https://ogma.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:37079 Wed 15 Dec 2021 16:07:28 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:15141 Wed 11 Apr 2018 13:54:12 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30590 Wed 11 Apr 2018 10:46:14 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34209 Wed 09 Feb 2022 15:53:11 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:38111 [BI] = 9.38 × 10^-25; p_[SSBI] = 5.23 × 10-14 for hypertension), smoking (p_[BI]= 4.4 × 10^-10; p_[SSBI] = 1.2 × 10^-4), diabetes (p_[BI] = 1.7 × 10 -8; p_[SSBI] = 2.8 × 10^-3), previous cardiovascular disease (p_[BI] = 1.0 × 10^-18; p_[SSBI] = 2.3 × 10^-7), stroke (p_[BI] = 3.9 × 10^-69; p_[SSBI] = 3.2 × 10^-24), and MRI-defined white matter hyperintensity burden (p_[BI]=1.43 × 10^-157; p_[SSBI] = 3.16 × 10^-106), but not with body mass index or cholesterol. GRS of BP traits were associated with BI and SSBI (p = 0.0022), without indication of directional pleiotropy. Conclusion: In this multiethnic GWAS meta-analysis, including over 20,000 population-based participants, we identified genetic risk loci for BI requiring validation once additional large datasets become available. High BP, including genetically determined, was the most significant modifiable, causal risk factor for BI.]]> Wed 04 Aug 2021 10:54:18 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30005 Mon 17 Oct 2022 12:06:14 AEDT ]]>