@article {8527,
	title = {{Genome-Wide Association Transethnic Meta-Analyses Identifies Novel Associations Regulating Coagulation Factor VIII and von Willebrand Factor Plasma Levels},
	journal = {Circulation},
	volume = {139},
	year = {2019},
	month = {01},
	pages = {620{\textendash}635},
	abstract = {Factor VIII (FVIII) and its carrier protein von Willebrand factor (VWF) are associated with risk of arterial and venous thrombosis and with hemorrhagic disorders. We aimed to identify and functionally test novel genetic associations regulating plasma FVIII and VWF.\ We meta-analyzed genome-wide association results from 46 354 individuals of European, African, East Asian, and Hispanic ancestry. All studies performed linear regression analysis using an additive genetic model and associated {\^a}{\textperthousand}{\textasciicircum}35 million imputed variants with natural log-transformed phenotype levels. In vitro gene silencing in cultured endothelial cells was performed for candidate genes to provide additional evidence on association and function. Two-sample Mendelian randomization analyses were applied to test the causal role of FVIII and VWF plasma levels on the risk of arterial and venous thrombotic events.\ We identified 13 novel genome-wide significant ( P{\^a}{\textperthousand}¤2.5{\~A}{\textemdash}10-8) associations, 7 with FVIII levels ( FCHO2/TMEM171/TNPO1, HLA, SOX17/RP1, LINC00583/NFIB, RAB5C-KAT2A, RPL3/TAB1/SYNGR1, and ARSA) and 11 with VWF levels ( PDHB/PXK/KCTD6, SLC39A8, FCHO2/TMEM171/TNPO1, HLA, GIMAP7/GIMAP4, OR13C5/NIPSNAP, DAB2IP, C2CD4B, RAB5C-KAT2A, TAB1/SYNGR1, and ARSA), beyond 10 previously reported associations with these phenotypes. Functional validation provided further evidence of association for all loci on VWF except ARSA and DAB2IP. Mendelian randomization suggested causal effects of plasma FVIII activity levels on venous thrombosis and coronary artery disease risk and plasma VWF levels on ischemic stroke risk.\ The meta-analysis identified 13 novel genetic loci regulating FVIII and VWF plasma levels, 10 of which we validated functionally. We provide some evidence for a causal role of these proteins in thrombotic events.},
	author = {Sabater-Lleal, M. and Huffman, J. E. and de Vries, P. S. and Marten, J. and Mastrangelo, M. A. and Song, C. and Pankratz, N. and Ward-Caviness, C. K. and Yanek, L. R. and Trompet, S. and Delgado, G. E. and Guo, X. and Bartz, T. M. and Martinez-Perez, A. and Germain, M. and de Haan, H. G. and Ozel, A. B. and Polasek, O. and Smith, A. V. and Eicher, J. D. and Reiner, A. P. and Tang, W. and Davies, N. M. and Stott, D. J. and Rotter, J. I. and Tofler, G. H. and Boerwinkle, E. and de Maat, M. P. M. and Kleber, M. E. and Welsh, P. and Brody, J. A. and Chen, M. H. and Vaidya, D. and Soria, J. M. and Suchon, P. and van Hylckama Vlieg, A. and Desch, K. C. and Kolcic, I. and Joshi, P. K. and Launer, L. J. and Harris, T. B. and Campbell, H. and Rudan, I. and Becker, D. M. and Li, J. Z. and Rivadeneira, F. and Uitterlinden, A. G. and Hofman, A. and Franco, O. H. and Cushman, M. and Psaty, B. M. and Morange, P. E. and McKnight, B. and Chong, M. R. and Fernandez-Cadenas, I. and Rosand, J. and Lindgren, A. and Gudnason, V. and Wilson, J. F. and Hayward, C. and Ginsburg, D. and Fornage, M. and Rosendaal, F. R. and Souto, J. C. and Becker, L. C. and Jenny, N. S. and M?rz, W. and Jukema, J. W. and Dehghan, A. and Tr?gou?t, D. A. and Morrison, A. C. and Johnson, A. D. and O{\textquoteright}Donnell, C. J. and Strachan, D. P. and Lowenstein, C. J. and Smith, N. L.}
}
@article {8277,
	title = {{Sex Differences in the Association Between Pentraxin 3 and Cognitive Decline: The Cardiovascular Health Study},
	journal = {J. Gerontol. A Biol. Sci. Med. Sci.},
	year = {2019},
	month = {Dec},
	abstract = {The importance of systemic inflammation, measured by C-reactive protein, in cognitive decline has been demonstrated; however, the role of vascular inflammation is less understood. Pentraxin 3 (PTX3) is a novel marker of vascular inflammation.\ We followed adults 65 and older, free of cardiovascular disease (CVD) for up to 9 years (n = 1,547) in the Cardiovascular Health Study. We evaluated the relationship between PTX3 and change in cognitive function, measured using the Modified Mini-Mental State Examination (3MSE), and incident cognitive impairment (3MSE < 80). Mediation by CVD events, and effect modification by sex and apolipoprotein E {\'E}{\guilsinglright}4 allele (APOE4) were also examined.\ The average decline in 3MSE was 0.77 points per year. The association between PTX3 and change in 3MSE differed between women and men (p = .02). In the adjusted model, each standard deviation higher in PTX3 was associated with a 0.20 greater decline in 3MSE score per year in women over follow-up (95\% CI: -0. 37, -0.03; p = .02), compared to no change in men ({\^I}{\texttwosuperior} = 0.07; 95\% CI: -0.08, 0.22). CVD events had a minor effect on the associations. No effect modification by APOE4 was found, although we observed the association of PTX3 and cognitive impairment in women was attenuated and nonsignificant after adjustment for APOE4. There was a paradoxical protective association between PTX3 and reduced cognitive impairment in men, even after adjustment for APOE4.\ We found that vascular inflammation was significantly associated with cognitive decline in older women, but not men.},
	author = {Miller, L. M. and Jenny, N. S. and Rawlings, A. M. and Arnold, A. M. and Fitzpatrick, A. L. and Lopez, O. L. and Odden, M. C.}
}
