An operator expansion for the elastic limit

A leading twist expansion in terms of bi-local operators is proposed for the structure functions of deeply inelastic scattering near the elastic limit $x \to 1$, which is also applicable to a range of other processes. Operators of increasing dimensions contribute to logarithmically enhanced terms which are supressed by corresponding powers of $1-x$. For the longitudinal structure function, in moment ($N$) space, all the logarithmic contributions of order $\ln^k N/N$ are shown to be resummable in terms of the anomalous dimension of the leading operator in the expansion.Comment: 9 pages, 1 figure, uses REVTEX 3.1 and axodra

Wide-angle elastic scattering and color randomization

Baryon-baryon elastic scattering is considered in the independent scattering (Landshoff) mechanism. It is suggested that for scattering at moderate energies, direct and interchange quark channels contribute with equal color coefficients because the quark color is randomized by soft gluon exchange during the hadronization stage. With this assumption, it is shown that the ratio of cross sections $R_{\overline{p} p/ p p}$ at CM angle $\theta = 90^0$ decreases from a high energy value of R_{\pbar p / pp} \approx 1/2.7, down to R_{\pbar p / pp} \approx 1/28, compatible with experimental data at moderate energies. This sizable fall in the ratio seems to be characteristic of the Landshoff mechanism, in which changes at the quark level have a strong effect precisely because the hadronic process occurs via multiple quark scatterings. The effect of color randomization on the angular distribution of proton-proton elastic scattering and the cross section ratio $R_{np/pp}$ is also discussed.Comment: 18 pages, latex2e, 4 uuencoded figures, include

Color Exchange in Near-forward Hard Elastic Ecattering

We study the large-$t$ small angle behavior of quark-quark elastic scattering. We employ a factorization procedure previously developed for fixed angle scattering, which depends on the color structure of the factorized hard subprocess. We find an evolution in $t$ that (in leading logarithmic approximation) becomes diagonal in a singlet-octet basis in the $t$-channel as $s\rightarrow \infty$. Octet exhange in the hard scattering is associated with the familiar `reggeized', $s^{\alpha_g(t)}$ behavior, which arises from $s$-dependence in Sudakov suppression. In contrast, Sudakov suppression for $t$-channel singlet exchange in the hard scattering is $s$-independent. In general, these contributions are mixed by soft corrections, which, however, cancel in many experimental amplitudes and cross sections.Comment: 24 pages, 4 figures (available upon request), LaTeX styl

Proton-Proton Near-Forward Hard Elastic Scattering

We calculate the leading twist contribution to near-forward proton-proton (and proton-antiproton) elastic scattering with large momentum transfer, in the multiple scattering (Landshoff) mechanism. The amplitude in the near-forward region is dominated by singlet exchange for all three valence quark-quark scatterings. We assume the existence of a hard singlet quark-quark amplitude, which we estimate to be ${\cal O}(\alpha_s^2/t)$. For a three-quark state whose transverse size is less than $1/\Lambda_{\rm QCD}$, Sudakov resummation accounts for both approximate \d \sigma^{pp}/ \d t \sim t^{-8} at moderate $t$, and \d \sigma^{pp}/ \d t \sim t^{-10} at larger $t$. The transition from approximate $t^{-8}$ to $t^{-10}$ behavior is strongly correlated with the transverse size of the valence three-quark state in the proton.Comment: 34 pages, LaTe

The Human Connectome Project's neuroimaging approach

Noninvasive human neuroimaging has yielded many discoveries about the brain. Numerous methodological advances have also occurred, though inertia has slowed their adoption. This paper presents an integrated approach to data acquisition, analysis and sharing that builds upon recent advances, particularly from the Human Connectome Project (HCP). The 'HCP-style' paradigm has seven core tenets: (i) collect multimodal imaging data from many subjects; (ii) acquire data at high spatial and temporal resolution; (iii) preprocess data to minimize distortions, blurring and temporal artifacts; (iv) represent data using the natural geometry of cortical and subcortical structures; (v) accurately align corresponding brain areas across subjects and studies; (vi) analyze data using neurobiologically accurate brain parcellations; and (vii) share published data via user-friendly databases. We illustrate the HCP-style paradigm using existing HCP data sets and provide guidance for future research. Widespread adoption of this paradigm should accelerate progress in understanding the brain in health and disease

Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies

Performance of the CMS muon trigger system in proton-proton collisions at √s = 13 TeV

The muon trigger system of the CMS experiment uses a combination of hardware and software to identify events containing a muon. During Run 2 (covering 2015-2018) the LHC achieved instantaneous luminosities as high as 2 × 10 cm s while delivering proton-proton collisions at √s = 13 TeV. The challenge for the trigger system of the CMS experiment is to reduce the registered event rate from about 40 MHz to about 1 kHz. Significant improvements important for the success of the CMS physics program have been made to the muon trigger system via improved muon reconstruction and identification algorithms since the end of Run 1 and throughout the Run 2 data-taking period. The new algorithms maintain the acceptance of the muon triggers at the same or even lower rate throughout the data-taking period despite the increasing number of additional proton-proton interactions in each LHC bunch crossing. In this paper, the algorithms used in 2015 and 2016 and their improvements throughout 2017 and 2018 are described. Measurements of the CMS muon trigger performance for this data-taking period are presented, including efficiencies, transverse momentum resolution, trigger rates, and the purity of the selected muon sample. This paper focuses on the single- and double-muon triggers with the lowest sustainable transverse momentum thresholds used by CMS. The efficiency is measured in a transverse momentum range from 8 to several hundred GeV

Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Abstract: Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies