https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:41167 Wed 21 Jun 2023 15:55:59 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:25486 Wed 11 Apr 2018 14:00:41 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53499 Thu 30 Nov 2023 15:57:52 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32703 Thu 12 Jul 2018 11:51:28 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49876 3 mg/L), and depression. In both trials, TT treatment led to a large, significant improvement in HRQOL compared with usual care (Cohen's d = 1.19; P < .001). Receiving a statin for systemic inflammation and oral corticosteroid for eosinophilic airway inflammation was associated with the largest HRQOL improvements. Treatments for exercise intolerance, anxiety, and obesity were associated with smaller improvements in HRQOL. Conclusions: This study contributes to identifying clinically impactful TTs by showing that TTs across pulmonary, extrapulmonary, and behavioral domains were associated with HRQOL impairment and treatment response.]]> Thu 08 Jun 2023 15:21:50 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:31408 Sat 24 Mar 2018 08:45:15 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:38338 -4, hazard ratio = 1.41). Moreover, rs7298096AA is associated with a higher NINJ2 expression in blood (p = 7.0 x 10^-6), which was confirmed in vitro (p = 0.009). Finally, NINJ2 expression is downregulated by IFNβ treatment and related to TTFR. Conclusions: Rs7298096 could influence MS disease activity during IFNβ treatment by modulating NINJ2 expression in blood. The gene encodes for an adhesion molecule involved in inflammation and endothelial cells activation, supporting its role in MS.]]> Mon 30 Aug 2021 13:46:38 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:54025 Mon 29 Jan 2024 13:33:41 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32298 Mon 23 Sep 2019 11:17:56 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:50980 Mon 14 Aug 2023 15:24:38 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:55070 Mon 08 Apr 2024 13:27:57 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47896 Mon 06 Feb 2023 13:46:00 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:39991 P = 0.013]. The G allele was associated with higher plasma serum ET-1 [least squares mean 1.59 pg/mL vs. 1.28 pg/mL; 95% confidence interval (CI) 0.10–0.53; P  = 0.005]. Patients with rs9349379-G allele had over double the odds of CMD [odds ratio (OR) 2.33, 95% CI 1.10–4.96; P  = 0.027]. Multimodality non-invasive testing confirmed the G allele was associated with linked impairments in myocardial perfusion on stress cardiac magnetic resonance imaging at 1.5 T (N = 107; GG 56%, AG 43%, AA 31%, P  = 0.042) and exercise testing (N = 87; −3.0 units in Duke Exercise Treadmill Score; −5.8 to −0.1; P  = 0.045). Endothelin-1 related vascular mechanisms were assessed ex vivo using wire myography with endothelin A receptor (ET_A) antagonists including zibotentan. Subjects with rs9349379-G allele had preserved peripheral small vessel reactivity to ET-1 with high affinity of ET_A antagonists. Zibotentan reversed ET-1-induced vasoconstriction independently of G allele status. Conclusion: We identify a novel genetic risk locus for CMD. These findings implicate ET-1 dysregulation and support the possibility of precision medicine using genetics to target oral ET_A antagonist therapy in patients with microvascular angina. Trial registration: ClinicalTrials.gov: NCT03193294.]]> Fri 15 Jul 2022 10:14:01 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34026 80%) for relapse incidence during the first year and for disability outcomes, moderate for relapse incidence in Years 2–4 and for the change in the cumulative disease burden, and low for conversion to secondary progressive disease and treatment discontinuation. External validation showed similar results, demonstrating high external validity for disability and relapse outcomes, moderate external validity for cumulative disease burden and low external validity for conversion to secondary progressive disease and treatment discontinuation. We conclude that demographic, clinical and paraclinical information helps predict individual response to disease-modifying therapies at the time of their commencement.]]> Fri 01 Feb 2019 10:45:46 AEDT ]]>