https://nova.newcastle.edu.au/vital/access/manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:40464 Wed 27 Jul 2022 13:10:26 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:40457 Wed 27 Jul 2022 11:14:03 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:45203  0.05). Multivariable gene-set association suggested that common variation enrichment within biologically constrained genes observed for schizophrenia also occurs across several psychiatric phenotypes. Pairwise meta-analysis of schizophrenia and each psychiatric phenotype was implemented and identified 330 significantly associated genes (PMeta < 2.7 × 10−6) that were only nominally associated with each disorder individually (P < 0.05). These analyses consolidate the overlap between the genomic architecture of schizophrenia and other psychiatric disorders, uncovering several candidate pleiotropic genes which warrant further investigation.]]> Wed 26 Oct 2022 14:40:02 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:45189 In situ hybridisation revealed that polyI:C offspring had: (1) SST mRNA reductions in the cingulate cortex and nucleus accumbens shell, regardless of MIA timing; (2) SSTR2 mRNA reductions in the cortex and striatum of GD19, but not GD10, MIA; (3) no alterations in cortical or striatal GAD1 mRNA of polyI:C offspring, but an expected reduction of PVALB mRNA in the infralimbic cortex, and; (4) no alterations in inhibitory markers in hippocampus. Maternal IL-6 response negatively correlated with adult offspring SST mRNA in cortex and striatum, but not hippocampus. These results show lasting inhibitory-related deficits in cortex and striatum in adult offspring from MIA. SST downregulation in specific cortical and striatal subregions, with additional deficits in somatostatin-related signalling through SSTR2, may contribute to some of the adult behavioural changes resulting from MIA and its timing.]]> Wed 26 Oct 2022 14:26:13 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:45103 Wed 26 Oct 2022 13:14:01 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:34987 Wed 24 Nov 2021 15:52:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:35669 Wed 24 Nov 2021 15:51:43 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:38769 Wed 20 Mar 2024 15:52:14 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:51035 Wed 16 Aug 2023 10:17:09 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:47091 Wed 14 Dec 2022 09:37:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:30417 Wed 11 Apr 2018 10:16:02 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:30677 p-values = 0.0326, FDR corrected) and an ROC analysis yielding an AUC of 0.87. Crucially, a GP regression revealed that MMN predicted global assessment of functioning (GAF) scores (correlation = 0.73, R² = 0.53, p = 0.0006).]]> Wed 10 Nov 2021 15:05:46 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:32814 Wed 09 Feb 2022 15:59:31 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:43092 C] within intron 2 of the zinc finger protein 804A gene (ZNF804A) is associated with schizophrenia at the genome-wide level, but its function in relation to the development of psychotic disorders, including its influence on brain morphology remains unclear. Methods: Using both univariate (voxel-based morphometry, VBM; cortical thickness) and multivariate (source-based morphometry, SBM) approaches, we examined the effects of variation of the rs1344706 polymorphism on grey matter integrity in 214 Caucasian schizophrenia cases and 94 Caucasian healthy individuals selected from the Australian Schizophrenia Research Bank. Results: Neither univariate nor multivariate analyses showed any associations between indices of grey matter and rs1344706 variation in schizophrenia or healthy participants. This was revealed in the context of the typical pattern of decreased grey matter integrity in schizophrenia compared to healthy individuals, including: (1) large grey matter volume reductions in the orbitofrontal and anterior cingulate cortices and the left fusiform/inferior temporal gyri; (2) decreased cortical thickness in the left inferior temporal and fusiform gyri, the left orbitofrontal gyrus, as well as in the right pars opercularis/precentral gyrus; and (3) decreased covariation of grey matter concentration in frontal and limbic brain regions emerging from the SBM analyses. Conclusions: Contrary to some – but not all – previous findings, this study of a large sample of schizophrenia cases and healthy controls reveals no evidence for association between grey matter alterations and variation in rs1344706 (ZNF804A). Differences in sample sizes and ethnicities may account for discrepant findings between the present and previous studies.]]> Wed 07 Jun 2023 14:36:02 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:28028 Wed 04 Sep 2019 09:48:07 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:34119 -4) with schizophrenia polygenic risk scores explaining up to 0.12% of the variance in ALS (P=8.4 × 10^-7). A modest increase in comorbidity of ALS and schizophrenia is expected given these findings (odds ratio 1.08-1.26) but this would require very large studies to observe epidemiologically. We identify five potential novel ALS-associated loci using conditional false discovery rate analysis. It is likely that shared neurobiological mechanisms between these two disorders will engender novel hypotheses in future preclinical and clinical studies.]]> Wed 04 Sep 2019 09:40:14 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:52173 Wed 04 Oct 2023 11:03:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:49052 Wed 03 May 2023 15:47:20 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:41435 Wed 03 Aug 2022 14:26:31 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:44959 Arx gene, critical to healthy neurodevelopment of PV interneurons, is reduced in the forebrain of MIA exposed mice. Finally, in a whole-genome sequenced patient cohort, we identified a novel missense mutation of ARX in a patient with schizophrenia and in the Psychiatric Genomics Consortium 2 cohort, a nominal association of proximal ARX SNPs with the disorder. This suggests MIA, as a risk factor for schizophrenia, may be influencing Arx expression to induce the GABAergic dysfunction seen in schizophrenia and that the ARX gene may play a role in the prenatal origins of schizophrenia pathophysiology.]]> Tue 25 Oct 2022 12:28:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:38872 1, whereas schizophrenia affects men with greater frequency and severity relative to women². All three illnesses have their strongest common genetic associations in the major histocompatibility complex (MHC) locus, an association that in SLE and Sjögren’s syndrome has long been thought to arise from alleles of the human leukocyte antigen (HLA) genes at that locus^3,4,5,6. Here we show that variation of the complement component 4 (C4) genes C4A and C4B, which are also at the MHC locus and have been linked to increased risk for schizophrenia⁷, generates 7-fold variation in risk for SLE and 16-fold variation in risk for Sjögren’s syndrome among individuals with common C4 genotypes, with C4A protecting more strongly than C4B in both illnesses. The same alleles that increase risk for schizophrenia greatly reduce risk for SLE and Sjögren’s syndrome. In all three illnesses, C4 alleles act more strongly in men than in women: common combinations of C4A and C4B generated 14-fold variation in risk for SLE, 31-fold variation in risk for Sjögren’s syndrome, and 1.7-fold variation in schizophrenia risk among men (versus 6-fold, 15-fold and 1.26-fold variation in risk among women, respectively). At a protein level, both C4 and its effector C3 were present at higher levels in cerebrospinal fluid and plasma^8,9 in men than in women among adults aged between 20 and 50 years, corresponding to the ages of differential disease vulnerability. Sex differences in complement protein levels may help to explain the more potent effects of C4 alleles in men, women’s greater risk of SLE and Sjögren’s syndrome and men’s greater vulnerability to schizophrenia. These results implicate the complement system as a source of sexual dimorphism in vulnerability to diverse illnesses.]]> Tue 22 Feb 2022 16:36:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:44746 Tue 21 Mar 2023 16:53:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:54330 Tue 20 Feb 2024 15:58:57 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:44630 Tue 18 Oct 2022 12:11:18 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:41878 Tue 16 Aug 2022 10:04:26 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:33797 Tue 15 Jan 2019 15:29:29 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:43160 Tue 13 Sep 2022 15:35:25 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:54261 Tue 13 Feb 2024 13:32:14 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:45935 Tue 08 Nov 2022 10:00:10 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:46890 Tue 06 Dec 2022 12:02:52 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:33669 Iba1, Gfap, IL1-β and TNF-α mRNA levels in the cingulate cortex (CC) in adult offspring exposed to maternal immune activation. Prenatal exposure to immune activation had a significant main effect on microglial IBA1-positive immunoreactive material (IBA1+IRM) in the corpus callosum; post-hoc analyses identified a significant increase in GD19 offspring, but not GD10. No change in was observed in the CC. In contrast, maternal immune activation had a significant main effect on GFAP+IRM in the CC at GD19 (not GD10); post-hoc analyses only identified a strong trend towards increased GFAP+IRM in the GD19 offspring, with no white matter changes. This suggests late gestation maternal immune activation causes subtle alterations to microglia and astrocytes in the adult offspring.]]> Tue 04 Jun 2019 13:36:19 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:34283 −15), which persisted after excluding loci implicated in previous studies (OR = 1.07, P = 1.7 × 10⁻⁶). CNV burden was enriched for genes associated with synaptic function (OR = 1.68, P = 2.8 × 10⁻¹¹) and neurobehavioral phenotypes in mouse (OR = 1.18, P = 7.3 × 10⁻⁵). Genome-wide significant evidence was obtained for eight loci, including 1q21.1, 2p16.3 (NRXN1), 3q29, 7q11.2, 15q13.3, distal 16p11.2, proximal 16p11.2 and 22q11.2. Suggestive support was found for eight additional candidate susceptibility and protective loci, which consisted predominantly of CNVs mediated by nonallelic homologous recombination.]]> Tue 03 Sep 2019 18:30:49 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:34909 Tue 03 Sep 2019 18:19:15 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:34980 Tue 03 Sep 2019 18:02:13 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:33388 Tue 03 Sep 2019 17:54:11 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:31502 Tue 02 Apr 2019 14:06:11 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:39146 Thu 30 Mar 2023 08:56:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:50043 Thu 29 Jun 2023 14:38:49 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:46136 Thu 29 Jun 2023 12:51:13 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:40876 Thu 28 Jul 2022 15:46:17 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:35402 Thu 27 Jan 2022 15:58:30 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:48621 Thu 23 Mar 2023 14:45:46 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:36040 Thu 22 Jun 2023 10:07:54 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:40024 Thu 21 Jul 2022 09:47:00 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:40979 Thu 21 Jul 2022 09:06:15 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:36530 Thu 17 Jun 2021 16:20:04 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:49926 Thu 15 Jun 2023 11:48:35 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:47202 Thu 15 Dec 2022 11:18:18 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:54811 Thu 14 Mar 2024 14:24:56 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:38640 Thu 14 Mar 2024 12:20:31 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:40564 Thu 14 Mar 2024 12:19:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:37069 Thu 13 Aug 2020 12:12:43 AEST ]]> 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:41990 Thu 10 Aug 2023 12:12:50 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:54644 Thu 07 Mar 2024 12:47:22 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:35546 Thu 03 Feb 2022 12:19:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:49523 Sat 20 May 2023 12:39:02 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:44131 Sat 08 Oct 2022 12:36:32 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:45764 Sat 05 Nov 2022 12:13:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:47780 Mon 30 Jan 2023 10:58:57 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:49693 Mon 29 May 2023 12:32:45 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:38937 SD = 2.6; out of 8-sessions). Seventeen participants (77%) completed at least half of the sessions, and nine participants (40%) completed all eight sessions. Participant satisfaction was high, with all participants followed up rating the quality of the service they received as 'good' or 'excellent'. When compared to the Control Condition, people in the Treatment Condition demonstrated greater treatment effects on smoking and leisure screen time. There was only a negligible effect on servings of fruit and vegetable. Conclusions: Results were promising regarding the feasibility of peer-workers delivering BHC. Good retention rates and high consumer satisfaction ratings in the Treatment Condition demonstrated that peer-workers were capable of delivering the intervention to the extent that consumers found it beneficial. The current results suggest that a sufficiently powered, peer delivered randomised controlled trial of BHC is warranted.]]> Mon 29 Jan 2024 18:03:28 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:38431 Mon 29 Jan 2024 18:00:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:34360 Mon 24 Feb 2020 11:21:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:32572 Mon 23 Sep 2019 12:39:53 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:32410 Mon 23 Sep 2019 12:12:49 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:32284 Mon 23 Sep 2019 10:58:58 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:33605 Mon 23 Sep 2019 10:26:50 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:42338 N = 29,125 cases and 34,836 controls), a robust polygenic signal was observed from gene sets based on TCF4, FMR1, upregulation from MIR137 and downregulation from CHD8. Additional analyses revealed a constant floor effect in the amount of variance explained, consistent with the omnigenic model. Thus, we report that putative core gene sets showed a significant effect above and beyond the floor effect that might be linked with the underlying omnigenic background. In addition, we demonstrate a method to quantify the contribution of specific gene sets within the omnigenic context.]]> Mon 22 Aug 2022 14:00:20 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:39125 p-value thresholds by summing methylation beta-values weighted by individual-CpG effect sizes from the meta-analysis of a previously published schizophrenia EWAS (comprising three separate cohorts with 675 [353 SZ and 322 HC] discovery cohort participants, 847 [414 SZ and 433 HC] replication cohort participants, and 96 monozygotic twin-pairs discordant for SZ). All SZ PMPSs were elevated in SZ participants relative to HCs, with the score calculated at a p-value threshold of 1 x 10⁻⁵ accounting for the greatest amount of variance. All PMPSs were elevated in SZ relative to BD and none of the PMPSs were increased in BD, or in a combined cohort of BD and SZ cases, relative to HCs. PMPSs were also not associated with positive or negative symptom severity. That this SZ-derived PMPSs was elevated in SZ, but not BD, suggests that epigenome-wide methylation patterns may represent distinct pathophysiology that is yet to be elucidated.]]> Mon 22 Apr 2024 08:42:29 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:46407 n = 299) and healthy controls (n = 131), we observed that the MIR137 4-repeats VNTR (VNTR₄) variant was enriched in a cognitive deficit subtype of schizophrenia and associated with altered brain morphology, including thicker left inferior temporal gyrus and deeper right postcentral sulcus. These findings suggest that the MIR137 VNTR₄ may impact neuroanatomical development that may, in turn, influence the expression of more severe cognitive symptoms in patients with schizophrenia.]]> Mon 21 Nov 2022 11:38:46 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:36121 Mon 20 Jul 2020 09:17:37 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:44569 Mon 17 Oct 2022 11:30:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:38229 Mon 16 Aug 2021 17:39:39 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:46272 Mon 14 Nov 2022 15:14:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:50977 Mon 14 Aug 2023 15:24:38 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:50972 Mon 14 Aug 2023 15:19:39 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:50953 Mon 14 Aug 2023 14:36:26 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:50935 Mon 14 Aug 2023 12:29:31 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:43035 Mon 12 Sep 2022 11:49:25 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:51593 Mon 11 Sep 2023 15:32:24 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:54759 Mon 11 Mar 2024 15:01:46 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:52269 Mon 09 Oct 2023 09:56:28 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:35822 Mon 09 Dec 2019 16:39:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:42814 Mon 05 Sep 2022 14:06:54 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:33142 Mon 03 Sep 2018 12:55:09 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:48305 Mon 01 May 2023 15:23:00 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:48732 Fri 31 Mar 2023 09:37:21 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:45466 n = 114 participants with completed cognitive outcomes at follow up were included in this analysis. Using the Cogstate Brief Battery, the following cognitive outcomes were assessed: psychomotor function, attention, visual learning and memory (visual and working). Subgroup analyses investigated whether baseline clinical parameters (baseline cognitive functioning, illness severity and duration, depressive symptoms) moderated the relationship between mangosteen pericarp extract intervention and change in cognitive outcomes. Results: There were no significant between-group changes in any cognitive outcomes assessed. Subgroup analysis based on baseline cognition and clinical characteristics did not reveal any significant between-group difference in change. Conclusions: Mangosteen pericarp extract did not affect cognitive outcomes in people with schizophrenia. Further investigation regarding optimal dosing strategies for mangosteen interventions and the testing of additional cognitive domains may be warranted.]]> Fri 28 Oct 2022 14:45:19 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:35646 Fri 27 Sep 2019 17:15:43 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:49672 Fri 26 May 2023 15:35:47 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:42186 n = 3,473) by performing identity-by-descent (IBD) mapping followed by exome sequencing of individuals identified as sharing risk haplotypes to search for rare risk variants in coding regions. We identified 45 rare haplotypes (>1 cM) that were significantly more common in cases than controls. By exome sequencing 105 haplotype carriers, we investigated these haplotypes for functional coding variants that could be tested for association in independent GWAS samples. We identified one rare missense variant in PCNT but did not find statistical support for an association with schizophrenia in a replication analysis. However, IBD mapping can prioritize both individual samples and genomic regions for follow-up analysis but genome rather than exome sequencing may be more effective at detecting risk variants on rare haplotypes.]]> Fri 26 Aug 2022 10:49:17 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:39019 Fri 22 Apr 2022 09:10:54 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:49494 Fri 19 May 2023 10:52:01 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:49352 Fri 12 May 2023 12:21:21 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:51559 Fri 08 Sep 2023 16:29:26 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:37045 Fri 07 Aug 2020 14:34:14 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:49142 Fri 05 May 2023 12:07:01 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:41596 Fri 05 Aug 2022 14:58:18 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:51364 Fri 01 Sep 2023 13:45:06 AEST ]]>