http://researchonline.federation.edu.au/vital/access/manager/Index ${session.getAttribute("locale")} 5 http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:14048 Wed 07 Apr 2021 14:02:08 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:13808 Wed 07 Apr 2021 14:01:55 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:13698 Wed 07 Apr 2021 14:01:48 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:13493 75 y), sex, and ethnicity. Results: Each unit increase in BMI corresponded to a-3.99 bp (95% CI: -5.17, -2.81 bp) difference in TL in the total pooled sample; among young adults, each unit increase in BMI corresponded to a -7.67 bp (95% CI:-10.03,-5.31 bp) difference. Each unit increase in BMI corresponded to a -1.58 × 10-3 unit T/S ratio (0.16% decrease; 95% CI: -2.14 × 10-3, -1.01 × 10-3) difference in ageand sex-adjusted relative TL in the total pooled sample; among young adults, each unit increase in BMI corresponded to a -2.58 × 10-3 unit T/S ratio (0.26% decrease; 95% CI: -3.92 × 10-3, -1.25 × 10-3). The associations were predominantly for the white pooled population. No sex differences were observed. Conclusions: A higher BMI is associated with shorter telomeres, especially in younger individuals. The presently observed difference is not negligible. Meta-analyses of longitudinal studies evaluating change in body weight alongside change in TL arewarranted.]]> Wed 07 Apr 2021 14:01:37 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:13241 Wed 07 Apr 2021 14:01:24 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:11392 Wed 07 Apr 2021 13:56:42 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:10772 Wed 07 Apr 2021 13:56:08 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:10766 Wed 07 Apr 2021 13:56:07 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:10534 Wed 07 Apr 2021 13:55:52 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:10465 Wed 07 Apr 2021 13:55:50 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:10341 Wed 07 Apr 2021 13:55:41 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:10162 Wed 07 Apr 2021 13:55:29 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:9618 Wed 07 Apr 2021 13:54:52 AEST ]]> 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 ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:7659 Wed 07 Apr 2021 13:47:08 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:7167 Wed 07 Apr 2021 13:46:40 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:5740 Wed 07 Apr 2021 13:45:18 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:5401 Wed 07 Apr 2021 13:45:02 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:5378 Wed 07 Apr 2021 13:45:01 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:5261 Wed 07 Apr 2021 13:44:54 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:5126 Wed 07 Apr 2021 13:44:45 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:5099 Wed 07 Apr 2021 13:44:43 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:4583 Wed 07 Apr 2021 13:44:04 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:4560 Wed 07 Apr 2021 13:44:02 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:4526 Wed 07 Apr 2021 13:43:59 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:4523 Wed 07 Apr 2021 13:43:59 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:4524 Wed 07 Apr 2021 13:43:59 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:4256 Wed 07 Apr 2021 13:43:42 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:4075 Wed 07 Apr 2021 13:43:24 AEST ]]> 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 ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:3886 Wed 07 Apr 2021 13:34:55 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:3688 Wed 07 Apr 2021 13:34:42 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:2909 Wed 07 Apr 2021 13:33:56 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:2883 Wed 07 Apr 2021 13:33:54 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:2458 Wed 07 Apr 2021 13:33:32 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:2460 Wed 07 Apr 2021 13:33:32 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:2459 Wed 07 Apr 2021 13:33:32 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:2136 = 0.1) single nucleotide polymorphisms in LRP6 were genotyped in 703 individuals from 213 Polish pedigrees (Silesian Cardiovascular Study families). The family-based analysis revealed that the minor allele of rs10845493 clustered with elevated LDL-C in offspring more frequently than expected by chance (P=0.0053). The quantitative analysis restricted to subjects free of lipid-lowering treatment confirmed the association between rs10845493 and age-, sex-, and BMI-adjusted circulating levels of LDL-C in families as well as 2 additional populations - 218 unrelated subjects from Silesian Cardiovascular Study replication panel and 1138 individuals from Young Men Cardiovascular Association cohort (P=0.0268, P=0.0476, and P=0.0472, respectively). In the inverse variance weighted meta-analysis of the 3 populations each extra minor allele copy of rs10845493 was associated with 0.14 mmol/L increase in age-, sex-, and BMI-adjusted LDL-C (SE=0.05, P=0.0038). Conclusions-Common polymorphism in the gene underlying monogenic form of coronary artery disease impacts on risk of LDL-C elevation. (Arterioscler Thromb Vasc Biol. 2009;29:1316-1321.)]]> Wed 07 Apr 2021 13:33:12 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:2137 Wed 07 Apr 2021 13:33:12 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:2129 Wed 07 Apr 2021 13:33:11 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:2115 Wed 07 Apr 2021 13:33:10 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:1772 Wed 07 Apr 2021 13:32:50 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:891 Wed 07 Apr 2021 13:31:53 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:890 Wed 07 Apr 2021 13:31:52 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:17327 Wed 01 Mar 2023 15:16:28 AEDT ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:17325 Tue 28 Feb 2023 14:32:09 AEDT ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:14703 = 18 years) recruited through opportunistic sampling were screened at sites in 92 countries during May 2019. Ideally, 3 blood pressure readings were measured for each participant, and data on lifestyle factors and comorbidities were collected. Hypertension was defined as a systolic blood pressure >= 140 mm Hg, or a diastolic blood pressure >= 90 mm Hg (mean of the second and third readings) or taking antihypertensive medication. When necessary, multiple imputation was used to estimate participants' mean blood pressure. Mixed-effects models were used to evaluate associations between blood pressure and participant characteristics. Of 1 508 130 screenees 482 273 (32.0%) had never had a blood pressure measurement before and 513 337 (34.0%) had hypertension, of whom 58.7% were aware, and 54.7% were on antihypertensive medication. Of those on medication, 57.8% were controlled to <140/90 mm Hg, and 28.9% to <130/80 mm Hg. Of all those with hypertension, 31.7% were controlled to <140/90 mm Hg, and 350 825 (23.3%) participants had untreated or inadequately treated hypertension. Of those taking antihypertensive medication, half were taking only a single drug, and 25% reported using aspirin inappropriately. This survey is the largest ever synchronized and standardized contemporary compilation of global blood pressure data. This campaign is needed as a temporary substitute for systematic blood pressure screening in many countries worldwide.]]> Tue 19 Oct 2021 16:23:32 AEDT ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:13276 Tue 19 Oct 2021 11:50:57 AEDT ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:17626 Tue 09 May 2023 12:01:48 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:17466 1000 common and rare genetic variants associated with BP and/or hypertension. The kidney is not only an organ of key relevance to BP regulation and the development of hypertension, but it also acts as the tissue mediator of genetic predisposition to hypertension. The identity of kidney genes, pathways, and related mechanisms underlying the genetic associations with BP has started to emerge through integration of genomics with kidney transcriptomics, epigenomics, and other omics as well as through applications of causal inference, such as Mendelian randomization. Single-cell methods further enabled mapping of BP-associated kidney genes to cell types, and in conjunction with other omics, started to illuminate the biological mechanisms underpinning associations of BP-associated genetic variants and kidney genes. Polygenic risk scores derived from genome-wide association studies and refined on kidney omics hold the promise of enhanced diagnostic prediction, whereas kidney omics-informed drug discovery is likely to contribute new therapeutic opportunities for hypertension and hypertension-mediated kidney damage. © 2022 International Society of Nephrology]]> Thu 23 Mar 2023 11:55:08 AEDT ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:14223 Thu 19 May 2022 12:38:25 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:14617 Thu 19 May 2022 12:02:09 AEST ]]> 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 ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:13014 Thu 07 Oct 2021 16:13:10 AEDT ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:17150 Mon 30 Jan 2023 13:43:48 AEDT ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:18726 Mon 18 Dec 2023 13:14:14 AEDT ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:5174 Fri 30 Apr 2021 15:48:56 AEST ]]>