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:13241 Wed 07 Apr 2021 14:01:24 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:9618 Wed 07 Apr 2021 13:54:52 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: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: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 ]]>