Multiplicative renormalizability of gluon and ghost propagators in QCD

We reformulate the coupled set of continuum equations for the renormalized gluon and ghost propagators in QCD, such that the multiplicative renormalizability of the solutions is manifest, independently of the specific form of full vertices and renormalization constants. In the Landau gauge, the equations are free of renormalization constants, and the renormalization point dependence enters only through the renormalized coupling and the renormalized propagator functions. The structure of the equations enables us to devise novel truncations with solutions that are multiplicatively renormalizable and agree with the leading order perturbative results. We show that, for infrared power law behaved propagators, the leading infrared behavior of the gluon equation is not solely determined by the ghost loop, as concluded in previous studies, but that the gluon loop, the three-gluon loop, the four-gluon loop, and even massless quarks also contribute to the infrared analysis. In our new Landau gauge truncation, the combination of gluon and ghost loop contributions seems to reject infrared power law solutions, but massless quark loops illustrate how additional contributions to the gluon vacuum polarization could reinstate these solutions. Moreover, a schematic study of the three-gluon and four-gluon loops shows that they too need to be considered in more detail before a definite conclusion about the existence of infrared power behaved gluon and ghost propagators can be reached.Comment: 13 pages, 1 figure, submitted to Phys. Rev.

Gauge Dependence of Mass and Condensate in Chirally Asymmetric Phase of Quenched QED3

We study three dimensional quenched Quantum Electrodynamics in the bare vertex approximation. We investigate the gauge dependence of the dynamically generated Euclidean mass of the fermion and the chiral condensate for a wide range of values of the covariant gauge parameter $\xi$. We find that (i) away from $\xi=0$, gauge dependence of the said quantities is considerably reduced without resorting to sophisticated vertex {\em ansatze}, (ii) wavefunction renormalization plays an important role in restoring gauge invariance and (iii) the Ward-Green-Takahashi identity seems to increase the gauge dependence when used in conjunction with some simplifying assumptions. In the Landau gauge, we also verify that our results are in agreement with those based upon dimensional regularization scheme within the numerical accuracy available.Comment: 14 pages, 11 figures, uses revte

Multiplicative renormalizability and quark propagator

The renormalized Dyson-Schwinger equation for the quark propagator is studied, in Landau gauge, in a novel truncation which preserves multiplicative renormalizability. The renormalization constants are formally eliminated from the integral equations, and the running coupling explicitly enters the kernels of the new equations. To construct a truncation which preserves multiplicative renormalizability, and reproduces the correct leading order perturbative behavior, non-trivial cancellations involving the full quark-gluon vertex are assumed in the quark self-energy loop. A model for the running coupling is introduced, with infrared fixed point in agreement with previous Dyson-Schwinger studies of the gauge sector, and with correct logarithmic tail. Dynamical chiral symmetry breaking is investigated, and the generated quark mass is of the order of the extension of the infrared plateau of the coupling, and about three times larger than in the Abelian approximation, which violates multiplicative renormalizability. The generated scale is of the right size for hadronic phenomenology, without requiring an infrared enhancement of the running coupling.Comment: 17 pages; minor corrections, comparison to lattice results added; accepted for publication in Phys. Rev.

Analytic properties of the Landau gauge gluon and quark propagators

We explore the analytic structure of the gluon and quark propagators of Landau gauge QCD from numerical solutions of the coupled system of renormalized Dyson--Schwinger equations and from fits to lattice data. We find sizable negative norm contributions in the transverse gluon propagator indicating the absence of the transverse gluon from the physical spectrum. A simple analytic structure for the gluon propagator is proposed. For the quark propagator we find evidence for a mass-like singularity on the real timelike momentum axis, with a mass of 350 to 500 MeV. Within the employed Green's functions approach we identify a crucial term in the quark-gluon vertex that leads to a positive definite Schwinger function for the quark propagator.Comment: 42 pages, 16 figures, revtex; version to be published in Phys Rev

Statistics and State-istics : exclusion categories in the population census (Belgium, 1846-1930)

Peer reviewe

Diving into the vertical dimension of elasmobranch movement ecology

Knowledge of the three-dimensional movement patterns of elasmobranchs is vital to understand their ecological roles and exposure to anthropogenic pressures. To date, comparative studies among species at global scales have mostly focused on horizontal movements. Our study addresses the knowledge gap of vertical movements by compiling the first global synthesis of vertical habitat use by elasmobranchs from data obtained by deployment of 989 biotelemetry tags on 38 elasmobranch species. Elasmobranchs displayed high intra- and interspecific variability in vertical movement patterns. Substantial vertical overlap was observed for many epipelagic elasmobranchs, indicating an increased likelihood to display spatial overlap, biologically interact, and share similar risk to anthropogenic threats that vary on a vertical gradient. We highlight the critical next steps toward incorporating vertical movement into global management and monitoring strategies for elasmobranchs, emphasizing the need to address geographic and taxonomic biases in deployments and to concurrently consider both horizontal and vertical movements

Analysis of shared heritability in common disorders of the brain

ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders

Detectable clonal mosaicism and its relationship to aging and cancer

In an analysis of 31,717 cancer cases and 26,136 cancer-free controls from 13 genome-wide association studies, we observed large chromosomal abnormalities in a subset of clones in DNA obtained from blood or buccal samples. We observed mosaic abnormalities, either aneuploidy or copy-neutral loss of heterozygosity, of >2 Mb in size in autosomes of 517 individuals (0.89%), with abnormal cell proportions of between 7% and 95%. In cancer-free individuals, frequency increased with age, from 0.23% under 50 years to 1.91% between 75 and 79 years (P = 4.8 × 10(-8)). Mosaic abnormalities were more frequent in individuals with solid tumors (0.97% versus 0.74% in cancer-free individuals; odds ratio (OR) = 1.25; P = 0.016), with stronger association with cases who had DNA collected before diagnosis or treatment (OR = 1.45; P = 0.0005). Detectable mosaicism was also more common in individuals for whom DNA was collected at least 1 year before diagnosis with leukemia compared to cancer-free individuals (OR = 35.4; P = 3.8 × 10(-11)). These findings underscore the time-dependent nature of somatic events in the etiology of cancer and potentially other late-onset diseases