https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53345 Wed 22 Nov 2023 10:19:25 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22648 Wed 22 May 2019 14:50:34 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:13672 Wed 11 Apr 2018 16:23:10 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:13671 Wed 11 Apr 2018 16:06:02 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:13673 Wed 11 Apr 2018 15:24:43 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24220 A and −174 G>C) correlate with MS susceptibility, but with varying results. In the present study, we analyzed these polymorphisms, together with an additional polymorphism (−572 G>C) in 279 healthy controls and 509 patients with MS. We found no significant differences between MS patients and healthy controls for the different −597 or −174 IL6 promoter alleles or genotypes. There was a slight reduction in the percentage of individuals with MS who carried a C allele at position −572, although this was not significant after correction for multiple comparisons. Interestingly, however, the −572 C allele showed a significant correlation with the MS severity score, suggesting a possible role in disease progression.]]> Wed 11 Apr 2018 15:18:27 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:28397 Wed 11 Apr 2018 15:14:13 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26643 Wed 11 Apr 2018 13:39:49 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:28923 Wed 11 Apr 2018 10:33:05 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:13692 Wed 11 Apr 2018 09:50:56 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:39516 Wed 10 Aug 2022 11:31:35 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:54378 Tue 20 Feb 2024 20:24:50 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:27384 Tue 13 Oct 2020 19:16:32 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:52120 Thu 28 Sep 2023 15:04:45 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46515 Thu 24 Nov 2022 15:50:23 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33303 Thu 04 Oct 2018 16:49:43 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:36736 Thu 02 Jul 2020 16:31:45 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:12845 T at 3p24.1 (odds ratio [OR], 1.17; p = 1.6 × 10⁻⁸) near EOMES, rs2150702^G in the second intron of MLANA on chromosome 9p24.1 (OR, 1.16; p = 3.3 × 10⁻⁸), and rs6718520^A in an intergenic region on chromosome 2p21, with THADA as the nearest flanking gene (OR, 1.17; p = 3.4 × 10⁻⁸). The 3 new loci do not have a strong cis effect on RNA expression in PBMCs. Ten other susceptibility loci had a suggestive p < 1 × 10⁻⁶, some of these loci have evidence of association in other inflammatory diseases (ie, IL12B, TAGAP, PLEK, and ZMIZ1). Interpretation: We have performed a meta-analysis of GWAS in MS that more than doubles the size of previous gene discovery efforts and highlights 3 novel MS susceptibility loci. These and additional loci with suggestive evidence of association are excellent candidates for further investigations to refine and validate their role in the genetic architecture of MS.]]> Sat 24 Mar 2018 08:17:22 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20798 Sat 24 Mar 2018 08:05:59 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17471 Sat 24 Mar 2018 08:04:07 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18887 Sat 24 Mar 2018 08:03:12 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18886 Sat 24 Mar 2018 08:03:11 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18888 Sat 24 Mar 2018 08:03:11 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:19533 95% of the identified indication bias. Slightly lower relapse incidence was found among patients treated with glatiramer acetate or subcutaneous interferon β-1a relative to intramuscular interferon β-1a and interferon β-1b (p≤0.001). No differences in 12-month confirmed progression of disability were observed. Conclusion: Small but statistically significant differences in relapse outcomes exist among the injectable immunomodulators. MSBase is sufficiently powered to identify these differences and reflects practice in tertiary MS centres. While the present study controlled indication, selection and attrition bias, centre-dependent variance in data quality was likely.]]> Sat 24 Mar 2018 08:02:06 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:19821 Sat 24 Mar 2018 07:56:56 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20620 Sat 24 Mar 2018 07:55:44 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20329 Sat 24 Mar 2018 07:55:11 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:19680 Sat 24 Mar 2018 07:53:39 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:28805 P < 10⁻¹²). However, the female-to-male ratio in patients with relapse-onset multiple sclerosis and zero relapses in any given year was double that of the patients with primary progressive multiple sclerosis. Patient age was a more important determinant of decline in relapse incidence than disease duration (P < 10⁻¹²). Females are predisposed to higher relapse activity than males. However, this difference does not explain the markedly lower female-to-male sex ratio in primary progressive multiple sclerosis. Decline in relapse activity over time is more closely related to patient age than disease duration.]]> Sat 24 Mar 2018 07:38:27 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30101 Sat 24 Mar 2018 07:37:59 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:29942 -23). A reciprocal relationship was seen for ambient ultraviolet radiation (UVR), with a significantly increasing AAO for patients with MS per each quartile increment of ambient UVR (p=1.56×10^-17). We found that the AAO of female patients was ~5 months earlier than male patients (p=0.002). AAO of progressive-onset patients with MS were ~9 years later than relapsing-onset patients (p=1.40×10^-265). Conclusions: An earlier AAO in higher latitude regions was found in this worldwide European-descent cohort and correlated inversely with variation in latitudinal UVR. These results suggest that environmental factors which act at the population level may significantly influence disease severity characteristics in genetically susceptible populations.]]> Sat 24 Mar 2018 07:31:01 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:25354 Sat 24 Mar 2018 07:24:42 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:23863 Sat 24 Mar 2018 07:12:10 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:36719 Mon 24 Aug 2020 10:45:35 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53246 Mon 20 Nov 2023 10:14:36 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46199 Mon 14 Nov 2022 11:22:52 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:25306 Mon 06 Mar 2023 17:55:37 AEDT ]]>