https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:42676 Wed 22 Mar 2023 14:34:07 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26719 -8). There were 693 and 219 independent loci with model-based replication rates ≥80% and ≥90%, respectively. Compared to analyses not incorporating relative enrichment scores, CM3 increased out-of-sample yield for SNPs that replicate at a given rate. This demonstrates that replication probabilities can be more accurately estimated using prior enrichment information with CM3.]]> Wed 11 Apr 2018 17:05:48 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:29013 P < 2 × 10⁻¹⁶). Further, the gene set analyses revealed several miRNAs regulating schizophrenia risk genes, with the strongest enrichment for targets of miR-9-5p (P = .0056 for enrichment among the top 1% most-associated single-nucleotide polymorphisms, corrected for multiple testing). It is further of note that MIR9-2 is located in a genomic region showing strong evidence for association with schizophrenia (P = 7.1 × 10⁻⁸). The second and third strongest gene set signals were seen for the targets of miR-485-5p and miR-137, respectively. Conclusions and Relevance: This study provides evidence for a role of miR-9-5p in the etiology of schizophrenia. Its implication is of particular interest as the functions of this neurodevelopmental miRNA tie in with established disease biology: it has a regulatory loop with the fragile X mental retardation homologue FXR1 and regulates dopamine D₂ receptor density.]]> Wed 11 Apr 2018 15:28:50 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:23292 Wed 11 Apr 2018 15:09:07 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26651 1.5 and FDR (false discovery rate) <0.05 for the comparisons of HCV versus co-infection, HIV versus co-infection, and HIV versus HCV were identified, respectively. Significantly altered pathways (FDR < 0.05), featured by those involved in immune system, signaling transduction, and cell cycle, were detected. Notably, the differential regulation of cytotoxicity pathway discriminated between HIV, HCV mono- and co-infection (up-regulated in the former versus the latter group: co-infection versus HIV or HCV, HIV versus HCV; FDR <0.001 ~ 0.019). Conversely, the cytokine-cytokine receptor interaction pathway was down-regulated in co-infection versus either HCV (FDR = 0.003) or HIV (FDR = 0.028). For the comparison of HIV versus HCV, the cell cycle (FDR = 0.016) and WNT signaling (FDR = 0.006) pathways were up- and down-regulated in HIV, respectively. Conclusions: Our study is the first to identify the differential regulation of cytotoxicity pathway discriminating between HIV, HCV mono- and co-infection, which may reflect the distinct patterns of virus-host cell interactions underlying disease progression. Further inspection of cytotoxicity pathway has pinned down to the expression of the KIR genes to be associated with specific patterns of particular virus-host interactions. Between HIV and HCV, the altered cell cycle and WNT signaling pathways may suggest the different impact of HIV and HCV on cell proliferation and differentiation.]]> Wed 11 Apr 2018 10:00:36 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:15118 Wed 11 Apr 2018 09:18:27 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:44746 Tue 21 Mar 2023 16:53:58 AEDT ]]> https://ogma.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://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47202 Thu 15 Dec 2022 11:18:18 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34615 Thu 04 Apr 2019 09:04:20 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20953 Sat 24 Mar 2018 08:06:07 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18520 Sat 24 Mar 2018 07:50:21 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:28049 Ginkgo biloba (EGb761), a potent antioxidant, may have neuroprotective effects. We hypothesized that there would be decreased BDNF expression in TD, but that treatment with EGb761 would increase BDNF expression and reduce TD manifestations in a rat model. Forty rats were treated with haloperidol (2 mg/kg/day via intraperitoneal injections) for 5 weeks. EGb761 (50 mg/kg/day) and vitamin E (20 mg/kg/day) were then administered by oral gavage for another 5 weeks, and we compared the effects of treatment with EGb761 or vitamin E on haloperidol-induced vacuous chewing movements (VCMs) and BDNF expression in four brain regions: prefrontal cortex (PFC), striatum (ST), substantia nigra (SNR), and globus pallidus (GP). Our results showed that haloperidol administration led to a progressive increase in VCMs, but both EGb761 and vitamin E significantly decreased VCMs. Haloperidol also decreased BDNF expression in all four brain regions, but both EGb761 and vitamin E administration significantly increased BDNF expression. Our results showed that both EGb761 and VE treatments exerted similar positive effects in a rat model of TD and increased BDNF expression levels in the four tested brain regions, suggesting that both EGb761 and vitamin E improve TD symptoms, possibly by enhancing BDNF in the brain and/or via their free radical-scavenging actions.]]> Sat 24 Mar 2018 07:41:01 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:29335 Sat 24 Mar 2018 07:34:19 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:29669 Sat 24 Mar 2018 07:32:21 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30079 Sat 24 Mar 2018 07:31:17 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26418 Sat 24 Mar 2018 07:27:57 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:28311 Sat 24 Mar 2018 07:27:06 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:23306 Sat 24 Mar 2018 07:16:19 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:23305 Sat 24 Mar 2018 07:16:19 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22607 2 = 3.48, p = 0.062 and X² = 0.036, p = 0.036, respectively). Cognitive test scores were significantly lower in patients than in controls on all scales (all p < 0.001) except for the visuospatial/constructional index (p > 0.05). There were significant genotype effects on delayed memory score (p = 0.013), the RBANS total score (p = 0.028) and language score (p = 0.034). Further analysis showed that the language score significantly differed according to the genotypic groups (A/A+T/A group versus T/T group) (p = 0.007) in patients but not in controls (p > 0.05), and the delayed memory score also significantly differed according to the genotypic groups (A/A+T/A group versus T/T group) (p = 0.021) in controls but not in patients (p > 0.05). Conclusions: This study found that the A allele of the TCF4 rs2958182 polymorphism was the risk allele of schizophrenia, and was associated with lower cognitive performance in language in schizophrenia and delayed memory in controls. In contrast, the T allele of this polymorphism was found to be the schizophrenia risk allele in another study in Han Chinese people.]]> Sat 24 Mar 2018 07:16:05 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22968 Sat 24 Mar 2018 07:15:20 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:25081 Sat 24 Mar 2018 07:15:04 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:23440 Sat 24 Mar 2018 07:12:55 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:44131 Sat 08 Oct 2022 12:36:32 AEDT ]]> https://ogma.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://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:42814 Mon 05 Sep 2022 14:06:54 AEST ]]>