268 research outputs found

    Measurement of the Proton and Deuteron Spin Structure Functions g2 and Asymmetry A2

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    We have measured the spin structure functions g2p and g2d and the virtual photon asymmetries A2p and A2d over the kinematic range 0.02 < x < 0.8 and 1.0 < Q^2 < 30(GeV/c)^2 by scattering 38.8 GeV longitudinally polarized electrons from transversely polarized NH3 and 6LiD targets.The absolute value of A2 is significantly smaller than the sqrt{R} positivity limit over the measured range, while g2 is consistent with the twist-2 Wandzura-Wilczek calculation. We obtain results for the twist-3 reduced matrix elements d2p, d2d and d2n. The Burkhardt-Cottingham sum rule integral - int(g2(x)dx) is reported for the range 0.02 < x < 0.8.Comment: 12 pages, 4 figures, 1 tabl

    Precision Measurement of the Proton and Deuteron Spin Structure Functions g2 and Asymmetries A2

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    We have measured the spin structure functions g2p and g2d and the virtual photon asymmetries A2p and A2d over the kinematic range 0.02 < x < 0.8 and 0.7 < Q^2 < 20 GeV^2 by scattering 29.1 and 32.3 GeV longitudinally polarized electrons from transversely polarized NH3 and 6LiD targets. Our measured g2 approximately follows the twist-2 Wandzura-Wilczek calculation. The twist-3 reduced matrix elements d2p and d2n are less than two standard deviations from zero. The data are inconsistent with the Burkhardt-Cottingham sum rule if there is no pathological behavior as x->0. The Efremov-Leader-Teryaev integral is consistent with zero within our measured kinematic range. The absolute value of A2 is significantly smaller than the sqrt[R(1+A1)/2] limit.Comment: 12 pages, 4 figures, 2 table

    Number of Affected Relatives, Age, Smoking, and Hypertension Prediction Score for Intracranial Aneurysms in Persons with a Family History for Subarachnoid Hemorrhage

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    Background: Persons with a positive family history of aneurysmal subarachnoid hemorrhage are at increased risk of aneurysmal subarachnoid hemorrhage. Preventive screening for intracranial aneurysms (IAs) in these persons is cost-effective but not very efficient. We aimed to develop and externally validate a model for predicting the probability of an IA at first screening in persons with a positive family history of aneurysmal subarachnoid hemorrhage. Methods: For model development, we studied results from initial screening for IA in 660 prospectively collected persons with ≥2 affected first-degree relatives screened at the University Medical Center Utrecht. For validation, we studied results from 258 prospectively collected persons screened in the University Hospital of Nantes. We assessed potential predictors of IA presence in multivariable logistic regression analysis. Predictive performance was assessed with the C statistic and a calibration plot and corrected for overfitting. Results: IA were present in 79 (12%) persons in the development cohort. Predictors were number of affected relatives, age, smoking, and hypertension (NASH). The NASH score had a C statistic of 0.68 (95% CI, 0.62-0.74) and showed good calibration in the development data. Predicted probabilities of an IA at first screening varied from 5% in persons aged 20 to 30 years with two affected relatives, without hypertension who never smoked, up to 36% in persons aged 60 to 70 years with ≥3 affected relatives, who have hypertension and smoke(d). In the external validation data IA were present in 67 (26%) persons, the model had a C statistic of 0.64 (95% CI, 0.57-0.71) and slightly underestimated IAs risk. Conclusions: For persons with ≥2 affected first-degree relatives, the NASH score improves current predictions and provides risk estimates for an IA at first screening between 5% and 36% based on 4 easily retrievable predictors. With the information such persons can now make a better informed decision about whether or not to undergo preventive screening

    Measurements of the Q2Q^2-Dependence of the Proton and Neutron Spin Structure Functions g1p and g1n

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    The structure functions g1p and g1n have been measured over the range 0.014 < x < 0.9 and 1 < Q2 < 40 GeV2 using deep-inelastic scattering of 48 GeV longitudinally polarized electrons from polarized protons and deuterons. We find that the Q2 dependence of g1p (g1n) at fixed x is very similar to that of the spin-averaged structure function F1p (F1n). From a NLO QCD fit to all available data we find Γ1pΓ1n=0.176±0.003±0.007\Gamma_1^p - \Gamma_1^n =0.176 \pm 0.003 \pm 0.007 at Q2=5 GeV2, in agreement with the Bjorken sum rule prediction of 0.182 \pm 0.005.Comment: 17 pages, 3 figures. Submitted to Physics Letters

    A historical perspective on the discovery of statins

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    Cholesterol is essential for the functioning of all human organs, but it is nevertheless the cause of coronary heart disease. Over the course of nearly a century of investigation, scientists have developed several lines of evidence that establish the causal connection between blood cholesterol, atherosclerosis, and coronary heart disease. Building on that knowledge, scientists and the pharmaceutical industry have successfully developed a remarkably effective class of drugs—the statins—that lower cholesterol levels in blood and reduce the frequency of heart attacks

    Precision measurement of the deuteron spin structure function g1dg^{d}_{1}

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    We report on a high-statistics measurement of the deuteron spin structure function g[sup d][sub 1] at a beam energy of 29 GeV in the kinematic range 0.029 < x < 0.8 and 1 < Q2 < 10 (GeV/c)2. The integral Gamma [sup d][sub 1] = (integral)[sup 1][sub 0]g[sup d][sub 1]dx evaluated at fixed Q2 = 3 (GeV/c)2 gives 0.042 ± 0.003(stat) ± 0.004(syst). Combining this result with our earlier measurement of g[sup p][sub 1], we find Gamma [sup p][sub 1]- Gamma [sup n][sub 1] = 0.163 ± 0.010(stat) ± 0.016(syst), which agrees with the prediction of the Bjorken sum rule with O( alpha [sup 3][sub s]) corrections, Gamma [sup p][sub 1]- Gamma [sup n][sub 1] = 0.171 ± 0.008. We find the quark contribution to the proton helicity to be Delta q = 0.30 ± 0.06

    Measurements of R=sigma_L/sigma_T for 0.03<x<0.1 and Fit to World Data

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    Measurements were made at SLAC of the cross section for scattering 29 GeV electrons from carbon at a laboratory angle of 4.5 degrees, corresponding to 0.03<x<0.1 and 1.3<Q^2<2.7 GeV^2. Values of R=sigma_L/sigma_T were extracted in this kinematic range by comparing these data to cross sections measured at a higher beam energy by the NMC collaboration. The results are in reasonable agreement with pQCD calculations and with extrapolations of the R1990 parameterization of previous data. A new fit is made including these data and other recent results.Comment: 8 pages, 4 figures, late

    Measurements of the Q2Q^2 dependence of the proton and neutron spin structure functions g1pg^p_1 and g1ng^n_1

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    he structure functions g1p and g1n have been measured over the range 0.014 < x < 0.9 and 1 < Q2 < 40 GeV2 using deep-inelastic scattering of 48 GeV longitudinally polarized electrons from polarized protons and deuterons. We find that the Q2 dependence of g1p (g1n) at fixed x is very similar to that of the spin-averaged structure function F1p (F1n). From a NLO QCD fit to all available data we find Γ1pΓ1n=0.176±0.003±0.007\Gamma_1^p - \Gamma_1^n =0.176 \pm 0.003 \pm 0.007 at Q2=5 GeV2, in agreement with the Bjorken sum rule prediction of 0.182 \pm 0.005

    Identification of a novel proinsulin-associated SNP and demonstration that proinsulin is unlikely to be a causal factor in subclinical vascular remodelling using Mendelian randomisation

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    Background and aims Increased proinsulin relative to insulin levels have been associated with subclinical atherosclerosis (measured by carotid intima-media thickness (cIMT)) and are predictive of future cardiovascular disease (CVD), independently of established risk factors. The mechanisms linking proinsulin to atherosclerosis and CVD are unclear. A genome-wide meta-analysis has identified nine loci associated with circulating proinsulin levels. Using proinsulin-associated SNPs, we set out to use a Mendelian randomisation approach to test the hypothesis that proinsulin plays a causal role in subclinical vascular remodelling. Methods We studied the high CVD-risk IMPROVE cohort (n = 3345), which has detailed biochemical phenotyping and repeated, state-of-the-art, high-resolution carotid ultrasound examinations. Genotyping was performed using Illumina Cardio-Metabo and Immuno arrays, which include reported proinsulin-associated loci. Participants with type 2 diabetes (n = 904) were omitted from the analysis. Linear regression was used to identify proinsulin-associated genetic variants. Results We identified a proinsulin locus on chromosome 15 (rs8029765) and replicated it in data from 20,003 additional individuals. An 11-SNP score, including the previously identified and the chromosome 15 proinsulin-associated loci, was significantly and negatively associated with baseline IMTmean and IMTmax (the primary cIMT phenotypes) but not with progression measures. However, MR-Eggers refuted any significant effect of the proinsulin-associated 11-SNP score, and a non-pleiotropic SNP score of three variants (including rs8029765) demonstrated no effect on baseline or progression cIMT measures. Conclusions We identified a novel proinsulin-associated locus and demonstrated that whilst proinsulin levels are associated with cIMT measures, proinsulin per se is unlikely to have a causative effect on cIMT
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