http://researchonline.federation.edu.au/vital/access/manager/Index ${session.getAttribute("locale")} 5 Uncovering genetic mechanisms of kidney aging through transcriptomics, genomics, and epigenomics http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:13808 Wed 07 Apr 2021 14:01:55 AEST ]]> Signatures of miR-181a on the renal transcriptome and blood pressure http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:10772 Wed 07 Apr 2021 13:56:08 AEST ]]> Renal Mechanisms of Association between Fibroblast Growth Factor 1 and Blood Pressure http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:10534 Wed 07 Apr 2021 13:55:52 AEST ]]> Runs of Homozygosity : Association with Coronary Artery Disease and Gene Expression in Monocytes and Macrophages http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:10162 Wed 07 Apr 2021 13:55:29 AEST ]]> Coronary artery disease predisposing haplogroup I of the Y chromosome, aggression and sex steroids - Genetic association analysis http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:9603 1000 young apparently healthy white men from the general population. Each Y chromosome was classified into one of 13 most common European lineages. Androgens (DHEA-S, androstenedione, total testosterone) and their metabolites (total estradiol, estrone) were measured by radioimmunoassays. Information on five dimensions of aggression (total, physical, verbal, anger and hostility) was collected using Buss and Perry questionnaire. Results: Approximately 17% men inherited haplogroup I from their fathers. Carriers of haplogroup I showed lower scores of verbal aggression than men with other haplogroups (beta = -0.72, SE = 0.29, P = 0.012) and when further compared to carriers of most common R1a lineage and other haplogroups (beta = -1.03, SE = 0.34, P = 0.003). However, these associations did not survive a correction for multiple testing. Sex steroids did not show even nominal level of association with haplogroup I. Conclusion: Our data show no overall association between haplogroup I and sex-related phenotypes in young white men. These results also suggest that the previously identified association between haplogroup I and coronary artery disease is not likely mediated by unfavourable profile of sex steroids or heightened aggression early in life. (C) 2014 Elsevier Ireland Ltd. All rights reserved.]]> Wed 07 Apr 2021 13:54:51 AEST ]]> Urotensin-II system in genetic control of blood pressure and renal function http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:5740 Wed 07 Apr 2021 13:45:18 AEST ]]> Longer leukocyte telomeres are associated with ultra-endurance exercise independent of cardiovascular risk factors http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:5126 Wed 07 Apr 2021 13:44:45 AEST ]]> Male-specific region of the y chromosome and cardiovascular risk phylogenetic analysis and gene expression studies http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:5099 Wed 07 Apr 2021 13:44:43 AEST ]]> Inheritance of coronary artery disease in men : An analysis of the role of the y chromosome http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:4526 Wed 07 Apr 2021 13:43:59 AEST ]]> Pathway analysis shows association between FGFBP1 and hypertension http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:4075 Wed 07 Apr 2021 13:43:24 AEST ]]> Genetic architecture of ambulatory blood pressure in the general population insights from cardiovascular gene-centric array http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:3910 2000 cardiovascular candidate loci. We found a strong association between rs13306560 polymorphism in the promoter region of MTHFR and CLCN6 and mean 24-hour diastolic blood pressure; each minor allele copy of rs13306560 was associated with 2.6 mm Hg lower mean 24-hour diastolic blood pressure (P=1.2 x 10(-8)). rs13306560 was also associated with clinic diastolic blood pressure in a combined analysis of 8129 subjects from the Genetic Regulation of Arterial Pressure of Humans in the Community Study, the CoLaus Study, and the Silesian Cardiovascular Study (P=5.4 x 10(-6)). Additional analysis of associations between variants in gene ontology-defined pathways and mean 24-hour blood pressure in the Genetic Regulation of Arterial Pressure of Humans in the Community Study showed that cell survival control signaling cascades could play a role in blood pressure regulation. There was also a significant overrepresentation of rare variants (minor allele frequency: <0.05) among polymorphisms showing at least nominal association with mean 24-hour blood pressure indicating that a considerable proportion of its heritability may be explained by uncommon alleles. Through a large-scale gene-centric analysis of ambulatory blood pressure, we identified an association of a novel variant at the MTHFR/CLNC6 locus with diastolic blood pressure and provided new insights into the genetic architecture of blood pressure.]]> Wed 07 Apr 2021 13:34:57 AEST ]]> Human Y Chromosome Exerts Pleiotropic Effects on Susceptibility to Atherosclerosis http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:14223 Thu 19 May 2022 12:38:25 AEST ]]> Molecular insights into genome-wide association studies of chronic kidney disease-defining traits http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:13555 100 loci of chronic kidney disease-defining traits (CKD-dt). Molecular mechanisms underlying these associations remain elusive. Using 280 kidney transcriptomes and 9958 gene expression profiles from 44 non-renal tissues we uncover gene expression partners (eGenes) for 88.9% of CKD-dt GWAS loci. Through epigenomic chromatin segmentation analysis and variant effect prediction we annotate functional consequences to 74% of these loci. Our colocalisation analysis and Mendelian randomisation in >130,000 subjects demonstrate causal effects of three eGenes (NAT8B, CASP9 and MUC1) on estimated glomerular filtration rate. We identify a common alternative splice variant in MUC1 (a gene responsible for rare Mendelian form of kidney disease) and observe increased renal expression of a specific MUC1 mRNA isoform as a plausible molecular mechanism of the GWAS association signal. These data highlight the variants and genes underpinning the associations uncovered in GWAS of CKD-dt.]]> Thu 19 May 2022 11:08:51 AEST ]]>