To investigate n-3 PUFA associations with spirometric measures of pulmonary function tests (PFTs) and determine underlying genetic susceptibility.\ Associations of n-3 PUFA biomarkers ({\^I}{\textpm}-linolenic acid, eicosapentaenoic acid, docosapentaenoic acid [DPA], and docosahexaenoic acid [DHA]) were evaluated with PFTs (FEV1, FVC, and FEV1/FVC) in meta-analyses across seven cohorts from the Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium (N = 16,134 of European or African ancestry). PFT-associated n-3 PUFAs were carried forward to genome-wide interaction analyses in the four largest cohorts (N = 11,962) and replicated in one cohort (N = 1,687). Cohort-specific results were combined using joint 2 degree-of-freedom (2df) meta-analyses of SNP associations and their interactions with n-3 PUFAs.\ DPA and DHA were positively associated with FEV1 and FVC (P < 0.025), with evidence for effect modification by smoking and by sex. Genome-wide analyses identified a novel association of rs11693320-an intronic DPP10 SNP-with FVC when incorporating an interaction with DHA, and the finding was replicated (P2df = 9.4 {\~A}{\textemdash} 10-9 across discovery and replication cohorts). The rs11693320-A allele (frequency, {\^a}{\textasciicircum}{\textonequarter}80\%) was associated with lower FVC (PSNP = 2.1 {\~A}{\textemdash} 10-9; {\^I}{\texttwosuperior}SNP = -161.0 ml), and the association was attenuated by higher DHA levels (PSNP{\~A}{\textemdash}DHA interaction = 2.1 {\~A}{\textemdash} 10-7; {\^I}{\texttwosuperior}SNP{\~A}{\textemdash}DHA interaction = 36.2 ml).\ We corroborated beneficial effects of n-3 PUFAs on pulmonary function. By modeling genome-wide n-3 PUFA interactions, we identified a novel DPP10 SNP association with FVC that was not detectable in much larger studies ignoring this interaction.},
	author = {Xu, J. and Gaddis, N. C. and Bartz, T. M. and Hou, R. and Manichaikul, A. W. and Pankratz, N. and Smith, A. V. and Sun, F. and Terzikhan, N. and Markunas, C. A. and Patchen, B. K. and Schu, M. and Beydoun, M. A. and Brusselle, G. G. and Eiriksdottir, G. and Zhou, X. and Wood, A. C. and Graff, M. and Harris, T. B. and Ikram, M. A. and Jacobs, D. R. and Launer, L. J. and Lemaitre, R. N. and O{\textquoteright}Connor, G. T. and Oelsner, E. C. and Psaty, B. M. and Vasan, R. S. and Rohde, R. R. and Rich, S. S. and Rotter, J. I. and Seshadri, S. and Smith, L. J. and Tiemeier, H. and Tsai, M. Y. and Uitterlinden, A. G. and Voruganti, V. S. and Xu, H. and Zilh?o, N. R. and Fornage, M. and Zillikens, M. C. and London, S. J. and Barr, R. G. and Dupuis, J. and Gharib, S. A. and Gudnason, V. and Lahousse, L. and North, K. E. and Steffen, L. M. and Cassano, P. A. and Hancock, D. B.}
}
@article {8917,
	title = {{Rare and low-frequency exonic variants and gene-by-smoking interactions in pulmonary function},
	journal = {Sci Rep},
	volume = {11},
	year = {2021},
	month = {09},
	pages = {19365},
	abstract = {. This study investigates the utility of assessing gene-by-smoking interactions and underscores their effects on potential pulmonary function.},
	author = {Yang, T. and Jackson, V. E. and Smith, A. V. and Chen, H. and Bartz, T. M. and Sitlani, C. M. and Psaty, B. M. and Gharib, S. A. and O{\textquoteright}Connor, G. T. and Dupuis, J. and Xu, J. and Lohman, K. and Liu, Y. and Kritchevsky, S. B. and Cassano, P. A. and Flexeder, C. and Gieger, C. and Karrasch, S. and Peters, A. and Schulz, H. and Harris, S. E. and Starr, J. M. and Deary, I. J. and Manichaikul, A. and Oelsner, E. C. and Barr, R. G. and Taylor, K. D. and Rich, S. S. and Bonten, T. N. and Mook-Kanamori, D. O. and Noordam, R. and Li-Gao, R. and Jarvelin, M. R. and Wielscher, M. and Terzikhan, N. and Lahousse, L. and Brusselle, G. and Weiss, S. and Ewert, R. and Gl{\"a}ser, S. and Homuth, G. and Shrine, N. and Hall, I. P. and Tobin, M. and London, S. J. and Wei, P. and Morrison, A. C.}
}
@article {9576,
	title = {{Genome-wide association study of preserved ratio impaired spirometry (PRISm)},
	journal = {Eur Respir J},
	volume = {63},
	year = {2024},
	month = {Jan},
	abstract = {{0.70. PRISm is associated with respiratory symptoms and comorbidities. Our objective was to discover novel genetic signals for PRISm and see if they provide insight into the pathogenesis of PRISm and associated comorbidities.\ We undertook a genome-wide association study (GWAS) of PRISm in UK Biobank participants (Stage 1), and selected single nucleotide polymorphisms (SNPs) reaching genome-wide significance for replication in 13 cohorts (Stage 2). A combined meta-analysis of Stage 1 and Stage 2 was done to determine top SNPs. We used cross-trait linkage disequilibrium score regression to estimate genome-wide genetic correlation between PRISm and pulmonary and extrapulmonary traits. Phenome-wide association studies of top SNPs were performed.\ =0.12},
	author = {Higbee, D. H. and Lirio, A. and Hamilton, F. and Granell, R. and Wyss, A. B. and London, S. J. and Bartz, T. M. and Gharib, S. A. and Cho, M. H. and Wan, E. and Silverman, E. and Crapo, J. D. and Lominchar, J. V. T. and Hansen, T. and Grarup, N. and Dantoft, T. and rhus, L. and Linneberg, A. and O{\textquoteright}Connor, G. T. and Dupuis, J. and Xu, H. and De Vries, M. M. and Hu, X. and Rich, S. S. and Barr, R. G. and Manichaikul, A. and Wijnant, S. R. A. and Brusselle, G. G. and Lahousse, L. and Li, X. and ndez Cordero, A. I. and Obeidat, M. and Sin, D. D. and Harris, S. E. and Redmond, P. and Taylor, A. M. and Cox, S. R. and Williams, A. T. and Shrine, N. and John, C. and Guyatt, A. L. and Hall, I. P. and Davey Smith, G. and Tobin, M. D. and Dodd, J. W.}
}
