Turbulence Measurements in Submerged Water Jets by Electromagnetic Induction Anemometry

This paper describes the measurement and data analysis of the turbulence in a two-dimensional water jet discharging from a thin slot into a large body of stationary water having the same width as the slot. Tap water without additives was used as the flow medium. The electromagnetic induction method (commonly known as magnetohydrodynamics, or the MHD method) was used to sense the fluctuation velocities in the diffusion zone of the jet. A DC magnet was placed outside the flow field with the magnetic flux density of 885 Gauss perpendicular to the plane of homogeneity of the two-dimensional flow field. A small probe in the flow field sensed voltage changes due to the turbulent velocities. The induced voltages picked up at the electrodes were fed into a high input 12 impedance (about 10 ohms) differential amplifier. The output from the amplifier was recorded on tape which was later read into a hybrid computer for analyzing the variances, autocorrelation and spectrum of the turbulence signal. Turbulent velocities induce fluctuating electric potentials everywhere in the flow field whenever a magnetic flux is present, and hence set up fluctuating currents between any two points of different potentials. These currents have an equalizing effect on the induced voltage, thus causing the differential fluctuating voltage sensed by the electrodes in a turbulent flow to be less than the true value. The voltage reduction effect was experimentally determined to be a constant value by comparing the measured variance of turbulence in a water jet by the MHD method with the variance in an air jet using hot-wire anemometry. The constant reduction factor should have no effect on the normalized autocorrelation and spectrum results of the water jet

Loci influencing blood pressure identified using a cardiovascular gene-centric array.

Blood pressure (BP) is a heritable determinant of risk for cardiovascular disease (CVD). To investigate genetic associations with systolic BP (SBP), diastolic BP (DBP), mean arterial pressure (MAP) and pulse pressure (PP), we genotyped ∼50 000 single-nucleotide polymorphisms (SNPs) that capture variation in ∼2100 candidate genes for cardiovascular phenotypes in 61 619 individuals of European ancestry from cohort studies in the USA and Europe. We identified novel associations between rs347591 and SBP (chromosome 3p25.3, in an intron of HRH1) and between rs2169137 and DBP (chromosome1q32.1 in an intron of MDM4) and between rs2014408 and SBP (chromosome 11p15 in an intron of SOX6), previously reported to be associated with MAP. We also confirmed 10 previously known loci associated with SBP, DBP, MAP or PP (ADRB1, ATP2B1, SH2B3/ATXN2, CSK, CYP17A1, FURIN, HFE, LSP1, MTHFR, SOX6) at array-wide significance (P < 2.4 × 10(-6)). We then replicated these associations in an independent set of 65 886 individuals of European ancestry. The findings from expression QTL (eQTL) analysis showed associations of SNPs in the MDM4 region with MDM4 expression. We did not find any evidence of association of the two novel SNPs in MDM4 and HRH1 with sequelae of high BP including coronary artery disease (CAD), left ventricular hypertrophy (LVH) or stroke. In summary, we identified two novel loci associated with BP and confirmed multiple previously reported associations. Our findings extend our understanding of genes involved in BP regulation, some of which may eventually provide new targets for therapeutic intervention

Gene-centric meta-analysis in 87,736 individuals of European ancestry identifies multiple blood-pressure-related loci.

Blood pressure (BP) is a heritable risk factor for cardiovascular disease. To investigate genetic associations with systolic BP (SBP), diastolic BP (DBP), mean arterial pressure (MAP), and pulse pressure (PP), we genotyped ~50,000 SNPs in up to 87,736 individuals of European ancestry and combined these in a meta-analysis. We replicated findings in an independent set of 68,368 individuals of European ancestry. Our analyses identified 11 previously undescribed associations in independent loci containing 31 genes including PDE1A, HLA-DQB1, CDK6, PRKAG2, VCL, H19, NUCB2, RELA, HOXC@ complex, FBN1, and NFAT5 at the Bonferroni-corrected array-wide significance threshold (p < 6 × 10(-7)) and confirmed 27 previously reported associations. Bioinformatic analysis of the 11 loci provided support for a putative role in hypertension of several genes, such as CDK6 and NUCB2. Analysis of potential pharmacological targets in databases of small molecules showed that ten of the genes are predicted to be a target for small molecules. In summary, we identified previously unknown loci associated with BP. Our findings extend our understanding of genes involved in BP regulation, which may provide new targets for therapeutic intervention or drug response stratification