https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52282 Wed 28 Feb 2024 15:49:01 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45164 Wed 26 Oct 2022 14:11:30 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45108 Wed 26 Oct 2022 13:19:35 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32803 Wed 23 Feb 2022 16:05:34 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30809 Wed 23 Feb 2022 16:03:23 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24073 -11). SNP rs727479 was also among those most strongly associated with circulating E₂ concentrations in 2767 post-menopausal controls (P=7.4x10^-8). The observed endometrial cancer odds ratio per rs727479 A-allele (1.15, CI=1.11-1.21) is compatible with that predicted by the observed effect on E₂ concentrations (1.09, CI=1.03-1.21), consistent with the hypothesis that endometrial cancer risk is driven by E₂. From 28 candidate-causal SNPs, 12 co-located with three putative gene-regulatory elements and their risk alleles associated with higher CYP19A1 expression in bioinformatical analyses. For both phenotypes, the associations with rs727479 were stronger among women with a higher BMI (P_interaction=0.034 and 0.066 respectively), suggesting a biologically plausible gene-environment interaction.]]> Wed 19 Apr 2023 16:42:45 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37352 Wed 17 Nov 2021 16:20:11 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24759 -11). The results were replicated in an independent cohort, the Hunter Community Study (p < 0.002) (n = 313). Conditional and joint analysis (COJO) confirmed the association of the chromosomal 17 region with ApoH levels. The set of independent SNPs identified by COJO explained 23% of the variance. The relationships between the top SNPs and cardiovascular/lipid/cognition measures and diabetes were assessed in Sydney MAS, with suggestive results observed for diabetes and cognitive performance. However, replication of these results in the smaller OATS cohort was not found. This work provides impetus for future research to better understand the contribution of genetics to ApoH levels and its possible impacts on health.]]> Wed 15 Dec 2021 16:09:56 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30306 Wed 15 Dec 2021 16:09:28 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37079 Wed 15 Dec 2021 16:07:28 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25770 Wed 15 Dec 2021 16:07:05 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27984 Wed 15 Dec 2021 16:06:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27319 Wed 11 Apr 2018 15:35:52 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23807 Wed 11 Apr 2018 15:03:55 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26195 Wed 11 Apr 2018 15:00:42 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16813 Wed 11 Apr 2018 14:42:05 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27318 Wed 11 Apr 2018 14:21:46 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25809 Wed 11 Apr 2018 13:52:40 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24574 Wed 11 Apr 2018 13:27:00 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30108 Wed 11 Apr 2018 12:12:57 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16952 Wed 11 Apr 2018 11:49:10 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16953 Wed 11 Apr 2018 11:42:24 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21811 Wed 11 Apr 2018 11:28:19 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16786 Wed 11 Apr 2018 11:23:35 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16780 Wed 11 Apr 2018 09:14:25 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32807 Wed 10 Nov 2021 15:12:32 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34942 Wed 09 Feb 2022 15:56:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30265 p < 0.001) as well as compared to their own baseline (5.37 ± 0.20 mmol/L vs 5.8 ± 0.09, p < 0.001). Beta cell function, insulin sensitivity and insulin resistance all showed a statistically significant improvement as well. Conclusion: To our knowledge this is the first trial to show an improvement in glucose handling using HOMA parameters in participants with prediabetes. Larger randomized controlled trials are warranted to confirm these findings and to explore clinical endpoints.]]> Wed 06 Apr 2022 14:00:37 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38655 Wed 04 May 2022 15:19:55 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31550 I² = 83.15%). BQ performance was poor to fair with pooled sensitivity and specificity of 0.66 (95%CI: 0.45, 0.83; I² = 78.65%) and 0.62 (95%CI: 0.48, 0.75; I² = 81.55%), respectively. BQ performance was heterogeneous depending on type of reference test and pregnancy. Sensitivity increased if diagnosis was based on polysomnography (0.90), and respiratory disturbance index (0.90). However, sensitivity decreased if screening was performed in early pregnancy (≤20 weeks gestation: 0.47), and high-risk pregnancy (0.44). Performance of ESS was poor with pooled sensitivity and specificity of 0.44 (95%CI: 0.33, 0.56; I² = 32.8%) and 0.62 (95%CI: 0.48, 0.75; I² = 81.55%), respectively. In conclusion, BQ and ESS showed poor performance during pregnancy, hence a new OSA screening questionnaire is needed.]]> Wed 02 Oct 2019 10:27:36 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30415 Wed 02 Oct 2019 10:27:18 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47841 Wed 01 Feb 2023 15:49:00 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54542 Tue 27 Feb 2024 20:40:53 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47632 Tue 24 Jan 2023 14:23:43 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53302  0.9). We observed the strongest evidence to date for OPRM1: lead SNP rs9478500 (p = 2.56 × 10–9). Gene-based analyses identified novel genome-wide significant associations with PPP6C and FURIN. Variants within these loci appear to be pleiotropic for addiction and related traits.]]> Tue 21 Nov 2023 12:03:34 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46467 P < 5 × 10⁻⁸) were identified as instrumental variables, and assessed using genome-wide association study data from the Endometrial Cancer Association Consortium (12 906 cases and 108 979 controls) and the Global Lipids Genetic Consortium (n = 188 578). Mendelian randomization analyses found genetically raised LDL cholesterol levels to be associated with lower risks of endometrial cancer of all histologies combined, and of endometrioid and non-endometrioid subtypes. Conversely, higher genetically predicted HDL cholesterol levels were associated with increased risk of non-endometrioid endometrial cancer. After accounting for the potential confounding role of obesity (as measured by genetic variants associated with body mass index), the association between genetically predicted increased LDL cholesterol levels and lower endometrial cancer risk remained significant, especially for non-endometrioid endometrial cancer. There was no evidence to support a role for triglycerides in endometrial cancer development. Our study supports a role for LDL and HDL cholesterol in the development of non-endometrioid endometrial cancer. Further studies are required to understand the mechanisms underlying these findings.]]> Tue 19 Sep 2023 15:34:26 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48300 Tue 14 Mar 2023 14:13:43 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43136 Tue 13 Sep 2022 15:14:51 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47028 Tue 13 Dec 2022 15:55:21 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47053 Tue 13 Dec 2022 15:25:32 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20561 Tue 10 Oct 2023 08:38:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30059 P for heterogeneity ≥0.36), although associations were strongest in relation to the POAG subtypes with IOP <22 mmHg (MVRR, 1.93; 95% CI, 1.09–3.43) and early paracentral VF loss (MVRR, 2.27; 95% CI, 1.32–3.88). Conclusions: Although the number of natural teeth was not associated with risk of POAG, recent tooth loss was associated with an increased risk of POAG. Because these findings may be due to chance, they need confirmation in larger studies.]]> Tue 03 Oct 2017 13:26:04 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30120 20,000 kJ/day, or they reported being overweight or obese at S3. Logistic regressions with discrete time survival analysis investigated the association between breakfast cereal intake and incident obesity and were adjusted for: area of residency, income, smoking, physical activity, hypertension, dietary intakes and a discrete measure of time. There were 308 incident cases of obesity. Any breakfast cereal intake was not associated with incident obesity (Odds Ratio (OR): 0.92; p = 0.68). Oat-based cereal (OR: 0.71; p = 0.01), muesli (OR: 0.57; p = 0.00) and All-Bran (OR: 0.62; p = 0.01) intakes were associated with a significant reduction in obesity risk. Among this cohort, muesli on its own, or as part of oat-based cereals, and All-Bran, were associated with a reduction in obesity. This effect may be due to particular characteristics of these cereal eaters, but the relationship warrants further investigation.]]> Tue 02 Apr 2019 14:06:34 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30456 Tue 01 May 2018 09:15:25 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30598 Thu 28 Oct 2021 13:05:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36199 Thu 27 Feb 2020 13:40:32 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34931 20,000 kJ. Logistic regression with discrete time survival analyses investigated the association between breakfast cereal intake and incident diabetes. Models were adjusted for income, BMI, smoking, physical activity, education, and dietary intakes and included a measure of time. There were 637 incident cases of diabetes. Breakfast cereal intake per se was not associated with incident diabetes (OR: 1.00; P =.98). Muesli consumption on its own (OR: 0.74; P =.00) or as a part of oats-based cereal (OR: 0.84; P =.047) was significantly associated with a decrease in the odds of developing diabetes. No other breakfast cereals were significantly associated with diabetes risk. Among mid-aged Australian women, muesli consumption was associated with a reduction in diabetes risk. This effect may be due to a particular profile of muesli eaters, but the relationship warrants further investigation.]]> Thu 24 Mar 2022 11:32:43 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26111 Thu 21 Oct 2021 12:51:05 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35094 Thu 20 Jun 2019 15:56:20 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38572 Thu 18 Nov 2021 12:07:16 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42115 Thu 18 Aug 2022 14:21:19 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25845 Thu 17 Mar 2022 14:40:27 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25914 Thu 17 Mar 2022 14:37:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34724 Thu 17 Feb 2022 09:27:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55127 Thu 11 Apr 2024 11:14:46 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36636 Thu 09 Dec 2021 11:03:23 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30531 Thu 09 Dec 2021 11:03:19 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46986 Thu 06 Jul 2023 15:13:05 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46812 n = 44 articles) and few studies comparing to the reference standard (n = 10 articles) of a diagnostic interview. This review shows that a variety of tools have been used to screen and identify disordered eating behaviours and eating disorders in people with T1D. Future research including comparison to a gold standard diagnostic interview is warranted to further evaluate the validity and reliability of available tools.]]> Thu 01 Dec 2022 10:32:13 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20858 Sat 24 Mar 2018 08:02:51 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18764 Sat 24 Mar 2018 08:02:46 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19446 Sat 24 Mar 2018 08:02:17 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19672 Sat 24 Mar 2018 08:01:12 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16922 Sat 24 Mar 2018 08:00:31 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20501 Sat 24 Mar 2018 07:59:03 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20622 Sat 24 Mar 2018 07:55:47 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19321 Sat 24 Mar 2018 07:51:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21021 N = 2088) and the Sydney Memory and Ageing Study (Sydney MAS, N = 541). Genotyping was undertaken using Affymetrix microarrays with imputation to HapMap2. Analyses were performed using linear regression. No genome-wide significant results were observed in HCS nor were any of the top signals replicated in Sydney MAS. Gene-based analyses in HCS identified two significant genes (ZNF295, C2CD2), but these results were not replicated in Sydney MAS. One out of eight SNPs previously associated with GS, rs550942, located near the CNTF gene, was significantly associated with GS (p = 0.005) in the HCS cohort only. Study differences may explain the lack of consistent results between the studies, including the smaller sample size of the Sydney MAS cohort. Our modest sample size also had limited power to identify variants of small effect. Our results suggest that similar to various other complex traits, many genetic variants of small effect size may influence GS. Future GWAS using larger samples and consistent measures may prove more fruitful at identifying genetic contributors for GS in middle-aged to older adults.]]> Sat 24 Mar 2018 07:50:32 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26880 -8). Limitations, Reasons for Caution: The meta-analysis for moderate-to-severe endometriosis included results of moderate-to-severe endometriosis cases from our European data sets and all endometriosis cases from the Japanese data sets, as disease stage information was not available for endometriosis cases in the Japanese data sets. Wider Implications of the Findings: SNP rs6542095 is located ~2.3 kb downstream of the IL1A gene and ~6.9 kb upstream of cytoskeleton-associated protein 2-like (CKAP2L) gene. The IL1A gene encodes the IL1a protein, a member of the interleukin 1 cytokine family which is involved in various immune responses and inflammatory processes. These results provide important replication in an independent Japanese sample and, for the first time, association of the IL1A locus in endometriosis patients of European ancestry. SNPs within the IL1A locus may regulate other genes, but if IL1A is the target, our results provide supporting evidence for a link between inflammatory responses and the pathogenesis of endometriosis. Study Funding/Competing Interest(s): The research was funded by grants from the Australian National Health and Medical Research Council and Wellcome Trust. None of the authors has competing interests for the study.]]> Sat 24 Mar 2018 07:41:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28053 Sat 24 Mar 2018 07:41:03 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26799 Sat 24 Mar 2018 07:36:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25826 PubMed and SCOPUS up to September 2015. Eligibility Criteria: RCTs comparing LIA with placebo or no infiltration after primary TKA in terms of pain score and opioid consumption at 24 and 48 h, mobilisation, LOS and complications were included. Results: In total 38 RCTs were included. LIA groups had lower pain scores, opioid consumption and postoperative nausea and vomiting, higher range of motion at 24 h and shorter LOS than no injection or placebo. After subgroup analysis, intraoperative peri-articular but not intra-articular injection had lower pain score at 24 h than no injection or placebo with the pooled mean difference of pain score at rest of -0.89 [95% CI (-1.40 to -0.38); I²=92.0%]. Continuing with postoperative injection or infusion reduced 24-h pain score with the pooled mean difference at rest of -1.50 [95% CI (-1.92 to -1.08); I²=60.5%]. There was no additional benefit in terms of pain relief during activity, opioid consumption, range of movement or LOS when LIA was used as an adjunct to regional anaesthesia. Four out of 735 patients receiving LIA reported deep knee infection, three of whom had had postoperative catheter placement. Conclusion: LIA is effective for acute pain management after TKA. Intraoperative peri-articular but not intra-articular injection may be helpful in pain control up to 24 h. The use of postoperative intra-articular catheter placement is still inconclusive. The benefit of LIA as an adjunctive treatment to regional anaesthesia was not demonstrated.]]> Sat 24 Mar 2018 07:34:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27149 -5): rs9478495, rs3778150, rs9384169, and rs562859. Rs3778150, located in OPRM1 intron 1, was significantly replicated (p = 6.3 x 10^-5). Meta-analysis across all case-control cohorts resulted in p = 4.3 x 10^-8: the rs3778150-C allele (frequency = 16%-19%) being associated with increased heroin addiction risk. Importantly, the functional SNP allele rs1799971-A was associated with heroin addiction only in the presence of rs3778150-C (p = 1.48 x 10^-6 for rs1799971-A/rs3778150-C and p = .79 for rs1799971-A/rs3778150-T haplotypes). Lastly, replication was observed for six other intron 1 SNPs that had prior suggestive associations with heroin addiction (smallest p = 2.7 x 10^-8 for rs3823010). Conclusions: Our findings show that common OPRM1 intron 1 SNPs have replicable associations with heroin addiction. The haplotype structure of rs3778150 and nearby SNPs may underlie the inconsistent associations between rs1799971 and heroin addiction.]]> Sat 24 Mar 2018 07:32:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28420 G-monomethyl-L-arginine (MMA), N^G,. N^G-dimethyl-L-arginine (ADMA) and N^G,. N^G'-dimethyl-L-arginine (SDMA), all of which have the capacity to alter NOS activity. Simultaneous assessment of these analytes, when assessing the impact of arginine metabolism in human disease states, is desirable. Methods: Analytes (ARG, ADMA, SDMA, MMA, HMA, CIT and ORN) were isolated from human plasma by solvent extraction, evaporated and reconstituted. Ultra-performance liquid chromatography (UPLC) was performed on a 150mm×2.1mm T3 HSS column using a gradient mobile phase comprising ammonium formate (10mM, pH3.8) in methanol (1% to 63%). Analytes were detected by time-of-flight mass spectrometry (Q-ToF-MS) in positive ion mode with electrospray ionisation (ESI+). Data were collected using MS^E. Results: Solvent extraction provided high recovery (>95%). UPLC-QToF-MS^E facilitated the separation and quantification of the 7 analytes in an analysis time of 6min. The approach has high sensitivity; LOQ range from 0.005µM (NMMA) to 0.25µM (ARG and ORN), and good precision; intra- and inter-day %RSD are <6% for all analytes. Conclusions: This approach provides the capacity to quantify 7 key compounds involved in ARG metabolism in a small sample volume, with a short total analysis time. These characteristics make this approach ideal for undertaking a comprehensive characterisation of this pathway in large data sets (e.g. population studies).]]> Sat 24 Mar 2018 07:29:06 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27532 Sat 24 Mar 2018 07:28:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25923 Sat 24 Mar 2018 07:27:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26944 0.05), but cases presented with an excess of rare germline deletions overlapping likely functional genomic regions including genes (P = 8 x 10^-10), CpG islands (P = 1 x 10^-7) and sno/miRNAs regions (P = 3 x 10^-9). On average, at least one additional gene and two additional CpG islands were disrupted by rare deletions in cases compared to controls. The most pronounced difference was that over 30 sno/miRNAs were disrupted by rare deletions in cases for every single disruption event in controls. A total of 13 DNA repair genes were disrupted by rare deletions in 19/1,209 cases (1.6 %) compared to one gene in 1/528 controls (0.2 %; P = 0.007), and this increased DNA repair gene loss in cases persisted after excluding five individuals carrying CNVs disrupting mismatch repair genes MLH1, MSH2 and MSH6 (P = 0.03). There were 34 miRNA regions deleted in at least one case but not in controls, the most frequent of which encompassed hsa-mir-661 and hsa-mir-203. Our study implicates rare germline deletions of functional and regulatory regions as possible mechanisms conferring endometrial cancer risk, and has identified specific regulatory elements as candidates for further investigation.]]> Sat 24 Mar 2018 07:27:02 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24437 Sat 24 Mar 2018 07:17:20 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47783 Mon 30 Jan 2023 14:03:27 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38396 Mon 29 Jan 2024 17:47:06 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39523 Mon 25 Jul 2022 15:19:59 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41100 Mon 25 Jul 2022 10:38:22 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32805 Mon 23 Sep 2019 10:39:48 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50306 Mon 17 Jul 2023 12:15:14 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38224 Mon 16 Aug 2021 15:26:47 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50955 Mon 14 Aug 2023 14:36:36 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46959 Mon 12 Dec 2022 11:04:28 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48810 Mon 10 Apr 2023 10:28:37 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42827 Mon 05 Sep 2022 11:56:26 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35710 4.5 but <20.0MJ/d). Linear regression models showed statistically significant associations between dietary intake of total n-6 fatty acids and improved cognitive performance measured by the ARCs (RC= 0.0043; P=0.0004; R²= 0.0084). Quartiles of n-6 fatty acid intakes where the lowest quartile of n-6 fatty acid intake (179.8-1150.3mg) and those in the highest quartile (2315.0-7449.4mg) had a total ARCs score 10.6 units greater (RC= 10.60466; P= 0.006; R²= 0.0081). Furthermore, when n-6 fatty acid intake was tested against each of the ARCs domains, statistically significant associations were observed for the Fluency (RC=0.0011432; P= 0.007; R²=0.0057), Visual (RC=0.0009889;P=0.034;R²=0.0050), Language (RC=0.0010651; P=0.047;R²=0.0068) and Attention (RC=0.0011605; P=0.017; R²=0.0099) domains, yet there was no association with Memory (RC= -0.000064; P= 0.889; R²= 0.0083). No statistically significant associations between any other fatty acids and ARCS, nor any fatty acids and MMSE were detected. A higher intake of total n-6 fatty acid, but no other types of fatty acids, was associated with better cognitive performance among a representative sample of older Australian adults.]]> Fri 25 Oct 2019 15:40:12 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40130 n = 20, I² = 90.3%) and obesity (RR = 1.58, CI: 1.34–1.85, n = 21, I² = 92.2) compared with a reference group with metabolically healthy normal weight. Cardiovascular disease risk was similar irrespective of the number of risk factors used to define metabolically healthy and the risk remained in the group with no metabolic risk factors. Cardiovascular disease risk is increased in populations with overweight and obesity classified as metabolically healthy even when there were no metabolic risk factors.]]> Fri 22 Jul 2022 13:48:22 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32802 Fri 22 Apr 2022 10:24:54 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:40026 2=0%), US$3857.34 (95% CI US$−7293.93 to US$15 008.61, I²=45.9%), US$37 577.74 (95% CI US$−649.02 to US$75 804.50, I²=92.4%) and US$14 062.42 (95% CI US$8168.69 to US$19 956.15, I²=86.4%), respectively. GLP1s were statistically significantly cost-effective compared with insulins, but not compared with DPP4i, sulfonylureas, and TZDs. Among GLP1s, liraglutide was more cost-effective compared with lixisenatide, but not compared with exenatide, with corresponding pooled INBs of US$4555.09 (95% CI US$3992.60 to US$5117.59, I²=0) and US$728.46 (95% CI US$−1436.14 to US$2893.07, I²=0), respectively. Conclusion: GLP1 agonists are a cost-effective choice compared with insulins, but not compared with DPP4i, sulfonylureas and TZDs. PROSPERO registration number: CRD42018105193.]]> Fri 15 Jul 2022 10:11:12 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41765 Fri 12 Aug 2022 11:49:26 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51506 Fri 08 Sep 2023 11:57:56 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32492 Fri 08 Jun 2018 14:22:16 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24983 Fri 03 Dec 2021 10:35:04 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34723 Fri 03 Dec 2021 10:32:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31991 1 year (RAAS2). An augmented inverse-probability weighting (AIPW) method was used to estimate potential-outcome mean (POM) and average treatment-effect (ATE). Multi-logit and Poisson regressions were used for treatment and outcome models, respectively. Analyses were stratified by ESRD, death before/after ESRD for diabetic and non-diabetic groups. STATA 14.0 was used for statistical analyses. Results: Among 15,032 diabetic patients, 2346 (15.6%), 2351 (18.5%), and 1607 (68.5%) developed ESRD, died before ESRD, and died after ESRD, respectively. Only RAAS2 effect was significant on ESRD, death before and after ESRD. The ESRD rates were 12.9%, versus 20.0% for RAAS2 and non-RAAS, respectively, resulted in significant risk differences (RD) of -7.2% (95% CI: -8.8%, -5.5%), and a numbers needed-to-treat (NNT) of 14. Death rates before ESRD for these corresponding groups were 14.4% (12.9%, 15.9%) and 19.6% (18.7%, 20.4%) with a NNT of 19. Death rates after ESRD in RAAS2 was lower than non-RASS group (i.e., 62.8% (55.5%, 68.9%) versus 68.1% (65.9%, 70.4%)) but this was not significant. RAAS2 effects on ESRD and death before ESRD were persistently significant in non-diabetic patients (n = 17,074) but not for death after ESRD with the NNT of about 15 and 16 respectively. Conclusions: Receiving RAAS blockade for 1 year or longer could prevent both CKD progression to ESRD and premature mortality.]]> Fri 01 Apr 2022 09:26:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31134 Fri 01 Apr 2022 09:21:14 AEDT ]]>