https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23230 Wed 24 Aug 2016 17:36:49 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16959 -7), with independent replication in a second population (p = 0.0048, OR(95% CI) = 1.18(1.05–1.32); meta-analysis p = 2.6×10^-8). The nearby gene, MMP12, was significantly over expressed in carotid plaques compared to atherosclerosis-free control arteries (p = 1.2×10^-15; fold change = 335.6). Permutation analyses demonstrated improved significance for associations when accounting for age-at-onset in all four stroke phenotypes (p<0.001). Our results show that a covariate-informed design, by adjusting for age-at-onset of stroke, can detect variants not identified by conventional GWAS.]]> Wed 11 Apr 2018 17:21:31 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42205 P=0.06). There was no evidence of heterogeneity between MR estimates produced by different instruments (Q P=0.26). Comparable MR estimates were obtained with weighted median MR (odds ratio, 2.57; 95% CI, 1.05-6.25; P=0.04) and MR pleiotropy residual sum and outlier (odds ratio, 1.81; 95% CI, 0.95-3.46; P=0.08). Conclusions: We found no MR evidence of genetically determined risk of depression affecting ischemic stroke risk but did find consistent MR evidence suggestive of a possible effect on functional outcome after ischemic stroke. Given the widespread prevalence of depression-related morbidity, these findings could have implications for prognostication and personalized rehabilitation after stroke.]]> Thu 25 Aug 2022 11:38:19 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13951 Sat 24 Mar 2018 10:41:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20171 Sat 24 Mar 2018 07:51:43 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27245 g=0.96, SE=0.47, P=9x10⁻⁴) and profile scores (r_g=0.72; 95% confidence interval, 0.52–0.93). Between LAA and cardioembolism and SVD and cardioembolism, correlation was moderate using linear mixed models but not significantly different from zero for profile scoring. Joint meta-analysis of LAA and SVD identified strong association (P=1x10⁻⁷) for single nucleotide polymorphisms near the opioid receptor μ1 (OPRM1) gene. Conclusions: Our results suggest that LAA and SVD, which have been hitherto treated as genetically distinct, may share a substantial genetic component. Combined analyses of LAA and SVD may increase power to identify small-effect alleles influencing shared pathophysiological processes.]]> Sat 24 Mar 2018 07:29:11 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:4666 Sat 24 Mar 2018 07:19:33 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25211 Sat 24 Mar 2018 07:14:02 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22678 Sat 24 Mar 2018 07:12:09 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48737 Fri 31 Mar 2023 16:23:23 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42223 P=0.0007; odds ratio=0.89; 95% CI, 0.82–0.95 and SiGN/GISCOME: P=0.0036; odds ratio=0.94; 95% CI, 0.91–0.98). The association was independent of age, sex, stroke severity on admission, stroke subtype, and ancestry. On subgroup analysis, imbalance affecting ohnologs was associated with outcome (CADISP: odds ratio=0.88; 95% CI, 0.80–0.95 and SiGN/GISCOME: odds ratio=0.93; 95% CI, 0.89–0.98) whereas imbalance without ohnologs lacked such an association. Conclusions: Increased genetic imbalance was associated with poorer functional outcome after IS in both study populations. Subgroup analysis revealed that this association was driven by presence of ohnologs in the respective copy number variations, suggesting a causal role of the deleterious effects of genetic imbalance.]]> Fri 26 Aug 2022 09:34:08 AEST ]]>