https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18827 Wed 11 Apr 2018 13:01:16 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28417 Wed 11 Apr 2018 11:52:24 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46991 Tue 04 Apr 2023 19:29:34 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25600 -28 for the LAS polygenic score in MO) and between MO and cardioembolic stroke (CE; p 2.7 x 10^-20 for the CE score in MO). Conclusions: Our findings indicate shared genetic susceptibility to migraine and IS, with a particularly strong overlap between MO and both LAS and CE pointing towards shared mechanisms. Our observations on MA are consistent with a limited role of common genetic variants in this subtype.]]> Sat 24 Mar 2018 07:28:03 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42483 p = 1.1 x 10⁻⁸). By contrast, the causal effect of LDL-C was much weaker for IS (OR 1.12, 95% CI 0.96−1.30, p = 0.14; p for heterogeneity = 2.6 x 10⁻³) and, in particular, for cardioembolic stroke (OR 1.06, 95% CI 0.84−1.33, p = 0.64; p for heterogeneity = 8.6 x 10⁻³) when compared with that for CHD. Conclusions: In contrast with the consistent effects of LDL-C-lowering therapies on IS and CHD, genetic variants that confer lifelong LDL-C differences show a weaker effect on IS than on CHD. The relevance of etiologically distinct IS subtypes may contribute to the differences observed.]]> Fri 26 Aug 2022 13:56:54 AEST ]]>