https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45256 1.4 million individuals, we show that FROH is significantly associated (p < 0.0005) with apparently deleterious changes in 32 out of 100 traits analysed. These changes are associated with runs of homozygosity (ROH), but not with common variant homozygosity, suggesting that genetic variants associated with inbreeding depression are predominantly rare. The effect on fertility is striking: FROH equivalent to the offspring of first cousins is associated with a 55% decrease [95% CI 44–66%] in the odds of having children. Finally, the effects of FROH are confirmed within full-sibling pairs, where the variation in FROH is independent of all environmental confounding.]]> Wed 26 Oct 2022 20:06:39 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50431 Tue 25 Jul 2023 19:01:27 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50411 Tue 25 Jul 2023 17:30:33 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53295 Tue 21 Nov 2023 11:54:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39718 270,000 independent mQTLs, of which 8.5% comprise long-range (trans) associations. Identified mQTL associations explain 15-17% of the additive genetic variance of DNAm. We show that the genetic architecture of DNAm levels is highly polygenic. Using shared genetic control between distal DNAm sites, we constructed networks, identifying 405 discrete genomic communities enriched for genomic annotations and complex traits. Shared genetic variants are associated with both DNAm levels and complex diseases, but only in a minority of cases do these associations reflect causal relationships from DNAm to trait or vice versa, indicating a more complex genotype-phenotype map than previously anticipated.]]> Tue 21 Mar 2023 17:20:57 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48599 Tue 04 Apr 2023 19:22:25 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41379 Tue 04 Apr 2023 19:08:51 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50952 overall) detected no genome-wide significant hits and showed low single nucleotide polymorphism (SNP) heritability (1.66%, 95% CI = 0.84-2.48%, n_effective = 132,260). Stratified analyses indicated rater-based heterogeneity in genetic effects, with self-reported internalizing symptoms showing the highest heritability (5.63%, 95% CI = 3.08%-8.18%). The contribution of additive genetic effects on internalizing symptoms appeared to be stable over age, with overlapping estimates of SNP heritability from early childhood to adolescence. Genetic correlations were observed with adult anxiety, depression, and the well-being spectrum (|r_g| > 0.70), as well as with insomnia, loneliness, attention-deficit/hyperactivity disorder, autism, and childhood aggression (range |r_g| = 0.42-0.60), whereas there were no robust associations with schizophrenia, bipolar disorder, obsessive-compulsive disorder, or anorexia nervosa. Conclusion: Genetic correlations indicate that childhood and adolescent internalizing symptoms share substantial genetic vulnerabilities with adult internalizing disorders and other childhood psychiatric traits, which could partially explain both the persistence of internalizing symptoms over time and the high comorbidity among childhood psychiatric traits. Reducing phenotypic heterogeneity in childhood samples will be key in paving the way to future GWAS success.]]> Mon 14 Aug 2023 14:36:09 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50392 0.49), but not with autism or the less common adult disorders (schizophrenia, bipolar disorder, or eating disorders) (rG < 0.01). Importantly, the total psychiatric problem score also showed at least a moderate genetic correlation with intelligence, educational attainment, wellbeing, smoking, and body fat (rG > 0.29). The results suggest that many common genetic variants are associated with childhood psychiatric symptoms and related phenotypes in general instead of with specific symptoms. Further research is needed to establish causality and pleiotropic mechanisms between related traits.]]> Mon 13 May 2024 11:16:33 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46603 Fri 25 Nov 2022 16:41:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41061 HHIP) gene and was previously associated with lung function and HHIP lung expression. We found HHIP expression was significantly different between the sexes (P=6.90x10⁻⁶), but we could not detect sex differential effects of rs7697189 on expression. Conclusions: We identified a novel genotype-by-sex interaction at a putative enhancer region upstream of the HHIP gene. Establishing the mechanism by which HHIP SNPs have different effects on lung function in males and females will be important for our understanding of lung health and diseases in both sexes.]]> Fri 22 Jul 2022 13:18:47 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53055 Fri 17 Nov 2023 11:47:02 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47296 Fri 13 Jan 2023 10:45:52 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39716 Fri 02 Jun 2023 09:38:38 AEST ]]>