Infrared Behaviour of Propagators and Vertices

We elucidate constraints imposed by confinement and dynamical chiral symmetry breaking on the infrared behaviour of the dressed-quark and -gluon propagators, and dressed-quark-gluon vertex. In covariant gauges the dressing of the gluon propagator is completely specified by P(k^2):= 1/[1+Pi(k^2)], where Pi(k^2) is the vacuum polarisation. In the absence of particle-like singularities in the dressed-quark-gluon vertex, extant proposals for the dressed-gluon propagator that manifest P(k^2=0)=0 and Max[P(k^2)]~10 neither confine quarks nor break chiral symmetry dynamically. This class includes all existing estimates of P(k^2) via numerical simulations.Comment: 10 pages, 2 figure

On Renormalized Strong-Coupling Quenched QED in Four Dimensions

We study renormalized quenched strong-coupling QED in four dimensions in arbitrary covariant gauge. Above the critical coupling leading to dynamical chiral symmetry breaking, we show that there is no finite chiral limit. This behaviour is found to be independent of the detailed choice of photon-fermion proper vertex in the Dyson-Schwinger equation formalism, provided that the vertex is consistent with the Ward-Takahashi identity and multiplicative renormalizability. We show that the finite solutions previously reported lie in an unphysical regime of the theory with multiple solutions and ultraviolet oscillations in the mass functions. This study supports the assertion that in four dimensions strong coupling QED does not have a continuum limit in the conventional sense.Comment: REVTEX 3.0, 15 pages,including 4 eps files comprising 3 figures. Submitted to Phys. Rev.

Chiral Symmetry Breaking in Quenched Massive Strong-Coupling QED4_4

We present results from a study of subtractive renormalization of the fermion propagator Dyson-Schwinger equation (DSE) in massive strong-coupling quenched QED$_4$. Results are compared for three different fermion-photon proper vertex {\it Ans\"{a}tze\/}: bare $\gamma^\mu$, minimal Ball-Chiu, and Curtis-Pennington. The procedure is straightforward to implement and numerically stable. This is the first study in which this technique is used and it should prove useful in future DSE studies, whenever renormalization is required in numerical work.Comment: REVTEX 3.0, 15 pages plus 7 uuencoded PostScript figure

Dynamical chiral symmetry breaking and confinement with an infrared-vanishing gluon propagator?

We study a model Dyson-Schwinger equation for the quark propagator closed using an {\it Ansatz} for the gluon propagator of the form \mbox{$D(q) \sim q^2/[(q^2)^2 + b^4]$} and two {\it Ans\"{a}tze} for the quark-gluon vertex: the minimal Ball-Chiu and the modified form suggested by Curtis and Pennington. Using the quark condensate as an order parameter, we find that there is a critical value of $b=b_c$ such that the model does not support dynamical chiral symmetry breaking for $b>b_c$. We discuss and apply a confinement test which suggests that, for all values of $b$, the quark propagator in the model {\bf is not} confining. Together these results suggest that this Ansatz for the gluon propagator is inadequate as a model since it does not yield the expected behaviour of QCD.Comment: 21 Pages including 4 PostScript figures uuencoded at the end of the file. Replacement: slight changes of wording and emphasis. ADP-93-215/T133, ANL-PHY-7599-TH-93, FSU-SCRI-93-108, REVTEX 3.

Renormalization and Chiral Symmetry Breaking in Quenched QED in Arbitrary Covariant Gauge

We extend a previous Landau-gauge study of subtractive renormalization of the fermion propagator Dyson-Schwinger equation (DSE) in strong-coupling, quenched QED_4 to arbitrary covariant gauges. We use the fermion-photon proper vertex proposed by Curtis and Pennington with an additional correction term included to compensate for the small gauge-dependence induced by the ultraviolet regulator. We discuss the chiral limit and the onset of dynamical chiral symmetry breaking in the presence of nonperturbative renormalization. We extract the critical coupling in several different gauges and find evidence of a small residual gauge-dependence in this quantity.Comment: REVTEX 3.0, 27 pages including 14 Extended Postscript files comprising 9 figures. Replacement: discussion of chiral limit corrected, and some minor typographical errors fixed. To appear in Phys. Rev.

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

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

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

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