https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47118 Wed 14 Dec 2022 12:25:36 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:50275 Wed 12 Jul 2023 15:07:08 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:36261 Tue 17 Mar 2020 17:05:31 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:42708 Thu 01 Sep 2022 10:02:33 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:6997 T-MTHFR, 1298A>C-MTHFR, 80G>A-RFC, 2756A>G-MS, 66A>G- MSR, 19bpDHFR and 1561C>T-GCPII), only 677C>T-MTHFR was a significant risk for hypertension: OR 1.89; 95% CI 1.07–3.32 (χ² p = 0.038). Additionally, hypertensive subjects had a significantly lower intake of dietary folate than normotensive individuals (p = 0.0221), although this did not markedly alter blood metabolite levels. Several significant linear associations between dietary folate and related blood metabolites were found in normotensive subjects (p<0.001 for Hcy, red cell and serum folate) and were as predicted on an a priori basis – generally weaker associations existed in hypertensive subjects (p<0.05 for serum folate). This was true for data examined collectively or by genotype. Multiple regression analysis for diastolic or systolic blood pressure showed significant interaction for gender and folate intake (p = 0.014 and 0.019, respectively). In both cases this interaction occurred only in females, with higher folate intake associated with decreased blood pressure. Regressing diastolic blood pressure and 677C>T-MTHFR genotype showed significance (males; p = 0.032) and borderline significance (all subjects). Conclusion: Dietary folate and 677C>T-MTHFR genotype may modify blood pressure.]]> Sat 24 Mar 2018 08:37:49 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:1162 Sat 24 Mar 2018 08:28:43 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:21751 Sat 24 Mar 2018 08:03:34 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20277 Sat 24 Mar 2018 07:59:53 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20873 Sat 24 Mar 2018 07:57:58 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:4945 Sat 24 Mar 2018 07:48:07 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:23953 Sat 24 Mar 2018 07:10:06 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32771 Mon 23 Jul 2018 15:44:21 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:42360 Mon 22 Aug 2022 14:01:23 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:51906 16-fold (from >125 μM to 15.6 μM) and greatly reduced cytotoxicity against mammalian cells (from ≤20 μM to ≥150 μM). These compounds showed significant disruption of preformed biofilms of S. aureus at micromolar concentrations.]]> Fri 22 Sep 2023 10:25:08 AEST ]]>