https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:36509 Wed 15 Dec 2021 16:07:52 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20390 Wed 11 Apr 2018 16:32:40 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18827 Wed 11 Apr 2018 13:01:16 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:28417 Wed 11 Apr 2018 11:52:24 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:21442 x10^-8) for the combined phenotype of IS or CAD and 17 loci passed genome-wide significance for LAS or CAD. Because these loci had prior evidence for genome-wide significance for CAD, we specifically analyzed the respective signals for IS and LAS and found evidence for association at chr12q24/SH2B3 (P_IS=1.62x10^-7) and ABO (P_IS=2.6x10^-4), as well as at HDAC9 (P_LAS=2.32x10-12), 9p21 (P_LAS=3.70x10^-6), RAI1-PEMT-RASD1 (P_LAS=2.69x10^-5), EDNRA (P_LAS=7.29x10^-4), and CYP17A1-CNNM2-NT5C2 (P_LAS=4.9x10^-4). Conclusions-Our results demonstrate substantial overlap in the genetic risk of IS and particularly the LAS subtype with CAD.]]> Sat 24 Mar 2018 08:05:46 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:19050 2-fold increased risk of IS compared with subjects in the lowest quintile. Addition of the combined GRS to a simple model based on sex significantly improved the prediction of IS in the combined clinic-based samples but not in the population-based studies, and there was no significant improvement in net reclassification. Conclusions - A multilocus GRS based on common variants for established cardiovascular risk factors was significantly associated with IS both in clinic-based samples and in the general population. However, the improvement in clinical risk prediction was found to be small.]]> Sat 24 Mar 2018 08:05:17 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20633 Sat 24 Mar 2018 07:55:46 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:21233 P < 5 × 10⁻⁸) with FVC in or near EFEMP1, BMP6, MIR129-2–HSD17B12, PRDM11, WWOX and KCNJ2. Two loci previously associated with spirometric measures (GSTCD and PTCH1) were related to FVC. Newly implicated regions were followed up in samples from African-American, Korean, Chinese and Hispanic individuals. We detected transcripts for all six newly implicated genes in human lung tissue. The new loci may inform mechanisms involved in lung development and the pathogenesis of restrictive lung disease.]]> Sat 24 Mar 2018 07:53:01 AEDT ]]> https://ogma.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://ogma.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 ]]>